ObjectiveTo understand dangerous factors causing child cerebral palsy and try to diagnose and treat cerebral palsy early, and decrease the ratio of cripple.MethodsTo analyze if the occurrence, style or complication of cerebral palsy having a relation to dangerous factors such as sexes, birth weight, premature delivery, twins, neonatal asphyxia, infection of newborn, nuclear icterus, mother's age, virus infection in the duration of pregnancy, threatened abortion and family history of cerebral palsy.ResultsThe ration of male and female is 1.47∶1 in 146 cases of child cerebral palsy. Factors causing cerebral palsy are low birth weight (79.45%), premature delivery (64.38%), neonatal asphyxia (41.78%), threatened abortion (32.89%), twins (31.53%), infection of newborn (12.33%), nuclear icterus (6.16%), parturient with advanced age (3.42%), having infection history in the duration of pregnancy (2.74%), and family history of cerebral palsy (0.68%). Both styles and complications of cerebral palsy have a relation to dangerous factors.ConclusionsThe low birth weight, premature delivery, neonatal asphyxia, twins and threatened abortion all are higher dangerous factors causing child cerebral palsy. In order to abstain the occurrence of these dangerous factors, it is important to educate people and doctors recognizing all dangerous factors. It is also helpful to lower the ratio of cripple that regularly examining child with dangerous factors, discovering symptoms and complications of cerebral palsy in time, and diagnosing and treating cerebral palsy as soon as possible.

Aged ; Female ; Humans ; Maxillary Sinus ; parasitology ; Myiasis ; Nasal Cavity ; parasitology

Actinin ; genetics ; Adolescent ; Adult ; Asian Continental Ancestry Group ; genetics ; Athletes ; Athletic Performance ; China ; Ethnic Groups ; genetics ; Female ; Humans ; Male ; Polymorphism, Genetic ; Young Adult

Reuse of waste oil in cooking has been the social concern for long time, but until now there is no reliable method to identify the gutter oil.In this work, based on the generation of long-chain aliphatic aldehydes in the refinement of gutter oil, gutter oil and adulterate cooking oil were identified by determining hexanal, heptanal, octanal, nonanal and decanal in oil sample with high perfomance liquid chromatography (HPLC) method using O-(3-(9H-carbazol-9-yl)propyl)hydroxylamine as the fluorescent derivative reagent.At first, 10 μL of oil sample was dissolved in 200 μL of isopropanol, then reacted with O-(3-(9H-carbazol-9-yl)propyl)hydroxylamine to form the stable derivatives, extracted with acetonitrile and injected into HPLC for analysis.The derivatives were separated on a C18 column within 15 min with ACN-H2O (90∶10, V/V) as mobile phase.The fluorescence detector was set at λex/λem=292 nm/348 nm.The linear range of 5 kinds of long-chain aliphatic aldehydes was 0.01-1.00 μmol/L with limit of detection (LOD, S/N=3) of 0.05-0.10 nmol/L, and the spiked recoveries were 95.6%-101.4%.The results showed that the edible oils obtained from supermarket almost had no hexanal, heptanal, octanal, nonanal, decanal, but these aldehydes increased significantly in gutter oil.Thus the 5 kinds of long-chain aldehydes could be used as the indictor of gutter oil.Taking the advantage of good specificity, higher sensitivity, good accuracy and simplicity, the method was suitable for the rapid identification of gutter oil.

AIM:To compare 2 environments , the subrenal capsule and oral submucosa , for producing well-formed teeth from mouse tooth germs and for exploring the ideal environment for tooth regeneration .METHODS: Two groups were set up .Group A was transplanted with the mouse embronic day ( ED) 14.5 first mandibular molar tooth germs into the subrenal capsule , while group B was transplanted with the ED 14.5 first mandibular molar tooth germs into the oral submucosa.After 3 weeks and 4 weeks, the host mice were sacrificed, and the transplanted explants were evaluated with morphologic observation , histological structures , hardness and elastictic modulus tests , and chemical compositions .RE-SULTS:(1) The explants isolated from both environments showed the tooth-like structures, but as to the group B, the crown was smaller, and the shape of the cusps was not significant .(2) HE staining showed that the dentin and enamel in group A were thicker than those in group B in which the ameloblasts and odontoblasts were differentiated not very well .(3) In the test of enamel hardness , only the hardness of 4 weeks in group B was lower than normal mouse tooth .In the test of enamel modulus , the elastic modulus of enamel in 3 weeks of group A was slightly lower than normal mouse tooth , but the difference was not significant .The elastic modulus of enamel in 4 weeks of group A and group B was significantly lower than normal mouse tooth and 3 weeks of group B .The hardness and elastic modulus of dentin in 3 groups was not significant . (4) Raman spectroscopy showed 2 groups grew in harmony in general , they all had the largest peak in the point of 961 cm-1 , but the 3 weeks of group B had an obvious peak in the point of 2 947 cm-1 .CONCLUSION:For the development of ED14.5 tooth germs, we obtain almost the whole tooth in subrenal capsule transplantation after 3 or 4 weeks.The buccal submucosa environment still has a certain influence on the tooth germ development , although there are some differences about the tooth development between this environment and subrenal capsule environment .

AIM:To investigate the effect of cigarette smoking condensate on histone deacetylase 2 (HDAC2) and inflammatory mediators in mouse myoblast C 2C12 cells.METHODS:C2C12 cells were treated with cigarette smoke extract (CSE).HDAC2 siRNA was transfected into the cells using Lipofectamine TM 2000.The levels of interleukin-8 (IL-8) and tumor necrosis factor-α( TNF-α) in the culture supernatants were measured by ELISA , and the expression of HDAC2 at mRNA and protein levels was determined by real-time PCR and Western blotting .RESULTS:The expression of HDAC2 at mRNA and protein levels in CSE group was lower than that in control group (P<0.05).The supernatant levels of IL-8 and TNF-αin CSE group were significantly higher than those in control group ( P<0.05 ) .When the cells were transfected with HDAC2 siRNA followed by CSE stimulation , the expression of HDAC2 at mRNA and protein levels was de-creased , and the supernatant levels of IL-8 and TNF-αwere significantly increased as compared with CSE group and control group (P<0.05).CONCLUSION: Under the oxidative stress condition , C2C12 cells generate high levels of IL-8 and TNF-αby down-regulating the expression of HDAC2.

Objective To investigate the relationship between cysteine-rich protein 61 ( Cyr61 ) and phosphatidylinositol 3-kinase ( PI3K ) signal pathway on cell proliferation and apoptotic in human ovarian carcinoma cells.Methods Recombinant human Cyr61 (rhCyr61) was pretreated with ovarian carcinoma cells.The expression of Cyr61 protein was detected by confocal spectral microscopy.Then treated the ovarian carcinoma cells with PI3K transduction inhibitors (LY294002) for 24 hours.Cell apoptosis was detected by flow cytometry (FCM).Cell viability was determined by methyl thiazolyl tetrazolium (MTT) method.The mRNA expressions of Cyr61,the protein levels of protein kinase B ( PKB),phospho-PKB and Cyr61 were assaved by real time-PCR and western blot analysis,respectively.Results The Cyr61 and phospho-PKB protein expression in two ovarian carcinoma cells (OV2008 and OVCAR-3 ) were increased in rhCyr61pretreated group.The decreasing of cell apoptosis [ ( 1.4 ±0.9)％,(2.1 ± 1.0)％ ] and increasing of cell proliferation [ ( 124.0 ± 1.8)％,( 133.0 ±2.2)％ ] was detected in the same time,compared with negative control group,there were significant difference ( P ＜ 0.05 ).After exposed to LY294002 for 24 hours,the apoptosis rate of OV2008 and OVCAR-3 in pretreated with rhCyr61 group exposed to LY294002 were (21.1 ± 1.6)％ and (26.4 ± 1.5 )％,respectively.Cells viability [ (59.0 ± 2.3 )％,(51.0 ± 2.0)％ ]was also significantly decreased in OV2008 and OVCAR-3 pretreated with rhCyr61 cells.Meanwhile,the mRNA expressions of Cyr61 (3.2 ± 0.8,6.2 ± 1.1 ) and the protein levels of phospho-PKB and Cyr61 were greatly decreased.Compared with negative control group,there were significant difference in OV2008 and OVCAR-3 cells (all P ＜ 0.0l ).Conclusions The activation of PI3K intracellular signaling pathways may lead to up-regulation of Cyr61 expression.Block PI3K signal pathway could significantly inhibit the expression of Cyr61,and may promote the apoptotic effects and inhibit the cell growth of ovarian carcinoma cells.

Objective To explore the effect of the simvastatin administration on the expression of connective tissue growth factor （CTGF） in fihrotic lungs of rats. Methods The cats were treated with single intratracheal instillation of bleomycin （BLM） or instillation of the same volume of normal saline （NS） as a control. The administration of simvastatin（20 mg/kg）began once a day immediately or 7 days later after intratracheal BLM instillation respectively with the same volume of NS was given as a vehicle control. The rats were killed on day 7,14 and 28 respectively. Pathological alteration of lung tissue was observed hy HE staining and Masson staining. Hydroxyproline（HYP）content in lung tissue was used to determine the severity of pulmonary fibrosis. The expression of CTGF in lung tissue was exanfined by immunohistochem- istry staining and photodeusitometry. Results Histopathological changes of pulmonary fibrosis emerged gradually after the instillation of BLM. The expression level of CTGF was increased in lungs of rats after intratracheal instillation of BLM, compared with the control. The administration of simvastatin immediately or 7 days after intratracheal instillation of BLM, attenuated the histopathological changes of bleomycin- induced puhnonary fibrosis and prevented the increased expression of CTGF in lung tissue on day 28. Conclusion The adntinistration of simvastatin, immediately or 7 days after intratracheal BLM instillation, prevented the up-regulation of CTGF in fibrotic lungs of rats, which ntight be one of the mechanisms of the anti-fihrosis of simvastatin in lungs.

Human kerotinocyte growth factor (hKGF) gene amplified by PCR was inserted into the shuttle vector pAdTrack-CMV to get the recombinant plasmid pAdTrack-CMV-hKGF, which was linearized with Pme I and transferred into Escherichia coli BJ5183 containing the adenoviral bone plasmid pAdEasy-1 to obtain the recombinant adenoviral plasmid pAdEasy-hKGF. The recombinant adenoviral plasmid was then transfected into HEK-293 cell lines via Lipofectamine 2000 to package and amplify the recombinant adenovirus containing hKGF gene detected by PCR. The recombinant adenovirus produced could effectively infect HaCat cells. The result of Western blotting showed that HaCat cells infected with the recombinant adenovirus expressed and secreted hKGF protein.

Objective To construct and express recombinant cecropin B-binding site of luteinizing hormone releasing hormone(CB-LHRH')gene,and to evaluate the anticancer function of CB-LHRH' on human ovarian cancer cell line SKOV3 and human endometrial cancer cell line HEC-1B.Methods The sequence of the cDNA encoding CB-LHRH' was designed,artificially synthesized,verified by DNA sequence analysis and expressed by Bac-to-Bac baculovirus expression system.The expression of CB-LHRH' proteins were identified by western dot blot using rabbit polyclonal antibody against LHRH as the primary antibody.To determine the anticancer effects of the CB-LHRH' protein,ovarian cancer cell line SKOV3 and endometrial adenocarcinoma cell line HEC-1B were treated by different doses of the CB-LHRH' protein.Cell growth inhibition assay was performed using the 2,3-bis(2-methoxy-4-nitro-5-sulfophenyl)5[(phenylamino) carbonyl]-2H-tetrazolium hydroxide(XTT)kit at different times,and cell morphologic changes were observed under the inverted microscope.Results The inhibitory rate of proliferation by CB-LHRH' increased with the increase of dose and time respectively:SKOV3 cell,from(5.03?0.08)% to(53.24 ?1.22)%;HEC-1B cell,from(5.13?0.37)% to(56.16?1.08)%.The inhibitory effect on HEC-1B cell was stronger than that on SKOV3 cell(P