Publications by authors named "Mohammed Nayeem"

Background: There exists a link between irritable bowel syndrome (IBS) and depression. Similarly, chronic depression is known to increase the risk of cancer in general. In this population-based analysis, we investigated the prevalence and the odds of colorectal cancer (CRC) in young-depressed patients with IBS.

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Coronary reactive hyperemia (CRH) is impaired in cardiovascular diseases, and angiotensin-II (Ang-II) exacerbates it. However, it is unknown how Ang-II affects CRH in Tie2-sEH Tr (human-sEH-overexpressed) versus wild-type (WT) mice. sEH-overexpression resulted in CRH reduction in Tie2-sEH Tr versus WT.

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The role of cytochrome P450-epoxygenase has been seen in cardiovascular physiology and pathophysiology. The aberration in CYP450-epoxygenase genes occur due to genetic polymorphisms, aging, or environmental factors, that increase susceptibility to cardiovascular diseases (CVDs). The actual role played by the CYP450-epoxygenases is the metabolism of arachidonic acid (AA) and linoleic acid (LA) into epoxyeicosatrienoic acids (EETs) and epoxyoctadecaenoic acid (EpOMEs) metabolites (oxylipins) and others, which is involved in vasodilation and myocardial-protection.

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Adenosine is a ubiquitous endogenous nucleoside or autacoid that affects the cardiovascular system through the activation of four G-protein coupled receptors: adenosine A receptor (AAR), adenosine A receptor (AAR), adenosine A receptor (AAR), and adenosine A receptor (AAR). With the rapid generation of this nucleoside from cellular metabolism and the widespread distribution of its four G-protein coupled receptors in almost all organs and tissues of the body, this autacoid induces multiple physiological as well as pathological effects, not only regulating the cardiovascular system but also the central nervous system, peripheral vascular system, and immune system. Mounting evidence shows the role of CYP450-enzymes in cardiovascular physiology and pathology, and the genetic polymorphisms in CYP450s can increase susceptibility to cardiovascular diseases (CVDs).

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Previously, we have reported that the coronary reactive hyperemic response was reduced in adenosine A receptor-null (AAR) mice, and it was reversed by the soluble epoxide hydrolase (sEH) inhibitor. However, it is unknown in aortic vascular response, therefore, we hypothesized that AAR-gene deletion in mice (AAR) affects adenosine-induced vascular response by increase in sEH and adenosine A receptor (AAR) activities. AAR mice showed an increase in sEH, A AR and CYP450-4A protein expression but decrease in CYP450-2C compared to C57Bl/6 mice.

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Backgrounds/aims: Lymph node (LN) metastasis though, is a poor prognostic factor for ampullary carcinoma (APC), the impact of Lymph node ratio (LNR) and Logarithm odds of positive lymph node (LODDS) in the long-term survival remains controversial. We evaluated the factors affecting the long-term outcome in APC patients with emphasis on LNR and LODDS.

Methods: The prospectively collected data of 198 patients who underwent pancreatoduodenectomy for APC was analyzed after excluding 12 patients for various reasons.

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Previously, we showed vascular endothelial overexpression of human-CYP2J2 enhances coronary reactive hyperemia in Tie2-CYP2J2 Tr mice, and eNOS mice had overexpression of CYP2J-epoxygenase with adenosine A receptor-induced enhance relaxation, but we did not see the response in CYP2J-epoxygenase knockout mice. Therefore, we hypothesized that -gene deletion affects acetylcholine- and 5'-N-ethylcarboxamidoadenosine (NECA) (adenosine)-induced relaxation and their response is partially inhibited by angiotensin-II (Ang-II) in mice. Acetylcholine (Ach)-induced response was tested with -(methylsulfonyl)-2-(2-propynyloxy)-benzenehexanamide (MS-PPOH, CYP-epoxygenase inhibitor; 10M) and Ang-II (10M).

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Previously, we showed that adenosine A receptor induces relaxation independent of NO in soluble epoxide hydrolase-null mice (Nayeem et al. in Am J Physiol Regul Integr Comp Physiol 304:R23-R32, 2013). Currently, we hypothesize that Ephx2-gene deletion affects acetylcholine (Ach)-induced relaxation which is independent of AAR but dependent on NO and CYP-epoxygenases.

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Globally, cardiovascular diseases (CVDs) are the number one cause of mortality. Approximately 18 million people died from CVDs in 2015, representing more than 30% of all global deaths. New diagnostic tools and therapies are eagerly required to decrease the prevalence of CVDs related to mortality and/or risk factors leading to CVDs.

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Background: To expand the donor pool, split liver transplantation is conventionally performed for one adult and one pediatric recipient. Application of this technique for two adult recipients can produce remarkable impact on the waiting list. Proper donor and recipient selection is crucial for the favorable outcome following full-right and full-left liver split.

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Coronary reactive hyperemia (CRH) protects the heart against ischemia. Adenosine AAR-deficient (AAR) mice have increased expression of soluble epoxide hydrolase (sEH); the enzyme responsible for breaking down the cardioprotective epoxyeicosatrienoic acids (EETs) to dihydroxyeicosatrienoic acids (DHETs). sEH-inhibition enhances CRH, increases EETs, and modulates oxylipin profiles.

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Adenosine is an endogenous mediator involved in a myriad of physiologic functions, including vascular tone regulation. It is also implicated in some pathologic conditions. Four distinct receptor subtypes mediate the effects of adenosine, such as its role in the regulation of the vascular tone.

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Cardiovascular diseases remain the number one diseases affecting patients' morbidity and mortality. The adenosine receptors are G-protein coupled receptors which have been of interest for drugs target for the treatment of multiple diseases ranging from cardiovascular to neurological. Adenosine receptors have been connected to several biological pathways affecting the physiology and pathology of the cardiovascular system.

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Arachidonic acid is metabolized to epoxyeicosatrienoic acids (EETs) by cytochrome (CYP) P450 epoxygenases, and to ω-terminal hydroxyeicosatetraenoic acids (HETEs) by ω-hydroxylases. EETs and HETEs often have opposite biologic effects; EETs are vasodilatory and protect against ischemia/reperfusion injury, while ω-terminal HETEs are vasoconstrictive and cause vascular dysfunction. Other oxylipins, such as epoxyoctadecaenoic acids (EpOMEs), hydroxyoctadecadienoic acids (HODEs), and prostanoids also have varied vascular effects.

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Cytochromes P450 metabolize arachidonic acid (AA) into two vasoactive oxylipins with opposing biologic effects: epoxyeicosatrienoic acids (EETs) and omega-(ω)-terminal hydroxyeicosatetraenoic acids (HETEs). EETs have numerous beneficial physiological effects, including vasodilation and protection against ischemia/reperfusion injury, whereas ω-terminal HETEs induce vasoconstriction and vascular dysfunction. We evaluated the effect of these oxylipins on post-ischemic vasodilation known as coronary reactive hyperemia (CRH).

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Vascular complications continue to have a devastating effect on liver transplantation recipients, even though their nature, incidence, and outcome might have actually changed with increasing experience and proficiency in high-volume centers. The aim of this study was to analyze the trends observed in vascular complications with changing protocols in adult and pediatric living donor liver transplantation over 10 years in 2 time frames in terms of nature, incidence, and outcome. It is a retrospective analysis of 391 (group 1, January 2006 to December 2010) and 741 (group 2, January 2011 to October 2013) patients.

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Living donor liver transplantation (LDLT) in obese patients raises concerns with regards to obtaining grafts of "adequate" graft-to-recipient weight ratio (GRWR) and the impact of obesity on the outcomes of LDLT. LDLT outcomes in patients weighing ≥100 kg were compared with those weighing <100 kg. Patients weighing ≥100 kg were divided into 3 categories based on the GRWR of the grafts they received.

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Soluble epoxide hydrolase (sEH) converts epoxyeicosatrienoic acids that are endothelium-derived hyperpolarizing factors into less active dihydroxyeicosatrienoic acids. Previously, we reported a decrease in adenosine A receptor (AAR) protein levels in sEH knockout (sEH) and an increase in sEH and AAR protein levels in AAR mice. Additionally, K channels are involved in adenosine receptor (AR)-dependent vascular relaxation.

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Coronary reactive hyperemia (CRH) is a physiological response to ischemic insult that prevents the potential harm associated with an interruption of blood supply. The relationship between the pharmacologic inhibition of soluble epoxide hydrolase (sEH) and CRH response to a brief ischemia is not known. sEH is involved in the main catabolic pathway of epoxyeicosatrienoic acids (EETs), which are converted into dihydroxyeicosatrienoic acids (DHETs).

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The relationship between soluble epoxide hydrolase (sEH) and coronary reactive hyperemia (CRH) response to a brief ischemic insult is not known. Epoxyeicosatrienoic acids (EETs) exert cardioprotective effects in ischemia/reperfusion injury. sEH converts EETs into dihydroxyeicosatrienoic-acids (DHETs).

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Introduction: Liver transplantation (LT) is the gold standard for decompensated Chronic Liver Disease (CLD) in individuals satisfying the selection criteria. Organ scarcity is the rate limiting step in liver transplantation across the globe. Expanding the donor pool is practiced by transplant surgeons across the globe in view of perennial donor organ scarcity and ever increasing organ demand.

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Despite advances in speciality care, mortality and morbidity remain the most important issues in the management of post-cholecystectomy bile duct injuries. We analysed the peri-operative management of post-cholecystectomy bile duct injuries to assess their outcomes. Of 150 patients with post-cholecystectomy bile duct injuries, 13 patients who presented with strictured hepaticojejunostomy were excluded from the analysis.

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Background And Purpose: Stimulation of the A1 adenosine receptor and angiotensin II receptor type-1 (AT1 receptor) causes vasoconstriction through activation of cytochrome P450 4A (CYP4A) and ERK1/2. Thus, we hypothesized that acute angiotensin II activation alters the vasomotor response induced by the non-selective adenosine receptor agonist, NECA, in mouse mesenteric arteries (MAs).

Experimental Approach: We used a Danish Myo Technology wire myograph to measure muscle tension in isolated MAs from wild type (WT), A1 receptor and A2B receptor knockout (KO) mice.

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This study aims to investigate the signaling mechanism involved in HS-induced modulation of adenosine-mediated vascular tone in the presence or absence of adenosine A2A receptor (A2AAR). We hypothesized that HS-induced enhanced vascular relaxation through A2AAR and epoxyeicosatrienoic acid (EETs) is dependent on peroxisome proliferator-activated receptor gamma (PPARγ) and ATP-sensitive potassium channels (KATP channels) in A2AAR(+/+) mice, while HS-induced vascular contraction to adenosine is dependent on soluble epoxide hydrolase (sEH) that degrades EETs in A2AAR(-/-) mice. Organ bath and Western blot techniques were conducted in HS (4 % NaCl) and normal salt (NS, 0.

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High salt (4% NaCl, HS) diet modulates adenosine-induced vascular response through adenosine A(2A) receptor (A(2A)AR). Evidence suggests that A(2A)AR stimulates cyp450-epoxygenases, leading to epoxyeicosatrienoic acids (EETs) generation. The aim of this study was to understand the vascular reactivity to HS and underlying signaling mechanism in the presence or absence of A(2A)AR.

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