Objective:To investigate the clinical characteristics of severe purulent meningitis in neonates.Methods:A retrospective study was conducted.One hundred and sixty-nine newborns with purulent meningitis diagnosed at the neonatal center of our hospital from January 2014 to December 2017 were selected.According to the severity of the disease, the cases were divided into severe group and mild group.The clinical data of all children were collected and analyzed, and the characteristics of severe purulent meningitis were summarized.Results:Among 169 cases of neonatal purulent meningitis, 43 cases(25.4%)were in severe group, and 126 cases(74.6%)were in mild group.Twenty-one cases were cured in severe group, 10 cases had complications, 9 cases abandoned and 3 cases died.Ninty-eight cases were cured in the mild group, 17 cases had complications and 11 cases were discharged automatically and 2 cases died.There were significant differences in respiratory failure requiring mechanical ventilation, convulsion, consciousness disorder, blood C-reactive protein, positive cerebrospinal fluid culture, severe abnormality of amplitude integrated electroencephalogram, cerebrospinal fluid/serum glucose ratio, the incidence rate of complications and mortality between two groups( P<0.05). Conclusion:Severe purulent meningitis not only has the manifestation of mild meningitis, but also often has the clinical characteristics of brain parenchymal damage and/or brain failure with more complications and higher mortality.

Caveolae, specialized vesicular invaginations of the plasma membrane ,have attracted increasing attentions to those who are studing siginal transduction .Many proteins involved in signal transduction have been found enriched in these microdomains.Caveolins,as marker proteins of caveolae,form a scaffold onto which many classes of signaling molecules can assemble at steady state or after ligand-induced activiton .In addition to concentrating these signal transducers within a distinct region of the plasma membrane ,caveolin binding may functionally regulate the activation state of caveolae-associated signaling molecules.Thus,an emerging notion is that caveolae are signaling processing centers which orchestrate signaling events at the cell surface that influence cell function .

[Objective]To explore the allograft,as a substitute for autograft,whether can be used to repair the defect of the tendon and restore the stability of joint and the dynamic biomechanical changes of allograft after transplantation.[Method]Deep-frozen allogeneic achilles tendons of rabbits were used as treatment group,and autogenous ones as control.The achilles tendon defects of back limbs were repaired by allograft and autograft separately.The macroscopic,microscopic observation and biomechanical test were performed on both of them before transplantation and in 2,4 and 8 weeks after transplantation.[Result]It was showed that there were no differences in macroscopy,microscopy and mechanical strength between allograft and autograft both before and after transplantation.They may have experienced the similar healing course.The mechanical strength of allograft(except failure strain) was reduced significantly after transplantation.But it had a rising trend with time passing,although it was fairly low in 8 weeks compared with the normal such as maximum load.[Conclusion]The results demonstrate that the deep-frozen allograft can substitute for autograft in repairing the tendon defect,and because of the weakness of allograft after transplantation,it needs appropriate protection to prevent failure by excessive strain in early stage.

Objective To investigate the value on clinical application of dynamic and combined detection of serum tumor markers alpha-fetoprotein (AFP),Golgi protein 73 (GP73),vascular endothelial growth factor (VEGF) and alpha-L-fucosidase (AFU) in early diagnosis and monitoring treatment of primary hepatocellular carcinoma.Methods Serum levels of AFP,GP73,VEGF,AFU in 98 patients with primary hepatocellular carcinoma (the malignant group) before and 3 months after treatment were detected by electrochemiluminescence immunoassay and enzyme-linked immunosorbent assay,which compared with the levels of 50 liver benign lesions (the benign group) and 50 healthy subjects (the normal group).Results The levels of serum AFP,GP73,VEGF,AFU in the malignant group before treatment were (219.16 ± 56.89) μg/L,(355.42 ± 109.26) μg/L,(88.21 ±24.22) μg/L,(276.51 ±83.20) U/L.These indexes in the benign group were (14.95 ± 3.26) μ g/L,(56.43 ± 15.72) μ g/L,(2.68 ± 1.27) μ g/L,(25.38 ± 11.17)U/L.These indexes in the normal group were (14.67 ± 3.07) μ g/L,(55.06 ± 14.21) μ g/L,(2.36 ± 1.14) μ g/L,(24.29 ± 10.10) U/L.There were statistical differences between the malignant group and the benign group,normal group (P ＜ 0.01).The levels of these indexes after treatment in the malignant group were (25.66 ±8.17) μg/L,(65.32 ±24.15) μg/L,(4.67 ± 1.89) μg/L,(35.23 ± 12.36) U/L,there were statistical differences between before treatment and after treatment (P ＜ 0.01).The sensitivity and accuracy of combined detection of these tumor markers in diagnosis of primary hepatocellular carcinoma were 95.92％ (94/98) and 93.24％(138/148),which were statistically higher than single detection(P＜ 0.05).Conclusion The dynamic and combined detection of serum tumor markers could be applied as supplementary means in early diagnosis and monitoring treatment of primary hepatocellular carcinoma.

Background Alkali burn-induced corneal neovascularization(CNV) usually leads to blindness.Recently,study determined that vascular endothelial growth factor(VEGF) and basic fibroblast growth factor(bFGF) were the main regulating factors inducing angiogenesis,and canstatin proteins can inhibit the growth of VEGF and bFGF and thereby inhibit CNV growth.Objective The present study was to investigate the effect of recombinant canstatin protein on mouse CNV induced by alkali burn and its mechanism.Methods CNV models were induced in the right eyes of 40 female BALB/c mice by sticking the 2.0 mm filtering paper with 1 mol/L NaOH at the central cornea for 10 seconds.The animals then were randomized into two groups.Recombinant canstatin protein drops(5 mg/L) was topically administered 4 times daily in the mice of the experimental group,and normal saline solution was used at the same way in the control group.Corneas of the mice were examined under the slit lamp to calculate the CNV area 1 day,3,7,14 days after modeling.The mice were sacrificed at above time points and corneas were obtained.The expressions of VEGF protein and bFGF protein in cornea were detected by Western blot,and the results were analyzed by enhanced chemiluminescence(ECL).The use of the experimental animals complied with the Instructive Notions with Respect to Caring for Laboratory Animals by State Ministry of Science and Technology.Results In 3,7 and 14 days after establishment of models,the area of CNV was (1.98-0.31) mm2,(6.21 ±0.44) mm2 and (9.83±0.72) mm2 in the experimental group,and that in the control group was (2.92 ± 0.41) mm2,(8.04 ± 0.56) mm2 and (11.78 ±0.84) mm2,showing significant reduce in the mice treated with recombinant canstatin protein(t3d =4.332,P=0.005 ;t7 d =11.729,P =0.000 ;t14 d =14.562,P =0.000).Western blot analysis showed that there was significant increase in the gray scale of VEGF protein 1 day,3,7,14 days following alkali burn in the experimental group compared with the control group(t1 d =-3.980,P＜0.001 ;t3d =-10.020,P＜0.001 ;t7d =-4.355,P＜0.001 ;t14 d =-8.156,P＜0.001),and the gray scale of bFGF was significantly ascent at various time points in the the experimental in comparison with the control groups (t1 d =-3.488,P＜0.001 ; t3 d =-2.124,P =0.013; t7 d =-1.977,P =0.028; t14 d =-4.542,P＜0.001).Conclusions Topical application of recombinant canstatin protein drops inhibits CNV growth induced by alkali burn by down-regulating the expressions of VEGF and bFGF proteins.

Objective To explore the inhibitory effect of rosiglitazone of peroxisome proliferator-activated receptor-?(PPAR?) agonist on aldosterone-induced mesangial cell(MC) proliferation.Methods Mouse primary MC were cultured and treated with aldosterone(100 nmol/L) in the presence or absence of rosiglitazone(1.0,2.5,5.0,10.0 ?mol/L).The incorporation of 3H-thymidine(3H-TdR) and cell count were used as the measure of MC proliferation.Cyclin D1 and cyclin A expression,PI3K and Akt phosphorylation were determined by Western blot analysis.Results 1.Aldosterone induced MC proliferation,as assessed by 3H-TdR incorporation and cell number,which were increased by 2.46-and 2.14-fold,respectively,in aldosterone-treated cells.Aldosterone-induced MC proliferation was inhibited by PPAR? agonist rosiglitazone in dose-dependent manner in mouse MC.2.Aldosterone induced cyclin D1 and cyclin A expression.Rosiglitazone reduced aldosterone-induced cyclin D1 and cyclin A expression in dose-dependent manner.3.Aldosterone induced PI3K/Akt activation in dose-dependent manner,incubation with 100 nmol/L aldosterone for 60 min,phosphorylation PI3K and Akt expression increased by above 3.0-fold.4.PI3K inhibitor LY294002 and Akt inhibitor significantly inhibited aldosterone-induced cyclin D1 and cyclin A expression.5.Rosiglitazone significantly inhibited aldosterone-induced PI3K/Akt activation,10 ?mol/L rosiglitazone almost completely blocked aldosterone-induced PI3K/Akt activation.Conclusion Rosiglitazone can block aldosterone-induced MC proliferation via inhibition of PI3K/Akt activation.

Objective To investigate the effect of c-Jun N-terminal kinase(JNK) specific inhibitor SP600125 on Angiotensin Ⅱ(AngⅡ)-induced transforming growth factor-?1(TGF-?1) and fibronectin (FN) expression in human mesangial cells (MC).Methods Human MC were isolated and cultured in vitro and were treated with AngⅡ in the presence or absence of JNK specific inhibitor SP600125.The protein was isolated or the supernate of medium was collected at the end of experiment.JNK,extracellular signal-regulated kinase(ERK1/2),and p38 mitogen-activated protein kinase(MAPK) activity were determined by Western blot method.TGF-?1 and FN were determined by enzyme linked immunosorbent assay(ELISA).Results SP600125 inhibited AngⅡ-induced Ser63 phosphorylation of c-Jun in a concentration-dependent manner,and JNK activity was reduced by 75% at 10 ?mol/L and by 90% at 20 ?mol/L.SP600125 had no effect on AngⅡ-induced ERK1/2 and p38 activity.TGF-?1 and FN protein were constitutively produced in MC,and production was significantly stimulated for 8 to 48 h after addition of AngⅡ.Preincubation of cells with SP600125(20 ?mol/L) significantly inhibited AngⅡ-induced TGF-?1 and FN production during this time period.SP600125 inhibited AngⅡ-induced production of TGF-?1 and FN in a concentration-dependent manner.Conclusion SP600125 inhibited AngⅡ-induced JNK activation and TGF-?1 and FN expression in human MC and may serve as the novel approach for the treatment of patients with chronic kidney disease.

Postoperative peritoneal adhesion represents a major complication of surgery. Recently, the angiogenesis which cyclooxygenase-2 enzyme induced was found to play an important role in the adhesion synthesis. This review summarized the relationship between COX-2 induced angiogenesis and peritoneal ad- hesion.

Humans ; Temporomandibular Joint Disorders ; diagnosis ; therapy

Objective To observe the expression of matrix metalloproteinase(MMP-2, MMP-9 and vascular endothelial growth factor (VEGF) in retinoblastoma (RB) and its relationship with the differentiation and optic nerve infiltration of RB. Methods Forty paraffin specimens of pathological confirmed RB were studied. They were divided into differentiated group (15 cases) and undifferentiated group (25 cases) , optic nerve infiltration group( 13 cases) and without optic nerve infiltration group(27cases). The expression of MMP-2, MMP-9 and VEGF were detected by immunohistochemistry, their relationships with the differentiation and optic nerve infiltration were also analyzed. Results The positive rate of MMP-2, MMP-9 and VEGF expression in 40 RB cases were 52.5%, 57.5% and 72.5%respectively. The expression of MMP-2, MMP-9 and VEGF in the undifferentiated group were significantly higher than those in the differentiated group (χ2= 9. 037, 9. 253, 8. 095;P＜0. 05). The expression ofMMP-2, MMP-9 and VEGF in RB with optic nerve infiltration group were significantly higher than those in RB without optic nerve infiltration group (χ2=11.045,10. 243, 8. 956;P＜0. 05). The expression of MMP-2,MMP-9 had a positive correlation with the expression of VEGF in RB (r= 0. 126, 0. 314;P ＜ 0. 05).Conclusions MMP-2, MMP-9 and VEGF expressed in RB tumor tissues. The expression of MMP-2,MMP-9 has a positive correlation with the expression of VEGF. The levels of MMP-2, MMP-9 and VEGF expression are related to optic nerve infiltration of RB cells.