China ; Environmental Exposure ; Heat Stress Disorders ; prevention & control ; Industry ; Occupational Health ; Temperature ; Workplace

Hot Temperature ; Humans ; Industry ; Occupational Exposure ; Occupational Health

Acetylcysteine ; analogs & derivatives ; urine ; Adolescent ; Adult ; Deoxyguanosine ; analogs & derivatives ; urine ; Female ; Furans ; urine ; Humans ; Hydrocarbons, Aromatic ; analysis ; Male ; Occupational Exposure ; analysis ; Young Adult

Adenocarcinoma, Follicular ; pathology ; surgery ; Aged ; Aged, 80 and over ; Carcinoma, Papillary ; pathology ; surgery ; Follow-Up Studies ; Humans ; Lymphatic Metastasis ; Middle Aged ; Neck Dissection ; Survival Analysis ; Thyroid Neoplasms ; pathology ; surgery ; Thyroidectomy ; methods

Animals ; Arterial Occlusive Diseases ; physiopathology ; therapy ; Dogs ; Genetic Therapy ; Hepatocyte Growth Factor ; genetics ; Hindlimb ; blood supply ; Ischemia ; physiopathology ; therapy ; Male ; Plasmids

Blood Platelets ; Humans ; MicroRNAs

Objective To investigate the expression of the hypoxia-inducible factor (HIF)-1α in rat brain neurons and the intervention of β-sodium aescinate after restoration of spontaneous circulation (ROSC).Methods Sixty SD adult rats were randomly (random number) divided into 3 groups (n =20),namely experiment group,control group and sham operation group.(1) The rats of experiment group were injected intraperitoneally with β-sodium aescinate (5 mg/kg) immediately after ROSC.(2) The rats of control group received normal saline injected intraperitoneally instead of β-sodium aescinate solution.(3)The rats of sham operation group did not have cardiac arrest and β-sodium aescinate intervention.Cardiac arrest rat model was established by using asphyxiation and intra-venous potassium chloride solution.Blood samples were taken 1 h,6 h,12 h and 24 h after ROSC,and subsequently rats were sacrificed and their brain tissues were harvested.The expressions of HIF-1 α mRNA,vascular endothelial growth factor (VEGF)mRNA and erythropoitin (EPO) mRNA and their protein levels in rat brain neurons were detected by using RT-PCR and immunohistochemistry,and the levels of serum neuron-specific enolase (NSE) and S100β proteins were determined by using enzyme-linked immunosorbent assay.The t test or one-way ANOVA was used to assess overall differences among groups for each of the variables,followed by Bonferroni test for multiple comparisons.Pearson method was used for correlation analysis.Results Compared with the sham operation group at intervals of 1 h,6 h,12 h and 24 h after ROSC,levels of serum S100β and NSE proteins were significantly increased in rats of the control group (P ＜ 0.05).Meanwhile,the expressions of HIF-1 α mRNA,VEGF mRNA and EPO mRNA and their protein levels in rat brain neurons were significantly increased in the control rats (P ＜0.05).Compared with the control group at intervals of 1 h,6 h,12 h and 24 h after ROSC,levels of serum NSE and S100β proteins were significantly decreased in rats of the experiment group (P ＜ 0.05).Whereas,the expressions of HIF-1 α mRNA,VEGF mRNA and EPO mRNA and their protein levels in rat brain neurons were significantly increased in rats of the experiment group (P ＜0.05).HIF-1 α mRNA was positively correlated with EPO mRNA and VEGF mRNAs (r =O.866,P ＜0.05 ; r =0.952,P ＜ O.01).Conclusions The expression of hypoxia-inducible factor-1 α is increased in rat brain cells after ROSC,and β-sodium aescinate up-regulates the expression of hypoxia-inducible factor1 α mRNA and protein levels.The up-regulated expression of hypoxia-inducible factor-1α improves the resistance of brain cells to ischemia and hypoxia contributing neuronal protection,which might be due to upregulated EPO and VEGF expressions induced by hypoxia-inducible factor-1α.

The DNA structures could be altered or even damaged by exogeous or endogenous factors during cell proliferation. Failure of effective and timely repair will lead to cell cycle arrest or apoptosis. By taking the advantage of the quick proliferation of cancer cells, DNA damage induction, cell cycle arrest and apoptosis promotion have become important strategies for ant-cancer chemotherapy. Previous reports showed that an array of natural compounds inhibit cancer cell proliferation by inducing DNA damage, which have therapeutic potentials for anti-cancer drug research and development.
Animals ; Biological Products ; pharmacology ; therapeutic use ; DNA Damage ; Drugs, Chinese Herbal ; therapeutic use ; Humans ; Neoplasms ; drug therapy

BACKGROUND: This study was undertaken to investigate the expression of hypoxia-inducible factor-1α (HIF-1α) in rat cerebral cortex and the effects of β-sodium aescinate (SA) administration after return of spontaneous circulation (ROSC).METHODS: Sixty rats were divided into three groups: SA group, injected intraperitoneally with SA instantly after ROSC; control group, injected intraperitoneally with normal saline; and sham-operated group, without cardiac arrest or SA. The cardiac arrest model was established using asphyxiation and intravenous potassium chloride. Blood was sampled 1, 6, 12, and 24 hours after ROSC. Protein and mRNA levels of HIF-1α, VEGF and EPO were detected in the cerebral cortex by immunohistochemistry and real-time RT-PCR; serum levels of NSE and S100β were determined by enzyme-linked immunosorbent assays.RESULTS: Serum S100β and NSE were signifi cantly increased in the control group versus the sham-operated group 1, 6, 12 and 24 hours after ROSC (P<0.05). Protein and mRNA levels of HIF-1α, VEGF and EPO were signifi cantly increased in the control rats (P<0.05). Serum NSE and S100β were significantly decreased in the SA group versus the control group 1, 6, 12 and 24 hours after ROSC (P<0.05). Protein and mRNA levels of HIF-1α, VEGF and EPO were signifi cantly increased in the SA group (P<0.05).CONCLUSIONS: The expression of HIF-1α is increased in rat cerebral cortex after ROSC, and SA up-regulates the expression of HIF-1α. The up-regulation of HIF-1α improves the resistance of the cortex to ischemia and hypoxia and contributes to neuroprotection, possibly because of up-regulation of EPO and VEGF expression.

Objective To analyze the CT findings of endobronchial spread in lung adenocarcinoma. Methods The CT findings of 15 lung adenocarcinomas or bronchioloalveolar carcinomas with endobronchial spread were reviewed,the distribution and the progression of the spread were evaluated.Results All of the primary tumors were consolidation form.The spread lesions distributed in one side of the lung or both sides along the bronchus.The pleural surface was spared.The CT findings of the spread included centrilobular nodules(n=5),tree-in-bud(n=7),acinar nodules(n=2),ground-glass opacities(n=10)and air- space consolidations(n=13)in the first CT examination.5 cases of the spread lesions only presented centrilobular nodules(single form)and 10 cases presented several appearances(complex form).All of the cases were diagnosed as tuberculosis or pneumonia,and antituberculotic or antibiotic therapy was taken with no effect.The follow-up CT scans showed progression in all cases,and the spread lesions with single form became multiple consolidations.The spread lesions with complex form deteriorated faster than the single one. Conclusion Although the CT findings of the endobronchial spread of the lung adenocarcinoma is specific, the clinical history and laboratory examination also are important for the differential diagnosis with tuberculosis and other infectious diseases.