Long-term impact of preeclampsia.
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More than half of the publishers listed alongside IntechOpen (18 out of 30) are Social Science and Humanities publishers. IntechOpen is an exception to this as a leader in not only Open Access content but Open Access content across all scientific disciplines, including Physical Sciences, Engineering and Technology, Health Sciences, Life Science, and Social Sciences and Humanities.
\\n\\nOur breakdown of titles published demonstrates this with 47% PET, 31% HS, 18% LS, and 4% SSH books published.
\\n\\n“Even though ItechOpen has shown the potential of sci-tech books using an OA approach,” other publishers “have shown little interest in OA books.”
\\n\\nAdditionally, each book published by IntechOpen contains original content and research findings.
\\n\\nWe are honored to be among such prestigious publishers and we hope to continue to spearhead that growth in our quest to promote Open Access as a true pioneer in OA book publishing.
\\n\\n\\n\\n
\\n"}]',published:!0,mainMedia:{caption:"IntechOpen Maintains",originalUrl:"/media/original/113"}},components:[{type:"htmlEditorComponent",content:'
Simba Information has released its Open Access Book Publishing 2020 - 2024 report and has again identified IntechOpen as the world’s largest Open Access book publisher by title count.
\n\nSimba Information is a leading provider for market intelligence and forecasts in the media and publishing industry. The report, published every year, provides an overview and financial outlook for the global professional e-book publishing market.
\n\nIntechOpen, De Gruyter, and Frontiers are the largest OA book publishers by title count, with IntechOpen coming in at first place with 5,101 OA books published, a good 1,782 titles ahead of the nearest competitor.
\n\nSince the first Open Access Book Publishing report published in 2016, IntechOpen has held the top stop each year.
\n\n\n\nMore than half of the publishers listed alongside IntechOpen (18 out of 30) are Social Science and Humanities publishers. IntechOpen is an exception to this as a leader in not only Open Access content but Open Access content across all scientific disciplines, including Physical Sciences, Engineering and Technology, Health Sciences, Life Science, and Social Sciences and Humanities.
\n\nOur breakdown of titles published demonstrates this with 47% PET, 31% HS, 18% LS, and 4% SSH books published.
\n\n“Even though ItechOpen has shown the potential of sci-tech books using an OA approach,” other publishers “have shown little interest in OA books.”
\n\nAdditionally, each book published by IntechOpen contains original content and research findings.
\n\nWe are honored to be among such prestigious publishers and we hope to continue to spearhead that growth in our quest to promote Open Access as a true pioneer in OA book publishing.
\n\n\n\n
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Hypertension is a common pregnancy-specific medical disorder, which is a significant cause of maternal and perinatal mortality [1]. There is disproportionate risk to the mother and fetus for further complications and long-term sequelae.
Preeclampsia is a hypertensive disorder of pregnancy causing multi-organ dysfunction syndrome with placental dysfunction occurring in the latter half of pregnancy, with major cause of maternal morbidity, maternal intensive care admissions, Cesarean section, end-organ damage, and fetal complications.
Preeclampsia is defined as new onset of hypertension with or without proteinuria or new onset hypertension with evidence of end organ dysfunction after 20 weeks gestation or postpartum in a previously normotensive woman [2].
Classification of hypertension in pregnancy by ACOG (American College of Obstetrician and Gynecologist) 2013 task force:
Preeclampsia
Preeclampsia without severe features
Severe preeclampsia with severe features
Progress of preeclampsia is divided into two stages:
It occurs early in pregnancy with impaired remodeling of the spiral arteries and abnormal placentation. This failure of normal angiogenesis results in superficial placentation.
It presents in late second or third trimester and is characterized by signs and symptoms distinguished by the release of excess of antiangiogenic factor from intervillous space into the maternal circulation, which causes widespread maternal endothelial dysfunction and accentuated systemic inflammatory response specific to each organ system.
It affects 6–12% of all pregnant women worldwide, with preeclampsia in 5–8% of pregnancy [3, 4]. The WHO (World Health Organization) has identified hypertension as the second most common cause of maternal death among the triad of hemorrhage and sepsis [5]. It is responsible for 70,000 maternal deaths (major cause of maternal morbidity and mortality) and 500,000 fetal deaths worldwide every year [5]. Nulliparous women are prone to develop preeclampsia, while older women are at higher risk of chronic hypertension with superimposed preeclampsia.
Hypertension is well known in pregnancy worldwide, including chronic, gestational, and possible dangerous preeclampsia [6]. It is considered as high-risk pregnancy when unfavorable conditions prevail for the well-being of mother, fetus, or both.
Effective antenatal care with good surveillance minimizes the risk of complications. Hypertensive disorders of pregnancy can result in life-threatening multisystem pathology, affecting nervous, hematological, renal, hepatic, and respiratory systems.
Preeclampsia presents with maternal features of hypertension, proteinuria, and systemic dysfunction with or without fetal syndrome. Thus, proteinuria is an objective marker and reflects the system-wide endothelial leak that characterizes the preeclampsia syndrome.
There has been an alarming 30% increase in incidence of hypertensive disorders of pregnancy [7], which is explained by the demographics of increase in maternal age, obesity, and increase in use of assisted reproductive techniques, which alters the maternal-fetal immune response. It is also influenced by genetic predisposition, race, and ethnicity.
Numerous preconceptional and pregnancy-related risk factors are identified and classified in development of preeclampsia.
There has been variation of maternal age of pregnancy from teenage to women who are 40 years or older, as compared with women between 20 and 29 years [8] of age, with approximately twofold increase in risk of preeclampsia. Hispanic ethnicity may be at increased risk of developing preeclampsia [9]. Women with advancing age and delayed childbirth show a substantial increase in chronic hypertension during pregnancy and are at increased risk of preeclampsia.
Maternal and fetal genetic factors carry strong risk for preeclampsia, with one-third attributable to maternal genetic factors [10]. Women are twice as likely to develop the disorder if they have a family history of preeclampsia, [11] and the risk increases with multiple affected pregnancies [12], potentially carrying high-risk outcomes of placental abruption and fetal growth restriction. Women with history of preeclampsia in previous pregnancy are at increased risk in subsequent pregnancy, particularly in the early onset of preeclampsia.
Partner-related risk factors are long considered a disease of primigravida in women due to limited paternal sperm antigens exposure before conception, which suggests an immunological role in pathophysiology of preeclampsia, with its incidence approximately threefold higher as compared to parous women [13]. A significant contribution of paternal genes (in the fetus) was identified as risk, with one-fifth of the variance in liability conferred through fetal genes in preeclampsia [14].
With worldwide increase in prevalence of obesity, risk of preeclampsia escalates with increasing body mass index (BMI) [15]. A systemic review found that an increase in BMI of 5–7 Kg/m was associated with a twofold increased risk of preeclampsia; it also has strong association with insulin resistance and chronic hypertension, elevating the risk of preeclampsia [16].
Other maternal medical conditions with recognized risk factors for preeclampsia are chronic renal disease, antiphospholipid antibody syndrome, and systemic lupus erythematosus [17] and pregnancy-related conditions with increased placental mass, including multiple fetal gestation and hydatidiform mole, are associated with higher rates of preeclampsia as well [18].
Associated metabolic syndrome, chronic disorders hypertension, preexisting diabetes, and renal diseases that cause endothelial injury are risk factors for preeclampsia. This explains the similar tendency of endothelial dysfunction and common factor for association of preeclampsia with increased future cardiovascular diseases [19].
Cigarette smoking during pregnancy decreases the risk of preeclampsia [20] by 30–40% as compared to women who do not smoke although biological mechanism remains unknown but probable mechanism may include nicotine inhibition of thromboxane A2 synthesis [21], simulation of nitric oxide release, or combination of both.
Physical activity during pregnancy is associated with decreased risk for preeclampsia in non-obese women [22]. This occurs by decreasing oxidative stress, enhancing endothelial function, and modulating the immune and inflammatory response.
The exact cause of initiation and progress of the disease process is not known, with placenta being the focus in pathogenesis.
Following theories have been proposed to explain mechanics causing preeclampsia.
Abnormal placentation with failure of trophoblast invasion of uterine vessels.
Immunological intolerance between maternal, paternal (placental), and fetal tissues.
Vascular endothelial damage.
Genetic-inherited predisposition and polygenic disorders.
In physiological pregnancy, embryo-derived endovascular cytotrophoblast invades the decidual (10–12 weeks) and myometrial (16–18 weeks) segment of spiral arterioles of uteroplacental bed, replacing endothelial lining [23] and causing remodeling of vascular smooth muscles and inner elastic lamina (Figure 1). These physiological changes lead the maternal spiral arterioles to distend the luminal diameter fourfold, resulting in creation of tortuous and funnel-shaped flaccid [23] tubes that provide a low-resistance, low-pressure, high-capacitance, high-flow pathway into intervillous space, which gets further remodeled and unresponsive to vasoactive stimuli. These alterations in maternal vasculature ensure adequate blood flow to nourish the growing fetus and placenta.
A-Normal pregnancy uterine spiral arteries are wide open and remodeled by endovascular trophoblast, thereby increasing blood flow B-Preeclampsia women spiral arteries fail to remodel due to defective trophoblast invasion.
In preeclampsia, endovascular cytotrophoblast invasion may be incomplete [24] and only the decidual vessels undergo change, while the deeper myometrial arterioles do not lose their endothelial lining and musculoelastic tissue, resulting in narrowing of maternal spiral arterioles (Figure 1), thus impairing placental blood flow and remaining hyperresponsive to vasomotor stimuli. Inadequate spiral arteriolar remodeling leads to narrowing of maternal vessels and relative placental ischemia.
The severity of the disease correlates with the magnitude of defective trophoblastic invasion [25]. Atherosclerotic changes in maternal radial arteries that supply decidua are observed in preeclampsia. Decidual vasculopathy lesions have high association in preeclampsia with placental insufficiency, including intrauterine growth restriction and small for gestational age [26]. These changes correspond to symptomatic second stage of the preeclampsia syndrome with systemic inflammatory response [27].
In association with defective remodeling of uteroplacental vasculature, there may be presence of agonistic autoantibodies to the angiotensin receptor-1 (AT1) [28]. These autoantibodies activate AT1 receptors, endothelial cells, and vascular smooth muscle cells [29]. The autoantibodies appear to block trophoblastic invasion and may induce the production of reactive oxygen species that plays a significant role in the pathogenesis of preeclampsia at several different stages [29].
Maternal immune tolerance to parentally derived placental and fetal antigens is lost at maternal-placental interface, which is suggestive of acute graft rejection. The abnormal uteroplacental development is not clearly understood but is likely due to complex interaction of immunologic, vascular, environmental, and genetic factors. The theory of immune maladaptation may play a central role in predisposition to abnormal placentation and subsequent preeclampsia, suggesting that long-term exposure to paternal antigens in sperm is protective.
In preeclamptic women, extravillous trophoblast in early pregnancy expresses reduced amounts of immunosuppressive non-classic human leukocyte antigen G (HLA G). These changes contribute to defective placental vascularization in stage 1 of preeclampsia syndrome [30].
Excess macrophages in the decidua are associated with impaired trophoblast invasion and impaired placentation, signifying excess inflammation. NK cells interact with fetal trophoblast cell markers
Etiology of preeclampsia is summarized in Figure 2.
Etiology of preeclampsia.
Inflammatory changes are said to be a continuation of stage 1 alternation. Placental factors are released in response to ischemia, and a cascade of events is provoked in response to antiangiogenic and metabolic factors and other inflammatory leukocyte mediators, commonly called endothelial cell activation or dysfunction. Systemic endothelial cell injury with intense vasospasm is from imbalance of vasodilators (PGI, NO), vasoconstrictors (Angiotensin-II, Thromboxane A2, and Endothelin-II), oxidative stress, and inflammatory mediators (Figure 3). Vasospasm exerts a damaging effect on blood vessels and causes endothelial cells to contract and, together with hypoxia, leads to hemorrhage, necrosis, and compromised end-organ function.
A: In normal pregnancy. B: Vasoconstriction in preeclampsia.
In preeclampsia, inflammatory mediators contributed by systemic oxidative stress are tumor necrosis factor [31] alpha (TNF-Alpha) and interleukins that in turn lead to formation of lipid peroxidases [32], producing toxic radicals that injure systemic vascular endothelial cells.
Mechanisms are precisely understood but proposed theory discussed are as follows:
Increase in circulatory pressor substances.
Increased sensitivity of the vascular system to normally circulating pressor substance.
First-time exposure to chorionic villi.
Superabundance of chorionic villi, exposed as with multifetal gestation or hydatidiform mole.
Have preexisting vascular diseases associated with endothelial cell activation or inflammation such as diabetes, obesity, cardiovascular or renal, immunological disorders, or hereditary influences.
Genetically predisposed to hypertension developing during pregnancy.
Imbalance of angiogenic and antiangiogenic proteins.
Injury to systemic endothelial cell is crucial in pathogenesis of preeclampsia and likely secretes placental protein factors into maternal circulation, which provokes activation and dysfunction of systemic vascular endothelium, producing less nitric oxide contributing to vasoconstriction, and promotes coagulation and greater sensitivity to vasopressors.
Normal pregnant women develop blunted vascular pressor response selectively to pressor agent angiotensin II, mediated by synthesis of endothelial prostaglandin and nitric oxide, which is a potent vasodilator. Following preeclampsia, angiotensinase activity is depressed, and the presence of autoantibodies to angiotensin AT1 receptor increases the vascular sensitivity to pressor agent angiotensin-II (Figure 4).
Imbalance of increased thromboxane and decreased prostacyclin in preeclampsia.
There is an imbalance of proangiogenic (VEGF) [33] and antiangiogenic (soluble fms-like tyrosine kinase sFlt-I) proteins in placental vascular bed. Soluble fms-like tyrosine kinase 1 (sFlt-1) has a receptor for VEGF (Figure 5).
Normal pregnancy: signaling of vascular hemostasias is maintained by physiological level of Vascular endothelial growth factor (VEGF) and Transforming growth factor (TGF). (B) In preeclampsia: excess secretion of Sflt1 (soluble fms- like tyrosine kinase) and sENG (soluble endoglin protein) inhibits VEGF (Vascular endothelial growth factor) and TGF (transforming growth factor) signaling of vasculature.
With the progress of pregnancy, the placenta becomes relatively hypoxic at uteroplacental interface and results in an overexpression and release of placentally derived antiangiogenic peptide factors from the trophoblastic tissue, including sFlt-1 and soluble endoglin protein (sEng) into the maternal circulation, which appears to be important in pathogenesis of preeclampsia and remains the underlying theory [34]. Endothelin-I is synthesized by endothelial cells and is a potent vasoconstrictor causing hypertension (Figure 5).
In preeclampsia, sFlt-1 is a soluble antiangiogenic protein that is elevated, which binds and inactivates or reduces biological activity of free-circulating proangiogenic proteins, vascular endothelial growth factor (VEGF), and placental growth factor (PIGF), causing endothelial dysfunction [35].
Severe manifestations of preeclampsia occur in all body systems because of widespread endothelial dysfunction, making diagnosis difficult due to similar clinical presentation despite complex differences in their underlying pathophysiology and prognosis.
Numerous factors combine to exert vasoactive effects in preeclampsia [36], causing resistance to blood flow and accounts for the development of arterial hypertension. Systemic organ dysfunction is explained in Figure 6.
Etiopathogenesis of preeclampsia.
Two marked cerebral pathologies are gross hemorrhage and ischemia, with other common variable lesions noted are edema, hyperemia, and thrombosis.
Manifestations of the central nervous system are severe headache, hyperexcitability, hyperreflexia, and coma attributable to hypoxia. Reversible vasogenic cerebral edema occurs commonly due to endothelial dysfunction of the brain in preeclampsia and eclampsia. Failure of autoregulation with reduced global cerebral blood flow and hyperperfusion commonly occurs in posterior circulation, such that the changes in the brain of patients with preeclampsia/eclampsia result in posterior reversible leukoencephalopathy syndrome (PRES) [37].
Intense ocular arteriolar constriction may cause visual disturbances, and may include blurred vision, scotoma, amaurosis [38], and retinal detachment (Figure 7).
PRES syndrome.
Airway: In normal healthy pregnancy, the internal diameter of the trachea is reduced because of mucosal capillary engorgement, which can be exaggerated with narrowing of upper airway, resulting in pharyngolaryngeal edema, and subglottic edema with signs of airway obstructions such as dysphonia, hoarseness, snoring, stridor, and hypoxemia; these changes may compromise visualization of airway landmarks during direct laryngoscopy making intubation difficult [39].
Pulmonary edema occurs in approximately 3% of preeclamptic women [40]. It is relatively infrequent in young healthy women than multiparous women. Decreased colloid osmotic pressure, in combination with increased permeability and the loss of intravascular fluid and protein into the interstitium, increases the risk for pulmonary edema [41]. Endothelial activations lead to extravasation of intravascular fluid into the extracellular space and, importantly, into the lungs. Excess intravenous fluid administration is an important risk factor for pulmonary edema in preeclampsia patients [42].
Common cardiovascular disturbances in preeclampsia syndrome are increased afterload caused by hypertension and reduced preload by pathologically diminished volume expansion during pregnancy.
Preeclampsia is a hyperdynamic state with increased vascular tone and increased sensitivity to vasoconstrictor, resulting in clinical manifestation of hypertension, vasospasm, and end-organ ischemia [43]. Hemodynamic response to circulatory catecholamine is exaggerated and characterized by severe vasospasm. Typically, blood pressure and systemic vascular resistance are elevated.
The majority of preeclamptic women show increased cardiac output [44], mild-to-moderate increased systemic vascular resistance [45], and hyperdynamic left ventricular function.
In summary, aggressive fluid administration in severe preeclampsia substantially elevates left-sided filling pressures and cardiac output to hyperdynamic levels. This elevates pulmonary capillary wedge pressure, causing pulmonary edema despite normal ventricular function.
Increase in blood volume is not evident in severe preeclampsia due to vasospastic state that follows endothelial activation and worsens with increased vascular permeability, and leakage of plasma into the interstitial space, resulting in increased hemoconcentration and hematocrit values that signify preeclampsia. These women with severe hemoconcentration are unduly sensitive to blood loss at delivery than normal [45].
Thrombocytopenia is the most common hematologic disorder with platelet count of less than 100,000/mm3 in severe preeclampsia disease or HELLP (hemolysis elevated liver function low platelets) syndrome [46] that creates a hypocoagulable state correlating with the severity of the disease process.
In preeclampsia [47], platelets are activated, subsequent degranulation accounting for decrease in platelet function, and aggregation appears to account for the decrease in platelet count.
HELLP syndrome: It is characterized by hemolysis, elevated levels of liver enzymes, and low platelet count. It is associated with increased rates of maternal and perinatal morbidity. Weinstein coined the acronym HELLP. Women who do not reveal one or more of the clinical features is called partial HELLP syndrome [48].
Clinical presentation of maternal signs and symptoms vary from right upper quadrant or epigastric pain, nausea and vomiting, headache, hypertension, and proteinuria, and 12–18% of women may be normotensive and 13% may be without proteinuria. Clinical management has to prioritize maternal stability, particularly, hypertension and Coagulation abnormalities, and assess the fetal condition
Severe preeclampsia is frequently accompanied by microangiopathic hemolysis that manifests as elevated lactate dehydrogenase, reduced haptoglobin levels, hemolytic anemia, and abnormal peripheral blood smear with schistocytes, spherocytes, and reticulocytosis [49].
Disseminated intravascular coagulation is a syndrome secondary to microthrombi formation in severe preeclampsia with liver derangement [50]. Activation of coagulation system is marked by consumptions of procoagulants, increased levels of fibrin degradation products, and end-organ dysfunction. In advanced stages of DIC (disseminated intravascular coagulation), it may cause spontaneous hemorrhage, intrauterine fetal demise, placental abruption, or postpartum hemorrhage.
Plasma levels of renin, angiotensin I & II, aldosterone, deoxycorticosterone, and atrial natriuretic peptide (ANP) are substantially increased during normal pregnancy, which is further enhanced in preeclampsia women.
Extracellular fluid manifests as edema with pathological fluid retention in women with severe preeclampsia due to endothelial injury. In addition to generalized edema and proteinuria, these women have reduced plasma oncotic pressure, which creates a filtration imbalance and further displaces intravascular fluid into the surrounding interstitium, creating intravascular dehydration and extravascular overhydration. Electrolyte concentration does not differ grossly in preeclampsia patients.
Defining component of preeclampsia is proteinuria, with its renal manifestations of persistent proteinuria, changes in glomerular filtration rate, renal blood flow, and hyperuricemia. In preeclampsia serum markers, blood urea nitrogen BUN, creatinine, and uric acid reflect a decrease in renal functions. Hyperuricemia (elevated uric acid levels) is one of the recognized early predictors of preeclampsia, with the primary mechanism of decreased renal clearance [51]. High level of serum uric acid correlates with the severity of the disease. Glomerular endotheliosis is the main feature of the preeclamptic kidney defined by endothelial swelling and glomerular capillary narrowing.
Oliguria is a probable late manifestation and parallels the severity of preeclampsia. Persistent oliguria (< 500-mL urine output in 24 hours) requires immediate attention for evaluation of intravascular volume status.
Major pathological process of acute renal failure in preeclampsia (83–90%) is from prerenal and intrarenal pathology (most commonly acute tubular necrosis), which resolves completely after delivery.
Reduced blood flow to the liver may lead to periportal necrosis and are at risk of periportal hemorrhage, fibrin deposit, subcapsular bleeding, and hepatic rupture.
Hepatic involvement frequently presents as right upper quadrant or epigastric pain and accounts for 32% maternal mortality rate [50].
Rupture of a subcapsular hematoma of the liver is a life-threatening complication that can manifest as abdominal pain, which worsens over time and becomes localized to the epigastric area or right upper quadrant associated with nausea, vomiting, and headache. Alarming hypotension and shock develop with enlarged and tender liver. Diagnosis of liver subcapsular hematoma is confirmed by ultrasonography, computerized tomography (CT), or magnetic resonant imaging (MRI). The most common cause of death is coagulopathy. Conservative management is recommended for subcapsular hematoma or intraparenchymal hemorrhage without capsular rupture in stable women with an important component to avoid all potential trauma to the liver.
Uteroplacental perfusion can be impaired in pregnancies complicated by preeclampsia with increased downstream resistance in the uteroplacental bed, decreased diastolic flow velocity, and increased systolic-diastolic flow velocity ratio [51]. Reduced uteroplacental malperfusion is considered one of the major causes of fetal compromise (IUGR, premature birth, and perinatal death). Risk of placental abruption is increased threefold with increased perinatal morbidity and mortality in preeclampsia women [51].
Definite treatment of preeclampsia is termination of pregnancy to prevent disease progression and reduce maternal complications and neonatal morbidity. Time of delivery is based on gestational age, severity of preeclampsia, and maternal and fetal condition.
Birth of infant who can then thrive subsequently.
Most patients with preeclampsia with or without severe features can be delivered vaginally. Cesarean delivery is indicated for obstetric indications.
Fluid balance must be titrated closely to avoid excessive administration and avoid pulmonary edema.
Expectant management of women with preeclampsia without severe features of disease process may be considered in tertiary care center setting with maternal-fetal medicine specialist (frequent laboratory monitoring, and clinical assessment of mother and fetus).
Complete restoration of mother’s health.
Table 1 describes long-term complications of preeclampsia syndrome.
Cardiovascular | Neurovascular | Metabolic | Renal | Central nervous system |
---|---|---|---|---|
Chronic hypertension | Stroke | Type 2 diabetes | Glomerular dysfunction | Cognitive dysfunction |
Ischemic heart disease | Retinal detachment | Metabolic syndrome | Proteinuria | Retinopathy |
Atherosclerosis | Diabetic retinopathy | Obesity | White-matter lesions | |
Cardiomyopathy | Dyslipidemia | |||
Thromboembolism |
Long-term impact of preeclampsia.
Preeclampsia is one of the hypertensive disorders of pregnancy with increased morbidity and mortality. It occurs in up to 12% of pregnancies. Advanced maternal age, genetic factors, obesity, and chronic renal impairment increase the risk of preeclampsia in pregnant patients. Abnormal placentation, immunological changes, endothelial injury and activation, and increased pressor response are the pathogenesis of preeclampsia.
Due to these generalized endothelial changes, the preeclampsia patients develop multiple organ dysfunction, including PRES (posterior reversible encephalopathy) syndrome, pulmonary edema, HELLP syndrome, acute kidney injury, and uteroplacental insufficiencies.
Management of preeclampsia is supportive therapy, blood pressure control, and seizures prevention and delivery of the fetus. Long-term effects of preeclampsia are chronic hypertension, stroke, and chronic kidney disease.
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",metaTitle:"About Open Access",metaDescription:"Open access contributes to scientific excellence and integrity. It opens up research results to wider analysis. It allows research results to be reused for new discoveries. And it enables the multi-disciplinary research that is needed to solve global 21st century problems. Open access connects science with society. It allows the public to engage with research. To go behind the headlines. And look at the scientific evidence. And it enables policy makers to draw on innovative solutions to societal challenges.\n\nCarlos Moedas, the European Commissioner for Research Science and Innovation at the STM Annual Frankfurt Conference, October 2016.",metaKeywords:null,canonicalURL:"about-open-access",contentRaw:'[{"type":"htmlEditorComponent","content":"The Open Access publishing movement started in the early 2000s when academic leaders from around the world participated in the formation of the Budapest Initiative. They developed recommendations for an Open Access publishing process, “which has worked for the past decade to provide the public with unrestricted, free access to scholarly research—much of which is publicly funded. Making the research publicly available to everyone—free of charge and without most copyright and licensing restrictions—will accelerate scientific research efforts and allow authors to reach a larger number of readers” (reference: http://www.budapestopenaccessinitiative.org)
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The Open Access publishing movement started in the early 2000s when academic leaders from around the world participated in the formation of the Budapest Initiative. They developed recommendations for an Open Access publishing process, “which has worked for the past decade to provide the public with unrestricted, free access to scholarly research—much of which is publicly funded. Making the research publicly available to everyone—free of charge and without most copyright and licensing restrictions—will accelerate scientific research efforts and allow authors to reach a larger number of readers” (reference: http://www.budapestopenaccessinitiative.org)
\n\nIntechOpen’s co-founders, both scientists themselves, created the company while undertaking research in robotics at Vienna University. Their goal was to spread research freely “for scientists, by scientists’ to the rest of the world via the Open Access publishing model. The company soon became a signatory of the Budapest Initiative, which currently has more than 1000 supporting organizations worldwide, ranging from universities to funders.
\n\nAt IntechOpen today, we are still as committed to working with organizations and people who care about scientific discovery, to putting the academic needs of the scientific community first, and to providing an Open Access environment where scientists can maximize their contribution to scientific advancement. By opening up access to the world’s scientific research articles and book chapters, we aim to facilitate greater opportunity for collaboration, scientific discovery and progress. We subscribe wholeheartedly to the Open Access definition:
\n\n“By “open access” to [peer-reviewed research literature], we mean its free availability on the public internet, permitting any users to read, download, copy, distribute, print, search, or link to the full texts of these articles, crawl them for indexing, pass them as data to software, or use them for any other lawful purpose, without financial, legal, or technical barriers other than those inseparable from gaining access to the internet itself. The only constraint on reproduction and distribution, and the only role for copyright in this domain, should be to give authors control over the integrity of their work and the right to be properly acknowledged and cited” (reference: http://www.budapestopenaccessinitiative.org)
\n\nOAI-PMH
\n\nAs a firm believer in the wider dissemination of knowledge, IntechOpen supports the Open Access Initiative Protocol for Metadata Harvesting (OAI-PMH Version 2.0). Read more
\n\nLicense
\n\nBook chapters published in edited volumes are distributed under the Creative Commons Attribution 3.0 Unported License (CC BY 3.0). IntechOpen upholds a very flexible Copyright Policy. There is no copyright transfer to the publisher and Authors retain exclusive copyright to their work. All Monographs/Compacts are distributed under the Creative Commons Attribution-NonCommercial 4.0 International (CC BY-NC 4.0). Read more
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\n\nOA Publishing Fees
\n\nThe Open Access publishing model employed by IntechOpen eliminates subscription charges and pay-per-view fees, enabling readers to access research at no cost. In order to sustain operations and keep our publications freely accessible we levy an Open Access Publishing Fee for manuscripts, which helps us cover the costs of editorial work and the production of books. Read more
\n\nDigital Archiving Policy
\n\nIntechOpen is committed to ensuring the long-term preservation and the availability of all scholarly research we publish. We employ a variety of means to enable us to deliver on our commitments to the scientific community. Apart from preservation by the Croatian National Library (for publications prior to April 18, 2018) and the British Library (for publications after April 18, 2018), our entire catalogue is preserved in the CLOCKSS archive.
\n\nOpen Science is transparent and accessible knowledge that is shared and developed through collaborative networks.
\n\nOpen Science is about increased rigour, accountability, and reproducibility for research. It is based on the principles of inclusion, fairness, equity, and sharing, and ultimately seeks to change the way research is done, who is involved and how it is valued. It aims to make research more open to participation, review/refutation, improvement and (re)use for the world to benefit.
\n\nOpen Science refers to doing traditional science with more transparency involved at various stages, for example by openly sharing code and data. It implies a growing set of practices - within different disciplines - aiming at:
\n\nWe aim at improving the quality and availability of scholarly communication by promoting and practicing:
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He is the president of the Travel Medicine Committee of the Pan-American Infectious Diseases Association (API), as well as the president of the Colombian Association of Infectious Diseases (ACIN). He is a member of the Committee on Tropical Medicine, Zoonoses, and Travel Medicine of ACIN. He is a vice-president of the Latin American Society for Travel Medicine (SLAMVI) and a Member of the Council of the International Society for Infectious Diseases (ISID). Since 2014, he has been recognized as a Senior Researcher, at the Ministry of Science of Colombia. He is a professor at the Faculty of Medicine of the Fundacion Universitaria Autonoma de las Americas, in Pereira, Risaralda, Colombia. He is an External Professor, Master in Research on Tropical Medicine and International Health, Universitat de Barcelona, Spain. He is also a professor at the Master in Clinical Epidemiology and Biostatistics, Universidad Científica del Sur, Lima, Peru. In 2021 he has been awarded the “Raul Isturiz Award” Medal of the API. Also, in 2021, he was awarded with the “Jose Felix Patiño” Asclepius Staff Medal of the Colombian Medical College, due to his scientific contributions to COVID-19 during the pandemic. He is currently the Editor in Chief of the journal Travel Medicine and Infectious Diseases. His Scopus H index is 47 (Google Scholar H index, 68).",institutionString:"Institución Universitaria Visión de las Américas, Colombia",institution:null},{id:"332819",title:"Dr.",name:"Chukwudi Michael",middleName:"Michael",surname:"Egbuche",slug:"chukwudi-michael-egbuche",fullName:"Chukwudi Michael Egbuche",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/332819/images/14624_n.jpg",biography:"I an Dr. Chukwudi Michael Egbuche. I am a Senior Lecturer in the Department of Parasitology and Entomology, Nnamdi Azikiwe University, Awka.",institutionString:null,institution:{name:"Nnamdi Azikiwe University",country:{name:"Nigeria"}}},{id:"284232",title:"Mr.",name:"Nikunj",middleName:"U",surname:"Tandel",slug:"nikunj-tandel",fullName:"Nikunj Tandel",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/284232/images/8275_n.jpg",biography:'Mr. Nikunj Tandel has completed his Master\'s degree in Biotechnology from VIT University, India in the year of 2012. He is having 8 years of research experience especially in the field of malaria epidemiology, immunology, and nanoparticle-based drug delivery system against the infectious diseases, autoimmune disorders and cancer. He has worked for the NIH funded-International Center of Excellence in Malaria Research project "Center for the study of complex malaria in India (CSCMi)" in collaboration with New York University. The preliminary objectives of the study are to understand and develop the evidence-based tools and interventions for the control and prevention of malaria in different sites of the INDIA. Alongside, with the help of next-generation genomics study, the team has studied the antimalarial drug resistance in India. Further, he has extended his research in the development of Humanized mice for the study of liver-stage malaria and identification of molecular marker(s) for the Artemisinin resistance. At present, his research focuses on understanding the role of B cells in the activation of CD8+ T cells in malaria. Received the CSIR-SRF (Senior Research Fellow) award-2018, FIMSA (Federation of Immunological Societies of Asia-Oceania) Travel Bursary award to attend the IUIS-IIS-FIMSA Immunology course-2019',institutionString:"Nirma University",institution:{name:"Nirma University",country:{name:"India"}}},{id:"334383",title:"Ph.D.",name:"Simone",middleName:"Ulrich",surname:"Ulrich Picoli",slug:"simone-ulrich-picoli",fullName:"Simone Ulrich Picoli",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/334383/images/15919_n.jpg",biography:"Graduated in Pharmacy from Universidade Luterana do Brasil (1999), Master in Agricultural and Environmental Microbiology from Federal University of Rio Grande do Sul (2002), Specialization in Clinical Microbiology from Universidade de São Paulo, USP (2007) and PhD in Sciences in Gastroenterology and Hepatology (2012). She is currently an Adjunct Professor at Feevale University in Medicine and Biomedicine courses and a permanent professor of the Academic Master\\'s Degree in Virology. She has experience in the field of Microbiology, with an emphasis on Bacteriology, working mainly on the following topics: bacteriophages, bacterial resistance, clinical microbiology and food microbiology.",institutionString:null,institution:{name:"Universidade Feevale",country:{name:"Brazil"}}},{id:"229220",title:"Dr.",name:"Amjad",middleName:"Islam",surname:"Aqib",slug:"amjad-aqib",fullName:"Amjad Aqib",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/229220/images/system/229220.png",biography:"Dr. Amjad Islam Aqib obtained a DVM and MSc (Hons) from University of Agriculture Faisalabad (UAF), Pakistan, and a PhD from the University of Veterinary and Animal Sciences Lahore, Pakistan. Dr. Aqib joined the Department of Clinical Medicine and Surgery at UAF for one year as an assistant professor where he developed a research laboratory designated for pathogenic bacteria. Since 2018, he has been Assistant Professor/Officer in-charge, Department of Medicine, Manager Research Operations and Development-ORIC, and President One Health Club at Cholistan University of Veterinary and Animal Sciences, Bahawalpur, Pakistan. He has nearly 100 publications to his credit. His research interests include epidemiological patterns and molecular analysis of antimicrobial resistance and modulation and vaccine development against animal pathogens of public health concern.",institutionString:"Cholistan University of Veterinary and Animal Sciences",institution:null},{id:"62900",title:"Prof.",name:"Fethi",middleName:null,surname:"Derbel",slug:"fethi-derbel",fullName:"Fethi Derbel",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/62900/images/system/62900.jpeg",biography:"Professor Fethi Derbel was born in 1960 in Tunisia. He received his medical degree from the Sousse Faculty of Medicine at Sousse, University of Sousse, Tunisia. He completed his surgical residency in General Surgery at the University Hospital Farhat Hached of Sousse and was a member of the Unit of Liver Transplantation in the University of Rennes, France. He then worked in the Department of Surgery at the Sahloul University Hospital in Sousse. Professor Derbel is presently working at the Clinique les Oliviers, Sousse, Tunisia. His hospital activities are mostly concerned with laparoscopic, colorectal, pancreatic, hepatobiliary, and gastric surgery. He is also very interested in hernia surgery and performs ventral hernia repairs and inguinal hernia repairs. He has been a member of the GREPA and Tunisian Hernia Society (THS). During his residency, he managed patients suffering from diabetic foot, and he was very interested in this pathology. For this reason, he decided to coordinate a book project dealing with the diabetic foot. Professor Derbel has published many articles in journals and collaborates intensively with IntechOpen Access Publisher as an editor.",institutionString:"Clinique les Oliviers",institution:null},{id:"300144",title:"Dr.",name:"Meriem",middleName:null,surname:"Braiki",slug:"meriem-braiki",fullName:"Meriem Braiki",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/300144/images/system/300144.jpg",biography:"Dr. Meriem Braiki is a specialist in pediatric surgeon from Tunisia. She was born in 1985. She received her medical degree from the University of Medicine at Sousse, Tunisia. She achieved her surgical residency training periods in Pediatric Surgery departments at University Hospitals in Monastir, Tunis and France.\r\nShe is currently working at the Pediatric surgery department, Sidi Bouzid Hospital, Tunisia. Her hospital activities are mostly concerned with laparoscopic, parietal, urological and digestive surgery. She has published several articles in diffrent journals.",institutionString:"Sidi Bouzid Regional Hospital",institution:null},{id:"229481",title:"Dr.",name:"Erika M.",middleName:"Martins",surname:"de Carvalho",slug:"erika-m.-de-carvalho",fullName:"Erika M. de Carvalho",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/229481/images/6397_n.jpg",biography:null,institutionString:null,institution:{name:"Oswaldo Cruz Foundation",country:{name:"Brazil"}}},{id:"186537",title:"Prof.",name:"Tonay",middleName:null,surname:"Inceboz",slug:"tonay-inceboz",fullName:"Tonay Inceboz",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/186537/images/system/186537.jfif",biography:"I was graduated from Ege University of Medical Faculty (Turkey) in 1988 and completed his Med. PhD degree in Medical Parasitology at the same university. I became an Associate Professor in 2008 and Professor in 2014. I am currently working as a Professor at the Department of Medical Parasitology at Dokuz Eylul University, Izmir, Turkey.\n\nI have given many lectures, presentations in different academic meetings. I have more than 60 articles in peer-reviewed journals, 18 book chapters, 1 book editorship.\n\nMy research interests are Echinococcus granulosus, Echinococcus multilocularis (diagnosis, life cycle, in vitro and in vivo cultivation), and Trichomonas vaginalis (diagnosis, PCR, and in vitro cultivation).",institutionString:"Dokuz Eylül University",institution:{name:"Dokuz Eylül University",country:{name:"Turkey"}}},{id:"71812",title:"Prof.",name:"Hanem Fathy",middleName:"Fathy",surname:"Khater",slug:"hanem-fathy-khater",fullName:"Hanem Fathy Khater",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/71812/images/1167_n.jpg",biography:"Prof. Khater is a Professor of Parasitology at Benha University, Egypt. She studied for her doctoral degree, at the Department of Entomology, College of Agriculture, Food and Natural Resources, University of Missouri, Columbia, USA. She has completed her Ph.D. degrees in Parasitology in Egypt, from where she got the award for “the best scientific Ph.D. dissertation”. She worked at the School of Biological Sciences, Bristol, England, the UK in controlling insects of medical and veterinary importance as a grant from Newton Mosharafa, the British Council. Her research is focused on searching of pesticides against mosquitoes, house flies, lice, green bottle fly, camel nasal botfly, soft and hard ticks, mites, and the diamondback moth as well as control of several parasites using safe and natural materials to avoid drug resistances and environmental contamination.",institutionString:null,institution:{name:"Banha University",country:{name:"Egypt"}}},{id:"99780",title:"Prof.",name:"Omolade",middleName:"Olayinka",surname:"Okwa",slug:"omolade-okwa",fullName:"Omolade Okwa",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/99780/images/system/99780.jpg",biography:"Omolade Olayinka Okwa is presently a Professor of Parasitology at Lagos State University, Nigeria. She has a PhD in Parasitology (1997), an MSc in Cellular Parasitology (1992), and a BSc (Hons) Zoology (1990) all from the University of Ibadan, Nigeria. She teaches parasitology at the undergraduate and postgraduate levels. She was a recipient of a Commonwealth fellowship supported by British Council tenable at the Centre for Entomology and Parasitology (CAEP), Keele University, United Kingdom between 2004 and 2005. She was awarded an Honorary Visiting Research Fellow at the same university from 2005 to 2007. \nShe has been an external examiner to the Department of Veterinary Microbiology and Parasitology, University of Ibadan, MSc programme between 2010 and 2012. She is a member of the Nigerian Society of Experimental Biology (NISEB), Parasitology and Public Health Society of Nigeria (PPSN), Science Association of Nigeria (SAN), Zoological Society of Nigeria (ZSN), and is Vice Chairperson of the Organisation of Women in Science (OWSG), LASU chapter. She served as Head of Department of Zoology and Environmental Biology, Lagos State University from 2007 to 2010 and 2014 to 2016. She is a reviewer for several local and international journals such as Unilag Journal of Science, Libyan Journal of Medicine, Journal of Medicine and Medical Sciences, and Annual Research and Review in Science. \nShe has authored 45 scientific research publications in local and international journals, 8 scientific reviews, 4 books, and 3 book chapters, which includes the books “Malaria Parasites” and “Malaria” which are IntechOpen access publications.",institutionString:"Lagos State University",institution:{name:"Lagos State University",country:{name:"Nigeria"}}},{id:"273100",title:"Dr.",name:"Vijay",middleName:null,surname:"Gayam",slug:"vijay-gayam",fullName:"Vijay Gayam",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/273100/images/system/273100.jpeg",biography:"Dr. Vijay Bhaskar Reddy Gayam is currently practicing as an internist at Interfaith Medical Center in Brooklyn, New York, USA. He is also a Clinical Assistant Professor at the SUNY Downstate University Hospital and Adjunct Professor of Medicine at the American University of Antigua. He is a holder of an M.B.B.S. degree bestowed to him by Osmania Medical College and received his M.D. at Interfaith Medical Center. His career goals thus far have heavily focused on direct patient care, medical education, and clinical research. He currently serves in two leadership capacities; Assistant Program Director of Medicine at Interfaith Medical Center and as a Councilor for the American\r\nFederation for Medical Research. As a true academician and researcher, he has more than 50 papers indexed in international peer-reviewed journals. He has also presented numerous papers in multiple national and international scientific conferences. His areas of research interest include general internal medicine, gastroenterology and hepatology. He serves as an editor, editorial board member and reviewer for multiple international journals. His research on Hepatitis C has been very successful and has led to multiple research awards, including the 'Equity in Prevention and Treatment Award” from the New York Department of Health Viral Hepatitis Symposium (2018) and the 'Presidential Poster Award” awarded to him by the American College of Gastroenterology (2018). He was also awarded 'Outstanding Clinician in General Medicine” by Venus International Foundation for his extensive research expertise and services, perform over and above the standard expected in the advancement of healthcare, patient safety and quality of care.",institutionString:"Interfaith Medical Center",institution:{name:"Interfaith Medical Center",country:{name:"United States of America"}}},{id:"93517",title:"Dr.",name:"Clement",middleName:"Adebajo",surname:"Meseko",slug:"clement-meseko",fullName:"Clement Meseko",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/93517/images/system/93517.jpg",biography:"Dr. Clement Meseko obtained DVM and PhD degree in Veterinary Medicine and Virology respectively. He has worked for over 20 years in both private and public sectors including the academia, contributing to knowledge and control of infectious disease. Through the application of epidemiological skill, classical and molecular virological skills, he investigates viruses of economic and public health importance for the mitigation of the negative impact on people, animal and the environment in the context of Onehealth. \r\nDr. Meseko’s field experience on animal and zoonotic diseases and pathogen dynamics at the human-animal interface over the years shaped his carrier in research and scientific inquiries. He has been part of the investigation of Highly Pathogenic Avian Influenza incursions in sub Saharan Africa and monitors swine Influenza (Pandemic influenza Virus) agro-ecology and potential for interspecies transmission. He has authored and reviewed a number of journal articles and book chapters.",institutionString:"National Veterinary Research Institute",institution:{name:"National Veterinary Research Institute",country:{name:"Nigeria"}}},{id:"158026",title:"Prof.",name:"Shailendra K.",middleName:null,surname:"Saxena",slug:"shailendra-k.-saxena",fullName:"Shailendra K. Saxena",position:null,profilePictureURL:"https://s3.us-east-1.amazonaws.com/intech-files/0030O00002bRET3QAO/Profile_Picture_2022-05-10T10:10:26.jpeg",biography:"Professor Dr. Shailendra K. Saxena is a vice dean and professor at King George's Medical University, Lucknow, India. His research interests involve understanding the molecular mechanisms of host defense during human viral infections and developing new predictive, preventive, and therapeutic strategies for them using Japanese encephalitis virus (JEV), HIV, and emerging viruses as a model via stem cell and cell culture technologies. His research work has been published in various high-impact factor journals (Science, PNAS, Nature Medicine) with a high number of citations. He has received many awards and honors in India and abroad including various Young Scientist Awards, BBSRC India Partnering Award, and Dr. JC Bose National Award of Department of Biotechnology, Min. of Science and Technology, Govt. of India. Dr. Saxena is a fellow of various international societies/academies including the Royal College of Pathologists, United Kingdom; Royal Society of Medicine, London; Royal Society of Biology, United Kingdom; Royal Society of Chemistry, London; and Academy of Translational Medicine Professionals, Austria. He was named a Global Leader in Science by The Scientist. He is also an international opinion leader/expert in vaccination for Japanese encephalitis by IPIC (UK).",institutionString:"King George's Medical University",institution:{name:"King George's Medical University",country:{name:"India"}}},{id:"94928",title:"Dr.",name:"Takuo",middleName:null,surname:"Mizukami",slug:"takuo-mizukami",fullName:"Takuo Mizukami",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/94928/images/6402_n.jpg",biography:null,institutionString:null,institution:{name:"National Institute of Infectious Diseases",country:{name:"Japan"}}},{id:"233433",title:"Dr.",name:"Yulia",middleName:null,surname:"Desheva",slug:"yulia-desheva",fullName:"Yulia Desheva",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/233433/images/system/233433.png",biography:"Dr. Yulia Desheva is a leading researcher at the Institute of Experimental Medicine, St. Petersburg, Russia. She is a professor in the Stomatology Faculty, St. Petersburg State University. She has expertise in the development and evaluation of a wide range of live mucosal vaccines against influenza and bacterial complications. Her research interests include immunity against influenza and COVID-19 and the development of immunization schemes for high-risk individuals.",institutionString:'Federal State Budgetary Scientific Institution "Institute of Experimental Medicine"',institution:null},{id:"238958",title:"Mr.",name:"Atamjit",middleName:null,surname:"Singh",slug:"atamjit-singh",fullName:"Atamjit Singh",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/238958/images/6575_n.jpg",biography:null,institutionString:null,institution:null},{id:"333753",title:"Dr.",name:"Rais",middleName:null,surname:"Ahmed",slug:"rais-ahmed",fullName:"Rais Ahmed",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/333753/images/20168_n.jpg",biography:null,institutionString:null,institution:null},{id:"252058",title:"M.Sc.",name:"Juan",middleName:null,surname:"Sulca",slug:"juan-sulca",fullName:"Juan Sulca",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/252058/images/12834_n.jpg",biography:null,institutionString:null,institution:null},{id:"191392",title:"Dr.",name:"Marimuthu",middleName:null,surname:"Govindarajan",slug:"marimuthu-govindarajan",fullName:"Marimuthu Govindarajan",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/191392/images/5828_n.jpg",biography:"Dr. M. Govindarajan completed his BSc degree in Zoology at Government Arts College (Autonomous), Kumbakonam, and MSc, MPhil, and PhD degrees at Annamalai University, Annamalai Nagar, Tamil Nadu, India. He is serving as an assistant professor at the Department of Zoology, Annamalai University. His research interests include isolation, identification, and characterization of biologically active molecules from plants and microbes. He has identified more than 20 pure compounds with high mosquitocidal activity and also conducted high-quality research on photochemistry and nanosynthesis. He has published more than 150 studies in journals with impact factor and 2 books in Lambert Academic Publishing, Germany. He serves as an editorial board member in various national and international scientific journals.",institutionString:null,institution:null},{id:"274660",title:"Dr.",name:"Damodar",middleName:null,surname:"Paudel",slug:"damodar-paudel",fullName:"Damodar Paudel",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/274660/images/8176_n.jpg",biography:"I am DrDamodar Paudel,currently working as consultant Physician in Nepal police Hospital.",institutionString:null,institution:null},{id:"241562",title:"Dr.",name:"Melvin",middleName:null,surname:"Sanicas",slug:"melvin-sanicas",fullName:"Melvin Sanicas",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/241562/images/6699_n.jpg",biography:null,institutionString:null,institution:null},{id:"337446",title:"Dr.",name:"Maria",middleName:null,surname:"Zavala-Colon",slug:"maria-zavala-colon",fullName:"Maria Zavala-Colon",position:null,profilePictureURL:"//cdnintech.com/web/frontend/www/assets/author.svg",biography:null,institutionString:null,institution:{name:"University of Puerto Rico, Medical Sciences Campus",country:{name:"United States of America"}}},{id:"338856",title:"Mrs.",name:"Nur Alvira",middleName:null,surname:"Pascawati",slug:"nur-alvira-pascawati",fullName:"Nur Alvira Pascawati",position:null,profilePictureURL:"//cdnintech.com/web/frontend/www/assets/author.svg",biography:null,institutionString:null,institution:{name:"Universitas Respati Yogyakarta",country:{name:"Indonesia"}}},{id:"441116",title:"Dr.",name:"Jovanka M.",middleName:null,surname:"Voyich",slug:"jovanka-m.-voyich",fullName:"Jovanka M. Voyich",position:null,profilePictureURL:"//cdnintech.com/web/frontend/www/assets/author.svg",biography:null,institutionString:null,institution:{name:"Montana State University",country:{name:"United States of America"}}},{id:"330412",title:"Dr.",name:"Muhammad",middleName:null,surname:"Farhab",slug:"muhammad-farhab",fullName:"Muhammad Farhab",position:null,profilePictureURL:"//cdnintech.com/web/frontend/www/assets/author.svg",biography:null,institutionString:null,institution:{name:"University of Agriculture Faisalabad",country:{name:"Pakistan"}}},{id:"349495",title:"Dr.",name:"Muhammad",middleName:null,surname:"Ijaz",slug:"muhammad-ijaz",fullName:"Muhammad Ijaz",position:null,profilePictureURL:"//cdnintech.com/web/frontend/www/assets/author.svg",biography:null,institutionString:null,institution:{name:"University of Veterinary and Animal Sciences",country:{name:"Pakistan"}}}]}},subseries:{item:{id:"12",type:"subseries",title:"Human Physiology",keywords:"Anatomy, Cells, Organs, Systems, Homeostasis, Functions",scope:"Human physiology is the scientific exploration of the various functions (physical, biochemical, and mechanical properties) of humans, their organs, and their constituent cells. The endocrine and nervous systems play important roles in maintaining homeostasis in the human body. Integration, which is the biological basis of physiology, is achieved through communication between the many overlapping functions of the human body's systems, which takes place through electrical and chemical means. Much of the basis of our knowledge of human physiology has been provided by animal experiments. Because of the close relationship between structure and function, studies in human physiology and anatomy seek to understand the mechanisms that help the human body function. The series on human physiology deals with the various mechanisms of interaction between the various organs, nerves, and cells in the human body.",coverUrl:"https://cdn.intechopen.com/series_topics/covers/12.jpg",hasOnlineFirst:!0,hasPublishedBooks:!0,annualVolume:11408,editor:{id:"195829",title:"Prof.",name:"Kunihiro",middleName:null,surname:"Sakuma",slug:"kunihiro-sakuma",fullName:"Kunihiro Sakuma",profilePictureURL:"https://mts.intechopen.com/storage/users/195829/images/system/195829.jpg",biography:"Professor Kunihiro Sakuma, Ph.D., currently works in the Institute for Liberal Arts at the Tokyo Institute of Technology. He is a physiologist working in the field of skeletal muscle. He was awarded his sports science diploma in 1995 by the University of Tsukuba and began his scientific work at the Department of Physiology, Aichi Human Service Center, focusing on the molecular mechanism of congenital muscular dystrophy and normal muscle regeneration. His interest later turned to the molecular mechanism and attenuating strategy of sarcopenia (age-related muscle atrophy). His opinion is to attenuate sarcopenia by improving autophagic defects using nutrient- and pharmaceutical-based treatments.",institutionString:null,institution:{name:"Tokyo Institute of Technology",institutionURL:null,country:{name:"Japan"}}},editorTwo:{id:"331519",title:"Dr.",name:"Kotomi",middleName:null,surname:"Sakai",slug:"kotomi-sakai",fullName:"Kotomi Sakai",profilePictureURL:"https://s3.us-east-1.amazonaws.com/intech-files/0033Y000031QtFXQA0/Profile_Picture_1637053227318",biography:"Senior researcher Kotomi Sakai, Ph.D., MPH, works at the Research Organization of Science and Technology in Ritsumeikan University. She is a researcher in the geriatric rehabilitation and public health field. She received Ph.D. from Nihon University and MPH from St.Luke’s International University. Her main research interest is sarcopenia in older adults, especially its association with nutritional status. Additionally, to understand how to maintain and improve physical function in older adults, to conduct studies about the mechanism of sarcopenia and determine when possible interventions are needed.",institutionString:null,institution:{name:"Ritsumeikan University",institutionURL:null,country:{name:"Japan"}}},editorThree:null,series:{id:"10",title:"Physiology",doi:"10.5772/intechopen.72796",issn:"2631-8261"},editorialBoard:[{id:"213786",title:"Dr.",name:"Henrique P.",middleName:null,surname:"Neiva",slug:"henrique-p.-neiva",fullName:"Henrique P. 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