\r\n\tThe book also covers the more specialized areas of energy consumption, riding comfort, noise and vibration. \r\n\tEscalators and passengers conveyors should also be addressed, as these devices complement elevator system in moving passenger around the building.
\r\n
\r\n\tModern developments are hope to be covered within the relevant chapters, some of which are listed as follows: Modern electrical safety systems,Modern shaft and motor feedback devices, Modern electrical drive system, Two elevator cars in the same shaft, Multiple elevator car systems in the same shaft, Evacuation systems using elevators, Modern calculation and simulation tools and software packages, Ropeless elevator systems.
",isbn:null,printIsbn:"979-953-307-X-X",pdfIsbn:null,doi:null,price:0,priceEur:0,priceUsd:0,slug:null,numberOfPages:0,isOpenForSubmission:!1,hash:"8d5766ef86475867198610aeb050233c",bookSignature:"Dr. Lutfi Al-Sharif",publishedDate:null,coverURL:"https://cdn.intechopen.com/books/images_new/10040.jpg",keywords:"Elevator Traffic Engineering, Simulation, Elevator Mechanical Engineering, Safety Gear System, Drive Systems, Control Systems, Energy Consumption, Power, Riding Comfort, Noise and Vibration, Escalators, Passenger Conveyors",numberOfDownloads:null,numberOfWosCitations:0,numberOfCrossrefCitations:1,numberOfDimensionsCitations:1,numberOfTotalCitations:2,isAvailableForWebshopOrdering:!0,dateEndFirstStepPublish:"November 14th 2019",dateEndSecondStepPublish:"February 28th 2020",dateEndThirdStepPublish:"April 28th 2020",dateEndFourthStepPublish:"July 17th 2020",dateEndFifthStepPublish:"September 15th 2020",remainingDaysToSecondStep:"a year",secondStepPassed:!0,currentStepOfPublishingProcess:5,editedByType:null,kuFlag:!1,biosketch:null,coeditorOneBiosketch:null,coeditorTwoBiosketch:null,coeditorThreeBiosketch:null,coeditorFourBiosketch:null,coeditorFiveBiosketch:null,editors:[{id:"314726",title:"Dr.",name:"Lutfi",middleName:null,surname:"Al-Sharif",slug:"lutfi-al-sharif",fullName:"Lutfi Al-Sharif",profilePictureURL:"https://mts.intechopen.com/storage/users/314726/images/system/314726.jpg",biography:"Lutfi Al-Sharif is currently Professor of Building Transportation Systems at of the Department of Mechatronics Engineering, The University of Jordan. He received his Ph.D. in lift traffic analysis in 1992 from UMIST (Manchester, U.K.). He worked for 9 years for London Underground, London, United Kingdom in the area of lifts and escalators.\r\nIn 2002, he formed Al-Sharif VTC Ltd, a vertical transportation consultancy based in London, United Kingdom. He has over 30 papers published in peer reviewed journals the area of vertical transportation systems and is co-inventor of four patents and co-author of the 2nd edition of the Elevator Traffic Handbook.\r\nHe is also a visiting professor at the University of Northampton (UK), member of the scientific committee of the annual Symposium on Lift & Escalator Technologies and a member of the editorial board of the journal Transportation Systems in Buildings. \r\nHe is a passionate believer in making higher education simple and accessible for engineering students and has a You Tube channel on engineering that has around 50 000 subscribers and around 7 million views. He has also been working as a member of the METHODS Project that aims to improve teaching methods in higher education in Jordan and Palestine. He is also the author of the Mechatronics Engineering Module on Saylor.org.",institutionString:"University of Jordan",position:null,outsideEditionCount:0,totalCites:0,totalAuthoredChapters:"1",totalChapterViews:"0",totalEditedBooks:"0",institution:{name:"University of Jordan",institutionURL:null,country:{name:"Jordan"}}}],coeditorOne:null,coeditorTwo:null,coeditorThree:null,coeditorFour:null,coeditorFive:null,topics:[{id:"11",title:"Engineering",slug:"engineering"}],chapters:null,productType:{id:"1",title:"Edited Volume",chapterContentType:"chapter",authoredCaption:"Edited by"},personalPublishingAssistant:{id:"194667",firstName:"Marijana",lastName:"Francetic",middleName:null,title:"Ms.",imageUrl:"https://mts.intechopen.com/storage/users/194667/images/4752_n.jpg",email:"marijana@intechopen.com",biography:"As an Author Service Manager my responsibilities include monitoring and facilitating all publishing activities for authors and editors. From chapter submission and review, to approval and revision, copyediting and design, until final publication, I work closely with authors and editors to ensure a simple and easy publishing process. I maintain constant and effective communication with authors, editors and reviewers, which allows for a level of personal support that enables contributors to fully commit and concentrate on the chapters they are writing, editing, or reviewing. I assist authors in the preparation of their full chapter submissions and track important deadlines and ensure they are met. I help to coordinate internal processes such as linguistic review, and monitor the technical aspects of the process. As an ASM I am also involved in the acquisition of editors. Whether that be identifying an exceptional author and proposing an editorship collaboration, or contacting researchers who would like the opportunity to work with IntechOpen, I establish and help manage author and editor acquisition and contact."}},relatedBooks:[{type:"book",id:"1591",title:"Infrared Spectroscopy",subtitle:"Materials Science, Engineering and Technology",isOpenForSubmission:!1,hash:"99b4b7b71a8caeb693ed762b40b017f4",slug:"infrared-spectroscopy-materials-science-engineering-and-technology",bookSignature:"Theophile Theophanides",coverURL:"https://cdn.intechopen.com/books/images_new/1591.jpg",editedByType:"Edited by",editors:[{id:"37194",title:"Dr.",name:"Theophanides",surname:"Theophile",slug:"theophanides-theophile",fullName:"Theophanides Theophile"}],productType:{id:"1",chapterContentType:"chapter",authoredCaption:"Edited by"}},{type:"book",id:"3161",title:"Frontiers in Guided Wave Optics and Optoelectronics",subtitle:null,isOpenForSubmission:!1,hash:"deb44e9c99f82bbce1083abea743146c",slug:"frontiers-in-guided-wave-optics-and-optoelectronics",bookSignature:"Bishnu Pal",coverURL:"https://cdn.intechopen.com/books/images_new/3161.jpg",editedByType:"Edited by",editors:[{id:"4782",title:"Prof.",name:"Bishnu",surname:"Pal",slug:"bishnu-pal",fullName:"Bishnu Pal"}],productType:{id:"1",chapterContentType:"chapter",authoredCaption:"Edited by"}},{type:"book",id:"3092",title:"Anopheles mosquitoes",subtitle:"New insights into malaria vectors",isOpenForSubmission:!1,hash:"c9e622485316d5e296288bf24d2b0d64",slug:"anopheles-mosquitoes-new-insights-into-malaria-vectors",bookSignature:"Sylvie Manguin",coverURL:"https://cdn.intechopen.com/books/images_new/3092.jpg",editedByType:"Edited by",editors:[{id:"50017",title:"Prof.",name:"Sylvie",surname:"Manguin",slug:"sylvie-manguin",fullName:"Sylvie Manguin"}],productType:{id:"1",chapterContentType:"chapter",authoredCaption:"Edited by"}},{type:"book",id:"371",title:"Abiotic Stress in Plants",subtitle:"Mechanisms and Adaptations",isOpenForSubmission:!1,hash:"588466f487e307619849d72389178a74",slug:"abiotic-stress-in-plants-mechanisms-and-adaptations",bookSignature:"Arun Shanker and B. Venkateswarlu",coverURL:"https://cdn.intechopen.com/books/images_new/371.jpg",editedByType:"Edited by",editors:[{id:"58592",title:"Dr.",name:"Arun",surname:"Shanker",slug:"arun-shanker",fullName:"Arun Shanker"}],productType:{id:"1",chapterContentType:"chapter",authoredCaption:"Edited by"}},{type:"book",id:"72",title:"Ionic Liquids",subtitle:"Theory, Properties, New Approaches",isOpenForSubmission:!1,hash:"d94ffa3cfa10505e3b1d676d46fcd3f5",slug:"ionic-liquids-theory-properties-new-approaches",bookSignature:"Alexander Kokorin",coverURL:"https://cdn.intechopen.com/books/images_new/72.jpg",editedByType:"Edited by",editors:[{id:"19816",title:"Prof.",name:"Alexander",surname:"Kokorin",slug:"alexander-kokorin",fullName:"Alexander Kokorin"}],productType:{id:"1",chapterContentType:"chapter",authoredCaption:"Edited by"}},{type:"book",id:"314",title:"Regenerative Medicine and Tissue Engineering",subtitle:"Cells and Biomaterials",isOpenForSubmission:!1,hash:"bb67e80e480c86bb8315458012d65686",slug:"regenerative-medicine-and-tissue-engineering-cells-and-biomaterials",bookSignature:"Daniel Eberli",coverURL:"https://cdn.intechopen.com/books/images_new/314.jpg",editedByType:"Edited by",editors:[{id:"6495",title:"Dr.",name:"Daniel",surname:"Eberli",slug:"daniel-eberli",fullName:"Daniel Eberli"}],productType:{id:"1",chapterContentType:"chapter",authoredCaption:"Edited by"}},{type:"book",id:"57",title:"Physics and Applications of Graphene",subtitle:"Experiments",isOpenForSubmission:!1,hash:"0e6622a71cf4f02f45bfdd5691e1189a",slug:"physics-and-applications-of-graphene-experiments",bookSignature:"Sergey Mikhailov",coverURL:"https://cdn.intechopen.com/books/images_new/57.jpg",editedByType:"Edited by",editors:[{id:"16042",title:"Dr.",name:"Sergey",surname:"Mikhailov",slug:"sergey-mikhailov",fullName:"Sergey Mikhailov"}],productType:{id:"1",chapterContentType:"chapter",authoredCaption:"Edited by"}},{type:"book",id:"1373",title:"Ionic Liquids",subtitle:"Applications and Perspectives",isOpenForSubmission:!1,hash:"5e9ae5ae9167cde4b344e499a792c41c",slug:"ionic-liquids-applications-and-perspectives",bookSignature:"Alexander Kokorin",coverURL:"https://cdn.intechopen.com/books/images_new/1373.jpg",editedByType:"Edited by",editors:[{id:"19816",title:"Prof.",name:"Alexander",surname:"Kokorin",slug:"alexander-kokorin",fullName:"Alexander Kokorin"}],productType:{id:"1",chapterContentType:"chapter",authoredCaption:"Edited by"}},{type:"book",id:"2270",title:"Fourier Transform",subtitle:"Materials Analysis",isOpenForSubmission:!1,hash:"5e094b066da527193e878e160b4772af",slug:"fourier-transform-materials-analysis",bookSignature:"Salih Mohammed Salih",coverURL:"https://cdn.intechopen.com/books/images_new/2270.jpg",editedByType:"Edited by",editors:[{id:"111691",title:"Dr.Ing.",name:"Salih",surname:"Salih",slug:"salih-salih",fullName:"Salih Salih"}],productType:{id:"1",chapterContentType:"chapter",authoredCaption:"Edited by"}},{type:"book",id:"872",title:"Organic Pollutants Ten Years After the Stockholm Convention",subtitle:"Environmental and Analytical Update",isOpenForSubmission:!1,hash:"f01dc7077e1d23f3d8f5454985cafa0a",slug:"organic-pollutants-ten-years-after-the-stockholm-convention-environmental-and-analytical-update",bookSignature:"Tomasz Puzyn and Aleksandra Mostrag-Szlichtyng",coverURL:"https://cdn.intechopen.com/books/images_new/872.jpg",editedByType:"Edited by",editors:[{id:"84887",title:"Dr.",name:"Tomasz",surname:"Puzyn",slug:"tomasz-puzyn",fullName:"Tomasz Puzyn"}],productType:{id:"1",chapterContentType:"chapter",authoredCaption:"Edited by"}}]},chapter:{item:{type:"chapter",id:"39391",title:"Regenerative Heat Treatment of Low Alloy Cast Steel",doi:"10.5772/50505",slug:"regenerative-heat-treatment-of-low-alloy-cast-steel",body:'
1. Introduction
Cylinder and valve chamber castings of large power steam turbines are usually made of low alloy Cr - Mo - V and Cr - Mo cast steels. Forming of the microstructure and mechanical properties of cast steels takes place through heat treatment, thus far mostly consisting of normalizing and tempering. As a result of such a treatment the cast steels of diverse wall thickness reveal microstructures from ferritic – pearlitic to bainitic – ferritic with various ferrite, pearlite and bainite amount.
Operation of the cast steels under creep conditions contributes to the occurrence of deformations, fractures and changes in the microstructure, decreasing their functional properties. The resistance to crack expressed by impact energy falls drastically. The value of impact energy of test pieces taken from cast steels after long-term service was considerably below the required level of 27J, frequently reaching the value of 6 - 10J (Fig. 1).
Figure 1.
Impact energy of turbine cylinder cast steel in the post-operating condition
Along with the fall of impact energy there is also a growth of nil ductility transition (NDT) temperature, frequently rising above 50 ÷ 60 oC. Large decrease in crack resistance is usually accompanied by a slight decrease in the strength properties (Fig. 2).
Unfavourable changes in mechanical properties of the castings are related to the changes in microstructure which occur during long term service at elevated temperatures, first and foremost to:
the preferential precipitation of carbides on grain boundaries, as well as changes in morphology and dispersion of precipitates;
segregation of phosphorus and other trace elements to grain boundaries and near boundary areas; disintegration of pearlite or/and bainite areas.
Figure 2.
Changes in tensile strength (TS) and yield strength (YS) depending on the time of service
Lowering of impact energy as a result of long-term service depends largely on the as received microstructure of a cast steel. The impact energy decrease is the smallest in the case of tempered bainite microstructure or bainitic – ferritic microstructure, with ferrite amount not higher than 5% (Fig. 3). High impact energy of quenched and tempered cast steel, considerably higher than 100J, guarantees that during long-term service of steel castings with low phosphorus volume fraction (≤ 0.015% P), the impact energy will not fall below the minimum required value of 27J.
Similar tendency has been noticed in new low-alloy bainitic 7CrWVMoNb9 – 6 (P23) steel. Impact energy in the case of this cast steel, whose microstructure is of tempered bainite in the as-received condition, after around 10 years of operation at the temperature of 555 oC and pressure 4.2MPa, was on the level of 70 – 80 J/cm2.
Degradation of the microstructure of castings and the related gradual decreasing of mechanical properties, however, do not limit the possibility of their further operation, especially as in most of the examined castings there were no irreversible creep changes observed. One of the conditions for extending the time of safe operation for cast steels above the calculated service time is running the process of revitalization of the castings.
Figure 3.
Influence of phosphorus amount and microstructure on impact energy KV of the Cr – Mo – V cast steel after long-term operation at the temperature of 535 oC
The revitalization process consists in heat treatment of turbine cylinders in order to regenerate the structure to the extent which allows the improvement of plastic properties (increase in impact energy, decrease in the nil ductility transition temperature). Regenerative heat treatment of castings applied in industry so far consists in normalizing/full annealing from the austenitizing temperature with the following high-temperature tempering/under annealing. The ferritic – pearlitic or ferritic – bainitic structure, obtained as a result of the above-mentioned heat treatment, provides the required impact energy of KV > 27J, however, with the strength properties being comparable to those after operation.
Modern hardening plants applying aqueous solutions of polymers as a cooling agent make the cooling of massive castings possible at programmed rate which provides an optimum structure throughout the whole casting section.
Regenerative heat treatment at costs not exceeding 40% of a new casting’s price, allows obtaining functional properties (yield strength, impact energy, NDT temperature) comparable to the properties of new castings. Regenerated cylinder is fit for further operation at least for another 100 000 hours.
In order to achieve an improvement in mechanical properties of cast steels after long-term operation, the following changes in the degraded microstructure are necessary:
grain refinement – leads to an increase in crack resistance, decreases the NDT temperature and raises yield strength;
eliminating irreversible brittleness caused by phosphorus segregation to grain boundaries and interphase boundary: matrix/carbides;
removal of the needle shaped ferrite (Widmannstätten’s ferrite);
removal of pearlite precipitated on ferrite grain boundaries;
dissolving of carbides in austenite, especially the carbides precipitated on grain boundaries, in order to obtain the required strength properties in the regenerated microstructure (hardness and tensile strength).
The research aim: The aim of the performed research was to determine the influence of regenerative heat treatment on the microstructure and properties of Cr – Mo – V cast steel with its microstructure degraded by long-term service and mechanical properties being lower than the minimum ones expected in the new castings.
2. Material for research
The material for study was Cr – Mo – V low-alloy L21HMF cast steel (designation according to Polish Standards) with its chemical composition given in Table 1. Test pieces for investigation were taken from an inner cylinder of a steam turbine serviced for around 186 000 hours at the temperature of 540 oC and pressure of 13.5MPa.
\n\t\t
\n\t\t
\n\t\t
\n\t\t
\n\t\t
\n\t\t
\n\t\t
\n\t\t
\n\t\t
\n\t\t\t
\n\t\t\t\tC\n\t\t\t
\n\t\t\t
\n\t\t\t\tMn\n\t\t\t
\n\t\t\t
\n\t\t\t\tSi\n\t\t\t
\n\t\t\t
\n\t\t\t\tP\n\t\t\t
\n\t\t\t
\n\t\t\t\tS\n\t\t\t
\n\t\t\t
\n\t\t\t\tCr\n\t\t\t
\n\t\t\t
\n\t\t\t\tMo\n\t\t\t
\n\t\t\t
\n\t\t\t\tV\n\t\t\t
\n\t\t
\n\t\t
\n\t\t\t
0.19
\n\t\t\t
0.74
\n\t\t\t
0.30
\n\t\t\t
0.017
\n\t\t\t
0.014
\n\t\t\t
1.05
\n\t\t\t
0.56
\n\t\t\t
0.28
\n\t\t
\n\t
Table 1.
Chemical composition of the L21HMF cast steel, % mass.
2.1. Microstructure and properties of the examined cast steel after service
In the post-operating condition the L21HMF cast steel was characterized by a degraded ferritic-pearlitic microstructure (Fig. 4). The dominant phase in the microstructure after operation was quasi-polygonal ferrite. The size of ferrite grain in the cast steel was diverse and ranged from 88.4 to 31.2μm, which corresponds to the grain size grade: 4 ÷ 7, according to ASTM standard scale.
Figure 4.
The microstructure of L21HMF cast steel after service
Long-term service of Cr – Mo – V cast steel contributed to the changes in microstructure, including:
preferential carbide precipitation of M23C6 carbides on ferrite grain boundaries. In some areas the number of carbides precipitated on boundaries was so large that they formed the so-called “continuous grid” of precipitates;
the process of degradation of pearlite grains consisting in fragmentation, spheroidization and coagulation of pearlitic carbides. Performed identifications have revealed the occurrence of the M3C and M7C3 type of precipitations in those areas (Fig. 5);
Figure 5.
Morphology and type of carbides in pearlite grain
precipitation of compound carbide complexes called „H – carbides”. The compound complexes of precipitates are created by MC and M2C carbides, where the MC carbide is a “horizontal” precipitation, while M2C carbides are precipitations of “vertical” type (Fig. 6). This sort of compound precipitations is defined as „H – carbide”. During long-term operation the MC carbide is enriched in molybdenum as a result of diffusion. The growth of molybdenum concentration in the interphase areas of MC/matrix makes it possible for the “needle-shaped” precipitations of M2C (rich in molybdenum) to nucleate on the interphase boundary: MC carbide/ferrite. These processes run more intensely in the border areas of grains, which results in the occurrence of precipitation free zones. The appearance of such zones may be the cause of slow reduction of the strength properties, the yield strength in particular, during long-term operation. The occurrence of this type of complexes results in a decay of fine-dispersion MC carbides which may lead to the fall of creep resistance in the serviced materials. A similar phenomenon can be seen at present in the new high-chromium cast steels for power industry, where the Z phase is being formed and developed at the expense of fine dispersion precipitates of the MX type, which causes a drastic drop of creep resistance of these cast steels.
Figure 6.
Precipitation of „H - carbide” type in the cast steel
Mechanical properties of L21HMF cast steel after long-term service are shown in Table 2.
\n\t\t
\n\t\t
\n\t\t
\n\t\t
\n\t\t
\n\t\t
\n\t\t
\n\t\t
\n\t\t
\n\t\t\t
Material
\n\t\t\t
TSMPa
\n\t\t\t
YSMPa
\n\t\t\t
El. %
\n\t\t\t
KV J
\n\t\t\t
HV30
\n\t\t\t
DBTT \n\t\t\t\toC
\n\t\t\t
Microstructure
\n\t\t
\n\t\t
\n\t\t\t
L21HMF
\n\t\t\t
545
\n\t\t\t
305
\n\t\t\t
26
\n\t\t\t
10
\n\t\t\t
156
\n\t\t\t
65
\n\t\t\t
ferritic-pearlitic
\n\t\t
\n\t\t
\n\t\t\t
Requirements of PN *
\n\t\t\t
500 ÷ 670
\n\t
min. 320
\n\t
min. 20
\n\t
min. 27
\n\t
140 ÷ 197**\n
\n
___
\n
___
\n
\n
Table 2.
Mechanical properties and microstructure of the L21HMF cast steels after service
Tensile strength and elongation of the examined cast steel after service were higher than the minimum values required for new castings, while the value of yield strength was lower than the minimum required by 15MPa. Hardness of the investigated cast steel after operation amounted to 156HV30.
A significant feature of the material proving its strain capacity, apart from elongation determined in the static test of tension, is the value of impact energy. Knowledge of this factor gives the possibility of assuming the right temperature for the hydraulic pressure tests used in industrial practice, as well as the right conditions of start-ups and shut-downs of a boiler, adjusted to the material state after long-term service. After operation the examined cast steel was characterized by low impact energy amounting to 10J, and the cracking of samples occurred through the transcrystalline fissile mechanism (typical for brittle fractures) with little energy absorbed due to the limited plastic strain preceding the decohesion. Fissile cracking requires little energy supply which is necessary for crack propagation, hence the low impact energy of the cast steel after service (Fig. 7). Low impact energy of the examined materials is related to the nil ductility temperature (brittle temperature). The fracture appearance transition temperature determined for the examined cast steel amounted to 65 oC.
Figure 7.
Transcrystalline ductile fracture with areas of microductility and secondary cracks
2.2. Influence of austenitizing parameters on the size of prior austenite grain
Influence of austenitization parameters on the prior austenite grain size has been described in a quantitative way using chosen stereological and statistical parameters, such as: mean diameter and mean area of grain, and also the coefficient of variation of grain size ν was calculated. The ν coefficient is characterized by the inhomogeneity of grain sizes: the more heterogeneous grains in terms of size within the casting, the higher the values of variation coefficient. The tests were run for the austenitizing temperature range of - 910 ÷970 oC with the „measurement step” – 15 oC and times of holding at the austenitizing temperature: 3 and 5 hours.
The character of austenite grain distributions was determined using the λ - Kolmogorov test of goodness of fit with normal distribution for logarithmed values (Fig. 8). The assumed significance level was α = 0.01, with its limiting statistics value amounting to 1.63. Selected logarithm-normal layouts of mean diameters and mean surface areas of former austenite grains for austenitization option of 925 oC and holding time 3 hours, are shown in Fig. 8. Obtained results of the tests are presented in Table 3 and 4 and graphically shown in Fig. 9 ÷ 11.
\n\t
\n\t
\n\t
\n\t
\n\t
\n\t
\n\t
\n\t
\n\t
\n\t
\n\t\t
\n\t\t\tHeat treatment parameters, oC/h\n\t\t
\n\t\t
\n\t\t\tAmount n\n\t\t
\n\t\t
\n\t\t\tMin. diameter of grain, μm\n\t\t
\n\t\t
\n\t\t\tMax. diameter of grain, μm\n\t\t
\n\t\t
\n\t\t\tDiameter of grain,μm\n\t\t
\n\t\t
\n\t\t\tStandard deviation\n\t\t
\n\t\t
\n\t\t\tλemp\n\t\t\t\n\t\t
\n\t\t
\n\t\t\tλα=0.01\n\t\t
\n\t\t
\n\t\t\tλempλα=0.01\n
\n
\n
\n\t
910/3
\n\t
976
\n\t
2
\n\t
29
\n\t
11.34
\n\t
6.36
\n\t
1.54
\n\t
1.63
\n\t
0.945
\n
\n
\n\t
925/3
\n\t
969
\n\t
2
\n\t
30
\n\t
9.84
\n\t
5.34
\n\t
1.36
\n\t
1.63
\n\t
0.834
\n
\n
\n\t
940/3
\n\t
954
\n\t
2
\n\t
31
\n\t
10.16
\n\t
6.22
\n\t
1.56
\n\t
1.63
\n\t
0.957
\n
\n
\n\t
955/3
\n\t
964
\n\t
2
\n\t
38
\n\t
14.08
\n\t
9.34
\n\t
1.36
\n\t
1.63
\n\t
0.834
\n
\n
\n\t
970/3
\n\t
2024
\n\t
2
\n\t
297
\n\t
22.14
\n\t
17.73
\n\t
2.26
\n\t
1.63
\n\t
1.387
\n
\n
\n\t
910/5
\n\t
946
\n\t
2
\n\t
27
\n\t
9.36
\n\t
5.70
\n\t
1.35
\n\t
1.63
\n\t
0.828
\n
\n
\n\t
925/5
\n\t
915
\n\t
2
\n\t
28
\n\t
11.00
\n\t
7.01
\n\t
1.55
\n\t
1.63
\n\t
0.951
\n
\n
\n\t
940/5
\n\t
959
\n\t
2
\n\t
32
\n\t
9.05
\n\t
5.41
\n\t
1.33
\n\t
1.63
\n\t
0.816
\n
\n
\n\t
955/5
\n\t
937
\n\t
2
\n\t
39
\n\t
12.02
\n\t
8.37
\n\t
1.18
\n\t
1.63
\n\t
0.724
\n
\n
\n\t
970/5
\n\t
2034
\n\t
2
\n\t
324
\n\t
23.67
\n\t
18.31
\n\t
1.43
\n\t
1.63
\n\t
0.877
\n
\n
Table 3.
The results of measurements and calculations of the size of prior austenite grains for the cast steel
\n\t
\n\t
\n\t
\n\t
\n\t
\n\t
\n\t
\n\t
\n\t
\n\t
\n\t\t
\n\t\t\tHeat treatment parameters, oC/h\n\t\t
\n\t\t
\n\t\t\tAmount n\n\t\t
\n\t\t
\n\t\t\tMin. area of grain,μm2\n\t\t\t\n\t\t
\n\t\t
\n\t\t\tMax. area of grain,μm2\n\t\t\t\n\t\t
\n\t\t
\n\t\t\tMean area of grain,μm2\n\t\t\t\n\t\t
\n\t\t
\n\t\t\tStandard deviation\n\t\t
\n\t\t
\n\t\t\tλemp\n\t\t\t\n\t\t
\n\t\t
\n\t\t\tλα=0.01\n\t\t
\n\t\t
\n\t\t\tλempλα=0.01\n
\n
\n
\n\t
910/3
\n\t
976
\n\t
4
\n\t
695
\n\t
142.67
\n\t
204.58
\n\t
1.74
\n\t
1.63
\n\t
1.067
\n
\n
\n\t
925/3
\n\t
969
\n\t
3
\n\t
741
\n\t
104.27
\n\t
173.60
\n\t
1.27
\n\t
1.63
\n\t
0.779
\n
\n
\n\t
940/3
\n\t
954
\n\t
3
\n\t
810
\n\t
121.34
\n\t
172.77
\n\t
1.40
\n\t
1.63
\n\t
0.859
\n
\n
\n\t
955/3
\n\t
964
\n\t
3
\n\t
1302
\n\t
187.41
\n\t
379.31
\n\t
1.59
\n\t
1.63
\n\t
0.975
\n
\n
\n\t
970/3
\n\t
2024
\n\t
3
\n\t
95722
\n\t
812.62
\n\t
2138.56
\n\t
1.99
\n\t
1.63
\n\t
1.221
\n
\n
\n\t
910/5
\n\t
946
\n\t
3
\n\t
608
\n\t
101.07
\n\t
162.93
\n\t
1.07
\n\t
1.63
\n\t
0.656
\n
\n
\n\t
925/5
\n\t
915
\n\t
2
\n\t
741
\n\t
144.72
\n\t
248.95
\n\t
1.61
\n\t
1.63
\n\t
0.988
\n
\n
\n\t
940/5
\n\t
959
\n\t
3
\n\t
842
\n\t
94.03
\n\t
147.10
\n\t
1.00
\n\t
1.63
\n\t
0.613
\n
\n
\n\t
955/5
\n\t
937
\n\t
2
\n\t
1533
\n\t
391.66
\n\t
423.09
\n\t
0.98
\n\t
1.63
\n\t
0.601
\n
\n
\n\t
970/5
\n\t
2034
\n\t
3
\n\t
102305
\n\t
915.33
\n\t
2408.43
\n\t
1.53
\n\t
1.63
\n\t
0.939
\n
\n
Table 4.
The results of measurements and calculations of the size of prior austenite grains for the cast steel
Figure 8.
Logarithm – normal layout of grains for : a) mean diameter; b) mean surface area
Figure 9.
Influence of austenitization temperature on: a) mean grain diameter; b) mean surface area depending on the time of holding (3hrs – orange, 5hrs – black) of L21HMF cast steel
The mean diameters of grains and their mean areas change continuously and reveal log-normal layouts on the significance level of α = 0.01 (λemp./ λ0.01 < 1). The exceptions were the treatment variants as follows: austenitization temperature of 910 oC and time - 3h for the mean area (fulfilled for lower significance level of α = 0.001) and the temperature of 970 oC and time - 3h for both: mean diameter and mean area of prior austenite grain. Within the range of austenitization temperatures: 910 ÷ 940 oC for holding times: 3 and 5 hrs, the mean diameters and areas of prior austenite grain do not reveal any considerable differences. (Fig. 9). The values of the mean diameters and areas for this range of austenitization amounted to: 9.05 ÷ 11.34 μm and 94.03 ÷ 144.72 μm2, respectively. The above-mentioned measurements can be confirmed by the calculated values of ν coefficient, specifying heterogeneity in terms of grain sizes, which are the lowest for this range of austenitizing temperatures (Fig. 10), and by the distributions of frequency of cumulated grains (Fig. 11).
Figure 10.
Interrelation between the heterogeneity factor (ν) of former austenite grain size in the cast steel and the austenitizing parameters for: a) mean diameter; b) mean grain area
Figure 11.
Distributions of frequency of cumulated grains
At the temperature of 970 oC the grain growth was observed – mean diameter increased over two times, while the mean area about five times in comparison with the temperature range of 910 ÷ 940 oC.
2.3. Determining the influence of cooling rate on the microstructure and properties
In order to determine the influence of cooling rates, allowing proper selection of parameters for the regenerative heat treatment, the TTT curves were plotted for L21HMF cast steel. On the basis of results achieved by means of dilatometric tests, a graph was drawn up, as shown in Fig 12. It illustrates the influence of cooling rate in the temperature range of 800 ÷ 500 oC on the structure and hardness of the investigated cast steel.
Figure 12.
Influence of the cooling rate on structure and hardness of the cast steel
Analysis of the curves presented in Fig. 10 allows to state that in the case of L21HMF cast steel, whose chemical composition is given in Table 1, austenite cooled at 0.004 K/s ≤ v8-5 ≤ 0.017 K/s gets transformed into ferrite and pearlite. The rate of cooling for austenite: 0.023 < v8-5 ≤ 0.869 K/s makes it possible to obtain ferritic – pearlitic – bainitic structures. Whereas after cooling of the cast steel at the range of 0.869 K/s < v8-5 ≤ 14.630 K/s bainitic – ferritic structures were obtained, with an increasing bainite volume fraction as the cooling rate increased. Bainitic structure with around 6% volume fraction was received for the cooling rate of v8-5 ≥ 14.630 K/s.
2.4. Influence of heat treatment on the microstructure and properties of L21HMF cast steel
The L21HMF cast steel was subject to heat treatment consisting in three-hour austenitizing of test pieces at the temperature of 910 oC and the following cooling at the rate corresponding to the processes of: bainitic hardening, normalizing and full annealing. The test pieces, bainite-hardened and normalized, were then tempered in the temperature range of 690 ÷ 730 oC and 690 ÷ 720 oC, respectively. While the test pieces cooled slowly from the austenitizing temperature (fully annealed), were subject to (α + γ) annealing (under annealing) at the temperatures of 780 ÷ 860 oC. Examples of microstructure of the examined cast steel after heat treatment are illustrated in Fig. 13.
Figure 13.
Microstructure of cast steel after: a) service; b) bainitic hardening and tempering; b) normalizing and tempering; c) full annealing and tempering
Bainitic hardening made it possible to obtain bainitic – ferritic microstructure in Cr – Mo – V cast steel. The amount of ferrite in the microstructure did not exceed 6%. In the tempered microstructure there were numerous precipitations of carbides on the lath boundaries, as well as inside and on the boundaries of prior austenite grain. Matrix after heat treatment was characterized by high dislocation density, however, some sparse polygonized areas were observed as well - showing lower density of dislocations (Fig. 14). Presence of the polygonized areas in the cast steel after heat treatment can be caused by the difference in chemical composition of particular grains resulting from a dendritic micro segregation or from the lack of austenite homogeneity during heat treatment. Differences of chemical composition may cause local decrease in the temperature of recrystallization.
Figure 14.
Microstructure of the L21HMF cast steel after heat treatment (bainitic hardening and high-temperature tempering)
Normalizing and tempering allowed obtaining tempered bainitic – ferritic structure with around 20% of ferrite in the Cr – Mo – V cast steel.
The observed microstructures after bainitic hardening and normalizing, apart from ferrite amount in the structure, differed in bainite morphology as well. After bainitic hardening only the “needle-shaped” form of bainite was observed, and it was morphologically similar to martensite, which indicates lower bainite presence in the structure (it can also be proved by the characteristic arrangement of carbides illustrated in Fig. 14). After normalization, however, the Cr – Mo – V cast steel microstructure showed the “feathery” bainite form, which indicates the presence of upper bainite. Apart from the “feathery” bainite also some single areas of „needle-shaped” bainite could be seen.
The identifications of precipitates performed by means of the extraction carbon replicas revealed in the investigated cast steel after heat treatment (in the tempered bainitic and bainitic – ferritic structure) the occurrence of the following carbide types: MC, M3C, M7C3 and M23C6.
The study of mechanical properties at room temperature has shown that the structure of high-temperature tempered bainite provides the combination of high strength properties and impact energy. Tensile strength and yield strength after tempering exceeded the minimum requirements considerably, and similarly, the impact energy was several times higher than the required minimum of 27J for the new castings (Table 5, Fig. 15). Tempering of L21HMF cast steel with bainitic structure at the temperatures which are 10 and 20 oC higher than the maximum tempering temperature recommended by the standard, i.e. at 720 and 730 oC, caused an increase in impact energy by 8 and 35%, respectively, with the hardness decrease by 2 ÷ 5% in comparison with the tempering temperature of 710 oC (Fig. 15).
Therefore, it can be concluded that for the cast steels of bainitic microstructure it is possible to apply higher temperatures of tempering compared to the ones recommended by the standards, without concern that the strength properties can go down below the required minimum. Apart form obtaining high impact energy with the required strength properties maintained, it also allows to achieve the microstructure of higher thermodynamic stability, which can guarantee slower process of its degradation.
Figure 15.
Influence of the tempering temperature on hardness and impact energy of the L21HMF cast steel with bainitic structure
The cast steel of tempered mixed (bainitic – ferritic) microstructure was characterized by the strength properties on a similar level as the cast steels with bainitic microstructure. However, the crack resistance of those cast steels was almost two times as low compared to that of cast steels with bainitic microstructure (Table 6).
High impact energy of the cast steel with the microstructure of tempered bainite isa consequence of large total amount of grain boundaries (boundaries of bainite packets) and high ductility of the tempered microstructure of lower bainite. Whilst, lower impact energy of the cast steel with mixed bainitic – ferritic structure results from the presence of ferrite in the microstructure, which favours the fissile cracking, and from the presence of upper bainite, characterized by greater brittleness than lower bainite.
Full annealing allows to obtain ferritic – pearlitic microstructure for the examined cast steel grade (Fig. 13d), with pearlite located mostly on ferrite grain boundaries. In pearlite the processes of fragmentation and spheroidization of carbides could be observed. The ferritic – pearlitic microstructure obtained as a result of repeated cooling from the austenitizing temperature was morphologically similar to the microstructure after long-term service.
\n\t
\n\t
\n\t
\n\t
\n\t
\n\t
\n\t
\n\t
\n\t\t
Heat treatment parameters
\n\t\t
TSMPa
\n\t\t
YS MPa
\n\t\t
El. %
\n\t\t
KV J
\n\t\t
HV30
\n\t\t
Microstructure
\n\t
\n\t
\n\t\t
after service
\n\t\t
545
\n\t\t
305
\n\t\t
26
\n\t\t
10
\n\t\t
156
\n\t\t
ferritic-pearlitic
\n\t
\n\t
\n\t\t
bainitic hardening + 720 oC/4h
\n\t\t
728
\n\t\t
620
\n\t\t
18
\n\t\t
104
\n\t\t
228
\n\t\t
bainitic
\n\t
\n\t
\n\t\t
normalizing + 720 oC/4h
\n\t\t
721
\n\t\t
594
\n\t\t
17
\n\t\t
62
\n\t\t
220
\n\t\t
bainitic-20%ferritic
\n\t
\n\t
\n\t\t
full annealing + 720 oC/4h
\n\t\t
558
\n\t\t
336
\n\t\t
27
\n\t\t
26
\n\t\t
153
\n\t\t
ferritic-20%pearlitic
\n\t
\n\t
\n\t\t
full annealing + 800 oC/4h
\n\t\t
552
\n\t\t
316
\n\t\t
31
\n\t\t
42
\n\t\t
162
\n\t\t
ferritic-20%pearlitic
\n\t
\n\t
\n\t\t
full annealing + 820 oC/4h
\n\t\t
550
\n\t\t
324
\n\t\t
28
\n\t\t
42
\n\t\t
164
\n\t\t
ferritic-20%pearlitic
\n\t
\n\t
\n\t\t
*PN requirements
\n\t\t
500 \n\t\t\t 670
\n\t\t
min. 320
\n\t\t
min. 20
\n\t\t
min. 27
\n\t\t
140 **\n\t\t\t \n\t\t\t 197
\n\t\t
___
\n\t
\n
Table 5.
Microstructure and properties of the L21HMF cast steel after heat treatment
Figure 16.
Change in the values of hardness and impact energy of the cast steel depending on the temperature of (α + γ) annealing
For the L21HMF cast steel of ferritic – pearlitic microstructure it is required to apply (α + γ) annealing (under annealing) instead of tempering which did not always provide the required impact energy. Applying under annealing causes: dissolution of carbides precipitated on grain boundaries during slow cooling from the temperature of austenitization, decrease of phosphorus segregation on ferrite grain boundaries and further reduction of austenite grain size. This allows to obtain the required strength properties and impact energy KV on the level ~ 40J. The influence of (α + γ) annealing temperature on the value of impact energy and hardness is presented in Fig.16.
The performed heat treatment, apart from the changes in microstructure and properties of the examined cast steels, also caused a change in the mechanism of cracking (Fig. 17). In the cast steel of high-temperature tempered bainite structure, on the entire surface under the fracture, there was a transcrystalline ductile fracture initiated by fine-dispersion precipitates of carbides and sulfide inclusions (Fig. 17a). The characteristic feature of plastic cracking is its ability to absorb significant amounts of energy connected with plastic deformations preceding the decohesion. The cast steel of bainitic – ferritic structure was subject to decohesion through mixed mechanism. Directly under the notch, at a depth of about 1.0 ÷ 1.5 mm, cracking proceeded in plastic manner through transcrystalline ductile mechanism. Below the area of plastic strain, fissile cracking could be observed, running through a transcrystalline fissile mechanism with micro fields of ductile character.
The cast steel with regenerated ferritic – pearlitic structure, obtained as a result of slow cooling and under annealing, was cracking through a mechanism similar to decohesion of the cast steel after service, i.e. transcrystalline fissile mechanism with micro fields of ductile character (Fig. 17b).
Figure 17.
Cracking mechanism of cast steel: a) transcrystalline ductile for tempered bainitic microstructure; b) transcrystalline fissile for ferritic – pearlitic microstructure
3. Summary
The research performed on the L21HMF cast steel, taken from a steam turbine cylinder serviced for around 186 000 hours at the temperature of 540 oC, has revealed that long-term service contributed to: the processes of recovery and polygonization of ferrite grains, preferential precipitation of M23C6 carbides on grain boundaries and formation of „H – carbide” complexes near the boundary areas of ferrite grains. During long-term operation the strength properties were decreasing slowly – yet faster in the case of yield strength than tensile strength, and the impact energy decreased drastically below the required minimum level of 27J.
Changes in the microstructure and properties of the long-term serviced cast steel do not eliminate the possibilities of their further safe operation. Extending the safe operation time beyond the calculative time of 100 000 hours (with the target up to 200 ÷ 250 000 hours) is possible thanks to regenerative heat treatment.
Performed research has proved that applying bainitic hardening instead of normalizing/full annealing, thus far applied in the castings, allows to achieve the best combination of high strength properties and very high impact energy. Moreover, the bainitic microstructure makes it possible to apply high temperatures of tempering, amounting to 710 ÷ 730 oC. This allows increasing the stability of microstructure of long-term serviced cast steels without concern for reduction in the strength properties below the required minimum. High impact energy KV > 100J of the cast steel with high-tempered bainite structure guarantees that after long-term operation the impact energy will not drop below the minimum required level of 27J.
Applying normalizing for the castings allows to obtain bainitic – ferritic microstructure, which is characterized by similar strength properties as the cast steel with tempered bainitic microstructure, with the impact energy, however, being almost two times as low. What seems evident here, is the negative influence of ferrite in the microstructure on the impact strength.
The ferritic – pearlitic microstructure, obtained as a result of slow cooling of the castings from the austenitizing temperature (full annealing), allows to obtain the strength properties comparable to those after service and impact energy on the level of 40J. After the process of full annealing it is recommended to apply the (α + γ) annealing (under annealing) instead of the process of tempering, which makes it possible to obtain the required impact energy.
\n',keywords:null,chapterPDFUrl:"https://cdn.intechopen.com/pdfs/39391.pdf",chapterXML:"https://mts.intechopen.com/source/xml/39391.xml",downloadPdfUrl:"/chapter/pdf-download/39391",previewPdfUrl:"/chapter/pdf-preview/39391",totalDownloads:3484,totalViews:321,totalCrossrefCites:1,totalDimensionsCites:3,hasAltmetrics:0,dateSubmitted:"December 20th 2011",dateReviewed:"June 6th 2012",datePrePublished:null,datePublished:"September 26th 2012",dateFinished:"September 25th 2012",readingETA:"0",abstract:null,reviewType:"peer-reviewed",bibtexUrl:"/chapter/bibtex/39391",risUrl:"/chapter/ris/39391",book:{slug:"heat-treatment-conventional-and-novel-applications"},signatures:"Grzegorz Golański",authors:[{id:"148598",title:"Dr.",name:"Grzegorz",middleName:null,surname:"Golański",fullName:"Grzegorz Golański",slug:"grzegorz-golanski",email:"grisza@mim.pcz.czest.pl",position:null,institution:null}],sections:[{id:"sec_1",title:"1. Introduction",level:"1"},{id:"sec_2",title:"2. Material for research",level:"1"},{id:"sec_2_2",title:"2.1. Microstructure and properties of the examined cast steel after service ",level:"2"},{id:"sec_3_2",title:"2.2. Influence of austenitizing parameters on the size of prior austenite grain",level:"2"},{id:"sec_4_2",title:"2.3. Determining the influence of cooling rate on the microstructure and properties",level:"2"},{id:"sec_5_2",title:"2.4. Influence of heat treatment on the microstructure and properties of L21HMF cast steel",level:"2"},{id:"sec_7",title:"3. Summary",level:"1"}],chapterReferences:[{id:"B1",body:'ZielińskiA.DobrzańskiJ.KrztońH.Structuralchanges.inlow.alloycast.steel-Mo-VCr.afterlong.timecreep.serviceJ. A. M. M. E. 2.2007'},{id:"B2",body:'StachuraS.Changesof.structuremechanicalproperties.insteels.caststeels.utilisedin.increasedtemperatures.Energetyka.1999\n\t\t\t'},{id:"B3",body:'Balyts’kyiO. I.RipeiI. V.ProtsakhKh. A.Degradationof.thecast.elementsof.steamturbines.ofthermal.powerplants.madeof. .KhM. F. 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F.BowenP.Kineticsof.phosphorussegregation.itseffect.onlow.temperaturefracture.behaviourin.2.Cr-Mo.pressurevessel.steelMaterials.and its effect on low temperature fracture behaviour in 2.25Cr- 1Mo pressure vessel steel, Materials Sc. and Techn., 21, 1, 2005\n\t\t\t'},{id:"B9",body:'MolinieE.PiquesR.PineauA.Behaviourof. a. .Cr--0.Mo.steelV.after-termlong.exposure-ICharpy impact toughness and creep properties, Fatique Fract. Eng. Mater. Struct., 14, 5, 1991'},{id:"B10",body:'Stachura S., Golański G., Metallographic and mechanical properties of steel and cast steel after long term service at elevated temperatures, Report BZ- 202- 1/01 unpublished researched'},{id:"B11",body:'Golański G., Stachura S., Kupczyk J., Kucharska- Gajda B., Heat treatment of cast steel using normalization and intercritical annealing, Arch.Foundry Eng., 7, 2007'},{id:"B12",body:'Komai N., Masuyama F., Igarashi M., 10 - year experience with T23(2.25Cr- 1.6W) and T122 (12Cr- 0.4Mo- 2W) in a power boiler, Transations of the ASME, 127,2005'},{id:"B13",body:'TrzeszczyńskiJ.GrzesiczekE..BrunneW.Effectivenessof.solutionsextending.operationtime.oflong.operatedcast.steelelements.ofsteam.turbinessteampipelines.Energetyka.2006\n\t\t\t'},{id:"B14",body:'Rehmus- Forc A., Change of structure after revitalization cylinders of a steam turbine, Inżynieria Materiałowa,2006\n\t\t\t'},{id:"B15",body:'GolańskiG.Influencetempering.temperatureon.mechanicalproperties.ofcast.steelsArchives.ofFoundry.Eng..2008'},{id:"B16",body:'Dobosiewicz J., Reasons for regenerating steam turbine cylinders, Energetyka,1996\n\t\t\t'},{id:"B17",body:'Łukowski J., Modern installations for quenching with the application of aqueous polimer solutions, Przegląd Odlewnictwa, 51,2001'},{id:"B18",body:'Bakalarski A., Nowarski A., Sus J., Wyszyński K., Theoretical investigation and experimental application of aqueous polymer solution for quenching products of low-alloy cast steel, Przegląd Odlewnictwa, 51,2001'},{id:"B19",body:'GolańskiG.StachuraS.GajdaB.KupczykJ.Influenceof.thecooling.rateon.structuremechanicalproperties.ofL.castH. M. F.steelafter.regenerativeheat.treatmentArchives.ofFoundary. .2.2006'},{id:"B20",body:'ZielińskiA.DobrzańskiJ.GolańskiG.Estimationof.residuallife.ofL.castH. M. F.steelelements.after-termlong.serviceJ.Achievements in Materials and Manufacturing Eng.., 34, 2, 2009'},{id:"B21",body:'GolańskiG.Microstructuremechanicalproperties.ofG.CrMo. V..caststeel.afterregenerative.heattreatment. J.Pressure Vessel Techn., 132201020100645031\n\t\t\t'},{id:"B22",body:'Golański G., Stachura S., Kupczyk J., Kucharska- Gajda B., Optimisation of regenerative heat treatment of G21CrMoV46 cast steel, Archives Mater.Sc. Eng., 28, 6, 2007'},{id:"B23",body:'MurphyM. C.BranchG. D.Themicrostructure.creepcreep-ruptureproperties.of-Mo-VCr.steamturbine.castingsJ. I. S. I.1969\n\t\t\t'},{id:"B24",body:'SeniorB. A.criticalA.reviewof.precipitationbehavior.in.Cr-Mo-Vrotor.steelsMater.Sc. Eng. A, 1988\n\t\t\t'},{id:"B25",body:'WilliamsK. R.WilshireB.Microstructuralinstability.of0.Cr-0Mo-0.creep-resistantV.steelduring.serviceat.elevatedtemperatures.MaterSci. Eng., 1981'},{id:"B26",body:'DanielsenH. K.HaldJ.Behaviourof. Z.phasein. ..Cr.steelsEnergy. ..2006'},{id:"B27",body:'Golański G., Mechanical Properties of G17CrMoV510 Cast Steel after Regenerative Heat Treatment, Solid State Phenom.2009'},{id:"B28",body:'Ryś J., Stereology of materials, FOTOBIT Publ., Cracow, 1995\n\t\t\t'},{id:"B29",body:'Taylor J.P., Blondeau R., The respective roles of the packet size and the lath width on toughness, Metall.Trans., 7A, 1976'},{id:"B30",body:'H. Kotilainen, The micromechanisms of cleavage fracture and their relationship to fracture toughness in a bainitie Low Alloy Steel, VTT, Espoo, Finland, 1980'},{id:"B31",body:'Bhadeshia H. K. D. H., Bainite in steels, 2nd edition, The University Press Cambridge, Cambridge, UK, 2001'},{id:"B32",body:'-8P. N.-831H.Caststeels.forelevated.temperatureapplications.Grades.\n\t\t\t'}],footnotes:[],contributors:[{corresp:null,contributorFullName:"Grzegorz Golański",address:null,affiliation:'
'}],corrections:null},book:{id:"2448",title:"Heat Treatment",subtitle:"Conventional and Novel Applications",fullTitle:"Heat Treatment - Conventional and Novel Applications",slug:"heat-treatment-conventional-and-novel-applications",publishedDate:"September 26th 2012",bookSignature:"Frank Czerwinski",coverURL:"https://cdn.intechopen.com/books/images_new/2448.jpg",licenceType:"CC BY 3.0",editedByType:"Edited by",isbn:null,printIsbn:"978-953-51-0768-2",pdfIsbn:"978-953-51-6238-4",editors:[{id:"16295",title:"Dr.",name:"Frank",middleName:null,surname:"Czerwinski",slug:"frank-czerwinski",fullName:"Frank Czerwinski"}],productType:{id:"1",title:"Edited Volume",chapterContentType:"chapter",authoredCaption:"Edited by"},chapters:[{id:"39393",title:"Design of Cooling Units for Heat Treatment",slug:"design-of-cooling-units-for-heat-treatment",totalDownloads:2320,totalCrossrefCites:0,signatures:"Michal Pohanka and Petr Kotrbáček",authors:[{id:"155021",title:"Dr.",name:"Michal",middleName:null,surname:"Pohanka",fullName:"Michal Pohanka",slug:"michal-pohanka"},{id:"162747",title:"Dr.",name:"Petr",middleName:null,surname:"Kotrbacek",fullName:"Petr Kotrbacek",slug:"petr-kotrbacek"}]},{id:"39391",title:"Regenerative Heat Treatment of Low Alloy Cast Steel",slug:"regenerative-heat-treatment-of-low-alloy-cast-steel",totalDownloads:3484,totalCrossrefCites:1,signatures:"Grzegorz Golański",authors:[{id:"148598",title:"Dr.",name:"Grzegorz",middleName:null,surname:"Golański",fullName:"Grzegorz Golański",slug:"grzegorz-golanski"}]},{id:"39388",title:"Deformation Reduction of Bearing Rings by Modification of Heat Treating",slug:"deformation-reduction-of-bearing-rings-by-modification-of-heat-treating",totalDownloads:4152,totalCrossrefCites:1,signatures:"Anton Panda, Jozef Jurko and Iveta Pandova",authors:[{id:"100571",title:"Prof.",name:"Jozef",middleName:"Jurko",surname:"Jurko",fullName:"Jozef Jurko",slug:"jozef-jurko"},{id:"110448",title:"Prof.",name:"Anton",middleName:null,surname:"Panda",fullName:"Anton Panda",slug:"anton-panda"},{id:"147783",title:"Dr.",name:"Iveta",middleName:null,surname:"Panda",fullName:"Iveta Panda",slug:"iveta-panda"}]},{id:"39389",title:"A Review on the Heat Treatment of Al-Si-Cu/Mg Casting Alloys",slug:"a-review-on-the-heat-treatment-of-al-si-cu-mg-casting-alloys",totalDownloads:7630,totalCrossrefCites:27,signatures:"A.M.A. Mohamed and F.H. 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Kim",authors:[{id:"16057",title:"Dr.",name:"Shae K.",middleName:null,surname:"Kim",fullName:"Shae K. 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\n
1. Introduction
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The gestation in the mare begins with the fertilization of the ovum, then the implantation of the blastocyst in the uterus followed by the development of the placenta and fetus until delivery. Therefore, gestation is a dynamic and coordinated process involving systemic and local changes in the mare that support the supply of nutrients and oxygen to the fetus for growth and development in the uterus [1]. In part, these changes occur through the secretion of hormones in the placenta, which in turn interact with each other and exert extensive effects on maternal tissues during gestation [2]. These endocrine changes in maternal physiology adaptations to gestational status result from modifications in the maternal environment of steroids such as progesterone (P4), estrogens, androgens, and other hormones such as relaxin and prostaglandins (PG). However, an inadequate adaptation of maternal physiology can lead to gestational complications, such as restriction or overgrowth of the fetus and premature delivery [3].
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Since an understanding of endocrinology in equine species is useful when considering hormone treatment of cyclic and pregnant mares, this chapter considers a basic review and applications of this information in clinical therapeutic situations. For this reason, this chapter aims to provide an overview of the endocrine changes that occur in the mare in response to gestation and to discuss the key role of hormones in mediating pathological processes.
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2. Neuroendocrine control of the estrus cycle in cycling mares
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The estrous cycle is defined as the interval of time between two consecutive ovulations. The approximate length varies between 18 and 22 days, considering on average a period of 21 days [4, 5]. The current nomenclature stipulates that the estrous cycle consists of two differentiated stages: estrus or follicular phase and diestrus or luteal phase. These phases are characterized by internal modifications of the sexual organs and glandular system as well as behavioral alterations based on the levels of oestradiol (E2) and P4 [6, 7].
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2.1 Follicular phase
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Estrus, heat or follicular phase is characterized by the presence of follicles at different stages of development, and the simultaneous increase in the secretion of E2. It has a duration of about 5–7 days, with a variability of 3–9 days related to the season. Thus, estrus is extended in autumn (7–10 days) and is shortened considerably, in late spring and early summer (4–5 days). During this period the mare is sexually receptive to the stallion genital tract and is ready to receive and transport of sperm and finally culminates with ovulation [5, 6, 8].
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2.1.1 Follicular dynamics
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Ovarian follicular development is a complex dynamic process, characterized by marked proliferation and differentiation of follicular cells, providing an optimal environment for oocyte maturation and preparation for fertilization after ovulation [9]. Among the recruited follicles in each follicular wave, dominance takes place and one follicle of the cohort acquires the ability to continue growing while others undergo atresia. The regulation of each wave and follicular selection involves interactions between specific circulating gonadotropins and intrafollicular factors, ensuring that each follicle is properly stimulated to grow or regress at any stage of development [8]. From an experimental point of view, the occurrence of a wave is defined as follicular growth or simultaneous emergence of a variable number of follicles below 6–13 mm in diameter [10, 11]. In the mare, these follicular waves are classified depending on their ability to develop the dominant follicle (primary waves) or, in contrast, generate only small follicles (smaller waves). Thus, the main waves or greater originate several follicles subordinate and a dominant follicle, while smaller waves, the follicles are not larger than 30 mm in diameter and then regress [12, 13].
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During each cycle produces 1 or 2 major follicular waves, differentiated according to time of onset at primary and secondary. The primary major wave occurs near the middle of the diestrus, in which the dominant follicle ovulates at the end or near the end of estrus. The largest wave precedes the previous secondary and emerges during late estrus or early diestrus. There are two anovulatory follicular waves followed by an ovulatory surge during the estrous cycle [14, 15].
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Steroidogenesis in the ovaries involves both theca and granulosa cells. The antral follicles acquire receptors for follicle-stimulating (FSH) and luteinizing (LH) hormones in the membranes of the granular cells and theca, respectively. Cholesterol passes through theca cell plasma membrane attached to a lipoprotein, is stored in cytoplasmic vacuoles, and is transported to the outer membrane of the mitochondria. The LH is released in a pulsating form from the anterior pituitary gland and binds to its receptor in the theca cell membrane, mobilizing cholesterol. Inside theca cells, the StAR protein helps transfer cholesterol to the internal mitochondrial membrane, where the cytochrome P450 (CYP) enzyme system divides cholesterol into pregnenalone (P5), and subsequently, P5 becomes to androstenedione (A4). The A4 produced in theca cells is transported through the basal membrane to the granulose cells. There FSH supports the steroidogenic pathway and converts A4 into E2 [16].
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Increased concentrations of estrogen stimulate the secretion of LH, which in turn induces greater estrogen synthesis. This progressive increase in estrogen also promotes the onset of LH receptors in granulosa cells, which facilitates the transition from the antral stage to the preovulatory stage, when the oocyte reaches the final stage of maturation. At 6 days after the emergence of major follicular wave deviation occurs. This event relates to the growth rate difference of the preovulatory follicle size (22.5 mm) compared to the subordinate follicles (19 mm) [12, 13, 17]. Deviation is related to inhibin secretion [12] and insulin-like growth factor-1 (IGF-1) [13, 17]. Specifically, inhibin reduces FSH secretion, making it impossible to continue the development of the subordinate follicle. However, the dominant follicle continues to grow at a constant rate of 2.3 mm per day until reaching a size of 40 mm in response to the increased sensitivity to FSH. As has been mentioned, at this stage of development, granulosa cells also develop receptors for LH required for final oocyte maturation and ovulation after the LH surge [18].
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As has been demonstrated in different horse breeds such as Quarter Horse, Arabian, Thoroughbred, and Spanish Purebred, the maximum diameter of the ovulatory follicle usually varies between 40 and 45 mm [19], although the range may be higher (30–70 mm) [7, 20]. Moreover, size differences were established concerning the breeding season or the presence of multiple ovulations. Thus, the follicles reach a size 5–8 mm higher in spring than in summer or autumn and are 4–9 mm lower in multiple ovulations compared to the simple [20, 21].
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The highest concentrations of estrogen secreted by the granulosa cells of the preovulatory follicle also induce the appearance of typical behavioral manifestations of estrus. Estrogens are also responsible for reproductive changes that ensure the reception, transport of sperm and oocyte fertilization [4, 6]. After the preovulatory LH surge, ovulation occurs spontaneously 24–48 h before the end of the follicular phase. The ovulatory process brings rapid evacuation of the oocyte and follicular fluid after follicular rupture at ovulation fossa. Once completed, E2 concentrations return to basal levels and at the same time completing the oestrus behavior in mares [11, 22, 23, 24].
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2.2 Luteal phase
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The diestrus or luteal phase begins at the time of ovulation with the formation of CL, which is responsible for the synthesis of P4. Unlike the follicular phase, the insensitivity of the corpus luteum (CL) photoperiod makes the length of this period more constant. Most research estimates an average duration of 14–15 days but can be more durable in mid-summer (16 days) than in spring or autumn (13 days) [5, 6].
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2.2.1 Formation of corpus luteum
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The disorganization of the follicular wall after ovulation allows blood vessels and fibroblasts invade the follicular cavity. Luteinization involves structural and functional changes in granulosa and theca cells. These are the same cells that initially produced E2 and become into luteal cells that produce P4. P4 remains high from day 5 post-ovulation until the end of the diestrus and exerts specific functions related to the preparation of the endometrium to accept and maintain pregnancy, endometrial gland development and inhibition of myometrial contractility [24].
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Have been described two types of CL regarding the presence or absence of central blood clot. In a high percentage of cases (50–70%) in place of ovulation, a core clot develops surrounded by luteal tissue. This type of condition is defined as a corpus hemorrhagic. The cavity begins to fill with blood, fibrin, and transudate for the first 24 h, reaching the maximum size at 3 days. Around day 5 post-ovulation CLs that develop a central cavity usually, have a significantly higher size (32.8 mm) to those without it (26.0 mm). The ratio of the maximum diameter of the CL is 65–80% compared to pre-ovulatory follicle size and has an outer wall thickness of 4–7 mm corresponding to the portion of luteinized tissue. As happens with the size, texture also changes depending on the type of CL. The CL that develops the central cavity is denser than those that lack it, in which the structure is more spongy [25]. Usually, the ratio of non-luteal luteal tissue of the corpus hemorrhagic is minimal during the early diestrus and maximum in halfway of diestrus. These events are associated with the gradual decrease of fluid as a result of the production and organization of connective tissue associated with the clotting mechanism [26, 27]. Notably, the formation of one type or another of CL is a random event. The morphology luteal repeatability is not always observed in subsequent ovulation [26, 27, 28].
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Furthermore, continuous P4 levels during diestrus reduce the frequency and intensity of gonadotrophin-releasing factor (GnRH) pulses by a feedback mechanism. However, because the pulses of FSH are higher than those of LH, a new follicular wave is developed during this period. In the absence of pregnancy, the end luteal phase culminates with the lysis of CL induced by the PGF2α of endometrial origin and decreased concentrations of P4 [5, 6]. Luteal regression involves several structural and functional events characterized by decreased vascularization, an increase of connective tissue, hyalinization, atrophy and fibrosis [29].
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2.3 Neuroendocrine control of the estrus cycle
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Physiological events that occur during the estrous cycle are regulated by the coordinated interaction of various hormones and releasing factors like GnRH, FSH, LH, E2, P4, and PGF2α, among others [22]. In this section we will describe a synthesis of the most notable changes and the physiological participation that all these factors have during the estral cycle in the mare.
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2.3.1 Gonadotrophin releasing factor
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The increased photoperiod during spring and summer causes decreased secretion of melatonin. This signal has a positive effect on the pulses of hypothalamic GnRH, which in turn controls the release of gonadotropins [27]. GnRH pulses produced every 45 min originate predominantly LH secretion whereas those occur every 6 h stimulate the secretion of FSH. The high-frequency pulses of GnRH (2 pulses per hour) during estrus favors an increase in LH and FSH decline, while reducing the frequency to 2 pulses per day, leads an increase of FSH and LH inhibition [30]. These endocrine events, allowing the emergence of follicular waves, E2synthesis, and ovulation during estrus and appearance of the CL with P4 release during diestrus [24].
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2.3.2 Follicle stimulating hormone
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Follicle-stimulating hormone describes two types of secretion patterns during the estrous cycle in the mare: uni or bimodal. The bimodal pattern occurs frequently during the spring transition period and the ovulatory season. The first peak of FHS appears between the 8th and 14th day of the cycle, the moment in which the largest follicle reached a diameter of 13 mm [18]. This initial increase precedes the beginning of the deviation and is associated with increased synthesis of inhibin by the largest follicle [8, 13, 15, 18, 31] and persists until the preovulatory follicle reaches 22 mm of diameter. The second peak of FSH begins on day 15 of the cycle and it is necessary to complete the development of the preovulatory follicle [19, 31]. Unlike the bimodal pattern, the first peak of FSH would be absent in the unimodal pattern [18]. In the latter pattern, FSH levels remain low during estrus, rise in times around ovulation, maintaining increased during diestrus [31].
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FSH is also involved in the development of the LH receptors in the preovulatory follicle [32, 33]. At the start of follicular growth, low levels of estradiol exert negative feedback on the hypothalamic-hypophysis axis (HHA) controlling the tonic or basal release of gonadotropin. This mechanism controls the follicular growth and E2 synthesis continuously preventing ovarian overstimulation. After the period of follicular growth, once the dominant follicle has been selected, the E2 and inhibin levels are significantly increased. This elevation of E2 is responsible for the characteristic changes of the genital tract and signs of heat during estrus. Furthermore, this response exerts positive feedback on the HHA, favoring the emergence of preovulatory LH surge, necessary to produce the ovulation. Additionally, the stimulatory effects of E2 on LH combined to the inhibitory action of inhibin on FSH create the ideal microenvironment for the final maturation of the oocyte, inhibiting the development of immature follicles [4].
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2.3.3 Luteinizing hormone
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LH levels gradually increase from day 5 to the day of ovulation, when it reaches the maximum concentration [7, 34]. The pre-ovulatory LH surge occurs as a result of the positive feedback mechanism exerted in the adenohypophysis by E2 concentrations secreted by the granulosa cells of the preovulatory follicle. However, the peak of E2 is reached 2 days before the LH surge. During diestrus, LH is released in a pulsatile manner, with a frequency of 1.4 pulses per 24 h and for a period of 20–40 min at the central level, or 2–4 h per pulse at the peripheral level [34]. Therefore, P4 secretion is maintained by basal levels of LH. The decline of LH at the end of diestrus is a result of the combined effect of decreased estrogen positive feedback, and the resurgence of negative feedback induced by P4 on the HHA. This gonadotropin not only participates in the development and maturation of the primary follicles but also in the development and maintenance of CL during the luteal phase [8, 13, 22].
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2.3.4 Estradiol-17β
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The ability of estrogen synthesis is dependent on the effect of FSH on granulosa cells. In the absence of P4, estrogens begin to be actively secreted by the preovulatory follicle 5–7 days before ovulation. This event coincides with the time of departure and reaches the peak 2 days before ovulation [5, 22], and will be responsible for the preovulatory release of LH. After ovulation, E2 levels begin to decrease, reaching basal levels at day 5 post-ovulation [13, 19].
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Although estrogen levels are directly related to the degree of ovarian activity, sexual receptivity and reproductive tract changes [4, 6, 13, 31, 35] there is no evidence of a direct relationship between the intensity of endometrial edema and E2 concentration. This situation is much clearer on P4. Swelling occurs when P4 levels are <1 ng/ml, so this hormone could be responsible in principle on the intensity of edema, among other behavioral and morphological changes of the cervix and uterus [35]. However, at the time of ovulation inverse correlations are established between E2 and FSH levels associated with the negative feedback effect of inhibin, as previously referred [31].
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2.3.5 Progesterone
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The steroidogenic activity of P4 depends on the action of LH on theca cells. As noted above, levels of P4 are <1 ng/ml during estrus [19, 36]. After ovulation, it increases progressively and significantly to the 5th or 6th day, with values similar to those of pregnant mares during the first 14 days of gestation. At this time the CL is fully functional and P4 levels remain high until day 9 [35, 37], consistent with the maximum diameter reached by the CL [7, 20, 35, 37]. However, peripheral concentrations of P4 are highly variable between mares. This variability is associated with secretory capacity CL and hormonal catabolic rate. Perhaps this fact may explain the differences in P4 levels between different breeds during the first 5 days of the luteal period, despite the similarity in length of estrous cycles. Among other factors related to variations in levels of P4 highlights the number of ovulations. In fact, double ovulations induce higher concentrations of P4 compared to simple ones [35].
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P4 inhibits the secretion and pulsatile release of GnRH and LH but does not modify the pattern of FSH [7, 13, 15]. This event, unlike what happens in other species, enabling a new wave of follicular growth and in some cases the presence of ovulation during diestrus related to high levels of this hormone [18, 22, 38]. After lysis of the CL at the end of diestrus, P4 is drastically reduced to levels <1 ng/ml, a fact which promotes the mare returns to estrus [19, 36].
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2.3.6 Prostaglandin F2α\n
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In the absence of pregnancy, the average life span of the CL is controlled by the release of endometrial PGF2α source, establishing a bimodal pattern of discharge around day 13–16 of diestrus. While the first 4-h peak precedes the decline of P4, the second occurs during and after luteolysis. Luteolysis involves decreased blood supply, leukocyte infiltration, cell disruption and loss of lutein steroidogenic capacity by apoptotic or non-apoptotic mechanisms intended to disintegrate the CL and therefore secretion P4 [39, 40].
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3. Recent advances in hormonal control of estrous cycle
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In mares, the natural breeding season extends from spring to early autumn. Until now, various methods have been used to advance the onset of the breeding season or to synchronize the estrus during the reproductive season. Ovulation induction protocols have also been developed for use in artificial insemination or embryo transfer programs [41, 42].
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3.1 Gonadotropin releasing hormone
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Seasonal reproductive inactivity in mares is due to reduced synthesis and storage in the hypothalamus of GnRH and decreased amounts of FSH and LH in the anterior pituitary gland [27]. Taking this physiological basis into account, it would be expected that the administration of gonadotropins to anestrous mares will restart reproductive capacity.
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The administration of a single dose of GnRH to mares causes an increase in the circulating concentrations of FSH and LH [43]. However, constant infusions result in a continuous release of both hormones [44]. An experience conducted in the late 1980s reported that 50% of mares treated during the seasonal anestrous had fertile estrous after infusion of GnRH for 28 days (100 ng/kg; SC). However, this same experiment showed that mares with transitional anestrous were more likely to respond to GnRH than mares with deep anestrous [45].
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In another study, daily but not continuous administration of GnRH to induce ovulation in anestrous mares only induced the development of preovulatory follicles [46]. Also, another report [47] showed that the administration of 0.5 mg GnRH three times daily for 7 or 7.5 days induced normal follicular maturation and normal luteinization in anestrous mares. From these studies, it has been demonstrated that the administration of GnRH in diverse protocols is not profitable and requires a lot of manpower. It also results in variable response to treatment among mares, especially deep anestrous mares.
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3.2 GnRH agonists
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GnRH is known to be responsible for the secretion of FSH and LH, but studies performed to evaluate the efficacy of GnRH-agonists are conflicting. GnRH agonists were used as injections or slow-releasing implants to induce estrus and ovulation in anestrous and transitional mares. The GnRH agonists available for mares include deslorelin, buserelin, and historelin [48].
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According to Allen et al. [49] two injections of GnRH agonists each day or continuous administration of GnRH agonists were able to induce follicular development and ovulation in acyclic mares. In the same way, Bergfelt and Ginther [26], demonstrate the same result where mares where about 60% of treated mares with GnRH-agonist ovulated within a 21-day long treatment.
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In a study conducted in transition mares for 28 days, Harrison et al. [50] administered buserelin twice daily (40 μg, IM, q 12 h) for 28 days, or as SC implants releasing 100 μg/day. 45% of the mares ovulated between the 10th and 25th day after the start of treatment, in response to the two daily injections. However, 60% of the mares ovulated between 4 and 30 days after implant treatment. The same results were observed when the GnRH agonist was combined with E2 [51].
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Deslorelin has also been used to induce cycle and ovulation in mares. Slow liberation subcutaneous deslorelin implants are effective in increasing LH and accelerating ovulation in mares [52, 53].
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It is important to indicate that the response is in correlation with the follicular size at the beginning of the treatment and the depth of anestrus. This means that due to the insensitivity of GnRH, mares that are already in the transition period are more likely to respond to the treatment compared to those who are in deep anestrus [54]. Another negative aspect of GnRH treatment in anestrous mares is the risk of early pregnancy losses due to inadequate luteal function [26].
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3.3 Progesterone and progestins
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The administration of P4 suppresses the release of LH from the anterior pituitary gland. Once P4 supplementation ceases, the so-called “rebound effect” induces follicular maturation and ovulation. Its use in equine reproduction is a common practice and the available protocols include progestogens administered orally or parenterally. However, its use in mares with seasonal anestrous is questionable.
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Different studies indicate that mares in deep anestrous or early transition do not anticipate the first ovulation of the year with P4 treatments [30, 55]. However, it has been shown that, if treatment is carried out at the end of the transition period and the mares have at least one follicle of more than 20 mm in diameter in the ovaries, they show regular post-treatment cycles [56].
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Intravaginal devices containing P4 (CIDR, PRID, and intravaginal sponges) have been used in mares. Indeed, Hanlon and Firth [57] examined the effect of intravaginal devices placed during 10 days in transitional Thoroughbred mares. The results of the experiment showed that the use of P4 has a positive effect in bringing forward the first estral cycle of the breeding season. Compared to control mares, in the first 21 days of the season, 95.2% treated mares were served and conceived sooner after the start of the breeding season.
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Regumate is the most commonly used orally administered progestogen. Its active ingredient is allyl trenbolone, also called Altrenogest. Allen et al. [55] evaluated the effect of oral P4 treatment in mares with seasonal anestrous. Within 8 days, 88% of the treated mares showed estrous behavior and within 18 days of treatment interruption, 84% had ovulated. Based on these figures, the treatment gave a positive result in the acceleration of cyclicity in mares, but its response depends on the depth of the anestrus.
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3.4 Recombinant equine FSH (reFSH) and LH (reLH)
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The use of recombinant equine FSH (reFSH) has been reported to induce follicular growth in cyclic mares [58, 59]. A study reviewed in 2013 however determined the efficacy of it in deep anestrous mares to be very successful with ovulation rate of 76.7% in response to FSH treatment followed by human chorionic gonadotropin (hCG) administration [60].
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Mares in deep anestrous treated with reFSH alone or reFSH and reLH in combination under natural photoperiod showed a significant increase in follicular development within 6 days on average and all of them ovulated within 10 days. In comparison, the control group needed a significantly longer time for follicular growth and only 30% of the control mares had ovulated at the end of the 14 days used for the experiment [61].
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3.5 Dopamine antagonists and prolactin
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Studies in sheep found that dopamine antagonists are effective in increasing LH secretion during estrus by inhibiting the release of dopamine in the brain [62]. In mares, the increased release of dopamine during winter anestrous has been confirmed in studies measuring a higher concentration of dopamine in the cerebrospinal fluid during deep anestrous. It has also been shown that inhibition of dopamine D2 receptors may accelerate the onset of the ovulatory season in mares. Sulpiride, domperidone, and perphenazine have been studied [63].
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Mari et al. [64] compared the efficacy of sulpiride and domperidone, two long-acting dopamine antagonists, to induce ovarian activity in mares with deep anestrous. The results showed that sulpiride administration was effective in accelerating the transition period and first ovulation in mares with deep anestrous.
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On the other hand, as daylight increases, the concentration of prolactin (PRL) also increases. Dopamine is an inhibitor of PRL release, and it has been suggested that the administration of this hormone may help stimulate cycling in mares in anestrus [65]. Various studies have confirmed that the administration of recombinant prolactin from different animal species (equine, porcine and ovine) has a stimulating effect on mares in anestrus. Thompson et al. [66] examined the effect of subcutaneous administration of recombinant porcine prolactin (rpPRL) pony mares for 45 days. About 17 days after the start of treatment, a high percentage of treated mares showed signs of heat and ovulation accelerated by more than 1 month. However, another study examined the effect of a single dose of recombinant ovine prolactin (ovPRL). As a result, significant stimulation of follicular development was observed, but only one mare ovulated [67].
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3.6 Induction of ovulation in mares
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A reliable ovulation-inducing drug is one that can trigger ovulation within a certain “fixed” period of time. This pharmacological action can provide enormous advantages in anticipating the right time for artificial insemination. Several pharmacological agents such as GnRH and GnRH agonist, hCG, recombinant equine LH, and equine pituitary extracts, prostaglandins and kisspeptin have been used to determine their efficacy in ovulation induction [68].
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3.6.1 GnRH
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The frequency of GnRH pulses is the main regulator of LH secretion by the adenohypophysis [69]. Because of this stimulation, they can be used as an ovulatory agent and therefore can be used to induce ovulation in mares. On the other hand, due to its natural origin, it does not cause an immune response after being administered in several sessions. There is also little risk of contamination as GnRH is a synthetic product. In the 1990s, several experiments were conducted to evaluate the efficacy of GnRH in ovulation induction in cyclic mares [70, 71]. In one of them, the effect of a single administration of 2 mg of synthetic GnRH was tested but did not affect ovulation induction. However, daily injections of the same compound from day 2 of heat to ovulation resulted in a shortening of the duration of heat and the time for ovulation [72]. Likewise, Duchamp et al. [73] conducted a study to try to identify a more suitable ovulatory agent. To do that, they compared the effect of an intramuscular injection of 2.500 i.u. hCG and 2 mg GnRH (not synthetic). The use of hCG, injected when the follicle reached 35 mm in diameter, induced ovulation in 24 or 48 h. However, GnRH was not effective in shortening ovulation time compared to the control group.
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On the other hand, the pulsatile infusion of endogenous GnRH was effective in advancing ovulation time in cyclic mares [70]. Treatments with low doses of endogenous GnRH (2.5 μg) continuous infusion for 14 days demonstrated increased LH and ovulation in all treated mares compared to controls [74].
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3.6.2 GnRH-agonist
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3.6.2.1 Deslorelin (ovuplant and other products)
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Deslorelin is a potent GnRH agonist and is marketed as a controlled-release subcutaneous implant under the trade name Ovuplant™. In the past, several authors have investigated the efficacy of Deslorelin in inducing ovulation in mares [29, 75, 76].
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It has been shown that between 84 and 93% of mares ovulate after 2 or 3 days of treatment, respectively [77]. However, adverse effects have been reported for this drug. Mares treated with Ovuplant™ showed a prolonged interovulatory interval and estrual cycles of 3–7 days longer than controls [78]. In this sense, it was suggested that the GnRH agonist may cause a decrease in the regulation of the pituitary gonadotropic cells [79]. Besides, additional studies reported suppression of follicular growth and decreased FSH levels in mares treated with Ovuplant™ [80]. A study conducted by McCue et al. [81] showed that the extraction of Ovuplant™ after 48 h prevented a prolonged interovulatory interval. These authors also observed an alteration in ovulation rates. However, Ovupant™ is currently not commercially available.
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A short-term release product of deslorelin was developed in a biocompatible liquid vehicle called BioRelease™ [82]. This product releases deslorelin for approximately 6–36 h. An increase in the number of ovulations within 48 h has been demonstrated (75% vs. 7% for controls). There was also no effect of fertility and the number of coverages per conception decreased in treated mares (1.6 vs. 2.9).
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Subsequently, a greater number of injectable deslorelin products have been developed. Many of them are suspensions in saline or sterile water and do not contain any slow-release mechanism. McCue et al. [83] compared several deslorelin formulations and reported that all of the formulations tested in their study resulted in a shortening of the follicular phase, acceleration of ovulation and a similar response to human chorionic gonadotropin (hCG). It is important to note that these studies were conducted in the middle of the breeding season.
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3.6.2.2 Buserelin
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Different works have also tested Buserelin for its effect of inducing ovulation in mares [84]. Treatment with 40 μg de buserelin (4 doses/12 h) caused ovulation without altering fertility in mares [84, 85]. Also, the effect of treatments with 20 μg or 13.3 μg of buserelin (4 doses/12 h; or 3 doses/6 h respectively) was comparable with treatment with 2.500 IU of hCG (iv).
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However, some problems with Buserelin to induce ovulation were also reported [86]. Mares treated with 40 μg iv. of Buserelin (2 times daily), 2.500 IU of hCG (single dose iv) and 2 ml of water distilled as placebo (iv) were compared. The highest ovulation rate was found in hCG treatments where 88% of the mares ovulated between 36 and 48 h. However, Buserelin treatment caused only 22.7% ovulation within 48 h.
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Buserelin has also been given during early diestrus to pregnant mares as a means of improving pregnancy rates [87, 88]. These studies used doses of 20–40 mg of Buserelin between days 8 and 12. The results showed that pregnancy rates after ovulation increased by approximately 10%. The exact mechanism of how GnRH increases pregnancy rates is unclear since P4 does not appear to be increased.
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3.6.2.3 Human chorionic gonadotropin
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hCG is a glycoprotein hormone and has a biological function like LH. It is composed of two subunits (α-subunit and β-subunit). The biological activity of hCG is determined by β-subunit, which is composed of 145 amino acids [89]. Several experiments have been conducted to test the efficacy of hCG in ovulation induction [73, 90, 91]. The results of these studies showed that administration of 1.500–3.300 IU of hCG to mares with a follicle in the ovary 35 mm in diameter, or after estrus day 2, induced ovulation within 48 h. The administration of hCG to mares with a follicle in the ovary 35 mm in diameter, or after estrus day 2, induced ovulation within 48 h. The administration of hCG to mares with a follicle in the ovary 35 mm in diameter, or after estrus day 2, induced ovulation within 48 h. However, the adverse effect of consecutive administration of hCG has been reported. The results demonstrate a null effect from the second administration of hCG.
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On the other hand, significant levels of antibodies to hCG were also observed after repeated injections [91, 92]. However, there is much conflicting evidence as to whether antibody formation affects the efficacy of hCG [93].
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3.6.2.4 Equine recombinant LH
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The recombinant equine LH (reLH) was successfully developed and tested for both in vitro and in vivo efficacy [94, 95]. To test the efficacy of reLH in ovulation induction, a study was performed in mares with 35 mm follicles that were treated with 0.3, 0.6, 0.75, 0.9 mg reLH, 2.500 IU hCG and the number of ovulations within 48 h of injection was monitored. With a total of 84 mares of various breeds 28.6, 50, 90, and 80% ovulated within 48 h in response to 0.3, 0.6, 0.75, and 0.9 mg reLH, respectively. Changes in hormonal profiles (LH, FSH, P4, E2) in response to 5, 0.65, or 10 mg reLH were similar to those of mares of the control group, except for the early increase in LH after reLH injection. The result of this study indicates that reLH is a drug that induces ovulation in mares with a follicle size of 35 mm in 48 h. It is important to point out that as a synthetic product it offers good potential by having, for example, a low production cost.
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3.6.2.5 Equine pituitary extracts
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The raw extract of equine gonadotropin (CEG) from the pituitary, contains FSH and LH. These extracts have been tested to determine if they can be used as agents to control the estrual cycles of mares. Also, due to their LH content, the effect of CEG for ovulation induction has been tested. Duchamp et al. [73] showed that 80% of ponies and 57% of mares ovulated 2 days after the administration of 50 mg and 25 mg of CEG, respectively. However, there is one major obstacle to these results; the FSH and LH relationship in cEG is not always consistent. Another important factor to keep in mind is that CEG may be contaminated with other pituitary hormones. Also, the potential transmission of certain associated diseases between animals or between animals and humans [96, 97, 98].
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3.6.2.6 Prostaglandins
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Savage and Liptrap [99], reported on the use of PGF2α was able to induce ovulation in mares. By administering 250 μg PGF2α synthetic (Fenprostalene) 60 h after the onset of estrus, the interval between treatment and ovulation and the duration of estrus were significantly reduced.
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Despite these good results, no other PGF2α could be found that could give similar results [100]. It is therefore believed that the prolonged action of Fenprostalene was responsible for these results. Another PGF2α (Luprostiol), has also been shown to induce a release of LH from the anterior pituitary gland [101].
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3.6.2.7 Kisspeptin
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Kisspeptin is a neuropeptide that induces the secretion of gonadotropins through the stimulation of GnRH secretion and has also been described as having a role in triggering the onset of puberty [102, 103]. A study in pony mares demonstrated the anticipated ovulation when treated with 10 mg of kisspeptin. Another report identified that the administration of 500 μg and 1.0 mg of kisspeptin induces indistinguishable LH and FSH responses to 25 μg GnRH. However, a single injection of 1.0 mg of kisspeptin (iv) was insufficient to induce ovulation in the mare in heat [104].
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4. Hormonal regulation of pregnancy in normal mares
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4.1 Progesterone
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“Maternal recognition of gestation-MGR” it is essential to establish a complete and uninterrupted interaction between the uterus and the conceptus to prevent the regression of primary CL as a result of the blocking of luteolysis. The mobility of the conceptus within the uterine lumen between days 11 and 15 (or “first luteal response of pregnancy”); [27] seem to compensate for the reduced contact surface due to the relatively small size of the equine trophoblast, demonstrating that restriction of movement only partially leads to early embryo loss [105]. The PGs synthesized and secreted by the concept itself stimulate myometrial contractions that promote their migration through the uterus, avoiding premature regression of CL. Additionally, the longitudinal direction of the uterine folds, as well as the spherical shape of the embryo due to the persistence of the glycoprotein capsule, contribute to facilitating this movement [106, 107]. During the mobility phase and its subsequent fixation uterine high amounts of estrogen, mainly oestrone sulfate (E1S) by the equine conceptus are synthesized, related to the development of the embryonic and endometrial vasculature and local effects on myometrial activity, uterine mobility and endometrial gland secretion [108, 109].
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Embryo implantation begins around day 36 post-ovulation and involves the development of the chorionic band from the trophoblast, whose cells invade the maternal endometrium giving rise to endometrial cups [110]. Ginther [28] reported that the embryonic cup cells produce a hormone called equine chorionic gonadotropin (eCG), formerly known as pregnant mare’s serum gonadotropin. This hormone is first detectable systemically between days 35 and 40 of pregnancy. The cups are mature and robustly secreting eCG at approximately days 50–60, but they will subsequently undergo sloughing by days 100–150 in most mares This resurgence phase of P4 secretion by the primary CL is termed the “secondary luteal phase or output 2,” whereas the production by supplementary CL is termed the “third luteal phase” or “output 3”. These accessory CLs formed, respectively, causing an increase in P4 secretion around the 75th day of gestation [27, 28, 111]. Thus, during this period, two secretion peaks of P4 are described, which gradually decreasing to undetectable levels at the 200 days of gestation [112, 113].
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Ovarian P4 is necessary for the early maintenance of gestation in the mare until 150 days of pregnancy. After the regression of CLs, the placenta is then the organ in charge of maintaining gestation [114]. Several studies describe maximum levels of P4 during the second and third months of gestation, followed by a significant decrease to minimum values (<1 ng/ml) from mid-gestation to term [115]. Additionally, the presence of eCG causes a change in luteal steroidogenesis. In this case, CL changes from synthesizing only P4 to secreting also estrogens and androgens, increasing plasma levels rapidly and tripling the basal values [116]. However, it is not until approximately day 35 that systemic estrogen rises. The source of this estrogen is the ovary, more specifically, the CL and possibly follicles. The stimulation of the ovaries by eCG is responsible for the timing of this increase in estrogen. It appears that estrogen is not actually necessary for pregnancy maintenance, because ovariectomized mares administered only exogenous progestins will maintain pregnancy without the administration of estrogens [28]. The origin of both steroids is found in the primary CL, since their increase takes place before the formation of the secondary CLs and is absent in mares without functional CL. Although the mechanism by which gonadotropin exerts this activity is unknown, an increase in the expression of the enzyme 17α-hydroxylase in charge of the conversion of P5 into dehydroepiandrosterone (DHEA) and P4 into A4 has been described. Both events coincide with the secretion of eCG, they seem to be limited to the first period since they are not detected towards the middle of gestation [116]. The increase in P4 responds primarily to the growth of primary CL and the development of secondary and accessory CLs [4, 117].
\n
During the period of endometrial cups activity, secretion peaks are described for testosterone (T) and A4 [118, 119], whose activity may be decisive in uterine processes related to cell transformation associated with decidualization [120]. In addition, estrogen production depends on the increased synthesis and availability of androgens that are subsequently metabolized by the enzyme aromatase, present in luteal tissue even before eCG secretion. Thus, total estrogen levels are like right-handed during the first 35 days of gestation and increase around day 40 due to follicular development before the formation of CL [121]. Additionally, primary gestational CL produces E1S in response to eCG stimulation [113, 115, 118].
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The regression of the endometrial cups to 100–120 days of gestation causes the cessation of eCG secretion and luteal development, observing a progressive decrease in plasma levels of P4 to reach basal values around 200 days of gestation [115]. Currently, all the luteal structures present in the ovary have completely involuted [27]. From this moment onwards, various metabolites derived from P4 (progestins) increase in the systemic circulation, that exceed 500 ng/ml during the last weeks of gestation, which subsequently fall in the 24–48 h prior to birth [122].
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4.2 Progestagens
\n
Progestins can be subclassified as pregnenes and 5α-pregnenes. The pregnenes includes P5, P4 and 5-pregnene-3β,20β-diol (P5ββ), while 5α-pregnenes includes 5α-pregnane-3,20-dione (5αDHP), 3β-hydroxy-5α-pregnan-3-one (3β5P), 20α-hydroxy-5α-pregnan-3-one (20α5P), 5α-pregnane-3β,20β-diol (ββ-diol) and 5α-pregnane-3β,20α-diol (βα-diol). Of them, the most important ones in maternal plasma during this period are the 5αDHP and its derivatives, 20α5P, and βα-diol. The origin of all of them is found in P5, synthesized mainly in the fetal adrenal gland, with a production rate exceeding 10 μmol/min. In the placenta, P5 is converted to P4 and this is transformed into 5αDHP in the endometrium [123]. The pattern of secretion of 5αDHP at beginning of gestation runs parallel to that of P4, while around 90 days the onset of P4 decline gives way to fetoplacental synthesis of the different progestogens whose concentrations continue to increase during the second half of gestation. Thus, 20α5P, which is initially at 5 ng/ml, reaches 69 ng/ml at 200 days of gestation and 300 ng/ml at term. In addition, the concentrations of βα-diol increase to 484 ng/ml [112], while 3β5P, P5ββ and ββ-diol reach values of 100, 10 and 100 ng/ml, respectively, towards the end of gestation [124].
\n
The 5αDHP is found primarily at the uterine level during midgestation, but as labor approaches, its distribution changes and is predominantly in fetal circulation. This metabolite is an immediate precursor of allopregnanolone, a potent gamma-aminobutyric acid (GABA) receptor agonist with activity on myometrial relaxation in other species [125, 126, 127]. Serum allopregnanolone increases similarly to its precursor, reaching maximum values at the middle of gestation and a term [112]. However, both P4 and 5αDHP prevent weakly myometrial contractions induced by oxytocin in vitro, suggesting the intervention of the other hormones in the maintenance of uterine quiescence [128]. On the other hand, an umbilical increase of P4 after 300 days of gestation related to a greater expression in the trophoblast of the enzyme necessary for the conversion of P5 into P4 has been described [129].
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Simultaneously with the production of progestagens, the feto-placental unit (FPU) synthesizes phenolic estrogens, E1S and E2 17β and 17α, through the aromatization of dihydroandrosterone (DHA), DHEA and its precursors (3β-hydroxyl C-19). The estrogens β unsaturated, equilin and echinelin, specific to the equine species, derive from farnesyl pyrophosphate, through a noncholesterol-dependent pathway. In general, the pattern of estrogen secretion during gestation is characterized by the first peak of secretion around day 40 in relation to follicular development before the formation of secondary and accessory CLs and a subsequent increase from day 80, reaching maximum levels around 210 days of gestation [130, 131, 132]. Thus, the initial plasma concentrations of E1S, corresponding to ovarian synthesis and are affected by ovariectomy. On the contrary, the subsequent peak of liberation comes only from fetoplacental synthesis, descending drastically after fetal death [108, 113, 115, 133].
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This increase in estrogens temporarily coincides with the hypertrophy of fetal gonads, which together with local expression of the enzyme 17α-hydroxylase, lead to elevated umbilical levels of P5, T and DHEA [134]. At the same time, maternal plasma concentrations of T and DHEA increase after 100 days of gestation, reaching maximum values at 6 months [116, 135] to promote greater perfusion in the fetal compartment and the uterine tonicity [27, 136]. Legacki et al. [112] describe DHEA values that increase since the first 2 months of gestation to at 6–8 months, decreasing afterward.
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The mitochondrial cytochrome P450 side-chain cleavage enzyme (P450scc), necessary for the conversion of cholesterol into P5 is present in the glomerulosa and reticularis zone of the fetal adrenals from 150 days of gestation. However, its expression increases noticeably at the end of gestation, is also found in the fasciculata zone, in the placenta, and the utero-placental tissues. At the same time, fetal plasma levels of P5 and its uteroplacental diffusion are doubled and tripled between 200 and 300 days of gestation and that subsequently descend in the days prior to birth [132, 137]. One of the main metabolites of P4, the 5α-DHP, returns to umbilical circulation after synthesis in the endometrium, excreting only 30% of its production to the maternal circulation. Thus, it has been suggested that it could play a relevant role within fetoplacental tissues [137].
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4.3 Estrogens
\n
Estrogen production can likewise be determined in serum obtained from the mare and used as an indicator of feto-placental health [136]. Although total estrogen levels decrease in term gestation, E2 increases dramatically hours before parturition with accentuated myoelectric activity at the uterine level, suggesting the involvement of E2 in myometrial activation [132, 138]. In fact, estrogens promote PGs synthesis and increase endometrial sensitivity to oxytocin, stimulating myometrial contractile activity during delivery [137].
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4.4 Cortisol
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A few days before parturition, fetal adrenals change from mainly synthesizing P5 to producing cortisol in response to the stimulation of adrenocorticotropic hormone (ACTH). The increase of fetal cortisol is related to preparing the fetus for extra-uterine life by stimulating different processes necessary for the maturation of organs such as the liver, thyroid gland, lungs, digestive system, bone marrow and cardiovascular system [137]. In addition, cortisol activates the enzymes responsible for the synthesis of PGs which, without the presence of progestogens, increase continuously stimulating the onset of myometrial contractions. In addition, E2 favors the uterine response to PGs and may also promote their synthesis [139].
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4.5 Prostaglandins
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PGF2α play an important role during delivery by promoting myometrial contractibility, along with oxytocin, and cervical ripening and relaxation (PGE2). Utero-placental tissues are capable of synthesizing PGs and can be found in maternal plasma, fetal plasma and allantoic fluid [140]. However, its bioactivity is controlled by the enzyme 15-hydroxyprostaglandin dehydrogenase (PGDH), which converts the PGs into inactive metabolites, present in the maternal endometrium since approximately 150 days of pregnancy. Since the labile nature of PGs makes it difficult to measure one of these metabolites, 13,14-dihydro-15-keto-prostaglandin F-2α (PGFM) remained at low levels until day 200, then increased to peak pregnancy levels by day 300 and remained at this value until parturition. PGFM uses one of its metabolites as an indicator of its circulating levels, with a term increasingly being described, although it is during the second labor stage when its value increases up to 50 times [141].
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4.6 Relaxin
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Relaxin is produced by the trophoblastic cells of the placenta and its activity is related to myometrial [137] as well as of the cervix and pelvic ligaments relaxation [142]. Maternal plasma levels increase at the end of gestation and during the second labor stage. After the expulsion of the placenta, it returns to basal values below the detection limit at 36 h, remaining elevated in cases of placental retention [143].
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5. High-risk mares and hormone supplementation
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5.1 Progesterone
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P4 concentrations above 4.0 ng/ml are considered adequate to support early pregnancy. However, when levels are <2.0 ng/ml, P4 supplementation is considered [137]. Several types of P4 products have been used to maintain pregnancies in mares. After oral administration altrenogest is readily absorbed, reaching peak levels after 3–6 h [144]. Altrenogest acts by binding to the P4 receptors but has little effect on endogenous plasma total progestagen concentrations. Specifically, altrenogest is not metabolized to 5α-pregnanes in the horse [128]. For this reason, the only scientific evidence that altrenogest prevents loss pregnancy in mares is during the first trimester, when it prevented abortion induced by repeated administration of PGF2α (cloprostenol) [145]. P4 may exert its effects by interfering with PG production stimulated by proinflammatory cytokines. Daels et al. [146] demonstrated that the rise in endogenous PGF2α concentrations was inhibited by altrenogest treatment. Indeed, when early pregnant mares (21–35 days post-ovulation) were exposed to Salmonella typhimurium endotoxin all mares supplemented with altrenogest until day 70 remained pregnant, whereas 6 out of 7 mares aborted when altrenogest therapy was discontinued on day 50 [147].
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Mares with suspected luteal insufficiency can be supplemented with altrenogest (0.044 mg/kg per os once or twice daily) or P4 (150 mg/day IM) starting on day 3 after ovulation and continuing until 100–120 days of pregnancy. Long-acting injectable formulations of P4 and altrenogest are available in some countries [148]. Administration of the GnRH analog, buserelin (40 μg), 10 or 11 days after ovulation has been reported to improve luteal function and reduce early pregnancy loss [149]. Panzani et al. [150] showed that the use of altrenogest improved recipient pregnancy rates compared to untreated controls. A recent clinical study showed a positive effect of altrenogest supplementation on embryonic growth rates between 35 and 45 days after ovulation in Warmblood mares older than 8 years [151]. P4 may need to be supplemented generally in early pregnant mares showing estrus signs, with a history of repeated pregnancy loss in case of endotoxemia and of stressful events. In mares under P4 supplementation continuation of pregnancy has to be monitored regularly, since many will lose their pregnancy despite supplementation of P4 and this will prevent those mares return to estrus [152].
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The latter sentence has been checked. It has been reported that the administration of a single dose of 20–40 μg of buserelin between day 9 and day 10 after ovulation increases the number of multiple ovulations and gestation up to 5–10% [153]. Buserelin does not increase circulating P4 levels or preventing the luteolysis, acting independently of CL in the mare [154]. These effects preventing pregnancy loss that operating between day 9 to day 10 and day 13 to day 14 of pregnancy.
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In a recent study Köhne et al. [155] reported that hCG administration for induction of ovulation in mares increased progestin concentration in plasma of early pregnancy as well as the embryo size at the time of the start of placentation. Periovulatory treatment of mares with hCG may thus be a valuable tool to enhance conceptus growth during early pregnancy by stimulation of endogenous P4 secretion. However, Biermann et al. [156] report that hCG-treatment of mares on day 5 or day 11 post-ovulation influenced peripheral P4 concentrations due to secondary luteal tissue but did not alter ovarian and uterine blood flow or increase pregnancy rates.
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5.2 Progestagens
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Several pathological conditions as placentitis, placental separation or fetus as, alteration in umbilical blood flow attributable to a cord pathologic condition stimulates inflammatory and immune responses leading disrupt the endocrine capacity of the FPU and alterations in endocrine profile in plasma maternal attributed to disturbances to the normal synthetic pathway for these pregnanes [126, 157].
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Fetal death or imminent fetal expulsión due to uterine torsion, colic, maternal stress, or acute cases of experimentally induced placentitis when the mares abort rapidly (within 7 days of infection) are related with the rapidly declining of P5 and P4 (less than the 95%), consistent with failure of the fetus and feto-placental tissues to produce and metabolize progestagens [158, 159].
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In mares with chronic placentitis, placental edema, and placentas with poorly developed or sparse microvilli [159, 160] unusually high concentrations of all the progestagens. This pattern indicates that the fetus and the uteroplacental tissues are metabolically active despite the presence of bacteria or their products. In addition, Shikichi et al. [157] demonstrated that mares with a high concentration of progestins and low concentration of estrogens after day 241 of pregnancy were likely to deliver aborted/dead foals with placentitis. These authors demonstrated elevated and low concentrations of progestins and estrogens in the maternal sera of all cases with placentitis in pregnant mares, respectively.
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The mare’s exposure to ergopeptine alkaloids from the endophyte fungus found on tall fescue grass (fescue toxicosis), ergot alkaloids inhibit fetal corticotropin-releasing hormone (CRH), inhibiting the normal function of the adrenal gland to produce the cortisol surge and associated changes in pregnane metabolism [137]. In mares with fescue toxicosis, prepartum total plasma progestagen concentrations remain low, their foals have low cortisol concentrations, indicating suppression of fetal adrenocortical activity and P5 production [161].
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Recent studies demonstrated that altrenogest, when given in combination with antimicrobials, pentoxifylline and nonsteroidal anti-inflammatory (NSAIDs) drugs to mares with placentitis, decreased the incidence of abortion [162]. In these cases, altrenogest counteracts uterine contractility induced by inflammation of the fetal membranes. In the same way, in bacterial placentitis, a combination of trimethoprim sulfamethoxazole, pentoxifylline and a double dose of altrenogest (0.088 mg/kg bwt per os s.i.d.) were successful in maintaining pregnancies to term [163], while that untreated control mares aborted. When mares were treated with trimpethoprim sulfamethoxazole and pentoxifylline without altrenogest, only one live foal was born [163, 164]. Despite this, it is not clear what role, if any, altrenogest plays within this multi-treatment approach. However, the mares can still abort while receiving altrenogest treatment in the last trimester of pregnancy.
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5.3 Estrogens
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In late gestation total estrogen (including E1S, E2, and its metabolites, equilin, and equilenin) may be used for fetal and placental health monitoring. However, it is doubtful that total estrogen concentration can predict fetal death as the fetal gonads are unlikely to respond to fetal stress [157, 165].
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Since the production of estrogens requires both contributions by the fetus and placental, reduced concentrations in maternal circulation may indicate or predict a stressed or hypoxic fetus that is not producing the estrogen precursors [165]. Indeed, E2 [166] and E1S [167] concentrations decreased sharply in mares with placental dysfunction and after the induction of abortion. If the fetus is severely compromised or die in the uterus, maternal plasma E1S are baseline because of the absence of the C19 precursors secreted by the fetal gonads. However, pregnancies compromised by equine herpesvirus-1 infection or severe colic can present normal or transiently decreased E1S concentrations [168]. Compared with the adrenal glands, the gonads are unlikely to respond to fetal stress; consequently, so it is doubtful that total estrogen concentrations can predict fetal death. Frequent blood sampling of mares induced to abort with PG between 90 and 150 days of pregnancy indicated that E1S levels did not decline until within 5 h of abortion [145].
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In cases of placentitis at gestational ages between 150 and 280 days, Douglas [169] and Shikichi et al. [157] showed hormonal alterations common as elevated progestogens and low estrogens in mares that aborted. Although the decline in E2 associated with placental dysfunction is thought to reflect placental disease per se, Esteller-Vico et al. [170] recommended the estrogen supplementation as a means to reduce the risk of abortion associated with placentitis in mares. Recently, Curcio et al. [171] showed that in addition to basic treatment with trimethoprim-sulfamethoxazole and flunixin meglumine, mares with experimentally induced ascending placentitis benefited from E2 cypionate supplementation. Conversely, altrenogest did not appear to make a difference in outcomes.
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After fetal death and stress or fetal weakness, androgens and estrogens levels drop rapidly. For better determination of the health state of the fetus, due to the metabolism of both steroids, it is recommended to monitor androgens and estrogens simultaneously [126].
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5.4 Relaxin
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Relaxin is a useful biomarker to assess placental health and can be monitored in high-risk mares. Ryan et al. [172] reported a positive relationship between circulating levels of relaxin and poor outcomes in high-risk pregnancies. Relaxin is detectable in the blood after the 80th day of pregnancy without any changes until the second stage of labor. In mares with impaired placental function, in cases of placentitis, placental abruption, hydroallantois, and hydramnios relaxin concentrations decrease below 4 ng/mL [143, 172]. Low circulating levels of relaxin have been reported both in pony mares affected by fescue toxicosis associated with placental disease and agalactia and in Thoroughbred mares, with other forms of placental disease or insufficiency [172].
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In the case of placental hydrops, the risk of spontaneous rupture of the fetal membranes increases significantly [173]. Relaxin has been explored as a potential marker of treatment success in placentitis due to its level decrease in cases of spontaneously occurring and experimentally induced pregnancy loss [174].
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5.5 Prostaglandins
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Placentitis is characterized by the production of proinflammatory cytokines (such as IL-6 and IL-8) and PGs [175, 176]. PG release increases uterine contractility and consequently the risk of premature delivery [138]. Proinflammatory cytokines and the PGs of the FPU increases both in response to inflammation/infection, inducing premature activation of the fetal hypothalamic-pituitary-adrenal (HPA) axis [177], accelerating fetal maturation before parturition [138, 178]. The fetal adrenal produces both progestins and, once sufficiently mature, cortisol. Fetal cortisol, in turn, enhances placental and uterine PGs production, further enhancing uterine contractility and resulting in fetal delivery. Since the maturation of the equine fetus occurs later in gestation [137] this implies that placentitis or maternal disease could be devastating to the newborn foal. However, early fetal maturation likely counterbalances premature delivery and may help improve the chances for foal survival [138, 178]. The supplementation with progestin and PG synthetase inhibitor can maintain equine pregnancy in the presence of PGF2 insults [146, 147]. In addition, Esteller-Vico et al. [170] showed that estrogen suppression resulted in a decrease in circulating PGFM, which suggests that estrogens partially regulate PG production during pregnancy since PGFM concentrations were lower but still increased during the last trimester of equine gestation in letrozole-treated mares.
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6. Conclusions
\n
Knowledge of the physiological basis of the estrous cycle allows us to understand the interaction of reproductive hormones and the factors or events that interact in the cyclicity of mares. These basic studies have made possible the correct manipulation of the estrous cycle, the advancement of the reproductive season or the synchronization of ovulation. A great contribution in this sense has been possible through the description of the follicular dynamics and the study of the different structures present in the ovaries of the mares throughout the year.
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Likewise, the adequate interaction between the ovary, the placenta, and the fetus guarantees the secretion of the correct hormonal patterns necessary for a successful pregnancy. Measurements of progestogens, estrogens, and relaxin, among other hormones, are useful for monitoring the health status of the placenta and fetal viability. This is mainly because placental pathologies or fetal death are mainly due to alterations of these hormones. On the other hand, the hormonal diagnosis allows temporizing and early detection of pathological conditions to propose an adequate treatment for the maintenance of gestation and with it, the production of a viable foal. Substantial progress has been made in recent years in the identification of risk pregnancies and their treatment.
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All this knowledge helps greatly to improve the work of professionals and achievements for the improvement of reproductive outcomes. It is important to bear in mind that the constant production of basic knowledge and applied in equine reproduction will allow in the future to improve and generate new guidelines in reproductive technologies.
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\n\n',keywords:"estrous, clinical endocrinology, mare, pregnancy",chapterPDFUrl:"https://cdn.intechopen.com/pdfs/70381.pdf",chapterXML:"https://mts.intechopen.com/source/xml/70381.xml",downloadPdfUrl:"/chapter/pdf-download/70381",previewPdfUrl:"/chapter/pdf-preview/70381",totalDownloads:234,totalViews:0,totalCrossrefCites:0,dateSubmitted:"September 9th 2019",dateReviewed:"November 5th 2019",datePrePublished:"June 10th 2020",datePublished:"January 20th 2021",dateFinished:"December 6th 2019",readingETA:"0",abstract:"The use of advanced reproductive endocrinology can generate important economic benefits for equine breeding farms. Pregnancy in the mare involves considerable endocrine changes, which can be explained in part by the development of different structures such as embryonic vesicles, primary and secondary CL, endometrial cups and development of fetoplacental units. Both the pregnant mare and the fetus adapt to this development with unique mechanisms, such as alterations in the maternal endocrine metabolism and hormonal feedback. Since the ability to produce a viable foal is critical for the broodmare, the maintenance of the gestation implies almost a year of physiological effort. Therefore, the joint knowledge of basic reproductive science and current clinical endocrinology allows veterinarians and breeders to be better positioned to achieve their objectives. This chapter reviews normal and abnormal endocrine patterns during the equine estrual cycle, pregnancy. We also consider hormonal evaluation related to placentitis, abortions, recurrent pregnancy loss, and premature deliveries. Also, several aspects associated with endocrinological control of the reproductive cycle, ovulation, parturition, high-risk mare, and hormone supplementation will be developed.",reviewType:"peer-reviewed",bibtexUrl:"/chapter/bibtex/70381",risUrl:"/chapter/ris/70381",signatures:"Katy Satué and Juan Carlos Gardon",book:{id:"8545",title:"Animal Reproduction in Veterinary Medicine",subtitle:null,fullTitle:"Animal Reproduction in Veterinary Medicine",slug:"animal-reproduction-in-veterinary-medicine",publishedDate:"January 20th 2021",bookSignature:"Faruk Aral, Rita Payan-Carreira and Miguel Quaresma",coverURL:"https://cdn.intechopen.com/books/images_new/8545.jpg",licenceType:"CC BY 3.0",editedByType:"Edited by",isbn:"978-1-83881-937-8",printIsbn:"978-1-83881-936-1",pdfIsbn:"978-1-83881-938-5",editors:[{id:"25600",title:"Prof.",name:"Faruk",middleName:null,surname:"Aral",slug:"faruk-aral",fullName:"Faruk Aral"}],productType:{id:"1",title:"Edited Volume",chapterContentType:"chapter",authoredCaption:"Edited by"}},authors:[{id:"125292",title:"Dr.",name:"Katy",middleName:null,surname:"Satué Ambrojo",fullName:"Katy Satué Ambrojo",slug:"katy-satue-ambrojo",email:"ksatue@uchceu.es",position:null,institution:null},{id:"251314",title:"Dr.",name:"Juan Carlos",middleName:null,surname:"Gardón",fullName:"Juan Carlos Gardón",slug:"juan-carlos-gardon",email:"jc.gardon@ucv.es",position:null,institution:null}],sections:[{id:"sec_1",title:"1. Introduction",level:"1"},{id:"sec_2",title:"2. Neuroendocrine control of the estrus cycle in cycling mares",level:"1"},{id:"sec_2_2",title:"2.1 Follicular phase",level:"2"},{id:"sec_2_3",title:"2.1.1 Follicular dynamics",level:"3"},{id:"sec_4_2",title:"2.2 Luteal phase",level:"2"},{id:"sec_4_3",title:"2.2.1 Formation of corpus luteum",level:"3"},{id:"sec_6_2",title:"2.3 Neuroendocrine control of the estrus cycle",level:"2"},{id:"sec_6_3",title:"2.3.1 Gonadotrophin releasing factor",level:"3"},{id:"sec_7_3",title:"2.3.2 Follicle stimulating hormone",level:"3"},{id:"sec_8_3",title:"2.3.3 Luteinizing hormone",level:"3"},{id:"sec_9_3",title:"2.3.4 Estradiol-17β",level:"3"},{id:"sec_10_3",title:"2.3.5 Progesterone",level:"3"},{id:"sec_11_3",title:"2.3.6 Prostaglandin F2α\n",level:"3"},{id:"sec_14",title:"3. Recent advances in hormonal control of estrous cycle",level:"1"},{id:"sec_14_2",title:"3.1 Gonadotropin releasing hormone",level:"2"},{id:"sec_15_2",title:"3.2 GnRH agonists",level:"2"},{id:"sec_16_2",title:"3.3 Progesterone and progestins",level:"2"},{id:"sec_17_2",title:"3.4 Recombinant equine FSH (reFSH) and LH (reLH)",level:"2"},{id:"sec_18_2",title:"3.5 Dopamine antagonists and prolactin",level:"2"},{id:"sec_19_2",title:"3.6 Induction of ovulation in mares",level:"2"},{id:"sec_19_3",title:"3.6.1 GnRH",level:"3"},{id:"sec_20_3",title:"3.6.2 GnRH-agonist",level:"3"},{id:"sec_20_4",title:"3.6.2.1 Deslorelin (ovuplant and other products)",level:"4"},{id:"sec_21_4",title:"3.6.2.2 Buserelin",level:"4"},{id:"sec_22_4",title:"3.6.2.3 Human chorionic gonadotropin",level:"4"},{id:"sec_23_4",title:"3.6.2.4 Equine recombinant LH",level:"4"},{id:"sec_24_4",title:"3.6.2.5 Equine pituitary extracts",level:"4"},{id:"sec_25_4",title:"3.6.2.6 Prostaglandins",level:"4"},{id:"sec_26_4",title:"3.6.2.7 Kisspeptin",level:"4"},{id:"sec_30",title:"4. Hormonal regulation of pregnancy in normal mares",level:"1"},{id:"sec_30_2",title:"4.1 Progesterone",level:"2"},{id:"sec_31_2",title:"4.2 Progestagens",level:"2"},{id:"sec_32_2",title:"4.3 Estrogens",level:"2"},{id:"sec_33_2",title:"4.4 Cortisol",level:"2"},{id:"sec_34_2",title:"4.5 Prostaglandins",level:"2"},{id:"sec_35_2",title:"4.6 Relaxin",level:"2"},{id:"sec_37",title:"5. High-risk mares and hormone supplementation",level:"1"},{id:"sec_37_2",title:"5.1 Progesterone",level:"2"},{id:"sec_38_2",title:"5.2 Progestagens",level:"2"},{id:"sec_39_2",title:"5.3 Estrogens",level:"2"},{id:"sec_40_2",title:"5.4 Relaxin",level:"2"},{id:"sec_41_2",title:"5.5 Prostaglandins",level:"2"},{id:"sec_43",title:"6. Conclusions",level:"1"}],chapterReferences:[{id:"B1",body:'\nFowden AL, Moore T. Maternal-fetal resource allocation: Co-operation and conflict. Placenta. 2012;33(2):e11-e15. DOI: 10.1016/j.placenta.2012.05.002\n'},{id:"B2",body:'\nNapso T, Yong HEY, Lopez-Tello J, Sferruzzi-Perri AN. 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Administration of sulpiride or domperidone for advancing the first ovulation in deep anestrous mares. Theriogenology. 2009;71(6):959-965. DOI: 10.1016/j.theriogenology.2008.11.001\n'},{id:"B65",body:'\nMcCue PM. Clinical cases in equine reproduction. In: Proceedings of the 52nd Annual Convention of the American Association of Equine Practitioners (AAEP); 2-6 December 2006; San Antonio, Texas. Vol. 52. pp. 591-596\n'},{id:"B66",body:'\nThompson DL, Hoffman R, Depew CL. Prolactin administration to seasonally anestrous mares: Reproductive, metabolic, and hair-shedding responses. Journal of Animal Science. 1997;75(4):1092-1099. DOI: 10.2527/1997.7541092x\n'},{id:"B67",body:'\nNequin LG, King SS, Johnson AL, Gow GM, Ferreira-Dias GM. Prolactin may play a role in stimulating the equine ovary during the spring reproductive transition. Journal of Equine Veterinary Science. 1993;13:631-635. DOI: 10.1016/S0737-0806(07)80391-1\n'},{id:"B68",body:'\nYoon M. 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Advancing the time of ovulation in the mare with a short-term implant releasing the GnRH analogue deslorelin. Equine Veterinary Journal. 1993;25:65-68. DOI: 10.1111/j.2042-3306.1993.tb02904.x\n'},{id:"B77",body:'\nFarquhar V, McCue P, Vanderwall DK, Squires EL. Efficacy of the GnRH agonist deslorelin acetate for inducing ovulation in mares relative to age of mare and season. Journal of Equine Veterinary Science. 2000;20:8-11. DOI: 10.1016/S0737-0806(00)80183-5\n'},{id:"B78",body:'\nVanderwall DK, Juergens TD, Woods GL. Reproductive performance of commercial broodmares after induction of ovulation with hCG or Ovuplant™ (deslorelin). Journal of Equine Veterinary Science. 2001;21:539-542. DOI: 10.1016/S0737-0806(01)70158-X\n'},{id:"B79",body:'\nJohnson CA, Thompson DL, Kulinski K, Guitreau AM. Prolonged interovulatory interval and hormonal changes in mares following the use of Ovuplant™ to hasten ovulation. Journal of Equine Veterinary Science. 2000;20:331-336. DOI: 10.1016/S0737-0806(00)70421-7\n'},{id:"B80",body:'\nFarquhar VJ, McCue PM, Nett TM, Squires EL. Effect of deslorelin acetate on gonadotropin secretion and ovarian follicle development in cycling mares. Journal of the American Veterinary Medical Association. 2001;218:749-752. DOI: 10.2460/javma.2001.218.749\n'},{id:"B81",body:'\nMcCue PM, Farquhar VJ, Carnevale EM, Squires EL. Removal of deslorelin (Ovuplant™) implant 48 h after administration results in normal interovulatory intervals in mares. Theriogenology. 2002;58(5):865-870. DOI: 10.1016/S0093-691X(02)00923-8\n'},{id:"B82",body:'\nStich KL, Wendt KM, Blandchard TL, Brinsko SP. Effects of a new injectable short-term release deslorelin in foal-heat mares. Theriogenology. 2004;62:831-836. DOI: 10.1016/j.theriogenology.2003.12.004\n'},{id:"B83",body:'\nMcCue PM, Magee C, Gee EK. Comparison of compounded deslorelin and hCG for induction of ovulation in mares. Journal of Equine Veterinary Science. 2007;27:58-61. DOI: 10.1016/j.jevs.2006.12.003\n'},{id:"B84",body:'\nBarrier-Battut I, Le Poutre N, Trocherie E, Hecht S, Grandchamp des Raux A, Nicaise JL, et al. Use of buserelin to induce ovulation in the cyclic mare. Theriogenology. 2001;55:1679-1695. DOI: 10.1016/s0093-691x(01)00512-x\n'},{id:"B85",body:'\nMiki W, Oniyama H, Takeda N, Kimura Y, Haneda S, Matsui M, et al. Effects of a single use of the GnRH analog buserelin on the induction of ovulation and endocrine profiles in heavy draft mares. Journal of Equine Science. 2016;27(4):149-156. DOI: 10.1294/jes.27.149\n'},{id:"B86",body:'\nCamillo F, Pacini M, Panzani D, Vannozzi I, Rota A, Aria G. Clinical use of twice daily injections of buserelin acetate to induce ovulation in the mare. Veterinary Research Communications. 2004;28(1):169-172. DOI: 10.1023/b:verc.0000045398.62134.e4\n'},{id:"B87",body:'\nNewcombe JR, Martinez TA, Peters AR. The effect of the gonadotropin-releasing hormone analog, buserelin, on pregnancy rates in horse and pony mares. Theriogenology. 2001;55:1619-1631. DOI: 10.1016/s0093-691x(01)00507-6\n'},{id:"B88",body:'\nKanitz W, Schneider F, Hoppen HO, Unger C, Nurmberg G, Becker K. Pregnancy rates, LH and progesterone concentrations in mares treated with GnRH agonist. Animal Reproduction Science. 2007;97:55-62. DOI: 10.1016/j.anireprosci.2005.12.011\n'},{id:"B89",body:'\nCole LA, Kardana A. Discordant results in human chorionic gonadotropin assays. Clinical Chemistry. 1992;38:263-270. PMID: 1371722\n\n'},{id:"B90",body:'\nKilicarslan MR, Horoz H, Senunver A, Konuk SC, Tek C, Carioglu B. Effect of GnRH and hCG on ovulation and pregnancy in mares. The Veterinary Record. 1996;139:119-120. DOI: 10.1136/vr.139.5.119\n'},{id:"B91",body:'\nWilson C, Downie C, Hughes J. Effects of repeated hCG injections on reproductive efficiency in mares. Journal of Equine Veterinary Science. 1990;10:301-308. DOI: 10.1016/S0737-0806(06)80015-8\n'},{id:"B92",body:'\nNewcombe JR, Wilson MC. The effect of repeated treatment with human chorionic gonadotrophin to induce ovulation in mares. In: Proceedings of the 46th Congress British Equine Veterinary Association (BEVA): 12-15th September 2007; Edinburgh. p. 291\n'},{id:"B93",body:'\nNewcombe JR. Human chorionic gonadotrophin. In: McKinnon AO, Squires EL, Vaala WE, Varner DD, editors. Equine Reproduction. United Kingdom: Blackwell Publishing Ltd.; 2011. pp. 1804-1810. ISBN: 978-0-813-81971-6\n'},{id:"B94",body:'\nJablonka-Shariff A, Roser JF, Bousfield GR, Wolfe MW, Sibley LE, Colgin M, et al. Expression and bioactivity of a single chain recombinant equine luteinizing hormone (reLH). Theriogenology. 2007;67:311-320. DOI: 10.1016/j.theriogenology.2006.06.013\n'},{id:"B95",body:'\nYoon MJ, Boime I, Colgin M, Niswender KD, King SS, Alvarenga M, et al. The efficacy of a single chain recombinant equine luteinizing hormone (reLH) in mares: Induction of ovulation, hormone profiles, and inter-ovulatory intervals. Domestic Animal Endocrinology. 2007;33:470-479. DOI: 10.1016/j.domaniend.2007.06.001\n'},{id:"B96",body:'\nGoldfarb LG, Cervenakova L, Gajdusek DC. Genetic studies in relation to kuru: An overview. Current Molecular Medicine. 2004;4(4):375-384. DOI: 10.2174/1566524043360627\n'},{id:"B97",body:'\nChakraborty C, Nandi S, Jana S. Prion disease: A deadly disease for protein misfolding. Current Pharmaceutical Biotechnology. 2005;6(2):167-177. DOI: 10.2174/1389201053642321\n'},{id:"B98",body:'\nZou WQ , Gambetti P. Prion: The chameleon protein. Cellular and Molecular Life Sciences. 2007;64(24):3266-3270. DOI: 10.1007/s00018-007-7380-8\n'},{id:"B99",body:'\nSavage NC, Liptrap RM. Induction of ovulation in cyclic mares by administration of a synthetic prostaglandin, fenprostalene, during oestrus. Journal of Reproduction and Fertility. Supplement. 1987;35:239-243. PMID: 3479578\n\n'},{id:"B100",body:'\nHarrison LA, Squires EL, McKinnon AO. Comparison of hCG, Burserelin and Luprostiol for induction of ovulation in cycling mares. Journal of Equine Veterinary Science. 1991;11:163-166. DOI: 10.1016/S0737-0806(07)80039-6\n'},{id:"B101",body:'\nJöchle W, Irvine CH, Alexander SL, Newby TJ. Release of LH, FSH and GnRH into pituitary venous blood in mares treated with a PGF analogue, luprostiol, during the transition period. Journal of Reproduction and Fertility. Supplement. 1987;35:261-267. PMID: 3119828\n\n'},{id:"B102",body:'\nCaraty A, Franceschini I. Basic aspects of the control of GnRH and LH secretions by kisspeptin: Potential applications for better control of fertility in females. Reproduction in Domestic Animals. 2008;43(2):172-178. DOI: 10.1111/j.1439-0531.2008.01158.x\n'},{id:"B103",body:'\nClarke H, Dhillo WS, Jayasena CN. Comprehensive review on Kisspeptin and its role in reproductive disorders. Endocrinology and Metabolism. 2015;30(2):124-141. DOI: 10.3803/EnM.2015.30.2.124\n'},{id:"B104",body:'\nMagee C, Foradori CD, Bruemmer JE, Arreguin-Arevalo JA, McCue PM, Handa RJ, et al. Biological and anatomical evidence for kisspeptin regulation of the hypothalamic-pituitary-gonadal axis of estrous horse mares. Biomedizinische Technik. 2009;150(6):2813-2821. DOI: 10.1210/en.2008-1698\n'},{id:"B105",body:'\nGinther OJ. Mobility of the early equine conceptus. Theriogenology. 1983;19(4):603-611. DOI: 10.1016/0093-691x(83)90180-2\n'},{id:"B106",body:'\nGinther OJ. Equine pregnancy: Physical interactions between the uterus and conceptus. In: Proceedings of the 44th Annual Convention of the American Association of Equine Practitioners (AAEP); 6-9 December 1998. Baltimore, Maryland. pp. 73-104\n'},{id:"B107",body:'\nStout TA, Allen WR. Role of prostaglandins in intrauterine migration of the equine conceptus. Reproduction. 2001;121(5):771-775. DOI: 10.1530/rep.0.1210771\n'},{id:"B108",body:'\nRaeside JI, Christie HL, Renaud RL, Waelchli RO, Betteridge KJ. Estrogen metabolism in the equine conceptus and endometrium during early pregnancy in relation to estrogen concentrations in yolk-sac fluid. Biology of Reproduction. 2004;71(4):1120-1127. DOI: 10.1095/biolreprod.104.028712\n'},{id:"B109",body:'\nRaeside JI, Christie HL, Waelchli RO, Betteridge KJ. Biosynthesis of oestrogen by the early equine embryo proper. Reproduction, Fertility, and Development. 2012;24(8):1071-1078. DOI: 10.1071/RD11275\n'},{id:"B110",body:'\nWilsher S, Allen WR. Factors influencing equine chorionic gonadotrophin production in the mare. Equine Veterinary Journal. 2011;43(4):430-438. DOI: 10.1111/j.2042-3306.2010.00309.x\n'},{id:"B111",body:'\nGinther OJ, Santos VG. Natural rescue and resurgence of the equine corpus luteum. Journal of Equine Veterinary Science. 2015;35:1-6. DOI: 10.1016/j.jevs.2014.10.004\n'},{id:"B112",body:'\nLegacki EL, Scholtz EL, Ball BA, Stanley SD, Berger T, Conley AJ. The dynamic steroid landscape of equine pregnancy mapped by mass spectrometry. Reproduction. 2016;151(4):421-430. DOI: 10.1530/REP-15-0547\n'},{id:"B113",body:'\nSatué K, Marcilla M, Medica P, Ferlazzo A, Fazio E. Sequential concentrations of placental growth factor and haptoglobin, and their relation to oestrone sulphate and progesterone in pregnant Spanish purebred mare. Theriogenology. 2018;115:77-83. DOI: 10.1016/j.theriogenology.2018.04.033\n'},{id:"B114",body:'\nDavies Morel MC. Equine Reproductive Physiology, Breeding and Stud Management. 3rd ed. Wallindorf, UK: CABI; 2008. ISBN: 9781845934507\n'},{id:"B115",body:'\nSatué K, Domingo R, Redondo JI. Relationship between progesterone, oestrone sulphate and cortisol and the components of renin angiotensin aldosterone system in Spanish purebred broodmares during pregnancy. Theriogenology. 2011;76(8):1404-1415. DOI: 10.1016/j.theriogenology.2011.06.009\n'},{id:"B116",body:'\nSatué K, Marcilla M, Medica P, Ferlazzo A, Fazio E. Testosterone, androstenedione and dehydroepiandrosterone concentrations in pregnant Spanish purebred mare. Theriogenology. 2019;1(123):62-67. DOI: 10.1016/j.theriogenology.2018.09.025\n'},{id:"B117",body:'\nAlbrecht BA, MacLeod JN, Daels PF. Differential transcription of steroidogenic enzymes in the equine primary corpus luteum during diestrus and early pregnancy. Biology of Reproduction. 1997;56(4):821-829. DOI: 10.1095/biolreprod56.4.821\n'},{id:"B118",body:'\nDaels PF, Chang GC, Hansen B, Mohammed HO. Testosterone secretion during early pregnancy in mares. Theriogenology. 1996;45(6):1211-1219. DOI: 10.1016/0093-691x(96)00076-3\n'},{id:"B119",body:'\nDaels PF, Albrecht BA, Mohammed HO. Equine chorionic gonadotropin regulates luteal steroidogenesis in pregnant mares. Biology of Reproduction. 1998;59(5):1062-1068. DOI: 10.1095/biolreprod59.5.1062\n'},{id:"B120",body:'\nKajihara T, Tanaka K, Oguro T, Tochigi H, Prechapanich J, Uchino S, et al. Androgens modulate the morphological characteristics of human endometrial stromal cells decidualized in vitro. Reproductive Sciences. 2014;21(3):372-380. DOI: 10.1177/1933719113497280\n'},{id:"B121",body:'\nFerraz LES, Vicente WRR, Ramos PRR. Progesterone and estradiol 17-β concentration, and ultrasonic images of the embryonic vesicle during the early pregnancy in Thoroughbred mares. Arquivo Brasileiro de Medicina Veterinária e Zootecnia. 2001;53(4):1-7. DOI: 10.1590/S0102-09352001000400015\n'},{id:"B122",body:'\nHoltan DW, Houghton E, Silver M, Fowden AL, Ousey J, Rossdale PD. Plasma progestagens in the mare, fetus and newborn foal. Journal of Reproduction and Fertility. Supplement. 1991;44:517-528. PMID: 1795295\n\n'},{id:"B123",body:'\nHan X, Rossdale PD, Ousey J, Holdstock N, Allen WR, Silver M, et al. Localisation of 15-hydroxy prostaglandin dehydrogenase (PGDH) and steroidogenic enzymes in the equine placenta. Equine Veterinary Journal. 1995;27(5):334-339. DOI: 10.1111/j.2042-3306.1995.tb04067.x\n'},{id:"B124",body:'\nOusey JC, Houghton E, Grainger L, Rossdale PD, Fowden AL. Progestagen profiles during the last trimester of gestation in Thoroughbred mares with normal or compromised pregnancies. Theriogenology. 2005;63(7):1844-1856. DOI: 10.1016/j.theriogenology.2004.08.010\n'},{id:"B125",body:'\nScholtz EL, Krishnan S, Ball BA, Corbin CJ, Moeller BC, Stanley SD, et al. Pregnancy without progesterone in horses defines a second endogenous biopotent progesterone receptor agonist, 5α-dihydroprogesterone. Proceedings of the National Academy of Sciences of the United States of America. 2014;111(9):3365-3370. DOI: 10.1073/pnas.1318163111\n'},{id:"B126",body:'\nConley AJ. Review of the reproductive endocrinology of the pregnant and parturient mare. Theriogenology. 2016;86(1):355-365. DOI: 10.1016/j.theriogenology.2016.04.049\n'},{id:"B127",body:'\nWynn MAA, Esteller-Vico A, Legacki EL, Conley AJ, Loux SC, Stanley SD, et al. A comparison of progesterone assays for determination of peripheral pregnane concentrations in the late pregnant mare. Theriogenology. 2018;106:127-133. DOI: 10.1016/j.theriogenology.2017.10.002\n'},{id:"B128",body:'\nOusey JC, Rossdale PD, Palmer L, Houghton E, Grainger L, Fowden AL. Effects of progesterone administration to mares during late gestation. Theriogenology. 2002;58:793-795. DOI: 10.1016/S0093-691X(02)00743-4\n'},{id:"B129",body:'\nOusey JC, Forhead AJ, Rossdale PD, Grainger L, Houghton E, Fowden AL. Ontogeny of uteroplacental progestagen production in pregnant mares during the second half of gestation. Biology of Reproduction. 2003;69(2):540-548. DOI: 10.1095/biolreprod.102.013292\n'},{id:"B130",body:'\nHenderson K, Stewart J. A dipstick immunoassay to rapidly measure serum oestrone sulfate concentrations in horses. Reproduction, Fertility, and Development. 2000;12(3-4):183-189. DOI: 10.1071/rd00062\n'},{id:"B131",body:'\nHenderson KM, Eayrs K. Pregnancy status determination in mares using a rapid lateral flow test for measuring serum oestrone sulphate. New Zealand Veterinary Journal. 2004;52(4):193-196. DOI: 10.1080/00480169.2004.36428\n'},{id:"B132",body:'\nFowden AL, Forhead AJ, Ousey JC. The endocrinology of equine parturition. Experimental and Clinical Endocrinology & Diabetes. 2008;116:393-403. DOI: 10.1055/s-2008-1042409\n'},{id:"B133",body:'\nPashen RL, Allen WR. The role of the fetal gonads and placenta in steroid production, maintenance of pregnancy and parturition in the mare. Journal of Reproduction and Fertility. Supplement. 1979;27:499-509. PMID: 289829\n\n'},{id:"B134",body:'\nHasegawa T, Sato F, Nambo Y, Ishida N. Expression of steroidogenic enzyme genes in the equine feto-placental unit. Journal of Equine Science. 2001;12(1):25-32. DOI: 10.1294/jes.12.25\n'},{id:"B135",body:'\nCanisso IF, Ball BA, Esteller-Vico A, Squires EL, Troedsson MH. Dehydroepiandrosterone sulfate and testosterone concentrations in mares carrying normal pregnancies. In: Proceedings of the Society for Theriogenology Annual Conference; 6-9 August 2014; Portland, OR, USA. p. 383\n'},{id:"B136",body:'\nOusey JC. Endocrinology of pregnancy. In: McKinnon AO, Squires EL, Vaala WE, Varner DD, editors. Equine Reproduction. Hoboken NJ: Wiley-Blackwell; 2011. pp. 2222-2231. ISBN: 978-0-813-81971-6\n'},{id:"B137",body:'\nOusey JC. Hormone profiles and treatments in the late pregnant mare. The Veterinary Clinics of North America. Equine Practice. 2006;22(3):727-747. DOI: 10.1016/j.cveq.2006.08.004\n'},{id:"B138",body:'\nMcGlothlin JA, Lester GD, Hansen PJ, Thomas M, Pablo L, Hawkins DL, et al. Alteration in uterine contractility in mares with experimentally induced placentitis. Reproduction. 2004;127(1):57-66. 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Endocrine Reviews. 1992;3(1):62-90. DOI: 10.1210/edrv-3-1-62\n'},{id:"B143",body:'\nStewart DR, Addiego LA, Pascoe DR, Haluska GJ, Pashen R. Breed differences in circulating equine relaxin. Biology of Reproduction. 1992;46(4):648-652. DOI: 10.1095/biolreprod46.4.648\n'},{id:"B144",body:'\nMachnik M, Hegger I, Kietzmann M, Thevis M, Guddat S, Schänzer W. Pharmacokinetics of altrenogest in horses. Journal of Veterinary Pharmacology and Therapeutics. 2007;30:86-90. DOI: 10.1111/j.1365-2885.2007.00820.x\n'},{id:"B145",body:'\nDaels PF, Hussni M, Montavon SME, Stabenfeldt GH, Hughes JP, Odensvik K, et al. Endogenous prostaglandin secretion during cloprostenol-induced abortion in mares. Animal Reproduction. 1995;40:305-321. DOI: 10.1016/0378-4320(95)01429-2\n'},{id:"B146",body:'\nDaels PF, Besognet B, Hansen B, Mohammed H, Odensvik K, Kindahl H. Effect of progesterone on prostaglandin F2 alpha secretion and outcome of pregnancy during cloprostenol-induced abortion in mares. American Journal of Veterinary Research. 1996;57:1331-1337. PMID: 8874729\n\n'},{id:"B147",body:'\nDaels PF, Stabenfeldt GH, Hughes JP, Odensvik K, Kindahl H. Evaluation of progesterone deficiency as a cause of fetal death in mares with experimentally induced endotoxemia. American Journal of Veterinary Research. 1991;52:282-288. PMID: 2012339\n\n'},{id:"B148",body:'\nVanderwall DK. Early embryonic loss in the mare. Journal of Equine Veterinary Science. 2008;28:691-702. DOI: 10.1016/j.jevs.2008.10.001\n'},{id:"B149",body:'\nPycock J, Newcombe J. The effect of the gonadotrophin-releasing hormone analog, buserelin, administered in diestrus on pregnancy rates and pregnancy failure in mares. Theriogenology. 1996;46:1097-1101. DOI: 10.1016/s0093-691x(96)00274-9\n'},{id:"B150",body:'\nPanzani D, Crisci A, Rota A, Camillo F. Effect of day of transfer and treatment administration on the recipient on pregnancy rates after equine embryo transfer. Veterinary Research Communications. 2009;33:113-116. DOI: 10.1007/s11259-009-9303-7\n'},{id:"B151",body:'\nWillmann C, Schuler G, Hoffmann B, Parvizi N. Effects of age and altrenogest treatment on conceptus development and secretion of LH, progesterone and eCG in early-pregnant mares. Theriogenology. 2011;75:421-428. DOI: 10.1016/j.theriogenology.2010.05.009\n'},{id:"B152",body:'\nSieme JL, Sielhorst J, Martinsson G, Bollwein H, Thomas S, Burger D. Improving the formation and function of the corpus luteum in the mare. Revista Brasileira de Reprodução Animal. 2015;39:117-120. DOI: 10.5167/uzh-116508\n'},{id:"B153",body:'\nNewcombe JR, Peters AR. The buserelin enigma: How does treatment with this GnRH analogue decrease embryo mortality? Journal of Veterinary Science and Technology. 2014;5:151. DOI: 10.4172/2157-7579.1000151\n'},{id:"B154",body:'\nStout TA, Tremoleda JL, Knaap J, Daels P, Kindahl H, Colenbrander B. Mid-diestrus GnRH-analogue administration does not suppress the luteolytic mechanism in mares. Theriogenology. 2002;58:567-570. DOI: 10.1016/S0093-691X(02)00860-9\n'},{id:"B155",body:'\nKöhne M, Ille N, Erber R, Aurich C. Treatment with human chorionic gonadotrophin before ovulation increases progestin concentration in early equine pregnancies. Animal Reproduction Science. 2014;149:187-193. DOI: 10.1016/j.anireprosci.2014.07.002\n'},{id:"B156",body:'\nBiermann J, Klewitz J, Otzen H, Martinsson G, Burger D, Meinecke-Tillmann S, et al. The effect of hCG, administered in diestrus, on luteal, ovarian and uterine blood flow, peripheral progesterone levels and pregnancy rates in mares. Journal of Equine Veterinary Science. 2014;34:166. DOI: 10.1016/j.jevs.2013.10.119\n'},{id:"B157",body:'\nShikichi M, Iwata K, Ito K, Miyakoshi D, Murase H, Sato F, et al. Abnormal pregnancies associated with deviation in progestin and estrogen profiles in late pregnant mares: A diagnostic aid. Theriogenology. 2017;98:75-81. DOI: 10.1016/j.theriogenology.2017.04.024\n'},{id:"B158",body:'\nLeBlanc MM, Macpherson M, Sheerin P. Ascending placentitis: What we know about pathophysiology, diagnosis and treatment. In: Proceedings of the Annual Convention of the American Association of Equine Practitioners (AAEP); 4-8 December 2004; Denver, Colorado, USA. pp. 127-143\n'},{id:"B159",body:'\nMorris S, Kelleman AA, Stawicki RJ, Hansen PJ, Sheerin PC, Sheerin BR, et al. Transrectal ultrasonography and plasma progestin profiles identifies feto-placental compromise in mares with experimentally induced placentitis. Theriogenology. 2007;67:681-691. DOI: 10.1016/j.theriogenology.2006.05.021\n'},{id:"B160",body:'\nWynn MAA, Ball BA, May J, Esteller-Vico A, Canisso I, Squires E, et al. Changes in maternal pregnane concentrations in mares with experimentally-induced, ascending placentitis. Theriogenology. 2018;122:130-136. DOI: 10.1016/j.theriogenology.2018.09.001\n'},{id:"B161",body:'\nBrendemeuhl JP, Williams MA, Boosinger TR, Ruffin DC. Plasma progestagen, trioiodothyronine and cortisol concentrations in postdate gestation foals exposed in utero to the tall fescue endophyte Acremonium coenophialum. Biology of Reproduction. 1995;1:53-59. DOI: 10.1093/biolreprod/52.monograph_series1.53\n'},{id:"B162",body:'\nTroedsson MHT, Miller LMJ. Equine placentitis. Pferdeheilkunde. 2016;32(1):49-53. DOI: 10.21836/PEM20160109\n'},{id:"B163",body:'\nBailey CS, Macpherson ML, Pozor MA, Troedsson MH, Benson SM, Giguere S, et al. Treatment efficacy of trimethoprim sulfamethoxazole, pentoxifylline and altrenogest in experimentally induced equine placentitis. Theriogenology. 2010;74:402-412. DOI: 10.1016/j.theriogenology.2010.02.023\n'},{id:"B164",body:'\nGraczyk J, Macpherson ML, Pozor MA, Troedsson MHT, Eichelberger AC, LeBlanc MM, et al. Treatment efficacy of trimethoprim sulfamethoxazole and pentoxifylline in equine placentitis. Animal Reproduction Science. 2006;94:434-435. DOI: 10.1016/j.theriogenology.2010.02.023\n'},{id:"B165",body:'\nLeBlanc MM. Ascending placentitis in the mare: An update. Reproduction in Domestic Animals. 2010;45:28-34. DOI: 10.1111/j.1439-0531.2010.01633.x\n'},{id:"B166",body:'\nCanisso IF, Ball BA, Esteller-Vico A, Williams NM, Squires EL, Troedsson MH. Changes in maternal androgens and oestrogens in mares with experimentally induced ascending placentitis. Equine Veterinary Journal. 2017;49(2):244-249. DOI: 10.1111/evj.12556\n'},{id:"B167",body:'\nKasman LH, Hughes JP, Stabenfeldt GH, Starr MD, Lasley BL. Estrone sulfate concentrations as an indicator of fetal demise in horses. American Journal of Veterinary Research. 1988;49(2):184-187. PMID: 2831761\n\n'},{id:"B168",body:'\nSantschi EM, LeBlanc MM, Weston PG. Progestagen, oestrone sulphate and cortisol concentrations in pregnant mares during medical and surgical disease. Journal of Reproduction and Fertility. Supplement. 1991;44:627-634. PMID: 1665522\n\n'},{id:"B169",body:'\nDouglas RH. Endocrine diagnostics in the broodmare: What you need to know about progestins and estrogens. In: Annual Meeting for the Society for Theriogenology and American College of Theriogenologists; 4-7 August, 2004; Lexington, KY. pp. 106-115\n'},{id:"B170",body:'\nEsteller-Vico A, Ball BA, Troedsson MHT, Squires EL. Endocrine changes, fetal growth, and uterine artery hemodynamics after chronic estrogen suppression during the last trimester of equine pregnancy. Biology of Reproduction. 2017;96:414-423. DOI: 10.1095/biolreprod.116.140533\n'},{id:"B171",body:'\nCurcio BR, Canisso IF, Pazinato FM, Borba LA, Feijo LS, Muller V, et al. Estradiol cypionate aided treatment for experimentally induced ascending placentitis in mares. Theriogenology. 2017;102:98-107. DOI: 10.1016/j.theriogenology.2017.03.010\n'},{id:"B172",body:'\nRyan PL, Christiansen DL, Hopper RM, Bagnell CA, Vaala WE, LeBlanc MM. Evaluation of systemic relaxin blood profiles in horses as a means of assessing placental function in high-risk pregnancies and responsiveness to therapeutic strategies. Annals of the New York Academy of Sciences. 2009;1160:169-178. DOI: 10.1111/j.1749-6632.2008.03802.x\n'},{id:"B173",body:'\nChristensen BW, Troedsson MHT, Murchie TA, Pozor MA, Macpherson ML, Estrada AH, et al. Management of hydrops amnion in a mare resulting in birth of a live foal. Journal of the American Veterinary Medical Association. 2006;228:1228-1233. DOI: 10.2460/javma.228.8.1228\n'},{id:"B174",body:'\nKlein C. The role of relaxin in mare reproductive physiology: A comparative review with other species. Theriogenology. 2016;86:451-456. DOI: 10.1016/j.theriogenology.2016.04.061\n'},{id:"B175",body:'\nLeBlanc MM, Giguere S, Lester GD, Bauer K, Paccamonti L. Relationship between infection, inflammation and premature parturition in mares with experimentally induced placentitis. Equine Veterinary Journal. Supplement. 2012;41:8-14. DOI: 10.1111/j.2042-3306.2011.00502.x\n'},{id:"B176",body:'\nLyle SK. Immunology of infective preterm delivery in the mare. Equine Veterinary Journal. 2014;46:661-668. DOI: 10.1111/evj.12243\n'},{id:"B177",body:'\nLyle SK, Hague M, Lopez MJ, Beehan DP, Staempfil S, Len JA, et al. In vitro production of cortisol by equine fetal adrenal cells in response to ACTH and IL-1b. Animal Reproduction Science. 2010;121:322. DOI: 10.1016/j.anireprosci.2010.04.127\n'},{id:"B178",body:'\nCanisso IF, Ball BA, Erol E, Squires EL, Troedsson MHT. Comprehensive review on equine placentitis. In: Proceedings of the 61st Annual Convention of the American Association of Equine Practitioners (AAEP); 5-9 December 2015; Las Vegas, Nevada, USA. pp. 490-509\n'}],footnotes:[],contributors:[{corresp:"yes",contributorFullName:"Katy Satué",address:"ksatue@uchceu.es",affiliation:'
Department of Animal Medicine and Surgery, Faculty of Veterinary, University CEU-Cardenal Herrera, Valencia, Spain
'},{corresp:null,contributorFullName:"Juan Carlos Gardon",address:null,affiliation:'
Department of Animal Medicine and Surgery, Faculty of Veterinary and Experimental Sciences, Catholic University of Valencia-San Vicente Mártir, Spain
'}],corrections:null},book:{id:"8545",title:"Animal Reproduction in Veterinary Medicine",subtitle:null,fullTitle:"Animal Reproduction in Veterinary Medicine",slug:"animal-reproduction-in-veterinary-medicine",publishedDate:"January 20th 2021",bookSignature:"Faruk Aral, Rita Payan-Carreira and Miguel Quaresma",coverURL:"https://cdn.intechopen.com/books/images_new/8545.jpg",licenceType:"CC BY 3.0",editedByType:"Edited by",isbn:"978-1-83881-937-8",printIsbn:"978-1-83881-936-1",pdfIsbn:"978-1-83881-938-5",editors:[{id:"25600",title:"Prof.",name:"Faruk",middleName:null,surname:"Aral",slug:"faruk-aral",fullName:"Faruk Aral"}],productType:{id:"1",title:"Edited Volume",chapterContentType:"chapter",authoredCaption:"Edited by"}}},profile:{item:{id:"75701",title:"Dr.",name:"T. V. Lakshmi",middleName:null,surname:"Kumar",email:"lkumarap@hotmail.com",fullName:"T. V. Lakshmi Kumar",slug:"t.-v.-lakshmi-kumar",position:null,biography:"Dr.T.V. Lakshmi Kumar, joined the Department of Physics, SRM Institute of Science and Technology (formerly known as SRM University) in 2009 after completing his Ph.D. from Andhra University in the year 2008. Lakshmi Kumar works in the areas of hydrometeorology and aerosol science. He has completed four projects sponsored by DST, ISRO, Govt of India. He has published around 40 papers in reputed journals and 4 candidates awarded Ph.D. under his guidance.",institutionString:null,profilePictureURL:"https://intech-files.s3.amazonaws.com/a043Y00000jzSbnQAE/Co1_Profile_Picture-1612241176857",totalCites:0,totalChapterViews:"0",outsideEditionCount:0,totalAuthoredChapters:"3",totalEditedBooks:"0",personalWebsiteURL:null,twitterURL:null,linkedinURL:null,institution:{name:"SRM Institute of Science and Technology",institutionURL:null,country:{name:"India"}}},booksEdited:[],chaptersAuthored:[{title:"Strengthening Regional Capacities for Providing Remote Sensing Decision Support in Drylands in the Context of Climate Variability and Change",slug:"strengthening-regional-capacities-for-providing-remote-sensing-decision-support-in-drylands-in-the-c",abstract:null,signatures:"Humberto A. Barbosa and T. V. Lakshmi Kumar",authors:[{id:"66233",title:"Prof.",name:"Humberto",surname:"Barbosa",fullName:"Humberto Barbosa",slug:"humberto-barbosa",email:"barbosa33@gmail.com"},{id:"75701",title:"Dr.",name:"T. V. Lakshmi",surname:"Kumar",fullName:"T. V. Lakshmi Kumar",slug:"t.-v.-lakshmi-kumar",email:"lkumarap@hotmail.com"}],book:{title:"International Perspectives on Global Environmental Change",slug:"international-perspectives-on-global-environmental-change",productType:{id:"1",title:"Edited Volume"}}},{title:"Validation of Satellite (TMPA and IMERG) Rainfall Products with the IMD Gridded Data Sets over Monsoon Core Region of India",slug:"validation-of-satellite-tmpa-and-imerg-rainfall-products-with-the-imd-gridded-data-sets-over-monsoon",abstract:"This work presents the validation of satellite (TMPA and IMERG) rainfall products against the India Meteorological Department (IMD) gridded data sets (0.25° × 0.25°) of dense network of rain gauges distributed over the monsoon core region of India. The validation uses the data sets covering the 20 years (1998–2017) and detects the time series bias; inter annual variations and Intra Seasonal Oscillations (ISO). The bias in the two data sets is found to be very less over the core region compared to whole India. The correlation between daily rainfall IMD and satellite is found to be +0.88 which is of 99% confidence level. The dominant periodicities in the rainfall patterns of IMD and satellite are Madden Julie Oscillation (30–60 days) and local oscillations (less than 20 days) are conspicuous and the normalized power varies from year to year. During the El Niño and La Niña years, the normalized power of rainfall pattern is low and high in satellite data sets which infer the suppressed and strongest activity of MJO over Indian Ocean that modulates the rainfall pattern over India.",signatures:"Tumuluru Venkata Lakshmi Kumar, Humberto Alves Barbosa, Manoj Kumar Thakur and Franklin Paredes-Trejo",authors:[{id:"66233",title:"Prof.",name:"Humberto",surname:"Barbosa",fullName:"Humberto Barbosa",slug:"humberto-barbosa",email:"barbosa33@gmail.com"},{id:"75701",title:"Dr.",name:"T. V. Lakshmi",surname:"Kumar",fullName:"T. V. Lakshmi Kumar",slug:"t.-v.-lakshmi-kumar",email:"lkumarap@hotmail.com"},{id:"291246",title:"Dr.",name:"Manoj",surname:"Kumar Thakur",fullName:"Manoj Kumar Thakur",slug:"manoj-kumar-thakur",email:"thakurmanoj2003@yahoo.com"},{id:"291318",title:"Dr.",name:"Franklin",surname:"Paredes",fullName:"Franklin Paredes",slug:"franklin-paredes",email:"franklinparedes75@gmail.com"}],book:{title:"Satellite Information Classification and Interpretation",slug:"satellite-information-classification-and-interpretation",productType:{id:"1",title:"Edited Volume"}}},{title:"Assessment of the CHIRPS-Based Satellite Precipitation Estimates",slug:"assessment-of-the-chirps-based-satellite-precipitation-estimates",abstract:"At present, satellite rainfall products, such as the Climate Hazards Group InfraRed Precipitation with Stations (CHIRPS) product, have become an alternative source of rainfall data for regions where rain gauge stations are sparse, e.g., Northeast Brazil (NEB). In this study, continuous scores (i.e., Pearson’s correlation coefficient, R; percentage bias, PBIAS; and unbiased root mean square error, ubRMSE) and categorical scores (i.e., probability of detection, POD; false alarm ratio, FAR; and threat score, TS) were used to assess the CHIRPS rainfall estimates against ground-based observations on a pixel-to-station basis, during 01 January 1981 to 30 June 2019 over NEB. Results showed that CHIRPS exhibits better performance in inland regions (R, PBIAS, and ubRMSE median: 0.51, −3.71%, and 9.20 mm/day; POD, FAR, and TS median: 0.59, 0.44, and 0.40, respectively) than near the coast (R, PBIAS, and ubRMSE median: 0.36, −5.66%, and 12.43 mm/day; POD, FAR, and TS median: 0.32, 0.42, and 0.26, respectively). It shows better performance in the wettest months (i.e., DJF) than in the driest months (i.e., JJA) and is sensitive to both the warm-top stratiform cloud systems and the sub-cloud evaporation processes. Overall, the CHIRPS rainfall data set could be used for some operational purposes in NEB.",signatures:"Franklin Paredes-Trejo, Humberto Alves Barbosa, Tumuluru Venkata Lakshmi Kumar, Manoj Kumar Thakur and Catarina de Oliveira Buriti",authors:[{id:"66233",title:"Prof.",name:"Humberto",surname:"Barbosa",fullName:"Humberto Barbosa",slug:"humberto-barbosa",email:"barbosa33@gmail.com"},{id:"75701",title:"Dr.",name:"T. V. Lakshmi",surname:"Kumar",fullName:"T. V. Lakshmi Kumar",slug:"t.-v.-lakshmi-kumar",email:"lkumarap@hotmail.com"},{id:"291246",title:"Dr.",name:"Manoj",surname:"Kumar Thakur",fullName:"Manoj Kumar Thakur",slug:"manoj-kumar-thakur",email:"thakurmanoj2003@yahoo.com"},{id:"291318",title:"Dr.",name:"Franklin",surname:"Paredes",fullName:"Franklin Paredes",slug:"franklin-paredes",email:"franklinparedes75@gmail.com"},{id:"318058",title:"Dr.",name:"Catarina",surname:"Buriti",fullName:"Catarina Buriti",slug:"catarina-buriti",email:"catarina.buriti@insa.gov.br"}],book:{title:"Inland Waters",slug:"inland-waters-dynamics-and-ecology",productType:{id:"1",title:"Edited Volume"}}}],collaborators:[{id:"54554",title:"Dr.",name:"Rajan",surname:"Patil",slug:"rajan-patil",fullName:"Rajan Patil",position:"Asst Professor",profilePictureURL:"https://mts.intechopen.com/storage/users/54554/images/332_n.jpg",biography:"Dr. Rajan R Patil is an epidemiologist, currently working as Asst Professor at SRM University at Chennai, India. He has a wide experience in public health research across northern and southern states of India. His core areas of research work include Vaccination Policy, Vector borne diseases and Occupational/Environmental health, Climate change and health Vaccine preventable diseases, Zoonotic diseases, Respiratory Health. He has over 60 publications to his credit including reputed\nInternational and national peer reviewed medical journals. He has served as consultant to UN agencies like UNDP-WHO in setting up Epidemic diseases surveillance systems in eastern Indian states of Orissa and Bihar. He is part of different national professional networks and is actively associated with various movements related to health. Has strong conviction that science and activism complement each other in evolving innovative and effective public health interventions",institutionString:null,institution:null},{id:"66656",title:"Dr.",name:"Maria Teresa",surname:"Alberdi",slug:"maria-teresa-alberdi",fullName:"Maria Teresa Alberdi",position:null,profilePictureURL:"//cdnintech.com/web/frontend/www/assets/author.svg",biography:null,institutionString:null,institution:{name:"Museo Nacional de Ciencias Naturales",institutionURL:null,country:{name:"Spain"}}},{id:"68580",title:"Dr.",name:"Hong",surname:"Ao",slug:"hong-ao",fullName:"Hong Ao",position:null,profilePictureURL:"//cdnintech.com/web/frontend/www/assets/author.svg",biography:null,institutionString:null,institution:null},{id:"69075",title:"Dr.",name:"Ali",surname:"Nefzaoui",slug:"ali-nefzaoui",fullName:"Ali Nefzaoui",position:null,profilePictureURL:"//cdnintech.com/web/frontend/www/assets/author.svg",biography:null,institutionString:null,institution:null},{id:"69747",title:"Dr.",name:"Cino",surname:"Pertoldi",slug:"cino-pertoldi",fullName:"Cino Pertoldi",position:null,profilePictureURL:"//cdnintech.com/web/frontend/www/assets/author.svg",biography:null,institutionString:null,institution:{name:"Aarhus University",institutionURL:null,country:{name:"Denmark"}}},{id:"75966",title:"Dr.",name:"Diogenes",surname:"Alves",slug:"diogenes-alves",fullName:"Diogenes Alves",position:null,profilePictureURL:"//cdnintech.com/web/frontend/www/assets/author.svg",biography:"Senior Researcher, Earth Observation Branch, National Space Research Institute (INPE); lecturer, remote sensing and earth system science post-graduate programs, INPE. Main areas of interest: land cover change, land use change, Amazonian deforestation, political ecology. Served as Manager, INPE Amazonian Deforestation Assessment Project (1990s); IPCC WG1 author (SAR); member, IGBP/IHDP LUCC project Scientific Steering Committee; member, Large-Scale Biosphere-Atmosphere Experiment on the Amazon International Scientific Committee.",institutionString:null,institution:{name:"National Institute for Space Research",institutionURL:null,country:{name:"Brazil"}}},{id:"76978",title:"Dr.",name:"Habib",surname:"Ketata",slug:"habib-ketata",fullName:"Habib Ketata",position:null,profilePictureURL:"//cdnintech.com/web/frontend/www/assets/author.svg",biography:null,institutionString:null,institution:null},{id:"76979",title:"Dr",name:"Mohammed",surname:"El Mourid",slug:"mohammed-el-mourid",fullName:"Mohammed El Mourid",position:null,profilePictureURL:"//cdnintech.com/web/frontend/www/assets/author.svg",biography:null,institutionString:null,institution:null},{id:"77302",title:"Dr.",name:"Lars",surname:"Bach",slug:"lars-bach",fullName:"Lars Bach",position:null,profilePictureURL:"//cdnintech.com/web/frontend/www/assets/author.svg",biography:null,institutionString:null,institution:{name:"Aarhus University",institutionURL:null,country:{name:"Denmark"}}},{id:"119133",title:"Dr.",name:"Guoqiao",surname:"Xiao",slug:"guoqiao-xiao",fullName:"Guoqiao Xiao",position:null,profilePictureURL:"//cdnintech.com/web/frontend/www/assets/author.svg",biography:null,institutionString:null,institution:{name:"China University of Geosciences",institutionURL:null,country:{name:"China"}}}]},generic:{page:{slug:"OA-publishing-fees",title:"Open Access Publishing Fees",intro:"
The Open Access model is applied to all of our publications and is designed to eliminate subscriptions and pay-per-view fees. This approach ensures free, immediate access to full text versions of your research.
As a gold Open Access publisher, an Open Access Publishing Fee is payable on acceptance following peer review of the manuscript. In return, we provide high quality publishing services and exclusive benefits for all contributors. IntechOpen is the trusted publishing partner of over 128,000 international scientists and researchers.
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10,000 GBP Monograph - Long Form
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Services included are:
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English language copyediting and proofreading, including the correction of grammatical, spelling, and other common errors
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XML Typesetting and pagination - web (PDF, HTML) and print files preparation
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Discoverability - electronic citation and linking via DOI
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Permanent and unrestricted online access to your work
What isn't covered by the Open Access Publishing Fee?
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If your manuscript:
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\\n\\t
Exceeds 20 pages (for chapters in Edited Volumes), an additional fee of 40 GBP per page will be required
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If a manuscript requires Heavy Editing or Language Polishing, this will incur additional fees.
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\\n\\n
Your Author Service Manager will inform you of any items not covered by the OAPF and provide exact information regarding those additional costs before proceeding.
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Open Access Funding
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To explore funding opportunities and learn more about how you can finance your IntechOpen publication, go to our Open Access Funding page. IntechOpen offers expert assistance to all of its Authors. We can support you in approaching funding bodies and institutions in relation to publishing fees by providing information about compliance with the Open Access policies of your funder or institution. We can also assist with communicating the benefits of Open Access in order to support and strengthen your funding request and provide personal guidance through your application process. You can contact us at oapf@intechopen.com for further details or assistance.
\\n\\n
For Authors who are still unable to obtain funding from their institutions or research funding bodies for individual projects, IntechOpen does offer the possibility of applying for a Waiver to offset some or all processing feed. Details regarding our Waiver Policy can be found here.
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Added Value of Publishing with IntechOpen
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Choosing to publish with IntechOpen ensures the following benefits:
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\\n\\t
Indexing and listing across major repositories, see details ...
\\n\\t
Long-term archiving
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Visibility on the world's strongest OA platform
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Live Performance Metrics to track readership and the impact of your chapter
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Dissemination and Promotion
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Benefits of Publishing with IntechOpen
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Proven world leader in Open Access book publishing with over 10 years experience
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+5,200 OA books published
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Most competitive prices in the market
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Fully compliant with OA funding requirements
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Optimized processes, enabling publication between 8 and 12 months
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Personal support during every step of the publication process
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+146,270 citations in Web of Science databases
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Currently strongest OA platform with over 150 million downloads
As a gold Open Access publisher, an Open Access Publishing Fee is payable on acceptance following peer review of the manuscript. In return, we provide high quality publishing services and exclusive benefits for all contributors. IntechOpen is the trusted publishing partner of over 128,000 international scientists and researchers.
\n\n
The Open Access Publishing Fee (OAPF) is payable only after your full chapter, monograph or Compacts monograph is accepted for publication.
\n\n
OAPF Publishing Options
\n\n
\n\t
1,400 GBP Chapter - Edited Volume
\n\t
10,000 GBP Monograph - Long Form
\n\t
4,000 GBP Compacts Monograph - Short Form
\n
\n\n
*These prices do not include Value-Added Tax (VAT). Residents of European Union countries need to add VAT based on the specific rate in their country of residence. Institutions and companies registered as VAT taxable entities in their own EU member state will not pay VAT as long as provision of the VAT registration number is made during the application process. This is made possible by the EU reverse charge method.
\n\n
Services included are:
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An online manuscript tracking system to facilitate your work
\n\t
Personal contact and support throughout the publishing process from your dedicated Author Service Manager
\n\t
Assurance that your manuscript meets the highest publishing standards
\n\t
English language copyediting and proofreading, including the correction of grammatical, spelling, and other common errors
\n\t
XML Typesetting and pagination - web (PDF, HTML) and print files preparation
\n\t
Discoverability - electronic citation and linking via DOI
\n\t
Permanent and unrestricted online access to your work
What isn't covered by the Open Access Publishing Fee?
\n\n
If your manuscript:
\n\n
\n\t
Exceeds 20 pages (for chapters in Edited Volumes), an additional fee of 40 GBP per page will be required
\n\t
If a manuscript requires Heavy Editing or Language Polishing, this will incur additional fees.
\n
\n\n
Your Author Service Manager will inform you of any items not covered by the OAPF and provide exact information regarding those additional costs before proceeding.
\n\n
Open Access Funding
\n\n
To explore funding opportunities and learn more about how you can finance your IntechOpen publication, go to our Open Access Funding page. IntechOpen offers expert assistance to all of its Authors. We can support you in approaching funding bodies and institutions in relation to publishing fees by providing information about compliance with the Open Access policies of your funder or institution. We can also assist with communicating the benefits of Open Access in order to support and strengthen your funding request and provide personal guidance through your application process. You can contact us at oapf@intechopen.com for further details or assistance.
\n\n
For Authors who are still unable to obtain funding from their institutions or research funding bodies for individual projects, IntechOpen does offer the possibility of applying for a Waiver to offset some or all processing feed. Details regarding our Waiver Policy can be found here.
\n\n
Added Value of Publishing with IntechOpen
\n\n
Choosing to publish with IntechOpen ensures the following benefits:
\n\n
\n\t
Indexing and listing across major repositories, see details ...
\n\t
Long-term archiving
\n\t
Visibility on the world's strongest OA platform
\n\t
Live Performance Metrics to track readership and the impact of your chapter
\n\t
Dissemination and Promotion
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Benefits of Publishing with IntechOpen
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Proven world leader in Open Access book publishing with over 10 years experience
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+5,200 OA books published
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Most competitive prices in the market
\n\t
Fully compliant with OA funding requirements
\n\t
Optimized processes, enabling publication between 8 and 12 months
\n\t
Personal support during every step of the publication process
\n\t
+146,270 citations in Web of Science databases
\n\t
Currently strongest OA platform with over 150 million downloads
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I am also a member of the team in charge for the supervision of Ph.D. students in the fields of development of silicon based planar waveguide sensor devices, study of inelastic electron tunnelling in planar tunnelling nanostructures for sensing applications and development of organotellurium(IV) compounds for semiconductor applications. I am a specialist in data analysis techniques and nanosurface structure. 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