Appearance of Inherited thrombophilia.
\\n\\n
These books synthesize perspectives of renowned scientists from the world’s most prestigious institutions - from Fukushima Renewable Energy Institute in Japan to Stanford University in the United States, including Columbia University (US), University of Sidney (AU), University of Miami (USA), Cardiff University (UK), and many others.
\\n\\nThis collaboration embodied the true essence of Open Access by simplifying the approach to OA publishing for Academic editors and authors who contributed their research and allowed the new research to be made available free and open to anyone anywhere in the world.
\\n\\nTo celebrate the 50 books published, we have gathered them at one location - just one click away, so that you can easily browse the subjects of your interest, download the content directly, share it or read online.
\\n\\n\\n\\n\\n"}]',published:!0,mainMedia:null},components:[{type:"htmlEditorComponent",content:'
IntechOpen and Knowledge Unlatched formed a partnership to support researchers working in engineering sciences by enabling an easier approach to publishing Open Access content. Using the Knowledge Unlatched crowdfunding model to raise the publishing costs through libraries around the world, Open Access Publishing Fee (OAPF) was not required from the authors.
\n\nInitially, the partnership supported engineering research, but it soon grew to include physical and life sciences, attracting more researchers to the advantages of Open Access publishing.
\n\n\n\nThese books synthesize perspectives of renowned scientists from the world’s most prestigious institutions - from Fukushima Renewable Energy Institute in Japan to Stanford University in the United States, including Columbia University (US), University of Sidney (AU), University of Miami (USA), Cardiff University (UK), and many others.
\n\nThis collaboration embodied the true essence of Open Access by simplifying the approach to OA publishing for Academic editors and authors who contributed their research and allowed the new research to be made available free and open to anyone anywhere in the world.
\n\nTo celebrate the 50 books published, we have gathered them at one location - just one click away, so that you can easily browse the subjects of your interest, download the content directly, share it or read online.
\n\n\n\n\n'}],latestNews:[{slug:"step-in-the-right-direction-intechopen-launches-a-portfolio-of-open-science-journals-20220414",title:"Step in the Right Direction: IntechOpen Launches a Portfolio of Open Science Journals"},{slug:"let-s-meet-at-london-book-fair-5-7-april-2022-olympia-london-20220321",title:"Let’s meet at London Book Fair, 5-7 April 2022, Olympia London"},{slug:"50-books-published-as-part-of-intechopen-and-knowledge-unlatched-ku-collaboration-20220316",title:"50 Books published as part of IntechOpen and Knowledge Unlatched (KU) Collaboration"},{slug:"intechopen-joins-the-united-nations-sustainable-development-goals-publishers-compact-20221702",title:"IntechOpen joins the United Nations Sustainable Development Goals Publishers Compact"},{slug:"intechopen-signs-exclusive-representation-agreement-with-lsr-libros-servicios-y-representaciones-s-a-de-c-v-20211123",title:"IntechOpen Signs Exclusive Representation Agreement with LSR Libros Servicios y Representaciones S.A. de C.V"},{slug:"intechopen-expands-partnership-with-research4life-20211110",title:"IntechOpen Expands Partnership with Research4Life"},{slug:"introducing-intechopen-book-series-a-new-publishing-format-for-oa-books-20210915",title:"Introducing IntechOpen Book Series - A New Publishing Format for OA Books"},{slug:"intechopen-identified-as-one-of-the-most-significant-contributor-to-oa-book-growth-in-doab-20210809",title:"IntechOpen Identified as One of the Most Significant Contributors to OA Book Growth in DOAB"}]},book:{item:{type:"book",id:"5901",leadTitle:null,fullTitle:"Testes and Ovaries - Functional and Clinical Differences and Similarities",title:"Testes and Ovaries",subtitle:"Functional and Clinical Differences and Similarities",reviewType:"peer-reviewed",abstract:"Male and female reproductive system similarities as well as differences should be taken into consideration by all scientists interested in this field. Some embryological, anatomical, histological, and clinical examples are addressed in this book. The message of the book is to increase orientation of all scientists interested in the field of similar and dissimilar issues in males and females. Reading this book will lead to a better understanding of management of both sexes, and the understanding of infertility that will hopefully reduce the effort, the time, the psychological, and the financial burden of the infertile couple and the society at large.",isbn:"978-953-51-3690-3",printIsbn:"978-953-51-3689-7",pdfIsbn:"978-953-51-3992-8",doi:"10.5772/65984",price:119,priceEur:129,priceUsd:155,slug:"testes-and-ovaries-functional-and-clinical-differences-and-similarities",numberOfPages:106,isOpenForSubmission:!1,isInWos:1,isInBkci:!1,hash:"a58d754113b9ce21f745d181a689b8e9",bookSignature:"Atef M. Darwish",publishedDate:"December 20th 2017",coverURL:"https://cdn.intechopen.com/books/images_new/5901.jpg",numberOfDownloads:7148,numberOfWosCitations:2,numberOfCrossrefCitations:3,numberOfCrossrefCitationsByBook:0,numberOfDimensionsCitations:9,numberOfDimensionsCitationsByBook:0,hasAltmetrics:0,numberOfTotalCitations:14,isAvailableForWebshopOrdering:!0,dateEndFirstStepPublish:"December 13th 2016",dateEndSecondStepPublish:"December 20th 2016",dateEndThirdStepPublish:"September 16th 2017",dateEndFourthStepPublish:"October 16th 2017",dateEndFifthStepPublish:"December 16th 2017",currentStepOfPublishingProcess:5,indexedIn:"1,2,3,4,5,6",editedByType:"Edited by",kuFlag:!1,featuredMarkup:null,editors:[{id:"29304",title:"Prof.",name:"Atef",middleName:"M.M.",surname:"Darwish",slug:"atef-darwish",fullName:"Atef Darwish",profilePictureURL:"https://mts.intechopen.com/storage/users/29304/images/1698_n.jpg",biography:"Dr. Atef Darwish graduated from Assiut School of Medicine in 1985 with an excellent grade with first class honors. He got his Master degree in 1989 with Excellent degree. Between 1992-1994, he spent 2 years at the Endoscopic Unit of Ulm University, Germany. Thereafter, he received his Medical Doctorate in 1995 through a combined program between the University of Ulm, Germany and the University of Assiut, Egypt with Excellent degree. He joined the Endoscopy Unit of Villach University Hospital in Austria, the Assisted Reproduction Unit in Düsseldorf University Hospital in Germany and the reproductive biology and minimally invasive surgery unit in the Cleveland Clinic Foundation, Clevland, Ohio, USA. Currently, he is a Professor of Obstetrics and Gynecology, Faculty of Medicine, Assiut University since July 2005. Moreover, he is a consultant of Obstetrics and Gynecology in three hospitals and he is the moderator and lecturer of many endoscopic societies. \nHe authored an internationally registered undergraduate book, presented 59 presentations in national and international meetings, delivered a lot of lectures in Egypt, some Arabian countries and the USA and published more than 40 papers in international medical journals, and 7 papers in national journals. He received some congress prizes and awards due to his work in the field of reproductive medicine since 1995. He is a reviewer of many international journals and an associate editor of two of them. \nIn 2009, he got a PhD degree in the reproductive medicine at the University of Utrichet, The Netherlands.",institutionString:null,position:null,outsideEditionCount:0,totalCites:0,totalAuthoredChapters:"8",totalChapterViews:"0",totalEditedBooks:"7",institution:null}],equalEditorOne:null,equalEditorTwo:null,equalEditorThree:null,coeditorOne:null,coeditorTwo:null,coeditorThree:null,coeditorFour:null,coeditorFive:null,topics:[{id:"1069",title:"Reproductive Endocrinology and Infertility",slug:"obstetrics-and-gynecology-reproductive-endocrinology-and-infertility"}],chapters:[{id:"56340",title:"Introductory Chapter: One-Stop Infertility Evaluation Unit",doi:"10.5772/intechopen.69631",slug:"introductory-chapter-one-stop-infertility-evaluation-unit",totalDownloads:1053,totalCrossrefCites:0,totalDimensionsCites:0,hasAltmetrics:0,abstract:null,signatures:"Atef Darwish and Essam-Eldn Mohamed",downloadPdfUrl:"/chapter/pdf-download/56340",previewPdfUrl:"/chapter/pdf-preview/56340",authors:[{id:"29304",title:"Prof.",name:"Atef",surname:"Darwish",slug:"atef-darwish",fullName:"Atef Darwish"}],corrections:null},{id:"55380",title:"The Impact of Aging on Fertility: Similarities and Differences between Ovaries and Testes",doi:"10.5772/intechopen.68905",slug:"the-impact-of-aging-on-fertility-similarities-and-differences-between-ovaries-and-testes",totalDownloads:1248,totalCrossrefCites:0,totalDimensionsCites:0,hasAltmetrics:0,abstract:"The increasing age seems to have a negative impact on reproductive functions not only in women but also in men. Therefore, our aim was to review the data available in the literature regarding the impact of advancing age on fertility and the mechanisms underlying this association in both genders. The available data suggest that the effects of age on ovarian function cause a decrease in fertility starting 13 years before menopause. Statistics show that 10% of women will have a decreased fertility starting with the age of 30. The impact of age on ovary is due to both decreased number and quality of the oocytes, resulting in a high rate of chromosomal aneuploidy in the embryo and mitochondria dysfunction. Assisted reproductive technologies aiming to identify competent embryo were created but for the moment the results are unsatisfactory. On the other hand, in men, the semen quality and testicular function were found to gradually decrease with age and most of the studies also describe a negative impact on fertility. The mechanisms underlying decreased fertility are mainly genetic and epigenetics changes. However, if the effects of age on male fertility in men can be overcome by assisted reproductive technologies is not clear yet as the results of the studies are inconsistent.",signatures:"Alice Ioana Albu and Dragos Albu",downloadPdfUrl:"/chapter/pdf-download/55380",previewPdfUrl:"/chapter/pdf-preview/55380",authors:[{id:"200829",title:"Dr.",name:"Alice",surname:"Albu",slug:"alice-albu",fullName:"Alice Albu"},{id:"207984",title:"Dr.",name:"Dragos",surname:"Albu",slug:"dragos-albu",fullName:"Dragos Albu"}],corrections:null},{id:"54578",title:"Diagnosis, Pathogenesis and Management of Polycystic Ovary Syndrome",doi:"10.5772/67877",slug:"diagnosis-pathogenesis-and-management-of-polycystic-ovary-syndrome",totalDownloads:1231,totalCrossrefCites:2,totalDimensionsCites:2,hasAltmetrics:0,abstract:"Polycystic ovary syndrome (PCOS) is one of the most common reproductive endocrine diseases occurs among women of childbearing age, which is affected by many factors, but its precise pathophysiology has not yet been determined. The heterogeneous of PCOS is reflected in its complex endocrine dysfunction of the hypothalamic-pituitary-gonadal axis (HPG axis) and its multiple clinical features, such as obesity, insulin resistance, hyperandrogenism and anovulation. Meanwhile, women with PCOS also have an increased risk of major cardiovascular events, most notably type 2 diabetes, cardiovascular disease and atherosclerosis. So far, many therapies are available for improving reproductive and metabolic abnormalities in PCOS patients, in which lifestyle modification and insulin-sensitizing agents are more effective management strategies.",signatures:"Fan Wang and Zhengchao Wang",downloadPdfUrl:"/chapter/pdf-download/54578",previewPdfUrl:"/chapter/pdf-preview/54578",authors:[{id:"204883",title:"Dr.",name:"Zhengchao",surname:"Wang",slug:"zhengchao-wang",fullName:"Zhengchao Wang"},{id:"205460",title:"Dr.",name:"Wang",surname:"Fan",slug:"wang-fan",fullName:"Wang Fan"}],corrections:null},{id:"55589",title:"Metabolic Disorders Associated with Biological Insulin Resistance in Congolese Woman with Polycystic Ovary Syndrome (PCOS)",doi:"10.5772/intechopen.69182",slug:"metabolic-disorders-associated-with-biological-insulin-resistance-in-congolese-woman-with-polycystic",totalDownloads:1216,totalCrossrefCites:1,totalDimensionsCites:1,hasAltmetrics:0,abstract:"We aimed to identify metabolic disorders associated with insulin resistance (IR) in Congolese women affected by polycystic ovary syndrome (PCOS). Fifty‐four PCOS women and 40 controls from three hospitals of Kinshasa were enrolled to our case‐control study. Blood samples were collected, and concentrations of high‐density lipoprotein (HDL) and low‐density lipoprotein (LDL) cholesterol, triglycerides (TG), fasting insulin, and glucose levels were measured. IR under basal conditions was evaluated with homeostasis model assessment (HOMA‐IR). Dyslipidemia was observed in 37.5 controls and 55.6% PCOS women (p < 0.05). The two main lipoproteins concerned were HDL and LDL; nevertheless, the difference in LDL levels between PCOS and controls was not significant. Higher TG (>150 mg/dl) was not found in the two groups, whereas TG levels in PCOS patients were significantly higher than in controls (p < 0.05). Impaired glucose tolerance (IGT) and metabolic syndrome were observed, respectively, in 1.9% of PCOS patients. Insulin resistance is associated with metabolic disorders in Congolese woman with PCOS. Dyslipidemia (55.6%), mainly due to low HDL levels, is the most common metabolic disorder. Impaired glucose tolerance and metabolic syndrome represent a small proportion.",signatures:"Chantal Amisi Anifa, Mputu Lobota, Mboloko Esimo and Paolo Pozzilli",downloadPdfUrl:"/chapter/pdf-download/55589",previewPdfUrl:"/chapter/pdf-preview/55589",authors:[{id:"201917",title:"Ph.D. Student",name:"Chantal",surname:"Amisi",slug:"chantal-amisi",fullName:"Chantal Amisi"},{id:"207191",title:"Prof.",name:"Mputu",surname:"Lobota",slug:"mputu-lobota",fullName:"Mputu Lobota"},{id:"207193",title:"Prof.",name:"Mboloko",surname:"Esimo",slug:"mboloko-esimo",fullName:"Mboloko Esimo"},{id:"207195",title:"Prof.",name:"Paolo",surname:"Pozzilli",slug:"paolo-pozzilli",fullName:"Paolo Pozzilli"}],corrections:null},{id:"57190",title:"Fertility Treatment for Women with PCOS",doi:"10.5772/intechopen.71188",slug:"fertility-treatment-for-women-with-pcos",totalDownloads:1249,totalCrossrefCites:0,totalDimensionsCites:2,hasAltmetrics:0,abstract:"Polycystic ovarian syndrome is the commonest cause of anovulatory infertility. This chapter will explore fertility treatment options for this condition including the risks, benefits and success rates for different treatment methods. The importance of close patient monitoring with hormone levels and pelvic ultrasounds to ensure mono-ovulation and to avoid ovarian hyperstimulation syndrome will be highlighted.",signatures:"Fiona Langdon, Jennifer Pontre and Roger J. Hart",downloadPdfUrl:"/chapter/pdf-download/57190",previewPdfUrl:"/chapter/pdf-preview/57190",authors:[{id:"187858",title:"Prof.",name:"Roger",surname:"Hart",slug:"roger-hart",fullName:"Roger Hart"},{id:"219734",title:"Dr.",name:"Fiona",surname:"Langdon",slug:"fiona-langdon",fullName:"Fiona Langdon"},{id:"219735",title:"Dr.",name:"Jenni",surname:"Pontre",slug:"jenni-pontre",fullName:"Jenni Pontre"}],corrections:null},{id:"54569",title:"Contribution of Autophagy to the Physiological and Pathophysiological Functions in the Mammalian Testis",doi:"10.5772/67878",slug:"contribution-of-autophagy-to-the-physiological-and-pathophysiological-functions-in-the-mammalian-tes",totalDownloads:1152,totalCrossrefCites:0,totalDimensionsCites:4,hasAltmetrics:0,abstract:"Mammalian spermatogenesis is a high regulated biological process occurring in the seminiferous tubules in the testis. The processing of this program requires delicate balance between cell proliferation, differentiation, apoptosis, and expedite cell interaction. Autophagy, an evolutionarily conserved cell reprograming machinery, had been shown to function as an important regulatory mechanism in spermatogenesis and steroid production in testis. Herein, we mainly focused on our understanding of autophagy in mammalian testis. By showing autophagy in physiological and pathophysiological conditions, we try to elicit the regulatory role of autophagy in spermatogenic cells and somatic cells of testis. Moreover, this review is intended to point out factors and mechanisms, which contribute to the initiation of autophagy in testicular cells.",signatures:"Zonghao Tang and Zhengchao Wang",downloadPdfUrl:"/chapter/pdf-download/54569",previewPdfUrl:"/chapter/pdf-preview/54569",authors:[{id:"204883",title:"Dr.",name:"Zhengchao",surname:"Wang",slug:"zhengchao-wang",fullName:"Zhengchao Wang"},{id:"205459",title:"Dr.",name:"Zonghao",surname:"Tang",slug:"zonghao-tang",fullName:"Zonghao Tang"}],corrections:null}],productType:{id:"1",title:"Edited Volume",chapterContentType:"chapter",authoredCaption:"Edited by"},subseries:null,tags:null},relatedBooks:[{type:"book",id:"5059",title:"Genital Infections and Infertility",subtitle:null,isOpenForSubmission:!1,hash:"ecb5e49241a0c218206e413b562a4909",slug:"genital-infections-and-infertility",bookSignature:"Atef M. 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It is well known that thromboembolic disease is an important cause of maternal morbidity and mortality [1, 2]. Moreover, pregnancy is a period of increased coagulation [1, 2]. The above underlines the need to assess thrombotic risk at all stages of pregnancy [3, 4]. To detect pregnancies with an increased risk of thromboembolic disease requires an individual, family history of thromboembolic events, obesity, or surgery [3, 4]. In order to reduce the incidence of this condition, it is necessary to identify women with multiple risk factors for thrombosis during pregnancy [5, 6]. In women with an individual or family history of proven thromboembolic disease, examination for thrombophilia should be performed at the beginning of pregnancy [5, 6].
\nThe term
Antithrombin III deficiency.
Protein C deficiency.
Protein S deficiency.
Mutation in factor V.
Prothrombin gene mutation.
High levels factor VIIIc.
Mild hyperhomocysteinemia.
Antithrombin and C protein are natural coagulation inhibitors, so any deficiency of them predispose for thrombosis. Leiden mutation of factor V is the most common thrombophilic abnormality making anticoagulant protein secreted enable to bind to factor V. Prothrombin G20210A gene mutation is also frequent, causing high levels of inactive prothrombin [15]. Increased factor VIII levels above the 75th position are also a strong risk factor for thromboembolic disease, as well as mild hyperhomocysteinemia (Table 1
\n | General population | \nThromboembolic history (%) | \n
---|---|---|
Antithrombin, C-protein and protein S deficiency | \n1% | \n7 | \n
Factor V Leiden | \nCaucasian: 4–7% Non-Caucasian: 0–1% | \n21 | \n
Prothrombin G20210A | \nCaucasian: 2–3% Non-Caucasian: 0–1% | \n6 | \n
High levels factor VIIIc | \n11% | \n25 | \n
Mild hypehomocysteinemia | \n55 | \n10 | \n
Appearance of Inherited thrombophilia.
Thrombophilia is a group of disorders that stimulate blood clotting. Patients with thrombophilia form clots very easily, either because they produce in excess certain proteins called coagulation factors or because they produce less anticoagulants [15, 16, 17, 18].
\nMost thrombophilic patients are unware for their disease because they do not demonstrate symptoms. However, some will develop a thrombus at some place. Usually clots present in the lower limbs, deep vein thrombosis, causing edema, redness, and dysphoria. These clots can lead into lethal events if they move and travel via blood circulation to vital organs (venous thromboembolism). When the clots block vessels in the lungs, brain, or heart, it can lead to embolism, stroke, or heart attack. A thrombophilia can also increase the risk of coronary artery disease. Clots are more frequent in patients with additional risk factors like immobility or undergoing surgery. Pregnancy is a status when the signs of thrombophilia are very common [15, 16, 17, 18].
\nIn general, women with thrombophilia do not have more pregnancies with complications, but late pregnancy loss in the first or later in the second trimester, placental abruption, and incomplete fetal development are the most frequent. Also, thrombophilia may be clots implicated in preeclampsia. These problems are believed to arise due to thrombus formation in the placenta, a phenomenon that leads to changes in the placenta and a reduced blood flow to the fetus. Pregnant patients with thrombophilia have a higher risk of developing thromboembolic disease than pregnant women without thrombophilia. Generally, pregnancy is a period of increased risk for thromboembolic disease even in women without thrombophilia. This is due to the changes accompanying normal pregnancy involving blood clotting and limiting the loss of blood during childbirth. In the USA, pulmonary embolism is the first cause of maternal death [7, 19, 20, 21].
\nDuring pregnancy, normal changes occur in the coagulation system. According to the literature, an increase in coagulation factors Vc, VIIIc, Xc, and von Willebrand factor antigen and reduction in total and free S protein have been observed. In addition, coagulation activation markers are increased particularly in the third trimester of pregnancy. There is no significant change in plasma levels of protein C or antithrombin III throughout pregnancy. The increase in platelet-derived inhibitor of typ. 2 plasminogen activation (PAI-2), which is produced in increased amounts during pregnancy, partly contributes to the attenuation of fibrinolytic activity. These physiological changes during pregnancy develop a relative thrombotic tendency. Moreover, during pregnancy, cesarean section, previous thromboembolic event, high BMI, multiple pregnancies, infections, preeclampsia, immobility, and maternal age are additional risk factors for venous thromboembolic events
Hereditary disorders | \nAcquired disorders | \n
---|---|
Prothrombin III deficiency | \nAntiphospholipid syndrome | \n
C & S protein deficiency | \nParoxysmal nocturnal hemoglobinuria | \n
Factor V Leiden Hyperhomocysteinemia | \nHyperhomocysteinemia Myeloproliferative disorders | \n
Prothrombin G20210A | \nCancer | \n
Dysfibrinogenemia | \nInflammatory bowel disease | \n
Factor VII, XII & plasminogen deficiency | \nNephrotic syndrome | \n
High levels of factor VII, IX, XI, tPA, PAI | \nCardiac insufficiency | \n
Risk factors leading to thrombosis disorders.
Inherited thrombophilia is present almost in the half of the cases of pregnancy-associated venous thromboembolic events (VTE). Homozygous women with Leiden or prothrombin gene mutation have double risk for recurrent miscarriage in the first trimester [22].
\nIt is well known that during pregnancy, levels of coagulation proteins like protein S, protein C, and antithrombin III are decreased, but deficiencies in these factors can easily lead to hypercoagulation. On the other hand, women with antithrombin deficiency and hyperhomocysteinemia may lead to higher risk of placental abruption. Finally, there is no evident correlation between high level VIIIc and preeclampsia, IUGR (intrauterine growth retardation), and HELLP syndrome [22, 23, 24].
\nEvery woman with vein thrombosis or pulmonary embolism history is thoroughly investigated by laboratory tests, but in the case of acute thromboembolic event during pregnancy, the treatment is not affected by the laboratory results. Therefore, diagnostic tests must be taken before anticoagulant regimen or 1 month after. The results must be evaluated keeping in mind that protein’s S levels are normally decreased in pregnancy. Furthermore, almost 40% of women with no mutation of factor V Leiden are presented with resistance of protein C. Moreover, decreased protein S, C, and antithrombin are widely observed if another disease like hepatopathy or nephritic syndrome coexists in pregnancy [25, 26, 27, 28, 29].
\nLow molecular weight heparin (LMWH) does not go through the placenta and is safe for the fetus, as well as decreases the risk of bleeding. In addition, LMWH is more stable and causes less platelet activation because of less binding of platelet factor 4. The risk of thrombocytopenia is decreased [25].
\nThe mechanism of thrombosis in most cases of congenital thrombophilia is the inability to inactivate thrombin or in the failure to control the production of thrombin. Natural anticoagulants, such as antithrombin, retain the fluidity of the blood. Antithrombin binds to heparin sulfate or endothelial cells and inactivates thrombin, factor XIa, factor IXa, and factor Xa. Another anticoagulant, protein C, controls the production of thrombin. When thrombin is bound to thrombomodulin in the blood vessels of the small blood vessels, thrombin is inactivated, and protein C is activated [30, 31, 32, 33].
\nIn large vessels, connection of protein C to its receptor increases the activation of protein C by thrombin. In turn activated protein C inactivates factors Va and VIII in the presence of free S protein and phospholipids to prevent the production of thrombin. Free S protein has anticoagulant effects: it prevents the prothrombinase complex (agents Xa, Va, and phospholipids) that converts prothrombin to thrombin and the supportive complex (factors IXa, VIIIa, and phospholipids) that converts factor X to Xa. The reduction in antithrombin activity prevents the inactivation of thrombin, and the reduced energy of protein C or protein S minimizes control of thrombin production. The aforementioned mechanisms increase the vulnerability to venous thrombosis [30, 31, 32, 33].
\nMutations in the involved genes endanger the human organism. Mutations in the factor V gene or prothrombin modify the thrombin production control. Replacement of Arg 506Gln factor V Leiden leads to a deceleration of proteolytic Va inactivation, which results in increased production of thrombin. The mutant factor V also decreases the action of the cofactor in the inactivation of VIIIa by activated protein C [30, 31, 32, 33].
\nMost types of thrombophilia are inherited, but there are some forms that appear later in life. The two most common forms are associated with mutations in factor V Leiden and prothrombin. Both of these forms are inherited in an autosomal dominant way. Another common form, mild hyperhomocysteinemia (MTHFR methylenetetrahydrofolate reductase), is inherited in an autosomal recessive status. More rare forms include deficiencies of antithrombin III and C and S proteins [34, 35, 36, 37, 38, 39].
\nAntiphospholipid syndrome (APS) is a thrombophilia that is not inherited but can later occur in life. In this syndrome, the body develops antibody to phospholipid-bound proteins. These antibodies are suspected of damaging the vessels, leading to clot formation. Therefore, the APS is considered as an autoimmune disease [40, 41, 42, 43, 44].
\nIn the question which women should be tested for thrombophilia, the answer is that all pregnant women with a history of thrombus should be controlled according to the American College of Obstetricians and Gynecologists. Doctors may suggest screening for women with a family history of thrombi, pulmonary embolism, or stroke that occurred before the age of 60 years or a history of complications during pregnancy (including two or more miscarriages, a fatal embryo, preeclampsia, placental abruption, or poor embryo development) [40, 41, 42, 43, 44].
\nThrombophilia is considered to be a major predictor of thrombosis. Acquired thrombophilia includes the lack of endogenous anticoagulants, protein C and S antithrombin, genetic mutations in procoagulants such as FV-Leiden (FVL), prothrombin G2021OA, and the methylenetetrahydrofolate reductase or methylenetetrahydrofolate methylene (MTHFR) gene [40, 41, 42, 43, 44].
\nAnother group of thrombophilic diseases combine hereditary and acquired characteristics such as factor VIIIc elevated, hyperhomocysteinemia, and acquired activated C protein. Hereditary thrombophilia is due to autosomal mutations of specific genes, which are inherited by one or both parents and are implicated in a significant rate of miscarriage [44, 45, 46, 47, 48, 49].
\nThe major of these genes are:
\nCoagulation factor V and mutation (FV-Leiden-G1691A)
This mutation is one of the most common and most important genetic factors of propensity for congenital thrombophilia. In the Greek population, it represents at 6–10%, while homozygous individuals are rarely detected.
In fact, heterozygous women have a 2–3 times increased risk of miscarriages, as well as other complications such as preeclampsia and delayed fetal development. Detection of a further mutation of A4044G in the same gene, although in itself, is a mild thrombophilic agent, however, in combination with the FV-Leiden mutation, increases the risk of thrombosis and, moreover, miscarriages [44, 45].
Prothrombin or coagulation factor II (FII) or F2
The detection of G2021OA mutation in the F2 gene is the second most common form of thrombophilia, after factor V Leiden, and in our country reaches 4%. The risk of vascular disease or auto-elimination in heterozygotes increases about threefold compared to the general population and homozygotes 20 times [46, 47, 48, 49].
Gene of hyperhomocysteinemia: methylenetetrahydrofolate reductase or methylene tetrahydrofolate (MTHFR).
Two important mutations, C677T and A1298C, have been implicated in the deficiency of this enzyme, which leads to elevated levels of plasma cytotoxic homocysteine. The C677T mutation is an important predictor of severe arterial and venous deep vein thrombosis and infertility in men and women.
\nThe risk of thrombosis is greater in subjects coexisting with the M77F mutation of the V77-Leiden mutant [46, 47, 48, 49].
\nThis deficiency is inherited by the autosomal dominant formula, presenting over 160 different mutations. Protein C deficiency is associated with familial thrombosis with phenotypic variation. The heterozygous disorder is associated with adverse events during pregnancy, such as deep vein thrombosis, preeclampsia, endometrial growth retardation, and abortions. In cases of homozygosity, they have been associated with a neonatal purple thunderbolt. Heterozygotes have an increased risk of deep vein thrombosis by 8–10 times [46, 47, 48, 49].
\nThis disorder is inherited by the autosomal dominant way. It is heterogeneous, numbering over 330 different mutations. The mechanism by which thrombosis is caused by abnormal fibrinogen production is not fully elucidated. Dysfibrinogenemia is sometimes manifested by a bleeding disposition or by a thrombotic and hemorrhagic image [39, 40, 41, 42, 43, 44, 45, 46, 47, 48, 49].
\nWith the recognition of factor V Leiden and the G20210A mutation of the prothrombin gene, the proportion of patients with venous thrombosis has increased, in which the diagnosis of hereditary thrombophilia can be established. The predominant areas of thrombosis during pregnancy are the luteal veins and veins of the foot [39, 40, 41, 42, 43, 44, 45, 46, 47, 48, 49].
\nThe term thrombophilia includes inherited or acquired lack of antithrombin, as well as secondary syndromes characterized by either reduced levels of coagulation inhibiting agents or elevated levels of coagulation factors. The age of the first thromboembolic event is 10 years less for the general population [39, 40, 41, 42, 43, 44, 45, 46, 47, 48, 49].
\nSeveral clinical forms of hereditary thrombophilia are associated with pregnancy complications such as abortions, preeclampsia, lethal newborns, endometrial growth retardation, and HELLP syndrome.
\nUniversal hereditary thrombophilia is due to antithrombin deficiency, protein C deficiency, protein S deficiency, factor V mutation, and mutation of the prothrombin gene 20210A. Increased factor VIIIc levels and mild hyperhomocysteinemia are linked to multifactorial or partial inherited thrombophilia.
\nThe natural inhibitors of coagulation are antithrombin and C and S proteins. Factor V Leiden mutation is the most frequent thrombophilic disorder. The prothrombin mutation 2010A generates higher levels of inactive prothrombin; elevated factor VIII levels above the 75th percentile are a risk factor for thromboembolic disease and mild hyperhomocysteinemia [39, 40, 41, 42, 43, 44, 45, 46, 47, 48, 49]. There is a double incidence of first trimester abortions in prothrombin or V Leiden factor mutants. For the other types, there is limited bibliographic data.
\nCardinally, the relationship between hereditary thrombophilia and the incidence of pregnancy loss appears to influence all stages of pregnancy. Concerning the other complications, preeclampsia, lethargy, placental detachment, and delayed intrauterine growth seem to be more associated with factor V mutation. The lack of protein S or C appears to be also associated more with preeclampsia and unexplained lethal neonates. Hyperhomocysteinemia and prothrombin mutation appear to be most associated with placental ablation. Finally, there seems to be no relationship between elevated factor VIIIc levels and preeclampsia, IUGR, and HELLP syndrome.
\nLaboratory findings include increased levels of factor VIII and fibrinogen, decreased levels of protein S, resistance to activated protein C, decreased fibrinolysis and Leiden factor V mutation, and G20210A antithrombin mutation. Monitoring of pregnant women with hereditary thrombophilia involves the implementation of a complete laboratory investigation. Laboratory testing is a common practice in women with a history of venous thrombosis or pulmonary embolism [39, 40, 41, 42, 43, 44, 45, 46, 47, 48, 49].
\nHowever, in the case of an acute thromboembolic event in pregnancy, the control is of limited value because it does not significantly affect the clinical response. Therefore, this laboratory investigation should be done either before anticoagulation treatment or 1 month after its discontinuation [39, 40, 41, 42, 43, 44, 45, 46, 47, 48, 49].
\nLaboratory findings should be interpreted with caution because levels of protein S show a normal decrease in pregnancy and resistance to protein C occurs in 40% of pregnancies without factor V Leiden disorder.
\nAlso the coexistence of some other disease (liver disease, nephrotic syndrome) can cause a decrease in C and S protein levels and antithrombin, respectively [39, 40, 41, 42, 43, 44, 45, 46, 47, 48, 49].
\nIn contrast to pregnancy, the genotypes for factor V Leiden and prothrombin G20210A can be safely interpreted. Treatment include thromboprophylaxis with low molecular weight heparin (enoxaparin 0.5-1mg/kg/12 hours or dalteparin 50-100 IU/kg/12 hours) in combination with compression stockings. It is more recommended for antithrombin and symptomatic patients [39, 40, 41, 42, 43, 44, 45, 46, 47, 48, 49]. Enoxaparin 40 mg or dalteparin 5000 IU should be given daily for 4–6 weeks. Low MB heparin does not penetrate the placenta, and so there is no risk of embryo or hemorrhage. Also in relation to classical heparin, it affects more favorably the anticholate (antithrombotic) anti-Xa versus anti-IIa (anticoagulant) effect resulting in a reduced risk of bleeding. It also exhibits stable and predictable pharmacological activity and causes less platelet activation due to less binding to platelet factor 4, reducing the risk of thrombocytopenia.
\nAntiphospholipid syndrome (APS) is common in patients with autoimmune diseases. Antiphospholipid antibodies are associated to these diseases (lupus, scleroderma, etc.) [39, 40, 41, 42, 43, 44, 45, 46, 47, 48, 49]. In pregnancy, the mechanism of increasing venous thrombosis in the antiphospholipid syndrome is not well known. The presence of lupus anticoagulant is severe and can cause fetal bradycardia around the 25th week of pregnancy and atrioventricular blockages [39, 40, 41, 42, 43, 44, 45, 46, 47, 48, 49].
\nAPS diagnostic criteria include:
Vascular thrombosis.
Gestational complications.
Anticardiolipin antibodies.
Diluted Russell viper venom time (dRVVT).
Clot-based LAC (which detects the in vitro inhibitory activity of aPL antibodies).
aPTT with silica as an activator (silica clotting time).
Kaolin clotting time (KCT).
Dilute prothrombin time (dPT).
Ecarin clotting time (ECT).
Textarin clotting time.
International Society on Thrombosis and Hemostasis (ISTH) and other guidelines recommend dRVVT as the first choice to confirm the diagnosis of APS and an aPTT with low phospholipids and silica activator as second choice [50, 51, 52, 53, 54]. Vascular thrombosis is the diagnosis of one or more clinical episodes of arterial, venous, or capillary thrombosis in any tissue or organ.
\nDiagnosis of the antiphospholipid syndrome needs the existence of at least one clinical and laboratory criteria [50, 51, 52, 53, 54]. Anticardiolipin or lupus anticoagulants are found in two or more measurements of moderate or high levels of IgG-IgM antibodies for a period of at least 6 weeks. In case of history with one or more unexplained endometrial deaths of normal morphological embryos from the 10th week of pregnancy or one or more premature births at week 34 and before or three unexplained consecutive abortions before the 10th week of pregnancy, anticardiolipin should be tested. As a consequence miscarriage is defined as the loss of three or more pregnancies before the 20th week of pregnancy [50, 51, 52, 53, 54].
\nThe mechanism in the abovementioned syndrome is not precisely specified. Potential microtubule mechanisms are included, including autoantibody failure to implant or develop embryo-fetal circulation. The abortions in the first trimester may be due to insufficient trophoblast development and failure to produce effective embryo-fetal circulation. They may also be due to thrombosis in the uterine-pulmonary circulation due to inadequate binding to factor V trophoblast [50, 51, 52, 53, 54]. In older gestational age, endometrial deaths are attributable to massive thrombosis in the placenta, while mechanisms associated with other complications (preeclampsia) are unknown.
\nDespite the lack of large cross-references, the treatment pathway includes corticosteroids, aspirin, heparin, and coumarin [55, 56, 57, 58, 59]. In addition, the treatments proposed are associated with a high risk for the mother and the fetus. Treatment should only be used when the risk of complications is considered to be greater and after a thorough discussion of pregnancy. Predictive poor outcome factors are the title of anticardiolipin antibodies and the obstetrical history. Corticosteroids have been extensively used in the past, but this practice was to a great extent abandoned after the publication of Laskin et al. which revealed increased maternal morbidity without sufficient evidence of improvement in perinatal outcome. Adoption is only recommended in cases where the syndrome is complicated by clinically manifest thrombocytopenia or lupus erythematosus. In these cases, a systematic check for the possibility of diabetes mellitus or gestational hypertension is necessary [55, 56, 57, 58, 59]. Aspirin inhibits the formation of thromboxane and reduces the risk of thrombosis due to platelet aggregation. It can be used during pregnancy because it usually does not cause complications in the mother and the fetus. The use of low-dose aspirin can be continued until delivery without significantly increasing the risk of epidural hemorrhage in the application of epidural anesthesia. Regarding the efficacy of the above treatment as monotherapy, there are currently no satisfactory conclusions according to two recent studies [55, 56, 57, 58, 59]. Low molecular weight heparin is considered to be safer than classical.
\nRegarding the duration of treatment, others recommend prophylactic administration until completion of the 37th week, suggesting then induction of labor and other administration until the birth occurs automatically with concomitant administration of vitamin K antagonists [55, 56, 57, 58, 59]. Over-the-counter gamma globulin is no longer recommended because there is no evidence of a clear improvement in perinatal outcomes.
\nCoumarins are not particularly administered in the first and third trimesters as potential teratogens and cause colonic disorders in the embryos due to easy passage through the placenta and because they are associated with greater maternal morbidity. Administration of these is indicated only in minimal cases of contraindication for the administration of heparin or aspirin [55, 56, 57, 58, 59]. The complications of antithrombotic therapy in pregnancy include embryo-phytopathy (nasal hypoplasia, stiff epiphyses), CNS abnormalities (Dandy-Walker syndrome, visual atrophy), embryonic hemorrhage, bleeding events, skin allergies, thrombocytopenia, and osteoporosis [60, 61, 62, 63, 64].
\nHyperhomocysteinemia is characterized by elevated fasting plasma homocysteine (> 100 μmol/L in severe cases). The mild to moderate form has less elevated fasting plasma homocysteine levels (>15–100 μmol/L). It causes homocystinuria, cataracts, skeletal abnormalities, early angiopathy, thromboembolic events, and mental retardation [60, 61, 62, 63, 64]. Characterized as a risk factor for thromboembolic disease. Homocysteine levels are higher in males and increase with age. On the contrary, pregnancy and estrogen decrease levels, due to genetic factors (lack of β-synthase of cystathionine, or 5,10-methylenetetrahydrofolate reductase) [60, 61, 62, 63, 64]. There are also environmental factors that affect homocysteine levels (decreased folic acid uptake and methionine intake, smoking, increased coffee intake, decreased renal function, hypothyroidism, and certain drugs such as methotrexate, steroids, cyclosporin, etc.). Homocysteine levels decrease during pregnancy because of increased renal infiltration and hemodilution. Moreover, the fetus increases the uptake of homocysteine. The high levels are linked to neural tube damages, placental thrombosis, preeclampsia, and placental abruption. Also, the rate of early abortion is increased [60, 61, 62, 63, 64].
\nThe proposed mechanisms include vascular endothelial dysfunction, cell apoptosis due to reduced nitrogen oxide bioactivity, decrease in antioxidant regulation, changes in platelet activity, elimination of prostacyclin biosynthesis pathway, decrease in antithrombin activity, inhibition of protein C activation, and inhibition of binding to the endothelium of the tissue plasminogen receptor [65, 66, 67, 68, 69].
\nTreatment includes substitution with vitamin B12 (0.5 mg/day) and folate (0.5–5 mg/day). It is a low-risk treatment that reduces homocysteine levels in most cases. Research clinical protocols have shown that B6 administration did not have significant results [65, 66, 67, 68, 69]. However, according to recent trials, vitamin administration did not contribute significantly to the reduction of complications. On the other hand, the administration of folic acid at a dose of 5 mg/day reduced the incidence of preeclampsia and prematurity and contributed to the increase in birth weight. The latest results have not been adequately proved [65, 66, 67, 68, 69].
\nConsequently, hyperhomocysteinemia is a common and easily treatable cause of arterial and venous thrombosis. The various treatments should be administered with caution because there is a risk of increased thrombus incidence. It is worth mentioning other acquired thrombophilia such as increased levels of coagulation factors VIII, IX, and sometimes factor XI. The levels of these factors increase in pregnancy with the main purpose of reducing the loss of blood in childbirth. The levels of these factors increase in pregnancy with the main purpose of reducing the loss of blood in labor [65, 66, 67, 68, 69].
\nIn Europe, the annual incidence of deep vein thrombosis is about 124/100.000 and 60–70/100.00 for pulmonary embolism (PE). Especially in Greece PE is affecting 1800 persons each year. In bibliography there are guidelines for prevention by the National Drug Organization and the Greek Society of Orthopedics and Trauma but not for diagnosis of thrombosis [65, 66, 67, 68, 69].
\nThe DVT diagnosis is based on Wells score for DVT, levels of d-dimmers, venous duplex or triplex ultrasonography and in rare cases on MRA. Wells score, EEG, chest X-ray, arterial gas blood values, D-dimers, CTPA, V/Q scan, PA, and MRA are used for PE diagnosis. D-dimer test has high sensitivity (80–85%), 99% negative predictive value, and 30% positive predictive value. The normal value of 500 μg/L depends on the age. In accord with ACP guidelines, the D-dimer value arises from the type: age x 10 μg/L. In general, d-dimers value used in patients with Wells score <2 or in patients with intermediate or with low pretest probability of PE who do not meet all Pulmonary Embolism Rule-Out Criteria (ACP guidelines) [65, 66, 67, 68, 69].
\nIn patients whose PE is unlike, D-dimer assay plays important role in diagnosis, as well as diagnosis is excluded in values under 500 ng/mL. On the other hand, spiral-CT pulmonary angiogram (CTPA) is a tool diagnosing PE in patients who are in high risk.
\nIn pregnancy, Wells test is not validated, but negative D-dimers are quite useful. Serial, proximal ultrasonography and iliac vein ultrasound or abdominal magnetic resonance venography can be also used. The treatment of acute VTE and PE includes UFH, LMWH, fondaparinux, DOACS (direct oral anticoagulants), and antivitamin K. Body weight-based LMWH or fixed dose of fondaparinux (7.5 mg) is initially used, and after 1 or 2 days VKA (acenocoumarol) is added. An alternative scheme includes rivaroxaban or apixaban from day 1 or dabigatran after 5–10 days of heparin administration. Anti-Xa monitoring is indicated in pregnant women, in patients with renal disease, and in underweight patients [65, 66, 67, 68, 69].
\nDOACS monitoring is not in routine. It is useful in the case of hemorrhage, before surgery, and before and after use of antidote. The available DOACS in Greece are dabigatran (DTI) and rivaroxaban, apixaban, and edoxaban (anti-Xa). Among acenocoumarol and dabigatran or rivaroxaban, the prices have extremely high difference [65, 66, 67, 68, 69].
\nWarfarin is still preferred in cases of mechanical valves, rheumatic mitral valve disease, advanced renal failure, cancer patients (if LMWH is not used), and high-risk thrombophilia. Quantitative monitoring of DOACS is not a routine but can be applied in special cases such as elderly, low body weight, and low renal function. It is well known that normal aPTT indicates that high dabigatran levels are not present. Rivaroxaban prolongs PT in a linear and concentration-dependent way. Idarucizumab is dabigatran antidote that can be used in life-threatening bleeding. Hemodialysis can also reduce the plasma levels by 60% within 2 hours. Andexanet is the anti-Xa antidote but is not yet approved [65, 66, 67, 68, 69].
\nTemporary inferior vena cava filters are an alternative method for fibrinolysis when patients with PE or DVT cannot have anticoagulation treatment or in patients with recurrent proximal DVT or PE, despite adequate anticoagulation treatment.
\nHIT II diagnosis is based on 4Ts score. Stop heparin and start alternative anticoagulation such as anti-Xa or DTIs are the first step of management. When PLTs >150.000/μL VKAs can be added. The treatment duration varies from 4 weeks up to 3 months in VTE [65, 66, 67, 68, 69].
\nAfter the first DVT episode, the decision for long-term anticoagulation is based on risk of thrombosis versus the risk of a major bleeding. At least a 3-month duration therapy is recommended except in the cases of active cancer, recurrent VTE, and high risk of thrombophilia as APS. Three different treatment phases in VTE and PE can be described: the initial, just for the first few days; the short term, up to 3–6 months; and the long term, beyond the first 6 months. HER DOO algorithm has been applied as a rule for clinical decisions. As a result, hyperpigmentation, edema or redness, D-dimers >250 μg/L, obesity (BMI > 30 kg/m2), and older age (>65yo) have major importance for the patient profile. Gender also plays important role, as men have 2.2-fold higher risk of recurrent disease than women.
\nDOACS are the first choice for the long-term therapy. Next choices are VKA and LMWH. In contrast, LMWH for 6 months is the first choice for cancer patients.
\nRegarding aspirin role, INSPIRE trial shows that after the first unprovoked VTE, it can reduce the overall risk for VTE recurrence more than one third, without significant increase of bleeding risk [65, 66, 67, 68, 69].
\nThe most common mutation associated with thrombophilia in Greece is MTHFR C677T (35%), whereas FV-Leiden and prothrombin G20210A have an incidence of about 2%.
\nCandidates for thrombophilia testing are people with family history of venous thrombosis, onset in young people (<45yo), thrombosis in unusual sites, people with secondary VTE in pregnancy, HTR or oral contraception intake, and patients with recurrent VTE. Although, the clinical practice is quite different and investigation of thrombophilia is much more frequent.
\nProtein C activity, free PS activity, antithrombin activity assay, activated protein C resistance, prothrombin G20210A mutation assay, anticardiolipin antibodies, and lupus anticoagulant testing are among diagnostic panel for thrombophilia.
\nIt is important to keep in mind that 3–5% of patients with an unprovoked DVT and no obvious sign of cancer has an occult cancer.
\nIn cases of acquired thrombophilia, diagnosis of antiphospholipid syndrome is based on revised Sapporo criteria. Primary prophylaxis is not recommended in APS. First-line treatment is VKAs and in pregnancy cases LMWH and aspirin.
\nAccording to recent studies, DOACS have no big importance in inherited thrombophilia treatment.
\nThrombophilia test aims to identify individuals at increased risk of VTE or relapse or complications in pregnancy associated with hereditary or acquired thrombophilia.
\nThe type of laboratory investigation is generally influenced by:
The age of occurrence of the first VTE episode.
The existence of a risk effector.
The number of recurrent of VTE episodes.
The presence of a family history.
Everyone who presented with first unprovoked episode of deep vein thrombosis at a young age and after the cancer diagnosis has been ruled out and is considered to be thrombophilic, regardless of whether or not there is a known thrombophilia and the risk of relapse is elevated. Thrombophilia check should not be massive. When a thrombophilia test is required, the investigation should include investigation for hematological disorders which at least doubling the risk of VTE.
\nThe most common of them are major thrombophilic mutations, deficiencies of normal inhibitors of coagulation, and the diagnosis of the antiphospholipid syndrome. If none of the common disorders associated with hereditary or acquired thrombophilia is found, investigation may be extended to other rare mutations or a combination of polymorphisms or to find out other acquired conditions that increase the risk of VTE.
\nIn any case, the investigation and the result evaluation should not be nonselective in population groups that do not fall under the criteria listed below. Laboratory investigation of hematologic disorders associated with hereditary or acquired thrombophilia includes:
Complete blood count.
Measurement of PT and aPTT.
Measurement of normal coagulation inhibitor levels:
Antithrombin (AT).
Protein C (PC).
Protein S (PS).
Test for the presence of resistance to activated protein C (APC-resistance) associated with Leiden factor V mutation.
Control for the presence of the G20210A mutation in the prothrombin gene (FIIG20210A).
Check for the presence of lupus anticoagulant, anticardiolipin antibodies, and antibodies against β2 glycoprotein I (anti-β2-GP1) [56, 70, 71, 72, 73, 74].
Control for mutation of factor V Leiden or the G20210A mutation in the prothrombin gene using PCR methods can be applied at any time relatively to the thrombotic episode and regardless of the administration of anticoagulant treatment. The levels of natural inhibitors of clotting are reduced in the acute phase of thrombosis (decrease in PS), pregnancy and labor (decrease in PS), and treatment with estrogenic contraceptives (reduction of PS).
\nPC and PS are reduced during treatment with vitamin K antagonists or when there is deficiency of vitamin K that is not associated with coumarin therapy. Administration of classical heparin causes a decrease in AT levels. The presence of hepatopathy, among other coagulation disorders, also causes a reduction in natural inhibitors. The presence of nephrotic syndrome causes a decrease in AT levels.
\nThe timing methods of clotting are affected by the newer anticoagulants that are active after oral administration and specifically inhibit thrombin (dabigatran) or factor Xa (rivaroxaban, apixaban, edoxaban).
\nAs a result, during treatment with these drugs, it is not necessary to measure the levels of protein S and control for the presence of activated protein C resistance or the presence of lupus anticoagulant [56, 70, 71, 72, 73, 74].
\nDiagnosis of the inherited lack of AT, PC, or PS should only be performed if all conditions that lead to their acquired lack are excluded. Examination of the antiphospholipid syndrome can also be performed during the acute phase of VTE during anticoagulation treatment with classical heparin, low molecular weight heparin, or fondaparinux, if a suitable method for controlling the lupus anticoagulant is selected and weighted to the minimum concentration of heparin or fondaparinux or INR, which does not affect it. Therefore, at least in patients taking its antagonist vitamin K, test for the lupus anticoagulant should be done in a specialized laboratory.
\nIn women with obstetric complications (such as miscarriages, preeclampsia, endometrial deaths, etc.), the investigation for obstetric antiphospholipid syndrome is preferable to occur close to the episode because it is possible for the levels of antiphospholipid antibodies to fall as far as we go away from pregnancy [56, 70, 71, 72, 73, 74].
\nAccording to the international guidelines, the laboratory investigation for the presence of hereditary or acquired thrombophilia is recommended in the following cases:
In patients with the first VTE episode occurred at the age of less than 40 years.
In patients younger than 60 years of age who present the first VTE episode without the presence of a significant risk factor or a known endogenous risk factor for VTE.
In patients who present as a single risk factor for VTE, oral contraceptive, or hormone replacement therapy or pregnancy.
Laboratory testing by techniques other than molecular biology (PCR) techniques for hereditary causes of thrombophilia should be performed at least 2 months after the stop of hormone therapy or labor [56, 70, 71, 72, 73, 74].
In patients with relapsing VTE, regardless of the presence of risk factors.
In patients without varicose veins exhibiting recurrent superficial thrombophlebitis.
In patients with VTE in unusual sites, such as retinal vein thrombosis or cerebral or mesenteric or hepatic vein thrombosis.
In patients with warfarin-induced skin necrosis and neonates with purpura fulminans not related with sepsis.
In asymptomatic relatives of first-degree patients with proven symptomatic thrombophilia or hematologic disorder that is linked with hereditary thrombophilia.
In women with a family history of adjusted VTE at <60 years, going to take hormonal medications for assisted reproduction.
In women with a history of recurrent unexplained abortions, growth retardation, or endometrial death.
The results of hematologic control should be analyzed by a hematologist. Patients with hereditary or acquired thrombophilia should be monitored by a hematology center. Screening for thrombophilia is not recommended in women who are going to take contraceptive treatment and in women who are going to undergo in vitro fertilization techniques if they do not meet any of the previous criteria or familial history of thromboembolism [56, 70, 71, 72, 73, 74].
\nConsidering all the risks and major obstetrics complications that thromboembolic events can lead during pregnancy, we can conclude that cooperation among obstetricians and hematologists is crucial for better outcomes. The careful history and appropriate laboratory investigation consist of the key point for the management of these patients.
\nThis chapter considers the relationship between inequalities in health with those in higher education, drawing on qualitative research undertaken with UK undergraduate students during the pandemic academic year, 2020–2021. Two sets of research were conducted at the same university – one by a lecturer and another by an undergraduate student – with a view to capturing the embedded inequalities in higher education, which was magnified, though not produced by, the situation of COVID-19. The chapter considers students’ experiences and argues that embracing and supporting material and emotional needs are essential for overcoming racial and ethnic inequalities in higher education. Taking a whole person approach, however, necessarily means redressing the structural racisms in society and in higher education, evidenced by the social determinants of health, so that all students, including those from ethnic minority groups, can have their potentials fulfilled as a matter of principle.
There have been increasing numbers of widening participation students entering higher education over the last few decades in the UK, in line with an increasing number of students overall [1]. Widening participation indicates those students who have not traditionally accessed higher education: those from low income or disadvantaged backgrounds, being mature, having disabilities and/or being from certain ethnic groups [2]. In the UK, widening participation has meant that since the 1980s, more working class and second-generation children from families arriving in post-World War II/end of the British Empire migrations have enrolled into university education [3, 4]. In the academic department where this research was undertaken, 71% of students identify as being from ethnic minority backgrounds [5]. Further, most are Black African, women, in their 30s, with families and work in the health system. They reflect the widening participation trend, by being mature, from minority ethnic backgrounds, of lower social and economic standing, who seek education and training [6] to improve their life circumstances.
While there have been increases among different social and economic groups accessing higher education over several decades, challenges remain in meeting the widening participation remit of addressing the unequal access to and progress through it [2]. These include “pronounced differences in continuation and degree awarding outcomes for white and BAME [Black, Asian and Minority Ethnic] students, with lower rates of BAME students continuing or qualifying and receiving a first/2:1 compared with their white peers [1]”. “Increasing access without increasing chances of success is becoming a new form of social exclusion within higher education [7]”. Social exclusion is one of the fundamental causes of inequality [8]. This exclusion is especially so when disaggregating data around race and ethnicity. Concerning continuation rates from one year to the next, in aggregate, there is a gap of 3.5 points between Black and Asian ethnic minority students and white students: 86.7% versus 90.2%, respectively [1]. However, when disaggregating the data, the lowest continuation rates were found among students from Other Black Backgrounds, with a gap of 8.7 points (81.5%) and Bangladeshi students, with a gap of 7.3 points (82.9%) compared with white students (90.2%). In terms of degree attainment and classifications (first/2:1 both of which constitutes a ‘good degree’ outcome), the gap between white students and all other students is 13.3 points. Once disaggregated, however, this number rises to 23.3 points for Black African students, 19.2 points for Black Caribbean students and 24.4 points for Other Black Background students in comparison to white students [1]. Ethnic/racial inequality is also evident in graduate employment, with 50.1% of white graduates working in professional roles within 15 months of graduation, whereas only 43.0% of BAME graduates had professional employment within the same time period [1]. These disparities represent endemic ethnic/racial inequalities in higher education whose impacts endure beyond graduation.
The blame for these differential outcomes across different racial and ethnic groups has often been laid at the feet of the students – in what is known as the deficit model. This model frames “students and their families of origin as lacking some of the academic and cultural resources necessary to succeed [9]” amid an assumption of equity across society. As will be explained below for health, many of the inequalities present in society are not the result of individual, family or community failings, but are the result of institutional and political structures [10, 11] that enable some to achieve success and disable others from the same. Laying the blame at the individual, their family and/or community is an example of prioritising values and expectations that the dominant population and calling these normal; this is white supremacy. White supremacy describes “the operation of forces that saturate the everyday mundane actions and policies that shape the world in the interests of white people [12]”. This prioritisation of a monocultural and monolinguistic society is an explicit act to “eradicate the linguistic, literate and cultural practices many students of colour brought from their homes and communities [13]”. Individuals, families and communities, who have other values, norms and expectations, instead of being acknowledged and embraced for these alternative sets of expertise and resources [13, 14] risk being classified as “subnormal [15]” or having deficiencies, due to operating from a different set of cultural mores and norms [16]. The deficit model does not interrogate the “multiple, intersecting factors” [17] within higher education that impact on the continuation and successful awarding of ethnic minority students. These factors include those from staff, such as implicit biases and low or lack of expectation for success, as well as from students, about their own fears of conforming to the negative lens through which society sees them and their potential [17]. The fault of who can be successful in higher education is a systemic problem and higher education needs to be conscious about its role in maintaining “barriers to student success [9]” through its assumptions and exclusive practices that reflect whiteness.
In February 2020, the UK’s Health Foundation published a report [18] on the social determinants of health, providing an update to its predecessor from a decade earlier [19]. Over the 10-year period, health inequalities were found to have widened, with declines in education funding, increases in precarious work, including zero-hour contracts, lack of affordable housing and increased use of food banks. Plus, life expectancy had plateaued after a century of increases [20], with outcomes worse for ethnic minority groups [18]. One month later, the World Health Organisation [21] announced the outbreak of a viral infection that began an unprecedented time throughout the world. From an equity perspective, the pandemic of COVID-19 has “exposed and amplified inequalities [22]”. At the time of writing, there have been upwards of 250 million cases and over 5 million deaths worldwide [23]. Although a pandemic, its responses have largely been at the level of the nation-state [4]. To tackle the virus’s spread, the UK government introduced strict measures, including social distancing, wearing masks, and nationwide lockdowns [24], with UK universities quickly shifting from face-to-face teaching to online learning [4, 25] and rapid adaptation to teaching and learning remotely [26].
However, these restrictions did not equalise the risks of exposure to or mortality from COVID-19. As several authors attest [10, 11, 27, 28], inherent racial and ethnic inequalities in the UK pre-date the pandemic. The fundamental risks from COVID-19 are situated firmly around “the role of systemic racism and socio-economic inequalities [27]” that pushes the burden of co-morbidities onto Black and Asian ethnic minority groups. Existing inequalities around health care standards, misdiagnoses, pain threshold assumptions, poorer maternal health outcomes, and an association of ill-health with poor personal choices have made health care facilities unsafe places for BAME groups [27]. Racism, not race, is a fundamental cause of these disparities, suggesting that poorer educational opportunities and outcomes, impacts of the criminal justice system, housing and employment together drive stress and contribute to co-morbidities [28]. These may increase risk of COVID-19 infection [29]. The inequalities surrounding COVID-19 in England and those related to geographical region, gender, age and deprivation are cumulative, and confer more risk onto minority ethnic groups in relation to COVID-19 [11]. Reference [10] effectively summaries these findings, by stating that “racism both shapes social determinants of health and has its own effect on the health of ethnic minorities”.
The linking of social and economic inequalities with health inequalities in England is not new. There have been several reports throughout the twentieth and twenty-first centuries calling out inequalities [19, 30, 31, 32]; with some authors linking inequalities to ethnic and racial discrimination [18, 33] and noting these as structural and institutional problems, rather than “individualised” issues [34]. “Systemic problems such as racism require structural interventions and reforms across the broad spectrum of society, including in healthcare, education, employment, and the criminal justice system [10]”. COVID-19 is yet another cog in the wheel of ethnic and racial inequalities, which impact students’ lives and their potential for success in higher education.
As a Public Health academic and student, we align ourselves within the social determinants of health ethic, to understand “the causes of the causes [8]”, which emphasise the foundational character of deprivation and exclusion as underlying health inequalities. The “responsibility for health is shared across society [35]”; similarly, the responsibility for equitable education is equally shared across society. Therefore, it is imperative to address the inequalities in the system of education – by changing educational and systemic cultures of practice [1] – to achieve equity of process and outcome for all.
Following on from these two frameworks – of recognising that systemic injustices in higher education negatively impact ethnic minority students and that social and economic inequalities underpin health equalities – this research proceeds with the following research question:
What were the impacts of the COVID-19 lockdowns on ethnic minority students at a widening participation university in the UK?
This research adopted a phenomenological, hermeneutic methodology of qualitative enquiry [36]. Exploratory and interpretative, qualitative methodologies seek to understand and explore the how participants perceived particular phenomenon [37, 38]. By doing so, researchers gain insight into the lived experiences of their participants [39]. Further, the research process undertaken was based in social constructionism [37, 38, 40, 41, 42, 43], wherein participants and researchers collectively identified key insights, enabling the process of research to be more democratic and participatory [44].
The purpose of this research was to interrogate how higher education needs to improve to meet the needs of ethnic minority students. Two separate but related research projects inform this work. The data for one was collected to understand the impact of remote delivery on student wellbeing and mental health, using one-to-one interviews; the data for the other was collected to understand the impact of pedagogical practices on student learning and belonging, using focus groups and anonymous module evaluations. Purposive sampling [45] was used for each, by inviting undergraduate students in the department to participate. Ethical approval was granted for each research project, and each participant consented to being included. All participants were fully informed about their rights, information security, intended use of data and that participation was fully voluntary [46].
The research comprised semi-structured one-to-one interviews, a focus group, anonymous pre- and post-module evaluations, and researcher reflections. Interviews lasted a median time of 20 mins. The focus group lasted 35 minutes. Each researcher used an interview guide but welcomed participant input which was relevant to the topic. The total number of participants was 20. Table 1 represents the participant list.
Participant | Gender | Age | Ethnicity |
---|---|---|---|
Participant 1 | Female | 18–25 | Black African / Black Caribbean |
Participant 2 | Female | 18–25 | Black African / Black Caribbean |
Participant 3 | Female | >46 | Black African / Black Caribbean |
Participant 4 | Female | 26–45 | Black African / Black Caribbean |
Participant 5 | Female | 26–45 | Black African / Black Caribbean |
Participant 6 | Female | 26–45 | Black African / Black Caribbean |
Participant 7 | Female | 26–45 | Black African / Black Caribbean |
Participant 8 | Female | >46 | Black African / Black Caribbean |
Participant 9 | Female | 26–45 | Black African / Black Caribbean |
Participant 10 | Female | 26–45 | Black African / Black Caribbean |
Participant 11 | Female | >46 | Black African / Black Caribbean |
Participant 12 | Female | >46 | Black African / Black Caribbean |
Participant 13 | Male | 18–25 | Black African / Black Caribbean |
Participant 14 | Female | 18–25 | White British |
Participant 15 | Male | 26–45 | Southeast Asian |
Participant 16 | Female | 26–45 | Black African / Black Caribbean |
Participant 17 | Female | >46 | Black African / Black Caribbean |
Participant 18 | Female | 26–45 | White British |
Participant 19 | Female | 26–45 | Black African / Black Caribbean |
Participant 20 | Female | >46 | Black African / Black Caribbean |
Participant demographics.
Eleven students took part in the one-to-one interviews and nine further students participated in the focus group and the module evaluations. Black African/Black Caribbean students (n = 17), white British (n = 2) and Southeast Asian students (n = 1) participated. Females (n = 18) outweighed males (n = 2). The demographics represented in the dataset weigh more heavily toward ethnic minority representation; this is due with the self-selection process for participation and remains in line with student demographics in the department.
Interviews were recorded, and the recordings were listened to repeatedly for accuracy. The interviews were then transcribed and read numerous times to familiarise and to begin interpretation of the data. The researchers used thematic analysis [47] and recursive analysis [48] to analyse the data and inform the coding. Based on these analyses, common themes were recognised. These themes were then compared across the two data sets and overarching themes were agreed upon by the two researchers. Consequently, a descriptive study has been chosen to represent the data because it helps summarise the essential features of the collected data. It also facilitated data management and its coded representation transparently and systematically [49].
The findings reveal limitations in resources and support for ethnic minority students in the shift to online learning during the pandemic. Peer-to-peer support was noted as particularly important and harder to attain. There was also fear that the consequences of the present situation would inhibit future prospects. Inclusive institutions and learning environments were revealed to be enablers for learning, even during the pandemic. In circumstances where students felt welcome, they were able to share more of themselves and their experiences and to collaboratively learn together.
In this section, access to learning and student support during the pandemic lockdowns are explored. Complexities around learning at home without adequate support and insufficient resources, such as not having access to a good broadband connection or the ability to gain technical skills, led to feelings of anxiety, stress and isolation.
These participants reflect that the shift to online learning created technical challenges that were hard to overcome. While personal change would be required to keep pace with new circumstances, the tangible support available to make those changes was expressed as lacking, with the consequence of students feeling lost and unable to learn.
Participant 15 provides an example of one of the learning challenges that was hard to elicit when online – peer-to-peer learning and support.
Here Participant 15 articulates how difficult it can be for students, who did not know already each other, to build connectivity and rapport from scratch and remotely. Learning alone is one of the challenges faced in the online environment, and even with technical access to lectures, peers learning from one another is important. Participants elaborated on the positive value of being on campus – for the moral boost of being with others, access to study materials and chance encounters. As they reflect,
Other participants also corroborated, stating that not having ready access to campus made them lose their daily structure and their peer-to-peer relationships, which then inhibited their motivation and initiative. However, even in compromised conditions of learning, opportunities can be made available for student connection. Participant 15 continues.
He notes that these interactions, which enable the students to seek what they need themselves, even whilst in an online learning context, can support students to learn from and support one another. Participant 20 notes that being able to engage with fellow students “helps us to meet others to help us”, again highlighting the value of peer support in learning. In online situations, this can be facilitated by lecturer assistance, to give time and space to students to connect with one another, enabling some of that isolation and stress to be overcome.
In addition to access and peer support issues, many students who are also parents, had to contend with educating their children whilst also studying full time themselves. This multiplied their burdens and took away time and energy from their own studies. Participant 6 reflects,
The impact of learning remotely, with inadequate technical support, barriers to peer support, while also raising and home-schooling own children created uncertainties about the future. Students were worried about not achieving the results they wanted to achieve and how this would affect their future aspirations and progress. Participant 1 summarises this concern:
The fears arising from COVID-19 also extended beyond grades and job prospects to existential concerns over life itself. Some participants expressed their worries about how the lockdown would not stop the spread of the virus, as transmission continued to escalate despite restrictions. Those participants who were lone parents expressed worry about catching the virus, dying from it, and on the fate of their children. Participant 11 expresses this, saying, she was fearful to catch COVID-19,
The reality of COVID-19 was not just that it impacted on student learning and future aspirations. It was also a fear of sickness and death, and the repercussions these would have on loved ones. The crisis of COVID-19 also revealed inequalities in access to education as well as barriers to learning and support, which particularly impinged on widening participation, ethnic minority students, who already suffer from economic, social and health inequalities. Within higher education, lack of technical support, lack of structured opportunities to engage with peers, being overly burdened by looking after children’s needs whilst also aiming to meet their own, combined with increased risk of sickness and death, lead to fear and uncertainty about the long-term consequences for themselves and their families.
This section focuses on the emotional wellbeing of ethnic minority students, through inclusive practices, and how their knowledge bases and experiences can be more fully valued within higher education institutions.
Considering mental health as one facet of emotional wellbeing, many participants revealed that they did not know that the university had a health and wellbeing team. Two participants who were aware of these services shared that they had used them before and found them useful. A further participant revealed that she had used private counselling services instead because it was offered in her native language, which made it easier for her to communicate effectively. As she says,
Participant 6 choose to go outside of the university for this service to achieve a higher level of self-expression. This insight reflects that students arrive at university with a range of knowledge bases and life experiences, many of which are unrecognised and not accommodated for by the university. This recognition of student knowledge from outside the university also relates to classroom learning. This is where the content discussed and the approach used can either include or exclude students, based on their experiences and capabilities. Participant 13 considers his sense of engagement with one of his classes as it related to his paid work, stating,
Enabling both the content of classes and the approach in classrooms to be inclusive is something many participants commented on. Regarding the latter, Participants 12, 13, 15 and 16 offered that they would like their teachers to be “more approachable”, “more supportive”, and “more welcoming, so [students] don’t feel condemned for being confused”. They also wanted teachers to create time and space for students “to have an input” and “express [their] feelings”. Participant 12 summarises, saying that the teaching flow should be an ongoing dialogue between the lecturer and the students, as it “allows us to really interact […] It draws us in”. Participant 13 shares again about what this inclusive approach looks like in practice.
Content and approach are both important for creating inclusive learning environments for students of diverse backgrounds, where in some cases, extra consideration may be needed to ensure everyone is together and some are not being left behind, especially, if English is not the first language, as is the case with Participant 6. Furthermore, inclusive content and approaches equally provide opportunities to refute negative stereotypes and create opportunities both for discussion and for learning, in the widest sense, as explored in the following example.
Some participants in the focus group recalled an experience they had had in a previous class. This related to a teaching session that was synchronously online and face-to-face, with students self-selecting how they wished to attend. The class was discussing communicable diseases and had considered data on the prevalence of domestic violence, as it links to sexually transmitted diseases (STDs) in different parts of the world. Participant 15, who was in the room, inferred from the data that Sub Saharan Africa had the highest prevalence of domestic violence in relation to STDs. Participant 12, who was online, disagreed with the interpretation, and talked the class through the data to show that it was Southeast Asia that had the higher prevalence. She then went onto challenge the class about the tendency to perceive Africa as a negative example; even reading data incorrectly to support the view. Participant 15 and the rest of the class agreed with Participant 12 and conceded the error. During the focus group, Participant 15 raised this incident for further discussion, reflecting how that difficult classroom situation became a teaching moment for him.
This vignette reveals that learning online can be as engaging as being in the room, provided that the material being discussed is as relevant to the students as people as it is to the intention of the session. It shows that learning possibilities span different ages, ethnicities, cultures, and genders. It also demonstrates that students explicitly learn from one another through discussions and working out their disagreements, which emphasises the importance of peer-to-peer learning. Further, gaining clarity on a specific issue and how it relates to pervasive systemic biases can have enduring impacts not just for academic education, but for social and cultural competence in general.
The discussion recounted above was prompted by the course material being explored. The session could have remained a dissemination style lecture, delivered by the teacher, which may have shut down any possibility of student-to-student dialogue. Instead, the session was open for participants to feel welcome to bring their contributions to the classroom space (even while online), whether as disagreement, consensus, or resolution.
This section has shown that emotional wellbeing in higher education for ethnically diverse students requires a range of potentials to be in place. The knowledge bases and experiences which ethnic minority students bring to the university need to be reflected within the university, whether this is in the services offered or the content of courses. Students’ emotional wellbeing is also affirmed by attentive teaching practices, which include the students in their learning, whether being led by their lecturer or directly addressing one another in class. This section demonstrates the importance of recognising and valuing ethnic minority students as complete persons, who can formulate significant learning experiences for themselves, their classmates, and their teachers.
This chapter has explored some of the challenges for equality that ethnic minority students face in higher education in the UK. Through qualitative research undertaken during the pandemic lockdowns in 2020–2021, this research has shown that access to learning, via technology, through peer-to-peer interactions, amid childcare responsibilities, coupled with negative impacts of COVID-19, limited student potential. It further found that inclusive support services and learning environments which valued student knowledges and life experiences beyond those limited by white supremacist ideologies [12], facilitated engaged learning and emotional wellbeing.
This is important because although widening participation initiatives aim to be inclusive of more diverse learners, in this case, of mature students, with families to look after, from minority ethnic backgrounds, and often of lower social and economic standing [2], inequalities remain. Education can reproduce existing social and economic inequalities, through failing to attend to what students need from their education and delivering in a way that is exclusive to these needs [50]. COVID-19 did not create the inequalities experienced by ethnic minority students; rather it exacerbated already existing inequalities [11, 18, 22, 28]. Without due attention to ensuring policies and practices are equitably designed for all students, as a matter of social justice, the system will continue to disadvantage and disenfranchise these groups [7, 12].
This chapter has proposed that a relationship exists between the social determinants of health and inequalities in access, support, and emotional wellbeing in higher education for ethnic minority students. One of the fundamental causes of health inequalities is social exclusion [8]. Lack of hope and limited opportunities to transform one’s circumstances are consequences of this exclusion [8]. Structural racism affects the social determinants of health and affects the health of ethnic minorities [10]. COVID-19 further impacted on student mental health due to isolated learning [4, 25, 51, 52, 53]. Although COVID-19 was the same storm everyone experienced [54], not everyone had the same vessel of resources through which to weather it. Additionally, ethnic minority students had to bear further burdens, including fears of sickness and death from COVID-19, and the consequences for families and loved ones. This was not unfounded, as statistical reports have shown that morbidity and mortality from COVID-19 were higher for ethnic minority groups than white groups [55].
When considering the factors impinging on emotional wellbeing at the university, small successes of inclusive and supportive practice have also been highlighted. Intangible qualities, such as feeling welcome, being able to share feelings, as well as being able to make mistakes, were noted as important. Being able to express oneself, linguistically and experientially, was also offered, which speaks to being recognised as unique individuals, rather than as receptacles of a standardised experience [12]. This inclusion is constitutive of the social justice project [13]. Creating enabling spaces where the whole student is welcomed and valued further arises through engendering and fostering humanistic dialogue [42, 56]. Discussing topics that “transgress [57]” the normative boundary of the classroom, including speaking about systemic racial inequalities [12, 58, 59], can move learning toward an interconnected project of co-construction among teachers and students [60, 61] and create opportunities where everyone learns.
This research has some limitations. As a qualitative exploration, the findings relate to those who chose to participate in the research and cannot necessarily be generalised to all students of ethnic minority backgrounds in the UK. A bias of females to males exists in the data set, and while this bias is reflective of national trends in higher education [1], the experiences reported cannot stand for students of all genders. The research took place within one academic department at one widening participation university, which may point to challenges faced in that specific department and/or university and not to higher education throughout the UK. As the researchers were known to the participants, with one holding power as a lecturer, participants may have not accurately represented their views due to influence or fear of consequences. Further research across the university, in comparison with other universities, and by researchers without connections to the participants, would increase robustness of the data and its interpretations.
Based on the findings from this research, there remain several challenges to be addressed if inequalities are to be overcome. There are inherent structural inequalities, particularly in relation to race and ethnicity, in UK society and in higher education institutions. Resistance to acknowledging that there are implicit structures of oppression against ethnic minority students and communities needs to be overcome through listening to and acting on the experiences of ethnic minority students and communities. Recognition of the rich and life affirming experiences, knowledge bases, and potentials of ethnic minority groups as valuable needs to be declared, supported and promoted, within the university and across society, as part of the dismantling of white supremacy. Restructuring policies and practices, from the highest domains of the state, down to the personal tenets held in one’s heart, needs to occur, so that ethnic minority students can have their potentials fulfilled as a matter of principle.
This research invoked a social determinants of health perspective with which to explore how structural racism in society continues to exclude ethnic minority students from achieving their potential in higher education. It has found that social exclusion, a fundamental cause for ill health, is likewise a fundamental cause for the inequalities ethnic minority students experience in higher education. While widening participation initiatives have sought to make higher education more accessible to the diversity of population groups within the UK, to which students from varied backgrounds have responded, there remains intractable inequalities that inhibit equitable progression through university and into graduate employment. Insufficient access to the resources for remote learning, including fellow students, combined with the burdens of child-care, home schooling and the increased risk of illness and death from COVID-19, placed substantial and unequal stresses on ethnic minority students in their quest for success in higher education. To effect change, countering white supremacist ideologies is needed in educational practice. Affirming and valuing the diverse skills, experiences, and needs of ethnic minority students, helps place wellbeing at the center. Recognising that students have much to teach one another, especially when able to engage in co-constructive dialogue, can further assist in countering current imbalances in higher education systems. Glimmers of good practice, however, will remain isolated and marginal until structural racism and the foundational inequality of social exclusion in the widest sense, are tackled at institutional and structural levels within higher education and across society.
We would like to thank the students who participated in this research, for sharing their time, their vulnerabilities and their experiences on higher education during this pandemic year with us. We are deeply indebted to you all and hope that your insights will help bring about much needed change.
The authors declare no conflict of interest.
IntechOpen is the first native scientific publisher of Open Access books, with more than 116,000 authors worldwide, ranging from globally-renowned Nobel Prize winners to up-and-coming researchers at the cutting edge of scientific discovery. Established in Europe with the new headquarters based in London, and with plans for international growth, IntechOpen is the leading publisher of Open Access scientific books. The values of our business are based on the same ones that any scientist applies to their research -- we have created a culture of respect, collegiality and collaboration within an atmosphere that’s relaxed, friendly and progressive.
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Chaban",coverURL:"https://cdn.intechopen.com/books/images_new/6092.jpg",editedByType:"Edited by",editors:[{id:"83427",title:"Prof.",name:"Victor",middleName:null,surname:"Chaban",slug:"victor-chaban",fullName:"Victor Chaban"}],equalEditorOne:null,equalEditorTwo:null,equalEditorThree:null,productType:{id:"1",chapterContentType:"chapter",authoredCaption:"Edited by"}},{type:"book",id:"5521",title:"Synaptic Plasticity",subtitle:null,isOpenForSubmission:!1,hash:"9eea3c7f926cd466ddd14ab777b663d8",slug:"synaptic-plasticity",bookSignature:"Thomas Heinbockel",coverURL:"https://cdn.intechopen.com/books/images_new/5521.jpg",editedByType:"Edited by",editors:[{id:"70569",title:"Dr.",name:"Thomas",middleName:null,surname:"Heinbockel",slug:"thomas-heinbockel",fullName:"Thomas Heinbockel"}],equalEditorOne:null,equalEditorTwo:null,equalEditorThree:null,productType:{id:"1",chapterContentType:"chapter",authoredCaption:"Edited by"}}],booksByTopicTotal:10,seriesByTopicCollection:[],seriesByTopicTotal:0,mostCitedChapters:[{id:"59437",doi:"10.5772/intechopen.74318",title:"Music and Brain Plasticity: How Sounds Trigger Neurogenerative Adaptations",slug:"music-and-brain-plasticity-how-sounds-trigger-neurogenerative-adaptations",totalDownloads:2085,totalCrossrefCites:5,totalDimensionsCites:14,abstract:"This contribution describes how music can trigger plastic changes in the brain. We elaborate on the concept of neuroplasticity by focussing on three major topics: the ontogenetic scale of musical development, the phenomenon of neuroplasticity as the outcome of interactions with the sounds and a short survey of clinical and therapeutic applications. First, a distinction is made between two scales of description: the larger evolutionary scale (phylogeny) and the scale of individual development (ontogeny). In this sense, listeners are not constrained by a static dispositional machinery, but they can be considered as dynamical systems that are able to adapt themselves in answer to the solicitations of a challenging environment. Second, the neuroplastic changes are considered both from a structural and functional level of adaptation, with a special focus on the recent findings from network science. The neural activity of the medial regions of the brain seems to become more synchronised when listening to music as compared to rest, and these changes become permanent in individuals such as musicians with year-long musical practice. As such, the question is raised as to the clinical and therapeutic applications of music as a trigger for enhancing the functionality of the brain, both in normal and impaired people.",book:{id:"6092",slug:"neuroplasticity-insights-of-neural-reorganization",title:"Neuroplasticity",fullTitle:"Neuroplasticity - Insights of Neural Reorganization"},signatures:"Mark Reybrouck, Peter Vuust and Elvira Brattico",authors:[{id:"196698",title:"Prof.",name:"Mark",middleName:null,surname:"Reybrouck",slug:"mark-reybrouck",fullName:"Mark Reybrouck"},{id:"209976",title:"Prof.",name:"Elvira",middleName:null,surname:"Brattico",slug:"elvira-brattico",fullName:"Elvira Brattico"},{id:"209977",title:"Prof.",name:"Peter",middleName:null,surname:"Vuust",slug:"peter-vuust",fullName:"Peter Vuust"}]},{id:"67730",doi:"10.5772/intechopen.86822",title:"Circadian Rhythms of the Autonomic Nervous System: Scientific Implication and Practical Implementation",slug:"circadian-rhythms-of-the-autonomic-nervous-system-scientific-implication-and-practical-implementatio",totalDownloads:1074,totalCrossrefCites:8,totalDimensionsCites:12,abstract:"Circadian rhythms are omnipresent in almost any biosignal. In this chapter, we join them with the need for practical tools for screening in preventive settings and point out heart rate variability (HRV), a measure of autonomic nervous system activity, as a chronobiologic, unspecific index of mental and physical health. We discuss methods to calculate the circadian variation of HRV measures, particularly the cosinor procedure. We present reference values for circadian variation parameters of HRV and data concerning reproducibility. Furthermore, we show data giving first evidence of HRV as a comprehensive health index by showing altered circadian variation patterns of HRV depending on mental (trait dysthymia) as well as physical (inflammatory markers) health. Finally, we present examples of disturbed chronobiology of HRV in clinical and preventive settings and its practical application in medical consultation.",book:{id:"6899",slug:"chronobiology-the-science-of-biological-time-structure",title:"Chronobiology",fullTitle:"Chronobiology - The Science of Biological Time Structure"},signatures:"Marc N. Jarczok, Harald Guendel, Jennifer J. McGrath and Elisabeth M. Balint",authors:[{id:"289160",title:"Dr.",name:"Marc",middleName:"N",surname:"Jarczok",slug:"marc-jarczok",fullName:"Marc Jarczok"},{id:"289379",title:"Dr.",name:"Elisabeth",middleName:null,surname:"Balint",slug:"elisabeth-balint",fullName:"Elisabeth Balint"},{id:"299975",title:"Prof.",name:"Jennifer J",middleName:null,surname:"McGrath",slug:"jennifer-j-mcgrath",fullName:"Jennifer J McGrath"},{id:"304667",title:"Prof.",name:"Harald",middleName:null,surname:"Gündel",slug:"harald-gundel",fullName:"Harald Gündel"}]},{id:"57827",doi:"10.5772/intechopen.71165",title:"A Role for the Longitudinal Axis of the Hippocampus in Multiscale Representations of Large and Complex Spatial Environments and Mnemonic Hierarchies",slug:"a-role-for-the-longitudinal-axis-of-the-hippocampus-in-multiscale-representations-of-large-and-compl",totalDownloads:1397,totalCrossrefCites:6,totalDimensionsCites:12,abstract:"The hippocampus is involved in spatial navigation and memory in rodents and humans. Anatomically, the hippocampus extends along a longitudinal axis that shows a combination of graded and specific interconnections with neocortical and subcortical brain areas. Functionally, place cells are found all along the longitudinal axis and exhibit gradients of properties including an increasing dorsal-to-ventral place field size. We propose a view of hippocampal function in which fine-dorsal to coarse-ventral overlapping representations collaborate to form a multi-level representation of spatial and episodic memory that is dominant during navigation in large and complex environments or when encoding complex memories. This view is supported by the fact that the effects of ventral hippocampal damage are generally only found in larger laboratory-scale environments, and by the finding that human virtual navigation studies associate ventral hippocampal involvement with increased environmental complexity. Other mechanisms such as the ability of place cells to exhibit multiple fields and their ability to scale their fields with changes in environment size may be utilized when forming large-scale cognitive maps. Coarse-grained ventral representations may overlap with and provide multi-modal global contexts to finer-grained intermediate and dorsal representations, a mechanism that may support mnemonic hierarchies of autobiographical memory in humans.",book:{id:"6250",slug:"the-hippocampus-plasticity-and-functions",title:"The Hippocampus",fullTitle:"The Hippocampus - Plasticity and Functions"},signatures:"Bruce Harland, Marcos Contreras and Jean-Marc Fellous",authors:[{id:"210681",title:"Dr.",name:"Bruce",middleName:null,surname:"Harland",slug:"bruce-harland",fullName:"Bruce Harland"},{id:"210682",title:"Dr.",name:"Marco",middleName:null,surname:"Contreras",slug:"marco-contreras",fullName:"Marco Contreras"},{id:"210683",title:"Prof.",name:"Jean-Marc",middleName:null,surname:"Fellous",slug:"jean-marc-fellous",fullName:"Jean-Marc Fellous"}]},{id:"68423",doi:"10.5772/intechopen.88232",title:"Polyunsaturated Fatty Acid Metabolism in the Brain and Brain Cells",slug:"polyunsaturated-fatty-acid-metabolism-in-the-brain-and-brain-cells",totalDownloads:1128,totalCrossrefCites:8,totalDimensionsCites:10,abstract:"Dietary polyunsaturated fatty acids (PUFAs) have gained more importance these last decades since they regulate the level of long-chain PUFAs (LC-PUFAs) in all cells and especially in brain cells. Because LC-PUFAs, especially those of the n-3 family, display both anti-inflammatory and pro-resolution properties, they play an essential role in neuroinflammation. Neuroinflammation is a hallmark of neurological disorders and requires to be tightly controlled or at least limited otherwise it can have functional consequences and negatively impact the quality of life and well-being of patients. LC-PUFAs exert these beneficial properties in part through the synthesis of specialized pro-resolving mediators (SPMs) that are involved in the resolution of inflammation and to the return of homeostasis. SPMs are promising relevant candidates to resolve brain inflammation and to contribute to neuroprotective functions and lead to novel therapeutics for brain inflammatory diseases. Here we present an overview of the origin and accumulation of PUFAs in the brain and brain cells and their conversion into SPMs that are involved in neuroinflammation and how nutrition induces variations in LC-PUFA and SPM levels in the brain and in brain cells.",book:{id:"6907",slug:"feed-your-mind-how-does-nutrition-modulate-brain-function-throughout-life-",title:"Feed Your Mind",fullTitle:"Feed Your Mind - How Does Nutrition Modulate Brain Function throughout Life?"},signatures:"Corinne Joffre",authors:[{id:"281107",title:"Dr.",name:"Corinne",middleName:null,surname:"Joffre",slug:"corinne-joffre",fullName:"Corinne Joffre"}]},{id:"61465",doi:"10.5772/intechopen.76603",title:"The Importance of Distinguishing Allocentric and Egocentric Search Strategies in Rodent Hippocampal-Dependent Spatial Memory Paradigms: Getting More Out of Your Data",slug:"the-importance-of-distinguishing-allocentric-and-egocentric-search-strategies-in-rodent-hippocampal-",totalDownloads:1419,totalCrossrefCites:4,totalDimensionsCites:8,abstract:"While the brain works as a dynamic network, with no brain region solely responsible for any particular function, it is generally accepted that the hippocampus plays a major role in memory. Spatial memory operates through the hippocampus with communication with the prefrontal and parietal cortices. This chapter will focus on two separate reference frames involved in spatial memory, egocentric and allocentric, and outline the differences of these reference frames and associated search strategies with relevance to behavioural neuroscience. The importance of dissociating these search strategies is put forward, and steps researchers can take to do so are suggested. Neurophysiological and clinical differences between these spatial reference frames are outlined to further support the view that distinguishing them would be beneficial.",book:{id:"6250",slug:"the-hippocampus-plasticity-and-functions",title:"The Hippocampus",fullTitle:"The Hippocampus - Plasticity and Functions"},signatures:"Adrienne M. Grech, Jay Patrick Nakamura and Rachel Anne Hill",authors:[{id:"230389",title:"Dr.",name:"Rachel",middleName:null,surname:"Hill",slug:"rachel-hill",fullName:"Rachel Hill"},{id:"230394",title:"Ms.",name:"Adrienne",middleName:null,surname:"Grech",slug:"adrienne-grech",fullName:"Adrienne Grech"},{id:"230395",title:"Mr.",name:"Jay",middleName:null,surname:"Nakamura",slug:"jay-nakamura",fullName:"Jay Nakamura"}]}],mostDownloadedChaptersLast30Days:[{id:"64482",title:"Neurodegenerative Diseases and Their Therapeutic Approaches",slug:"neurodegenerative-diseases-and-their-therapeutic-approaches",totalDownloads:1324,totalCrossrefCites:1,totalDimensionsCites:2,abstract:"Alzheimer’s disease and Parkinson’s disease are characterized as a chronic and progressive neurodegenerative disorder and are manifested by the loss of neurons within the brain and/or spinal cord. In the present chapter, we would like to summarize the molecular mechanism focusing on metabolic modification associated with neurodegenerative diseases or heritable genetic disorders. The identification of the exact molecular mechanisms involved in these diseases would facilitate the discovery of earlier pathophysiological markers along with substantial therapies, which may consist (of) mitochondria-targeted antioxidant therapy, mitochondrial dynamics modulators, epigenetic modulators, and neural stem cell therapy. Therefore, all these therapies may hold particular assurance as influential neuroprotective therapies in the treatment of neurodegenerative diseases.",book:{id:"6991",slug:"neurons-dendrites-and-axons",title:"Neurons",fullTitle:"Neurons - Dendrites and Axons"},signatures:"Farhin Patel and Palash Mandal",authors:[{id:"217215",title:"Dr.",name:"Palash",middleName:null,surname:"Mandal",slug:"palash-mandal",fullName:"Palash Mandal"}]},{id:"75762",title:"Structural and Biological Basis for Proprioception",slug:"structural-and-biological-basis-for-proprioception",totalDownloads:474,totalCrossrefCites:1,totalDimensionsCites:1,abstract:"The proprioception is the sense of positioning and movement. It is mediate by proprioceptors, a small subset of mechanosensory neurons localized in the dorsal root ganglia that convey information about the stretch and tension of muscles, tendons, and joints. These neurons supply of afferent innervation to specialized sensory organs in muscles (muscle spindles) and tendons (Golgi tendon organs). Thereafter, the information originated in the proprioceptors travels throughout two main nerve pathways reaching the central nervous system at the level of the spinal cord and the cerebellum (unconscious) and the cerebral cortex (conscious) for processing. On the other hand, since the stimuli for proprioceptors are mechanical (stretch, tension) proprioception can be regarded as a modality of mechanosensitivity and the putative mechanotransducers proprioceptors begins to be known now. The mechanogated ion channels acid-sensing ion channel 2 (ASIC2), transient receptor potential vanilloid 4 (TRPV4) and PIEZO2 are among candidates. Impairment or poor proprioception is proper of aging and some neurological diseases. Future research should focus on treating these defects. This chapter intends provide a comprehensive update an overview of the anatomical, structural and molecular basis of proprioception as well as of the main causes of proprioception impairment, including aging, and possible treatments.",book:{id:"10554",slug:"proprioception",title:"Proprioception",fullTitle:"Proprioception"},signatures:"José A. Vega and Juan Cobo",authors:[{id:"59892",title:"Prof.",name:"José A.",middleName:null,surname:"Vega",slug:"jose-a.-vega",fullName:"José A. Vega"},{id:"100648",title:"Dr.",name:"Juan",middleName:null,surname:"Cobo",slug:"juan-cobo",fullName:"Juan Cobo"}]},{id:"62564",title:"Inflammation and Autonomic Function",slug:"inflammation-and-autonomic-function",totalDownloads:1785,totalCrossrefCites:2,totalDimensionsCites:3,abstract:"Inflammation is generally a temporary and limited condition but may lead to a chronic one if immune and physiological homeostasis are disrupted. The autonomic nervous system has an important role in the short- and, also, long-term regulation of homeostasis and, thus, on inflammation. Autonomic modulation in acute and chronic inflammation has been implicated with a sympathetic interference in the earlier stages of the inflammatory process and the activation of the vagal inflammatory reflex to regulate innate immune responses and cytokine functional effects in longer processes. The present review focuses on the autonomic mechanisms controlling proinflammatory responses, and we will discuss novel therapeutic options linked to autonomic modulation for diseases associated with a chronic inflammatory condition such as sepsis.",book:{id:"6808",slug:"autonomic-nervous-system",title:"Autonomic Nervous System",fullTitle:"Autonomic Nervous System"},signatures:"Ângela Leal, Mafalda Carvalho, Isabel Rocha and Helder Mota-Filipe",authors:[{id:"227590",title:"Prof.",name:"Isabel",middleName:null,surname:"Rocha",slug:"isabel-rocha",fullName:"Isabel Rocha"},{id:"253537",title:"Ph.D.",name:"Ângela",middleName:null,surname:"Leal",slug:"angela-leal",fullName:"Ângela Leal"},{id:"253581",title:"MSc.",name:"Mafalda",middleName:null,surname:"Carvalho",slug:"mafalda-carvalho",fullName:"Mafalda Carvalho"},{id:"253701",title:"Prof.",name:"Hélder",middleName:null,surname:"Mota-Filipe",slug:"helder-mota-filipe",fullName:"Hélder Mota-Filipe"}]},{id:"62850",title:"Anatomy of the Human Optic Nerve: Structure and Function",slug:"anatomy-of-the-human-optic-nerve-structure-and-function",totalDownloads:2939,totalCrossrefCites:2,totalDimensionsCites:5,abstract:"The optic nerve (ON) is constituted by the axons of the retinal ganglion cells (RGCs). These axons are distributed in an organized pattern from the soma of the RGC to the lateral geniculated nucleus (where most of the neurons synapse). The key points of the ON are the optic nerve head and chiasm. This chapter will include a detailed and updated review of the ON different parts: RGC axons, glial cells, connective tissue of the lamina cribrosa and the septum and the blood vessels derivate from the central retina artery and from the ciliary system. There will be an up-to-date description about the superficial nerve fibre layer, including their organization, and about prelaminar, laminar and retrolaminar regions, emphasizing the axoplasmic flow, glial barriers, biomechanics of the lamina cribrosa and the role of the macro- and microglia in their working.",book:{id:"6786",slug:"optic-nerve",title:"Optic Nerve",fullTitle:"Optic Nerve"},signatures:"Juan J. Salazar, Ana I. Ramírez, Rosa De Hoz, Elena Salobrar-Garcia,\nPilar Rojas, José A. Fernández-Albarral, Inés López-Cuenca, Blanca\nRojas, Alberto Triviño and José M. Ramírez",authors:null},{id:"68362",title:"Carbohydrates and the Brain: Roles and Impact",slug:"carbohydrates-and-the-brain-roles-and-impact",totalDownloads:1398,totalCrossrefCites:1,totalDimensionsCites:1,abstract:"Even if its size is fairly small (about 2% of body weight), the brain consumes around 20% of the total body energy. Whereas organs such as muscles and liver may use several sources of energy, under physiological conditions, the brain mainly depends on glucose for its energy needs. This involves the need for blood glucose level to be tightly regulated. Thus, in addition to its fueling role, glucose plays a role as signaling molecule informing the brain of any slight change in blood level to ensure glucose homeostasis. In this chapter, we will describe the fueling and sensing properties of glucose and other carbohydrates on the brain and present some physiological brain functions impacted by these sugars. We will also highlight the scientific questions that need to be answered in order to better understand the impact of sugars on the brain.",book:{id:"6907",slug:"feed-your-mind-how-does-nutrition-modulate-brain-function-throughout-life-",title:"Feed Your Mind",fullTitle:"Feed Your Mind - How Does Nutrition Modulate Brain Function throughout Life?"},signatures:"Xavier Fioramonti and Luc Pénicaud",authors:[{id:"281112",title:"Ph.D.",name:"Xavier",middleName:null,surname:"Fioramonti",slug:"xavier-fioramonti",fullName:"Xavier Fioramonti"},{id:"281113",title:"Dr.",name:"Luc",middleName:null,surname:"Pénicaud",slug:"luc-penicaud",fullName:"Luc Pénicaud"}]}],onlineFirstChaptersFilter:{topicId:"213",limit:6,offset:0},onlineFirstChaptersCollection:[],onlineFirstChaptersTotal:0},preDownload:{success:null,errors:{}},subscriptionForm:{success:null,errors:{}},aboutIntechopen:{},privacyPolicy:{},peerReviewing:{},howOpenAccessPublishingWithIntechopenWorks:{},sponsorshipBooks:{sponsorshipBooks:[],offset:8,limit:8,total:0},allSeries:{pteSeriesList:[{id:"14",title:"Artificial Intelligence",numberOfPublishedBooks:8,numberOfPublishedChapters:87,numberOfOpenTopics:6,numberOfUpcomingTopics:0,issn:"2633-1403",doi:"10.5772/intechopen.79920",isOpenForSubmission:!0},{id:"7",title:"Biomedical Engineering",numberOfPublishedBooks:12,numberOfPublishedChapters:98,numberOfOpenTopics:3,numberOfUpcomingTopics:0,issn:"2631-5343",doi:"10.5772/intechopen.71985",isOpenForSubmission:!0}],lsSeriesList:[{id:"11",title:"Biochemistry",numberOfPublishedBooks:27,numberOfPublishedChapters:286,numberOfOpenTopics:4,numberOfUpcomingTopics:0,issn:"2632-0983",doi:"10.5772/intechopen.72877",isOpenForSubmission:!0},{id:"25",title:"Environmental Sciences",numberOfPublishedBooks:1,numberOfPublishedChapters:9,numberOfOpenTopics:4,numberOfUpcomingTopics:0,issn:"2754-6713",doi:"10.5772/intechopen.100362",isOpenForSubmission:!0},{id:"10",title:"Physiology",numberOfPublishedBooks:11,numberOfPublishedChapters:139,numberOfOpenTopics:4,numberOfUpcomingTopics:0,issn:"2631-8261",doi:"10.5772/intechopen.72796",isOpenForSubmission:!0}],hsSeriesList:[{id:"3",title:"Dentistry",numberOfPublishedBooks:8,numberOfPublishedChapters:129,numberOfOpenTopics:0,numberOfUpcomingTopics:2,issn:"2631-6218",doi:"10.5772/intechopen.71199",isOpenForSubmission:!1},{id:"6",title:"Infectious Diseases",numberOfPublishedBooks:13,numberOfPublishedChapters:105,numberOfOpenTopics:3,numberOfUpcomingTopics:1,issn:"2631-6188",doi:"10.5772/intechopen.71852",isOpenForSubmission:!0},{id:"13",title:"Veterinary Medicine and Science",numberOfPublishedBooks:9,numberOfPublishedChapters:101,numberOfOpenTopics:3,numberOfUpcomingTopics:0,issn:"2632-0517",doi:"10.5772/intechopen.73681",isOpenForSubmission:!0}],sshSeriesList:[{id:"22",title:"Business, Management and Economics",numberOfPublishedBooks:1,numberOfPublishedChapters:11,numberOfOpenTopics:2,numberOfUpcomingTopics:1,issn:null,doi:"10.5772/intechopen.100359",isOpenForSubmission:!0},{id:"23",title:"Education and Human Development",numberOfPublishedBooks:0,numberOfPublishedChapters:0,numberOfOpenTopics:2,numberOfUpcomingTopics:0,issn:null,doi:"10.5772/intechopen.100360",isOpenForSubmission:!1},{id:"24",title:"Sustainable Development",numberOfPublishedBooks:0,numberOfPublishedChapters:9,numberOfOpenTopics:4,numberOfUpcomingTopics:1,issn:null,doi:"10.5772/intechopen.100361",isOpenForSubmission:!0}],testimonialsList:[{id:"6",text:"It is great to work with the IntechOpen to produce a worthwhile collection of research that also becomes a great educational resource and guide for future research endeavors.",author:{id:"259298",name:"Edward",surname:"Narayan",institutionString:null,profilePictureURL:"https://mts.intechopen.com/storage/users/259298/images/system/259298.jpeg",slug:"edward-narayan",institution:{id:"3",name:"University of Queensland",country:{id:null,name:"Australia"}}}},{id:"13",text:"The collaboration with and support of the technical staff of IntechOpen is fantastic. The whole process of submitting an article and editing of the submitted article goes extremely smooth and fast, the number of reads and downloads of chapters is high, and the contributions are also frequently cited.",author:{id:"55578",name:"Antonio",surname:"Jurado-Navas",institutionString:null,profilePictureURL:"https://s3.us-east-1.amazonaws.com/intech-files/0030O00002bRisIQAS/Profile_Picture_1626166543950",slug:"antonio-jurado-navas",institution:{id:"720",name:"University of Malaga",country:{id:null,name:"Spain"}}}}]},series:{item:{id:"11",title:"Biochemistry",doi:"10.5772/intechopen.72877",issn:"2632-0983",scope:"Biochemistry, the study of chemical transformations occurring within living organisms, impacts all areas of life sciences, from molecular crystallography and genetics to ecology, medicine, and population biology. Biochemistry examines macromolecules - proteins, nucleic acids, carbohydrates, and lipids – and their building blocks, structures, functions, and interactions. Much of biochemistry is devoted to enzymes, proteins that catalyze chemical reactions, enzyme structures, mechanisms of action and their roles within cells. Biochemistry also studies small signaling molecules, coenzymes, inhibitors, vitamins, and hormones, which play roles in life processes. Biochemical experimentation, besides coopting classical chemistry methods, e.g., chromatography, adopted new techniques, e.g., X-ray diffraction, electron microscopy, NMR, radioisotopes, and developed sophisticated microbial genetic tools, e.g., auxotroph mutants and their revertants, fermentation, etc. More recently, biochemistry embraced the ‘big data’ omics systems. Initial biochemical studies have been exclusively analytic: dissecting, purifying, and examining individual components of a biological system; in the apt words of Efraim Racker (1913 –1991), “Don’t waste clean thinking on dirty enzymes.” Today, however, biochemistry is becoming more agglomerative and comprehensive, setting out to integrate and describe entirely particular biological systems. The ‘big data’ metabolomics can define the complement of small molecules, e.g., in a soil or biofilm sample; proteomics can distinguish all the comprising proteins, e.g., serum; metagenomics can identify all the genes in a complex environment, e.g., the bovine rumen. This Biochemistry Series will address the current research on biomolecules and the emerging trends with great promise.",coverUrl:"https://cdn.intechopen.com/series/covers/11.jpg",latestPublicationDate:"May 15th, 2022",hasOnlineFirst:!0,numberOfPublishedBooks:27,editor:{id:"31610",title:"Dr.",name:"Miroslav",middleName:null,surname:"Blumenberg",slug:"miroslav-blumenberg",fullName:"Miroslav Blumenberg",profilePictureURL:"https://mts.intechopen.com/storage/users/31610/images/system/31610.jpg",biography:"Miroslav Blumenberg, Ph.D., was born in Subotica and received his BSc in Belgrade, Yugoslavia. He completed his Ph.D. at MIT in Organic Chemistry; he followed up his Ph.D. with two postdoctoral study periods at Stanford University. Since 1983, he has been a faculty member of the RO Perelman Department of Dermatology, NYU School of Medicine, where he is codirector of a training grant in cutaneous biology. Dr. Blumenberg’s research is focused on the epidermis, expression of keratin genes, transcription profiling, keratinocyte differentiation, inflammatory diseases and cancers, and most recently the effects of the microbiome on the skin. He has published more than 100 peer-reviewed research articles and graduated numerous Ph.D. and postdoctoral students.",institutionString:null,institution:{name:"New York University Langone Medical Center",institutionURL:null,country:{name:"United States of America"}}},editorTwo:null,editorThree:null},subseries:{paginationCount:4,paginationItems:[{id:"14",title:"Cell and Molecular Biology",coverUrl:"https://cdn.intechopen.com/series_topics/covers/14.jpg",isOpenForSubmission:!0,editor:{id:"165627",title:"Dr.",name:"Rosa María",middleName:null,surname:"Martínez-Espinosa",slug:"rosa-maria-martinez-espinosa",fullName:"Rosa María Martínez-Espinosa",profilePictureURL:"https://mts.intechopen.com/storage/users/165627/images/system/165627.jpeg",biography:"Dr. Rosa María Martínez-Espinosa has been a Spanish Full Professor since 2020 (Biochemistry and Molecular Biology) and is currently Vice-President of International Relations and Cooperation development and leader of the research group 'Applied Biochemistry” (University of Alicante, Spain). Other positions she has held at the university include Vice-Dean of Master Programs, Vice-Dean of the Degree in Biology and Vice-Dean for Mobility and Enterprise and Engagement at the Faculty of Science (University of Alicante). She received her Bachelor in Biology in 1998 (University of Alicante) and her PhD in 2003 (Biochemistry, University of Alicante). She undertook post-doctoral research at the University of East Anglia (Norwich, U.K. 2004-2005; 2007-2008).\nHer multidisciplinary research focuses on investigating archaea and their potential applications in biotechnology. She has an H-index of 21. She has authored one patent and has published more than 70 indexed papers and around 60 book chapters.\nShe has contributed to more than 150 national and international meetings during the last 15 years. Her research interests include archaea metabolism, enzymes purification and characterization, gene regulation, carotenoids and bioplastics production, antioxidant\ncompounds, waste water treatments, and brines bioremediation.\nRosa María’s other roles include editorial board member for several journals related\nto biochemistry, reviewer for more than 60 journals (biochemistry, molecular biology, biotechnology, chemistry and microbiology) and president of several organizing committees in international meetings related to the N-cycle or respiratory processes.",institutionString:null,institution:{name:"University of Alicante",institutionURL:null,country:{name:"Spain"}}},editorTwo:null,editorThree:null},{id:"15",title:"Chemical Biology",coverUrl:"https://cdn.intechopen.com/series_topics/covers/15.jpg",isOpenForSubmission:!0,editor:{id:"441442",title:"Dr.",name:"Şükrü",middleName:null,surname:"Beydemir",slug:"sukru-beydemir",fullName:"Şükrü Beydemir",profilePictureURL:"https://s3.us-east-1.amazonaws.com/intech-files/0033Y00003GsUoIQAV/Profile_Picture_1634557147521",biography:"Dr. Şükrü Beydemir obtained a BSc in Chemistry in 1995 from Yüzüncü Yıl University, MSc in Biochemistry in 1998, and PhD in Biochemistry in 2002 from Atatürk University, Turkey. 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He is a member of the Turkish Biochemical Society, American Chemical Society, and German Genetics society. Dr. Ekinci published around ninety scientific papers, reviews and book chapters, and presented several conferences to scientists. He has received numerous publication awards from several scientific councils. 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He worked on the structure-function relationships of glycoconjugates and his main project was the investigations on the biological roles of the de-N-glycosylation enzymes (Endo-N-acetyl-β-D-glucosaminidase and peptide-N4-(N-acetyl-β-glucosaminyl) asparagine amidase). From 2002 he contributes to the understanding of the Blood-brain barrier functioning using proteomics approaches. He has published more than 70 papers. 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Since then, he has been working as an Adjunct Professor in the same Department at the University of Pavia. His research activity during the first years was primarily focused on the purification and structural characterization of enzymes from animal and plant sources. During this period, Prof. Iadarola familiarized himself with the conventional techniques used in column chromatography, spectrophotometry, manual Edman degradation, and electrophoresis). Since 1995, he has been working on: i) the determination in biological fluids (serum, urine, bronchoalveolar lavage, sputum) of proteolytic activities involved in the degradation processes of connective tissue matrix, and ii) on the identification of biological markers of lung diseases. 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The applications of this research cover many related fields, such as biotechnology and medicine, where, for example, Bioinformatics contributes to faster drug design, DNA analysis in forensics, and DNA sequence analysis in the field of personalized medicine. Personalized medicine is a type of medical care in which treatment is customized individually for each patient. Personalized medicine enables more effective therapy, reduces the costs of therapy and clinical trials, and also minimizes the risk of side effects. Nevertheless, advances in personalized medicine would not have been possible without bioinformatics, which can analyze the human genome and other vast amounts of biomedical data, especially in genetics. The rapid growth of information technology enabled the development of new tools to decode human genomes, large-scale studies of genetic variations and medical informatics. 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