From the aspects of formation mechanism,illness position character,disease attribute and laws and prescriptions of heat excess accumulated in chest,the author gave a profound analysis of the internal relations between heat excess accumulated in chest and the sanjiao fu syndrome.Furthermore it proved sanjiao fu viscera's objective existing and its independent significance from treatment based on syndrome differentiation.

Based on the viewpoint of six meridians separately varying with the pathogenesis of exterior-interior and cold-heat,which is separately dominated by different meridians,this article systematically analyzes and generalizes the connotation of the treatment based on differentiation of various syndromes of cold-heat complication involved in Treatise on Cold Pathogenic Diseases.By delimiting which meridian the cold-heat complication syndrome belong to in six meridians and what the pathogenesis is,the article further promotes the signifi cance of six-meridian theory guiding the treatment based on differentiation of miscellaneous diseases.

This article proposes the integrated outline of excessive heat accumulated in chest syndrome from the view of Fu-viscera disease of sanjiao based on numbers of clinical experiences,which can prove that the objective existence and theory of sanjiao fu-viscera has specific significance.

Three problems of treatment based on syndrome differentiation, TBSD are discussed here. Firstly, in allusion to the diversity of the concept of TBSD, the due medical concept of it are discussed and analyzed. Hence, the actual difference and sameness, the due relationship as well as the principle of management between syndrome differentiation and disease differentiation are fully compared. Finally, the concrete operation procedure of syndrome differentiation and disease differentiation are expounded. The author detailedly introduced particular cognition to standardized operation of TBSD attained from Yao Hesheng, a famous physician in Jiangxi Province.

In view of the contradictory phenomenon between yingfen dominating the interior when suffering exogenous epidemic febrile disease and ying disease dominating the exterior in cold pathogenic diseases,the authors revealed the misunderstanding of yingfen dominating the interior in epidemic febrile disease by a systematical analysis on the headstream of the theory,the connotation for diagnosis and treatment and logical relation. Based on the requirement of the theory guiding the clinical effectively,at the same time,the authors put forward a new opinion on classification of diagnosis and treatment on wei,qi,ying,blood system by the theory of the cold integrating the warm,which was a courageous exploration for the purpose of seeking unity of thinking on syndrome differentiation and treatment of external infection diseases.

In view of the contradictory phenomenon between yingfen dominating the interior when suffering exogenous epidemic febrile disease and ying disease dominating the exterior in cold pathogenic diseases,attemping to get the logical demonstration that cold pathogenic diseases and exogenous epidemic febrile diseases can be integrated by yingfen diseases,the authors made a systematic classification and comparison on basis of the collection of related diagnosis and treatment in respective yingfen diseases of cold pathogenic diseases and exogenous epidemic febrile disease. It was of vital importance to connecting cold pathogenic diseases with exogenous epidemic febrile diseases in classification of diagnosis and treatment in wei,qi,ying,blood system.

AIM: Coding microsphere suspension chip is a novel protein chip technology, which is considered as the developing direction of medical tests. This study investigated the feasibility of coding microsphere suspension chip to detect coronary heart disease (CHD)-associated protein factors. METHODS: The serum samples of 30 patients with CHD were collected including 19 males and 11 females, with average age of (63?10) years in the Department of Cardiology, Zhujiang Hospital of Southern Medical University from August to September 2007. Patients did not have hepatic or renal dysfunction, cerebrovascular accident, acute infection or any anticoagulation medication. The regional ethics committee approved the study protocol and the informed consents were obtained from all subjects. The integrated detection method was established by coding microsphere suspension chip to detect CHD-associated protein factors including high sensitivity C reactive protein (hs-CRP), lipoprotein a (Lpa) and adiponectin (ADPN). Meanwhile, these three factors from 30 CHD cases were detected by the enzyme-linked immunosorbent assay (ELISA). The detection results by both methods were compared. RESULTS: The serum samples of 30 CHD cases were all included in final analysis. The detection results by coding microsphere suspension chip integrated detection method were hs-CRP (2.54?1.97) mg/L, Lpa (102.41?76.74) mg/L and ADPN (15.43? 9.87) mg/L. The detection results by ELISA were hs-CRP (3.93?2.52) mg/L, Lpa (208.63?81.23) mg/L, and ADPN (16.63? 8.21) mg/L. The detection results by coding microsphere suspension chip integrated detection method were correlated significantly to that of ELISA (hs-CRP: r=0.979, P

Objective To investigate the effects of edaravone on myocardial fibrosis induced by isoproterenol (ISO) in rats, and to discuss the correlation between the level of transforming growth factor-β1 (TGF-β1) and the myocardial fibrosis. Methods Forty male SD rats were randomly divided into five groups, namely control group, model group and edaravone groups (low, medium and high doses). Isoproterenol was used to establish the rat model of myocardial fibrosis. Edaravone groups were given edaravone [3, 5 and 10 mg/(kg · d)] to intervene for 14 days. The activity of superoxide dismutase (SOD) and the level of malondialdehyde (MDA) were examined after 15-d treatment. The left ventricular mass index (LVMI) and collagen volume fraction (CVF) were examined. The expression of TGF-β1 was detected by Western blot assay and immuno-fluorescence method. Results The content of MDA and LVMI were significantly higher in model group than those of the control group (P<0.01),whereas the content of SOD was significantly lower in model group than that of the control group (P<0.01). Compared with model group, the expression level of MDA decreased with the increased intervention dose of edara-vone (P<0.05), while SOD expression level increased (P<0.05). There was no significant difference in the level of SOD be-tween middle dose edaravone group and the control group. LVMI was decreased with the increased doses of edaravone ( P<0.01). There was no significant difference in LVMI between the high dose of edaravone group and the control group. Com-pared with the control group, the expression level of TGF-β1 was significantly increased in model group (P<0.01). The ex-pression level of TGF-β1 was reduced with the increased doses of edaravone. CVF was significantly increased in model group compared with that of control group (P<0.001). CVF decreased with the increased doses of edaravone in medium and high doses of edaravone groups, but they were higher than that of control group (P<0.01). TGF-β1 was positively correlated with MDA, LVMI and CVF (r=0.931, 0.879 and 0.930, P<0.001). SOD was negatively correlated with TGF-β1 (r=-0.892, P<0.001). Conclusion Edaravone can relieve myocardial fibrosis by inhibiting oxidative stress and TGF-β1 in rats.

Objective To explore the effects of nicorandil on cardiac function and clinical outcomes in patients with acute myocardial infarction (AMI) undergoing percutaneous coronary intervention (PCI). Method Sixty-six patients with AMI were randomized into a control group and nicorandil group (n = 33 for each group). In the nicorandil group, nicorandil (4 mg as a bolus injection followed by constant infusion at 8 mg/hour for 24 hours) was administered immediately after admission. Reactive oxygen species (ROS) formation was assessed by measuring urinary excretion of 8-epi-prostaglandin F2α (PGF2α) and compared between the two groups; cardiac function and cardiac events were also compared. Results Urinary 8-epi-PGF2αexcretion was increased 2-fold at 60 to 90 minutes after PCI in the control group, whereas it was unchanged in the nicorandil group (P < 0.001). Left ventricular ejection fraction and cardiac index immediately after PCI and at 6 months were greater in the nicorandil group than in the control group(P < 0.05). Rates of total inhospital cardiac events and rehospitalization were lower in the nicorandil group than in the control group (P<0.05). Conclusions Nicorandil improves cardiac function and clinical outcomes in patients with AMI undergoing primary percutaneous coronary intervention. Suppression of ROS formation may be involved in the potential mechanism.

Objective To observe the expression of caspase-3 and transposition of Omi/HtrA2 in H9C2 by erythropoietin and/or Omi/HtrA2 silencing to explore the related anti-apoptotic mechanisms.Methods The cultured H9C2 cardiomyocytes were divided into control group,H/R group (anoxia 2 h and re-oxygenation 24 h), and different concentrations of EPO treatment groups.The release rate of lactate dehydrogenase (LDH)in cell supernatant was measured in each group.Expressions of cleaved caspase-3 and Omi/HtrA2 were measured by Western blot;then the transposition of Omi/HtrA2 between cytoplasm and mitochondria was observed.Specific siRNA interfering fragment was transfected into H9C2 cardiomyocytes by liposome method.Its silencing effect on Omi/HtrA2 was measured by RT-PCR and Western blot.The survival rate,release rate and expression of cleaved caspase-3 were measured.And the expression of Omi/HtrA2 was measured in cytoplasm and mitochondria in H9C2 (transposition of Omi/HtrA2 ).Results Compared with H/R group,the release of LDH and expression of cleaved caspase-3 were decreased; the transposition of Omi/HtrA2 from mitochondria to cytoplasm in H/R treatment groups was increased compared with control group,while that in EPO (20 IU/mL)group decreased.si-HtrA2 group transfected with siRNA showed a decreased release of LDH and expression of cleaved caspase-3 with all significant variances (P <0.05).Conclusion EPO exerts a cytoprotective effect by inhibiting the transposition of Omi/HtrA2 and hence the activation of caspases-3 pathway.