Objective To investigate serum leptin and adiponectin levels and their relationship in elderly coronary artery disease (CAD).Methods A total of 88 subjects aged 55 yeas or older were enrolled in which coronary angiograms were performed.The subjects were divided into CAD group (52 patients) and control group (36 patients) by angiography.Serum concentrations of leptin and adiponectin were evaluated by ELISA system.Results Serum concentrations of leptin were significantly increased in CAD group compared with that in control group [(9.38 ±3.51) μg/L vs.(7.27 ±3.25) μg/L,P ＜0.05].On the contrary,serum concentrations of adiponectin were significantly decreased in CAD group compared with that in control group [(11.08 ±3.87) mg/L vs.(13.34 ±4.94) mg/L,P＜0.05].Logistic regression analysis revealed that only serum leptin was the independent risk factor for CAD.Serum adiponectin concentrations had a negative relationship with leptin concentrations (r =-0.320,P =0.002).Conclusion Lower serum adiponectin levels are related to higher serum leptin concentrations.Elevated serum leptin but not decreased serum adiponectin is the independent risk factor for CAD.

Objective:To observe the effect of Tangshenning on renal function and LOX-1 mRNA expression in the kidney of early diabetic nephropathy rats model. Methods:Early diabetic nephropathy rats model was made with high fat diet, STZ and unilateral ne-phregtomy. After the 12-week drug intervention, the rats were sacrificed, the kidneys were removed and the mRNA expressions of LOX-1 in the kidney were observed by the method of RT-PCR. Results:Early diabetic nephropathy rats model was successfully made by the triple-modeling method. The mRNA expression of LOX-1 in the kidney was significantly increased, and Tangshenning could low-er the expression of LOX-1 in the kidney in a dose-dependent manner. Conclusion:The abnormal expression of LOX-1 could be one of the mechanisms for diabetic nephropathy. Tangshening has good kidney protective effect through decreasing LOX-1 abnormal expression in the kidneys, which deserves further research.

Objective To observe the effect of Tanggankang on the expression of CREB in diabetic-fatty liver rats;To investigate the mechanism of Tanggankang. Methods STZ and feeding high fat forage induced diabetic rats were randomly divided into model group, Huganning group, Tanggankang high dose group, Tanggankang medium dose group, Tanggankang low dose group, 10 rats in each group, with 10 normal rats as control. After 12 weeks of drug intervention, rats were killed, the livers were removed, and the expression of CREB was detected by Western blot. Results Compared with normal group, the level of CREB of model group was significantly decreased (P<0.01). Compared with model group, Tanggankang low, medium and high dose group significantly decreased the level of CREB (P<0.01). Conclusion Tanggankang may play an active role in glucose and lipid metabolism by affecting the expression of CREB.

AIM: To investigate the effects of leptin (LEP) on the alveolar type Ⅱ cells(AECⅡ) apoptosis induced by Na2S2O4 and explore the molecular mechanisms. METHODS: Primary AECⅡ culture was prepared according to a specific immunosorption procedure with slight modification and the cells were identified by transmission electron microscope and immunocytochemistry. AECⅡ damage was induced by 5 mmol/L Na2S2O4. LEP group cells were treated with LEP at concentrations from 100 ?g/L to 1 600 ?g/L. The cell survival rate was evaluated by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assays. Cell cycle and apoptosis were analyzed by flow cytometry and the level of caspase-3 was measured by Western blotting. RESULTS: Highly purified AECⅡ, obtained by the method of modified immunosorption, were identified with the positive expression of SP-A and intracellular lamellarbodies were found under electron micrography. The cells, exposed to 5 mmol/L Na2S2O4, showed characteristic changes of apoptosis and activation of caspase 3. These damages were relieved by the treatment of LEP (100-1 600 ?g/L), with survival increasing, apoptosis peak decreasing, cell morphology restoring and caspase 3 activation inhibiting.CONCLUSION: Leptin prevents AECⅡ from apoptosis induced by Na2S2O4 or hypoxia. The potential mechanism of its action may be related to promoting cell cycle from G1 phase to S phase and inhibiting the activating of caspase 3.

AIM: To observe whether arachidonic acid (AA) could induce apoptosis in mouse fibroblast cell line L929 and the potential mechanism involved. METHODS: The viability and damaged degree of L929 was monitored by MTT and the release of lactate dehydrogenase (LDH). Lipid peroxidation in L929 was measured as malondialdehyde (MDA) content by colorimetric assay. Hoechst 33258 staining was used to observe AA-induced morphological changes. Agarose gel electrophoresis was used to detect DNA fragmentation. RESULTS: Treatment of L929 cell with AA for 24 h, in the range of 40-160 ?mol/L, caused a great decrease in cell survival and increased MDA contents and the release of LDH simultaneously( P

Objective To investigate the protective effect of protocatechuic acid(PCA)on the PC12 cell model of Alzheimer’s disease(AD)and to explore its mechanism . Methods Amyloid beta peptide 1-42(Aβ1-42)fiber polymers were identified by immunofluorescence. After PC12 cells were stimulated with the Aβ1-42 fiber polymers, the cellular morphology was observed at different time points of hour 0, 3, 6, 9, 12, 24 , and the cellular viability was tested by methyl thiazolyl tetrazolium(MTT)assay to monitor the modeling condition. The effect of PCA on PC12 cells was detected after PC12 cells were pretreated with the different contentions of PCA. Autophagy-related marker Beclin1 protein level was detected by Western blotting method to investigate the protective mechanism of PCA. Results Aggregated white Aβ1-42 mass was stable at hour 12 and 24, and showed no significant difference between the two time points, the cell damage rate being 40%. Therefore, we defined culturing time being 12 and 24 hours as the modeling condition of AD model. The cell viability was increased with 200-800 μmol/L of PCA after culturing for 24 hours(P<0.01) , and the Western blotting results showed that the Beclin1 protein expression was up-regulated by PCA. Conclusion PCA prevents PC12 cells from Aβ1-42-induced toxicity, the mechanism being related with the increase of cellular autophagy.

Objective To explore the feasibility of mechanical chest compression to establish a rat model of car?diopulmonary resuscitation ( CPR) . Methods 4?month old healthy male Sprague Dawley rats were randomly divided into control group ( n=6 ) and model group ( n=10 ) . After induction of anaesthesia with 10% chloraldurate ( 3 ml/kg, i. p. ) , tracheal intubation and left femoral artery cannulation were performed. Under electrocardiographic and artery blood pressure monitoring, tracheal obstruction ( TO) was performed to rats in model group. At 2 min after the cardiac arrest ( CA) occurred, CPRs were administered to the rats using a self?made animal chest compressor, which provided chest?com?pression at a rate of 200 bpm. Results Shortly after TO, rats in the model group had respiratory arrest, cyanosis and ar?rhythmia. Electrocardiography indicated that CA occurred within 4-5 min, with a decreased artery systolic blood pressure ( <40 mmHg) and a zero pulse pressure. Return of spontaneous circulation ( ROSC) after the CPR was successfully a?chieved in 8 rats (80%), with a transient reperfusion arrhythmia. Finally, 60% of the rats (n=6) recovered to con?sciousness and survived for 24 hrs. The serum biochemical analysis indicated that there were electrolyte disturbances, aci?dosis, impaired renal functions and increased myocardial enzyme spectrum. Pathological examination revealed cardiac rhab? domyolysis, no?reflow phenomenon in renal glomeruli, decrease of neurons and pulmonary congestion in the model group rats. Conclusions Mechanical chest compression can provide minimal cardiac output for the requirement of CPR incardiac arrestin rats. It is feasible to establish rat CPR model with the mechanical chest compression.

Objective To observe the effect of penetrating electro-acupuncture at scalp-acupoints on the motor function and oxidative stress action of mice with Parkinson's disease (PD).Methods Mouse model of PD was established by 5-day intraperitoneal injection of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP,30 mg/kg),and then PD mice were given electro-acupuncture set at different parameters.The effect of the electroacupuncture on the behavior and expression of tyrosine hydroxylase (TH) of mice were observed to screen out the appropriate treatment parameters.Healthy C57BL/6 mice were randomly divided into blank group,model group,positive group (madopar,6.25 mg/kg) and electro-acupuncture group.The mice except for blank group were given intraperitoneal injection of MPTP to induce PD,and then the PD mice of positive group and electroacupuncture group were treated with madopar(6.25 mg/kg) and electro-acupuncture respectively from the 6th day for 7 continuous days.Behavioral test was carried out on the 5~ modeling day and on the Th electro-acupuncture treatment day to evaluate the motor function of the mice.After the mice were killed and their brains were isolated,mitochondrial complex Ⅰ ～Ⅳ activities,reactive oxygen species(ROS) level,malondialdehyde (MDA) content,and total activities of superoxide dismutase (SOD) in the cerebral mitochondria were determined to evaluate the effect of electro-acupuncture at acupoints on anti-oxidative stress of PD mice.Results The motor function of PD mice was improved,the activity of mitochondrial complex Ⅰ was increased,the contents of ROS and MDA in cerebral mitochondria were decreased,and the activity of SOD was increased in the electro-acupuncture group,the differences being significant compared with those of the model group (P ＜ 0.05 or P ＜ 0.01).Conclusion Penetrating electro-acupuncture at scalp-acupoints can increase the anti-oxidative ability of the cerebral mitochondria and improve the motor function of PD mice.

BACKGROUND:Currently, limb salvage therapy has become the standard treatment of malignant bone tumors way, but improper treatments wil result in tumor recurrence, secondary infection, internal fixation or prosthesis loosening.
OBJECTIVE:Based on the traditional surgical principle for metastatic bone tumors of the limbs, this study designed a user-friendly, individualized, simplistic pal iative treatment regimen from the actual conditions of patients to observe the reasonability, clinical efficacy and prognosis of bone cement fil ing combined with internal fixation in the treatment of metastatic malignant bone tumors.
METHODS:Thirty-one patients with metastatic malignant bone tumors who required salvage treatment were screened from the Department of Orthopedics, the 421 Hospital of Chinese PLA, and their clinical data were retrospectively analyzed. Al the 31 patients were divided into two groups:tumor removal+internal fixation group (non-chemoradiotherapy group, n=11) treated with bone cement fil ing plus plate internal fixation (pal iative
treatment);tumor removal+internal fixation+chemoradiotherapy group (chemoradiotherapy group, n=20), treated with radiotherapy before internal fixation plus plate internal fixation with limb salvage. The fol ow-up period was 4-38 months, averagely 18 months.
RESULTS AND CONCLUSION:The fol ow-up results showed that in the non-chemoradiotherapy group, al the 11 patients survived, who could live independently and have good motor functions;in the chemoradiotherapy
group, 17 of the 20 patients survived and the rest three patients died of tumor metastasis, their poor conditions and complications at 9 and 13 months after internal fixation. In patients undergoing tumor removal+plate internal fixation with limb salvage, the integrated scores for nerve and motor functions were increased by more than
level 1. These findings confirm that a simple pal iative therapy of bone cement fil ing and internal fixation without chemoradiotherapy is better for metastatic malignant bone tumors patients who require limb salvage.

Objective To investigate the clinical manifestations, laboratory and imaging features, treatments and prognosis of anti GABA-B receptor encephalitis. Methods We performed a retrospective analysis of the clinical data of five cases with anti GABA-B receptor encephalitis diagnosed by cerebrospinal fluid immunological examination. Results Five cases had acute onset. The initial clinical symptom was epileptic seizure. After epileptic attack, patients developed different degrees of cognition dysfunction, mental and behavioral disorders. Neuroimaging showed that the lesions mainly involved medial temporal lobe and hippocampus. The lesions ware equal or low density shadows in CT scan and long T 1 and T2 signals, T2 high signals on Flair, equal or high signals on DWI in MRI scan. Cranial MRI enhancement showed lesions with no enhancement in two tested cases. One case took PET-CT and data showed a low density shadow of temporal lobe and hippocampus with increased metabolism. CSF and blood immunological examinations showed CSF GABAB-R-AB positive (+), blood GABAB-R-AB positive (+). Five cases were associated with increased NSE. EEG was nonspecific and related to the conscious state of the patient. Lung CT showed enlarged mediastinal lymph nodes in 5 tested cases. Central lung cancers were found in five cases including three cases at onset and two cases during three month follow-up. Bronchoscopic biopsy identified small cell lung cancer in two examined cases. Conclusion Epileptic seizure is the most frequent initial symptoms of anti GABA-B encephalitis. Inflammatory response signals in the medial temporal lobe and hippocampus are image features of anti GABA-B encephalitis. The disease is closely related to lung cancer (Especially c small cell lung cancer, SCLC). Immunological examination of cerebrospinal fluid and the above characteristics are helpful for diagnosis.