MicroRNAs that are causally implicated in PH.
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\\n\\nLaunching 2021
\\n\\nArtificial Intelligence, ISSN 2633-1403
\\n\\nVeterinary Medicine and Science, ISSN 2632-0517
\\n\\nBiochemistry, ISSN 2632-0983
\\n\\nBiomedical Engineering, ISSN 2631-5343
\\n\\nInfectious Diseases, ISSN 2631-6188
\\n\\nPhysiology (Coming Soon)
\\n\\nDentistry (Coming Soon)
\\n\\nWe invite you to explore our IntechOpen Book Series, find the right publishing program for you and reach your desired audience in record time.
\\n\\nNote: Edited in October 2021
\\n"}]',published:!0,mainMedia:{caption:"",originalUrl:"/media/original/132"}},components:[{type:"htmlEditorComponent",content:'With the desire to make book publishing more relevant for the digital age and offer innovative Open Access publishing options, we are thrilled to announce the launch of our new publishing format: IntechOpen Book Series.
\n\nDesigned to cover fast-moving research fields in rapidly expanding areas, our Book Series feature a Topic structure allowing us to present the most relevant sub-disciplines. Book Series are headed by Series Editors, and a team of Topic Editors supported by international Editorial Board members. Topics are always open for submissions, with an Annual Volume published each calendar year.
\n\nAfter a robust peer-review process, accepted works are published quickly, thanks to Online First, ensuring research is made available to the scientific community without delay.
\n\nOur innovative Book Series format brings you:
\n\nIntechOpen Book Series will also publish a program of research-driven Thematic Edited Volumes that focus on specific areas and allow for a more in-depth overview of a particular subject.
\n\nIntechOpen Book Series will be launching regularly to offer our authors and editors exciting opportunities to publish their research Open Access. We will begin by relaunching some of our existing Book Series in this innovative book format, and will expand in 2022 into rapidly growing research fields that are driving and advancing society.
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\n\nDentistry (Coming Soon)
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\n\nNote: Edited in October 2021
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At physiologically normal oxygen levels, the pulmonary vasculature of healthy individuals is highly distensible, allowing the cardiac output to adjust to levels of activity. In varying degrees of oxygen availability, as in different altitudes, adaptive cardiovascular responses are employed. In acute hypoxia (short, transient reduction in oxygen tension), the pulmonary vascular bed constricts rapidly [1]. When oxygen levels are restored, it dilates again in a swift and reversible manner. With a sustained hypoxic exposure (hours to days), the response is different. There is a loss of pulmonary distensibility, increased arterial pressure, tachycardia and increased workload for the right cardiac ventricle. In return to normoxic conditions, there is, at least in the short term, a limited reversibility of these effects. The Operation Everest II study [2] demonstrated this phenomenon by monitoring the pulmonary vascular pressure of healthy individuals who were exposed to progressive partially pressured oxygen over a period of a few weeks. However, for high-altitude populations, such as the Tibetans, this is not the case. Due to natural selection and adaptation over many thousands of years living under low oxygen conditions, Tibetans have altered oxygen-sensing mechanisms and pulmonary vascular resistance to sustained hypoxia (discussed later in this chapter) [3].
\nHealthy, native sea-level dwellers, who move to high altitude, develop high pulmonary arterial pressure, but with time, in the majority of cases, it stabilises and becomes well tolerated [4]. By contrast, people with pre-existing lung pathologies, such as chronic obstructive pulmonary disease (COPD), cystic fibrosis, idiopathic pulmonary fibrosis, bronchiectasis or restrictive chest wall abnormalities, are at risk of developing pulmonary hypertension (PH). Chronic PH lowers quality of life and decreases life expectancy for the affected individuals [5–8].
\nThe pathophysiology of hypoxia-associated PH is characterised by extensive vascular remodelling that leads to arterial narrowing rather than reversible vessel vasoconstriction (Figure 1). Processes that take place include endothelial cell dysfunction, muscularisation of normally non-muscular arteries, phenotypic switching and proliferation of vascular smooth muscle cells (VSMCs), increased extracellular matrix deposition and erythrocytosis [7, 9, 10]. In this chapter, recent developments in mechanistic aspects underlying hypoxia-induced pathophysiological changes in PH will be briefly summarised.
Schematic representation of pulmonary arterial responses to normoxia, acute hypoxia and chronic hypoxia. With acute and chronic hypoxia, the pulmonary artery undergoes vasoconstriction. In the case of acute hypoxia, the artery can reversibly dilate. But in chronic hypoxia, the artery undergoes nonreversible vascular remodelling characterised by intimal thickening due to VSMC dedifferentiation (loss of contractility, hypertrophy and hyperplasia). Additionally, there is distal muscularisation of non-muscular vessels, a settled-in endothelial cell dysfunction and erythrocytosis. Activation of HIF-1α and HIF-2α as well as over-activation of mTORC1 contributes to VSMC dedifferentiation and the establishment of hypoxic PH. Abbreviations: HIF-1α, hypoxia-inducible factor 1α; HIF-2α, hypoxia-inducible factor 2α; mTORC1, mechanistic target of rapamycin complex 1; PH, pulmonary hypertension.
Endothelial cells in pulmonary vessels first sense hypoxic stress. Having a role in maintaining homeostasis, endothelial cells contribute to reducing the vascular tone in order for vasoconstriction to take place and regulate vessel adaptation to increased blood flow [11]. In healthy individuals, the endothelium is responsible for the balanced expression of vasoactive mediators that have either vasodilator ability, such as nitric oxide (NO) and prostacyclin (PGI2), or vasoconstrictive properties, such as endothelin-1 (ET-1) [11–14]. ET-1 is released abluminally and triggers vasoconstriction through binding to its VSMC receptors ETA and ETB [15]. However, when ET-1 binds to its endothelial ETB receptor, it can induce vasodilation through NO and PGI2 recruitment [15], while this route also serves for ET-1 clearance from the lung [16].
\nIn pathological PH, as in COPD, endothelial cell dysfunction is one of the major contributing factors for the progression of the condition. It has been found that endothelial NO synthase (eNOS), the enzyme responsible for NO production, as well as prostacyclin synthase, the enzyme responsible for PGI2 production, is markedly diminished in patients with COPD [12, 17]. Furthermore, ET-1 has been reported to have an increased expression in the lungs of patients with PH and is a therapeutic target [14]. ET-1, as well as being a potent vasoconstrictor, is also a VSMC mitogen, acting through smooth muscle ETA and ETB receptors [15]. So in effect, during hypoxic endothelial dysregulation, the pathogenic excess of ET-1 maintains vessel constriction and VSMC proliferation.
In hypoxia, the highly plastic VSMCs switch from a contractile to a synthetic phenotype, which is characterised by increased proliferation and extracellular matrix deposition [18]. Differentiated smooth muscle cells express a repertoire of contractile proteins, signalling molecules and receptors for their primary function of vessel contraction. These contractile VSMCs have little capacity for proliferation, protein synthesis or migration [18]. However, pulmonary VSMCs, under chronic hypoxic stimulation, switch to a synthetic state exhibiting hypertrophy, hyperplasia, loss of contractility and migration, contributing to the enlargement of the arterial intimal layer (Figure 1) and in the muscularisation of non-muscular pulmonary vessels [9]. Additionally, there is a deposition of collagen and elastic fibres. In extreme cases, the excessive VSMC proliferation can progress from vascular lesions to calcification. These phenomena seem to correlate with the degree of PH extent and COPD severity [19–21].
\nThe endothelial dysfunction that takes place in PH may also contribute to the dedifferentiation and proliferation of VSMCs [22]. Specifically, dysregulated endothelial cells can cause alterations in AKT signalling in VSMCs, which in turn triggers their phenotypic switch [23]. This pathway is also affected by aberrant regulation of the mechanistic target of rapamycin (mTOR) pathway (discussed later in this chapter).
The major cellular oxygen-sensing mechanism implicated in hypoxia-induced pulmonary hypertension is the hypoxia-inducible factor (HIF) pathway. HIFs are transcription factors that induce the activation of some several hundred genes in response to hypoxia [24]. Initially identified as regulators of erythropoietin (EPO), the hormone responsible for increased red blood cells in response to low oxygen levels, HIFs have since been found to regulate expression of genes that are important for angiogenesis, cellular metabolism, cardiovascular development and cardiovascular control [24–26].
\nIn low oxygen conditions, HIFs bind DNA as heterodimeric complexes of alpha (HIF-α) and beta (HIF-β) subunits, with HIF-α being the subunit regulated by oxygen tension [27]. Higher animals have a series of isoforms for each of the HIF subunits as a result of gene evolutionary duplications [24]. In humans, there are three paralogs of HIF-α—HIF-1α, HIF-2α and HIF-3α—with the first two members being the best characterised [24, 25]. The expression of HIF-1α and HIF-2α is differentially regulated, while their balance is believed to be important for tissue-specific differences in oxygen sensing [25]. They both bind to the same DNA consensus (RCGTG) in hypoxia-response elements of the genome, but they only induce partially overlapping sets of genes [27, 28].
\nIn normoxic conditions, the HIF-α subunit is hydroxylated by Fe(II) prolyl hydroxylase domain (PHD) enzymes (PHD1, PHD2 and PHD3 or otherwise known as Egln2, Egln1 and Egln3) that use 2-oxoglutarate and Fe2+ as substrates [29]. After hydroxylation by PHDs, HIF-α is recognised and bound by the von Hippel-Lindau (VHL) protein, a ubiquitin E3 ligase, which marks HIF-α for proteasomal degradation. In hypoxia, PHD enzymes are inactive allowing HIF-α subunits to translocate to the nucleus and activate HIF target genes. HIFs are further regulated by factor-inhibiting HIF (FIH)-mediated asparaginyl hydroxylation, which impairs their recruitment to transcriptional complexes [30].
\nMouse models of HIF-1α and HIF-2α have illustrated that the HIF pathway is critically important for the pulmonary hypoxic response and the development of PH. Heterozygous deficiency of either HIF-1α or HIF-2α allele in mice does not affect their life span, and these animals are largely normal in unstressed, normal oxygen conditions. In response to chronic hypoxia (10% for 3 weeks), HIF-1α+/− mice exhibit an attenuated PH with a low rise in right ventricular pressure and right ventricular hypertrophy [31]. Interestingly, heterozygous HIF-2α+/− mice, exposed to 10% oxygen for 10 weeks, showed a complete lack of any PH manifestation [32]. Of note, animals with hetero- or homozygous mutations in stabilising HIF-2α spontaneously developed progressive PH [33]. These studies all indicate a pathological role of both HIF-α subunits in PH development.
\nCell-type-specific inactivation of HIF-α with the use of a variety of promoters has also been studied but with some variable results, which may be due to the method of HIF-α manipulations and/or the use of different mouse strains [34–36]. Nevertheless, there seems to be a clear link between HIFs and PH, since studies from human genetics, including several populations that have adapted to different altitudes, have demonstrated the importance of HIF-2α in pulmonary response to hypoxia and PH pathophysiology [37].
\nThe Tibetans, who have lived for at least 25,000 years in 4000 m elevation and continuously inspired partially pressured oxygen (~80 mmHg), have been identified to have a number of single-nucleotide polymorphisms in close-to-one-another loci near the gene
Further evidence for a role for HIF-2α in PH comes from another human genetic study, which showed that an activating HIF-2α mutation (G→A substitution in position 2097) caused erythrocytosis with elevated total red cell volume and PH in an affected family [42].
The VHL protein is a tumour suppressor and an essential component for the clearance of HIF-α through the ubiquitin-proteasomal degradation pathway [24, 43]. A number of VHL mutations have been described that result in aberrant induction of HIF target genes, due to the loss of function of VHL and in turn to the loss of HIF-α regulation. VHL mutations are associated with VHL syndrome, which is a hereditary condition, characterised by highly vascularised tumours within specific tissues, including the renal, retinal and central nervous system [44]. However, a small number of VHL mutations (R200W, D126N, S183L, D126N) are associated with development of Chuvash polycythemia (CP) [45–47]. CP is a rare autosomal recessive condition that is endemic to the population in Chuvashia, Russia and in the island of Ischia, Italy [46, 48]. Chuvash patients manifest increased haemoglobin and haematocrit with elevated levels of EPO, as well as increased expression of vascular endothelial growth factor (VEGF) and ET-1, which are HIF-α target genes [45–49]. In addition, these patients are highly susceptible to both arterial and venous thrombosis and can develop mild to severe PH [45–49].
\nThe importance of HIF-2α isoform in the regulation of pulmonary vascular control has also been demonstrated by the use of a mouse model of CP [50]. This model carries a hypomorphic VHL allele (with an R200W substitution) and recapitulates all symptoms of the human CP phenotype. Interestingly, when these mice are crossed with HIF-2α+/− or HIF-1α+/− strains for heterozygous deficiency in either of the two HIF-α, they manifest an ameliorated PH phenotype for suppressed HIF-2α, but not for HIF-1α.
\nComparison of CP and HIF-2α gain-of-function mutation human phenotypes has additionally shown that the latter condition somehow manifests more moderate symptoms than the first. The explanation for this may be that, in CP, both HIF-α subunits are upregulated, and therefore, there may be an additive effect [51]. Furthermore, VHL has a number of HIF-α-independent functions that may also play a role in the CP phenotype.
Zinc, an essential dietary element, plays an important cytoprotective role for the lung by sheltering the pulmonary epithelium from extrinsic activation of apoptotic pathways following acute lung injury [52]. Zinc transporters are responsible for zinc cellular uptake and homeostasis [53]. A recent linkage analysis study that compared a PH-resistant rat strain, Fisher 344 (F344), with the Wistar Kyoto (WKY) strain identified the gene
Zinc-binding motifs have been considered as potential PH drug-therapeutic targets with phosphodiesterase type 5 (PDE5) and histone deacetylases as examples [54, 55]. Zinc is a structural component of a number of intracellular enzymes, transcription factors, other proteins and cofactors and is a putative drug target for PH.
MicroRNAs (miRNAs) are small non-coding RNA molecules (about 21 nucleotides long) that regulate gene expression post-transcriptionally. Hypoxic stimulation of a variety of human cell types has shown induction of more than 90 miRNAs [56], with altered expression of some of these miRNAs involved in VSMC remodelling and endothelial cell dysfunction in PH [57].
\nMiRNAs that have been causally implicated in PH include miR-204, miR-138, miR-21 and miR-130/miR-301, among others (Table 1). MiR-204 has been shown to be downregulated in VSMCs of patients suffering from PH, as well as in mouse models of the disease [58, 59]. The degree of miR-204 suppression has been found to be inversely proportional to the degree of pulmonary artery resistance and pressure, while compensating for the loss of miR-204 through nebulisation in PH patients has been shown to reverse the VSMC proliferative and anti-apoptotic phenotype [59]. MiR-204 is involved in the activation of the nuclear factor of activated T cell (NFAT) pathway, the Rho pathway, VSMC proliferation and resistance to apoptosis, as well as downregulation of transcripts such as bone morphogenetic protein receptor type II (BMPR2) and interleukin-6 (IL-6) [60–62]. Also, miR-204 regulates the expression of the Runt-related transcription factor 2 (RUNX2), which has been shown to stabilise HIF-1α in chondrocytes by competing with VHL [20, 63]. In the context of hypoxia, RUNX2 is upregulated, since miR-204 is downregulated, and therefore sustains HIF-1α activation, which in turn contributes to aberrant VSMC proliferation, resistance to apoptosis and their transdifferentiation to osteoblast-like cells [20].
MicroRNA | Change in PH | Target transcripts | Cellular function, process or pathway affected | Ref. |
---|---|---|---|---|
miR-204 | ↓ | BMPR2, IL-6, RUNX2 among others | Activation of NFAT pathway, VSMC proliferation, resistance to apoptosis, Rho pathway, HIF-1α pathway | [20, 58–63] |
miR-138 | ↑ | HIF-1α, S100A1 | HIF-1α pathway, endothelial regulation of vasomotor tone | [64] |
miR-21 | ↑ | PDCD4, SPRY2, PPARα | VSMC proliferation, resistance to apoptosis | [61, 65–67] |
miR-130/301 | ↑ | PPARγ which leads to subordinate gene targets and other miRNAs | Master regulator of cell proliferation and apoptosis in PH ↓ miR-204 | [68] |
MicroRNAs that are causally implicated in PH.
MiR-138 is upregulated by hypoxia and suppresses HIF-1α [64]. However, its upregulation also contributes to endothelial cell dysfunction in PH by downregulating the small EF-hand Ca2+-binding protein S100A1 that relays Ca2+ oscillations, controlling vascular tone responses [64].
\nMiR-21 expression has been found to be upregulated in both pulmonary VSMC and endothelial cells during hypoxic conditions [61, 65]. This upregulation, in turn, leads to downregulation of programmed cell death protein 4 (PDCD4), sprouty homolog 2 (SPRY2) and peroxisome proliferator-activated receptor-α (PPARα), which when dysregulated play a role in the increased proliferation and resistance to apoptosis [65–67]. Treatment of mice with anti-miR-21 during hypoxia showed an improvement in distal pulmonary artery muscularisation [69]. However, miR-21 has also been shown to have a protective effect during PH [61]. Using VHL-null mice, IL-6 transgenic mice, pulmonary vessels from patients with PH as well as deficient (miR-21−/−) or miR-21 overexpression (miR-21+/+) mouse models, it has been demonstrated that miR-21 loss of function causes onset of PH [61]. Specifically, miR-21 deletion showed exaggerated pulmonary vascular remodelling, whereas in mice overexpressing miR-21, these disease-associated phenotypes were abolished [61].
\nThe family of miR-130/301 is also upregulated in pulmonary VSMCs and the endothelium in hypoxia, as well as in the lungs of mice with PH due to chronic hypoxic exposure [68]. This upregulation is mediated by HIF-2α and Oct-4. MiR-130/301 is a master regulator miRNA subordinating other miRNA pathways, and, for instance, it suppresses miR-204 [68].
\nmiR-223, miR-17, miR-130, miR-145, miR-424 and miR503 are also involved in the pathophysiology of PH (reviewed in Ref. [70]). So far, PH animal models have helped greatly in these studies, but the exact role and balance for each of these miRNAs in human PH have not been fully elucidated.
Mechanistic target of rapamycin (mTOR) is a cellular hub that controls growth factor signalling and nutrient sensing to regulate cell growth, proliferation, metabolism and survival [71]. mTOR is a protein kinase that is the catalytic component of two functionally distinct complexes, mTOR complex 1 (mTORC1) and mTOR complex 2 (mTORC2) [72, 73]. mTORC1 is composed of mTOR, Raptor, LST8/GβL, PRAS40 and DEP domain containing mTOR-interacting protein (DEPTOR), and its activity is stimulated by growth factor signals to regulate protein synthesis through 4E-BP1/BP2 and the S6 kinases, S6K1 and S6K2 [74, 75]. By contrast, mTORC2, which comprises mTOR, Rictor, LST8/GβL, DEPTOR, SIN1 and PRR5, regulates cytoskeletal organisation [76, 77] and has a role in phosphorylation of protein kinase C (PKC), protein kinase B (PKB) and serum- and glucocorticoid-induced protein kinase (SGK) to promote cell survival and cell cycle progression [78–80].
\nAberrant mTOR activity has a well-characterised role in promoting proliferative diseases including cancer and smooth muscle cell pathologies [71]. mTORC1 signalling is activated following vascular injury promoting Vinhibitor, rapamycin, promotes smooth muscle cell (SMC) remodelling. Accordingly, mTOR inhibitors are widely used in drug-eluting stents to prevent restenosis. In addition, mTOR also regulates the differentiation state of VSMCs since the mTOR inhibitor, rapamycin, promotes SMC differentiation and expression of contractile proteins [81]. mTORC1 activity is low in differentiated contractile VSMCs but becomes activated by growth factors and is thought to contribute to the change towards a synthetic phenotype that is characterised by increased SMC proliferation and migration. As such, rapamycin analogues may have therapeutic potential for treating PH.
\nThe relationship between hypoxic conditions and mTOR is complex and depends, in part, on cellular context. Many cell types respond to prolonged periods of hypoxia by inactivating energy-intensive processes such as protein synthesis and proliferation, and accordingly mTOR is downregulated [82]. By contrast, the vasculature responds to long-term hypoxia by promoting new blood vessel growth—angiogenesis, which in turn, restores O2 to deprived tissues. Hypoxic stress is a key driving force in the vascular remodelling observed in pulmonary hypertension, and HIFs activate pulmonary artery endothelial and smooth muscle cell proliferation, which is mediated by both mTORC1 and mTORC2 [83–85]. Currently, the mechanisms by which hypoxia/HIFs signal to activate mTOR in ECs and VSMCs are poorly understood [86–90].
Severe PH associated with hypoxic lung disease is a life-threatening condition with poor survival rates. Despite significant advances in targeted therapeutics for PH, randomised clinical trial data for this particular group of patients are scarce, and it is not clear whether endothelin receptor antagonists will benefit patients with hypoxia-associated PH. Importantly, recent genetic studies identifying mutations in the oxygen-sensing machinery have provided new mechanistic insights into the aetiology of PH. Further studies are required to determine whether specific targeting of HIF-2α will provide additional therapeutic benefit for this complex disease.
Cardiovascular disease (CVD) is a notable cause of death globally [1]. One main contributing factor to cardiovascular disease development is arteriosclerosis and it is the key cause of morbidity and mortality [2]. Blood pressure (BP) measurement is the most commonly utilized method of assessing arteriosclerosis activity [3]. Systolic blood pressure (SBP) difference between arms (inter-arm difference/IAD) is one risk marker that is easy to measure since it does not require extra equipment and seems acceptable to patients. Circumstances in which differences in BP were found in clinical settings were infrequent [4, 5].
When undetected, varying measurements of BP between arms can lead to inaccuracies in the interpretation and management of blood pressure consequently putting individuals in an avoidable risk through sub-optimal blood pressure control [6]. Furthermore it has been reported that systolic BP difference of 10 mmHg or greater between both arms was related with cardiovascular risk/complications [7, 8]. Moreover an inter arm difference is mostly encountered with differences in systolic of 10 mmHg or greater prevalent in 11% of hypertensive patients, 7% diabetic patients as well as 4% of the general population [5].
Past studies have discovered a rise in the incidence of big inter arm difference in hypertensive [9] and diabetic patients [10]. The association between inter arm difference and atherosclerosis-related diseases, such as coronary artery disease [11], and other peripheral artery disease were also reported [12, 13]. Nevertheless, the majority of these studies took place in populations that were Westernized/urbanized with little sample sizes and comprising of certain disease groups. The prevalence of selected cardiovascular risk factors has been reported in young adults at Ellisras including BP/hypertension [14], but the inter arm BP difference was not investigated. Furthermore as far as we are aware, such a study was not reported among black South Africans in Limpopo Province. Therefore the study aimed to determine the blood pressure difference between arms and its association to cardiovascular risk in young adults at Ellisras.
The study constituted of 624 young adults (306 males; 318 females) aged 18 to 29 years old from the Ellisras Longitudinal Study (ELS) in Lephalale, Limpopo province in South Africa. The details of ELS are explained elsewhere [15]. The study was approved by the Ethics Committee at the University of Limpopo prior to the study commencing. Consent forms were also signed by the participants.
Participants with factors that could influence the reliability of the study including pregnancy and chronic diseases or hospitalization were excluded.
Prior to being measured the participants rested for approximately 5 minutes. Afterwards, three blood pressure (BP) readings of systolic blood pressure (SBP) And diastolic blood pressure (DBP) were measured five minutes apart in both the left and right arms using an electronic Micronta monitoring kit, [16, 17]. Average BP was calculated for both arms. Then the difference between the average SBP and DBP in the left and right arms was calculated.
All participants underwent height and weight measurements according to the standard procedures [18]. The weight and height were then used to determine the body mass index (BMI) [18].
There was fasting of between 8–10 hours before the collection of blood samples. All blood sample collections were carried out in schools by qualified nurses from the Witpoort Hospital at Ellisras in the morning. The samples were collected, stored, transported, and analyzed according to standard procedures [14].
Blood glucose (fasting) was drained into fluoride tubes and measured using an Accu-chek [19]. The total cholesterol (TC) and high-density lipoprotein cholesterol (HDL-C) levels were both measured using standard procedure that utilizes spectrophotometry. The Friedewald equation was then used to determine low density lipoprotein cholesterol (LDL-C) (LDL-C = TC - HDL-C - TG/2.2) [20]. Triglycerides (TG) measurement was done through standard enzyme-based colorimetric technique. These measurements were all accomplished using an AU480 Chemistry System from Beckman Coulter (Brea, Calif).
All apparatuses underwent calibration based on standard procedures. These blood analysis was carried out by workers in the Department of Pathology and Medical Science Unit at University of Limpopo.
The cut-off points were as follows: hypertension was defined as systolic and diastolic blood pressure ≥ 140/90 mmHg. Diabetes was defined as elevated FBG ≥7.8 mmol/L while obesity was defined as BMI (kg/m2) ≥25 kg/m2 [21].
Inter arm systolic blood pressure difference (IASBPD) and inter arm diastolic blood pressure difference (IADBPD) were described as the absolute value of the left arm SBP/DBP minus the right arm SBP/DBP respectively. Both the IASBPD and IADBPD were grouped into two categories based on a cut-off point: <10 mmHg which is normal and ≥ 10 mmHg which is the category increasing cardiovascular risk [22]. Continuous variables were articulated as mean ± standard deviation while categorical variables were articulated as frequencies and percentages. Moreover comparisons of the variables were performed between the two cut-off groups using independent
Table 1 represents the Descriptive statistics of the general characteristics. There was significant (p ≤ 0.05) mean difference of diastolic blood pressure of the <10 mmHg and ≥ 10 mmHg groups. The prevalence of obesity, diabetes and hypertension was insignificantly (p > 0.05) higher in the <10 mmHg group (1.8–30.9%) than the ≥10 mmHg (0–16.7%).
Variables | <10 mmHg | ≥10 mmHg | P-value |
---|---|---|---|
Height (cm) | 168.26 ± 13.15 | 169.52 ± 10.19 | 0.743 |
Weight (Kg) | 66.99 ± 14.22 | 67.74 ± 22.54 | 0.859 |
BMI (Kg/m2) | 23.51 ± 5.47 | 23.58 ± 7.39 | 0.964 |
SBP (mmHg) | 119.99 ± 12.88 | 117.92 ± 20.38 | 0.585 |
DBP (mmHg) | 70.03 ± 9.62 | 81.50 ± 15.41 | 0.000 |
Fasting glucose (mmol/L) | 5.54 ± 1.27 | 5.38 ± 0.87 | 0.677 |
TC (mmol/L) | 4.14 ± 1.03 | 4.39 ± 1.05 | 0.406 |
TG (mmol/L) | 1.01 ± 0.59 | 1.05 ± 0.48 | 0.827 |
HDL-C(mmol/L) | 1.15 ± 0.34 | 1.18 ± 0.33 | 0.724 |
LDL- C (mmol/L) | 2.80 ± 0.87 | 3.00 ± 0.84 | 0.429 |
Gender | m = 301(49.2%) f = 311(50.8%) | m = 5 (41.7%) f = 7(58.3%) | 0.606 |
Obesity | 189(30.9%) | 2(16.7%) | 0.716 |
Diabetes | 10(1.66%) | 0(0%) | 0.655 |
Hypertension | 11(1.8%) | 1(8.3%) | 0.103 |
Descriptive statistics showing general characteristics.
P ≤ 0.05.
Table 2 shows the association between risk factors and inter arm differences in systolic blood pressure among Ellisras young adults. There was a positive significant association between IASBPD and hypertension (B = 5.331; 95%CI = 12.260–23.183; P = 0.026). There was also a positive significant association found between gender and IASBPD (B = 1.998; 95%CI = 0.022–3.903; P = 0.043).
Variables | B | 95%CI | P-value | |
---|---|---|---|---|
Lower | upper | |||
Age (years) | 0.929 | 0.825 | 1.046 | 0.222 |
Gender | 1.998 | 0.022 | 3.903 | 0.043 |
Height (cm) | 1.002 | 0.981 | 1.024 | 0.853 |
Weight (kg) | 1.038 | 0.986 | 1.092 | 0.159 |
BMI (Kg/m2) | 0.882 | 0.764 | 1.018 | 0.087 |
SBP (mmHg) | 1.000 | 0.974 | 1.026 | 0.983 |
DBP (mmHg) | 1.012 | 0.980 | 1.045 | 0.464 |
Fasting glucose(mmol/L) | 1.093 | 0.822 | 1.454 | 0.540 |
TC(mmol/L) | 0.000 | 0.000 | — | 1.000 |
TG (mmol/L) | 23.905 | 0.000 | — | 1.000 |
HDL-C (mmol/L) | 1174525.430 | 0.000 | — | 1.000 |
LDL-C (mmol/L) | 7854389.463 | 0.000 | — | 1.000 |
Diabetes | 0.000 | 0.000 | — | 0.999 |
Hypertension | 5.331 | 12.260 | 23.183 | 0.026 |
The association between risk factors and inter arm differences in SBP.
P ≤ 0.05.
Table 3 shows the association between risk factors and interarm differences in diastolic blood pressure among Ellisras young adults. There was a positive significant association found between SBP and IADBPD (B = 1.003; 95%CI = 0.967–1.041; P = 0.001) while there was no significant association found between DBP and IADBPD (B = 1.081; 95%CI = 1.032–1.131; P = 0.920).
Variables | B | 95%CI | P-value | |
---|---|---|---|---|
Lower | upper | 0.105 | ||
Age (years) | 0.858 | 0.713 | 1.032 | 0.203 |
Gender | 1.970 | 0.963 | 5.596 | 0.596 |
Height (cm) | 1.023 | 0.940 | 1.113 | 0.851 |
Weight (kg) | 1.013 | 0.889 | 1.153 | 0.654 |
BMI (Kg/m2) | 0.920 | 0.640 | 1.323 | 0.853 |
SBP (mmHg) | 1.003 | 0.967 | 1.041 | 0.001 |
DBP (mmHg) | 1.081 | 1.032 | 1.131 | 0.920 |
Fasting gucose(mmol/L) | 1.024 | 0.624 | 1.632 | 1.000 |
TC(mmol/L) | 187307.604 | 0.000 | — | 1.000 |
TG (mmol/L) | 0.072 | 0.000 | — | 1.000 |
HDL-C (mmol/L) | 0.000 | 0.000 | — | 1.000 |
LDL-C (mmol/L) | 0.000 | 0.000 | — | 1.000 |
Diabetes | 0.000 | 0.000 | — | 0.999 |
Hypertension | 0.261 | 0.022 | 3.132 | 0.290 |
The association between risk factors and inter arm differences in diastolic blood pressure among Ellisras young adults.
P ≤ 0.05.
In the current study, 12 participants (5 males and 7 females; 1.92% of the sample size) showed an inter arm difference ≥ 10 mmHg. A previous study has suggested that interarm BP difference was more usual among young healthy study participants, with an interarm blood pressure difference > 10 mm Hg reported in 111 (12.6%) and 77 (8.8%) participants for SBP and DBP respectively [23]. The current study did not find similar results due to a low prevalence found. Another study conducted among hypertensive patients reported a prevalence of 7.7% (285 patients with a systolic interarm difference of ≥10 mm Hg), while 1.5% (57 patients) had a ≥ 10 mmHg diastolic interarm blood pressure difference. Furthermore, a study by Kim et al. [22] reported a 0.6% (21 patients) prevalence for both systolic and diastolic interarm difference ≥ 10 mmHg.
The different findings found between the current and other related studies could be because of the varying age groups, diseases profile of the participants (some being healthy and others suffering from hypertension and other chronic diseases) or even the different methods used to measure the interarm BP difference. The difference in systolic blood pressure between arms is considered a risk marker and advantageous due to that it is easy to measure clinically without additional equipment and is more acceptable to patients. Furthermore, studies have associated a systolic inter arm difference ≥ 15 mmHg [24], and ≥ 10 mmHg with cardiovascular risk and mortality [7]. The inability to detect the interarm BP difference may result in insufficient treatment of people suffering from hypertension and interrupt hypertension diagnosis. Hence, it is vital to measure blood pressure in both arms. A previous study has reported that blood pressure measured in only one arm would lead to approximately 30% misdiagnosis of hypertensive patients being wrongfully classified as normotensive [25].
In multivariate logistic regression of the current study, a positive significant association was found between systolic interarm blood pressure and hypertension as well as gender. In addition there was also a positive significant association found between SBP and diastolic interarm blood pressure difference in the current study. A previous study by Kimura et al. [26], reported a positive association between systolic interarm systolic blood pressure > 10 mm Hg and SBP and BMI. This was different from the findings of the current study since we found a non-significant association between BMI and both IASBPD and IADBPD. Furthermore, another study by Grossman et al. [27], reported that interarm BP difference was not associated with age, BMI, and heart rate, but was in association with SBP in both young and healthy patients [27]. The latter findings are similar to the current study since we found an association between SBP and IADBPD. Moreover, A study by Grossman et al. [27] which is supported by another study by Ma et al. [28], reported that high inter arm systolic blood pressure difference seems to be more common in older than in younger people.
The study had several limitations. The study had limited variables to broadly represent the large spectrum of cardiovascular risk/health. The effect of controlling interarm blood pressure difference on cardiovascular risk could not be evaluated at this stage. The study did not have a large range in terms of the age hence the effect of age on the inter arm blood pressure difference could not be adequately determined. The cardiovascular health status of the participants was determined on a cross sectional basis hence some factors that can temporarily affect measurements may have affected the readings. The nature of the study cannot fully establish a cause and effect relationship, hence possible bias cannot be ruled out.
The current study found a low prevalence of interarm BP difference and showed positive associations between inter arm differences and a few cardiovascular risk factors including hypertension and gender. More similar studies should include a variety of risk factors and diseases as well as a broader age group. Carrying out such an investigation on a longitudinal basis is also necessary for exclusion of factors that can temporarily affect the findings. Detection of an interarm BP difference that is ≥10 mmHg should motivate the need for a thorough cardiovascular/health assessment to prevent late diagnosis and other related complications.
The Ellisras Longitudinal Study (ELS) administrators, Mr. Makata, Mrs. Makgae, as well as Mr. T Tselapedi are greatly acknowledged. The ELS participants and community coordinators are gratefully recognized for their assistance.
ELS | Ellisras Longitudinal Study |
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MRI is commonly used once treating brain, prostate cancers, ankle and foot. The Magnetic Resonance Imaging (MRI) images are usually liable to suffer from noises such as Gaussian noise, salt and pepper noise and speckle noise. So getting of brain image with accuracy is very extremely task. An accurate brain image is very necessary for further diagnosis process. During this chapter, a median filter algorithm will be modified. Gaussian noise and Salt and pepper noise will be added to MRI image. A proposed Median filter (MF), Adaptive Median filter (AMF) and Adaptive Wiener filter (AWF) will be implemented. The filters will be used to remove the additive noises present in the MRI images. The noise density will be added gradually to MRI image to compare performance of the filters evaluation. 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Particularly in the case of motor imagery BCIs, users may need several training sessions before they learn how to generate desired brain activity and reach an acceptable performance. A typical training protocol for such BCIs includes execution of a motor imagery task by the user, followed by presentation of an extending bar or a moving object on a computer screen. In this chapter, we discuss the importance of a visual feedback that resembles human actions, the effect of human factors such as confidence and motivation, and the role of embodiment in the learning process of a motor imagery task. Our results from a series of experiments in which users BCI-operated a humanlike android robot confirm that realistic visual feedback can induce a sense of embodiment, which promotes a significant learning of the motor imagery task in a short amount of time. We review the impact of humanlike visual feedback in optimized modulation of brain activity by the BCI users.",book:{id:"6610",slug:"evolving-bci-therapy-engaging-brain-state-dynamics",title:"Evolving BCI Therapy",fullTitle:"Evolving BCI Therapy - Engaging Brain State Dynamics"},signatures:"Maryam Alimardani, Shuichi Nishio and Hiroshi Ishiguro",authors:[{id:"11981",title:"Prof.",name:"Hiroshi",middleName:null,surname:"Ishiguro",slug:"hiroshi-ishiguro",fullName:"Hiroshi Ishiguro"},{id:"231131",title:"Dr.",name:"Maryam",middleName:null,surname:"Alimardani",slug:"maryam-alimardani",fullName:"Maryam Alimardani"},{id:"231134",title:"Dr.",name:"Shuichi",middleName:null,surname:"Nishio",slug:"shuichi-nishio",fullName:"Shuichi Nishio"}]}],mostDownloadedChaptersLast30Days:[{id:"29764",title:"Underlying Causes of Paresthesia",slug:"underlying-causes-of-paresthesia",totalDownloads:193348,totalCrossrefCites:3,totalDimensionsCites:7,abstract:null,book:{id:"1069",slug:"paresthesia",title:"Paresthesia",fullTitle:"Paresthesia"},signatures:"Mahdi Sharif-Alhoseini, Vafa Rahimi-Movaghar and Alexander R. 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Precise anatomical description along with a correct characterization of the component structures is essential for understanding its functions.",book:{id:"6331",slug:"hypothalamus-in-health-and-diseases",title:"Hypothalamus in Health and Diseases",fullTitle:"Hypothalamus in Health and Diseases"},signatures:"Miana Gabriela Pop, Carmen Crivii and Iulian Opincariu",authors:null},{id:"57103",title:"GABA and Glutamate: Their Transmitter Role in the CNS and Pancreatic Islets",slug:"gaba-and-glutamate-their-transmitter-role-in-the-cns-and-pancreatic-islets",totalDownloads:3565,totalCrossrefCites:4,totalDimensionsCites:10,abstract:"Glutamate and gamma-aminobutyric acid (GABA) are the major neurotransmitters in the mammalian brain. Inhibitory GABA and excitatory glutamate work together to control many processes, including the brain’s overall level of excitation. The contributions of GABA and glutamate in extra-neuronal signaling are by far less widely recognized. In this chapter, we first discuss the role of both neurotransmitters during development, emphasizing the importance of the shift from excitatory to inhibitory GABAergic neurotransmission. The second part summarizes the biosynthesis and role of GABA and glutamate in neurotransmission in the mature brain, and major neurological disorders associated with glutamate and GABA receptors and GABA release mechanisms. The final part focuses on extra-neuronal glutamatergic and GABAergic signaling in pancreatic islets of Langerhans, and possible associations with type 1 diabetes mellitus.",book:{id:"6237",slug:"gaba-and-glutamate-new-developments-in-neurotransmission-research",title:"GABA And Glutamate",fullTitle:"GABA And Glutamate - New Developments In Neurotransmission Research"},signatures:"Christiane S. Hampe, Hiroshi Mitoma and Mario Manto",authors:[{id:"210220",title:"Prof.",name:"Christiane",middleName:null,surname:"Hampe",slug:"christiane-hampe",fullName:"Christiane Hampe"},{id:"210485",title:"Prof.",name:"Mario",middleName:null,surname:"Manto",slug:"mario-manto",fullName:"Mario Manto"},{id:"210486",title:"Prof.",name:"Hiroshi",middleName:null,surname:"Mitoma",slug:"hiroshi-mitoma",fullName:"Hiroshi Mitoma"}]},{id:"35802",title:"Cross-Cultural/Linguistic Differences in the Prevalence of Developmental Dyslexia and the Hypothesis of Granularity and Transparency",slug:"cross-cultural-linguistic-differences-in-the-prevalence-of-developmental-dyslexia-and-the-hypothesis",totalDownloads:3622,totalCrossrefCites:2,totalDimensionsCites:7,abstract:null,book:{id:"673",slug:"dyslexia-a-comprehensive-and-international-approach",title:"Dyslexia",fullTitle:"Dyslexia - A Comprehensive and International Approach"},signatures:"Taeko N. Wydell",authors:[{id:"87489",title:"Prof.",name:"Taeko",middleName:"N.",surname:"Wydell",slug:"taeko-wydell",fullName:"Taeko Wydell"}]},{id:"58597",title:"Testosterone and Erectile Function: A Review of Evidence from Basic Research",slug:"testosterone-and-erectile-function-a-review-of-evidence-from-basic-research",totalDownloads:1370,totalCrossrefCites:2,totalDimensionsCites:3,abstract:"Androgens are essential for male physical activity and normal erectile function. Hence, age-related testosterone deficiency, known as late-onset hypogonadism (LOH), is considered a risk factor for erectile dysfunction (ED). This chapter summarizes relevant basic research reports examining the effects of testosterone on erectile function. Testosterone affects several organs and is especially active on the erectile tissue. The mechanism of testosterone deficiency effects on erectile function and the results of testosterone replacement therapy (TRT) have been well studied. Testosterone affects nitric oxide (NO) production and phosphodiesterase type 5 (PDE-5) expression in the corpus cavernosum through molecular pathways, preserves smooth muscle contractility by regulating both contraction and relaxation, and maintains the structure of the corpus cavernosum. Interestingly, testosterone deficiency has relationship to neurological diseases, which leads to ED. Testosterone replacement therapy is widely used to treat patients with testosterone deficiency; however, this treatment might also induce some problems. Basic research suggests that PDE-5 inhibitors, L-citrulline, and/or resveratrol therapy might be effective therapeutic options for testosterone deficiency-induced ED. Future research should confirm these findings through more specific experiments using molecular tools and may shed more light on endocrine-related ED and its possible treatments.",book:{id:"5994",slug:"sex-hormones-in-neurodegenerative-processes-and-diseases",title:"Sex Hormones in Neurodegenerative Processes and Diseases",fullTitle:"Sex Hormones in Neurodegenerative Processes and Diseases"},signatures:"Tomoya Kataoka and Kazunori Kimura",authors:[{id:"219042",title:"Ph.D.",name:"Tomoya",middleName:null,surname:"Kataoka",slug:"tomoya-kataoka",fullName:"Tomoya Kataoka"},{id:"229066",title:"Prof.",name:"Kazunori",middleName:null,surname:"Kimura",slug:"kazunori-kimura",fullName:"Kazunori Kimura"}]}],onlineFirstChaptersFilter:{topicId:"18",limit:6,offset:0},onlineFirstChaptersCollection:[{id:"82953",title:"Early Visual Areas are Activated during Object Recognition in Emerging Images",slug:"early-visual-areas-are-activated-during-object-recognition-in-emerging-images",totalDownloads:1,totalDimensionsCites:0,doi:"10.5772/intechopen.105756",abstract:"Human observers can reliably segment visual input and recognise objects. However, the underlying processes happen so quickly that they normally cannot be captured with fMRI. We used Emerging Images (EI), which contains a hidden object and extends the process of recognition, to investigate the involvement of early visual areas (V1, V2 and V3) and lateral occipital complex (LOC) in object recognition. The early visual areas were located with a retinotopy scan and the LOC with a localiser. The participants (N=8) then viewed an EI, followed by the hidden object’s silhouette (disambiguation), and then, the EI was repeated. BOLD responses before and after disambiguation were compared. The retinotopy parameters were used to back-project the BOLD response onto the visual field, creating spatially detailed maps of the activity change. V1 and V2 (but not V3) showed stronger response after disambiguation, while there was no difference in the LOC. The back-projections revealed no distinct pattern or changes in activity on object location, indicating that the activity in V1 and V2 is not specific for voxels corresponding to the object location. We found no difference before and after disambiguation in the LOC, which may be repetition suppression counteracting the effect of recognition.",book:{id:"11374",title:"Sensory Nervous System - Computational Neuroimaging Investigations of Topographical Organization in Human Sensory Cortex",coverURL:"https://cdn.intechopen.com/books/images_new/11374.jpg"},signatures:"Marleen Bakker, Hinke N. Halbertsma, Nicolás Gravel, Remco Renken, Frans W. Cornelissen and Barbara Nordhjem"},{id:"82931",title:"Neuroinflammation in Traumatic Brain Injury",slug:"neuroinflammation-in-traumatic-brain-injury",totalDownloads:3,totalDimensionsCites:0,doi:"10.5772/intechopen.105178",abstract:"Neuroinflammation following traumatic brain injury (TBI) is an important cause of secondary brain injury that perpetuates the duration and scope of disease after initial impact. This chapter discusses the pathophysiology of acute and chronic neuroinflammation, providing insight into factors that influence the acute clinical course and later functional outcomes. Secondary injury due to neuroinflammation is described by mechanisms of action such as ischemia, neuroexcitotoxicity, oxidative stress, and glymphatic and lymphatic dysfunction. Neurodegenerative sequelae of inflammation, including chronic traumatic encephalopathy, which are important to understand for clinical practice, are detailed by disease type. Prominent research topics of TBI animal models and biomarkers of traumatic neuroinflammation are outlined to provide insight into the advances in TBI research. We then discuss current clinical treatments in TBI and their implications in preventing inflammation. To complete the chapter, recent research models, novel biomarkers, and future research directions aimed at mitigating TBI will be described and will highlight novel therapeutic targets. Understanding the pathophysiology and contributors of neuroinflammation after TBI will aid in future development of prophylaxis strategies, as well as more tailored management and treatment algorithms. This topic chapter is important to both clinicians and basic and translational scientists, with the goal of improving patient outcomes in this common disease.",book:{id:"11367",title:"Traumatic Brain Injury",coverURL:"https://cdn.intechopen.com/books/images_new/11367.jpg"},signatures:"Grace Y. Kuo, Fawaz Philip Tarzi, Stan Louie and Roy A. Poblete"},{id:"82876",title:"Oxygen Tissue Levels as an Effectively Modifiable Factor in Alzheimer’s Disease Improvement",slug:"oxygen-tissue-levels-as-an-effectively-modifiable-factor-in-alzheimer-s-disease-improvement",totalDownloads:9,totalDimensionsCites:0,doi:"10.5772/intechopen.106331",abstract:"Despite the advance in biochemistry, there are two substantial errors that have remained for at least two centuries. One is that oxygen from the atmosphere passes through the lungs and reaches the bloodstream, which distributes it throughout the body. Another major mistake is the belief that such oxygen is used by the cell to obtain energy, by combining it with glucose. Since the late nineteenth century, it began to be published that the gas exchange in the lungs cannot be explained by diffusion. Even Christian Bohr suggested that it looked like a cellular secretion. But despite experimental evidence to the contrary and based only on theoretical models, the dogma that our body takes the oxygen it contains inside from the air around it has been perpetuated to this day. The oxygen levels contained in the human body are high, close to 99%, and the atmosphere only contains between 19 and 21%. The hypothesis that there is a supposed oxygen concentrating mechanism has not been experimentally proven to date, after almost two centuries. The mistaken belief, even among neurologists, that our body takes oxygen from the atmosphere is widespread, even though there is no experimental basis to support it, just theoretical models. Our finding that the human body can take oxygen from the water it contains, not from the air around it, like plants, comes to mark a before and after in biology in general, and the CNS is no exception. Therefore, establishing the true origin of the oxygen present within our body and brain will allow us to better understand the physio pathogenesis of neurodegenerative diseases.",book:{id:"11637",title:"Neuropsychology of Dementia",coverURL:"https://cdn.intechopen.com/books/images_new/11637.jpg"},signatures:"Arturo Solís Herrera"},{id:"82859",title:"Impact of Hypoxia on Astrocyte Induced Pathogenesis",slug:"impact-of-hypoxia-on-astrocyte-induced-pathogenesis",totalDownloads:6,totalDimensionsCites:0,doi:"10.5772/intechopen.106263",abstract:"Astrocytes are the most abundant cells of the central nervous system. These cells are of diverse types based on their function and structure. Astrocyte activation is linked mainly with microbial infections, but long-term activation can lead to neurological impairment. Astrocytes play a significant role in neuro-inflammation by activating pro-inflammatory pathways. Activation of interleukins and cytokines causes neuroinflammation resulting in many neurodegenerative disorders such as stroke, growth of tumours, and Alzheimer’s. Inflammation of the brain hinders neural circulation and compromises blood flow by affecting the blood–brain barrier. So the oxygen concentration is lowered, causing brain hypoxia. Hypoxia leads to the activation of nuclear factor kappa B (NFkB) and hypoxia-inducible factors (HIF), which aggravates the inflammatory state of the brain. Hypoxia evoked changes in the blood–brain barrier, further complicating astrocyte-induced pathogenesis.",book:{id:"10744",title:"Astrocytes in Brain Communication and Disease",coverURL:"https://cdn.intechopen.com/books/images_new/10744.jpg"},signatures:"Farwa Munir, Nida Islam, Muhammad Hassan Nasir, Zainab Anis, Shahar Bano, Shahzaib Naeem, Atif Amin Baig and Zaineb Sohail"},{id:"82839",title:"Neurophysiology of Emotions",slug:"neurophysiology-of-emotions",totalDownloads:2,totalDimensionsCites:0,doi:"10.5772/intechopen.106043",abstract:"Emotions are automatic and primary patterns of purposeful cognitive-behavioral organizations. They have three main functions: coordination, signaling, and information. First, emotions coordinate organs and tissues, thus predisposing the body to peculiar responses. Scholars have not reached a consensus on the plausibility of emotion-specific response patterns yet. Despite the limitations, data support the hypothesis of specific response patterns for distinct subtypes of emotions. Second, emotional episodes signal the current state of the individual. Humans display their state with verbal behaviors, nonverbal actions (e.g., facial movements), and neurovegetative signals. Third, emotions inform the brain for interpretative and evaluative purposes. Emotional experiences include mental representations of arousal, relations, and situations. Every emotional episode begins with exposure to stimuli with distinctive features (i.e., elicitor). These inputs can arise from learning, expressions, empathy, and be inherited, or rely on limited aspects of the environment (i.e., sign stimuli). The existence of the latter ones in humans is unclear; however, emotions influence several processes, such as perception, attention, learning, memory, decision-making, attitudes, and mental schemes. Overall, the literature suggests the nonlinearity of the emotional process. Each section outlines the neurophysiological basis of elements of emotion.",book:{id:"11742",title:"Neurophysiology",coverURL:"https://cdn.intechopen.com/books/images_new/11742.jpg"},signatures:"Maurizio Oggiano"},{id:"82172",title:"Neuroimaging in Common Neurological Diseases Treated by Anticoagulants",slug:"neuroimaging-in-common-neurological-diseases-treated-by-anticoagulants",totalDownloads:7,totalDimensionsCites:0,doi:"10.5772/intechopen.105128",abstract:"Stroke imaging/Cerebral Venous sinus thrombosis/Arterial dissecting disease in Head and Neck regions/Neurocomplication of anticoagulation therapy. Nowsday, anticoagulant drugs are common drugs used in daily practice for patients in neurology clinic. Anticoagulant treatment used for treated symptomatic patients as well as for prophylaxis therapy in asymptomatic patients. The purpose of this chapter based on the review of essential neuroimaging in the most common neurological conditions that benefit from treatment with anticoagulant drugs such as ischemic stroke, cerebral venous sinus thrombosis, and arterial dissecting disease of head and neck arteries and will be enclosed with neuroimaging in case of neurocomplication by anticoagulant therapy.",book:{id:"11742",title:"Neurophysiology",coverURL:"https://cdn.intechopen.com/books/images_new/11742.jpg"},signatures:"Pipat Chiewvit"}],onlineFirstChaptersTotal:12},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:9,numberOfPublishedChapters:90,numberOfOpenTopics:6,numberOfUpcomingTopics:0,issn:"2633-1403",doi:"10.5772/intechopen.79920",isOpenForSubmission:!0},{id:"7",title:"Biomedical Engineering",numberOfPublishedBooks:12,numberOfPublishedChapters:107,numberOfOpenTopics:3,numberOfUpcomingTopics:0,issn:"2631-5343",doi:"10.5772/intechopen.71985",isOpenForSubmission:!0}],lsSeriesList:[{id:"11",title:"Biochemistry",numberOfPublishedBooks:33,numberOfPublishedChapters:330,numberOfOpenTopics:4,numberOfUpcomingTopics:0,issn:"2632-0983",doi:"10.5772/intechopen.72877",isOpenForSubmission:!0},{id:"25",title:"Environmental Sciences",numberOfPublishedBooks:1,numberOfPublishedChapters:19,numberOfOpenTopics:4,numberOfUpcomingTopics:0,issn:"2754-6713",doi:"10.5772/intechopen.100362",isOpenForSubmission:!0},{id:"10",title:"Physiology",numberOfPublishedBooks:14,numberOfPublishedChapters:145,numberOfOpenTopics:4,numberOfUpcomingTopics:0,issn:"2631-8261",doi:"10.5772/intechopen.72796",isOpenForSubmission:!0}],hsSeriesList:[{id:"3",title:"Dentistry",numberOfPublishedBooks:9,numberOfPublishedChapters:139,numberOfOpenTopics:2,numberOfUpcomingTopics:0,issn:"2631-6218",doi:"10.5772/intechopen.71199",isOpenForSubmission:!0},{id:"6",title:"Infectious Diseases",numberOfPublishedBooks:13,numberOfPublishedChapters:122,numberOfOpenTopics:4,numberOfUpcomingTopics:0,issn:"2631-6188",doi:"10.5772/intechopen.71852",isOpenForSubmission:!0},{id:"13",title:"Veterinary Medicine and Science",numberOfPublishedBooks:11,numberOfPublishedChapters:112,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:21,numberOfOpenTopics:3,numberOfUpcomingTopics:0,issn:"2753-894X",doi:"10.5772/intechopen.100359",isOpenForSubmission:!0},{id:"23",title:"Education and Human Development",numberOfPublishedBooks:0,numberOfPublishedChapters:10,numberOfOpenTopics:1,numberOfUpcomingTopics:1,issn:null,doi:"10.5772/intechopen.100360",isOpenForSubmission:!0},{id:"24",title:"Sustainable Development",numberOfPublishedBooks:1,numberOfPublishedChapters:19,numberOfOpenTopics:5,numberOfUpcomingTopics:0,issn:"2753-6580",doi:"10.5772/intechopen.100361",isOpenForSubmission:!0}],testimonialsList:[{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"}}}},{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"}}}}]},series:{item:{id:"6",title:"Infectious Diseases",doi:"10.5772/intechopen.71852",issn:"2631-6188",scope:"This series will provide a comprehensive overview of recent research trends in various Infectious Diseases (as per the most recent Baltimore classification). Topics will include general overviews of infections, immunopathology, diagnosis, treatment, epidemiology, etiology, and current clinical recommendations for managing infectious diseases. Ongoing issues, recent advances, and future diagnostic approaches and therapeutic strategies will also be discussed. This book series will focus on various aspects and properties of infectious diseases whose deep understanding is essential for safeguarding the human race from losing resources and economies due to pathogens.",coverUrl:"https://cdn.intechopen.com/series/covers/6.jpg",latestPublicationDate:"August 2nd, 2022",hasOnlineFirst:!0,numberOfPublishedBooks:13,editor:{id:"131400",title:"Prof.",name:"Alfonso J.",middleName:null,surname:"Rodriguez-Morales",slug:"alfonso-j.-rodriguez-morales",fullName:"Alfonso J. Rodriguez-Morales",profilePictureURL:"https://mts.intechopen.com/storage/users/131400/images/system/131400.png",biography:"Dr. Rodriguez-Morales is an expert in tropical and emerging diseases, particularly zoonotic and vector-borne diseases (especially arboviral diseases). 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},editorTwo:null,editorThree:null},subseries:{paginationCount:5,paginationItems:[{id:"3",title:"Bacterial Infectious Diseases",coverUrl:"https://cdn.intechopen.com/series_topics/covers/3.jpg",editor:{id:"205604",title:"Dr.",name:"Tomas",middleName:null,surname:"Jarzembowski",slug:"tomas-jarzembowski",fullName:"Tomas Jarzembowski",profilePictureURL:"https://s3.us-east-1.amazonaws.com/intech-files/0030O00002bRKriQAG/Profile_Picture_2022-06-16T11:01:31.jpg",biography:"Tomasz Jarzembowski was born in 1968 in Gdansk, Poland. He obtained his Ph.D. degree in 2000 from the Medical University of Gdańsk (UG). After specialization in clinical microbiology in 2003, he started studying biofilm formation and antibiotic resistance at the single-cell level. In 2015, he obtained his D.Sc. degree. His later study in cooperation with experts in nephrology and immunology resulted in the designation of the new diagnostic method of UTI, patented in 2017. He is currently working at the Department of Microbiology, Medical University of Gdańsk (GUMed), Poland. Since many years, he is a member of steering committee of Gdańsk branch of Polish Society of Microbiologists, a member of ESCMID. He is also a reviewer and a member of editorial boards of a number of international journals.",institutionString:"Medical University of Gdańsk, Poland",institution:null},editorTwo:{id:"484980",title:"Dr.",name:"Katarzyna",middleName:null,surname:"Garbacz",slug:"katarzyna-garbacz",fullName:"Katarzyna Garbacz",profilePictureURL:"https://s3.us-east-1.amazonaws.com/intech-files/0033Y00003St8TAQAZ/Profile_Picture_2022-07-07T09:45:16.jpg",biography:"Katarzyna Maria Garbacz, MD, is an Associate Professor at the Medical University of Gdańsk, Poland and she is head of the Department of Oral Microbiology of the Medical University of Gdańsk. She has published more than 50 scientific publications in peer-reviewed journals. She has been a project leader funded by the National Science Centre of Poland. Prof. Garbacz is a microbiologist working on applied and fundamental questions in microbial epidemiology and pathogenesis. Her research interest is in antibiotic resistance, host-pathogen interaction, and therapeutics development for staphylococcal pathogens, mainly Staphylococcus aureus, which causes hospital-acquired infections. Currently, her research is mostly focused on the study of oral pathogens, particularly Staphylococcus spp.",institutionString:"Medical University of Gdańsk, Poland",institution:null},editorThree:null,editorialBoard:[{id:"190041",title:"Dr.",name:"Jose",middleName:null,surname:"Gutierrez Fernandez",slug:"jose-gutierrez-fernandez",fullName:"Jose Gutierrez Fernandez",profilePictureURL:"//cdnintech.com/web/frontend/www/assets/author.svg",institutionString:null,institution:{name:"University of Granada",institutionURL:null,country:{name:"Spain"}}},{id:"156556",title:"Prof.",name:"Maria Teresa",middleName:null,surname:"Mascellino",slug:"maria-teresa-mascellino",fullName:"Maria Teresa Mascellino",profilePictureURL:"https://mts.intechopen.com/storage/users/156556/images/system/156556.jpg",institutionString:"Sapienza University",institution:{name:"Sapienza University of Rome",institutionURL:null,country:{name:"Italy"}}},{id:"164933",title:"Prof.",name:"Mónica Alexandra",middleName:null,surname:"Sousa Oleastro",slug:"monica-alexandra-sousa-oleastro",fullName:"Mónica Alexandra Sousa Oleastro",profilePictureURL:"https://mts.intechopen.com/storage/users/164933/images/system/164933.jpeg",institutionString:"National Institute of Health Dr Ricardo Jorge",institution:{name:"National Institute of Health Dr. Ricardo Jorge",institutionURL:null,country:{name:"Portugal"}}}]},{id:"4",title:"Fungal Infectious Diseases",coverUrl:"https://cdn.intechopen.com/series_topics/covers/4.jpg",editor:{id:"174134",title:"Dr.",name:"Yuping",middleName:null,surname:"Ran",slug:"yuping-ran",fullName:"Yuping Ran",profilePictureURL:"https://s3.us-east-1.amazonaws.com/intech-files/0030O00002bS9d6QAC/Profile_Picture_1630330675373",biography:"Dr. Yuping Ran, Professor, Department of Dermatology, West China Hospital, Sichuan University, Chengdu, China. Completed the Course Medical Mycology, the Centraalbureau voor Schimmelcultures (CBS), Fungal Biodiversity Centre, Netherlands (2006). International Union of Microbiological Societies (IUMS) Fellow, and International Emerging Infectious Diseases (IEID) Fellow, Centers for Diseases Control and Prevention (CDC), Atlanta, USA. Diploma of Dermatological Scientist, Japanese Society for Investigative Dermatology. Ph.D. of Juntendo University, Japan. Bachelor’s and Master’s degree, Medicine, West China University of Medical Sciences. Chair of Sichuan Medical Association Dermatology Committee. General Secretary of The 19th Annual Meeting of Chinese Society of Dermatology and the Asia Pacific Society for Medical Mycology (2013). In charge of the Annual Medical Mycology Course over 20-years authorized by National Continue Medical Education Committee of China. Member of the board of directors of the Asia-Pacific Society for Medical Mycology (APSMM). Associate editor of Mycopathologia. 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He also obtained an MSc in Molecular and Genetic Medicine, and a Ph.D. in Clinical Immunology and Human Genetics from the University of Sheffield, UK. He also completed a short-term fellowship in Pediatric Clinical Immunology and Bone Marrow Transplantation at Newcastle General Hospital, England. Dr. Rezaei is a Full Professor of Immunology and Vice Dean of International Affairs and Research, at the School of Medicine, Tehran University of Medical Sciences, and the co-founder and head of the Research Center for Immunodeficiencies. He is also the founding president of the Universal Scientific Education and Research Network (USERN). Dr. Rezaei has directed more than 100 research projects and has designed and participated in several international collaborative projects. He is an editor, editorial assistant, or editorial board member of more than forty international journals. He has edited more than 50 international books, presented more than 500 lectures/posters in congresses/meetings, and published more than 1,100 scientific papers in international journals.",institutionString:"Tehran University of Medical Sciences",institution:{name:"Tehran University of Medical Sciences",country:{name:"Iran"}}},{id:"180733",title:"Dr.",name:"Jean",middleName:null,surname:"Engohang-Ndong",slug:"jean-engohang-ndong",fullName:"Jean Engohang-Ndong",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/180733/images/system/180733.png",biography:"Dr. Jean Engohang-Ndong was born and raised in Gabon. After obtaining his Associate Degree of Science at the University of Science and Technology of Masuku, Gabon, he continued his education in France where he obtained his BS, MS, and Ph.D. in Medical Microbiology. He worked as a post-doctoral fellow at the Public Health Research Institute (PHRI), Newark, NJ for four years before accepting a three-year faculty position at Brigham Young University-Hawaii. Dr. Engohang-Ndong is a tenured faculty member with the academic rank of Full Professor at Kent State University, Ohio, where he teaches a wide range of biological science courses and pursues his research in medical and environmental microbiology. Recently, he expanded his research interest to epidemiology and biostatistics of chronic diseases in Gabon.",institutionString:"Kent State University",institution:{name:"Kent State University",country:{name:"United States of America"}}},{id:"188773",title:"Prof.",name:"Emmanuel",middleName:null,surname:"Drouet",slug:"emmanuel-drouet",fullName:"Emmanuel Drouet",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/188773/images/system/188773.png",biography:"Emmanuel Drouet, PharmD, is a Professor of Virology at the Faculty of Pharmacy, the University Grenoble-Alpes, France. As a head scientist at the Institute of Structural Biology in Grenoble, Dr. Drouet’s research investigates persisting viruses in humans (RNA and DNA viruses) and the balance with our host immune system. He focuses on these viruses’ effects on humans (both their impact on pathology and their symbiotic relationships in humans). He has an excellent track record in the herpesvirus field, and his group is engaged in clinical research in the field of Epstein-Barr virus diseases. He is the editor of the online Encyclopedia of Environment and he coordinates the Universal Health Coverage education program for the BioHealth Computing Schools of the European Institute of Science.",institutionString:null,institution:{name:"Grenoble Alpes University",country:{name:"France"}}},{id:"131400",title:"Prof.",name:"Alfonso J.",middleName:null,surname:"Rodriguez-Morales",slug:"alfonso-j.-rodriguez-morales",fullName:"Alfonso J. Rodriguez-Morales",position:null,profilePictureURL:"https://mts.intechopen.com/storage/users/131400/images/system/131400.png",biography:"Dr. Rodriguez-Morales is an expert in tropical and emerging diseases, particularly zoonotic and vector-borne diseases (especially arboviral diseases). 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:{name:"University of Agriculture Faisalabad",country:{name:"Pakistan"}}},{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:{name:"University of Agriculture Faisalabad",country:{name:"Pakistan"}}},{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). 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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. 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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. 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