AIM : To investigate the effects of FFBHQH on the level of expression of caspase 3 protein of middle cerebral artery in ischemia / reperfusion model and to study its mechanisms in preventing and treating ischemic apoplexy. METHODS : The model of focal cerebral ischemia / reperfusion in rats was established with the suture occluded method. The effects of FFBHQH on the behavior obstacle of rats after MCAO/R 24, 48, and 72 h were observed, and the levels of expression of caspase 3 protein were observed by immunoassay method in rats treated with FFBHQH after the cerebral ischemia / reperfusion. RESULTS : Different degrees of behavior obstacle appeared in rats after MCAO/R 24,48,72 h, and FFBHQH reduced the behavior obstacle grade. After MCAO/R, the expression of caspase 3 protein increased obviously, but FFBHQH reduced the expression. CONCLUSION : FFBHQH can prevent and treat the ischemic apoplexy, and the mechanisms may relate to the calcium antagonism and the prevention of the apoptosis correlated gene such as caspase 3 after cerebral ischemia.

BACKGROUND: Peroxisome proliferation-activated receptor-gamma (PPARγ) is the member of nuclear receptor superfamily, and closely related with the formation of atherosclerosis.OBJECTIVE: To investigate the relationship between PPARγ C161→T gene polymorphism and coronary atherosclerotic heart disease (CAHD).DESIGN: Randomized controlled experiment SETTING: Department of Cardiology, Tonai Hospital of Huazhong University of Science and Technology; Department of Cardiology, Zhongnan Hospital of Wuhan University; Center for Human Genome Research,Huazhong University of Science and Technology; Department of Internal Medicine, Affiliated Hospital of Hubei University of Traditional Chinese Medicine; Institute of Geriatrics, Dongzhimen Hospital, Beijing University of Chinese Medicine PARTICIPANTS: Totally 203 CAHD patients aged (65±11) years, including 129 males and 74 females, were the inpatients and outpatients of Zhongnan Hospital of Wuhan University and Tonai Hospital of Huazhong University of Science and Technology from June 2002 to December 2005.And 156 cases of them were diagnosed by coronary arteriongraphy, among which 43 patients without coronary artery affection or with coronary stricture ＜ 50%, and 113 patients with coronary stricture ＞ 50 %. While 89 healthy physical examinees of Han race and mean (59±9) years old were enrolled as control group, including 56 males and 33 females. There was no blood relationship between controls and patients.METHODS: The experiment was conducted at Tongji Hospital of Huazhong University of Science and Technology from June 2002 to December 2005. PPARγ C161→T gene polymorphism was determined by polymerase chain reaction and restriction endonuclease fragment length polymorphisms. The radio-immunity technique, coronary angiography and clinical routine biochemical index were applied to analyze the genotypic frequency and allele frequency distributions as well as the relation between clinical data, biochemical index and different genotypes. The risk factors of CAHD were estimated in the patients of different genotypes.MAIN OUTCOME MEASURES: The genotypic frequency and allele frequency distributions, the relation between clinical data, biochemical index and different genotypes, along with the blood lipid, blood glucose, fasting insulin and body mass index (BMI).RESULTS: Totally 103 CAHD patients and 89 controls were involved in the result analysis of gene polymorphism and yielded different gene distribution frequencies.① In control group, "T" allele frequency was 0.213 and "C" allele frequency was 0.787, and in CAHD group, "T" allele frequency was 0.192 and "C" allele frequency was 0.808. There was no significant difference in the genotypic frequency and C, T allele frequencies between two groups (P ＞ 0.05).② The CC genotype was dominant in CAHD patients with coronary artery lesions, and showed significant differences from "T"allele carriers (CT+TT) (P ＜ 0.05). The CAHD risk in the "T" allele carries (OR: 0.56, 95% CI: 0.24-0.63) was much lower than that in the CC homozygote (OR: 1.92, 95% CI: 1.09-2.54).③ Apolipoprotein B in patients with CC genotype was obviously higher than that in patients with "T" allele (CT+TT) (P ＜ 0.05), and there was insignificant difference in the insulin resistance index (P ＞ 0.05).CONCLUSION: There is an important correlation between the substitution of PPARγ C161→T and CAHD, and "T" allele carriers demonstrate a lower risk of CAHD.

To summarize Professor TU Jinwen's clinical experience in the treatment of severe influenza based on the “heat toxin theory”. He believed that “heat toxin” is the main disease mechanism of severe influenza， emphasized the pathogenesis process that toxin enters with the pathogenic qi， heat generates by the toxin， and changes initiate from the toxin， and proposed simultaneous treatment of warmth and toxin and combination of multiple methods as the treatment principles. Syndrome differentiation in clinic should combine with wei-qi-ying-blood. The disease in the early stage located in wei （defensive） and qi level， treated by clearing heat and resolving toxins， releasing the exterior and expelling pathogen， harmonizing the exterior and interior， dredging the bowels with diarrhea， and combining other methods to get rid of the heat and toxin， and modified Self-Prescribed Tuire No. 1 Formula （自拟退热1号方） is recommended； the disease in progression stage located in ying-blood， treated by relieving heat and resolving toxins， and clearing the ying level and cool the blood， with prescriptions as modified Self-Prescribed Tuire No. 1 Formula plus Qingying Decoction （清营汤）， or Xijiao Dihuang Decoction （犀角地黄汤）； the disease in the late stage with of yin fluid consumption， and heat toxin in the blood level， treated by eliminating heat and resolving toxins， and enriching yin and cooling the blood， with prescriptions as modified Shashen Maidong Decoction （沙参麦冬汤） and Zhuye Shigao Decoction （竹叶石膏汤）. At the same time， it is emphasised that heat-clearing and fire-draining method and harmonising methods are important， and that dispelling pathogen should not injure healthy qi， and that the selection of prescriptions and medicines need consider syndrome differentiation and treatment.