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

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.

Blood Platelets ; Humans ; MicroRNAs

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

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

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

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

Objective:To report the preliminary results of intensity modulated radiation therapy(IMRT)for 20 nasopharyngeal carcinoma patients.Methods:A total of 20 patients with nasopharyngeal carcinoma received IMRT in our hospital between January 2007 and April 2008.Five patients were of stage Ⅱ,13 patients were of stage Ⅲ,and 2 patients were of stage Ⅳ.The prescribed dose 69.96 Gy was delivered to the gross tumor volume(PTV)and positive neck nodes(PTVnd);59.36 Gy to the clinical target volume(PTV1),covering the upper neck and area around the nasopharynx;and 50.96 Gy to the low neck and supreclavicular area (PTV2).The dose to 50% of the parotid was≤35 Gy.The maximum dose to the lens.pituitary gland,temporo-mandibular joint,mandible,and temporal lobe was 9,54,60,70,and 60 Gy.The maximum dose to the brainstem,spinal cord,optic nerve and optic chiasma(PRV)was 54,40,54,and 54 Gy,respectively.All of the patients received 1 or 2 circles of chemothrapy before IMRT.Results:The median follow-up time was 14 months.The one-year overall survival was 94.1%.One patient died of osseous metastasis and respiratory failure and 3 patients developed distant metastasis.Acute toxicity was mostly Grade Ⅰ to Grade Ⅱ.Seventeen patients had grade Ⅰ xerostomia.Three patients suffered from grade Ⅰ acute oral mucosa reaction and 12 patients had grade Ⅱ acute oral mucosa reaction.Analysis of the dose-volume histograms (DVHs) showed that the mean dose delivered to the PTV,PTVnd,PTV1 and PTV2 was 73.4,74.1,67.8,and 54.1 Gy,respectively.The median dose to 50% of the right and left parotid glands was 43.9 Gy and 41.9 Gy,respcetively.The average value of maximum dose to the left and right lens was 8.06 and 8.12 Gy,respectively.The average value of maximum dose to the brainstem,spinal cord,left and right optic nerve and optic chiasma PRV was 60.6,46.6,50.0,55.0,and 56.0 Gy,respectively.Conclusion:IMRT can achieve satisfactory dose distdbution to nasopharyngeal carcinoma and surrounding tissues in NPC patients,protect normal tissues during the treatment and improve local control rate.

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.