The exponents of formula (3).
\\n\\n
Released this past November, the list is based on data collected from the Web of Science and highlights some of the world’s most influential scientific minds by naming the researchers whose publications over the previous decade have included a high number of Highly Cited Papers placing them among the top 1% most-cited.
\\n\\nWe wish to congratulate all of the researchers named and especially our authors on this amazing accomplishment! We are happy and proud to share in their success!
\\n"}]',published:!0,mainMedia:null},components:[{type:"htmlEditorComponent",content:'IntechOpen is proud to announce that 179 of our authors have made the Clarivate™ Highly Cited Researchers List for 2020, ranking them among the top 1% most-cited.
\n\nThroughout the years, the list has named a total of 252 IntechOpen authors as Highly Cited. Of those researchers, 69 have been featured on the list multiple times.
\n\n\n\nReleased this past November, the list is based on data collected from the Web of Science and highlights some of the world’s most influential scientific minds by naming the researchers whose publications over the previous decade have included a high number of Highly Cited Papers placing them among the top 1% most-cited.
\n\nWe wish to congratulate all of the researchers named and especially our authors on this amazing accomplishment! We are happy and proud to share in their success!
\n'}],latestNews:[{slug:"stanford-university-identifies-top-2-scientists-over-1-000-are-intechopen-authors-and-editors-20210122",title:"Stanford University Identifies Top 2% Scientists, Over 1,000 are IntechOpen Authors and Editors"},{slug:"intechopen-authors-included-in-the-highly-cited-researchers-list-for-2020-20210121",title:"IntechOpen Authors Included in the Highly Cited Researchers List for 2020"},{slug:"intechopen-maintains-position-as-the-world-s-largest-oa-book-publisher-20201218",title:"IntechOpen Maintains Position as the World’s Largest OA Book Publisher"},{slug:"all-intechopen-books-available-on-perlego-20201215",title:"All IntechOpen Books Available on Perlego"},{slug:"oiv-awards-recognizes-intechopen-s-editors-20201127",title:"OIV Awards Recognizes IntechOpen's Editors"},{slug:"intechopen-joins-crossref-s-initiative-for-open-abstracts-i4oa-to-boost-the-discovery-of-research-20201005",title:"IntechOpen joins Crossref's Initiative for Open Abstracts (I4OA) to Boost the Discovery of Research"},{slug:"intechopen-hits-milestone-5-000-open-access-books-published-20200908",title:"IntechOpen hits milestone: 5,000 Open Access books published!"},{slug:"intechopen-books-hosted-on-the-mathworks-book-program-20200819",title:"IntechOpen Books Hosted on the MathWorks Book Program"}]},book:{item:{type:"book",id:"463",leadTitle:null,fullTitle:"A Comprehensive Book on Autism Spectrum Disorders",title:"A Comprehensive Book on Autism Spectrum Disorders",subtitle:null,reviewType:"peer-reviewed",abstract:'The aim of the book is to serve for clinical, practical, basic and scholarly practices. In twentyfive chapters it covers the most important topics related to Autism Spectrum Disorders in the efficient way and aims to be useful for health professionals in training or clinicians seeking an update. Different people with autism can have very different symptoms. Autism is considered to be a "spectrum" disorder, a group of disorders with similar features. Some people may experience merely mild disturbances, while the others have very serious symptoms. This book is aimed to be used as a textbook for child and adolescent psychiatry fellowship training and will serve as a reference for practicing psychologists, child and adolescent psychiatrists, general psychiatrists, pediatricians, child neurologists, nurses, social workers and family physicians. A free access to the full-text electronic version of the book via Intech reading platform at http://www.intechweb.org is a great bonus.',isbn:null,printIsbn:"978-953-307-494-8",pdfIsbn:"978-953-51-4434-2",doi:"10.5772/975",price:139,priceEur:155,priceUsd:179,slug:"a-comprehensive-book-on-autism-spectrum-disorders",numberOfPages:490,isOpenForSubmission:!1,isInWos:1,hash:null,bookSignature:"Mohammad-Reza Mohammadi",publishedDate:"September 15th 2011",coverURL:"https://cdn.intechopen.com/books/images_new/463.jpg",numberOfDownloads:113886,numberOfWosCitations:19,numberOfCrossrefCitations:39,numberOfDimensionsCitations:128,hasAltmetrics:1,numberOfTotalCitations:186,isAvailableForWebshopOrdering:!0,dateEndFirstStepPublish:"October 20th 2010",dateEndSecondStepPublish:"November 17th 2010",dateEndThirdStepPublish:"March 24th 2011",dateEndFourthStepPublish:"April 23rd 2011",dateEndFifthStepPublish:"June 22nd 2011",currentStepOfPublishingProcess:5,indexedIn:"1,2,3,4,5,6,8",editedByType:"Edited by",kuFlag:!1,editors:[{id:"62755",title:"Dr.",name:"Mohammad-Reza",middleName:null,surname:"Mohammadi",slug:"mohammad-reza-mohammadi",fullName:"Mohammad-Reza Mohammadi",profilePictureURL:"https://mts.intechopen.com/storage/users/62755/images/1662_n.jpg",biography:"Professor Mohammad-Reza Mohammadi works as a child and adolescent psychiatrist at Tehran University of Medical Sciences (TUMS), and is the chair of Psychiatry and Psychology Research Centre of Iran. 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Kumavath",coverURL:"https://cdn.intechopen.com/books/images_new/5867.jpg",editedByType:"Edited by",editors:[{id:"163692",title:"Dr.",name:"Ranjith",surname:"Kumavath",slug:"ranjith-kumavath",fullName:"Ranjith Kumavath"}],productType:{id:"1",chapterContentType:"chapter",authoredCaption:"Edited by"}},{type:"book",id:"554",title:"Bacterial Artificial Chromosomes",subtitle:null,isOpenForSubmission:!1,hash:"3092adcfb46acf538c9ef38530f92d8f",slug:"bacterial-artificial-chromosomes",bookSignature:"Pradeep Chatterjee",coverURL:"https://cdn.intechopen.com/books/images_new/554.jpg",editedByType:"Edited by",editors:[{id:"91537",title:"Dr.",name:"Pradeep",surname:"Chatterjee",slug:"pradeep-chatterjee",fullName:"Pradeep Chatterjee"}],productType:{id:"1",chapterContentType:"chapter",authoredCaption:"Edited by"}},{type:"book",id:"6764",title:"Cyanobacteria",subtitle:null,isOpenForSubmission:!1,hash:"87c7d8f86f7c1185aa4dd47c6492951a",slug:"cyanobacteria",bookSignature:"Archana Tiwari",coverURL:"https://cdn.intechopen.com/books/images_new/6764.jpg",editedByType:"Edited by",editors:[{id:"186791",title:"Dr.",name:"Archana",surname:"Tiwari",slug:"archana-tiwari",fullName:"Archana Tiwari"}],productType:{id:"1",chapterContentType:"chapter",authoredCaption:"Edited by"}}]},chapter:{item:{type:"chapter",id:"67845",title:"Abortions in First Trimester Pregnancy, Management, Treatment",doi:"10.5772/intechopen.86194",slug:"abortions-in-first-trimester-pregnancy-management-treatment",body:'\nSpontaneous abortions are considered as one of the most common complications in pregnancy. Abortion is defined as the ejection of the fetus until the 20th week and is clinically classified based on ultrasound evaluation. Threatened abortion is usually accompanied by vaginal bleeding without affecting the pregnancy. Incomplete miscarriage is described as incomplete passage of conception products. Complete, when all pregnancy products are spontaneously aborted. Septic abortion when endometrial infection coexists. Finally, recurrent abortions that are defined when three consecutive abortions occur before 20th weeks of gestation [1, 2, 3, 4, 5].
\nMore than 80% of miscarriages occur up to 12 weeks. The percentage of clinically recognized abortions (appeared after 6th week) is estimated to be 12–15%. More analytically, 2 miscarriages occurred in 5% of women and ≥3 miscarriages in 1–3% of women [1, 2, 3, 4, 5]. Recurrent miscarriages consist of a serious problem for women with physical and psychological consequences. Abortions and especially recurrent miscarriages are considered as heterogeneous groups in regard to etiology [1, 2, 3, 4, 5]. Two or more causes can coexist, whereas about 50% of cases are characterized as idiopathic as a result of genetic, anatomical, endocrine, genetic, anatomical, endocrine, autoimmune factors or infections exclusion [1, 2, 3, 4, 5].
\nThe number of clinically recognized miscarriages to total number of pregnancies is about 10–15%, while the equivalent of early abortions based only on human chorionic gonadotropin (hCG) measurements is actually much higher (50–60%) and interestingly before and after the implantation it is 30% but are not perceived [1, 6, 7, 8, 9, 10].
\nA positive correlation has been identified between the mother’s biological age and the incidence rate of spontaneous abortions. So, a progressive increase of 10-fold afterwards the age of 40 is observed compared to younger women aged <35 years [1, 6, 7, 8, 9, 10].
\nRegarding the gestational age in first trimester and the abortion risk, this counts to 4 and 2%, respectively, in 6th and 8th week of gestation [1, 6, 7, 8, 9, 10]. The risk of recurrence in the next pregnancy is minor except of cases diagnosed with congenital uterine abnormalities [1, 6, 7, 8, 9, 10].
\nRecurrent miscarriages are defined as three or more consecutive embryos losses weighing under 500 g. According to bibliography we can find different definitions for miscarriages [1, 11, 12]: two or more miscarriages of clinical pregnancies [7]; three or more miscarriages of the first trimester or one or more miscarriages of the second trimester; three or more miscarriages <14 weeks [1, 11, 12]. Frequency appearance is of quite large (1 in every 300 pregnancies).
\nRecurrent miscarriages (frequency 1–3% among couples of reproductive age) usually occur during the first trimester and relative risk increases with the number of previous miscarriages [1, 11, 12]. Consequently, after the first miscarriage, this risk reaches 24%, after the second one to 26% and after the third it amounts to 32% [1, 11, 12]. About 10–15% of all clinical recognized pregnancies are aborted and the theoretical risk for three consecutive pregnancy losses is 0.34% [1, 11, 12].
\nReceiving history includes:
the gestational age of spontaneous abortions
the certification in the presence of embryonic pole and heart function
the symptoms related to the antiphospholipid syndrome and family history of automatic abortions
The possibility to predict the risk of recurrence depends on several factors like as maternal age, fetal parental karyotypes gestational age, presence of various maternal laboratory findings [1, 11, 12].
\nAbout 80% of abortions occur during the first trimester, 50–60% of them are based on genetic abnormalities. The risk of pregnancy loss is 2–5% after the recognition of heart function, 5% for women who report two miscarriages and finally 1% of women mentioning more than three miscarriages [1, 11, 12].
\nInvestigation of recurrent pregnancy loss (RPL) begins with personal history, followed by laboratory, genetic, hormonal, anatomic, immunologic, thrombophilic factors and infective reasons that can affect pregnancy outcome. It is quite often that 2 or more factors coexist [11, 12, 13, 14, 15, 16, 17, 18, 19, 20]. In half of cases, etiology cannot be identified, so it is described as “Recurrent miscarriages of unknown etiology” [1, 11, 16].
\nDuring the clinical examination, a gynecological examination and a check for hyperandrogenemia and hyperprolactinemia signs should be done [1, 17].
\nA laboratory control includes:
Karyotype in couple
Hysteroscopy or hysterosalpingography (HSG)
Anticardiolipins and LA
Control of progesterone levels in the middle of the luteal phase cycle
Check the levels of FSH,LH,PRL and testosterone (2–5th day of period)
TVS (transvaginal ultrasound) [1, 13, 14, 15, 16, 17, 18, 19, 20].
It is of great importance in thrombophilia examinations control to include V Leiden factor and prothrombin 20210 mutation [1, 15, 16, 17, 18, 19, 20].
\nAnatomical abnormalities that can cause miscarriages are typically recognized using hydrosonohysterography (HSG), hysteroscopy, laparoscopy, possible in same cases magnetic resonance and recently three-dimensional ultrasonography.
\nCongenital anomalies malformations of the female reproductive tract uterine anatomical abnormalities, such as bicornuate uterus or uterine diaphragm, polyps, heart-shaped ultrasound fibroids are results from failure completion of bilateral duct elongation, fusion, septal resorption of müllerian ducts [13, 14, 15].
\nEspecially with regard to fibroids, they may block the development of early pregnancy, but their influence on spontaneous abortions is also affected by other factors such as age and hormonal disorders. Müllerian anomalies occurred in 8–10% of women, who had three or more consecutive spontaneous abortions. The fibromuscular tissue in septate uterus is poorly vascularized fibromuscular tissue that is associated with the highest pregnancy loss rate in some studies reporting an average of 65%. Except the above-mentioned abnormality, high frequency for pregnancy loss is noticed in didelphys, bicornuate and unicornuate uterus [13, 14, 15].
\nIntrauterine adhesions (Asherman syndrome) are acquired uterine defect resulting from infection, endometritis and unsuccessful curettage, which is associated with recurrent miscarriage, oligomenorrhea and amenorrhea and bad prognosis. Recommended treatment in these cases includes balloon catheter, administration of estrogen and progestin medication [1, 16, 17, 18].
\nUterine cavity abnormalities including submucosal, intramural >40 myomas, polyps are associated to poorly vascularization of endometrium led to failure of implantation, placenta tissue development and contribute to pregnancy loss. Cervical insufficiency is described as an acquired uterine anomaly, which is depending in painless cervical dilatation, effacement and inability of the uterine cervix to retain the amniosac is the commonest reason for abortion in the second trimester [16, 17, 18]. Exposure of the embryo in diethylstilbestrol DES and a variety of environmental factors like thalidomide, infectious agents and ionizing radiation affects the uterine morphology by triggering changes in both the location and amount of HOXA/Hoxa expression in the development of Müllerian ducts. No prospective studies exist. The HOXA genes along the Müllerian ducts, influencing the development of Müllerian ducts are: HOXA9 Oviduct, HOXA10, HOXA11 Uterus, HOXA11, HOXA13 Cervix and HOXA13 Upper vagina [1, 19, 20, 21].
\nGenetics reasons of recurrent pregnancy loss be subdivided in embryo abnormalities resulting of known parental genetic pathology and embryo aneuploidy in parents to be chromosomally normal A variety of genetic factors including aneuploidy (gain or loss of a chromosomal), chromosomal imbalance resulting from harbored translocations, inversions, deletions, duplications within chromosomes, single gene mutations led to recurrent pregnancy loss (RPL) [1, 22, 23, 24, 25, 26, 27, 28, 29, 30, 31, 32, 33]. In 3–5% of couples with RPL, the ratio of parental chromosome abnormalities in contrast to the general population is 0.7%. The most common chromosomal abnormalities leading to RPL are balanced translocations. The first chromosomally abnormal abortion was reported in 1961. Chromosomal abnormality is approximately responsible for half of the clinically diagnosed abortions in the first trimester. About 50% of them are autosomal trisomy, 20% monosomy XO, 20% polyploidy and 10% variety of other abnormalities [33, 34, 35].
\n\n
Karyotype in couple
No need for molecular karyotype
No need for microdeletions control
About 25% of cases exist in the first trimester, in which although the embryos are normal and euploid, they cannot develop properly. The reasons include women with müllerian agenesis and other significant anatomic abnormalities. In the second trimester, the abortion incidence due to a chromosomal abnormality is <20%. Structural chromosome abnormalities (Robertson-type balancing and translocations).
X-inactivation chromosome (?)
aneuploidy of spermatozoa (?).
Recurrent abortion (RA) as well as repeated IVF failure (RIF) has a common underlying factor which is the significant increase in the rate of chromosomal abnormality [35]. The results also suggest that in women with recurrent abortions, the transfer of normal embryos improves the pregnancy rate and live-birth rate in both younger and older women. In these cases, preimplantation genetic diagnosis is recommended, testing for structural chromosomal aberrations like translocations, inversions, removing cells from the resultant embryo or oocyte evaluating the cells for genetic abnormalities and determine the optimal embryos for uterine transfer [35, 36, 37]. Last year, novel technologies like microarrays, fluorescence in situ hybridization and biopsy of embryo blastocyst are widely used [34, 35, 36].
\nWomen with RPL have reproductive difficulties because they are concerned about various toxins and agents within the environment. It is of great importance to counseling these couples in health care institutions to have current and accurate information and to avoid exposures to these substances [37, 38]. The rate of spontaneous abortion is positively associated to cigarette smoking, alcohol consumption, obesity, body mass index (BMI, weight in kilograms divided by square of height in meters) >30 kg/m2, caffeine intake (excess of 300 mg/day) and ionizing radiation [37, 38].
\nIn some case, a failure to activate a normal control mechanism to prevent an immune reaction against self is observed and this subsequently led to autoimmune response. Natural killer cells are attached to the cytotrophoblast of the embryo. However, the mechanism by which such cells may or may not affect the embryo is not proven. When implantation occurs, there is a slight inflammatory response. Patient with infertility and recurrent miscarriages develop less prominent reaction that may prevent the embryo from implanting [39, 40]. Autoimmune abortions are thought to be caused by the presence of autoantibodies that already exist in the woman against membrane phospholipids, thyroid antigens, nuclear antigens, syncytiotrophoblast cells or against other organelles or tissues [39, 40].
\nAbout 10–15% of all women have antinuclear antibodies regardless of medical history of RPL. In cases of presence of antinuclear antibodies, the possibility of successful pregnancy outcome is independent of antibodies existence [39, 40].
\nAutoimmune factors causing RPL are: antiphospholipid antibody syndrome, aPL antibodies (anticardiolipin antibodies and lupus anticoagulant), ß2 glycoprotein antibodies, phosphatidyl serine. Antibody hemeostasis in systemic circulation is different between men and women, just because women need to be better equipped, so that they can cope with the required immune tolerance in fetal antigens derived from them [39, 40].
\nThe “thermostat” is therefore positioned higher in women, as a result, autoimmune diseases have much higher incidence in women. If autoantibodies are found in relation to a pathological condition, this means: whether they are the pathogenetic factors of the disease (autoimmune hemolytic anemia); whether it is the result of a previous pathological process (autoantibodies against cardiac muscle after its destruction) and whether they are causative agents without damaging themselves, which is the most common, as is believed [40, 41].
\nIf the antibodies are present in the mother’s serum as a result of allogeneic stimulation during pregnancy, then they are not considered to be autoantibodies unless they exist previously [40, 41]. Until now, there is no common point of the effect of pregnancy on the production of autoantibodies. Although no clear increase in autoantibodies has been found during normal pregnancy, an increase in some of them has been reported in pathological pregnancies, most of which have been described as antiphospholipid antibodies [40, 41]. In the group of recurrent miscarriages, 15% were certified positive findings for the lupus anticoagulant or antiphospholipid antibodies or both of them. It is important to notice that lupus anticoagulant is not synonymous with systemic lupus erythematosus (SLE), where it is found in only 5–15% [40, 41].
\nAntiphospholipid antibodies (APAs) are a family of immunoglobulins which react with anions of phospholipids or anions of phospholipid-protein complexes in the cell membrane of the syncytiotrophoblast [1, 41, 42].
\nThe finding of aPL antibodies is associated to adverse pregnancy outcomes such inducing vessel thrombosis of the surrounding placental maternal unit, placenta infarction, and fetal death. The primary mechanism in the first trimester depends on a deleterious effect directly on trophoblastic cells, inhibition of secretion of human placental chorionic gonadotropin, and the expression of trophoblast cell adhesion molecules (a1, a5 integrins, E, VE-cadherins). The most widely used are anti-cardiolipin (diphosphatidyl-glycerol) [1, 41, 42].
\nOthers are anti-phosphatidylserine anti-phosphatidylethanolamine, anti-phosphatidylcholine, anti-phosphatidylinositol, and phosphatidic acid. Large variation in APHA measurements between laboratories and in the same laboratory for the same patient and great fluctuation in the values during pregnancy are observed.
\nIt is questionable whether the same or other substnces (anti-β2-glycoprotein I) have similar impact according to recurrent pregnancy loss [42, 43, 44, 45].
\nPossible action of APAs on miscarriages:
\nAbnormalities in endothelial cell function of vessels (decrease in production of arachidonic acid prostacyclin and a relative increase of thromboxane which is a potent vasoconstrictor and promotes platelet aggregation).
\nObstructive angiopathy (reaction with anion phospholipids exposed after vessel damage).
\nPlatelet stimulation and/or adhesion (in damaged platelets, APAs bind phosphatidylserine to the structural element of the inner membrane of the platelets and promote platelet aggregation and thrombus formation).
\nPlacental infarction (microscopic arterial thrombosis and necrotic fibrous deposition have been found). It also appears to be due to reduced flow in the vessels, as has been found to occur in the umbilical and maternal arteries in patients with lupus or APS. This situation resembles a destruction of the vessels through antibodies after heart transplantation, coronary bypass, or angioplasty [42, 43, 44, 45].
\nInhibition of protein C stimulation in S. These two proteins, after their activation, inactivate clotting factors Va and VIIa. Stimulating their stimulation creates an increased tendency for coagulation.
\nReduction of levels of annexin V, a protein with potent antithrombotic effect on the surface between trophoblast and endothelial cells.
\nEffect on placental function: (ACA inhibits the secretion of gonadotropin secretion from placenta, which can act on the secretion of hormones from the placenta, negatively affecting the viability of the fetus).
\nPhospholipids bind to the surface of trophoblast, and this results in direct destruction of cells, inhibition of syncytia formation, decrease of hCG production and defective penetration into maternal peristalsis.
\nAntiphospholipid syndrome: high levels of antiphospholipid antibodies and history of miscarriages and/or endometrial death and/or thrombosis—risk of autoimmune in subsequent pregnancy ~90% [46, 47].
\nVascular thrombosis (one or more clinical episodes of venous, arterial, or small vessel thrombosis in any tissue or organ).
\nGestational complications (one or more recurrent miscarriages after the 10th week of gestation, one or more preterm births and one or more recurrent miscarriages before the 10th week of gestation).
\nLaboratory criteria: cardiolipin antibodies (IgG or IgM anti-cardiolipins, at moderate or high levels in two or more measurements over a period of at least 6 weeks between them).
\nLupus anticoagulant (in two or more measurements at least 6 weeks apart) [44, 45, 46, 47].
\nSteroids (complications: pregnancy and prematurity) are not recommend based on current publication evidence. It is reported that the maternal and fetal complications increase without affecting the pregnancy outcome and live births [43, 44, 45, 46, 47].
\nIt may prevent recycling in the circulation of cardiolipins or suspend the discharge of embryo toxic factors or factors associated with HLA. In addition, it lowers NK (CD56+/CD16+) cell percentage. It has been associated with pregnancy hypertension, diabetes mellitus, and mainly with premature labor and low-weight new-born babies. Aspirin should be given preconceptually. Aspirin in low dosage (80–100 mg daily) may suspend cyclooxygenase (COX) action on platelets, by suspending the composition of thromboxane thrombosis and thus preventing vascular thrombosis in placental blood vessels. At discontinuance after around 32 weeks, heparin (does not pass the placenta) should be started after the first positive pregnancy test and should be continued until of labor to avoid thrombosis risk: hypo-heparin, for example, heparin of low molecular weight, one injection daily. Anticoagulant action (reinforces the action of antithrombin III), while it may bind AFAs, thus prevents chorionic villus sampling (CVS) phospholipids from being destroyed, by assisting in the successful implantation in the early stages of pregnancy [43, 44, 45, 46, 47]. Thrombocytopenia and osteoporosis check-up. Discontinuation after 34 weeks of pregnancy and prior to giving birth. (Now in labor).
\nIt appears that combining aspirin and heparin has the best results. Patients should start taking heparin as early as possible when pregnant and continue until labor and during puerperium [42, 43, 44, 45, 46, 47, 48, 49, 50]. Combination of aspirin and heparin is associated with better results. Heparin subcutaneously, for example, low molecular weight heparin one injection per day may prevent recycling of circulating anti-cardiolipins or suppress the secretion of embryotoxic agents or HLA-related agents. It also reduces the percentage of NK (CD56+/CD16+) cells [46, 47, 48, 49, 50]. It has been associated with gestational hypertension and diabetes mellitus and mainly with premature labor and low birth weight neonates. Combination of aspirin with heparin, aspirin with prednisolone, or all three is associated to satisfactory results. It seems that the combination of aspirin and heparin works best. Heparin should be started as soon as possible in pregnancy and should be maintained until the labor and postpartum especially when the risk of thrombosis is high [42, 43, 44, 45, 46, 47, 48, 49, 50]. Intravenous immunoglobulin therapy IVIG (no superior to the combination of aspirin and heparin) Intravenous injection of high doses of gamma globulin (300–500 mg/kg body weight). An increase inT-immunosuppressive cells, decreases the activity of natural killer cells, inhibition of transport by the mother’s placenta of IgG, inhibition of Fc receptors in macrophages and, especially, multivalent immunosuppression. To avoid the adverse reactions of heparin therapy, it is recommended to add calcium 600 mg twice daily and vitamin D supplementation 400 IU daily to decrease the osteoporosis risk. The platelet count should be weekly examined in the first two weeks after treatment with heparin because bleeding could occur due to heparin induced thrombocytopenia [42, 43, 44, 45, 46, 47, 48, 49, 50].
\nMentioned here are polycystic ovary syndrome (PCOS) due to high levels of luteinizing hormone (LH), corpus luteum (CL) deficiency, nonregulated diabetes mellitus during conception period, thyroid malfunction, thrombophilic factors, alloimmunological factors: PCOS, menstrual complications, hypertrichosis, polycystic ovaries, and resistance to insulin. The contribution of endocrinological factor as reasons of RPL including luteal phase deficiency, untreated hypothyroidism, abnormal glucose metabolism hyperprolactinemia, and diminished ovarian reserve is average by 8–12% [51, 52, 53, 54].
\nCorpus luteum malfunction association with RPLs still remains a hypothesis, despite the fact that there are studies that reveal that it is responsible for 12–28% of cases. Luteal phase deficiency is defined as an inability of the corpus luteum to secrete progesterone either in increased satisfactory amounts or for too short duration. This inability to function is established by alteration of preovulatory estrogen stimulation, which led to poor oocyte quality and a poorly functioning corpus luteum. The diagnosis should be confirmed either with endometrial biopsy which is not recommended as diagnostic modality or if serum progesterone levels are <10 ng/ml [51, 52, 53, 54]. Strategy of treatments of corpus luteum malfunction has a wide variation and includes administration of progesterone or human chorionic gonadotropin induction or a combination of these. Progesterone administration either as intravaginal suppositories 50–100 mg or as intramuscular injections 50 mg IM is considered necessary only within RCTs [51, 52, 53, 54].
\nHyperprolactinemia is an endocrinopathy which led to infertility and abortions due to anovulation. It is not clear whether it is associated with RPLs. Increased prolactin levels interact with the hypothalamic pituitary ovarian axis, reducing the folliculogenesis or leading to a small duration of luteal phase. Studies reveal that it affects progesterone discharge at luteal stage; however, this situation has not been confirmed in humans. A randomized control trial including 64 hyperprolactinemic women with RPL treated with bromocriptine was associated with a higher rate of successful pregnancy, whereas PRL levels were significantly higher in women that miscarried (85.7 vs. 52.4%) [55, 56, 57, 58].
\nCurrently, there is no sufficient evidence for effectiveness of dopamine agonist evaluation in preventing future miscarriage in women with idiopathic hyperprolactinemia and a history of recurrent miscarriage [55, 56, 57].
\nWomen with nonregulated DM I: diabetes mellitus (DM) in women with RPLs is associated with a higher incidence of spontaneous abortions in relation to women with euglycemic metabolism preconceptually. A well controlled diabetes mellitus decreases the rates of recurrent pregnancy loss. Testing for fasting insulin and glucose and hemoglobin A1c usually have an increased modality for the evaluation of insulin resistance. The metformin administration seems to improve pregnancy outcome and is it safe in the first trimester [55, 56, 57].
\nIt is well known that hypothyroidism without therapy increases the risk of abortion. Treatment before attempting a pregnancy is clearly recommend as well as keeping a TSH level between 1.0–2.5 UIU/ml in the first trimester. In cases with TSH levels higher than 2.5 MIU/ml, levothyroxine should be started at a minimum dose of 50 μg/d.
\nAnti-thyroid Abs is associated with RPLs when detected before the start of pregnancy or at an early stage.
\nHypothyroidism is involved with obstetric complications like infertility, abortions, anemia, preeclampsia, placental abruption, fetal death, preterm birth, and low birth weight [55, 56, 57, 58].
\n\n
Elevated CD56+ lymphocyte levels
Increased NK cell levels in the secretory phase of endometrium
Higher levels in NK cells during the endometrium secretory phase. Strong association between maternal type Th2-cell immunity and successful pregnancy outcome. Recurrent abortions: associated with immunity type Th1 (lF-γ, TNF, lL-12, 58)
Increased levels of FSH in the early follicular phase of menstrual cycle are significant for diminished ovarian reserve. In the least years, another marker antimüllerian hormone is better to identify the number of follicular units for recruitment. It is recommended that women with RPL visit healthcare services to have appropriate counselling to treat endocrinological disorders [59].
\nPolycystic ovary syndrome (PCOS) is associated with increased frequency of RPL and has an uncertain prevalence, because factors associated with PCOS such as obesity, insulin resistance, LH rise, and hyperandrogenemia may be the reason and not PCOS as a whole [60, 61, 62, 63, 64, 65, 66, 67, 68]. The incidence of abortions in spontaneous ovulation is difficult to determine. Diagnostic criteria for this heterogeneous disorder have not been present in the past. Hypersecretion of LH and elevate androgen levels possibly led to RPL [60, 61, 62, 63, 64, 65, 66, 67, 68]. The association of excess androgens and RPL is not clear. The hyperinsulinemia in PCOS that is a consequence of insulin resistance involving plasminogen activator inhibitor-1(PAI-1) which inhibits plasminogen activation and subsequent fibrinolysis, has potential thromboembolic effect that makes women with PCOS in high risk for recurrent pregnancy loss [60, 61, 62, 63, 64, 65, 66, 67, 68].
\n\n
premature oocyte maturation
hyperandrogenemia may impact on oocytes
high androgens may affect endometrium
\n
\n\n
gene hoxa10 is thought to be essential for implantation.
the expression of this gene is decreased when testosterone is elevated.
Preimplantation environment is affected by decreasing:
expression of glycodelin—which inhibits endometrial immune response to the embryo and
IGF—binding protein-1, which facilitates adhesion progress at the fetomaternal interface. Plasma plasminogen activator inhibitor-1 concentrations are increased in hyperinsulinemia leading to hypofibrinolytic state and thrombophilia [60, 61, 62, 63, 64, 65, 66, 67, 68]
Plasminogen activator inhibitor gene (PAI-1) activity (i.e., hypofibrinolysis) is elevated in PCO.
\nMetformin reduces gene activity from 42.5 to 12.4 U/ml, that is, correct tendency for thrombosis which improves uteroplacental flow.
\nPAI-1 activity fell 44% in women with live births.
\nPAI-1 activity increased 19% in women with abortion.
\n\n
Decreased levels of androgen may improve endometrial function; IR resistance is decreased
Glycodelin and IGF-1 protein expression is corrected
Glycodelin inhibits endometrial immune response to the embryo
IGF-1 improves the adhesion process at the fetomaternal interface
Hypofibrinolytic activity is reduced by decreased PAI-1 activity (which induces hypofibrinolytic activity) [60, 61, 62, 63, 64, 65, 66, 67, 68].
\n
Obesity very probably implicated
Insulin resistance probably but may INDIRECTLY affect the parameters which are influenced by metformin
The role of LH needs to be elucidated
Endometrial factor probable
Oocyte factor probable
PAI-1 factor probable
Further prospective studies needed to elucidate the significance of these factors
Usually, women with PCOS require different treatments due to variety of reasons so we can use metformin, diet and infertility drugs. Therapeutic management combines normalization of weight and administration of metformin to reduce mainly the RPL rate [60, 61, 62, 63, 64, 65, 66, 67, 68].
\nAny infection with high fever can lead to miscarriage rubella virus, cytomegalovirus passing the placenta and affecting the fetus, malaria, mycoplasma, and trypanosomiasis.
\nSeveral studies have confirmed the role of infections as a cause of miscarriage especially in the second trimester of pregnancy; however, their role in the first trimester miscarriages remains unclear [69, 70, 71, 72, 73, 74].
\nToxic metabolic bio-products, endotoxins, exotoxins, or cytokines may have a direct effect on the uterus and the fetoplacental unit chronic endometrial infection following after lineal infection (M. hominis, Chlamydia, Ureaplasma urealyticum, and HSV) may affect the fetus implantation. Fetal infections are possible to cause fetal death or severe malformations incompatible with fetal livability (rubella, parvovirus B19, CMV, HSV, and syphilis). Placental infection probably causes placental deficiency with consequent fetal death. Amnionitis in the first trimester may have a similar effect on chorioamnionitis in the third trimester (causing premature labor). Various microorganisms with such effect, as L. monocytogenes, are suspected [69, 70, 71, 72, 73, 74].
\nMechanisms:
Embryotoxicity
Placental deficiency
Endometritis/endocervicitis
Amnionitis
Microorganisms: rubella, parvovirus B19, CMV, HSV, syphilis, Chlamydia, Mycoplasma, Ureaplasma, and various Gram-positive or Gram-negative bacteria (L. monocytogenes).
\nNone of the above-mentioned infectious agents are usually confirmed to lead to RPL. Each high fever infection may lead to pregnancy loss. Viruses such as rubella and cytomegalovirus infection (CMV) go through the placenta and affect the embryo, as well as lead to malaria, chlamydia, mycoplasma, and trypanosomiasis [69, 70, 71, 72, 73, 74].
\nQuite a few studies have confirmed that infections are to blame when it comes to miscarriages, especially during the second trimester of pregnancy; however, their role in the first trimester miscarriages remains unspecified.
\nNew techniques in molecular biology and genetics could recognize the importance of “locality” for mutations. Detection of new mutations in immunological and other molecules is involved in the pathophysiology of abortions. It is of great importance to immediately start appropriate antibiotic therapy based on a test of cure culture, when cervical and vaginal infections are identified and to extend the treatment for both parents [75, 76].
\nPregnancy is a condition that predisposes to hypercoagulation. The pregnant woman is in a state of increased tendency for coagulation (hypercoagulable state). The action of the fibrinolytic system decreases during pregnancy, particularly in the placenta, mainly due to an increase in inhibitors of the plasminogen activator [77, 78, 79, 80, 81, 82, 83, 84].
\nPregnancy and coagulation mechanisms include the following:\n
Increase of coagulation precursors (procoagulant factors)
Decrease in levels of physiologically existing anticoagulant factors (naturally occurring anticoagulants)
Reduction of fibrinogenolysis
“Modified” maternal response to hemostasis (‘disordered’ maternal hemostatic response) [77, 78, 79, 80, 81, 82, 83, 84]
Correlation not quite clear!
\nPregnancy is a state of hypercoagulation (hypercoagulable state). This hypercoagulable state do not necessarily causes thrombosis and the miscarriage is not due to thrombosis.and a lot of patients with miscarriages. This predisposition for thrombosis may lead to malfunction in the fetoplacental unit. A disorder in the balance between activators and inhibitors of plasminogen can lead to defective placentation [77, 78, 79, 80, 81, 82, 83, 84]. The infiltration of trophoblast in arcuate arteries is essential for implantation, placentation, and consequently a regular continuation of pregnancy. Defective penetration is a common pathological finding in placenta preparations by women with excretion and also preeclampsia or intrauterine fetal growth delay [77, 78, 79, 80, 81, 82, 83, 84].
\nPlacenta abnormalities include excessive implantation and placenta accreta.
\nIncreasing thrombophilic factors and five more frequent thrombophilic polymorphisms: a) V Leiden factor; b) MHTHFRC 677T; c) MTHFRA1298C; d) Factor VA1299H; and e) factor II G20210A are predisposition to venous thromboembolism (VTE). None of the five thrombophilic mutations, alone or in combination, was found to significantly increase the risk of miscarriages [77, 78, 79, 80, 81, 82, 83, 84].
\nV Leiden: women with RPLs and V Leiden mutation: there is no discrimination test for those who will have recurrent miscarriages from those that have a term pregnancy.
\nTreatment: prophylactic administration of heparin without the confirmation of RCT is prescribed for known mutations of the factor V Leiden and also for the cases that there is indication of placental thrombosis [77, 78, 79, 80, 81, 82, 83, 84].
\nC677T MTHFR polymorphism: previous studies have shown conflicting results between the MTHFR C677T genotype and the recurrent miscarriages.
\n5,10-methylentetrahydrofolate reductase catalyzes the conversion of 5,10-methylentetrahydrofolic acid to 5-methyltetrahydrofolic acid.
\n5-methyltetrahydrofolic acid takes part in the methylation of homocysteine in methionine.
\nSubstitution of a cytosine molecule by a thymine molecule at position 677 increases the incidence of homocysteine and thrombophilia.
\nThe reduced activity of MTHFR and hyperhomocysteinemia is clinically manifested when lack of folic acid coexists [77, 78, 79, 80, 81, 82, 83, 84].
\nTreatment: administration of 0.5–2 mg of folic acid leads to homocysteine normal levels [77, 78, 79, 80, 81, 82, 83, 84].
\nIncreased activity of PAI: genetic factors, metabolic disorders of insulin resistance syndrome, hypertension, smoking, etc.
\nPAI-1: the major physiological inhibitor of plasminogen activation plays a central role in fibrinolysis.
\nPAI-2: trophoblast and macrophages. Increased PAI activity has been linked to recurrent miscarriages.
\n4G polymorphism of PAI-1 gene is associated with high levels of PAI-1 and reduced fibrinolytic activity.
\nHomozygous for 4G has been complicated with preeclampsia, prematurity, IUGR, and placental ablation.
\n\n
low molecular weight heparin (LMWH)
heparin
LMWH vs. heparin
one injection per day
anti-Xa follow-up is not necessary
decreased risk of osteoporosis
reduced risk of thrombocytopenia
safe for the fetus as it does not pass the placenta
more likely outcome in obstetric complications [77, 78, 79, 80, 81, 82, 83, 84]
As mentioned before, decreased MTHFR activity and hyperhomocysteinemia are only obvious as long as there is folic acid deficiency. Substitution with folic acid prevents any phenotypic expression of C677T polymorphism.
\nPrediction for women with polymorphism who are going to have a spontaneous abortion [77, 78, 79, 80, 81, 82, 83, 84]:
\nTreatment: the administration of 0.5–2 mg folic acid reduces homocysteine levels to normal [77, 78, 79, 80, 81, 82, 83, 84].
\nHomocysteine: homocysteine is an amino acid formed as an intermediate of metabolism of methionine. Elevated blood levels of homocysteine (hyperhomocysteinemia) consist an important cardiovascular risk factor, which in recent years have significance similar to hypercholesterolemia [85, 86, 87, 88, 89, 90].
\nThe detection of women with congenital hyperthyroidism that have much more frequent complications in gestation has led to an investigation of the association between homocysteine and pregnancy complications associated with placental vascular lesions such as placental abruption, preeclampsia, abortions, fetal death, and restriction of intrauterine fetal growth. Hyperhomocysteinemia is also associated with spinal tube deficits due to folic acid insufficiency. The result that women with hyperhomocysteinemia of relative cause show complications much more frequently has led to the investigation of obstetric complications with homocysteine, which are relevant with vascular placental failure such as placental abruption, pre-eclampsia, recurrent miscarriages, stillbirth, and intrauterine growth restriction [85, 86, 87, 88, 89, 90].
\nMethionine consist of an important amino-acid that participates in cell growth and division by providing methyl groups in the biosynthesis of t-RNA, DNA, and proteins. Methionine constitutes a necessary amino acid that plays a crucial role in cellular increase and division by providing methyl groups to t-RNA, DNA, and protein biosynthesis. Homocysteine is synthesized after a methyl group transposition from methionine. The 50% could be catalyzed with a sulfureted group transposition into cystathionine. The remaining 50% of homocysteine may be reformed to methionine by removing a methyl group from two sources: (1) the metabolism of tetrahydrofolic acid (THF) and (2) the catabolism of betaine. Three enzymes take part in these metabolic pathways: methionine synthetase (MS), cysteine synthetase (CBS), and methyl-tetrahydrofolic acid reductase (MTHFR). Vitamin B6 (pyridoxine) consists of a coenzyme in the CBS and MTHFR function, while B12 is a coenzyme in the MS function. The adequacy of folic acid is necessary for both functions. The vascular endothelium may only produce CBS and MTHFR, rendering it more sensitive to disturbances in homocysteine metabolism [85, 86, 87, 88, 89, 90].
\nHomocysteine levels >15–16 μmol/l in nonpregnant women and >6–8 μmol/l in the third trimester of pregnancy are considered abnormal. In pregnancy, homocysteine levels decrease progressively and reach a minimum in the second trimester, while increasing slightly in the third trimester. Causes of fluctuations are estrogen, blood dilution, and increased metabolism of homocysteine in the liver, as well as its removal to the fetus. Mild disturbances in homocysteine metabolism can be detected if its levels are measured 6 hours after methionine administration. In this case, levels >51 μmol/l are considered pathologically out of pregnancy, but for pregnancy, there are no measurements [85, 86, 87, 88, 89, 90].
\nGenerally, the increase in basal levels of homocysteine represents deficits in remethylation, whereas the increase in homocysteine after methionine loading reveals deficiencies related to the transfer of the sulfur group.
\nHyperhomocysteinemia may be related to mutations in genes controlling the production of CBS and MHTFR and environmental factors such as B6, B12, and folic acid deficiency. Drugs that interfere with the metabolism or absorption of these vitamins, decreased homocysteine excretion in chronic renal failure, and other causes (hypothyroidism, hepatic failure, malignant anemia, and cancer) cause hypercholesterolemia [85, 86, 87, 88, 89, 90].
\nIt is worth highlighting cases with genetic mutations of the enzymes that cause hyperomyeloidemia, because they are common and appear to play a role in the course of pregnancy [85, 86, 87, 88, 89, 90].
\nAntibodies vs. cardiolipins: anti-cardiolipins lgG or lgM, in medium or high levels in 2 or more cases, with a time distance of at least 6 weeks between them.
\nLupusanticoagulant: in two or more cases with a time distance of at least weeks between them.
Antiphospholipid antibodies
Acute infections
Medicine (chlorpromazine and hydralazine)
Chronic infections (syphilis and hepatitis C)
No thrombotic effects
Antiphospholipid syndrome
Recurrent abortions
Endometrial death
Pre-eclampsia
IUGR
B2 glycoprotein 1
Annexin-V: a protein with strong, anticoagulant action.
Multiple placental micro-thrombosis [85, 86, 87, 88, 89, 90].
The existence of high homocysteine levels in the blood has a harmful effect on the placenta and decidua and is associated with the appearance of recurrent abortion and placental abruption. Hyperhomocysteinemia has been found to cause more complications such as pre-eclampsia, stillbirth, and deceleration of intrauterine growth [85, 86, 87, 88, 89, 90].
\nHyperhomocysteinemia and spinal tube deficiency (NTD) are associated with insufficient MS and MFTHR function, leading to homocysteine accumulation. Reduced methionine methylation and methyl group (necessary for myelin creation) deficiency are responsible for the above complications and not homocysteine effects [10]. Low folic acid levels or reduced intake in cases with increased need (heat sensitive MTHFR) are responsible for spinal tube deficiencies, but also homocysteine level increase. Hyperhomocysteinemia has also been associated with congenital abnormalities on the face and body. Administering 500 mg folic acid for 4 weeks prior to conception or even at the first stage of pregnancy has been found to reduce homocysteine levels by 22% [90, 91, 92, 93, 94, 95].
\nThe gene C677T and MTHFR frequency combined with the dietary habits of a population are the reason for variety in NTD appearance in different populations. In Holland, homozygous C677T of MTHFR polymorphism carriers is at 10–16% NTD risk compared to 5% of witnesses. A1298C, a second type of polymorphism, was discovered with just as high risk NTD levels in case of homozygosity [90, 91, 92, 93, 94, 95].
\nSeveral researchers compared patient groups with witnesses, found an increased hyperhomocysteinemia frequency, as well as increased C677T of MTHFR mutation frequency in women with pre-eclampsia. So, they were led to the conclusion that it may also constitute a genetic factor in pre-eclampsia manifestation [90, 91, 92, 93, 94, 95].
\nIn large woman study groups where homocysteine levels were evaluated in the second trimester of gestation either prospectively or recursively, it was found that the relevant pre-eclampsia risk in women with hyperhomocysteinemia was between 1.32 and 3.2%, while in primigravida, it reached 9.7% and in those who were obese, it reached 6.9%. Certainly, patient choice (with heavy, premature pre-eclampsia) has a lot to do with the various levels of pre-eclampsia in incidence of appearance of hyperhomocysteinemia in the bibliography. In a prospective study of 1049 pregnant women, at their 16th week of gestation, homocysteine levels did not appear to be different amongst patients with an uncomplicated course of gestation and those with pre-eclampsia. It is undetermined whether homocysteine levels should be evaluated in all women with a history of serious pre-eclampsia in a previous pregnancy. Repeated studies in women with angiopathy and high homocysteine levels have proved that pre-eclampsia was seven times more frequent in their pregnancies when compared to those with normal homocysteine levels. Homocysteine does not appear to activate the endothelium as there was not found a comparison between fibronectin and homocysteine during the episode of pre-eclampsia. A study revealed that administration of folic acid and vitamins in women with a history of heavy early course pre-eclampsia decreases its frequency and severity in the subsequent pregnancy, but because these studies were quite small and not random, other greater ones are in progress. At the moment, no specific genotype has been associated with more severe or premature types of the disease. Therefore, homozygosity in C677T had an applicable pre-eclampsia risk of 2.6% (95% CI 1.4–5.1) and a hyperhomocysteinemia risk of 20.6% (95% CI 3.6–121.6) [90, 91, 92, 93, 94, 95].
\nHigh homocysteine levels have proven to be embryo toxic in guinea pigs through the vascular decidua and villi network destruction. Steegers-Theunissen and Co. found that between 8th and 12th week of pregnancy, there are high methionine levels and low homocysteine levels in the extra-embryonic cavity and amniotic fluid compared to the mother, suggesting that homocysteine accumulation may be toxic. Increased miscarriages in the first trimester are not linked to angiopathy, but to methyl group deficiency and defective DNA composition. Wouters and Co. were the first to notice the high hyper-homocysteinemia frequency in the 14% of cases with recurrent abortion with no prior normal pregnancies and in 33% of those with a history of normal pregnancy. Another study in 100 patients with a history of consecutive spontaneous abortions found homocysteinaemia in 12% of them, C677T of MTHFR mutation in 20%, and decreased folic acid levels in 15% of patients. Supplementation of high levels (15 mg) of folic acid and vitamin B6 (750 mg) to 28 patients with recurrent abortion cases improved homocysteine levels and the 17 pregnancies that followed had a successful outcome. In an after-analysis, homocysteine presence with or without methionine loading showed an increased hyper-homocysteinaemia risk by 4.2 and 2.7%, respectively. In another study where MTHFR genotypes were sought after in embryonic tissues and newborns, all genotype associations were found in embryonic tissue, while in newborns, there were no combinations of three or more mutant alleles. This reveals that embryos with a lot of mutations may be miscarried. As a result, it is proved that there is a correlation between homocysteine metabolic disorder and habitual abortions, but it is not clear whether administering vitamins before conception may prevent them [95, 96, 97, 98, 99, 100].
\nPlacental biopsy in cases with abruption shows vasculopathy compatible with stenosis, necrosis, thrombosis, and atherosclerosis in the spinal arteries. Homocysteine in blood vessels acts by removing the methyl groups necessary for the DNA composition of multiplying cells. In many studies, hyperhomocysteinemia has been linked to placental abruption. In an after-analysis, folic acid deficiency was found to increase placental abruption frequency by 25.9% (95% CI-736.3) and hyperhomocysteinemia by 5.3% (95% CI 1.8–15.9). The presence of C677T of MTHFR polymorphism increases placental angiopathy risk by 2.45% (95% CI 1.00–6.02). In placental angiopathy cases, endothelium proteins are released in the blood, such as the von Willebrand factor (vWF), the activator of plasma tissue tPA (tissue plasma activator), the inhibitor of this activator PAI-1 (plasma activator inhibitor-1), fibronectin, and thrombomodulin that act as malfunction indicators. Women with hyperhomocysteinemia appeared to have a disproportionate tPA/PAI-1 ratio and a high vWF, while women with a placental abruption history had a high vWF and thrombomodulin. Thrombomodulin levels were in proportion with homocysteine levels. Administering antioxidant vitamins (folic acid, pyridoxine, and hydroxocobalamin) reduced the tPA/PAI-1 ratio but did not affect vWF, while the sole administration of folic acid reduced vWF levels. Combining hyperhomocysteinemia with thrombophilia, increases placental abruption risk by 3.4 [95, 96, 97, 98, 99, 100].
\nFinally, angiopathy resulting from hyperhomocysteinemia may be at least theoretically involved in placental abruption, therefore it may be useful for cases with abruption in the future to be checked for thrombophilia and hyperhomocysteinemia and receive antioxidant vitamin treatment [95, 96, 97, 98, 99, 100].
\nHyperhomocysteinemia may be associated with increased endometrial death by different mechanisms such as congenital disorders and pre-eclampsia, but its significance as an independent factor is in question. In a small group of patients, it was found to coexist with 11% frequency, while in a different group it was no more apparent than the rest of the population. The findings for its role in slowing intrauterine growth are contradictory. In another group of patients, hyperhomocysteinemia levels were as high as 38% and in a different group that was checked after methionine loading in women with a history of slowing intrauterine growth, hyperhomocysteinemia levels reached 19.2%. On the contrary, in a recursive review of the course of pregnancy in women who were CBS mutation carriers, newborns did not appear to have lower birth weight [95, 96, 97, 98, 99, 100].
\nTreatment with vitamin B6, B12, and folic acid on its own or combined with other vitamins has been evaluated on small groups of patients with coronary artery disease and obstetrical complications and has been found to induce homocysteine levels and incidents by 30–50% in these groups. In other studies, vitamin C and E were given as antioxidant factors. The significance of adding aspirin or heparin in these groups still remains questionable, even though we can conclude that normalizing homocysteine levels should be enough, in order to achieve the therapeutic response. From the above-mentioned factors, we can estimate that even if there is no unanimity, it is within reason to check homocysteine levels in cases with a history of NTD, pre-eclampsia, recurrent abortions, and perhaps in cases with placental abruption and endometrial death. It is valuable to look further into the results from administering vitamins in these cases [95, 96, 97, 98, 99, 100].
\nWe and other researchers have been searching for such predictive blood biomarkers of miscarriage. Macrophage inhibitory cytokine 1 (MIC-1), which is During the first trimester of gestation macrophage inhibitory cytokine 1 (MIC-1), which is presented in the syncytiotrophoblast and deciduas increases in serum and it is proposed to play an immunomodulatory role in the progression of the pregnancy. Pregnancy is considered as an ideal condition to study the regulation mechanisms of vascular growth under physiologic circumstances. Fetal vasculogenesis, angiogenesis, and vascular adaptation of the uterine circulation are one of a kind [101, 102, 103, 104]. There is strong evidence bracing a close relationship between embryonic development and the state of vascularization of the chorionic villi. Normal chorionic villous vascularization is crucial for the normal development of pregnancy. However, it is not well known whether abnormal changes in utero-placental vascular development predispose to abortions [101, 102, 103, 104]. The development of a normal functioning placental vascular network requires an important degree of coordination between various angiogenic and angiostatic factors and is exquisitely dependent on signals exchanged between these factors. Abnormalities in the development of placental vasculature may generate a number of gestational pathologies including miscarriages, intrauterine fetal death (IUFD), intrauterine growth restriction (IUGR), placental abruption, and preeclampsia. The importance of angiogenesis and angiogenetic factors in pregnancy is well known, and it has been proved that chemokines and their receptors are implicated in pregnancy and abortion, while cytokines and chemokines have a crucial part in controlling immune cells; these molecules are synthesized at the maternal-fetal interface where they have been implicated to play critical roles in the establishment and maintenance of pregnancy. In addition, they take part in other biological processes, such as cellular lymphoid organogenesis, and expression of adhesion molecules. The role of chemokines in angiogenesis during pregnancy has been experimentally demonstrated in cultures of leukocyte-free first trimester gestational decidual cells and in spontaneous miscarriage in mice, but the angiogenetic and angiostatic role of chemokines in the placental growth and decidua has not been well demonstrated [101, 102, 103, 104]. These preliminary results propose a disturbance of the chemokine-associated angiogenetic network with a significant number of spontaneous abortions during the 1st trimester of gestation.
\nMiscarriage is the most usual complication of pregnancy. There are currently no definite predictive tests and treatments that can prevent spontaneous miscarriage. While 50% of miscarriages are associated with fetal chromosomal faults, most of the remaining cases are likely to be euploid fetuses that have failed due to implantation problems. Numerous investigators have previously figured that developing an accurate predictive test for miscarriage may open the window for identifying euploid pregnancies that are still viable but intended to miscarry. It follows therefore that possibly, emerging therapeutics could be targeted at such high risk euploid pregnancies so that some of them may continue to viability, (i.e., rescuing some from miscarriage). The treatment of miscarriages and especially RPL has a wide variety and should be targeted at the reason. It could be complicated to recommend general therapeutic management especially if they are unproven, invasive, and expensive, because most couples with unexplained recurrent miscarriages have a good outcome. Further investigation of the factors that regulate the possible transcriptional repression of angiogenic chemokines and/or the overexpression of the angiostatic chemokines could cooperate in early prediction and prevention of spontaneous abortions. We assume that an accurate investigation of chemokine networks possibly taking part in the angiogenetic mechanisms of pregnancy would assist in the design of more accurate and possibly individualized angiogenesis-associated strategies for improving the early prediction and prevention of spontaneous abortion.
\nBetween the interacting surfaces can be continuous or discontinuous third body. Until 70s of the last century the oil layer of hydrodynamic generation existent in the contact zone, was considered as a parameter determining a working capacity of the heavy loaded frictional contact. Many experimental and theoretical works are devoted to study of thickness of this layer [1, 2, 3, 4, 5]. An approximate (digital) solution of the elasto-hydrodynamic problem considering thermal processes is given in the work [6], where the temperature, pressure and thickness of the oil layer between the cylinders interacting with the rolling-sliding friction, are determined. However, in spite of many attempts, ascertainment of the reliable relations between the thickness of the oil layer and tribological properties of the contact zone turned out to be problematic [7]. The supplements to the lubricants developed in succeeding years and technical means of study the processes proceeding in the contact zone have radically widened direction of the researches.
\nThe fundamentals of materials science and contact mechanics are developed in works [8, 9, 10] and in recent years a new direction of tribology – nano-tribology appeared [11, 12]. New materials were created (graphene etc.) [13]. For tribological modeling are used the methods of mechanics and multiphysics [14, 15, 16, 17, 18], methods of finite and boundary elements [19, 20, 21], discrete dynamics of dispositions [22], and atomistic methods [23]. However, in spite of this, some engineer aspects of the problems of tribology are not yet properly studied and their solution needs additional researches.
\nAt common operational conditions, various types of boundary films - products of interaction with the environment that prevent the direct contact of rubbing surfaces, cover these surfaces with thin layers. Depending on the friction conditions, properties of the surfaces and environment, these layers may have various tribological properties that will have the great influence on the boundary friction [24, 25, 26]. This is confirmed by the results of the experimental researches in the inert gas environment and vacuum, that excludes the possibility of oxidation during friction. Under such conditions, the seizure and intensive wear rate are observed. To prevent these undesirable phenomena, it is necessary to provide the presence of the third body in the contact zone with due properties, control of the friction factor and protection of the third body from destruction.
\nWhen the interacting surfaces are separated by the continuous third body, the friction forces mainly depend on the rheological properties of the third body [25, 26] or on the third body viscosity and area of the contact zone: F = f(η, \n
Usually, the surfaces are covered with various types of natural and artificial coatings, which represent the components of the third body in the contact zone of the interacting surfaces, are subjected to heavy power and thermal loads. This causes deformations of these coatings, their destruction, activation of the physical and chemical processes proceeding between them and the surfaces and generation of new coatings. Thus, during the interaction of surfaces, the processes of the third body destruction and restoration takes place in the contact zone continuously. When the intensity of destruction of the third body is greater than the intensity of its restoration, the amount of the micro-asperities coming into direct interaction leads to seizure and the wear rate increase because of various kinds of surface damage.
\nA part of micro-asperities of the heavy loaded interacting surfaces are in direct contact with each other causing their seizure and the remaining part interact with each other through the third body that is schematically shown in Figure 1.
\nTypes of interaction of the surfaces.
For heavy loaded interacting surfaces is typical seizure. This can happen when continuity of the third body is disrupted in individual places; the parts of the direct contact are cleansed from various coatings and boundary layers and are approached to each other at the distance of several atom diameters. As molecular dynamics [27] and atom microscope [28] show, in such conditions they will attract each other generating electron-pair bindings.
\nAdhesive approach to the friction means invasion of micro-asperities into each other in the contact zone, their close contact without the third body and adhesive scuffing of micro-asperities. The thermal effects accompanying the process have direct influence on the deformation area and value, volume of the deformed material, variation of the surface structure and physical and mechanical characteristics and damage of various types proceeding simultaneously.
\nThe friction forces between interacting surfaces (at lack of the third body in the places of actual contact) depend on the total area of the actual contacts Ff = ψ (∑τAasp) [24], where τ is effective strength on shear of the actual contact area of interacting surfaces; Aasp – seizure area of the actual contact that depends on the thermal load of the contact zone, thickness of the heated up layer, properties of the surfaces and environment of individual micro-asperities etc.
\nHence, the friction forces depend on the contact area in both cases, when the surfaces are separated from each other by the third body fully or partially.
\nThe surfaces are the weakest places of the rigid body from which their destruction begins [29]. Displacement of the coupled places of surfaces relative to each other causes sharp increase of the shear stresses and corresponding deformations, value and instability of the friction forces and rupture of the coupled places. It is possible in this case transfer of the pulled out material from on surface on the other, sharp change of roughness of these surfaces and development of the process of catastrophic wear – scuffing. The shear deformation generated on the surface sharply decreases towards the depth and multiple repetition of such processes results in superficial plastic deformations, lamination and fatigue damage (Figure 2) [30, 31].
\nThe scheme of the surface plastic deformation (a); appearance of cracks and lamination (b); appearance of fatigue pits (c).
The damage scales and dominant types in such cases depend on the working conditions. Thus, for providing the interacting surfaces with due tribological properties, their separation from each other by the continuous third body with corresponding properties is necessary.
\nIt should be noted that various types of surface take place simultaneously and proceed with various intensity and a dominant type of damage ascertained visually. The experimental researches have shown that damage intensity and type, of interacting surfaces are especially sensitive to the relative sliding velocity and shear stresses. Thereat, at low total and relative sliding velocities of the surfaces, when power of the thermal action, velocity and resistance of the shear deformation in the contact zone are comparatively small, stability of the third body and its resistance to scuffing are high and a main type of damage is fatigue wear [4]. With increase of the total and relative sliding velocities of surfaces, thermal load of the actual contact zone and destruction intensity of the third body increases. However, time of action of this load, thickness of the heated up layer and sizes of micro-asperities generated because of the scuffing and subsequent rupture of the seized places, decrease. Such phenomena take place on tread surfaces of the train wheel, near the pitch point of the gear drives, in the rolling bearings etc. (Figure 3). At increase of the relative sliding velocity, share of the adhesive wear and scuffing increases and it often becomes a dominant type of damage. For example, a steering surface of the train wheel, places of tooth profile of the gear drive distant from the pitch point, cam mechanisms etc.
\nThe damage types: (a) train wheel with fatigue damage of the tread surface and adhesive wear (scuffing) of the flange; (b) gear wheel with the traces of scuffing on the tooth face; (c) inner ring of the rolling bearing with the traces of fatigue damage.
For avoiding the above-mentioned non-desirable phenomena, providing the contact zone with the third body having due properties, its protection against destruction and control of the friction coefficient are necessary. However, despite the great number of scientific works this direction could not attract due attention of the scientists until today.
\nVariation of tribological properties of the surfaces is a result of various mechanical, physical and chemical processes proceeding simultaneously in the contact zone whose essence and mechanism of action are not properly studied [20, 21, 22]. This complicates control of the mentioned processes that needs consideration of many factors acting simultaneously. Such factors are:
Initial tribological properties of the third body and surfaces; influence of interaction of the friction modifier and other materials existent in the contact zone and the surfaces on the properties and stability of the third body and surfaces.
Structural, physical and mechanical peculiarities and tendency to scuffing of the clean (juvenile) surfaces in the places of the third body destruction; destruction peculiarities of the seized places;
Influence of the contact zone working conditions on the wear type and rate, variation of the micro- and macro-geometry etc.
Various interacting surfaces of machines should have different tribological properties: tooth gear drives, cam mechanisms, guides of various types etc., should have stable and as small as possible friction coefficient (≤ 0.1) and friction clutch and brakes – comparatively high and stable friction coefficient (0.25-0.4).
\nEspecially should be noted operational peculiarities of the wheel and rail interacting surfaces. The existent profiles of wheels and rails can be divided into the tread surfaces (which take part in the “free” rolling, traction and braking) and steering surfaces (the wheel flange and rail gauge, which take part in the steering mainly in curves and prevent the wheel-set from derailment). The flange root can roll on the rail corner, and it can take part in traction, braking and steering (Figure 4).
\nComponents of the wheel and rail interacting surfaces.
But traction (braking) and steering require mutually excluding properties and the “ideal” value of the friction coefficient (μ < 0,1) in the contact zone of the flange root and the rail corner is not acceptable for both cases.
\nAs it is seen from Figure 5, the power and thermal loads of tread surfaces are relatively low. At working of wheels in the modes of traction and braking, the lateral displacement, rotation about vertical axis and skidding, sliding velocity and distance increase. The flange root and rail corner in the contact zone are characterized by the increased creeping, that at destruction of the third body results in the increased shearing stresses and temperatures.
\nThe ideal values of the friction coefficients and stress distribution in the contact zone of the wheel and rail according to [32] and the thermal loads.
For interacting surfaces of some mechanisms, such as tooth gear drives, cam mechanisms, wheel and rail etc., the main types of wear are adhesive wear (and its heavy form – scuffing, whose nature is not studied sufficiently and under heavy working conditions it is followed by sharp increase of the friction coefficient instability and wear rate or catastrophic wear) and fatigue wear, that proceed simultaneously and are quite different processes.
\nFor revealing the factors influencing tribological properties of the interacting surfaces, the experimental researches were carried out on the high-speed and serial twin-disk machines.
\nA great number of scientific works are devoted to ascertainment of laws of variation of tribological properties of the interacting surfaces and with perfection of machines, actuality of such works increases. Despite the considerable quantity of works in this direction, the expected results are not obtained yet. The unexpected and catastrophic failure, unlike fatigue, corrosion and other slowly progressing wear types, are subjected some heavy loaded interacting surfaces of gear teeth, cams and followers, sleeve bearings etc. The wheel and rail contact zone is characterized by heavy operational conditions [33] (direct impact of the environmental conditions, high relative sliding and contact stresses) that enhances adhesive and fatigue processes. The wheel and rail contact zone is characterized by the heavy operational conditions (direct impact of the environmental conditions, high relative sliding and contact stresses) that enhances adhesive and fatigue processes raise the problems to be solved for many-sided study of these processes.
\nFor some heavy loaded interacting surfaces of machines are typical unpredictable change of tribological properties and sharp increase of the friction coefficient and wear intensity, so called catastrophic wear. As main cause of the latter is considered the heaviest form of the adhesive wear – scuffing [4] that is not properly studied yet [34] and whose signs are appearance of pits and scratches on the surfaces and transfer of the material from one surface on the other. The various aspects of the complex physical, tribo-chemical and mechanical processes proceeding in the contact zone are not properly studied yet that is accordingly reflected on the operation quality and resource. As an example can be cited interaction of the wheel and rail that occurs on: the tread surfaces during rolling, traction and braking; steering surfaces mainly in curves; flange root and rail corner at rolling, traction, braking and steering. The friction coefficient for wheel-rail interaction can vary in the range 0.05 - 0.8. The values of the friction coefficient for the tread and steering surfaces must be correspondingly in the ranges of 0.25-0.4 and <0.1 [32]. The optimal value of the friction factor for tread surfaces is 0.35 [32] and for steering surfaces - as low as possible. The scuffing on the wheel and rail steering surfaces causes rise of the friction coefficient, energy consumed on rolling, vibrations, nose, wear intensity and probability of derailment.
\nFor more detailed study of the properties and state of the third body in the contact zone we performed the experimental researches on the twin disk machine MT − 1 (Figure 6) with the use of existing lubricants and ecologically friendly friction modifiers, developed by us.
\nThe twin disk machine model MT1 and measuring means: 1 - twin disk machine, 2 - tribo-elements, 3 - the wear products, 4 - tester, 5 - personal computer, 6 – vibrometer.
The tests were performed at single application of the friction modifier on the rolling surface of the roller. After certain number of revolutions, a thin layer of the friction modifier was destroyed that was revealed by sharp increase of the friction moment and initial signs of scuffing on the surfaces. Without repeated feeding the friction modifier, the damage process was progressed. The rollers with various degree of damage are shown in Figure 7: (a) with initial signs of damage; (b) damage in the form of a narrow strip; (c) damage on the whole contacting area.
\nThe stages of damage of the interacting surfaces: (a) damage in the separate points; (b) damage in the form of the narrow strip; (c) damage on the whole area of the contacting surfaces.
Experimental research was performed at rolling of discs with up to 20% of sliding. The rollers had diameters of 40 mm and widths of 10 and 12 mm. The tests were performed at single application of the friction modifier on the interacting surface of the rollers. After certain number of revolutions, a thin layer of the friction modifier (FM) was destroyed that was revealed by sharp increase of the friction moment and initial signs of scuffing on the surfaces. Without repeated feeding of the friction modifier the damage process were progressed. The rollers with various degrees of damage are shown in Figure 7: (a) with initial signs of damage; (b) damage in the form of a narrow strip; (c) damage of the whole contacting area.
\nThe graphs of dependences of the friction coefficient and number of revolutions of rollers until appearance of the first signs of scuffing on the contact stress for initial linear contact of disks are shown in Figure 8. It is seen from these graphs that for the initial linear contact, when the contact stress is in the range of 0.65-0.77 GPa increase of the contact stress leads to decrease of the friction coefficient. It can also be seen that increase of the contact stress leads to decrease of number of revolutions until the destruction of the third body and onset of scuffing.
\nDependences of friction coefficients (a) and numbers of revolutions (b) until appearance of the first signs of scuffing on the contact stress for initial linear contact of disks and different anti-frictional friction modifiers.
The graphs of dependences of the friction coefficient and number of revolutions of rollers until appearance of the first signs of scuffing on the contact stress for initial point contact of disks and anti-frictional friction modifiers are shown in Figure 9.
\nDependences of friction coefficients (a) and numbers of revolutions (b) until appearance of the first signs of destruction of the third body (first signs of scuffing) on the contact stress for initial point contact of disks and three different frictional FM-s.
When the contact stress is in the range of 2.42-3.96 GPa the friction coefficient increases with increase of the contact stress. It can also be seen that increase of the contact stress leads to decrease of the number of revolutions until the destruction of the third body and onset of scuffing more intensive than in the previous case.
\nAt high working velocities, the maximal power and thermal stresses approach to the surfaces and intensity of the third body destruction/restoration and sensitivity of the contact zone tribological properties to working conditions, increase. To promote the mentioned problem, the experimental researches were carried out on the high-speed twin disk machine with independent drive of rollers (Figure 10).
\nHigh speed twin disk machine (a), experimental pieces (b) and a working surface of the roller with traces of scuffing (c) at total speed of rolling 7 m/s, sliding speeds of 3 m/s, linear load 100 N/m.
During experiments were studied the character of the wear process of working surfaces, influence of various parameters on the lubricant film thickness and friction coefficient at the use of popular mineral lubricants. The researches were executed with the use of the high-speed roller machine with independent drive of rollers. Conditions of the experiments and measured sizes were:
Rolling speed – up to 70 m/s;
Diameters of rollers 183 mm and 143,3 mm; width of rollers 12 mm and 17 mm;
Sliding velocity- up to 35 m/s;
Contact pressure – 5 × 105 – 2 × 106 N/м;
Dynamic viscosity 49-140 mNs/m2;
During experiments at the given loading and rolling velocity, the friction torque, sliding velocity and lubricant film thickness were measured. For measurement of speeds of rotation was utilized magnetic pickups, for measurement of the friction torque was utilized the strain gage transducer and contactless skate. The lubricant film thickness was measured by capacitance method [35]. The beginning of scuffing was revealed by the surges of the friction moment. Development of the friction process was accompanied by sharp rise of temperature and characteristic noise. Results of experimental research are shown in Figure 11.
\nDependence of relative lubricant film thickness (h/R), linear scuffing load (Pllsc) and coefficient of friction (f) until the appearance of the first signs of scuffing from rolling speed (Vr) and sliding velocity (Vs) at various viscosities (ν) of lubricants: (1) h/R = φ(Vr), Pll = 106 H/m; ν = 157 cSt, (2) h/R = φ(Vsl), Pll = 2 × 106 H/m, ν = 157 cSt, Vr = 50 m/s, (3) Pllsc = φ(Vsl), ν = 49 cSt, Vr = 50 m/s, (4) Pllsc = φ(Vr), ν = 157 cSt, Vsl = 22 m/s, (5) f = φ(Vsl), Pll = 1.5 × 106 H/m, ν = 49 cSt; Vr = 50 m/s, (6) f = φ(Vr), Pll = 106 H/m, ν = 157 cSt.
The studies have shown that with increase of the rolling speed, the thickness of the lubricating film initially increases (in our case up to 14 m/s) and then decreases slightly.
\nWith increase of the sliding velocity, sharp decrease of the lubricated film thickness is observed. Though measurement of the particularly thin film (boundary film) is technically difficult, its presence in the contact zone is indicated by the magnitude and stability of the friction coefficient. Further worsening of the working conditions leads to destruction of the third body in individual places of interacting surfaces.
\nA particular instability of the friction coefficient was observed at low velocities and high loads: intensive impulses of low frequency were marked and the scuffing marks of significant sizes – scratches and pits were noticed on the rollers surfaces. With increase of the velocity, the time of dwelling of the surfaces in the real contact zone and duration of the thermal impact, values of the amplitude of the friction force variable component decrease; the frequency increases and the individual impulses turn into noise. With further increase of the velocity the friction process is progressed, the temperature on the actual contact area of the interacting surfaces reaches the metal melting point, tonality of the noise rises and turns into whistle and when the frequency exceeds 20 KHz it becomes imperceptible for man.
\nThe complex physical, mechanical and tribo-chemical processes proceeding in the contact zone of interacting surfaces at direct impact of the environmental conditions raise the problems whose solution demands many-sided approach to these processes. There are many works devoted to these problems [36, 37, 38] but they are not solved properly yet. Namely, prediction of the friction coefficient in the contact zone, its control and character of influence of many parameters on its variation are still problematic.
\nAt heavy working conditions, when destruction of the third body is irreversible and scuffing is spread over the factual contact area of the whole surface relative displacement of the surfaces causes sharp increase of the shear stresses, corresponding deformations, values and instability of the friction forces and rupture of the seized places. Strength of the seized places may exceed the strength of the interacting bodies because of which the material pulled out from one surface can form a wear product or can be transferred on the other surface and attached to it that is followed by development of the scuffing process.
\nMultiple repetition of the shear deformation generated on the surfaces (that sharply decreases towards the depth) causes appearance of cracks on the surfaces, their development and fatigue damage, superficial plastic deformations and lamination. The area of each seized place in the contact zone depends on its power and thermal load; initial micro-geometry of the surfaces; value, velocity and resistance of the deformation etc. Therefore, various working conditions are characterized by corresponding variation of the tribological parameters, namely friction forces, amplitude and frequency of their variable component, wear intensity and roughness of the surfaces. Development of these processes leads to the catastrophic wear due to scuffing.
\nAt low velocities of interacting surfaces, the thermal load of the factual contact zone, velocity of the surface and environment tribo-chemical reaction and resistance of deformation decrease and time of the thermal action and thickness of the superficial heated up layer increase. In such conditions, at destruction of the third body, due to rupture of the seized places, the jerks of low frequency and high amplitudes and sharp instability of the friction coefficient take place and relatively large-size asperities (pits, scratches, asperities, cracks and layers) appear on the surfaces. This is correspondingly reflected on the damage type and roughness of the surfaces.
\nAt high velocities of interacting surfaces, despite several works in this area [39, 40, 41, 42, 43], some problems have not yet been resolved. The thermal load of the factual contact zone, velocity of the surface, tribo-chemical reaction of the environment and resistance of deformation increase, whereas time of the thermal action and thickness of the superficial heated up layer decrease. In such conditions, at destruction of the third body, due to rupture of the seized places, the jerks of high frequency and comparatively low amplitudes and instability of the friction coefficient take place and relatively small-size asperities (pits, scratches, asperities, cracks and layers) appear on the surfaces. This is correspondingly reflected on the damage type and roughness of the surfaces. Under the conditions of our experiments at a high rolling speed (more than 40 m/s), traces of fatigue damage and scuffing are not visually observed, however, a high wear rate remains.
\nThus, destruction of the third body causes sharp worsening of tribological properties of the interacting surfaces and necessary condition of its avoidance is separation of these surfaces from each other by continuous third body with due properties.
\nIt was ascertained by the experimental researches that destruction of the third body begins in individual points of the factual contact zone that is revealed by appearance of signs of the scuffing in these points. Restoration of the individual damaged points was often observed at unchanged operational conditions but at worsening, the operational conditions the superficial damage quantity increased and multiple damages appeared. At further worsening the operational conditions, a narrow strip of damage is generated spreading afterwards over the whole surface that causes worsening of the tribological parameters and catastrophic wear. The above-mentioned damage stages of the third body are shown in Figure 12.
\nThe damage stages of the interacting surfaces. (a) Unit seizures; (b) multiple seizures; (c) seizures on the narrow strip; (d) seizures on the whole area.
Usually the friction process proceeds at presence of the continuous or discontinuous (restorable or progressively destructible) third body stipulating the character of variation of the friction coefficient. Experimentally it was revealed that to negative friction corresponds the continuous or discontinuous but restorable third body; to neutral friction – multiple seizures of the interacting surfaces and to positive friction – increasing scuffing process that is spread on the whole surface. In Figure 13 is shown variation of the tractive (friction) force with creep [37].
\nFriction/creep relationship.
As it were shown by our experimental researches, at presence of the continuous third body increase of the relative sliding velocity leads to increase of the friction power and contact temperature; decrease of the lubricant viscosity, film thickness and friction force (Figure 13, “negative friction”), stable (or smoothly variable) friction torque and low destruction rate of the surfaces. Worsening of the working conditions caused by the partial, non-progressive damage of the third body in the separate unit places corresponds to the separate small impulses of the friction moment. Destruction of the third body in the multiple places leads to the multiple damage of the third body, multiple adhesive junctions of micro-asperities, disruption of these junctions, and a bit little increased impulses of the friction torque and to “neutral friction.”
\nAt progressive damage of the third body, the friction torque increases and corresponds to positive friction. Our experimental researches have shown that in other equal conditions the variation of the friction coefficient mainly depends on degree of destruction of the third body. Therefore, preservation of the third body between interacting surfaces and avoidance the scuffing, has a crucial importance for decrease of the friction coefficient, wear rate, etc. This issue became burning especially for wheels and rails in the last 50 years and many works appeared that are devoted to enhancing stability of the wheel flanges against the operational impacts.
\nIn Figure 14 are shown dependences of the friction factor and various damage types on relative sliding velocity (a) and of the wear rate (types) on slip (b) [32].
\nDependences of the friction factor and various damage types on relative sliding velocity (a) and of the wear rate (types) on slip (b).
Three zones can be distinguished in Figure 14a. The low relative sliding velocity, full separation of the interacting surfaces and continuous third body provide high wear resistance of the interacting surfaces and relatively stable friction coefficient (zone 1, Figure 14a) that corresponds to “mild” [32] wear rate (Figure 14b). In such conditions, the main damage types are the fatigue and plastic deformations.
\nSmall increase of the sliding velocity leads to appearance of small damage sources in multiple places and emergence of small surges of the friction torque (zone 2, Figure 14a). The rise of the third body destruction, as well as the magnitude of the friction coefficient and its instability, are clearly reflected in the oscillogram of the friction torque and may be predicted on the base of results of the experimental researches. The typical damage types of this zone are fatigue, plastic deformation, adhesive wear and limited rate of scuffing and correspond to “severe” wear rate (Figure 14b).
\nAt further increase of the relative sliding velocity, destruction of the third body becomes irreversible and extending and multiple seizures becomes uninterrupted (causing scuffing) and they propagate on the whole width of the interacting surfaces. The typical damage types of this zone are scuffing, plastic deformation and fatigue (zone 3, Figure 14a, and “catastrophic” wear rate Figure 14b). In this case, the scuffing can be avalanche in nature that quickly disables the machine.
\nDestruction of the third body makes especially heavy the working conditions of the interacting surfaces and is characterized by increased instability, high wear rate (‘catastrophic wear”), vibrations and noise, change of structure and micro-geometry of the surfaces at operation etc.
\nAt low velocities, time of dwelling of individual places of the surfaces in the contact zone and power and thermal actions, variable components of the friction torque and scales of the superficial damage increase and inversely, decrease with increasing speed, although the high wear rate is maintained.
\nFor each operational mode and frictional pairs, this stipulates corresponding micro-geometry and tribological properties.
\nThe methods of calculation of the contact zone power and thermal loads, friction coefficient, wear rate etc., are characterized by low informativeness and precision. This complicates prediction and realization of proper tribological properties of surfaces at various working conditions that prevents machines from reliable and effective operation.
\nFor heavy loaded interacting surfaces are typical destruction of the third body, direct contact of the surfaces and cohesion. The shearing forces, rate of the adhesive and fatigue wear rise sharply in the contact zone at such conditions and friction forces become instable causing the vibrations and noise.
\nThe mentioned types of wear in the contact zone are the results of quite different processes proceeding simultaneously. Besides, identification of the wear type according to the wear signs is often ambiguous that hinders selection of methods for its decrease.
\nDependence of tribological properties of the interacting surfaces on the properties of the third body and degree of its destruction were ascertained on the base of results of the experimental researches.
\nAt existence of a continuous third body between interacting surfaces, tribological properties of the contact zone are stipulated by the properties of the third body and at existence of a discontinuous third body, tribological properties of the contact zone are mainly stipulated by the properties of the third body and degree of its destruction.
\nThe signs of onset and development of the third body destruction and a criterion of its destruction are given there. The reasons of the negative, neutral and positive friction, mild, severe and catastrophic wear and types of surface damage at various relative sliding velocities are revealed.
\nThe most complete mathematical model of lubrication is the elastohydrodynamic (EHD) theory of lubrication [44]. The effectiveness of the EHD theory of lubrication is described by ratio λ or film parameter [45], which is the ratio of film minimum thickness at the Hertzian contact zone to the r.m.s. of the rolling element surface finish:
\nwhere Ra1 and Ra2 are the mean roughnesses of the surfaces.
\nBelow are given the integro-differential equations of EHD theory of lubrication with the consideration of the thermal processes that take place in the lubricant film and on the boundaries of surfaces, and the corresponding boundary conditions:
\nwhere p is pressure; V\n1 and V\n2 – peripheral speeds; μ – dynamic viscosity of lubricant oil in normal conditions; h – clearance; h\n0 – minimum clearance; R – radius of curvature; E\n1 and E\n2 – modulus of elasticity; ν – Poisson’s ratio of body materials; t – temperature; ρ, c, ζ, ρ\n1, c\n1, ζ\n1, ρ\n2, c\n2, ζ\n2 – correspondingly density, specific heat capacity and thermal conductivity of lubricant and interacting surfaces; μ\n0 – dynamic viscosity of the lubricant; β – piezo coefficient of lubricant viscosity; ζ – lubricant thermal conductivity; α – thermal coefficient of lubricant viscosity; ξ, ε – complementary variables; x\n0 – abscissa in the place of lubricant outlet from the gap.
\nCalculation of the oil film thickness, which separates the bodies, is the main problem of the EHD lubrication theory and there are numerous literature sources about it (Dowson, 1995; Ham rock and Dowson, 1981, etc.). There are various formulas for isothermal and anisothermal solutions for EHD problems describing the behavior of oil film thickness with various accuracies.
\nThe modern friction modifiers contain tribochemically active products that have great influence on their operational properties. The various aspects of properties of these components are not sufficiently studied and they cannot be expressed mathematically. EHD theory of lubrication only considers the mechanical phenomena proceeding in the lubricant film of the contact zone, ignoring other layers.
\nThe thickness of the rough surface boundary layers cannot be measured with the use of the modern methods of measurement of the oil layer thickness. Information about destruction of the boundary layers (and about onset of scuffing as well) can be obtained by sharp increase of the friction torque on the oscillogram. Therefore, onset of the friction torque sharp increase is considered as beginning of the third body destruction.
\nOn the base of system of equations of EHD, theory of lubrication and results of experimental researches considering formula (1), criterion of the third body destruction was developed that has a form:
\nAs it follows from the formula (2), a criterion of the third body destruction depends on the mechanical and thermo-physical characteristics of interacting surfaces, geometric and kinematic parameters, thermo-physical and tribological parameters of the third body. The properties and stability of the boundary layers are revealed in values of coefficient K and exponent e. The researches have also shown special sensitivity of the third body stability to thermal loads and relative sliding velocities, which must be taken into account to improve working conditions.
\nThe criterion of the third body destruction that is developed on the base of EHD theory of lubrication and results of experimental researches considering stability of the boundary layers has the form:
\nwhere VΣk is a total rolling velocity; Vsl – sliding velocity; Pll – linear load; μ - dynamic viscosity of the lubricant; R – reduced radius of curvature of the surfaces; Ra1 and Ra2- average standard deviation of the interacting surfaces; β – piezo coefficient of the lubricant viscosity; ζ– the lubricant thermal conductivity; α – thermal coefficient of the lubricant viscosity; a – thermal diffusivity; The exponents a, b, c, …, n and coefficient K are specified on the base of the experimental data obtained by T.I. Fowle, Y.N. Drozdov, Vellawer, G. Niemann, A.I. Petrusevich, I.I. Sokolov, K. Shawerhammer, G. Tumanishvili and are given in the Table 1.
\na | \nb | \nc | \nd | \nl | \nf | \ng | \nh | \ni | \nj | \nn | \n
---|---|---|---|---|---|---|---|---|---|---|
0.37 to 0.7 | \n(−0.36) to (−1.32) | \n(−0.15) to (−0.265) | \n0.04 to 0.52 | \n0.25 to 0.36 | \n−1 | \n0.6 | \n0.18 to 0.66 | \n(−0.18) to (−0.66) | \n0.09 to 0.33 | \n0.045 to 0.165 | \n
The exponents of formula (3).
As it is seen from the Table 1, destruction of the third body is especially sensitive to the degree b of sliding velocity. It follows from formulae (2) and (3) that with increase of the rolling velocity, radius of curvature, piezo-coefficient of viscosity, heat conductivity factor, thermal diffusivity and coefficient of elasticity, the stability of the third body increases and with increase of the sliding velocity, linear loading, roughness of surfaces and thermal coefficient of viscosity it decreases.
\nAs it was already mentioned, one of the indicators of the third body destruction (scuffing) is appearance of signs of scuffing on the surfaces. According to criteria of destruction of the third body, its destruction is supposed when values of the corresponding criteria are less than 1. K. Schauerhammer experimentally ascertains the conditions of the third body destruction (scuffing) for the gear drive on the gear drive test bench TUME 11 [46]. To predict the destruction of the third body (scuffing), we used the well-known Dowson and Higginson formulas to determine the lubricating layer parameter (λ) [44, 45] and the criterion C developed by us at the values of the coefficient K = 2.7 and the exponent e = 0.336 in formula (3). Dependences of the fields of deviations of the values of these criteria on the gear wheels circular velocity are shown in Figure 15.
\nDependences of the fields of deviations of the values of λ parameter (1) and criterion C of destruction of the third body (2) developed by us, on the gear wheels circular velocity.
As it is seen from the graphs, deviations of the criterion C of destruction of the third body developed by us, are small and constant, while deviations of the parameter λ and its values increase with increase of the gear wheels velocity.
\n\nFigure 16 shows the results of similar calculations using the C criterion with the values of the coefficient K = 1.55 and the exponent e = 0.29 in formula (3) and the formulas of H. Block [47] and Niemann G. and Saitzinger K. [48]. The studies were carried out on gear drive test bench FZG for transmissions A, L, N 141, 142, 143, 201, 202, and 203 with lubricant k1.
\nDependences of the fields of deviations of the temperature criterion (θ, 1) of H. block, criterion (SF, 2) of G. Niman and Saitzinger and offered criterion (C, 3) of destruction of the third body, on the gear wheels circular velocity.
It is seen from the graphs that deviations of the offered criterion C of destruction of the third body little differ from the unit in the whole range of variation of the circular velocity, while deviations of other criteria significantly differ from the unit and they increase with increase of the circular velocity.
\n\n
Tribological properties of the interacting surfaces mainly depend on tribological properties of the third body, degree of its destruction, disposition of the surfaces to seizure etc. The researches have shown that the continuous or discontinuous but restorable third body at the initial stage of destruction and progressively destructing third body have quite different properties. In the first case the said properties are stable and depend on the properties of the third body and in the second case, these properties are instable and worsened that are characterized by increasing friction coefficient, catastrophic wear and typical noise.
Prediction of destruction of the third body is possible in the laboratory conditions by estimation of the friction torque variation and with the use of the criterion of destruction of the third body, with ascertained beforehand values of the experimental coefficients;
The friction coefficient (negative, neutral and positive), wear rate of the interacting surfaces (mild, severe and catastrophic), damage types (scuffing, fatigue, plastic deformation, adhesive wear) and vibrations and noise generated in the contact zone depend on tribological properties of the third body, its degree of destruction and area of the factual contact zone seized places;
For the improvement of tribological properties of the interacting surfaces, it is necessary to provide the contact zone with continuous or restorable third body having due tribological properties at the initial stage of destruction.
This work was supported by Shota Rustaveli National Science Foundation of Georgia (SRNSFG) under GENIE project CARYS-19-588.
\nThe authors declare no conflict of interest.
As this section deals with legal issues pertaining to the rights of individual Authors and IntechOpen, for the avoidance of doubt, each category of publication is dealt with separately. Consequently, much of the information, for example definition of terms used, is repeated to ensure that there can be no misunderstanding of the policies that apply to each category.
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\\n\\nIntechOpen only publishes manuscripts for which it has publishing rights. This is governed by a publication agreement between the Author and IntechOpen. This agreement is accepted by the Author when the manuscript is submitted and deals with both the rights of the publisher and Author, as well as any obligations concerning a particular manuscript. However, in accepting this agreement, Authors continue to retain significant rights to use and share their publications.
\\n\\nHOW COPYRIGHT WORKS WITH OPEN ACCESS LICENSES?
\\n\\nAgreement samples are listed here for the convenience of prospective Authors:
\\n\\n\\n\\nDEFINITIONS
\\n\\nThe following definitions apply in this Copyright Policy:
\\n\\nAuthor - in order to be identified as an Author, three criteria must be met: (i) Substantial contribution to the conception or design of the Work, or the acquisition, analysis, or interpretation of data for the Work; (ii) Participation in drafting or revising the Work; (iii) Approval of the final version of the Work to be published.
\\n\\nWork - a Chapter, including Conference Papers, and any and all text, graphics, images and/or other materials forming part of or accompanying the Chapter/Conference Paper.
\\n\\nMonograph/Compacts - a full manuscript usually written by a single Author, including any and all text, graphics, images and/or other materials.
\\n\\nCompilation - a collection of Works distributed in a Book that IntechOpen has selected, and for which the coordination of the preparation, arrangement and publication has been the responsibility of IntechOpen. Any Work included is accepted in its entirety in unmodified form and is published with one or more other contributions, each constituting a separate and independent Work, but which together are assembled into a collective whole.
\\n\\nIntechOpen - Registered publisher with office at 5 Princes Gate Court, London, SW7 2QJ - UNITED KINGDOM
\\n\\nIntechOpen platform - IntechOpen website www.intechopen.com whose main purpose is to host Monographs in the format of Book Chapters, Long Form Monographs, Compacts, Conference Proceedings and Videos.
\\n\\nVideo Lecture – an audiovisual recording of a lecture or a speech given by a Lecturer, recorded, edited, owned and published by IntechOpen.
\\n\\nTERMS
\\n\\nAll Works published on the IntechOpen platform and in print are licensed under a Creative Commons Attribution 3.0 Unported License, a license which allows for the broadest possible reuse of published material.
\\n\\nCopyright on the individual Works belongs to the specific Author, subject to an agreement with IntechOpen. The Creative Common license is granted to all others to:
\\n\\nAnd for any purpose, provided the following conditions are met:
\\n\\nAll Works are published under the CC BY 3.0 license. However, please note that book Chapters may fall under a different CC license, depending on their publication date as indicated in the table below:
\\n\\n\\n\\n
LICENSE | \\n\\t\\t\\tUSED FROM - | \\n\\t\\t\\tUP TO - | \\n\\t\\t
\\n\\t\\t\\t Creative Commons Attribution-NonCommercial-ShareAlike 3.0 Unported (CC BY-NC-SA 3.0) \\n\\t\\t\\t | \\n\\t\\t\\t\\n\\t\\t\\t 1 July 2005 (2005-07-01) \\n\\t\\t\\t | \\n\\t\\t\\t\\n\\t\\t\\t 3 October 2011 (2011-10-03) \\n\\t\\t\\t | \\n\\t\\t
Creative Commons Attribution 3.0 Unported (CC BY 3.0) | \\n\\t\\t\\t\\n\\t\\t\\t 5 October 2011 (2011-10-05) \\n\\t\\t\\t | \\n\\t\\t\\tCurrently | \\n\\t\\t
The CC BY 3.0 license permits Works to be freely shared in any medium or format, as well as the reuse and adaptation of the original contents of Works (e.g. figures and tables created by the Authors), as long as the source Work is cited and its Authors are acknowledged in the following manner:
\\n\\nContent reuse:
\\n\\n© {year} {authors' full names}. Originally published in {short citation} under {license version} license. Available from: {DOI}
\\n\\nContent adaptation & reuse:
\\n\\n© {year} {authors' full names}. Adapted from {short citation}; originally published under {license version} license. Available from: {DOI}
\\n\\nReposting & sharing:
\\n\\nOriginally published in {full citation}. Available from: {DOI}
\\n\\nRepublishing – More about Attribution Policy can be found here.
\\n\\nThe same principles apply to Works published under the CC BY-NC-SA 3.0 license, with the caveats that (1) the content may not be used for commercial purposes, and (2) derivative works building on this content must be distributed under the same license. The restrictions contained in these license terms may, however, be waived by the copyright holder(s). Users wishing to circumvent any of the license terms are required to obtain explicit permission to do so from the copyright holder(s).
\\n\\nDISCLAIMER: Neither the CC BY 3.0 license, nor any other license IntechOpen currently uses or has used before, applies to figures and tables reproduced from other works, as they may be subject to different terms of reuse. In such cases, if the copyright holder is not noted in the source of a figure or table, it is the responsibility of the User to investigate and determine the exact copyright status of any information utilised. Users requiring assistance in that regard are welcome to send an inquiry to permissions@intechopen.com.
\\n\\nAll rights to Books and all other compilations published on the IntechOpen platform and in print are reserved by IntechOpen.
\\n\\nThe copyright to Books and other compilations is subject to separate copyright from those that exist in the included Works.
\\n\\nAll Long Form Monographs/Compacts are licensed under the Creative Commons Attribution-NonCommercial 4.0 International (CC BY-NC 4.0) license granted to all others.
\\n\\nCopyright to the individual Works (Chapters) belongs to their specific Authors, subject to an agreement with IntechOpen and the Creative Common license granted to all others to:
\\n\\nUnder the following terms:
\\n\\nThere must be an Attribution, giving appropriate credit, provision of a link to the license, and indication if any changes were made.
\\n\\nNonCommercial - The use of the material for commercial purposes is prohibited. Commercial rights are reserved to IntechOpen or its licensees.
\\n\\nNo additional restrictions that apply legal terms or technological measures that restrict others from doing anything the license permits are allowed.
\\n\\nThe CC BY-NC 4.0 license permits Works to be freely shared in any medium or format, as well as reuse and adaptation of the original contents of Works (e.g. figures and tables created by the Authors), as long as it is not used for commercial purposes. The source Work must be cited and its Authors acknowledged in the following manner:
\\n\\nContent reuse:
\\n\\n© {year} {authors' full names}. Originally published in {short citation} under {license version} license. Available from: {DOI}
\\n\\nContent adaptation & reuse:
\\n\\n© {year} {authors' full names}. Adapted from {short citation}; originally published under {license version} license. Available from: {DOI}
\\n\\nReposting & sharing:
\\n\\nOriginally published in {full citation}. Available from: {DOI}
\\n\\nAll Book cover design elements, as well as Video image graphics are subject to copyright by IntechOpen.
\\n\\nEvery reproduction of a front cover image must be accompanied by an appropriate Copyright Notice displayed adjacent to the image. The exact Copyright Notice depends on who the Author of a particular cover image is. Users wishing to reproduce cover images should contact permissions@intechopen.com.
\\n\\nAll Video Lectures under IntechOpen's production are subject to copyright and are property of IntechOpen, unless defined otherwise, and are licensed under the Attribution-NonCommercial-NoDerivatives 4.0 International (CC BY-NC-ND 4.0) license. This grants all others the right to:
\\n\\nShare — copy and redistribute the material in any medium or format
\\n\\nUnder the following terms:
\\n\\nUsers wishing to repost and share the Video Lectures are welcome to do so as long as they acknowledge the source in the following manner:
\\n\\n© {year} IntechOpen. Published under CC BY-NC-ND 4.0 license. Available from: {DOI}
\\n\\nUsers wishing to reuse, modify, or adapt the Video Lectures in a way not permitted by the license are welcome to contact us at permissions@intechopen.com to discuss waiving particular license terms.
\\n\\nAll software used on the IntechOpen platform, any used during the publishing process, and the copyright in the code constituting such software, is the property of IntechOpen or its software suppliers. As such, it may not be downloaded or copied without permission.
\\n\\nUnless otherwise indicated, all IntechOpen websites are the property of IntechOpen.
\\n\\nAll content included on IntechOpen Websites not forming part of contributed materials (such as text, images, logos, graphics, design elements, videos, sounds, pictures, trademarks, etc.), are subject to copyright and are property of, or licensed to, IntechOpen. Any other use, including the reproduction, modification, distribution, transmission, republication, display, or performance of the content on this site is strictly prohibited.
\\n\\nPolicy last updated: 2016-06-08
\\n"}]'},components:[{type:"htmlEditorComponent",content:'Copyright is the term used to describe the rights related to the publication and distribution of original Works. Most importantly from a publisher's perspective, copyright governs how Authors, publishers and the general public can use, publish, and distribute publications.
\n\nIntechOpen only publishes manuscripts for which it has publishing rights. This is governed by a publication agreement between the Author and IntechOpen. This agreement is accepted by the Author when the manuscript is submitted and deals with both the rights of the publisher and Author, as well as any obligations concerning a particular manuscript. However, in accepting this agreement, Authors continue to retain significant rights to use and share their publications.
\n\nHOW COPYRIGHT WORKS WITH OPEN ACCESS LICENSES?
\n\nAgreement samples are listed here for the convenience of prospective Authors:
\n\n\n\nDEFINITIONS
\n\nThe following definitions apply in this Copyright Policy:
\n\nAuthor - in order to be identified as an Author, three criteria must be met: (i) Substantial contribution to the conception or design of the Work, or the acquisition, analysis, or interpretation of data for the Work; (ii) Participation in drafting or revising the Work; (iii) Approval of the final version of the Work to be published.
\n\nWork - a Chapter, including Conference Papers, and any and all text, graphics, images and/or other materials forming part of or accompanying the Chapter/Conference Paper.
\n\nMonograph/Compacts - a full manuscript usually written by a single Author, including any and all text, graphics, images and/or other materials.
\n\nCompilation - a collection of Works distributed in a Book that IntechOpen has selected, and for which the coordination of the preparation, arrangement and publication has been the responsibility of IntechOpen. Any Work included is accepted in its entirety in unmodified form and is published with one or more other contributions, each constituting a separate and independent Work, but which together are assembled into a collective whole.
\n\nIntechOpen - Registered publisher with office at 5 Princes Gate Court, London, SW7 2QJ - UNITED KINGDOM
\n\nIntechOpen platform - IntechOpen website www.intechopen.com whose main purpose is to host Monographs in the format of Book Chapters, Long Form Monographs, Compacts, Conference Proceedings and Videos.
\n\nVideo Lecture – an audiovisual recording of a lecture or a speech given by a Lecturer, recorded, edited, owned and published by IntechOpen.
\n\nTERMS
\n\nAll Works published on the IntechOpen platform and in print are licensed under a Creative Commons Attribution 3.0 Unported License, a license which allows for the broadest possible reuse of published material.
\n\nCopyright on the individual Works belongs to the specific Author, subject to an agreement with IntechOpen. The Creative Common license is granted to all others to:
\n\nAnd for any purpose, provided the following conditions are met:
\n\nAll Works are published under the CC BY 3.0 license. However, please note that book Chapters may fall under a different CC license, depending on their publication date as indicated in the table below:
\n\n\n\n
LICENSE | \n\t\t\tUSED FROM - | \n\t\t\tUP TO - | \n\t\t
\n\t\t\t Creative Commons Attribution-NonCommercial-ShareAlike 3.0 Unported (CC BY-NC-SA 3.0) \n\t\t\t | \n\t\t\t\n\t\t\t 1 July 2005 (2005-07-01) \n\t\t\t | \n\t\t\t\n\t\t\t 3 October 2011 (2011-10-03) \n\t\t\t | \n\t\t
Creative Commons Attribution 3.0 Unported (CC BY 3.0) | \n\t\t\t\n\t\t\t 5 October 2011 (2011-10-05) \n\t\t\t | \n\t\t\tCurrently | \n\t\t
The CC BY 3.0 license permits Works to be freely shared in any medium or format, as well as the reuse and adaptation of the original contents of Works (e.g. figures and tables created by the Authors), as long as the source Work is cited and its Authors are acknowledged in the following manner:
\n\nContent reuse:
\n\n© {year} {authors' full names}. Originally published in {short citation} under {license version} license. Available from: {DOI}
\n\nContent adaptation & reuse:
\n\n© {year} {authors' full names}. Adapted from {short citation}; originally published under {license version} license. Available from: {DOI}
\n\nReposting & sharing:
\n\nOriginally published in {full citation}. Available from: {DOI}
\n\nRepublishing – More about Attribution Policy can be found here.
\n\nThe same principles apply to Works published under the CC BY-NC-SA 3.0 license, with the caveats that (1) the content may not be used for commercial purposes, and (2) derivative works building on this content must be distributed under the same license. The restrictions contained in these license terms may, however, be waived by the copyright holder(s). Users wishing to circumvent any of the license terms are required to obtain explicit permission to do so from the copyright holder(s).
\n\nDISCLAIMER: Neither the CC BY 3.0 license, nor any other license IntechOpen currently uses or has used before, applies to figures and tables reproduced from other works, as they may be subject to different terms of reuse. In such cases, if the copyright holder is not noted in the source of a figure or table, it is the responsibility of the User to investigate and determine the exact copyright status of any information utilised. Users requiring assistance in that regard are welcome to send an inquiry to permissions@intechopen.com.
\n\nAll rights to Books and all other compilations published on the IntechOpen platform and in print are reserved by IntechOpen.
\n\nThe copyright to Books and other compilations is subject to separate copyright from those that exist in the included Works.
\n\nAll Long Form Monographs/Compacts are licensed under the Creative Commons Attribution-NonCommercial 4.0 International (CC BY-NC 4.0) license granted to all others.
\n\nCopyright to the individual Works (Chapters) belongs to their specific Authors, subject to an agreement with IntechOpen and the Creative Common license granted to all others to:
\n\nUnder the following terms:
\n\nThere must be an Attribution, giving appropriate credit, provision of a link to the license, and indication if any changes were made.
\n\nNonCommercial - The use of the material for commercial purposes is prohibited. Commercial rights are reserved to IntechOpen or its licensees.
\n\nNo additional restrictions that apply legal terms or technological measures that restrict others from doing anything the license permits are allowed.
\n\nThe CC BY-NC 4.0 license permits Works to be freely shared in any medium or format, as well as reuse and adaptation of the original contents of Works (e.g. figures and tables created by the Authors), as long as it is not used for commercial purposes. The source Work must be cited and its Authors acknowledged in the following manner:
\n\nContent reuse:
\n\n© {year} {authors' full names}. Originally published in {short citation} under {license version} license. Available from: {DOI}
\n\nContent adaptation & reuse:
\n\n© {year} {authors' full names}. Adapted from {short citation}; originally published under {license version} license. Available from: {DOI}
\n\nReposting & sharing:
\n\nOriginally published in {full citation}. Available from: {DOI}
\n\nAll Book cover design elements, as well as Video image graphics are subject to copyright by IntechOpen.
\n\nEvery reproduction of a front cover image must be accompanied by an appropriate Copyright Notice displayed adjacent to the image. The exact Copyright Notice depends on who the Author of a particular cover image is. Users wishing to reproduce cover images should contact permissions@intechopen.com.
\n\nAll Video Lectures under IntechOpen's production are subject to copyright and are property of IntechOpen, unless defined otherwise, and are licensed under the Attribution-NonCommercial-NoDerivatives 4.0 International (CC BY-NC-ND 4.0) license. This grants all others the right to:
\n\nShare — copy and redistribute the material in any medium or format
\n\nUnder the following terms:
\n\nUsers wishing to repost and share the Video Lectures are welcome to do so as long as they acknowledge the source in the following manner:
\n\n© {year} IntechOpen. Published under CC BY-NC-ND 4.0 license. Available from: {DOI}
\n\nUsers wishing to reuse, modify, or adapt the Video Lectures in a way not permitted by the license are welcome to contact us at permissions@intechopen.com to discuss waiving particular license terms.
\n\nAll software used on the IntechOpen platform, any used during the publishing process, and the copyright in the code constituting such software, is the property of IntechOpen or its software suppliers. As such, it may not be downloaded or copied without permission.
\n\nUnless otherwise indicated, all IntechOpen websites are the property of IntechOpen.
\n\nAll content included on IntechOpen Websites not forming part of contributed materials (such as text, images, logos, graphics, design elements, videos, sounds, pictures, trademarks, etc.), are subject to copyright and are property of, or licensed to, IntechOpen. Any other use, including the reproduction, modification, distribution, transmission, republication, display, or performance of the content on this site is strictly prohibited.
\n\nPolicy last updated: 2016-06-08
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