Archives ; China ; Humans ; Occupational Health ; Residence Characteristics

Humans ; Occupational Diseases ; epidemiology ; prevention & control ; Occupational Health Services

Archives ; Humans ; Occupational Health

For the problems that 3 first-class ternary hospitals which are not directly affiliated to medical universities are facing in cultivating high-educated staff's scientific abilities,analyze the importance to carry out scientific work in clinic and discuss how to improve their scientific abilities from hospitals,departments and high-educated staff themselves.

OBJECTIVETo investigate the protective effect of ginsenoside Rg1 on oxygen-glucose deprivation (OGD) in PC-12 cells, and preliminarily discuss the potential molecular mechanism of mTOR/Akt/FoxO3 signaling pathway.

METHODThe OGD PC-12 cell model was established. The cell viability was measured by MTT assay. After the pretreatment with Rg1 with the concentration of 10, 20, 40 micromol x L(-1) for 24 h, the cell viability was observed. Lactate dehydrogenase (LDH) release, superoxide dismutase (SOD) ac- tivity and malondialdehyde (MDA) level were detected by colorimetry assay. mTOR, p-Akt(ser473), p-Akt(tjr308), Akt, p-FoxO3, FoxO3 in cytoplasm and nucleus, and total FoxO3 protein expression were detected by Western blot assay.

RESULTOGD could significantly in- hibit cell proliferation in 4-24 h in a time-dependent manner. After pretreatment for 24 h, Rg1 (20, 40 micromol x L(-1)) could notably elevate the cell viability and SOD viability and reduce the LDH release and MDA content. Besides, Rg1 also inhibited OGD-induced mTOR and p-Akt(ser473) decreases. After treatment for 6 h, OGD could reduce FoxO3 phosphorylation and promote FoxO3 in cytoplasm. This data suggested that Rg1 could protect PC-12 cell injury through mTOR/p-Akt/FoxO3 signaling pathway.

CONCLUSIONGinsenoside Rg1 could attenuate OGD-induced PC-12 cell injury. Its action mechanism may be closely related to activation of mTOR/p-Akt/FoxO3 signaling pathway.

Animals ; Apoptosis ; drug effects ; Cell Proliferation ; drug effects ; Cell Survival ; drug effects ; Drugs, Chinese Herbal ; pharmacology ; Forkhead Box Protein O3 ; Forkhead Transcription Factors ; genetics ; metabolism ; Ginsenosides ; pharmacology ; Glucose ; metabolism ; Oxygen ; metabolism ; PC12 Cells ; Protective Agents ; pharmacology ; Proto-Oncogene Proteins c-akt ; genetics ; metabolism ; Rats ; Signal Transduction ; drug effects ; TOR Serine-Threonine Kinases ; genetics ; metabolism

Objective To study the different effects of valsartan and extended realse nifedipine tablets on lowering blood pressure of essential hypertension patients and their reversal effects on left ventricular hypertrophy. Methods 100 cases of essential hypertension patients with left ventricular hypertrophy were randomly divided into valsartan group(group A) and adalt group(group B).Other antihypertensive drugs except diuretic were removed for 3 weeks.There were 50 cases in group A using valsartan 4～8mg qd,and 50 cases in group B using adalt 30～60 mg qd,the stud),lasted for 24 weeks.The blood pressure was measured and the altrasowic cardiogram examed in baseline and 24 weeks later.Results BP could be significantly reduced after treatment(P

OBJECTIVETo study the efficacy and safety of Naoxintong capsule treatment of stroke recovery with Qi-deficiency and blood-stasis syndrome (cerebral infarction), and to compared the non-inferiority analysis with the positive drug Tongxinluo capsule.

METHODTaking Tongxinluo capsules as control, randomized, double-blind, controlled, multi-center clinical experiments were studied. The evaluating indexes included the decrease of integral value of stroke patients, changes in traditional Chinese medicine, the improvement of the patient viability status (disability level), Chinese stroke scale (CSS), activities of daily living (DAL) scale and barthel index (BI ) points.

RESULTThe total effect of the two groups, Chinese and other symptoms, showed no significant statistical significance.

CONCLUSIONNaoxintong capsule stroke recovery, with Qi-deficiency and blood-stasis syndrome (cerebral infarction) has a therapeutic effect, and more secure.

Activities of Daily Living ; Adult ; Aged ; Capsules ; Double-Blind Method ; Drugs, Chinese Herbal ; therapeutic use ; Female ; Humans ; Male ; Middle Aged ; Qi ; Stroke ; drug therapy ; Treatment Outcome

OBJECTIVETo investigate the effect of Shenshao Decoction on the inflammatory status: in the aorta in a rat model of atherosclerosis.

METHODSForty Sprague-Dawley rats were randomly divided into: five groups, 8 rats in each group: control untreated group, atherosclerosis group, atherosclerosis with Shenshao Decoction (low dose) group, atherosclerosis with Shenshao Decoction (high dose) group, atherosclerosis with simvastatin group. To stimulate atherosclerosis, the rats were fed vitamin D3 and a high-cholesterol diet. Four weeks later, treatments were maintained for eight weeks. Morphology changes were investigated by hematoxylin and eosin staining. Serum levels of total cholesterol (TC), triglycerides (TG), and low-density lipoprotein cholesterol (LDL-C) were obtained by enzymatic assays with use of an automated biochemical analyzer. The expression of malondialdehyde (MDA), glutathione peroxidase (GSH-PX) were detected by enzyme-enzymelinked immunosorbent assay. The expression levels of interleukin (IL)-1β, IL-17A, and IL-23 were detected by linked immunoblotting.

RESULTSShenshao Decoction treatment decreased TC, TG, LDL-C and MDA and increased: GSH-PX levels (P<0.01). Compared with the control group, IL-1β, IL-17A, and IL-23 were lower in the high and

CONCLUSIONShenshao Decoction: could attenuate the progression of aortal atherosclerotic plaques by inhibiting the inflammatory response in a rat atherosclerotic model.

Animals ; Aorta, Thoracic ; drug effects ; pathology ; Atherosclerosis ; blood ; drug therapy ; pathology ; Cholesterol ; blood ; Cholesterol, LDL ; blood ; Disease Models, Animal ; Drugs, Chinese Herbal ; therapeutic use ; Glutathione Peroxidase ; blood ; Immunohistochemistry ; Inflammation ; drug therapy ; pathology ; Interleukin-17 ; metabolism ; Interleukin-1beta ; metabolism ; Interleukin-23 ; metabolism ; Male ; Malondialdehyde ; blood ; Rats ; Rats, Sprague-Dawley ; Triglycerides ; blood

OBJECTIVETo investigate the effect of short hairpin RNA (shRNA) targeting hypoxia-inducible factor-1 alpha (HIF-1 alpha) on the human breast carcinoma MCF-7 cell line.

METHODSThe hypoxia environment was achieved by treating cells with cobalt chloride. The shRNA eukaryotic expression vector targeting HIF-1 alpha was constructed, and transfected into MCF-7 cells through lipofectamine 2000. Semi-quantitative reverse transcription-polymerase chain reaction (RT-PCR) was used to study the expression of vascular endothelial growth factor (VEGF). The mRNA and protein level of HIF-1 alpha were detected by real-time PCR and Western blot. Sub-G1 apoptotic population analysis, Annexin V/PI binding assay, and DNA ladder analysis were applied to investigate the cell apoptosis. The cell cycle was detected by flow cytometry.

RESULTSThe mRNA and protein level of HIF-1 alpha increased after exposure of MCF-7 cells to hypoxia (P < 0.01). However, apoptosis was lower in hypoxia compared with normoxia (P < 0.05). The HIF-1 level of MCF-7 transfected with HIF-1 alpha shRNA decreased approximately 91.63% (P < 0.01). When the cells were treated with or without apoptosis inducer Ara-C, the apoptosis of MCF-7 cells transfected with HIF-1 alpha shRNA increased by 1.75 times (P < 0.01) and 61. 31 times (P < 0.01), respectively. The expression of VEGF in MCF-7 cells transfected with HIF-1 alpha shRNA decreased 66.8% compared with untransfected cells (P < 0.05). Cell cycle progression was inhibited when the MCF-7 cells were transfected with HIF-1 alpha shRNA.

CONCLUSIONSHIF-1 alpha plays an anti-apoptotic role in human breast carcinoma MCF-7 cell line. The shRNA we designed targeting HIF-1 alpha in MCF-7 can promote cell apoptosis, inhibit the expression of VEGF, and delay cell cycle progression.

Apoptosis ; Breast Neoplasms ; genetics ; metabolism ; pathology ; Cell Cycle ; Cell Line, Tumor ; Down-Regulation ; Female ; Humans ; Hypoxia-Inducible Factor 1, alpha Subunit ; genetics ; RNA Interference ; RNA, Messenger ; genetics ; RNA, Small Interfering ; genetics ; Transfection ; Vascular Endothelial Growth Factor A ; metabolism

OBJECTIVETo explore the mechanism of tanshinol on alleviate the inflammatory injury of lung tissue in rat hepatopulmonary syndrome (HPS).

METHODSSD rats were randomly divided into normal control group (n = 8), hepatopulmonary syndrome (HPS) group (n = 11) and tanshinol intervention group (n = 9). HE staining was used to observe the histopathology changes of pulmonary and hepatic tissues, and to count the number of macrophages in lung tissues. The activity of alanine transferase (ALT) and concentrations of endotoxin, tumor necrosis factor-a (TNF-alpha) and homocystein (Hcy) in plasma were detected. The concentrations of TNF-alpha, nitric oxide (NO) and malondialdehyde (MDA) and the activity of inducible nitric oxide synthase (iNOS) in the lung tissues were measured, respectively.

RESULTSThickened alveolar septum and increased macrophages were observed in lungs in HPS rat. After administered with tanshinol, the pulmonary pathological changes were alleviated and the number of macrophages in lung tissue was decreased compared with HPS group. The activity of ALT and the concentrations of endotoxin, TNF-alpha and Hcy in plasma ,and TNF-alpha, iNOS, NO and MDA in lung tissue in HPS group were higher than those of normal control group; meanwhile, those tanshinol group were less those that of HPS group.

CONCLUSIONTanshinol may play an important role in delaying the development of HPS through protecting liver or directly antagonizing the effect of intestinal endotoxemia so as to alleviate the inflammatory reaction in lung tissue.

Alanine Transaminase ; metabolism ; Animals ; Caffeic Acids ; pharmacology ; Disease Models, Animal ; Endotoxins ; blood ; Hepatopulmonary Syndrome ; drug therapy ; pathology ; Homocysteine ; blood ; Liver ; drug effects ; pathology ; Lung ; drug effects ; pathology ; Macrophages ; drug effects ; pathology ; Male ; Malondialdehyde ; metabolism ; Nitric Oxide ; metabolism ; Nitric Oxide Synthase Type II ; metabolism ; Rats ; Rats, Sprague-Dawley ; Tumor Necrosis Factor-alpha ; blood