Objective To investigate the effects of exposure of gravid rats to the persistent organic pollutants (POPs), methoxychlor (MXC), on the placenta and their progeny during gestation periods. Methods According to different dosage levels of MXC [16, 32, 64 and 0 mg/(kg?d)], forty female SD rats aged 3-month were randomly divided into low-dosage group, mid-dosage group, high-dosage group and control group, with 10 animals for each. All the rats received intraperitoneal injection of MXC for 20 days. The influence of MXC on placenta of gravid rats and their progeny were observed in all aspects. Results With the increase in MXC dosage, intense changes were found in the rats, including an inerease in the number of corpus luteum of ovary, the number of nidation, fetal death and merging fetal (P

Objective To approach the relationship of the expression of hepatocyte growth factor (HGF)/c-met and clinical characteristics of patients with ovarian tumor. Methods Immunohistochemistry (SABC)was used to detect the expressions of HGF and c-met in different pathology group with ovarian cancer. Results HGF positive cells are chromatosised to yellow and take strong expression in the ovarian cancer tissue. C-met takes strong expression in epithelial cell and amply-chromatosis in interstitial cell. HGF and c-met have significant deviation in ovarian tumors, commissurotome tumors and benign tumors (P

0.05),but the integrated arthoplasty group had significant differences from the other two groups(P

Cell culture, Fluo-3 AM loading and laser scanning confocal microscope(LSCM), flow cytometer(FCM)and Western blot were employed to detect the regulation effect of retinoic acid on signal transduction pathway of gap junction gene connexin cx43 in HeLa. The results showed that after treated by ATRA , the second intercellular messenger [Ca 2+]i was much higher in HeLa cells(58.16 nmol/L)than in untreated cells(35.73 nmol/L). A detectable and up-regulation of Cx43 in 43kDa protein in HeLa cells increased from 1.9% to 26.3% in RA-treated cells than in untreated cells examined by FCM and Western blot. Immunoblot showed that only the treated cells had phosphorylated Cx43 protein of 43 kDa. The results suggest that the anti-tumor effect of ATRA in HeLa might be due to up-regulation of cx43 gene and its signal transduction pathway which mediates GJIC. The decreased expression of Cx genes, and the disorder and abnormal signal transduction pathway of Cx gene should be responsible for the uncontrolled tumor cell growth.

Objective To design and synthesize an antitubercular compound,24-ketoarguesterol.Methods The target compound was synthesized via 8 steps,including methyl esterification,grignard isopropylation,deportation,etc.,using hyodeoxycholic acid as the starting material.3?-tert-butyldimethylsilyoxyl-5?-hydroxyl-6?-di-me-thoxylmethyl-24-keto-B-norcholanate was the key intermediate and grignard isopropylation as the key step.Results The target compound was synthesized in a total yield of 42% and identified by mass spectrometry(MS),proton magnetic resonance spectroscopy(1HNMR),carbon magnetic resonance spectroscopy,(13CNMR)and infrared spectroscopy(IR).Conclusion The synthetic route is characterized by atomic economy and high efficiency and laid the foundation for development of novel antituberculous drugs.

Objective Our purpose in this study is to investigate genes involved in the development of diabetes-induced embryonic malformations. Methods Two groups of 70-90 day old Sprague-Dawley rats were employed in our study: group 1 was normal control rats receiving a normal diet (n=3); group 2 consisted of experimentally-induced diabetic rats by intravenous injection of 65mg/kg of streptozotocin(STZ) on pregnancy day 6 with an attempt to reproduce malformations in embryos (n=3). Embryos were examined on day 12 under light microscopy to look for morphological defect of the neural tube (NTD). Yolk sac cells were harvested from each group and RNA was isolated. Genes expression profiles in yolk sac cells were analyzed using a DNA microarray technique. Results Gene expression patterns were compared in a total of 1200 genes between experimentally-induced diabetic rats and normal control rats, and 79 of genes were found to express differently between the two groups. Forty-two of genes were up-regulated in yolk sac cells of diabetic rats, such as apoptosis related genes BAX, bcl-2, heat shock 70kD protein and glucose-transporter 3; 37 of genes were down-regulated, such as phospholipase A2, insulin-like growth factor II receptor. Conclusion Understanding of differently expressed genes should help us disclose the potential molecular mechanisms underlying the developmental process during diabetes-associated embryonic morphogenesis, and it also might provide a useful tool in rapid diagnosis and prevention of malformation in early gestation stage of diabetic subjects.

BACKGROUND:Previous studies have confirmed that healing of in vivo tendon is the outcome of interaction between endogenous healing and exogenous healing. Exogenous healing is a main reason for tendon adhesion, and affects the recovery of tendon function.OBJECTIVE: To explore application of tissue engineering technique and its materials in prevention and treatment of tendon adhesion induced by movement injury.METHODS: Using the key words of "movement injury, biomaterial, tissue engineering, tendon adhesion", we retrieved randomized animal controlled studies and clinical application literatures addressing tendon biomechanics function, adsorbable biomaterial polyglycolic acid, tendon cells-constructed tissue engineered tendon in vitro, biomembrane, chitosan, adsorbable antistick membrane, sodium hyaluronate, bioprotein gel and so on in prevention of tendon adhesion in Chinese Journal Full-text Database published from January 1990 to December 2000. By aggregate analysis of literature data, follow-up and function evaluation, this article summarized clinical application of tissue engineered techniques and materials in prevention of tendon adhesion.RESULTS AND CONCLUSION: A total of 61 literatures were primarily obtained. Following reading titles and abstracts, 31 literatures of irrelevant objectives and contents, and 9 literatures of repetitive contents were excluded. Totally 21 literatures were included for analysis. Tendon adhesion refers to hyperplasia and invasion of surrounding tissues during repair of tendon damage. With the deep understanding of tendon repair healing, application of tissue engineering to preventing tendon adhesion became more and more. Tendon healing is an interaction between endogenous healing and exogenous healing, and mainly endogenous healing, which was simultaneously associated with tendon sheath, vincula tendinum and synovial fluid. Tendon adhesion is mainly induced by excessive action of exogenous healing and damage to surrounding tissues. Tissue engineering is a novel technique. Novel biomaterials are widely used in tissue engineering performance to solve problems such as tendon injury andchondronecrosis. Presently, it Is important to reconstruct tissues, which can reach clinical outcomes of preventing adhesion.

Objective To investigate the effects of gestrinone on growth and apoptosis, as well as the expression of phosphatase and tension homologue deleted on chromosome 10(PTEN) in isolated ectopic endometrium cells in vitro and the underlying mechanisms. Methods Ectopic endometrium cells were cultured and exposed to gestrinone of different doses of 0, 10 -6 and 10 -4 mol/L respectively. The inhibition of the cells during 48 hours was determined by methylthiazolyl tetrazolium (MTT) assay, and the cell growth curve was made. Gestrinone was administered to the cells and at 24 hours the morphological changes were observed by transmission electron microscopy and the apoptosis rate, cell cycle and PTEN expression were monitored by flow cytometry (FCM) at the same time. Results Gestrinone at different concentrations could inhibit the growth and proliferation of ectopic endometrium cells in a dose- and time-dependent manner. The inhibition rate of cell growth after exposed to gestrinone for 8,16,24,32,40 and 48 h was 99.6%,87.3%,79.8%,62.3%,51.7% and 44.2% in the 10 -6 mol/L group,and 99.2%,77.1%,69.6%,51.1%,33.7% and 23.6% in the 10 -4 mol/L group (P

BACKGROUND: Multiple applications of opium medicines can induce the accommodative changes of morphology and function in some intracerebral nerve positions. These accommodative changes are important neurobiological bases inducing drug-desire and re-addiction after detoxification. However, the actual molecular mechanism is unclear at present.OBJECTIVE: To investigate the impacts of the generation of heroin-dependence and detoxification on brain-derived neurotrophic factor (BDNF) in rat to provide a laboratorial gist for the participation of BDNS in heroin-dependence and detoxification.DESIGN: A randomized controlled study by employing experimental animals as subjectsSETTING: Mental health center of a medical university affiliated hospital MATERIALS: The study was conducted in the Laboratory of Pharmacology,Faculty of Pharmacology, Chongqing Medical University between March 2004and July 2004. Totally 30 inbreeding clean male SD rats with a bodymass between 200 g and 250 g were obtained from the Experimental Animal Center of the Third Military Medical University of Chinese PLA. Rats were randomly divided into blank control group(control group), heroin-dependent group (heroin group), and naloxone detoxification group(naloxone group) with 10rats each.METHODS: Morphine was subcutaneously injected into the rat with dose-increasing method to establish heroin-dependence rat model. Rats of naloxone group received subcutaneously injection of 2 mg/kg of naloxone to excite abstinent symptoms. The same dose of normal saline (NS) was injected in rats of control group. Model rats of each group were observed biologically and behaviorally. BDNF expression at different brain zone of rats in three different groups was tested with immunohistochemistry and digoxin-labeled oligonucleoide probe in situ hybridization technique.Comparison of the evaluation of abstinent symptoms in rats of each group.RESULTS: In the heroin group, the relative content of BDNF protein was higher in frontal lobe cortex, locus caeruleus and hippocampus than that of the control group( P ＜ 0.05); BDNFmRNA relative content was higher in frontal lobe cortex than that of the control group( P ＜ 0. 05) . In naloxone group, BDNF and its mRNA relative contents in frontal lobe cortex, locus caeruleus and hippocampus were higher than that of heroin group and control group ( P ＜ 0.05 ).CONCLUSION: Chronic administration of heroin could affect BDNF protein and its mRNA expressions in the corresponding brain areas of the rats, which suggests that the change of BDNF expression participates in heroin-dependence and detoxification.

OBJECTIVE:To investigate the influences of Schwann cells-alginic acid sodium hydrogel transplantation on cellular apoptosis,Bcl-2 expression,and lower limb locomotor function in a rat model of spinal cord injury.METHODS:SD rats of clean grade were randomly divided into 4 groups:normal control,simple injury,Schwann cells,and Schwann cells-alginic acid sodium hydrogel.Spinal cord transaction model was established in the latter 3 groups.Gelatin sponge blocks containing Schwann cells suspension were transplanted into the Schwann cells group.Schwann cells-alginic acid sodium hydrogel was transplanted into Schwann cells-alginic acid sodium hydrogel group.No treatments were performed in the normal control and simple injury groups.At 12 hours,1,3,7,and 21 days after surgery,animals were assessed using Basso,Beattie and Bresnahan (BBB) locomotor rating scale and were sacrificed.The spinal cord-transected segments were taken to prepare paraffin sections for TUNEL and Bcl-2 staining to quantitate apoptotic cells and Bcl-2 cells in the injured spinal cord and to investigate their distributions.RESULTS:A small number of slightly stained Bcl-2 positive cells were observed in the normal control group.In the simple injury group,Bcl-2 immunoreactive cells peaked at 3 days after surgery,and the expression level was close to normal level at 14 days.Following Schwann cells-alginic acid sodium hydrogel transplantation,Bcl-2 immunoreactive cells in the spinal cord-transected segments were significantly increased till 7 days (P＜0.05) and remained this level for more than 14 days.In the simple injury group,apoptotic cells were most as compared with the remaining 3 groups,and peaked at 1 and 7 days following spinal cord injury,and they were mostly distributed in the white matter.BBB scores were significantly higher in the Schwann cells-alginic acid sodium hydrogel transplantation group than in the simple injury and Schwann cells groups (P＜0.05).CONCLUSION:Schwann cells-alginic acid sodium hydrogel transplantation could inhibit cellular apoptosis and enhance Bcl-2 expression in the spinal cord-transected segments,and thereby promote the recovery of locomotor function after spinal cord injury but did not reach normal levels.