Objective To investigate the relationship between metabolic syndrome(MS) and severity of coronary atherosclerosis. Methods Sixty-four hospitalized patients diagnosed as coronary heart disease were divided into MS group(n=26)and non-MS group(n=38).All the patients underwent 16-row multi-slice CT coronary angiography,and cardiovascular risk factors were evaluated. Results The prevalence of MS increased with the number of stenosed coronary arteries(P

OBJECTIVEEndothelial apoptosis plays an important role in the initiation of atherosclerosis. It would be useful to clarify whether activation of non-neuronal muscarinic receptor (NNMR) could prevent endothelial apoptosis and atherosclerosis. We investigated the effects of NNMR activation on regulating rat aortic endothelial cells (RAECs) apoptosis induced by homocysteine, an independent risk factor of atherosclerosis, and further studied its molecular mechanism.

METHODSRAECs were incubated using homocysteine at the concentration of 2.7 mmol/L for 36 h. RAECs were also pre-treated with carbachol or arecoline to examine their effects. RT-PCR was used to assess changes in the gene expression related to cell apoptosis.

RESULTSIncubation of RAECs with homocysteine at the concentration of 2.7 mmol/L resulted in morphologic changes, such as cellular shrinkage, membrane blebbing, chromatin condensation and margination. These could be attenuated by pretreatment with carbachol and arecoline at the concentration of 10 micromol/L for 12 h. Homocysteine induced apoptosis in RAECs and the molecular mechanisms were associated with the regulation of fas, fas-L and caspase-8 in the death receptor pathway, bcl-2, bcl-xL and bax in the mitochondrial pathway, caspase-12 in the endoplasmic reticulum pathway and caspase-3, caspase-6 and p53 as downstream effectors. Carbachol and arecoline attenuated the effects of homocysteine on genes in the death receptor pathway, in the mitochondrial pathway and in the downstream pathway. Atropine could reverse all of the effects of arecoline.

CONCLUSIONActivation of NNMR by carbacol and arecoline inhibits homocysteine-induced endothelial cell apoptosis mainly through regulation of death receptor pathway, mitochondrial pathway and downstream effectors.

Animals ; Aorta ; cytology ; Apoptosis ; Apoptosis Regulatory Proteins ; metabolism ; Arecoline ; Carbachol ; Cell Cycle ; Endoplasmic Reticulum ; metabolism ; Endothelial Cells ; cytology ; drug effects ; Homocysteine ; adverse effects ; Mitochondria ; metabolism ; Rats ; Receptors, Muscarinic ; metabolism

China ; epidemiology ; Humans ; Pneumoconiosis ; epidemiology ; Retrospective Studies

Objective To explore the effects of transcranial magnetic stimulation (TMS) on motor function in patients with Parkinson's disease (PD) using meta-analysis. Methods Eight comparative studies of the effects of TMS were meta-analyzed. Results The combined studies confirmed a significant difference before and after TMS treatment. Between the experimental and control groups the effect was also highly significant. Conclusion TMS may play an active role in the rehabilitation of motor function for patients with Parkinson's disease.

AIM:To observe the expression and tissue localization of matrix metalloproteinase 9 (MMP-9) and transforming growth factor beta 1 ( TGF-β1 ) in the rat acute cerebral ischemia model.METHODS:Male Wistar rats were used to establish acute cerebral ischemia model by a suturing method.The rats were divided into normal control group, sham group and ischemia 6 h, 12 h, 1 d, 2 d, 6 d and 14 d groups.The rat cerebral cortex and hippocampus of the brain were collected at different time points.The mRNA and protein levels of MMP-9 and TGF-β1 in the brain tissues were detec-ted by real-time PCR and in situ histochemistry staining, respectively.The levels of MMP-9 and TGF-β1 in the plasma were also measured by ELISA.RESULTS:The results of real-time PCR showed that the mRNA levels of MMP-9 began to in-crease 6 h after acute ischemia and reached to a peak 2 d after acute ischemia.Similarly, the mRNA level of TGF-β1 began to rise 12 h after acute ischemia and reached to the highest level 6 d after acute ischemia.Compared with the sham rats, the mRNA levels of MMP-9 and TGF-β1 in the rat brains that collected at ischemic time of 12 h, 1 d, 2 d, 6 d and 14 d were significantly increased.Moreover, results of in situ histochemical staining showed that the expression of MMP-9 was detected at cerebral cortex and hippocampus 1 d after acute cerebral ischemia.Further studies showed that MMP-9 dyeing of the rat cerebral cortex was most obvious 2 d after the acute cerebral ischemia.Similarly, the rat cortex and hippocampus began to express TGF-β1 2 d after acute ischemia and TGF-β1 staining at rat cerebral cortex was most obvious 6 d after the acute cerebral ischemia.In addition, ELISA showed that the increase in MMP-9 and TGF-β1 was detected in the plasma 12 h after ischemia.Compared with the sham rats, the level of these 2 factors significantly upregulated since 1 d after ischemia. CONCLUSION:The brain tissue itself contributes to the upregulation of MMP-9 and TGF-β1 post acute cerebral ischemia, which shed light on the related research in the field.

Daiwenjiu Gao plasters were stuck onto the following two groups of acupoints,group 1 including acupoints Guanyuan (CV 4), Shenshu (BL 23) and Zusanli (ST 36) and group2 including acupoints Zhongji (CV 3), Pangguangshu (BL 28) and Sanyinjiao (SP 6), to treat 100 cases of infantile enuresis, the results showed that 92 cases were cured, 6 cases got remarkable effect, 2 cases got effect, with total effective rate being 100%.

ObjectiveTostudy the value of color Doppler sonography in diagnosisof rhabdomyolysis.Methods The color Doppler sonography images of twenty-one patients with diagnosed rhabdomyolysis were retrospective analyzed.The pathological changes of the muscle were observed.Results The appearance of ultrasound was cloundness and rough-cast glass change in the diseased area of rhabdomyolysis.The diseased region can be found by ultrasound,and location and scope can be displayed clearly.There were major differences in the location of rhabdomyolysis because of etiological factor.The muscle volume and tension of rhabdomyolysis were increased for trauma,the individual patients will lead to the osteofascial compartment syndrome.There was no blood flow signal or little blood flow signal in the diseased area of rhabdomyolysis.Conclusions The color Doppler sonography is an efficient method for diagnosis of rhabdomyolysis.

Objective To investigate the role of surfactant protein (SP)-A and SP-D in urinary tract infection mouse model,and evaluate the effects of SP-A and SP-D absence on urinary tract infection.Methods SP-A and SP-D double knockout (SP-A/D KO) mice were made.SP-A/D KO and wild-type (WT) C57BL/6 female mice were used for this study.The expression of SP-A and SP-D in kidney was detected by immunohistochemistry (IHC).The levels of p-p38 and p38 protein in kidneys were measured by Western blotting.Uropathogenic Escherichia coli or buffer was delivered into the bladder of female mice.At 24 and 48 h after inoculation,CFU of Escherichia coli in the kidney and urine of the treated and control mice were measured.Histological,cellular and molecular analysis were performed by several methods of H/E staining,IHC and Western blotting.The effects of SP-A and SP-D on bacterial growth were studied in vitro.Results SP-A and SP-D in kidney were located in the proximal tubules and collecting tubules.Compared with WT mice,infected SP-A/D KO mice with UPEC had higher CFU in kidneys and urine at 24 h and 48 h,increased inflammatory cells infiltration in kidneys (P＜0.05).Compared with WT mice,SP-A/D KO mice had higher p38 MAPK phosphorylation levels in kidneys (P ＜ 0.05).Growth of Escherichia coli was greatly inhibited by both SP-A and SP-D (P＜0.05).Conclusions Both SP-A and SP-D are expressed in kidney.SP-A and SP-D can attenuate UTI induced by UPEC which may be through inhibiting bacterial growth and modulating renal inflammation.

Objective To explore the differentiation potential of bone marrow stromal cells (BMSC) to enteric neuron in vitro and to seek proper induction methods.Methods BMSC were harves- ted from male rats and cultured in DMEM supplemented with 20% fetal bovine serum,and characterized by flow cytometry.At passage 6,BMSC were pre-induced by basic fibroblast growth factor (bFGF,10 ng/ml) for 24 h,then induced in two groups:glial cell-line derived neurotrophic factor (GDNF) group, 10 ng/ml GDNF in fetal gut condition medium (FGCM) for 10 d.Vitamin A acid (VA) group,VA, zinc in FGCM for 10 d.The expressions of neuronal markers,neural specific enolase (NSE) and neu- rofilament (NF),glial cell marker,glial fibrillary acidic protein (GFAP),enteric neuronal marker,pro- tein gene production 9.5(PGP9.5),nitric oxide synthase (nNOS),enteric neural transmitter,vasoactive intestinal peptide (VIP) were detected by fluorescent immunohistochemistry method.Results The cul- tured BMSC were CD90 positive and CD45 negative on flow cytometry.After 10 d of induction,a certain number of cells adopted neuron-like morphological changes and showed the expressions of NSE,NF, PGPg.5,nNOS and VIP without the expression of GFAP by fluorescent immunohistoehemistry method in both groups.But in GDNF group,the positive rate of NF,PGP9.5,nNOS and VIP was significantly higher than that in VA group (75.6%?8.4% vs 48.5?7.5%;57.7%?6.5% vs 35.7%?7.2% 46.6%?5.4% vs 30.5%?6.6%;72.3%?6.7% vs 40.4%?7.4%;P＜0.01).Conclusion BMSC can be induced to differentate into enteric neuron in vitro by different methods.GDNF with FGCM can induce higher rate of enteric neuron like cells compared with VA etc.

The microbial populations and community structure characterization technologies of the enhanced biological phosphate removal system were reviewed comprehensively in this paper, and their future research directions were outlined.