Effect Of Diabetes On Endothelial And Plateletts 2019 Pdf
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- Coagulatory Defects in Type-1 and Type-2 Diabetes
- Pathological effects of ionizing radiation: endothelial activation and dysfunction
- Platelets Are at the Nexus of Vascular Diseases
Diabetes both type-1 and type-2 affects millions of individuals worldwide.
Diabetes mellitus is associated with an enhanced risk for cardiovascular disease and its prevalence is increasing. Diabetes induces metabolic stress on blood and vascular cells, promoting platelet activation and vascular dysfunction. The level of vascular cell activation can be measured by the number and phenotype of microparticles found in the circulation. The aim of this study was to investigate the effect of a platelet-inhibitory dose of aspirin on the number and type of microparticles shed to the circulation.. Forty-three diabetic patients were enrolled in the study and received a daily dose of mg of aspirin for 10 days to cover the average platelet life-span in the circulation.
Coagulatory Defects in Type-1 and Type-2 Diabetes
The mean P2Y 12 reaction units PRU on empagliflozin was significantly less than without empagliflozin at baseline The mean difference in PRU was No patients experienced any serious adverse events SAEs. Significantly attenuated platelet reactivity was observed on empagliflozin as compared to without empagliflozin. Further studies are required to confirm these exploratory findings. Funded by the University of the West Indies, St.
Pathological effects of ionizing radiation: endothelial activation and dysfunction
The endothelium, a tissue that forms a single layer of cells lining various organs and cavities of the body, especially the heart and blood as well as lymphatic vessels, plays a complex role in vascular biology. It contributes to key aspects of vascular homeostasis and is also involved in pathophysiological processes, such as thrombosis, inflammation, and hypertension. Epidemiological data show that high doses of ionizing radiation lead to cardiovascular disease over time. The aim of this review is to summarize the current knowledge on endothelial cell activation and dysfunction after ionizing radiation exposure as a central feature preceding the development of cardiovascular diseases. For many years after its discovery in the s, the vascular endothelium was believed to be a mere inert, semipermeable barrier between circulating blood and underlying subendothelial tissues. Numerous subsequent studies have led to the current view of the endothelium as a dynamic heterogeneous and distributed organ with essential secretory, synthetic, metabolic, and immunologic functions [ 1 ]. In the presence of irritant stimuli, such as dyslipidemia [ 2 , 3 ], hypertension [ 4 , 5 , 6 , 7 ], and pro-inflammatory agents [ 8 , 9 , 10 , 11 ], the normal physiological functions of the arterial endothelium are adversely affected [ 12 , 13 ], starting a chain of molecular changes that leads to atherosclerosis and cardiovascular diseases CVDs , including coronary artery disease, carotid artery disease, peripheral artery disease, and ischemic stroke [ 14 , 15 , 16 ].
Although, effects of intensive glycemic control were well profound for prevention of micro-vascular complications as compared to macro-vascular.
Platelets Are at the Nexus of Vascular Diseases
The evidence that exposure to ozone air pollution causes acute cardiovascular effects is mixed. We postulated that exposure to ambient levels of ozone would increase blood markers of systemic inflammation, prothrombotic state, oxidative stress, and vascular dysfunction in healthy older subjects, and that absence of the glutathione S-transferase Mu 1 GSTM1 gene would confer increased susceptibility. This double-blind, randomized, crossover study of 87 healthy volunteers 55—70 years of age was conducted at three sites using a common protocol. Subjects were exposed for 3 h in random order to 0 parts per billion ppb filtered air , 70 ppb, and ppb ozone, alternating 15 min of moderate exercise and rest. Blood was obtained the day before, approximately 4 h after, and approximately 22 h after each exposure.
Platelets are important actors of cardiovascular diseases CVD. Current antiplatelet drugs that inhibit platelet aggregation have been shown to be effective in CVD treatment. However, the management of bleeding complications is still an issue in vascular diseases.
Box , Al-Ahsa, Saudi Arabia. Box , Doha, Qatar. Microparticles MPs are small vesicles shed from the cytoplasmic membrane of healthy, activated, or apoptotic cells.
Metrics details. The incidence and prevalence of diabetes mellitus is rapidly increasing worldwide at an alarming rate. Besides affecting the ability of body to use glucose, it is associated with micro-vascular and macro-vascular complications. Augmented atherosclerosis is documented to be the key factor leading to vascular complications in T2DM patients. The metabolic milieu of T2DM, including insulin resistance, hyperglycemia and release of excess free fatty acids, along with other metabolic abnormalities affects vascular wall by a series of events including endothelial dysfunction, platelet hyperactivity, oxidative stress and low-grade inflammation. Activation of these events further enhances vasoconstriction and promotes thrombus formation, ultimately resulting in the development of atherosclerosis. All these evidences are supported by the clinical trials reporting the importance of endothelial dysfunction and platelet hyperactivity in the pathogenesis of atherosclerotic vascular complications.
Сокращенно NDAKOTA. Подумать. - Что вы имеете в виду. - Да он смеялся над нами. Это же анаграмма. Сьюзан не могла скрыть изумления.
In this review, we try to describe in an organized way the pathophysiological continuity between diabetes mellitus, endothelial dysfunction, and platelet.
Вам нужен ключ. Я поняла так, что весь смысл в том, чтобы его уничтожить. - Верно.
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Невероятно, - подумала она, - двадцать шесть тысяч служащих, двадцатимиллиардный бюджет - и они не могут обойтись без меня в уик-энд. Она поставила машину на зарезервированное за ней место и выключила двигатель.
Клушар проснулся лишь на несколько секунд. Он успел бы вскрикнуть от боли, если бы сильная рука не зажала ему рот. Старик не мог даже пошевелиться.
Беккер не раздумывая просунул ногу в щель и открыл дверь. Но сразу же об этом пожалел. Глаза немца расширились.