Mahatma Jyotiba Phule Rohilkhand University
Bareilly, India

Mahatma Jyotiba Phule Rohilkhand University is a public university in Uttar Pradesh, India. More than 215 colleges are affiliated to the university and approximately three lakh students enroll every year for examinations. The university has taken an overall perspective of development plan. The university headquarters is in Bareilly with territorial jurisdiction extending over the districts of Bareilly, Moradabad, Rampur, Bijnore, Jyotibaphule Nagar, Budaun, Pilibhit, Shahjahanpur, Noida and Sitapur. The administrative block is on the outskirts of Bareilly city along Pilibhit bypass road. Wikipedia.

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Denimal D.,Mahatma Jyotiba Phule Rohilkhand University
Arteriosclerosis, Thrombosis, and Vascular Biology | Year: 2017

OBJECTIVE—: High-density lipoprotein (HDL) from nondiabetic patients with metabolic syndrome (MetS) displays abnormalities in their lipidome, such as triglyceride enrichment and sphingosine-1-phosphate depletion. We hypothesized that these abnormalities could impair the ability of HDL to stimulate endothelial nitric oxide synthase (eNOS). APPROACH AND RESULTS—: Compared with HDL from control subjects, HDL from normoglycemic patients with MetS was 39% richer in triglycerides (P<0.01) and 15% poorer in sphingosine-1-phosphate (P<0.05; n=23 in each group). eNOS activity, assessed by the conversion of L-[H]arginine to L-[H]citrulline, was 69% lower in human umbilical vein endothelial cells incubated with HDL from MetS patients than in cells incubated with HDL from controls (P<0.0001). In addition, the activating phosphorylation of eNOS at serine (Ser) 1177 and of Akt at Ser473 was 37% (P<0.001) and 39% (P<0.05) lower, respectively, with HDL from MetS patients. Sphingosine-1-phosphate enrichment of HDL from MetS patients restored their ability to stimulate eNOS activity (P<0.05), in relation with a significant increase in eNOS phosphorylation at Ser1177 (P<0.05) and in Akt phosphorylation at Ser473 (P=0.05). By contrast, triglyceride enrichment of HDL from control subjects did not modify eNOS activity (P=0.90) and phosphorylation at Ser1177 (P=0.87). CONCLUSIONS—: We provide evidence that the activation of eNOS by HDL is decreased in MetS patients before the appearance of diabetes mellitus and that sphingosine-1-phosphate depletion of HDL is the main factor responsible for this defect. This has important consequences on the impairment of HDL functionality and antiatherogenic properties in these patients. © 2017 American Heart Association, Inc.

Shabeeh H.,Mahatma Jyotiba Phule Rohilkhand University
Hypertension | Year: 2017

NO is physiologically generated by endothelial and neuronal NO synthase (nNOS) isoforms. Although nNOS was first identified in brain, it is expressed in other tissues, including perivascular nerves, cardiac and skeletal muscle. Increasing experimental evidence suggests that nNOS has important effects on cardiovascular function, but its composite effects on systemic hemodynamics in humans are unknown. We undertook the first human study to assess the physiological effects of systemic nNOS inhibition on basal hemodynamics. Seventeen healthy normotensive men aged 24±4 years received acute intravenous infusions of an nNOS-selective inhibitor, S-methyl-L-thiocitrulline, and placebo on separate occasions. An initial dose-escalation study showed that S-methyl-L-thiocitrulline (0.1–3.0 µmol/kg) induced dose-dependent changes in systemic hemodynamics. The highest dose of S-methyl-L-thiocitrulline (3.0 µmol/kg over 10 minutes) significantly increased systemic vascular resistance (+42±6%) and diastolic blood pressure (67±1 to 77±3 mm Hg) when compared with placebo (both P<0.01). There were significant decreases in heart rate (60±4 to 51±3 bpm; P<0.01) and left ventricular stroke volume (59±6 to 51±6 mL; P<0.01) but ejection fraction was unaltered. S-methyl-L-thiocitrulline had no effect on radial artery flow-mediated dilatation, an index of endothelial NOS activity. These results suggest that nNOS-derived NO has an important role in the physiological regulation of basal systemic vascular resistance and blood pressure in healthy humans.Hypertension is published on behalf of the American Heart Association, Inc., by Wolters Kluwer Health, Inc. This is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution, and reproduction in any medium, provided that the original work is properly cited. © 2017 American Heart Association, Inc

Zhu L.-P.,Mahatma Jyotiba Phule Rohilkhand University
Arteriosclerosis, Thrombosis, and Vascular Biology | Year: 2017

OBJECTIVE—: To identify circulating microRNAs that are differentially expressed in severe coronary heart disease with well or poorly developed collateral arteries and to investigate their mechanisms of action in vivo and in vitro. APPROACH AND RESULTS—: In our study, we identified a circulating microRNA, miR-15b-5p, with low expression that, nevertheless, characterized patients with sufficient coronary collateral artery function. Moreover, in murine hindlimb ischemia model, in situ hybridization identified that miR-15b-5p was specifically expressed in vascular endothelial cells of adductors in sham group and was remarkably downregulated after femoral artery ligation. Overexpressed miR-15b-5p significantly inhibited arteriogenesis and angiogenesis in mice. In vitro, both under basal and vascular endothelial growth factor stimulation, loss-of-function or gain-of-function studies suggested that miR-15b-5p significantly promoted or depressed the migration and proliferation of endothelial cells. We identified AKT3 (protein kinase B-3) as a direct target of miR-15b-5p. Interestingly, AKT3 deficiency by injection with Chol-AKT3-siRNA obviously suppressed arteriogenesis and the recovery of blood perfusion after femoral ligation in mice. CONCLUSIONS—: These results indicate that circulating miR-15b-5p is a suitable biomarker for discriminating between patients with well-developed or poorly developed collaterals. Moreover, miR-15b-5p is a key regulator of arteriogenesis and angiogenesis, which may represent a potential therapeutic target for ischemic disease. © 2017 American Heart Association, Inc.

BACKGROUND AND PURPOSE—: There is great interest in how endovascular clot retrieval hubs provide services to a population. We applied a computational method to objectively generate service boundaries for such endovascular clot retrieval hubs, defined by traveling time to hub. METHODS—: Stroke incidence data merged with population census to estimate numbers of stroke in metropolitan Melbourne, Australia. Traveling time from randomly generated addresses to 4 endovascular clot retrieval–capable hubs (Royal Melbourne Hospital [RMH], Monash Medical Center [MMC], Alfred Hospital [ALF], and Austin Hospital [AUS]) estimated using Google Map application program interface. Boundary maps generated based on traveling time at various times of day for combinations of hubs. RESULTS—: In a 2-hub model, catchment was best distributed when RMH was paired with MMC (model 1a, RMH 1765 km and MMC 1164 km) or with AUS (model 1c, RMH 1244 km and AUS 1685 km), with no statistical difference between models (P=0.20). Catchment was poorly distributed when RMH was paired with ALF (model 1b, RMH 2252 km and ALF 676 km), significantly different from both models 1a and 1c (both P<0.05). Model 1a had the greatest proportion of patients arriving within ideal time of 30 minutes followed by model 1c (P<0.001). In a 3-hub model, the combination of RMH, MMC, and AUS was superior to that of RMH, MMC, and ALF in catchment distribution and travel time. The method was also successfully applied to the city of Adelaide demonstrating wider applicability. CONCLUSIONS—: We provide proof of concept for a novel computational method to objectively designate service boundaries for endovascular clot retrieval hubs. © 2017 American Heart Association, Inc.

Borst O.,Mahatma Jyotiba Phule Rohilkhand University
Arteriosclerosis, Thrombosis, and Vascular Biology | Year: 2015

OBJECTIVE—: Atherosclerosis, an inflammatory disease of arterial vessel walls, requires migration and matrix metalloproteinase (MMP)-9–dependent invasion of monocytes/macrophages into the vascular wall. MMP-9 expression is stimulated by transcription factor nuclear factor-κB, which is regulated by inhibitor κB and thus inhibitor κB-kinase IκB kinase. Regulators of nuclear factor-κB include serum- and glucocorticoid-inducible kinase 1 (SGK1). The present study explored involvement of SGK1 in vascular inflammation and atherogenesis.APPROACH AND RESULTS—: Gene-targeted apolipoprotein E (ApoE)–deficient mice without (apoesgk1) or with (apoesgk1) additional SGK1 knockout received 16-week cholesterol-rich diet. According to immunohistochemistry atherosclerotic lesions in aorta and carotid artery, vascular CD45 leukocyte infiltration, Mac-3 macrophage infiltration, vascular smooth muscle cell content, MMP-2, and MMP-9 positive areas in atherosclerotic tissue were significantly less in apoesgk1mice than in apoesgk1mice. As determined by Boyden chamber, thioglycollate-induced peritonitis and air pouch model, migration of SGK1-deficient CD11bF4/80 macrophages was significantly diminished in vitro and in vivo. Zymographic MMP-2 and MMP-9 production, MMP-9 activity and invasion through matrigel in vitro were significantly less in sgk1 than in sgk1macrophages and in control plasmid–transfected or inactive SGK1-transfected than in constitutively active SGK1-transfected THP-1 cells. Confocal microscopy revealed reduced macrophage number and macrophage MMP-9 content in plaques of apoesgk1 mice. In THP-1 cells, MMP-inhibitor GM6001 (25 μmol/L) abrogated SGK1-induced MMP-9 production and invasion. According to reverse transcription polymerase chain reaction, MMP-9 transcript levels were significantly reduced in sgk1macrophages and strongly upregulated in SGK1-transfected THP-1 cells compared with control plasmid–transfected or SGK1-transfected THP-1 cells. According to immunoblotting and confocal microscopy, phosphorylation of IκB kinase and inhibitor κB and nuclear translocation of p50 were significantly lower in sgk1macrophages than in sgk1macrophages and significantly higher in SGK1-transfected THP-1 cells than in control plasmid–transfected or SGK1-transfected THP-1 cells. Treatment of SGK1-transfected THP-1 cells with IκB kinase-inhibitor BMS-345541 (10 μmol/L) abolished SGK1-induced increase of MMP-9 transcription and gelatinase activity.CONCLUSIONS—: SGK1 plays a pivotal role in vascular inflammation during atherogenesis. SGK1 participates in the regulation of monocyte/macrophage migration and MMP-9 transcription via regulation of nuclear factor-κB. © 2015 American Heart Association, Inc.

Panday S.K.,Mahatma Jyotiba Phule Rohilkhand University
Tetrahedron Asymmetry | Year: 2011

Non-proteinogenic prolines have been acknowledged as an important pool for the synthesis of conformationally rigid bioactive peptides, angiotensin converting enzyme inhibitors and as pharmacological probes. Proline and its derivatives are often used as asymmetric catalysts in organic reactions, such as CBS reductions and proline catalyzed aldol reactions, Mannich reactions, and so on. Furthermore l-proline is an osmoprotectant and is therefore frequently used in many pharmacological as well as biotechnological applications. The wide range of chemical and biological applications associated with l-proline has prompted researchers to develop new methodologies for the synthesis of prolines and substituted prolines and to further explore their chemical and biological applications. The present article is an attempt to discuss all the major advances available till date, describing the use of proline in organic asymmetric synthesis, the synthesis of various bioactive molecules or proline as a constituent part of bioactive molecules. © 2011 Elsevier Ltd. All rights reserved.

Mustian K.M.,Mahatma Jyotiba Phule Rohilkhand University
Journal of clinical oncology : official journal of the American Society of Clinical Oncology | Year: 2013

Thirty percent to 90% of cancer survivors report impaired sleep quality post-treatment, which can be severe enough to increase morbidity and mortality. Lifestyle interventions, such as exercise, are recommended in conjunction with drugs and cognitive behavioral therapy for the treatment of impaired sleep. Preliminary evidence indicates that yoga-a mind-body practice and form of exercise-may improve sleep among cancer survivors. The primary aim of this randomized, controlled clinical trial was to determine the efficacy of a standardized yoga intervention compared with standard care for improving global sleep quality (primary outcome) among post-treatment cancer survivors. In all, 410 survivors suffering from moderate or greater sleep disruption between 2 and 24 months after surgery, chemotherapy, and/or radiation therapy were randomly assigned to standard care or standard care plus the 4-week yoga intervention. The yoga intervention used the Yoga for Cancer Survivors (YOCAS) program consisting of pranayama (breathing exercises), 16 Gentle Hatha and Restorative yoga asanas (postures), and meditation. Participants attended two 75-minute sessions per week. Sleep quality was assessed by using the Pittsburgh Sleep Quality Index and actigraphy pre- and postintervention. In all, 410 survivors were accrued (96% female; mean age, 54 years; 75% had breast cancer). Yoga participants demonstrated greater improvements in global sleep quality and, secondarily, subjective sleep quality, daytime dysfunction, wake after sleep onset, sleep efficiency, and medication use at postintervention (all P ≤ .05) compared with standard care participants. Yoga, specifically the YOCAS program, is a useful treatment for improving sleep quality and reducing sleep medication use among cancer survivors.

Jakovljevic D.G.,Mahatma Jyotiba Phule Rohilkhand University
Circulation. Cardiovascular imaging | Year: 2015

BACKGROUND: Higher levels of physical activity are associated with reduced cardiovascular mortality but its effect on age-related changes in cardiac structure and function is unknown. The present study defines the effect of daily physical activity on age-related changes in cardiac structure, function, metabolism, and performance in healthy women.METHODS AND RESULTS: Sixty-three healthy women were grouped according to age (young, 20-30 years, n=21; middle, 40-50 years, n=22; and older, 65-81 years, n=20) and daily physical activity level (low active<7500 and high active>12,500 steps/d). Participants underwent cardiac MRI including tissue tagging and 31P spectroscopy and exercise testing with noninvasive central hemodynamic measurements. Aging was associated with increased concentric remodeling (P<0.01) and left ventricular torsion (P<0.01), and a decline in diastolic function (P<0.01), cardiac phosphocreatine:ATP ratio (P<0.01), peak exercise cardiac power output (P<0.01), and O2 consumption (P<0.01). Older high-active women demonstrated a phosphocreatine:ATP ratio and relative peak O2 consumption similar to young low-active women, and 23% and 26% higher than older low-active women (phosphocreatine:ATP ratio, 1.9±0.2 versus 1.4±0.1; P<0.05 and O2 consumption, 24.1±3.8 versus 17.8±2.0 mL/[kg·min]; P<0.01). In older women, physical activity had no effect on eccentricity ratio (0.9±0.2 versus 0.8±0.1 g/mL; P=0.19), E/A ratio (1.3±0.5 versus 1.4±0.5; P=0.66), torsion (7.6±1.7 versus 8.0°±2.1°; P=0.20), and peak cardiac power output (3.4±0.7 versus 3.4±0.8 W; P=0.91).CONCLUSIONS: A higher level of daily physical activity preserves cardiac metabolism and exercise capacity with aging but has limited effect on age-related changes in concentric remodeling, diastolic function, and cardiac performance. © 2014 American Heart Association, Inc.

Yeung E.H.,Mahatma Jyotiba Phule Rohilkhand University
Hypertension | Year: 2014

Copeptin, a surrogate biomarker of vasopressin, has been associated with renal function decline and may serve as a useful early biomarker for preeclampsia. We measured serum copeptin using samples collected longitudinally during pregnancy among unaffected controls (n=136) and cases of preeclampsia (n=169), gestational diabetes mellitus (n=92), gestational hypertension (n=101), and preterm birth (n=86) in the Calcium for Preeclampsia Prevention trial (1992–1995). Preeclampsia and gestational hypertension were defined as having a diastolic blood pressure ≥90 mm Hg on 2 occasions with and without proteinuria, respectively. The risk of pregnancy complications associated with copeptin was estimated by logistic regression adjusting for maternal age, race, body mass index, insurance status, marital status, current smoking, and clinical site. Baseline copeptin levels, at mean 16 weeks of gestation, were associated with increased preeclampsia risk (adjusted odds ratios and 95% confidence interval being 1.55 per log unit; 1.03–2.31) when compared with controls (P=0.03). The association was stronger among cases diagnosed before 37 weeks (1.86; 1.08–3.20) than those diagnosed later (1.45; 0.91–2.32). Copeptin levels rose with increasing gestational age in both cases and controls but remained significantly higher among those who were diagnosed with preeclampsia. Differences in levels of copeptin between cases and controls became more apparent closer to time of diagnosis. No significant associations were found for gestational hypertension without proteinuria, gestational diabetes mellitus, or preterm birth without preeclampsia. Copeptin levels are elevated in pregnant women before diagnosis of preeclampsia with elevation specific to this pregnancy complication rather than hypertension alone. © 2014 American Heart Association, Inc

Wong M.K.Y.,Mahatma Jyotiba Phule Rohilkhand University
Circulation | Year: 2014

BACKGROUND—: Out-of-hospital cardiac arrest (OHCA) is associated with a poor prognosis and poses a significant burden to the healthcare system, but few studies have evaluated whether OHCA incidence and survival have changed over time.METHODS AND RESULTS—: A population-based cohort study was conducted, including 34 291 OHCA patients >20 years ofage who were transported alive to the emergency department of an acute-care hospital from April 1, 2002, to March 31, 2012, in Ontario, Canada. Patients with life-threatening trauma and those who died before hospital arrival were excluded. The overall age- and sex-standardized incidence of OHCA patients who were transported alive was 36 cases per 100 000 persons and did not significantly change over the study period. Cardiac risk factor prevalence increased significantly, whereas the rate of most cardiovascular conditions decreased significantly. The 30-day survival improved from 9.4% in 2002 to 13.6% in 2011; 1-year survival improved from 7.7% to 11.8% (P<0.001). Patients hospitalized in 2011 were significantly more likely to survive 30 days (adjusted odds ratio, 1.47 [95% CI, 1.22–1.77]) and 1 year (adjusted odds ratio, 1.55 [95% CI, 1.27–1.91]) compared with 2002. A significant interaction between temporal trends in survival improvement and age group was observed in which the improvement in survival was largest in the youngest age groups.CONCLUSIONS—: OHCA patients who were transported alive are increasingly likely to have cardiovascular risk factors but less likely to have previous cardiovascular conditions. The overall incidence of OHCA patients transported to hospital alive did not change over the past decade. Short- and longer-term survival after OHCA has substantially improved, with younger patients experiencing the greatest improvement. © 2014 by the American College of Cardiology Foundation and the American Heart Association, Inc.

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