1.Exploration on Sanjiao Fu Syndrome from Heat Excess Accumulated in Chest
China Journal of Traditional Chinese Medicine and Pharmacy 2005;0(06):-
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.
2.Treatment based on differentiation of cold-heat complication syndrome with six-meridian theory in Treatise on Cold Pathogenic Diseases
China Journal of Traditional Chinese Medicine and Pharmacy 2005;0(03):-
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.
3.Diagnosis and treatment of excessive heat accumulated in chest syndrome which belongs to Fu-viscera disease of sanjiao and its application
China Journal of Traditional Chinese Medicine and Pharmacy 2005;0(01):-
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.
4.Feasibility of integrated detection for coronary heart disease-associated protein factors by coding microsphere suspension chip
Jianhong LI ; Yingfeng LIU ; Fei MIU
Chinese Journal of Tissue Engineering Research 2007;0(22):-
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
5.An exposition of yingfen with connection of cold pathogenic diseases and exogenous epidemic febrile disease (Part 1)——Historical review
Yingfeng LIU ; Lixing HUANG ; Wei ZHAN
China Journal of Traditional Chinese Medicine and Pharmacy 2005;0(07):-
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.
6.An exposition of yingfen with connection of cold pathogenic diseases and exogenous epidemic febrile disease (Part 2): logical integration
Lixing HUANG ; Wei ZHAN ; Yingfeng LIU
China Journal of Traditional Chinese Medicine and Pharmacy 2005;0(08):-
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.
7.Re-discussion on Treatment based on Syndrome Differentiation and its Standardized Operation
Lixing HUANG ; Yingfeng LIU ; Guangrong ZHANG
China Journal of Traditional Chinese Medicine and Pharmacy 2005;0(02):-
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.
8.Effects of edaravone on the expression of TGF-β1 and myocardialfibrosis in rats
Shixiang WANG ; Hongchao WU ; Yingfeng LIU
Tianjin Medical Journal 2016;44(1):67-70
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.
9.Effects of nicorandil on cardiac function and clinical outcomes in patients with acute myocardial infarction undergoing percutaneous coronary intervention
Zhengxin HUANG ; Xianbao WANG ; Yingfeng LIU
The Journal of Practical Medicine 2016;32(4):544-547
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.
10.Effect of esmolol on myocardial apoptosis and cardiac function in rats with sepsis
Dehong LIU ; Yingfeng LIU ; Xinke MENG ; Zhiwei XU
Chongqing Medicine 2014;(31):4181-4184
Objective To investigate the effect of esmolol on myocardial apoptosis and cardiac function in rats with sepsis .Meth‐ods Ninety six SD rats were randomly divided into sham group (n= 32 ,for sham operation) ,sepsis group (n= 32 ,sepsis model) and treatment group (n= 32 ,intravenous infusion with esmolol after sepsis modeling) .At 3 h ,6 h ,12 h ,24 h after operation ,sam‐ples were conserved to measure serum cardiac troponin I (cTnI) ,caspase‐3 ,cardiomyocytes apoptosis index ,and myocardial patho‐morphology was observed by optical microscope .At 24 h after operation ,echocardiography was performed .Results The serum cT‐nI ,caspase‐3 ,cardiomyocytes apoptosis index were increased significantly in sepsis group and treatment group compared with sham group (all P< 0 .05) .After using esmolol ,cTnI and cardiomyocytes apoptosis index were relatively decreased in treatment group compared with sepsis group at the four time‐points(all P < 0 .05) .Caspase‐3 of treatment group decreased at 12 h after operation compared with sepsis group (P< 0 .05) .Treatment group had a higher LVEF than sepsis group at 24 h(P< 0 .05) .Conclusion Es‐molol could inhibit myocardial apoptosis and mitigate the damage of cardiac function in rats with sepsis .The decrease in caspase‐3 may be the mechanism of anti‐apoptosis .