Disaster Planning ; organization & administration ; Emergencies ; Emergency Medical Services ; organization & administration ; Humans ; Public Health ; methods

0.05],significantly higher than stage Ⅲ,Ⅳ[60%(6/10),50%(5/10);P

ObjectiveTo observe the effect of sport walking on heart and lungs functions in old women.MethodsForty-two old women aged from 60 to 69 had sport walking for 4 months; the speed and intensity were controlled according to their heart rate respectively. The indexes of respiration, circulation and rheoencephalography were measured before and after exercise.ResultsAfter exercise, blood-pumping function of heart improved obviously, stroke volume increased from (65.22±11.41)ml to (72.10± 10.78)ml, ejection fraction increased from (60.10±5.03)% to (68.78±6.25)%, while heart rate declined from (77.45±8.69) times/min to (7.89±8.21)times/min, capacity increased from (2.86±0.36)L to (3.34±0.53)L, and maximal voluntary ventilation for every minute increased from (96.14± 15.21)L to (114.02±16.01)L, significantly different compared with that before treatment ( P<0.01). The fluid time of rheoencephalography reduced from (0.171±0.058)s to (0.128±0.049)s ( P<0.01).ConclusionSport walking under proper intensity can improve the function of respiration and circulation system in old women, so it is a good way to keep health for the elders.

OBJECTIVETo study the effects of treatment with gonadotropin-releasing hormone analogs (GnRHa) on final height, weight and pubertal development in girls with central precocious puberty.

METHODSTwenty-six girls with central precocious puberty were treated with GnRHa for an average of 19.2+/- 8.4 months. Pretreatment and posttreatment predicted adult heights (PAH) were evaluated based on the Bayley-Pineau table. The patients, heights and weights were measured monthly. Bone age (BA) was evaluated using Greulich-Plyle. Height standard deviation score for BA [HtSDS (BA)] was measured. After discontinuation of treatment, the patients were followed-up for the observation of height, weight, BA and menstruation.

RESULTSFinal height averaged 158.0+/- 4.0 cm in the 26 girls, which was greater than their target height (155.3+/- 4.4 cm; P< 0.01) and consistent with their posttreatment PAH (158.4+/- 5.2 cm). The final height was positively corrrelated with initial height, PAH and HtSDS(BA). There was a positive correlation in the body mass index before and after treatment (r=0.724, P< 0.01). Menarche occurred 13.2+/- 6.1 months after discontinuation of treatment, with a mean menarche age of 12.2+/- 0.7 years.

CONCLUSIONSGnRHa may increase final height in girls with central precocious puberty. Their final heights may be correlated with their initial heights and PAH. The pubertal development after GnRHa treatment in girls with central precocious puberty may be matched with normal children.

Age Determination by Skeleton ; Body Height ; drug effects ; Body Mass Index ; Child ; Child Development ; drug effects ; Female ; Gonadotropin-Releasing Hormone ; adverse effects ; analogs & derivatives ; Humans ; Puberty, Precocious ; drug therapy ; physiopathology

OBJECTIVETo observe the evolutionary tendency of brain derived neurotrophic factor (BDNF) of the limbic system in post-stroke model rats and the intervention effect of Yinao Jieyu Recipe (YJR).

METHODSMale Wistar rats were randomly divided into the normal control group (n =6), the sham-operation group (n =7), the multiple cerebral infarction (MCI) group (n =10), the post-stroke depression (PSD) group (n =10), the Chinese medicine (CM) treatment group (n =10), and the Western medicine (WM) treatment group (n =10) according to random digit table after open-field testing. Rats in the normal control group were routinely fed. 0. 3 mL normal saline was intravenously pushing from the external carotid artery to rats in the sham-operation group, and distilled water administered to them by gastrogavage. Each dose allogenic microthrombi were in vitro pushed to rats in the rest groups from the external carotid artery. The PSD model was duplicated by 21-day chronic unpredictable mild stress (CUMS) and single cage feeding in the PSD group 7 days after surgery. After preparing models rats in the CM group and the WM group were administered with YJR and Nimodipine respectively for 4 successive weeks. Changes of BDNF and the intervention effect of YJR were observed at week 1, 2, and 4 after intervention.

RESULTSImmunohistochemical results of BDNF showed, compared with the normal control group, expression levels of BDNF in the hippocampus, hypothalamus, and amygdala decreased in the MCI group at week 2 and 4 (P <0. 01 , P <0. 05) ; expression levels of BDNF in each part decreased in the PSD group at week 1-4 (P <0.01). Compared with the MCI group, expression levels of BDNF in each part decreased in the PSD group at week 1-4 (P <0. 01). Compared with the PSD group, expression levels of BDNF in each part increased in the CM group at week 1-4 (P <0. 01).

CONCLUSIONBDNF changes existed in post-stroke model rats, and YJR could slow down this progress.

Amygdala ; Animals ; Brain-Derived Neurotrophic Factor ; metabolism ; Depression ; Depressive Disorder ; Drugs, Chinese Herbal ; pharmacology ; therapeutic use ; Hippocampus ; Male ; Models, Animal ; Rats ; Rats, Wistar ; Stroke ; drug therapy

Objective To compare the differences of electrical activity in calf muscle of children with growing pains from normal children when standing and heel raising. Methods 32 children with growing pains and foot pronation were as growing pains group, and 32 normal children as control group. All the children were measure with surface electromyography (sEMG) of tibialis anterior, peroneus longus, medial gastrocnemius and tibialis posterior when standing and heel raising. Results The root mean square (RMS) of peroneus longus increased significantly in growing pains group when standing (P<0.01). The RMS decreased significantly in medial gastrocnemius (P<0.05) and increased significantly in tibialis posterior (P<0.01) when heel raising. Conclusion The characteristics of electrical activity in calf muscle is difference from the normal in the growing pains children with foot pronation during standing and heel raising.

Homo sapiens longevity assurance homologue 2 (LASS2) is a novel gene isolated from a human liver cDNA library by our laboratory, and it is a human homologue of the yeast longevity assurance gene LAG1 (Saccharomyces cerevisiae longevity assurance gene). According to our previous results, LASS2 could interact with subunit c of vacuolar type H(+)-ATPase (V-ATPase), and the overexpression of LASS2 could inhibit the cell growth of a human hepatocellular carcinoma (HCC) cell line, SMMC-7721. In order to understand the role of the interaction between LASS2 and V-ATPase in HCC cell growth, we transiently transfected plasmid pCMV-HA2-LASS2 into HCCLM3, a HCC cell line without the significant expression of endogenous LASS2. The pH-sensitive fluorescence probes, BCECF and BCECF-AM, were used to measure the intracellular and extracellular H(+) concentrations of HCCLM3 cells respectively. The effect of LASS2 gene on apoptosis was evaluated with Annexin-V/FITC and propidium iodide (PI) by flow cytometry. Western blot was used to detect cytochrome c (Cyt c) in the cytosol and mitochondria, as well as pro-caspase-3 in cytosol. The results showed that the cell growth of LASS2-transfected HCCLM3 cells was significantly inhibited compared with that of the mock control. LASS2 transfection increased intracellular H(+) concentration of HCCLM3 cells, while decreased extracellular H(+) concentration. Moreover, LASS2 transfection significantly enhanced the apoptosis of HCCLM3 cells. In LASS2-transfected cells, the amounts of Cyt c increased in the cytosol, while decreased in the mitochondria. Meanwhile, the expression of pro-caspase-3 in the cytosolic extracts was decreased. These results implicate that LASS2 gene might increase intracellular H(+) of HCC cells via the interaction with V-ATPase, thereby inducing cell apoptosis through mitochondrial pathway.
Apoptosis ; Carcinoma, Hepatocellular ; pathology ; Caspase 3 ; metabolism ; Cell Line, Tumor ; Cell Proliferation ; Humans ; Liver Neoplasms ; pathology ; Membrane Proteins ; metabolism ; RNA, Small Interfering ; Sphingosine N-Acyltransferase ; metabolism ; Transfection ; Tumor Suppressor Proteins ; metabolism ; Vacuolar Proton-Translocating ATPases ; metabolism

OBJECTIVETo investigate the protective effects of the natural medicinal monomer isopsoralen (ISR) with estrogenic activity against oxidative damage in human lens epithelial cells B3 (HLE-B3) caused by hydrogen peroxide (H(2)O(2)) and to pursue the possible mitochondrial proteomic regularity of the protective effects.

METHODSHLE-B3 cells were treated with H(2)O(2) (300 μ mol/L), β-estradiol (E(2): 10(-8) mol/L) and H(2)O(2), ISR (10(-5) mol/L) and H(2)O(2), or left untreated. Altered expressions of all mitochondrial proteins were analyzed by protein array and surfaceenhanced laser desorption ionization time of flight mass spectrometry (SELDI-TOF-MS). The mass/charge (m/z) ratios of each peak were tested by the Kruskal-Wallis rank sum test, and the protein peak value of the m/z ratio for each treatment by pair comparison was analyzed with the Nemenyi test.

RESULTSH(2)O(2) up-regulated the expressions of two protein spots (with m/z of 6532 and 6809). E(2) mitigated the oxidative damage, and the expression of one protein spot (m/z 6532) was down-regulated. In contrast, ISR down-regulated both of protein spots (m/z 6532 and 6809).

CONCLUSIONSISR could effectively inhibit H(2)O(2)-induced oxidative damage in HLE-B3 cells. The protein spot at m/z of 6532 might be the target spot of ISR against oxidative damage induced by H(2)O(2).

Cell Line ; Epithelial Cells ; drug effects ; metabolism ; pathology ; Estradiol ; pharmacology ; Furocoumarins ; pharmacology ; Humans ; Hydrogen Peroxide ; toxicity ; Lens, Crystalline ; pathology ; Mitochondria ; metabolism ; Oxidation-Reduction ; drug effects ; Oxidative Stress ; drug effects ; Protective Agents ; pharmacology ; Proteome ; metabolism ; Proteomics ; methods

BACKGROUNDPrevious investigations indicate that cooks are exposed to polycyclic aromatic hydrocarbons (PAH) from cooking oil fumes (COF). However, Emission of PAH and their carcinogenic potencies from cooking oil fumes sources have not been investigated among cooks.

AIMSTo investigate the urinary excretion of a marker for oxidative DNA damage, 8-hydroxydeoxyguanosine (8-OHdG), in different groups of cooks and different exposure groups, and to study the association between 8-OHdG and 1-hydroxypyrene (1-OHP), a biological marker for PAH exposure.

METHODSUrine samples were collected from different groups of cooks (n = 86) and from unexposed controls (n = 36), all are male with similar age and smoking habits. The health status, occupational history, smoking, and alcohol consumption 24 hours prior to sampling was estimated from questionnaires. The urinary samples were frozen for later analyses of 8-OHdG and 1-OHP by high performance liquid chromatography.

RESULTSExcretion in urine of 8-OHdG were similar for controls (mean 1.2 µmol/mol creatinine, n = 36), and for those who had been in the kitchen room with exhaust hood operation (mean 1.5 µmol/mol creatinine, n = 45). COF exposed cooks without exhaust hood operation had increased excretion of 8-OHdG (mean 2.3 µmol/mol creatinine, n = 18). The difference between this group and the unexposed controls was significant. The urinary levels of ln 1-OHP and ln 8-OHdG were still significantly correlated in a multiple regression analysis.

CONCLUSIONResults indicate that exposure to PAH or possibly other compounds in COF may cause oxidative DNA damage.

Adult ; Air Pollutants, Occupational ; urine ; Cooking ; DNA Damage ; Deoxyguanosine ; analogs & derivatives ; urine ; Humans ; Male ; Occupational Exposure ; Oils ; adverse effects ; Oxidative Stress ; Polycyclic Aromatic Hydrocarbons ; adverse effects ; Surveys and Questionnaires ; Young Adult