OBJECTIVE: To observe the changes of cell gap junction ultrastructure of gastric epithelial cells in patients with gastric cancer(GC) and precancerous lesion(PL),and to investigate the relation between these changes and H.pylori infection. METHODS: Seventy patients with GC, 88 with PL, and 33 with chronic superfial gastritis (CSG) were studied. H.pylori was detected by rapid urease test,basic fuchsin stain and 14C-urea breath test. The CagA gene of H.pylori was determined by polymerase chain reaction(PCR).The cell gap junction ultrastructure was observed under transmission electronic microscope. RESULTS: Length of junction/unit perimeter of gastric epithelial cells in patients with PL was smaller than that in CSG patients, and the smallest width of the intercellular space was bigger than that in CSG patients. The number of cell junction, the number of junction/unit perimeter, and the length of junction/unit perimeter in patients with GC were all smaller than those in patients with CSG or PL, and its smallest width of the intercellular space was bigger than that in patients with CSG. In patients with GC, the number of cell junction, the number of junction/unit perimeter and the length of junction/unit perimeter in CagA+ H.pylori group were smaller than those in CagA(-) H.pylori group, and its smallest width of the intercellular space was bigger than that in CagA(-) H.pylori group. In PL patients, the intercellular space decreased, and the length of cell junction of gastric epithelial cells became bigger after H.pylori eradication. The length of junction/unit perimeter in patients of H.pylori eradication was bigger than that in patients without eradication, and the smallest width of the intercellular space was smaller than that in patients without eradication. CONCLUSION The changes of cell gap junction of gastric epithelial cells in patients with GC and PL are associated with H.pylori infection especially CagA+ H.pylori infection. Eradication of H.pylori can promote the formation of cell junction.
Adenocarcinoma ; microbiology ; ultrastructure ; Epithelial Cells ; ultrastructure ; Female ; Gastric Mucosa ; ultrastructure ; Helicobacter Infections ; pathology ; Helicobacter pylori ; Humans ; Intercellular Junctions ; ultrastructure ; Male ; Precancerous Conditions ; microbiology ; ultrastructure ; Stomach Neoplasms ; microbiology ; ultrastructure

OBJECTIVETo understand the reproductive health status of female workers in pharmaceutical industry of Gansu Province, to explore influencing factors, and to propose some reference basis of intervening measures.

METHODSThe cluster sampling method was used to study 1801 female workers from 16 pharmaceutical industries in 6 cities (Pingliang, Qingyang, Lanzhou, Dingxi, Zhangye and Jiuquan cities) of Gansu Province. The investigation was performed by interviewing and adopting questionnaires.

RESULTSThere were the problems of labor and organization, which included the overtime work, continuous work, standing for long periods, rapid monotonous action assignments, the loading work and a variety of harmful factors in the working environment of the pharmaceutical industry in Gansu Province. There were many problems in the reproductive health status of female workers. The morbidities of abnormal menstruation and breast diseases in female workers were 43.25% and 20.43%. The order of high morbidities was hyperplasia of mammary glands (91.30%), breast adenofibroma (5.43%) and mastitis (2.99%). The order of morbidities for three reproductive system disease was adnexitis (21.57%), cervical erosion (20.06%) and vaginitis (11.09%). The rates of abnormal menstrual cycle, abnormal menstrual amount and cervical erosion increased with the length of service (P < 0.01). The taking breaks, long standing, loading work, exposure to harmful factors were related to abnormal menstruation (P < 0.05). The rapid repeat monotonous action was an important influencing factor for female reproductive system disease (OR = 1.255, 95%CI = 1.031 ∼ 1.528).

CONCLUSIONThere are relatively serious occupational hazards in the pharmaceutical industry of Gansu Province. The reproductive health status of female workers is not improved. Social public should pay attention to the protection for female workers.

Adolescent ; Adult ; China ; Drug Industry ; Female ; Health Status ; Humans ; Middle Aged ; Occupational Exposure ; Reproductive Health ; Surveys and Questionnaires ; Workplace ; Young Adult

BACKGROUNDPrenatal hyperglycaemia may increase metabolic syndrome susceptibility of the offspring. An underlying component of the development of these morbidities is hepatic gluconeogenic molecular dysfunction. We hypothesized that maternal hyperglycaemia will influence her offsprings hepatic peroxisome proliferator-activated receptor coactivator-1α (PGC-1α) expression, a key regulator of glucose production in hepatocytes.

METHODWe established maternal hyperglycaemia by streptozotocin injection to induce the maternal hyperglycaemic Wistar rat model. Offspring from the severe hyperglycemia group (SDO) and control group (CO) were monitored until 180 days after birth. Blood pressure, lipid metabolism indicators and insulin resistance (IR) were measured. Hepatic PGC-1α expression was analyzed by reverse transcription polymerase chain reaction and Western blotting. mRNA expression of two key enzymes in gluconeogenesis, glucose-6-phosphatase (G-6-Pase) and phosphoenolpyruvate carboxykinase (PEPCK), were analyzed and compared.

RESULTSIn the SDO group, PGC-1α expression at protein and mRNA levels were increased, so were expression of G-6-Pase and PEPCK (P < 0.05). The above effects were seen prior to the onset of IR.

CONCLUSIONThe hepatic gluconeogenic molecular dysfunction may contribute to the metabolic morbidities experienced by this population.

Animals ; Female ; Hyperglycemia ; chemically induced ; physiopathology ; Insulin Resistance ; physiology ; Liver ; metabolism ; Male ; Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha ; Peroxisome Proliferator-Activated Receptors ; metabolism ; Pregnancy ; Prenatal Exposure Delayed Effects ; RNA-Binding Proteins ; Rats ; Rats, Wistar ; Streptozocin ; toxicity ; Transcription Factors

OBJECTIVETo investigate the clinical manifestations, complications and treatment of medicament-like dermatitis due to trichloroethylene (TCE), so as to provide basis for studying its etiology and mechanism.

METHODSFifty patients with dermatitis due to TCE from 1997 to 2000 were analysed retrospectively.

RESULTSThe occurrence of the dermatitis was not parallel to TCE exposure levels, without significant dose-effect relationship. This disease could be caused by both inhalation and skin exposure. The latency period of TCE dermatitis ranged from 5 to 66 days, and the average was 31.5 d (Medium). The major clinical manifestations included skin lesions, fever, superficial lymph node swelling and liver dysfunction. Infection was the major complication. Glucocorticoid was effective for treatment of this disease.

CONCLUSIONThe clinical manifestations due to TCE exposure were similar to dermatitis medicamentosa. The major clinical types of TCE dermatitis included exfoliative dermatitis and erythema multiforme. The dermatitis is considered to be mediated by delayed-type (IV) hypersensitivity. The key factors to treat this disease successfully included the use of glucocorticoid in time with sufficient dose and full course, professional skin care, active treatment to protect the liver and to avoid infection.

Adolescent ; Adult ; Allergens ; adverse effects ; Dermatitis, Exfoliative ; diagnosis ; etiology ; therapy ; Drug Eruptions ; diagnosis ; etiology ; therapy ; Female ; Humans ; Male ; Occupational Exposure ; adverse effects ; Retrospective Studies ; Trichloroethylene ; adverse effects

OBJECTIVETo study DNA damages of liver cells in rats exposed to vinyl chloride monomer (VCM), and the expressions of DNA damage repair enzymes including O(6)-methyl guanine-DNA methyl transferase (MGMT), X-ray repair cross-complementing group 1 (XRCC1) and X-ray repair cross-complementing group 3 (XRCC3); and to explore the repair mechanism of DNA damage induced by VCM.

METHODSRats were exposed to VCM by intraperitoneal injection. DNA damages were detected by single cell gel electrophoresis (comet assay). The expressions of DNA damage repair enzymes were measured by immunohistochemical methods.

RESULTSThe percentages of comet cells in low, moderate, and high dose groups (11.75%, 12.38%, and 17.63%, respectively) were greater than that of control (5.67%). The latter two groups were significantly different from that of control (P < 0.05, P < 0.01). The expressions of MGMT and XRCC1 decreased, and XRCC3 increased with the dose of VCM increased. DNA damage was correlated with the expression of XRCC3 (r = 0.438, P = 0.067).

CONCLUSIONVCM can cause DNA damage of liver cells with dose-response relationship. DNA damage repair enzymes take part in the repairing of DNA damage induced by VCM.

Animals ; Carcinogens ; toxicity ; DNA Damage ; drug effects ; DNA Repair ; DNA-Binding Proteins ; genetics ; metabolism ; Dose-Response Relationship, Drug ; Liver ; cytology ; metabolism ; Male ; O(6)-Methylguanine-DNA Methyltransferase ; genetics ; metabolism ; Rats ; Rats, Sprague-Dawley ; Vinyl Chloride ; toxicity ; X-ray Repair Cross Complementing Protein 1

Background Prenatal hyperglycaemia may increase metabolic syndrome susceptibility of the offspring.An underlying component of the development of these morbidities is hepatic gluconeogenic molecular dysfunction.We hypothesized that maternal hyperglycaemia will influence her offsprings hepatic peroxisome proliferator-activated receptor coactivator-1α (PGC-1α) expression,a key regulator of glucose production in hepatocytes.@@Method We established maternal hyperglycaemia by streptozotocin injection to induce the maternal hyperglycaemic Wistar rat model.Offspring from the severe hyperglycemia group (SDO) and control group (CO) were monitored until 180 days after birth.Blood pressure,lipid metabolism indicators and insulin resistance (IR) were measured.Hepatic PGC-1α expression was analyzed by reverse transcription polymerase chain reaction and Western blotting.mRNA expression of two key enzymes in gluconeogenesis,glucose-6-phospha-tase (G-6-Pase) and phosphoenolpyruvate carboxykinase (PEPCK),were analyzed and compared.@@Results In the SDO group,PGC-1α expression at protein and mRNA levels were increased,so were expression of G-6-Pase and PEPCK (P<0.05).The above effects were seen prior to the onset of IR.@@Conclusion The hepatic gluconeogenic molecular dysfunction may contribute to the metabolic morbidities experienced by this population.

Aim To observe the effect of capsaicin on the experimental autoimmune neuritis (EAN) in rats and explore the mechanism.Methods To induce EAN,male Lewis rats were immunized with peripheralnerve myelin sheath antigen (P257481) peptide and complete Freund's adjuvant (CFA) mixed liquor.Rapamycin (RAPA,2.5 mg · kg-1) was administered by intraperitoneal injection 0.5 h after immunization and capsaicin (1 mg · kg-1 · d-1) was administered by intragastric administration 1.0 h after immunization for 15 days.The incidence and clinical characteristics of EAN were observed.The clinical scores of neurological signs were completed and body weight was measured.Pathological morphology of sciatic nerve was observed by HE staining and Lauck fast blue staining.Ultrastructure of sciatic nerve was observed by transmission electron microscope.Levels of serum tumor necrosis factor alpha (TNF-α),interferon gamma (IFN-γ),interleukin 1β (IL-1β) and intedeukin-6 (IL-6) were tested by enzyme linked immunosorbent assay (ELISA).Expressions of autophagy related protein were measured by Western blot.Results Compared with EAN group,the clinical scores of neurological signs significantly decreased from day 7 to day 16 of post-immunization (P ＜ 0.05),body weight significantly increased from day 3 to day 16 of post-immunization (P ＜ 0.05),demyelination obviously decreased,inflammatory cell infiltration number obviously decreased (P ＜ 0.05),the levels of TNF-α,IFN-γ,IL-1β and IL-6 significantly decreased (P ＜ 0.05),the number of autophagosome in axon of sciatic nerve significantly decreased (P ＜ 0.05),and expressions of Beclin-1 and LC3-Ⅱ and the ratio of LC3-Ⅱ and LC3-Ⅰ were significantly down-regulated,and the expression of p62 was significantly up-regulated (P ＜ 0.05) in EAN + capsaicin group.Rapamycin partially reversed the action of capsaicin.Conclusions Capsaicin inhibits EAN in rats,and the mechanism may be related with the inhibition of autophagy activity.

Objective To analyze the patterns of incidence and mortality on larynx cancer in China.Methods Data from 32 Cancer Registries in China were examined,sorted,and analyzed by the National Cancer Registry,to obtain the crude,Chinese national and world age- standardized rates (ASR) of incidence and mortality and their trends.Results The crude incidence and mortality rates of larynx cancer wcrc 2.04/105 and 1.06/105 in China during 2003-2007.The rates were higher in males than those in females,and also higher in urban areas than those in rural areas.The highest Chinese ASRs of incidence and mortality of larynx cancer in 32 cancer registries in China were 2.08/105 in Zhongshan city,Guangdong province,and 1.58/105 in She county,Hebei province respectively.The trend of incidence and mortality of larynx cancer was stable from 2003 to 2007.Conclusion Although both the incidence and mortality of larynx cancer in China were still in low level,comprehensive measures should be carried out to prevent the increase on both the incidence and mortality of larynx cancer.

Objective To investigate the presence and genetic background of 16S rRNA methylase gene and Aminoglycoside modifying enzymes(AMEs) genes in Klebsiella pneumoniae isolated from the People's Liberation Army 98th HospitaI,Huzhou district,Zhejiang province,China.Methods 25 strains of Klebsiella pneumoniae were isolated from the inpatienta between September,2005 and April,2006.6 kinds of 16S rRNA methylase gene (including armA,rmtA,rmtB,rmtC,rmtD and npmA ),6 kinds of AMEs genes [ including aac (3)-Ⅰ,sac (3)-Ⅱ,sac (6')-Ⅰ,aac (6')-Ⅱ,ant (3")-Ⅰand ant(2")-Ⅰ],intI1,intI2,intI3,mercuric reductase gene merA (merA gene were the collective genetic markers of transposona of Tn21 and Tn501 ) and tnpA ( tnpA gene were the collective genetic markers of transposons of Tn1,Tn2,Tn3 and Tn1000) were analyzed by PCR and verificated by DNA sequencing.Results In 25 strains of Klebsiella pneumoniae,the positive rate of genes of rmtB,sac (3)-Ⅱ,sac (6')-Ⅰ,ant(3")-Ⅰ and intI1 were 60.0%(15/25),4.0%(1/25),48.0%(12/25),60.0%(15/25) and 96.0%(24/25),respectively.The rest 12 kinds of genes were all tested negative.The total positive rate of 6 kinds of AMEs gene was 84.0%(21/25).Conclusion There were very high positive rate on both genes of rmtB and AMEs genotypes in Klebsiella pneumoniae isolated from inpatients,and this was the first report of the emergence of 16S rRNA methylase gene rmtB in Klebsiella pneumoniae identified in Zhejiang province,China.

In order to reveal variation and evolution of M genes of human avian H5N1 influenza strains, the M genes of human avian H5N1 strains in Guangdong were sequenced and the M genes of global strains were searched out from Internet. They were analyzed by DNAStar 5. 0 and their revolutionary speeds were studied by means of combining the epidemiological data. It was found that M1 genes of 53 H5N1 strains and M2 genes of 51 strains during 1997-2006 were homologously classified into two groups: the strains from Hong Kong during 1997 (G I) were one group and the strains from Hong Kong, Vietnam, Thailand, Indonesia, China mainland, Turkey, Iraq, Azerbaijan, Egypt during 2003-2006 (G II ) were the another group. There were 20 substitutions of amino acids in M1 gene of all strains (7.94%, 20/252), where there were 9 amino acids in strains during 2003-2006 differing from the strains in 1997, meanwhile there were 22 substitutions of amino acids in M2 gene of all strains (22.7%, 22/97), where there were 4 amino acids in strains during 2003-2006 differing from the strains in 1997. In the synonymous variation, Ks values in M1 were 26.8 x 10(-6)-42.6 x 10(-6) Nt/d, and Ka values 4.39 x 10(-6)-6.98 x 10(-6) Nt/d, where there was more rapid speed of synonymous substitution than that of replacement, which showed that there existed less human immunological pressure and negative selective pressure by biological test. Ks values in M2 were 13.1 x 10(-6)-23.4 x 10(-6) Nt/ d, and Ka values 9.1 x 10(-6)-16.2 x 10(-6) Nt/d; where the ratios of Ks to Ka was 1.0-1.6 times as there was the neutral selective pressure in TL-676-05 strain. There was an amino acid substitution of S224, N in M1 gene of strains during 2003-2006 and an increas in a glycoprotein domain NSS224-226. The secondary structure of M2 protein varied as the substitution of C50 F of eight strains from Indonesia in 2005. The strains G I did not reemerge after Hong Kong human avian H5N1 influenza event. An increase of a glycoprotein domain NSS224-226 in M1 protein during 2003-2006 might be related with virus pathogenicity. Human avian H5N1 influenza M gene evolved frequently in nature, which might have an impact on its capacity of human-to-human transmission.
Amino Acid Sequence ; China ; Genetic Variation ; Humans ; Influenza A Virus, H5N1 Subtype ; genetics ; Molecular Sequence Data ; Phylogeny ; Viral Matrix Proteins ; chemistry ; genetics