BackgroundRheological disorders of red blood cells (RBC) and decreased RBC deformability have been involved in the development of diabetic microangiopathy. However, few studies have evaluated the association of RBC count with microvascular complications in patients with type 2 diabetes mellitus (T2DM). The purpose of this study was to investigate the association of RBC count with microvascular complications in patients with T2DM.MethodsThis study involved 369 patients with T2DM: 243 with one or more microvascular complications and 126 without microvascular complications. Anticoagulated blood was collected and analyzed in an automated blood cell counter. The presence of risk factors for microvascular complications was determined.ResultsThe proportion of patients with microvascular complications increased as the RBC count decreased (P < 0.001). After adjustment for known risk factors for microvascular complications by logistic regression analysis, lower quartiles of RBC count were associated with a higher risk of microvascular complications compared with the reference group composed of the highest quartile (first quartile, odds ratio 4.98, 95% confidence interval 1.54–6.19, P = 0.008; second quartile, odds ratio 3.21, 95% confidence interval 1.17–5.28, P = 0.024).ConclusionA decreased RBC count is associated with microvascular complications in Chinese patients with T2DM. The RBC count is a potential marker to improve further the ability to identify diabetic patients at high risk of microvascular complications.
Myocarditis is an inflammatory disease of the heart and a major cause of dilated cardiomyopathy that can lead to heart failure and sudden death in young adults. Giant cell myocarditis is a severe heart disease of unknown causes and is defined histopathologically as diffuse myocardial necrosis with multinucleated giant cells in the absence of sarcoid-like granulomata. Giant cell myocarditis is often studied using a model of experimental autoimmune myocarditis (EAM) in rats. Emodin is an important component of traditional Chinese herb rhubarb, and has well-documented anti-inflammatory effect. The current study determined the potential efficacy of emodin using a rat model of EAM. Male Lewis rats (6 weeks of age) were immunized on days 0 and 7 with a porcine cardiac myosin at both footpads to induce EAM. Simultaneously with the immunization, rats received emodin (50 mg/kg/day) or distilled water by intragastric administration for 3 weeks (8 animals/group). Likewise, eight animals were immunized with adjuvant alone and treated with distilled water. The immunization significantly enlarged the hearts due to inflammatory lesions. Emodin treatment significantly improved left ventricular (LV) function and reduced the severity of myocarditis, as reflected by echocardiographic and histopathological examination. Emodin treatment decreased the serum levels of proinflammatory cytokines tumor necrosis factor (TNF)-α and interleukin (IL)-1β . Nuclear factor-κBp65 (NF-κBp65), a rapid-response transcription factor that regulates proinflammatory cytokines, in the myocardial tissue was also suppressed in the treated rats. In conclusion, emodin could ameliorate EAM, at least in part, by decreasing the production of proinflammatory cytokines TNF-α and IL-1β.
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