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Gernot Beutel Ronny Perthel Mayuren Suntharalingam Stefanie M. Bode-Böger Jens Martens-Lobenhoffer Jan T. Kielstein Heike Kielstein 《Annals of hematology》2013,92(4):505-508
The endogenous nitric oxide synthase inhibitor asymmetric dimethylarginine (ADMA) is elevated in both animal models of chronic inflammatory disorders as well as in patients with chronic inflammatory disease. In vivo data suggest that ADMA can increase the number of circulating monocytes and possibly affect their adhesion potential in vitro. The aim of our study was to evaluate possible effects of chronically elevated levels of ADMA on white blood cell count (WBC), leukocyte subsets, and WBC distribution pattern using a model of chronic exogenous ADMA infusion. Male Sprague–Dawley rats (n?=?20, 10 weeks of age) were randomized to receive either (1) isotonic saline or (2) ADMA applied by osmotic mini pumps. After 28 days of infusion, all animals were sacrificed for blood and tissue sampling. WBC count, flow cytometry for subtype assessment, and histological assessment were performed. Over a time period of 28 days, continuous ADMA infusion significantly increased mean plasma levels (1.26?±?0.07 μmol/l) as compared to saline infusion (0.57?±?0.02 μmol/l). Clinical side effects were not observed. Despite a physiologically relevant rise in ADMA plasma levels, measured by decrease of the l-arginine/AMDA ratio—a surrogate parameter of NO production capacity—there was no effect on WBC count or pattern of leukocyte subsets. Numbers and morphology of peripheral blood cells as well as number of NK-cells leveling liver and spleen were not affected by chronic ADMA infusion. Chronically elevated ADMA levels in otherwise healthy rats did not affect WBC counts or leukocyte subsets. Furthermore, anemia frequently found in patients with progressive renal failure and elevated ADMA levels, was not observed. In a chronic inflammatory state, elevated ADMA levels themselves are rather the result than the cause of the underlying inflammatory process. 相似文献
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Pandey Manisha Choudhury Hira Vijayagomaran Prathiba A/P Lian Pauline Ng Poh Ning Tan Jing Wai Ng Zing Xian-Zhuang Ng Le Er Chong Rahmah Nur Suraiza Nabila Kamaruzzaman Nur Dayana Binti Mayuren Jayashree Candasamy Mayuren Gorain Bapi Chawla Pooja A. Amin Mohd Cairul Iqbal Mohd 《Pharmaceutical research》2022,39(6):1115-1134
Pharmaceutical Research - Cancer is associated with a comprehensive burden that significantly affects patient’s quality of life. Even though patients’ disease condition is improving... 相似文献
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Safa Abdelgadir Mohamed Elhassan Mayuren Candasamy Elaine Wan Ling Chan Subrat Kumar Bhattamisra 《Diabetes & Metabolic Syndrome: Clinical Research & Reviews》2018,12(6):1109-1116
Background
Autophagy is a process devoted to degrade and recycle cellular components inside mammalian cells through lysosomal system. It plays a main function in the pathophysiology of several diseases. In type 2 diabetes, works demonstrated the dual functions of autophagy in diabetes biology. Studies had approved the role of autophagy in promoting different routes for movement of integral membrane proteins to the plasma membrane. But its role in regulation of GLUT4 trafficking has not been widely observed. In normal conditions, insulin promotes GLUT4 translocation from intracellular membrane compartments to the plasma membrane, while in type 2 diabetes defects occur in this translocation.Method
Intriguing evidences discussed the contribution of different intracellular compartments in autophagy membrane formation. Furthermore, autophagy serves to mobilise membranes within cells, thereby promoting cytoplasmic components reorganisation. The intent of this review is to focus on the possibility of autophagy to act as a carrier for GLUT4 through regulating GLUT4 endocytosis, intracellular trafficking in different compartments, and translocation to cell membrane.Results
The common themes of autophagy and GLUT4 have been highlighted. The review discussed the overlapping of endocytosis mechanism and intracellular compartments, and has shown that autophagy and GLUT4 utilise similar proteins (SNAREs) which are used for exocytosis. On top of that, PI3K and AMPK also control both autophagy and GLUT4.Conclusion
The control of GLUT4 trafficking through autophagy could be a promising field for treating type 2 diabetes. 相似文献6.
Vikram Rao B. Vasanth Rao Mayuren Candasamy Subrat Kumar Bhattamisra 《Diabetes & Metabolic Syndrome: Clinical Research & Reviews》2019,13(3):2112-2120
Obesity is a complex disorder that is linked to many coexisting disorders. Recent epidemiological data have suggested that the prevalence of obesity is at an all-time high, growing to be one of the world's biggest problems. There are several mechanisms on how individuals develop obesity which includes genetic and environmental factors. Not only does obesity contribute to other health issues but it also greatly affects the quality of life, physical ability, mental strength and imposes a huge burden in terms of healthcare costs. Along with that, obesity is associated with the risk of mortality and has been shown to reduce the median survival rate. Obesity is basically when the body is not able to balance energy intake and output. When energy intake exceeds energy expenditure, excess calories will be stored as fat leading to weight gain and eventually obesity. The therapeutic market for treating obesity is composed of many different interventions from lifestyle intervention, surgical procedures to pharmacotherapeutic approaches. All of these interventions have their respective benefits and disadvantages and are specifically prescribed to a patient based on the severity of their obesity as well as the existence of other health conditions. This review discusses the genetic and environmental causes of obesity along with the recent developments in anti-obesity therapies. 相似文献
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