Objective To investigate the effects of malnutrition, nephrosis itself and glucocorticoid therapy on serum IGF-l and liver IGF-l mRNA, and illustrate relationship between growth failure in nephrotic rats and turbulence of serum IGF-l. Methods Twenty-four male SD rats were randomly divided into control, pair-fed, doxorubincin-induced nephrotic(nephrotic) and dexamethasone-treated nephrotic (des-treated) rats. Serum IGF-1 and liver IGF-l mRNA were measured by RIA and RT-PCR respectively. Results 1. Serum IGF-l was reduced and liver ICF-l mRNA was increased in pair-fed and nephrotic rats, but no significant difference was found between two groups. 2. Serum IGF-l and liver IGF-l mRNA were lower in des-treated rats than in nephritic rats. 3. There was a positive correlation of serum IGF-l with nose-tail length and weight. Conclusions Reduced serum IGF-1 induced by secondary malnutrition is the cause of growth failure in nephrotic syndrome. Glucocorticoid therapy deteriorates growth failure in nephrotic syndrome by further decreased liver IGF-1 synthesis.

Objective To investigate the effects of malnutrition,nephrosis itself and glucocorticoid therapy on serum thyroid hormone,illustrate the relationship between serum thyroid hormone and renal IGF-I/IGFBPs autocrine/paracrine in nephrotic rats.Methods Twenty-four male Sprague-Dawley(SD) rats were randomly divided into control,pair-fed,doxorubicin(5mg/kg)-induced nephrotic and dexamethasone treated nephrotic(des-treated) rats.Serum T 3,T 4 and GH were measured by RIA,renal GHR and IGF-I/IGFBPs mRNA were analyzed by radioreceptor assay and RT-PCR respectively.Results ⑴Serum thyroid hormone levels were decreased by degrees according normal rats,pair-fed rats,nephrotic rats and lowest in des-treated rats except for high serum T 4 in pair-fed rats showed increasing trendency.⑵Reduced serum thyroid hormone was parallel well with decreased renal GHR and IGFBP-2 mRNA,and correlated negatively with increased renal IGFBP-3 mRNA.⑶There was some significant correlation positively between nose-tail length or weight and serum thyroid hormone.Conclusions The hypothyroidism is a possible mechanism of IGFBPs autocrine/paracrine disorder and further growth retardation in nephrotic syndrome.

Objective To study the neuropathological changes of gastrin and substance P(SP) in the intermuscular and submucous nerve plexus of the colonic walls in patients with delayed motor constipation(DMC). Methods Gastrin and rabbit SP polyclonal antibiotics were used to make an immunohistochemical staining of the samples of different segments obtained from 10 patients with DMC and 8 normal subjects(control group) for a comparative observation as well as a relative semi-quantitative analysis. Results The immune positive nerve cells of gastrin and SP in the intermuscular nerve plexus of colon with DMC were markedly reduced; no differences in the immune response of gastrin and SP in the mucous nerve plexus were found between the two groups(P＜0.01). With routine HE staining, focal inflammation occurred in the mucous membrane of DMC colon and that the neuronal vacuolus of the intermuscular nerve plexus degenerated, reduced and even disappeared. Conclusion The abnormal changes of the neural structure in the immune reponse of gastrin and SP in the intermuscular nerve plexus of colon with DMC might be related to reduction of gastrin and SP peptide neuron or dysfunctional.

Objective To investigate the effects of malnutrition, nephrosis itself and glucocorticoid therapy on serum growth hormone binding protein(GHBP) and liver growth hormone receptor(GHR), and elucidate the relationship between growth failure in nephrotic rats and serum GHBP or liver GHR. Methods Twenty-four male Sprague-Dawley(SD) rats were randomly divided into control, pair-fed, doxoruhincin-induced nephrotic (nephrotic) and dexamethasone-treated nephrotic (des-treated ) rats. Serum GHB P, GHB P- 1 and liver GHR were measured by dextran-coated charcoal technique, gel filtration and radioreceptor assay respectively. Results (1) Serum GHBP and liver GHR were reduced in nephrotic and des-treated rats compared with control and pair-fed rats, but no significant difference was found between control and pair-fed rats or between nephrotic and des-treated rats. (2)Serum GHBP-1 was lower in pair-fed rats, even lower in nephrotic rats and lowest in des-treated rats than in control. (3) There was some significantly positive correlations between nose-tail length or weight and serum GHBP or liver GHR. Conclusion GH resistance, due to decreasd liver GHR, is an important cause of growth failure induced by secondary malnutrition and nephrosis itself Glucocorticoid therapy deteriorates growth failure by further decreased hepatic GHR.

DNA in the livers of rats was isolated 24 h af-ter oral administration of benzidine, Congo red andEvan's blue, DNA adducts in the livers of ratswere investigated by a ~(32)P-postlabeling assay. Thelevel of DNA adducts in the livers of rats after oraladministration of benzidine, congo red andEvan'blue were 18. 17, 1. 03 and 1. 74?mol/kgDNA respectively. The results showed that themetabolites of the benzidine derivative azo dyes canform adducts with DNA in the livers of rats.These DNA adducts probably are one of the rea-sons that the incidence of the bladder cancer rosein the people group who are only exposed to benzi-dine derivative azo dyes.

This study is to investigate the effects of ubenimex on tumor cell invasion and apoptosis, dose relationship and mechanism. Immunofluorescence staining was performed to detect the expression of CD13 in HT-1080 cells. MTT assay was used to analyze the effect of ubenimex on cell proliferation. Annexin V-EGFP/PI was used to detect apoptotic cells by flow cytometry. Cell cycle was analyzed using flow cytometry. Ala-pNA was used as substrate to evaluate the effect of ubenimex on the aminopeptidase activity. Transwell assay was used to analyze the effect of ubenimex on cell invasion and migration ability. Western blotting was used to detect the expression level of CD13. MMP activity was analyzed using gelatin zymography. The results showed that ubenimex at high concentration inhibited the proliferation of HT-1080 cells (IC50: 3.8 mg x mL(-1)), and induced cell apoptosis. Cell cycle was blocked at G1 phase. Ubenimex at low concentration inhibited the aminopeptidase activity of HT-1080 cells (IC50: 8.3 microg x mL(-1)) and inhibited cell invasion, but it had no effects on the cell migration and proliferation. Ubenimex had no effects on CD13 expression and MMP activity. In conclusion, ubenimex at low concentration can inhibit the invasion ability of tumor cells by directly inhibiting the aminopeptidase activity; ubenimex at high concentration can inhibit the proliferation of tumor cells and induce cell apoptosis by a CD13-independent pathway.

Objective To evaluate influence of patient-controlled intravenous analgesia (PCIA) and patient-controlled epidural analgesia (PCEA) on expressions of serum inflammatory cytokines in elderly patients with hemi or whole hip replacement using cemented artificial joint. Methods Elderly patients undergoing hip replacement were selected and were divided into PCIA group and PCEA group. VAS scores were calculated at 12 h postoperatively. Patients whose VAS scores were not more than 2 at postoperative 12h were included. 30 cases in each group were finally included. Fifteen cases were randomly chosen in each group and underwent sample blood drawing for assays. Expressions of serum inflammatory cytokines were detected by ELISA , RT-PCR and Western-blot. Results Gene and protein expressions of TNF-a as well as IL-6 in group PCEA were lower and expression of IL-10 was higher than that in group PCIA. Serum level of TGb-β was higher in group PCEA detected by ELISA. There was no significant difference in expression of IL-8 between groups. Conclusions PCEA may better promote expressions of anti-inflammatory cytokines and inhibit expressions of proinflammatory cytokines. PCEA is superior in maintenance of inflammatory cytokine balance.

Objective To investigate the value of intravital fluorescence microscopy in the observation of the changes of hepatic microcirculation in the rat model with hepatic cirrhosis and portal hypertension.Methods Seventy male SD rats were selected.According to the random number table,40 SD rats were randomly divided into the sham operation group,bile duct ligation (BDL) 2 weeks group,4 weeks group and 6 weeks group,there were 10 rats in each group,and the hepatic microcirculation of the rats was observed with intravital fluorescence microscope; the remaing 30 SD rats were randomly divided into the normal saline (NS) group,endothelin-1 (ET-1) group and the S-nitrosoglutathion (GSNO) group at 4 weeks later after the establishment of BDL model.The changes of hepatic microcirculation of the 3 groups were observed.All data were analyzed using the one-way analysis of variance (ANOVA) or paired samples t test.Results Nine rats died in the BDL model groups,and the survival rate was 85.0％ (51/60).All rats in the sham operation group were survived.The hepatic sinusoid diameters were decreased as time passed by.The hepatic sinusoid diameters of the BDL 2 weeks group,4 weeks group and 6 weeks group were (13.6 ± 1.0) μm,(8.8 ± 0.7) μm and (8.0 ± 0.5) μm,respectively,which were significantly shorter than (17.4 ± 1.0) μm of the sham operation group (t =5.86,18.24,15.57,P ＜ 0.05).The hepatic sinusoid densities of the BDL 2 weeks group,4 weeks group and 6 weeks group were (6.8 ±0.8)/ 200 μm,(4.3 ± 1.8)/200 μm and (4.0 ± 1.2)/200 μm,which were significandy lesser than (8.8 ± 0.5)/200 μm (t =3.25,2.77,2.12,P ＜ 0.05).At 15 minutes after injection of NS,the hepatic sinusoid diameter of the NS group was (7.2 ± 1.2) μm,which was significantly different from (6.9 ± 0.5) μm before injection of NS (t =0.89,P ＞ 0.05) ; the hepatic sinusoid density of the NS group before and after injection of NS were (6.6 ± 0.4) / 200 μm and (6.8 ± 1.4)/200 μm,with no significant difference(t =1.12,P ＞0.05).At 15 minutes after injection of ET-1,the hepatic sinusoid diameter of the ET-1 group was (5.4 ±0.5) μm,which was significantly different from (7.9 ± 0.6) μm before injection of ET-1 (t =7.39,P ＜ 0.05) ; the hepatic sinusoid density of the ET-1 group before and after ET-1 injection were (5.8 ± 1.2)/200 μm and (5.4 ± 1.8)/200 μm,with no significant difference(t =0.84,P ＞0.05).At 15 minutes after injection of the GSNO,the hepatic sinusoid diameter of the GSNO group was (11.4 ± 1.3) μm,which was significantly different from (7.5 ± 1.7) μm before injection of GSNO (t =5.95,P ＜ 0.05) ; the hepatic sinusoid density of the GSNO group before and after GSNO injection were(5.6 ± 0.8)/200 μm and (6.4 ± 1.6)/200 μm,with no significant difference (t =0.54,P ＞ 0.05).Conclusions The changes of hepatic microcirculation observed under intravital fluorescence microscope could reflect the progress of hepatic cirrhosis,and the changes of hepatic sinusoid diameters caused by drugs could be dynamically monitored under the intravital fluorescence microscope.

manual beam orientation selection, beam orientation optimization which is feasible in IMRT planning may significantly improve the efficiency and result.

Objective To observe the effect of Weidongfang and hydrotalcite in treatment of bile reflux gastrifis.Methods Bile reflux gastritis were randomly assigned to 2 groups.30 eases in the Weidongfang group were treated with Weidongfang and hydrotalcite;30 cases in the mosapride group were treated with mosapride and hydrotalcite;and the course of treatment was 4 weeks for all.The clinical symptoms of bile reflux gastritis,the classify of extent of bile reflux and the accumulated points of pathological change of the gastric mucosa below gastroscope were evalumed before and after treatment.Results The significant and total effective rate in the Weidongfang group were 33.3% and 86.7%.Mosapride group 43.3% and 83.3%.Butthe classify of extent of bile reflux and the accumulated points of pathological change of the gastric mucosa of Weidongfang group were Similar to Mosapfide group below gastroscope.Conclusion Weidongfang and hydrotalcite were effective medicine in treatment of bile reflux gastritis.