[Objective] To study effects of the velvet antler polypeptides on spinal nerve cell apoptosis induced by ?-amyloid peptide. [Method]Spinal nerve cells were performed serial subcultivation,and entered into experiment during the exponential phase of growth.The viability of spinal nervecells 24h after induction by ?-amyloid peptide with different concentrations were detected by MTT assay,percentages of the cell apoptosis and expression of casepase-3 were detected after induction by 25?mol/L ?-amyloid peptide.[Result]It was revealed that 24 h after treatment with ?-amyloid peptide of different concentrations,the viability of spinal nerve cells was significantly decreased in a dose-dependent manner(P

Background and objectives Proliferation of human vascular smooth muscle cells (VSMCs) induced by hyperinsulinemia is a very common clinical pathology. Extensive research has focused on PKC (Protein kinase C)-MAPK (mitogen-activated protein kinase)intracellular signal transduction and the phenotypic modulation accompanied by reorganization of intracellular F-actins in VSMCs.Methods DNA synthesis, signaling of ERK1/2 MAPKs, and changes in α-smooth muscle (SM) actin and F-actin were studied in hypertensive and normotensive human arterial VSMCs exposed to insulin and PMA with and without the PKC inhibitor, GF109203X.Results Differences among cell types in MAPK signaling, α-SM actin, and F-actin isoforms in VSMCs harvested from the arteries of patients with essential hypertension (EH) and normotension (NT) were identified in response to insulin treatment. Proliferation and activation of MAPK were more pronounced in EH VSMCs than in NEH VSMCs. Insulin exposure decreased expression of α-SM actin and was accompanied by rearrangement of intracellular F-actins in VSMCs, especially in the EH group. These effects were reversed by treatment with the PKC inhibitor. Conclusions Human mesenteric VSMCs of EH and NT patients differed in proliferation, MAPK signaling, and degree of changes in α-SM actin and F-actin isoforms immediately following insulin exposure in vitro.

Objective To evaluate the clinical effect of the upper lip defect with lower cross-lip flap (Abbe-Estlander flap).Methods A total of 68 cases of upper lip defect underwent the reconstruction with cross-lip flaps.We applied Abbe flap in upper lip defect in the center,and Estlander flap in lateral upper lip defect.This method was a two-stage procedure:the first stage was to rotate flap 180 degrees into the upper lip defect and to suture with the created defect of the upper lip,with careful maintenance of blood supply from the pedicle; the second was to undertake the division of bridged pedicle and paid more attention to creation of the vermilion border.Results The flaps survived in all cases.Evaluation from 3 to 12 months after the operation showed that the shape of lips were obviously repaired with excellent aesthetic and functional results.Conclusions Abbe-Estlander flap could reconstruct anatomical features and function of the lip precisely.It seems that within certain limits (probably between one-third and one-half of total upper lip length),this flap appears to be the preferred method for upper lip reconstruction.

Objective To determine the effect of different doses vitamin D supplementation to the change of bone metabolism in 6 months after Roux-en-Y gastric bypass ( RYGB) .Methods The change of body weight and body mass index ( BMI ) in 36 patients in 6 months after RYGB WAS analyzed.Then,the effect of low-dose (n=11,400 IU/day) and high-dose (n=12,1 600 IU/day) vitamin D to the serum calcium,25-hydroxyvitamin D and bone density were observed ,and 15 patients as control .Results In 6 months after RYGB,the body weight and BMI were decreased ,and the differences were statistical significance (P<0.05).The serum calcium,25-hydroxyvitamin D and bone density were increased in high-dose group,and the differences were statistical significance (P<0.05).Conclusion High-dose (1 600 IU/day) vitamin D supplementation is effective to the bone loss of patients undergoing RYGB .

Objective To evaluate the effects on blood pressure and vascular endothelial-1 function of combined therapy of atrovastin and nifedipine controlled released tablet in essential hypertension.Methods A randomized,double-blind,controlled trial was performed.Eighty-two patients with essential hypertension were randomly divided into two groups,receiving nifedipine controlled released tablet 30 mg once daily,or atrovastin 10 mg once daily and nifedipine controlled released tablet 30 mg once daily for 12 weeks.Another 30 subjects with normal blood pressure served as normal blood pressure control.Antihypertensive efficiency was observed during the whole study period.The concentration of plasma endothelin-1(ET-1) nitric oxide(NO) were measured before and after treatment.Results Blood pressure decreased significantly in both groups,but more significant in combined therapy group.In the combined therapy group,atrovastin resulted in a significant reduction of plasma ET-1 and a rise of nitric oxide(NO)(P

AIM: To identify proteins involved in insulin stimulation and the molecular mechanism of proliferation and migration in vascular smooth muscle cells (VSMCs). METHODS: A series of methods, including 2-D electrophoresis, PDQuest software analysis of 2-DE gels, peptide mass fingerprinting based on matrix-assisted laser desorption/ionization time of flight mass spectrometry (MALDI-TOF-MS) and SWISS-PROT database searching, were used to separate and identify the differentially expressed proteins. The difference of some proteins was proved by Western blotting. Proliferation and migration of VSMCs treated with insulin were also observed. RESULTS: DNA synthesis were increased in VSMCs. ~3H-thymidine incorporation in VSMCs from SHR (14.40?0.85) was higher than that in VSMCs from WKY (9.21?0.93, P

AIM: To investigate the changes of intracellular calcium ion (Ca2+) concentration in mouse H9c2 (2-1) cells transfected with or without FK506 binding protein 12.6(FKBP12.6) gene by ultrasound mediated destruction of microbubbles. METHODS: The pcDNA3.1-FKBP12.6 plasmid, mingled with albumin-coated microbubbles agents, was transfected into H9c2 (2-1) cells by ultrasound-mediated destruction of microbubbles. The H9c2 (2-1) cell growth state was investigated by inverted microscope. The changes of intracellular Ca2+ concentration was determined by laser scanning confocal microscope. The FKBP12.6 protein expression was checked by immunohistochemistry. RESULTS: As compared with control cells, the H9c2 (2-1) cells, transfected with FKBP12.6 gene, grew better, had higher gross intracellular Ca2+ concentration. CONCLUSION: FKBP12.6 gene augments Ca2+ concentration in mouse H9c2 (2-1) cells, enhances the contractibility of the myocardial cell, which may be helpful to improve the myocardial dysfunction.

AIM:To explose the possible existing pathway of intracellular signaling transduction in hypertensive induced by insulin in rat vascular smooth muscle cells proliferation which involved mitogen-activated protein kinase. METHODS:Male spontaneously hypertensive rat (SHR) aorta and WKY(6 weeks old) were isolated and then cultured to make the purified vascular smooth muscle cells.6-8th generation of VSMC were interfered with insulin in vitro . MAPK activity was determined by myelin basic protein method and its volume was measured with Western Blot. And [ 3 H]-TdR was used to measure DNA synthesis in VSMC proliferation. RESULTS: After the interfered with insulin the DNA synthesis was increased obviously in SHR group. MAPK activity and its contains in SHR were increased more than the control group. Protein kinase C inhibitor decreased MAPK activity induced by insulin. CONCLUSION:Proliferation of SHR VSMC in vitro was correlated with increased activity of MAPK. Insulin can affect MAPK induced activity. So an insulin-PKC-MAPK axis may exist in hypertensive VSMC.

PBL (Problem-based learning) is a kind of teaching method, which is helpful for guiding students to solve practical and complex problems. The compiling of PBL teaching plans is the key to the implementation of PBL teaching. According to the teaching outline of internal medicine, we set the PBL teaching plan, formulated the teaching goal, collected the clinical real cases, finished the compiling of PBL cases of student version and teacher version, and preceded teaching practice accord-ing to the PBL cases. Improving and constructing the compiling framework of internal medicine PBL teaching plan laid the theoretical foundation for carrying out internal medicine PBL teaching.

AIM: To explore the effect of endoplasmic reticulum stress on cardiac myocyte apoptosis in mouse congestive heart failure induced by myocardial infraction.METHODS: The mouse model of heart failure was established by ligating the left anterior descending coronary to produce acute myocardial infarction.Thirty-two mice were divided into 4 groups: sham group and groups of post-operation at time points of 2,4 or 6 weeks,respectively.The ventricular dilatation and left ventricular functions were assessed by echocardiography.The expression of GRP78,CHOP,caspase-12,cleaved caspase-12,JNK and phosphorylated-JNK was detected by Western blotting.The cardiac myocyte apoptosis was determined by terminal deoxynucleotidyl transferase mediated dUTP-biotin nick end labeling(TUNEL).RESULTS: The cardiac expression of endoplasmic reticulum chaperones GRP78 was significantly increased in the hearts with functional failure.The upregulated expression of CHOP,phosphorylated-JNK and cleaved caspase-12 illuminated that the CHOP-JNK-caspase-12 dependent pathways for endoplasmic reticulum-initiated apoptosis were activated in the heart with functional failure by myocardial infraction.CONCLUSION: These findings suggest that the congestive heart failure induced by myocardial infraction is associated with endoplasmic reticulum stress and activation of CHOP,JNK,caspase-12 dependent pathways for endoplasmic reticulum-initiated apoptosis.