Time in seconds, for both Reynolds numbers and the two methods described for the lid-driven cavity problem.
\r\n\t
",isbn:"978-1-80356-495-1",printIsbn:"978-1-80356-494-4",pdfIsbn:"978-1-80356-496-8",doi:null,price:0,priceEur:0,priceUsd:0,slug:null,numberOfPages:0,isOpenForSubmission:!0,isSalesforceBook:!1,hash:"2d409a285bea682efb34a817b0651aba",bookSignature:"Dr. Saeed El-Ashram, Dr. Guillermo Téllez and Dr. Firas Alali",publishedDate:null,coverURL:"https://cdn.intechopen.com/books/images_new/11635.jpg",keywords:"PCR, Genotyping, ELISA, Cell Lines, 2D Culture, 3D Culture, PRRs, CD4 Responses, CD8 Responses, Behavior Manipulation, Parasite Cysts, Psychiatric Disorders",numberOfDownloads:null,numberOfWosCitations:0,numberOfCrossrefCitations:null,numberOfDimensionsCitations:null,numberOfTotalCitations:null,isAvailableForWebshopOrdering:!0,dateEndFirstStepPublish:"March 4th 2022",dateEndSecondStepPublish:"May 6th 2022",dateEndThirdStepPublish:"July 5th 2022",dateEndFourthStepPublish:"September 23rd 2022",dateEndFifthStepPublish:"November 22nd 2022",remainingDaysToSecondStep:"16 days",secondStepPassed:!0,currentStepOfPublishingProcess:3,editedByType:null,kuFlag:!1,biosketch:"Dr. El-Ashram's research focuses on apicomplexan parasites, such as Toxoplasma and Eimeria. He has more than 96 SCI publications, he acted as an academic editor, reviewer, and he holds several registered patents.",coeditorOneBiosketch:"Researcher in enteric health, most notably probiotics and their relationship to nutrition and disease protection in poultry as well as the design of avian enteric inflammation models for the study of the impact of diet and microbiome on growth and development.",coeditorTwoBiosketch:"My research focuses mainly on apicomplexan parasites, such as Toxoplasma Cryptosporidium, Eimeria, and minor on nematodes. Prof.Alali has more than 30 publications and he acts as a reviewer in many journals.",coeditorThreeBiosketch:null,coeditorFourBiosketch:null,coeditorFiveBiosketch:null,editors:[{id:"209746",title:"Dr.",name:"Saeed",middleName:null,surname:"El-Ashram",slug:"saeed-el-ashram",fullName:"Saeed El-Ashram",profilePictureURL:"https://mts.intechopen.com/storage/users/209746/images/system/209746.jpg",biography:"Saeed El-Ashram (BSc, MSc, PhD Vet. Med.), Professor at School of Life Sciences and Engineering, Foshan University (Xianxi Campus), Shishan Town, Naihai district of Foshan City, Guangdong Province, China. The primary focus of his research is to understand how the animal immune system recognizes and responds to parasitic infections with and/or without microbial community, because some of them are the causative agents of major diseases of humans, such as toxoplasmosis, cryptosporidiosis, alveolar echinococcosis and fasciolosis. Others are a huge financial burden to food producers because of the effects these parasites have on domestic animals, for example, coccidiosis and cryptosporidiosis (livestock and poultry), and fasciolosis and haemonchosis (livestock). Another area of research in Dr. El-Ashram laboratory investigates the inter-species dynamics in mixed parasitic-bacterial, fungal, or viral infections particularly those with clinical and therapeutic implications. The overall target of his research is to provide information that will aid in the design of novel therapeutic strategies aimed at the prevention and/or treatment of these complicated infections. To achieve this objective, they are utilizing new technology, including Proteomics, Immunoproteomics, Mass Spectrometry, Next Generation Sequencing, Tetramers, Real-time PCR, Immunohistochemistry and Bioinformatic and Flow Cytometry Analyses to dissect the host-pathogen interactions in single or combined infections. Dr. El-Ashram's laboratory deciphers the formation and evolution of host specialization in the foodborne illnesses, such as Salmonella spp., Clostridium perfringens, Campylobacter jejuni and Bacillus cereus by building a genome-based phylogeny and studying the Whole genome sequencing (WGS) as an effective and rapid surveillance tool of foodborne disease.",institutionString:"Foshan University",position:null,outsideEditionCount:0,totalCites:0,totalAuthoredChapters:"0",totalChapterViews:"0",totalEditedBooks:"0",institution:{name:"Foshan University",institutionURL:null,country:{name:"China"}}}],coeditorOne:{id:"73465",title:"Dr.",name:"Guillermo",middleName:null,surname:"Téllez",slug:"guillermo-tellez",fullName:"Guillermo Téllez",profilePictureURL:"https://mts.intechopen.com/storage/users/73465/images/system/73465.jpg",biography:"Guillermo Tellez-Isaias was born in Mexico City, in 1963. He received his Doctor in Veterinary Medicine degree in 1986 and his Master in Science degree in Veterinary Sciences in 1989 from the National Autonomous University of Mexico (UNAM), College of Veterinary Medicine. He worked as a full Professor at UNAM for 16 years, 8 as head of the Avian Medicine Department at the College of Veterinary Medicine. Tellez was President of the National Poultry Science Association of Mexico, is a member of the Mexican Veterinary Academy and the Mexican National Research System. Currently, he works as a Research Professor at the Center of Excellence in Poultry Science of the University of Arkansas. His research is focused on the advantages of the poultry gastrointestinal model to evaluate the beneficial effects of functional foods to enhance intestinal health and disease resistance.",institutionString:"University of Arkansas at Fayetteville",position:null,outsideEditionCount:0,totalCites:0,totalAuthoredChapters:"8",totalChapterViews:"0",totalEditedBooks:"0",institution:{name:"University of Arkansas at Fayetteville",institutionURL:null,country:{name:"United States of America"}}},coeditorTwo:{id:"437285",title:"Dr.",name:"Firas",middleName:null,surname:"Alali",slug:"firas-alali",fullName:"Firas Alali",profilePictureURL:"https://mts.intechopen.com/storage/users/437285/images/17927_n.jpg",biography:"Academic reviewer for many journals.\r\nAssociate Professor at University of Kerbala, Iraq. Firas Alali works at the Department of Veterinary Parasitology of Veterinary Medicine college, Kerbala University. Firas does research in Parasitology, Entomology, and Vector-Borne Diseases including zoonoses.",institutionString:"University of Kerbala",position:null,outsideEditionCount:0,totalCites:0,totalAuthoredChapters:"0",totalChapterViews:"0",totalEditedBooks:"0",institution:null},coeditorThree:null,coeditorFour:null,coeditorFive:null,topics:[{id:"13",title:"Immunology and Microbiology",slug:"immunology-and-microbiology"}],chapters:null,productType:{id:"1",title:"Edited Volume",chapterContentType:"chapter",authoredCaption:"Edited by"},personalPublishingAssistant:{id:"453623",firstName:"Silvia",lastName:"Sabo",middleName:null,title:"Mrs.",imageUrl:"https://mts.intechopen.com/storage/users/453623/images/20396_n.jpg",email:"silvia@intechopen.com",biography:null}},relatedBooks:[{type:"book",id:"1591",title:"Infrared Spectroscopy",subtitle:"Materials Science, Engineering and Technology",isOpenForSubmission:!1,hash:"99b4b7b71a8caeb693ed762b40b017f4",slug:"infrared-spectroscopy-materials-science-engineering-and-technology",bookSignature:"Theophile Theophanides",coverURL:"https://cdn.intechopen.com/books/images_new/1591.jpg",editedByType:"Edited by",editors:[{id:"37194",title:"Dr.",name:"Theophile",surname:"Theophanides",slug:"theophile-theophanides",fullName:"Theophile Theophanides"}],productType:{id:"1",chapterContentType:"chapter",authoredCaption:"Edited by"}},{type:"book",id:"3161",title:"Frontiers in Guided Wave Optics and Optoelectronics",subtitle:null,isOpenForSubmission:!1,hash:"deb44e9c99f82bbce1083abea743146c",slug:"frontiers-in-guided-wave-optics-and-optoelectronics",bookSignature:"Bishnu Pal",coverURL:"https://cdn.intechopen.com/books/images_new/3161.jpg",editedByType:"Edited by",editors:[{id:"4782",title:"Prof.",name:"Bishnu",surname:"Pal",slug:"bishnu-pal",fullName:"Bishnu Pal"}],productType:{id:"1",chapterContentType:"chapter",authoredCaption:"Edited by"}},{type:"book",id:"371",title:"Abiotic Stress in Plants",subtitle:"Mechanisms and Adaptations",isOpenForSubmission:!1,hash:"588466f487e307619849d72389178a74",slug:"abiotic-stress-in-plants-mechanisms-and-adaptations",bookSignature:"Arun Shanker and B. 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\nThe idea behind this iterative method was to work with a symmetric and positive definite matrix. The scheme worked very well, as shown in [1, 2, 3, 4], but the processing time was, in general, very large especially for high Reynolds numbers. Working with matrixes A and B, we are dealing with a non-symetric matrix, but it can be proved that it is strictly diagonally dominant for Δt sufficiently small. The processing time with the second method was reduced in approximately 30 or 35%.
\nAdditionally, in order to show that the fixed point iterative method works well for moderate and high Reynolds numbers, we report results for the lid-driven cavity problem and Reynolds numbers in the range of 3200 ≤
Results, in both formulations, are obtained using the fixed point iterative method reported in [5], which is applied to a non-linear elliptic system resulting after time discretization. The method has shown to be robust enough to handle moderate and high Reynolds numbers, which is not an easy task, see [1, 2].
\nAs the Reynolds number increases, the mesh has to be refined and a smaller time step has to be used, in order to capture the fast dynamics of the flow and, numerically, because of stability reasons, as mentioned in [6], although, with the velocity-vorticity formulation [7, 8], a finer mesh has to be used, both in time and in space.
\nThe computing time is, in general, very large with this numerical scheme and for both formulations, so that is why we are looking forward to reduce computing time working with both matrixes A and B resulting from the discretization of the Laplacian and the advective term, respectively, instead of working just with matrix A, which is symmetric and positive definite.
\nWith the Stream function-vorticity formulation, and for moderate and high Reynolds numbers, the second scheme was faster than the fixed point iterative method (see [9, 10]). With respect to the velocity-vorticity formulation, we are just showing results using the fixed point iterative method, and for lower Reynolds numbers, but we are looking forward to modify the scheme also in order to reduce computing time.
\nLet \n
These are the Navier-Stokes equations in primitive variables. This system must be provided with appropriate initial conditions \n
When working in a two-dimensional region \n
followed by (Eq. (1b)), with ψ the Stream function, \n
The following system of equations is then obtained:
\nwhere ω is the vorticity given by ω = \n
This system represents the Navier-Stokes equations in the Stream function-vorticity formulation. The incompressibility condition (Eq. (1b)), because of (Eq. (2)), is automatically satisfied and the pressure does not appear any more.
\nTaking the curl in
\nand using the identity \n
Two Poisson type equations for the velocity are obtained, which together with the equation for the vorticity give us:
\nThese are the Navier-Stokes equations in the velocity-vorticity formulation.
\nThe following second-order approximation for the time derivative is used:
\nwhere \n
The resulting discretization system reads:
\nwhere \n
At each time level, the following non-linear system has to be solved.
\nTo obtain \n
For solving this system of equations, two strategies were used in this work: First, we used the fixed point iterative method described in [5]:
\nDenoting \n
our system is equivalent to
\nThen, at each time level, the following the fixed point iterative process (see [5]) is used:
\nGiven \n
and then take \n
To reduce the computing time, we worked in solving the system by the following method at each time step:
\nwhere A and B are the matrixes resulting from the discretization of the Laplacian and the advective term respectively, and (Eq. (13b)) is solved using Gauss-Seidel method.
\nThe second-order approximation (Eq. (7)) for the time derivative is used and the following non-linear system is obtained in Ω
\nwhere
\nUsing again the fixed point iterative method previously described, we have:
\nGiven \n
and then take \n
With respect to the lid-driven cavity problem and using the Stream function-vorticity formulation \n
where \n
In \nFigures 1\n and \n2\n, we show results for the lid-driven cavity problem with \n
Streamlines (left) and isovorticity contours (right) for
Streamlines (left) and isovorticity contours (right) for
For the Taylor vortex problem, results are shown in \nFigures 3\n and \n4\n for \n
Stream function and vorticity for
Exact stream function and vorticity for
The exact Stream function and the vorticity are also shown in \nFigure 5\n, for \n
Stream function and vorticity for
In the primitive variables formulation, we have as initial conditions:
\nFor the Stream function, the boundary conditions are:
\nFor the vorticity, the boundary conditions are:
\nIn \nTables 1\n and \n2\n, we show computing times for the above-mentioned problems with both the methods; the Fixed Point Iterative Method and working with matrixes A and B.
\n\n | \nFixed point iterative method (s) | \nWorking with A and B (s) | \n
---|---|---|
5000 | \n153 | \n120 | \n
7500 | \n801 | \n610.25 | \n
Time in seconds, for both Reynolds numbers and the two methods described for the lid-driven cavity problem.
\n | \nFixed point iterative method (s) | \nWorking with A and B (s) | \n
---|---|---|
5000 | \n15.5 | \n12.75 | \n
7500 | \n15.5 | \n12.75 | \n
Time in seconds, for both Reynolds numbers and the two methods for the Taylor vortex problem.
In \nFigure 6\n, we show the streamlines and isovorticity contours for \n
Streamlines (left) and isovorticity contours (right) for
Streamlines (left) and isovorticity contours (right) for
Then, in \nFigure 8\n, we show just the isovorticity contours for \n
Isovorticity contours (left) for
In the case of the velocity-vorticity formulation and the lid-driven cavity problem, the boundary condition for u is given by
Not all the results were obtained using the second-order discretization. In some cases, a fourth-order discretization has to be used, using the fourth-order option of Fishpack [12] (used in this work for solving the elliptic problems appearing).
\nIn \nFigure 9\n, we show the streamlines and the isovorticity contours for \n
Streamlines (left) and isovorticity contours (right) for
In \nFigure 10\n, we show the isovorticity contours for \n
Isocontours for the vorticity for
As can be noticed with the Stream function-vorticity formulation, we are using a value of h half of the size of the one used with the velocity-vorticity formulation. We assume the results obtained with the first-mentioned formulation are more reliable. Computing time for the velocity-vorticity formulation was much larger. We think there are still some numerical problems with this formulation and for very high Reynolds numbers.
\nFor the lid-driven cavity problem results agree very well with those reported in the literature [1, 2, 3, 4, 13, 14], and by working with matrixes A and B it was possible to reduce computing time between a 30 and 35%.
\nAs can be seen in \nFigures 1\n and \n2\n, numerical oscillations occurred, given the high Reynolds numbers used in such a way that it is necessary to use smaller values of h [6], numerically because of stability of the method and physically in order to capture the fast dynamics of the flow.
\nFor high Reynolds numbers and small values of h the computational work takes a lot of time, so reducing computing time becomes a very important fact. For the Taylor Vortex Problem [8, 15], processing time was also reduced between 30 and 35%.
\nWith the velocity-vorticity formulation, as already mentioned, we only show results using the Fixed Point Iterative Method, and we are looking forward working with both matrixes A and B, in order to reduce computing time also with this formulation. This is the reason why we only show results till
In conclusion, the numerical scheme applied with the stream function-vorticity formulation is not as good with the velocity-vorticity formulation, although, the way it behaves with some values of the parameters and the order of discretization, gives us another point of view about the behavior of the fluids under different numerical methods and different formulations.
\nWe must also say that our code has not been parallelized since it is difficult to do this. It must be taken into account that the equations, in both formulations, are coupled. We are looking forward to use a solver for the system of linear equations that can be parallelized. This can be viewed as a future work.
\nThe authors would like to acknowledge the support received by the National Laboratory of Supercomputing from of the southeast of Mexico BUAP-INAOE-UDLAP (Laboratorio Nacional de Supercómputo del Sureste de México).
\nThe neurohypophyseal nonapeptide hormone oxytocin (OT), the first peptide hormone to have its structure determined [1], plays an important role in social behavior across a wide variety of species [2, 3]. The word ‘oxytocin’ was coined from the Greek words (ω k ν ξ, τ o k ox ξ) meaning ‘quick birth’ after its uterine-contracting properties were discovered by Dale [4]. OT’s repertoire has expanded to maintain a central role in more complicated aspects of reproductive behavior. For these reasons, it is called the great facilitator of life [5] (Figure 1).
A simple cycle of life illustrates numerous points at which OT may affect behaviors and physiology to facilitate the propagation of the species [
OT is synthesized at the paraventricular (PVN), supraoptic nuclei (SON), and intermediate accessory nuclei of the hypothalamus and transported through the axons of these cells to the posterior pituitary gland [6]. From the posterior pituitary, OT reaches the general blood circulation. It is also produced by different peripheral tissues, such as skin, placenta, ovary, testis, thymus, pancreas, adipocytes, kidney, heart, and blood vessels [7]. OT acts as a hormone in the peripheral circulation and as a neurotransmitter/neuromodulator in the central nervous system [8].
The neurohormone OT is an effective stimulant of the uterine contraction and is used primarily to induce or reinforce labor in obstetrics [9]. OT facilitates the expulsion of milk from the mammary gland during nursing. The release of OT from the posterior pituitary is stimulated by tactile sensory inputs from the nipple. Milk-ejection is the only physiological function known to absolutely require OT [10]. For both men and women, OT is released during sexual stimulation and orgasm, may reduce urine volume and induce natriuresis through co-activation of vasopressin receptors, and is involved in the modulation and regulation of the hypothalamic–pituitary–adrenal (HPA) axis [11]. Moreover, OT plays a role in the endocrine and paracrine activities such as various sexual and maternal behaviors, social recognition, aggression, neuromodulation, cognition, and tolerance development; however, the mechanism is still unclear [2, 12, 13].
The central neuropeptidergic effect of OT has continued to be studied in the social behavior of various species (in humans and animal models) to date. Nagasawa
“Summary of the role of the oxytocin system in reciprocal communication” Nagasawa et al. [
According to the figure, the central OT secretion is stimulated by multiple sensory signals in mammals. Increased OT release is important in the development of physiology and behavioral functions, and also causes a decrease in pain and stress.
Oxytocin (seq;CYIQNCPLG), a neurohypophysial peptide hormone, consists of nine amino acids (H-Cys(1)-Tyr-Ile-Gln-Asn-Cys(1)-Pro-Leu-Gly-NH2) linked with a [1-6] disulfide bond and a semi-flexible carboxy amidation tail [15] (Figure 3). This results in a peptide constituted of a rigid N-terminal cyclic 6-residue ring structure and a flexible COOH-terminal alpha amidated three-residue tail [5].
Chemical structure depiction of oxytocin (OT). Molecular formula: C43H66N12O12S2/Molecular weight: 1007.2 g/mol [
Biological description of IUPAC (International Union of Pure and Applied Chemistry);
L-cysteinyl-L-tyrosyl-L-isoleucyl-L-glutaminyl-L-asparagyl-L-cysteinyl-L-prolyl-L-leucyl-glycinamide (1->6)-disulfide [15].
The structure of OT is very similar to another nonapeptide, entitled vasopressin (AVP/arginine vasopressin), which differs from OT by only two amino acids in positions 3 and 8 (Figure 4) [16], (Figure 5) [9]. OT and AVP genes in the mouse, rat, and human genomes are located on the same chromosome separated by a short (3.5–12 kbp) intergenic region but are in opposite transcriptional orientations [17, 18, 19, 20]. They are synthesized in the brain’s hypothalamic paraventricular and supraoptic nuclei [21].
“Schematic diagram of the oxytocin (OT) and vasopressin (AVP) genes (large arrows), preprohormones (boxes), and neuropeptides (bottom)” [
“Organization of the oxytocin (OT) and vasopressin (VP) gene structure including a schematic depiction of the putative cell-specific enhancers (open circle, enhancer of OT gene; shaded circle, enhancer of VP gene)” [
OT is currently known to have only one receptor (OTR/oxytocin receptor), which forms together with the related V1a, V1b, and V2 vasopressin receptor subtypes a subfamily of the large G protein-coupled receptor (GPCR) superfamily, one of the most abundant protein classes in the mammalian genome [16, 22]. OT shows its biological activity through the GPCR, which is widely expressed throughout the body, including the central and peripheral nervous systems. Heterotrimeric G-proteins are composed of α, β, and γ subunits [23]. These receptors are characterized by seven putative transmembrane domains, three extracellular, and three intracellular loops (Figure 6) [9, 22, 24].
“Schematic model of the structure of the OT receptor and its interaction with the ligand” (Zingg HH and Laporte SA, 2003) [
The group of OT and vasopressin receptors is well suited for receptor structure–function analysis, because it comprises four related receptors that bind, with varying degrees of specificity, the two closely related peptide ligands, OT and vasopressin [25].
OTR can be coupled to different G proteins, leading to different intracellular pathways. It is possible that these various signaling pathways are differentially expressed in neuronal versus peripheral tissues [26].
The quality of specific acute or long-term neuronal effects of OT is dependent on the regional and subcellular presence of OTR, the characteristics of OT-OTR binding, and subsequent activation of intraneuronal signaling cascades. In addition, the formation of OTR homodimers or heterodimers with other receptors is likely to influence OTR affinity and downstream signaling [23]. The classical signaling pathway associated with the OTR involves a phospholipase C-mediated increase in phosphoinositide hydrolysis, activation of protein kinase C, and a rise in intracellular calcium [27, 28]. The proliferative effects of OT are mediated primarily by the activation of the MAP kinase pathway, involving different G protein-linked pathways as well as receptor tyrosine kinase transactivation [29].
OT-induced Ca2 influx also seems to play a role in neuronal OT responses. On a cellular level, the OTR activates numerous Ca2-related and MAPK-related signaling cascades in a variety of cell types [23].
Given the multiple signaling pathways in which OTR binds, the development of pathway-specific ligands will be important in elucidating the different OTR-linked pathways, as well as developing more specific agonists and antagonists for future therapeutic applications.
In mammals, increasing brain OT levels promotes attachment and attachment behavior, facilitates parental behavior, social recognition, and memory between relatives, and establishes emotional bonds between animals and caregivers [11, 30, 31, 32]. In humans, it has been also shown to increase trust and generosity, strengthen emotional and cognitive empathy, and reduce social-anxiety and fear-related behavior [33, 34]. In line with these findings, impaired social behavior profiles have been associated with reduced central endogenous OTergic activity. Depletion of OTergic signaling through genetic change of the OT gene or receptor has caused convincing social deficiencies, social amnesia, malfunctions in breastfeeding and maternal nutrition, and decreased infant ultrasonic sounds in response to social isolation, but normal birth and sexual behavior [35, 36, 37].
Abnormal brain development, during embryogenesis, fetal development, or early postnatal periods, can generate cognitive dysfunction as well as neurological, emotional, and behavioral disorders. Disturbed brain OTergic signaling has been implicated in several psychiatric disorders where social dysfunction is a core symptom (autism spectrum disorder, social anxiety, borderline personality disorder, addiction, and schizophrenia) [31, 37, 38].
There are several animal studies in the literature showing neuroprotective effects of OT. These neuroprotective effects of OT hormone include social neuroprotection, oxygen–glucose deprivation resistance, immune system modulation, anti-apoptotic, anti-inflammatory, and antioxidative functions [38, 39].
Due to the therapeutic properties and health benefits of OT, it can be thought that OT and OT-like molecules are a part of ‘natural medicine’ that can both prevent and treat diseases and affect the course of many diseases [20].
Understanding the complex actions of OT requires awareness that OT regulates not only the brain and reproductive system but also the immune and autonomic nervous systems. For example, evidence supporting the coordinated effects of acetylcholine (the neurotransmitter in the preganglionic sympathetic and parasympathetic neurons) and OT regulate the autonomic nervous system [40].
The therapeutic effects of the OT hormone have been studied in a variety of pathological conditions, both
OT treatment in rats induces several long-lasting anti-stress effects, for example, subchronic OT treatment of males and females rats produces a long-lasting change in spontaneous motor activity, nociception threshold, and weight gain [41].
In many studies, the antiepileptic properties of OT have been emphasized which have positive effects on neurobehavioral pathologies such as autism and psychosis, and it has been shown that it has healing effects on these diseases with its anti-inflammatory and antioxidant properties [42].
It has been revealed that OT modulates the immune and anti-inflammatory response thus reducing inflammatory cytokines production (TNFα; tumor necrosis factor-alpha; is a multifunctional cytokine and IL-6 (interleukin 6)); added to its remarkable anabolic properties on many peripheral organs and on the immune system development [38, 43, 44].
Studies demonstrate the therapeutic effects of both melatonin and OT on critical disease polyneuropathy (CIP) are remarkable. These effects appear to be associated with suppression of cytokine production and improvement in antioxidant capacity [45].
In a study, scientists evaluated the therapeutic potential of OT and liraglutide (LIR), which is a long-acting human glucagon-like peptide-1 (GLP-1) analog, in a rat model of vincristine-induced neuropathy [46]. Vincristine (VCR) is a vinca alkaloid, is known to cause various neurological dysfunctions, antitumoral, and the most neurotoxic agent and it has been used for the treatment of numerous tumors [47, 48]. GLP-1 is a polypeptide hormone composed of 30 amino acids, which is mainly secreted from intestinal L cells in response to nutrient ingestion [49]. Recent studies have indicated that GLP-1 analogs may have therapeutic effects against central and peripheral degenerative changes in animal models of neurodegenerative diseases [50]. GLP-1 exerts its neurotrophic effects through GLP-1 receptors (GLP-1Rs), which are detected particularly on neurons throughout the central and peripheral nervous system [51]. Histological and biochemical findings of the study revealed that both OT and liraglutide significantly prevented neuronal damage by suppressing lipid peroxidation and inducing NGF (nerve growth factor) expression in VCR-received rats [46].
Platinum drugs are compounds containing metal ions that form binding sites for proteins, nucleic acids, and other cellular molecules. This property is largely responsible for the biological activity of drugs as well as their toxicity [52]. Peripheral neurotoxicity is the dose-limiting factor for clinical use of platinum derivatives, a class of anticancer drugs that includes cisplatin, induce decreased neural transmission rate, loss of vibration and position senses, tingling paresthesia, dysesthesia, loss of tendon reflexes, tremor, ataxia, and muscle weakness [53, 54].
Cisplatin (CP) was the first heavy metal compound to be used as antineoplastic, and since its approval by the FDA in 1978, it is one of the most widely used for the treatment of various solid tumors such as lung, ovary, testis, bladder, head, and neck, and cervical and endometrial cancers [55, 56].
The mechanisms suggested explaining the neurotoxicity of these drugs are dorsal root ganglia alteration, oxidative stress involvement, and mitochondrial dysfunction. These alterations are able to stop DNA replication and cell cycle, inhibit DNA repair mechanisms, and induce cell death through apoptosis [57]. Oxidative stress, DNA damage, and inflammatory cytokines play a major role in the mechanism of cisplatin-induced cytotoxicity. Cisplatin increases the production of free oxygen radicals and decreases the antioxidants, thus resulting in the deterioration of the oxidant/antioxidant balance and accumulation of reactive oxygen radicals (ROS) in tissues [58]. Akman
Present results also demonstrate that OT appears to alleviate the harmful effects of hyperglycemia on peripheral neurons by suppressing inflammation, oxidative stress, and apoptotic pathways [63]. Excessive ROS accumulation leads to an increase in mitochondrial inner membrane permeability. Hyperglycemia also increases oxidative stress and inhibits mitochondrial biogenesis [64]. The depletion of growth factors and the activation of caspase 3 and caspase 8 trigger intrinsic apoptotic cell death in neurons [65, 66].
Diabetic polyneuropathy (DNP) is the most common complication of diabetes with a prevalence of 60–70%. DNP represents a heterogeneous group of syndromes with clinical and subclinical disorders and abnormalities such as distal symmetrical polyneuropathy, mononeuropathy, diabetic amyotrophy, autonomic dysfunction, or cranial neuropathies [67]. Hyperglycemia-induced metabolic changes affect tissues and microvascular systems and lead to ischemic pathological changes in the nerve tissue [68]. Erbas
The brain is the most complex human organ and is extremely sensitive to the action of external chemicals and/or physical factors during its ontogenesis. Exposure to xenobiotics has raised great concern about the increasing prevalence of neurodevelopmental disorders and the possible unknown developmental neurotoxic effects of certain chemicals and drugs [69, 70].
Rotenone is a commonly used plant-derived pesticide that inhibits mitochondrial complex I of the electron transport chain [71]. Rotenone has been suggested as one of the most important environmental risk factors for Parkinson’s Disease (PD) [72, 73]. Clinical and experimental studies have strongly supported that it is not only the SNc (substantia nigra pars compacta) and striatum, but also other regions, such as ventral tegmental area (VTA), have important roles in the pathophysiology of PD [74, 75, 76]. Accumulating evidence indicates that OT exerts its cytoprotective effects via anti-oxidative, anti-apoptotic, and anti-inflammatory pathways [44, 77, 78]. In recent years, rotenone-induced PD model in rats is commonly used to study the mechanisms of neuronal degeneration in PD. Erbas
The factors that cause brain damage are varied. These factors include inflammation, birth trauma, tumors, stroke, ischemia, and hypoxia, as well as metabolic and genetic disorders. Hypoxia is the insufficient oxygen supply of the cell. It leads to neurodegeneration by causing mitochondrial dysfunction. Disruption of aerobic respiration mechanism causes different degrees of hypoxia in the tissue. As a result of damage, neurodegeneration, and brain dysfunction accompanied by cognitive impairment are observed [82, 83, 84]. Depending on the degree of hypoxia, activation of potassium channels, increase in perivascular PH, elevated blood and tissue concentrations of CO2, variation in intracellular calcium levels may contribute to neurodegeneration [85]. Regardless of neuronal damage, another factor underlying hypoxia-induced neonatal seizures may be a decrease in gamma-aminobutyric acid (GABA) activity [42, 86]. The cerebral cortex, hippocampus, striatum, and cerebellum have been shown to be the primary areas that are significantly affected by hypoxia and these regions have been associated with the resultant long-term cognitive problems in animal models [87]. In 2018, Panaitescu
Stroke is a sudden decrease or cessation of blood flow to the brain. It can occur when one of the brain vessels ruptures and blood bleeds into the brain tissue or brain membranes. This is known as “brain hemorrhage”. Depending on the affected brain region, speech, muscle strength, coordination-balance, vision, or memory loss occur. Technical advances in neuroimaging and neuropathology have facilitated the understanding of ischemia, infarction, and hemorrhage in the brain [94]. Neuronal injury in stroke is caused by different mechanisms, including excitotoxicity, inflammation, oxidative stress, and apoptosis [95].
Cerebral ischemia induces microglial activation by a strong inflammatory reaction with peripheral leukocyte influx into the cerebral parenchyma. Interruption of cerebral blood flow causes necrotic neuron death by affecting energy metabolism. In addition, different immune responses occur and inflammatory cell activation develops. Inflammatory cells can release a variety of cytotoxic agents including more cytokines, matrix metalloproteinases (MMPs), nitric oxide (NO), and more ROS (Figure 7) [95, 96].
“Brain ischemia triggers inflammatory responses due to the presence of necrotic cells, generation of reactive oxygen species (ROS), and production of inflammatory cytokines even within neurons” (Wang Q et al. 2007) [
One of the dramatic events during ischemia is the increase in intracellular calcium (Ca + 2), which leads to the activation of calpain proteases [97]. A study shows that calpain-1 increases reactive oxygen species levels and inflammatory cytokines [98]. Increased oxidative stress followed by calcium influx, mitochondrial dysfunction, and the loss of cytoskeletal proteins are phenotypes commonly observed in Alzheimer, Huntington, and Parkinson’s diseases, as well as amyotrophic lateral sclerosis, stroke, ischemia, spinal cord injury, and TBI (traumatic brain injury) [99].
Neuroprotective effects of OT and the underlying molecular mechanisms are under discussion after different ischemia–reperfusion models [100, 101]. Jankowski
The effect of oxytocin as a neuromodulator is a subject that has been studied in many different ways. It effectively provides nerve regeneration in nerve damage is a known issue. In addition, its anti-epileptic attack or reducing attack power effect in epilepsy models has also been shown in some studies. It plays an important role in the regulation of spinal autonomic functions. Although it regulates urination reflex and uterine motility, it can increase heart rate and renal sympathetic activity. Considering the positive effects of OT on the brain, reproductive system, immune and autonomic nervous system it shows promise as future treatment agents on the spectrum of anxiety, autism, personality disorders, and neurodegenerative disorders. Studies reveal that oxytocin shows its cytoprotective effects through its anti-inflammatory, anti-apoptotic and antioxidant properties. In chronic inflammation, immune cells constantly attack healthy tissues, resulting in conditions such as obesity, cancer, diabetes, heart disease, autoimmune diseases, Alzheimer’s, and some other diseases. Increasing the effectiveness of anti-inflammatory agents such as OT will improve the quality of life by changing the course of many diseases.
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