[Distribution characteristics of traditional Chinese medicine syndromes and their elements in people with subhealth fatigue].

OBJECTIVE: To investigate the characteristics of traditional Chinese medicine (TCM) syndromes and their elements in people with subhealth fatigue. METHODS: The TCM symptoms in line with the diagnostic criteria of subhealth fatigue status were collected by clinical investigations and using information collection form based on TCM four diagnostic methods. Referred to Clinical Guidelines of Chinese Medicine on Subhealth and other related standards, the syndrome type was identified in accordance with clinical symptoms of each patient with subhealth fatigue by two physicians. The data of syndrome differentiation were analyzed by descriptive statistical analysis. RESULTS: There were 81 syndrome types from 495 cases of subhealth fatigue. There were 24 syndrome types after separation, and the top ten were liver stagnation and spleen deficiency, stagnation of liver qi, hyperactivity of liver fire, disharmony between liver and stomach, damp obstruction due to spleen deficiency, deficiency of both heart and spleen, yin deficiency of liver and kidney, yang deficiency of spleen and kidney, stagnation of gallbladder and disturbance of phlegm, and internal disturbance of phlegm-heat. There were 17 syndrome elements, including seven disease location elements and ten disease nature elements. The disease location elements were liver, spleen, kidney, stomach, heart, gallbladder and lung. The disease nature elements were qi stagnation, qi deficiency, exuberance of fire (heat), damp obstruction, phlegm obstruction, yin deficiency, adverse flow of qi, yang deficiency, blood deficiency, and blood stasis. CONCLUSION: Syndrome types of subhealth fatigue involve in deficiency syndrome, excess syndrome, and mixture of deficiency and excess syndromes. The syndrome elements of disease location involve five zang organs and two fu organs, and the liver and spleen were the most frequently involved organs. The syndrome elements of disease nature involve deficiency and excess. Qi stagnation is most frequently involved in the excess syndrome, and qi deficiency is most frequently involved in the deficiency syndrome.

Impairment of cardiac function and remodeling induced by myocardial infarction in rats are attenuated by the nonpeptide angiotensin-(1-7) analog AVE 0991.

AIMS: We evaluated effects of the nonpeptide angiotensin (ANG)-(1-7) analog AVE 0991 (AVE) on cardiac function and remodeling as well as transforming growth factor-beta1 (TGF-ß1)/tumor necrosis factor-alpha (TNF-α) expression in myocardial infarction rat models. METHODS AND RESULTS: Sprague-Dawley rats underwent either sham surgery or coronary ligation. They were divided into four groups: sham, control, AVE, and AVE+A-779 [[D-Ala(7) ]-ANG-(1-7), a selective antagonist for the ANG-(1-7)] group. After 4 weeks of treatment, the AVE group displayed a significant elevation in left ventricular fractional shorting (LVFS) (25.5 ± 7.3% vs. 18.4 ± 3.3%, P < 0.05) and left ventricular ejection fraction (LVEF) (44.8 ± 7.6% vs. 32.7 ± 6.5%, P < 0.05) when compared to the control group, but no effects on the left ventricular end-diastolic and end-systolic diameters (LVDd and LVDs, respectively) were observed. In addition, we found that the myocyte diameter (18 ± 2 µm vs. 22 ± 4 µm, P < 0.05), infarct size (42.6 ± 3.6% vs. 50.9 ± 4.4%, P < 0.001) and collagen volume fraction (CVF) (16.4 ± 2.2% vs. 25.3 ± 3.2%, P < 0.001) were significantly reduced in the AVE group when compared to the control group. There were no differences in LVFS, LVEF, myocyte diameter, and infarct size between the control and AVE+A-779 groups. AVE also markedly attenuated the increased mRNA expression of collagen I (P < 0.001) and collagen III (P < 0.001) and inhibited the overexpression of TGF-ß1 (P < 0.05) and TNF-α (P < 0.05) compared to the control group. CONCLUSION: AVE could improve cardiac function and attenuate ventricular remodeling in MI rat models. It may involve the inhibition of inflammatory factors TGF-ß1/TNF-α overexpression and the action on the specific receptor Mas of ANG-(1-7).