There should be two systems studying from complex human system:pleurodiaphragmatic interspace systems of narrow-meaning and broad-meaning.The narrow-meaning one's connotation:a vertical hidden pleurodiaphragmatic interspace,the structure of 2 horizontal pleurodiaphragmatic interspace;the broad-meaning one's connotation:the relation structure of ① 9 fault horizontal pleurodiaphragmatic interspaces,② 9 straight vertical pleurodiaphragmatic interspaces,③pleurodiaphragmatic interspaces of 18 horizontal-wheel cross sections.Tri-jiao is the human's giant system of Qi function of essential Qi,deciding the functional level of pleurodiaphragmatic interspace.The large system of functional level governs all the sub-systems.All levels of systems control the relation net knob of intersected pleurodiaphragmatic interspaces;the relation net knob corresponds to unit deciding the special structures of all systems of pleurodiaphragmatic interspaces.The systemic pleurodiaphragmatic interspace theory is based on the classic subject of tri-jiao—the door of pleurodiaphragmatic interspace.Mr.Xue Shengbai's principle has outstanding initial achievement in analyzing the subject,opening the secret gate of tri-jiao,guiding the sealed and blurred pleurodiaphragmatic interspace theory into complex systemic research,activating the horizontal confusing pleurodiaphragmatic interspace into dimensional structural space,promoting it stand up and walk and be alive,also bringing it into the big system of tri-jiao Qi function,making the integrated constant move theory connected in levels of governing,abiding,being through,collateral and simplicity,finally falling down the spot of effective clinical treatment,with decoction corresponding to sign,developing creative modern model of TCM systemic pleurodiaphragmatic interspace theory.

Apply systemic complex study method to make multi-level and visual field study on Pleurodiaphragmatic Interspace Principle of febrile disease,aiming to expose occurrence principle of Pleurodiaphragmatic Interspace syndrome science,its form position,physiological function and pathological mechanism,syndrome state as well.Its syndrome types;explore its connotation in broad and narrow meanings,define the relation structure and functional level of Pleurodiaphragmatic Interspace and Shaoyang,half superficial and inner of triple energizer,offer reference and effective resource for modern clinical infectious disease,acute contagion,type A H1N1,esp.the treatment based on differentiation of signs of "latent pathogeny in Pleurodiaphragmatic Interspace",one of wet hot febrile and pestilence diseases in Jiangnan,Lingnan and Liangguang region.

Objective To investigate the effects of methycobal on the expression of Caspase-3 in brain tissue after cerebral ischemia reperfusion in rats. Methods Rats were randomly divided into sham-operation group, model control group, nimodipine group and low-dose methycobal group, high-dose methycobal group(n=30 in each group).Rats in the sham-operation group and model control group were administered intragastrically with 0.9% sodium chloride solution, rats in the nimodipine group were treated with 1 mg . kg-1 . d-1 of nimodipine, rats in the low- and high-dose of methycobal groups were given 50 and 100 μg.kg-1 .d-1 of methycobal, respectively. The rat model of cerebral ischemia reperfusion was established by middle cerebral artery occlusion with suture method for 3 h.Neurological deficit scores were evaluated 24 h after reperfusion.The apoptosis of perifocal cortex cells was detected by TUNEL method and the expression of Caspase-3 was analyzed by RT-PCR 6, 12 and 24 h after reperfusion. Results Neurological deficit scores in model control group, nimodipine group, low-dose methycobal group and high-dose methycobal group were 2.70±0.52, 1.30±0.51, 2.20±0.75 and 1.30±0.81, respectively.Compared with model control group, neurological deficit scores were significantly different in the nimodipine group, low-dose methycobal group and high-dose methycobal group(P<0.05 or P<0.01).There were no significant differences between the high-dose methycobal group and nimodipine group ( P>0. 05 ) . There was a significant difference between the high-dose methycobal group and low-dose methycobal group( P<0. 05 ) . The results of apoptosis by TUNEL were as follows: compared with model control group, the apoptosis decreased obvsiouly in the nimodipine group, low-dose methycobal group, and high-dose methycobal group at each time point.There was significant difference between the high-dose methycobal group and nimodipine group at the end of the 24th hours (P<0.01).Compared with low-dose methycobal group, there were significant differences in the high-dose methycobal group at the end of 6th, 12th and 24th hours(P<0.01 or P<0.05).The results of RT-PCR were as follows: there was expression of caspase-3 mRNA in the perifocal cortex of all groups, with weak expression in the sham-operation group.Compared with the sham-operation group, the expression of caspase-3 mRNA was increased significantly in the model control group(P<0.01).The expression of caspase-3 mRNA was reduced significantly in the nimodipine group, the low-dose methycobal group and high-dose methycobal group as compared with model control group at each time point( P<0.05 or P<0.01) , but it was not significantly different in the low-dose methycobal group and high-dose methycobal group as compared with that of the nimodipine group(P>0.05).There were significant differences between the high-dose methycobal group and low-dose methycobal group at the end of 24 h(P<0.05). Conclusion Methycobal can protect the brain cells from injury after cerebral ischemia reperfusion by adjusting the expression of Caspase-3m RNA, and the high-dose methycobal is more effective.

Objective To evaluate the effects of sinomenine on the expression of hypoxia-inducible factor-1α (HIF-1α) and vascular endothelial growth factor (VEGF) during renal ischemia-reperfusion (I/ R) in rats.Methods Fifty-four male Wistar rats, weighing 180-220 g, were randomly divided into 3 groups (n=18 each) using a random number table: sham operation group (group S) , group I/R and sinomenine group (group SIN).Renal I/R was induced by clamping the left renal pedicle for 45 min followed by reperfusion in I/R and SIN groups.In group S, the bilateral renal pedicels were only exposed.Sinomenine 60 mg/kg was intraperitoneally injected at 30 min before reperfusion in group SIN, while the equal volume of normal saline was given in group S and group I/R.At 6, 12 and 24 h (T1-3) of reperfusion, 6 rats from each group were chosen, and blood samples were drawn from the hearts for determination of the serum creatinine (Cr) and blood urea nitrogen (BUN) concentrations.The animals were then sacrificed, and the left kidney was removed and embedded into a paraffin block for determination of the expression of HIF-1α and VEGF in the renal tissues (by immuno-histochemistry).Results Compared with group S, the serum Cr and BUN concentrations were significantly increased at T1-3 , and the expression of HIF-1α was significantly up-regulated at T2,3 in group I/R and group SIN, and the expression of VEGF was significantly upregulated at T2,3in group I/R, and at T1-3 in group SIN.Compared with group I/R, the serum Cr concentration at T1-3 and serum BUN concentration at T2,3 were significantly decreased and the expression of HIF-1α at T2,3and VEGF at T1-3was significantly up-regulated in group SIN.Conclusion The mechanism by which sinomenine attenuates renal I/R injury is related to up-regulation of the expression of HIF-1α and VEGF in the renal tissues of rats.

Objective To investigate the effect of sinomenine on the levels of nuclear factor kappa B (NF-κB) and inducible nitric oxide synthase (iNOS) during renal ischemia-reperfusion (I/R) in rats.Methods Seventy-two healthy male Wistar rats, aged 6-9 weeks, weighing 180-220 g, were randomly assigned into 4 groups (n =18 each) using a random number table: control group (group C), sinomenine group (group SIN), group I/R, and sinomenine+I/R group (group SIN+I/R).The animals were anesthetized with 10％ chloral hydrate 350 mg/kg.The left renal pedicles were clamped with atraumatic microclips for 45 min followed by reperfusion, and the right kidney was removed immediately after onset of reperfusion to establish the model of renal I/R injury.Sinomenine 60 mg/kg was injected intraperitoneally at 30 min before reperfusion in group SIN +I/R, and at the corresponding time point in group SIN.At 6, 8 and 12 h of reperfusion, the blood samples were drawn by cardiac puncture for measurement of serum creatinine (Cr) and blood urea nitrogen (BUN) concentrations.The left renal specimens were obtained for examination of pathological changes (with light microscopes) and for determination of the rate of NF-κB-positive cells and iNOS expression in renal tissues (by immunohistochemistry).Results Compared with group C, the concentrations of serum Cr and BUN, and rate of NF-κB-positive cells were significantly increased, and the expression of iNOS was up-regulated in I/R and SIN+I/R groups, and no significant change was found in the parameters mentioned above in group SIN.Compared with group I/R, the concentrations of serum Cr and BUN, and rate of NF-κB-positive cells were significantly decreased, and the expression of iNOS was down-regulated in group SIN+I/R.The microscopic examination showed that the pathological changes of kidney were significantly attenuated in group SIN+I/R compared with group I/R.Conclusion The mechanism by which sinomenine attenuates renal I/R injury is related to inhibited activity of NF-κB and down-regulated expression of iNOS in rats.

Objective To evaluate the effect of sinomenine on apoptosis in renal tubular epithelial cells of rats subjected to renal ischemia-reperfusion (I/R), and the relationship with C-Jun N-terminal kinase (JNK) signaling pathway.Methods Fifty-four male Wistar rats, aged 6-8 weeks, weighing 180-220 g, were randomly divided into 3 groups (n =18 each) using a random number table: sham operation group (group S), I/R group and sinomenine group (group SIN).Renal ischemia was induced by occlusion of the left renal pedicle for 45 min followed by reperfusion, and the right kidney was removed immediately after onset of reperfusion in anesthetized rats in I/R and SIN groups.In group SIN, sinomenine 60 mg/kg was injected intraperitoneally at 30 min before reperfusion, while the equal volume of normal saline was given instead of sinomenine at the same time point in S and I/R groups.Six animals in each group were selected at 0.5, 6 and 24 h of reperfusion, blood samples were collected by cardiac puncture for determination of serum creatinine (Cr) and blood urea nitrogen (BUN) concentrations.Immediately after blood sampling, the left kidney was removed for examination of pathological changes in renal tissues (with light microscopes) and for determination of phosphorylated JNK (p-JNK) and caspase-3 expression (by immune-histochemistry) and apoptosis in renal tubular epithelial cells (by TUNEL).The apoptotic rate was calculated.Results Compared with group S, the serum Cr and BUN concentrations were significantly increased, the expression of p-JNK and caspase-3 was up-regulated, and the apoptotic rate was increased in I/R and SIN groups.Compared with group I/R, the serum Cr and BUN concentrations were significantly decreased, the expression of p-JNK and caspase-3 was down-regulated, and the apoptotic rate was decreased in group SIN.The microscopic examination showed that the pathological changes of kidney were significantly attenuated in group SIN compared with group I/R.Conclusion The mechanism by which sinomenine attenuates renal I/R injury is related to inhibited activation of p-JNK signaling pathway and reduced apoptosis in renal tubular epithelial cells of rats.

Objective To evaluate the effect of lappaconitine on renal ischemia-reperfusion (I/R) injury in mice.Methods Thirty-six male Wistar rats,weighing 180-220 g,were randomly divided into 3 groups (n=12 each) using a random number table:sham operation group (group S),group I/R and lappaconitine group (group LA).Renal I/R was induced by occlusion of the left renal pedicle for 45 min with atraumatic microclips followed by reperfusion,and the right kidney was removed after atraumatic microclips were released.At 30 min before reperfusion,lappaconitine 4 mg/kg was injected intraperitoneally in group LA,and normal saline 2 ml was given in S and I/R groups.In group S,the left renal pedicle was only isolated.At 5 and 24 h of reperfusion,blood samples were taken from the inferior vena cava for determination of serum creatinine (Cr) and blood urea nitrogen (BUN) concentrations,and kidney specimens were obtained for histopathologic examination (with light microscope) and for determination of the expression of cyclooxygenase-2 (COX-2) and matrix metalloproteinase-2 (MMP-2) in renal tissues (by immunohistochemistry).Results Compared with group S,the serum Cr and BUN concentrations were significantly increased,and the expression of COX-2 and MMP-2 in renal tissues was up-regulated at 5 and 24 h of reperfusion in I/R and LA groups.Compared with group I/R,the serum Cr and BUN concentrations were significantly decreased,the expression of COX-2 and MMP-2 in renal tissues was down-regulated at 5 and 24 h of reperfusion and histopathologic changes were reduced in group LA.Conclusion Lappaconitine can attenuate renal I/R injury through inhibiting the expression of COX-2 and MMP-2 in rats.

OBJECTIVETo investigate the role of K(Ca)3.1 channel in the proliferation and migration of rat vascular smooth muscle cells of the proliferative phenotype.

METHODSRat vascular smooth muscle cells (VSMCs) were cultured with tissue adhesion method. The morphological characteristics of the fist and ninth passages of VSMCs were observed with light and electron microscopy and immunocytochemistry. The expressions of K(Ca)3.1 channel mRNA and protein in the cells were detected using RT-PCR and immunocytochemistry, respectively. MTT and transwell assay were employed to assess the effect of the K(Ca)3.1 channel blocker TRAM-34 on the proliferation and migration of VSMCs.

RESULTSThe first and ninth passages of VSMCs showed morphological characteristics of contractile and proliferative phenotypes, respectively. Compared with the first- passage cells, the ninth-passage VSMCs exhibited significantly increased K(Ca)3.1 channel mRNA and protein expressions with enhanced cell proliferation and migration (P<0.01), which was inhibited by the application of TRAM-34 (P<0.01). TRAM-34 produced no obvious effect on the first-passage VSMCs.

CONCLUSIONUpregulated expression of K(Ca)3.1 channel can promote the proliferation and migration of rat VSMCs of the proliferative phenotype.

Animals ; Cell Movement ; Cell Proliferation ; Cells, Cultured ; Large-Conductance Calcium-Activated Potassium Channels ; metabolism ; Muscle, Smooth, Vascular ; cytology ; metabolism ; Myocytes, Smooth Muscle ; cytology ; metabolism ; Potassium Channel Blockers ; pharmacology ; Pyrazoles ; pharmacology ; Rats ; Rats, Sprague-Dawley

OBJECTIVE To investigate the effect of diallyl sulfide (DAS) in protection against acute lung injury in rats induced by paraquat(PQ). METHODS A total of 100 male Wistar rats were randomly divided into normal control group,PQ 70 mg·kg-1 model group,and DAS 25,50 and 100 mg·kg-1 treatment groups,with 20 rats in each group. A poisoning model was estalolished after administration ig at a single dose of PQ 70 mg·kg-1,while the normal control group was ip given the same volume of normal saline. DAS 25,50 and 100 mg · kg-1 was intraperitoneally injected 30 min before and after PQ exposure. Five rats in each group were sacrificed at 1,3,6 and 12 h,respectively. The inferior lobe of the right lung was observed by HE staining under an optical microscope. Tissue of the upper lobe of the right lung was used to detect the content of nitric oxide (NO). Alveolar macrophages (AMs) were collected and cultured for 24 h,and the content of nitric oxide synthase(iNOS)in the supernatant was detected. AMs were cultured for 72 h and the expression of iNOS protein in AMs was detected by immunocytochemistry method. RESULTS Compared with normal control group,the alveolar structure of PQ group was severely damaged and the pathological score was significantly increased(P<0.01). The NO content of PQ group was significantly higher than in normal control group(P<0.01). The content and protein expression of iNOS were significantly increased in PQ group(P<0.01). Compared with PQ group,the lung injury score of rats in DAS 50 mg·kg-1 group at 3,6 and 12 h and in the DAS 100 mg·kg-1 group at each time point was decreased(P<0.05). Compared with PQ group,the NO content of DAS 25 and 50 mg · kg-1 group was decreased(P<0.05),and the NO content of DAS 100 mg · kg-1 group was significantly reduced(P<0.01). The content of iNOS was reduced in DAS 100 mg · kg-1 group(P<0.05). Compared with PQ group,the expression of iNOS protein in DAS groups was decreased(P<0.05). CONCLUSION DAS can inhibit the oxidative damage in rats induced by PQ.

Objective To understand patient pathway and clinical characteristics of chronic diseases in urban areas of Shanghai. Methods A total of 10 002 residents were enrolled and assigned to the chronic disease group (including hypertension, diabetes, coronary heart disease, myocardial infarction, and ischemic stroke) and the non-chronic disease group. Body mass index,fasting blood glucose, triglyceride,total cholesterol, high-density lipoprotein cholesterol and low-density lipoprotein cholesterol were tested.Difference of patient pathway and clinical characteristics of those chronic diseases was compared. Results Above chronic diseases were observed in 37.7% participants. About 2/3 diseases were confirmed and 80% patients were followed up in healthcare units not far away from home. Patients with coronary heart disease and myocardial infarction showed more outpatient visit to tertiary hospitals (P＜0. 05 ). However, patients with ischemic stroke had health check, rehabilitation and pharmacy done mainly in local healthcare centers (P＜0. 05 ). Diastolic blood pressure of patients visiting local doctors was significantly decreased (P＜0. 05). Conclusion Some differences in patient pathway were found in this study. Communication and cooperation between medical institutions should be intensified for effective chronic disease control.