0 05) between the two groups in the patient′s age, pregnancy age, parities, the cavity volume of uterine, hemoglobin and blood platelet count The bleeding volume was (51 6?17 2) ml for the treated group and (63 3?17 1) ml for the control group ( P 2 months It could decrease the volume of bleeding during the operation and benefit for patients recovering

Objective To develop the detection method of common fungal pathogens by general primer PCR.Methods The primers were designed from the target genes of 5.8S rDNA and 28S rDNA of fungi,and the specificity and sensitivity were observed.Results The general primer PCR can be used to detected C.albicans,C.parapsilosis,C.krusei,C.glabrata,C.tropicalis,C.neoformans,A.fumigatus,A.flavus,A.nidulans,A.niger,C.carrionii,P.verrucosa,S.schenckii,F.pedrosoi,T.rubrum,T.mentagrophytes,M.gypseum,M.canis,E.floccosum,M.racemosus,the sensitivity was 15 pg/ml of DNA.Conclusion The general primer PCR can be used to detect common fungal pathogens.

0.05),but the average levels of DNMT1 mRNA of mild and moderate groups were significantly lower than that of the control group(P

Objective To study the relationship between the invasion of pituitary adenomas and expressions of MMP-9,Ki-67 and nm23. Methods The expressions of MMP-9,Ki-67 and nm23 were examined by immunohistochemical Elivision methods in 78 cases of pituitary adenomas. Of them,40 cases were invasive pituitary adenomas and, 38 cases were noninvasive pituitary adenomas. Results The expression levels of MMP-9 and Ki-67 in the invasive pituitary adenomas were significantly higher than those in the noninvasive ones (P

Objective To study the content difference of naringin in Fructus Aurantii Immaturus of different specifications.Methods HPLC was performed on the Merck- Lichrospher RP-C18(4.6 mm? 250 mm, 5 ? m) with temperature of 35 ℃ .The chromatographic conditions for naringin:the mobile phase consisting of acetonitrile-0.3 % Phosphoric acid(20 ∶ 80), at the flow rate of 1 mL/min, and the detection wavelength at 283 nm. Results The content of naringin increased with the diameter of Fructus Aurantii Immature slices.Conclusion It is suggested that there exists significant differences in intrinsic quality among Fructus Aurantii Immaturus of different specifications.

Objective To construct a ciaR gene-knockout (ΔciaR) mutant of Streptococcus pneu-moniae ( S. pneumoniae) and to investigate the effects of CiaR in CiaH/CiaR, a streptococcal two-component signal-transducing system, on the expression of genes encoding penicillin-binding proteins ( pbps genes) and cia-dependent small RNAs (csRNAs). Methods Electrophoretic mobility shift assay (ESMA) was per-formed to detect the recombinant CiaR (rCiaR)-binding pbps genes. A suicide plasmid pEVP3ciaR for ciaR gene knockout was constructed and then aΔciaR mutant was obtained through homologous recombination and insertion inactivation of the suicide plasmid, and screening with chloromycin. The mutant was identified using PCR and sequencing analysis. E-test was used to detect the minimal inhibitory concentrations ( MIC) of penicillin ( PCN) and cefotaxime ( CTX) against S. pneumoniae strains. Changes and differences in the expression of pbps genes and csRNAs in theΔciaR mutant and its wild-type strain before and after treatment with 1/4 MIC of PCN or CTX were detected using real-time quantitative RT-PCR. Results The rCiaR could bind to the promoter regions in pbp1a, pbp1b and pbp2b genes of S. pneumoniae. The ciaR gene in ΔciaR mutant was inactivated by insertion according to the results of PCR and sequencing analysis. After treatment with 1/4 MIC of PCN or CTX, the expression of pbps genes at mRNA level ( pbps-mRNAs) in theΔciaR mu-tant was significantly increased (P<0. 05), but the levels of csRNAs were significantly decreased (P<0. 05);whereas a significantly decreased pbps-mRNAs (P<0. 05) and increased csRNAs (P<0. 05) were observed in its wild-type strain. The result of E-test showed that the MICs of PCN and CTX against ΔciaR mutant were increased by 250-fold as compared with those against its wild-type strain. Conclusion The CiaR can enhance the drug resistance of S. pneumoniae to PCN and CTX through down-regulating the expres-sion of PBP1a, PBP1b and PBP2b and up-regulating the expression of csRNAs to inhibit the expression of PBPs.

ObjectiveTo study the curative effects of using oxygen treatment combined mixture to Ⅲ-Ⅳ bedsore. Methods Divided 63 patients into the observation group (32 cases) and the traditional group (31 cases) randomly. Oxygen treatment combined mixture was used in the observation group and the traditional nursing measures were used in the traditional group. Compared the curative effects of bedsore between the 2 groups.Results The cure rate of Ⅲ-Ⅳ bedsore in the observation group was significant higher than that of in the traditional group,P

OBJECTIVE To investigate DNA hypermethylation of human 8-hydroxyguanine glycosy-lase(hOGG1 )gene and and the level of oxidative stress and DNA oxidative damage relations with arse-nic poisoning.METHODS In ende mic coal-pollution-borne arsenism area,Xinren county,Guizhou Province,according to the diagnostic criteria of ende mic arsenism(WS /T21 1 -2001 ),207 people with ende mic arsenism were selected and divided into four groups(The arsenic exposure group:46 cases, mild arsenism group:46 cases,moderate arsenism group:60 cases and severe arsenism group:55 cases).64 residents were selected as controls in a village about 12 km away fro m the ende mic arsenism area.With the informed consent principle,peripheral blood of all respondents was collected in order to analyze DNA methylation.Methylation-specific poly merase chain reaction were respectively performed to analyze hOGG1 Hypermethylation in arsenism respondents.Che mical methods were performed on the activity of super oxide dis mutase (SOD)and glutathione peroxidase (GSH-Px),while the contents of malondialdehyde (MDA)in the blood of patients were measured,and the contents of 8-hydroxy-2′-deox-yguanine(8-OHdG)urine of patients were measured and analysed.On the basis of methylation status are divided into hOGG1 gene methylation group (34 cases)and hOGG1 gene no methylation group (237cases).Analysis was performd on hOGG1 gene DNA methylation and the relationship between oxi-dative stress and arsenic poisoning.RESULTS The positive rates of hypermethylation of hOGG1 were associated with the degree of arsenic poisonin (co mpared with control group,χ2 =23.916,P <0.05, Co mpared with the Ende mic area normal group,χ2 =12.039,P <0.05 ).Co mparing with negative group,SOD〔(85 ±25)kU·L -1 〕,GSH-Px〔(70 ±26)kU·L -1 〕activity and 8-OHdG 〔(22.5 ±6.8)μg·L -1 〕contents were lower〔(1 18 ±41 )kU·L -1 ,(171 ±56)kU·L -1 ,(28.4 ±6.5)μg·L -1 ,P <0.05)〕in positive group.There was no significant difference between the MDA content(P>0.05).CONCLUSION Coal arsenic exposure can cause hOGG1 gene high methylation and oxidation and anti-oxidation system imbalance,causing DNA oxidative damage,it is one of the reasons to pro mote the develop ment of arsenic poisoning occurred.

China ; Female ; Hepatitis A Vaccines ; administration & dosage ; Hepatitis B ; prevention & control ; Hepatitis B Vaccines ; administration & dosage ; Humans ; Male ; Vaccination ; methods ; Vaccines, Combined ; administration & dosage

Objective To investigate the association of the expression level of anti-apoptosis protein p-AKT and gastric mucasal injury induced by indomethacin in mice.Methods The cytotoxicity induced by indomethacin was measured by LDH assay.The p-AKT expression levels were measured in the gastric mucosal tissues from C57BL/6 mice and rat gastric mucosal (RGM-1) cell lines treated with indomethacin lay western blotting.Results The cytotoxicity induced by indomethacin was in a dose dependent manner.Compared with the control,a typical histological appearance of gastric ulcer was observed in the gastric mucosa of in domethacin-administered mice;p-AKT protein expression in the gastric mucosa of mice and RGM-1 cell lines was decreased after treated with indomethacin.Conclusion The reduction of Anfi-apoptesis protein p-AKT expression may be a new mechanism for the gastric mucosal injury induced by indomethacin.