M
Muhammad M. Yaqoob
Researcher at Queen Mary University of London
Publications - 220
Citations - 8649
Muhammad M. Yaqoob is an academic researcher from Queen Mary University of London. The author has contributed to research in topics: Kidney disease & Renal function. The author has an hindex of 48, co-authored 202 publications receiving 7977 citations. Previous affiliations of Muhammad M. Yaqoob include University of London & University of Colorado Denver.
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Bicarbonate Supplementation Slows Progression of CKD and Improves Nutritional Status
TL;DR: It is demonstrated that bicarbonate supplementation slows the rate of progression of renal failure to ESRD and improves nutritional status among patients with CKD and Nutritional parameters improved significantly with bic carbonate supplementation, which was well tolerated.
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Erythropoietin Protects the Kidney against the Injury and Dysfunction Caused by Ischemia-Reperfusion
Edward Sharples,Nimesh S. A. Patel,Paul A.J. Brown,Keith Nicol Stewart,Helder Mota-Philipe,Michael Sheaff,Julius Kieswich,David A. Allen,Steven Harwood,Martin Raftery,Christoph Thiemermann,Muhammad M. Yaqoob +11 more
TL;DR: It is shown that a single systemic administration of EPO either preischemia or just before reperfusion prevents ischemia-reperfusion injury in the rat kidney and may have major implications in the treatment of acute renal tubular damage.
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Hematopoietic prostaglandin D2 synthase controls the onset and resolution of acute inflammation through PGD2 and 15-deoxyDelta12 14 PGJ2.
Ravindra Rajakariar,Mark Hilliard,Toby Lawrence,Seema G. Trivedi,Paul Colville-Nash,G. Bellingan,Desmond J. Fitzgerald,Muhammad M. Yaqoob,Derek W. Gilroy +8 more
TL;DR: This work provides definitive proof that 15d-PGJ2 is synthesized during mammalian inflammatory responses, and highlights DP1 receptor activation as a potential antiinflammatory strategy.
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Mechanisms of high glucose-induced apoptosis and its relationship to diabetic complications
TL;DR: The relationship between high glucose-induced oxidative stress and apoptosis are discussed here with reference to additional regulators of apoptosis such as the mitogen-activated protein kinases (MAPKs) and cell-cycle regulators.
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High glucose-induced oxidative stress causes apoptosis in proximal tubular epithelial cells and is mediated by multiple caspases
TL;DR: It is demonstrated that high glucose causes the generation of ONOO−, leading to caspase‐mediated apoptosis, implicating OnOO− as a proapoptotic ROS in early diabetic nephropathy.