Objective To investigate the association of expressions of neutrophil extracellular trap (NET) and B lymphocyte in renal tissue with lupus activity in patients with lupus nephritis (LN). Methods Immunohistochemistry was.used to detect the expression of NET (citrullinated histone H3 as the marker) and the infiltration of B lymphocyte (CD19 as the marker)in renal specimens of three groups [LN group,n=20; minimal change disease (MCD) group,n=8;healthy control group,n=3].The chronic index and SLE-disease activity index (SLE-DAI) in renal tissues of LN and their correlations with NET and B lymphocytes were examined. Results The expression of NET was not found in the renal tissues of healthy control group and MCD group,while it increased significantly in LN group,especially in glomeruli with moderate and severe mesangial cells proliferation, cellular crescents, and tubulointerstitium with inflammatory cell infiltration.Compared with other types of glomeruli,the expression of NET was significantly upregulated in glomeruli with moderate and severe mesangial cell proliferation (P＜0.01).In the glomeruli with moderate and severe glomerular mesangial cell proliferation,the mean number of =NET positive cells was positively correlated with renal pathological active index (r=0.620,P=0.004),the score of SLE-DAI (r=0.492,P=0.027) and the mean number of NET positive tubular cells (r=0.558,P=0.011).In renal interstitium,the NET positive cells were positively correlated with CD19 positive B lymphocytes (r=0.573,P=0.008) and renal pathological chronic index (r=0.645,P=0.002). Conclusion NET is widely expressed in the renal tissues of lupus nephritis,which may play a role in the active damage of glomeruli.

A few of patients with lumbar disk herniation having a separation of clinical symptoms and signs and imaging features, can be found in clinic, but the traditional theory of direct mechanical compression of nerve roots by herniated nucleus pulposus can't be used to explain this abnormal protrusion of lumbar intervertebral disc. The clinical symptoms and signs of the atypical lumbar disk herniation are affected by multiple factors. The indirect mechanical compression and distraction effect of spinal nerve roots may play an important role in the occurrence of the separation, and the appearance of abnormal clinical symptoms and signs is closely related to the migration of herniated nucleus pulposus tissue, transmission of injury information in the nervous system, and the complex interactions among the nucleus pulposus, dural sac and nerve roots. Moreover,the changes of microcirculation and inflammation secondary to the herniated nucleus pulposus tissue, the hyperosteogeny in the corresponding segment of the lumbar vertebrae and the posture changes all results in a diversity of symptoms and signs in patients with lumbar intervertebral disc herniation. Besides, there exist congenital variation of lumbosacral nerve roots and vertebral bodies in some patients, and the misdiagnosis or missed diagnosis of imaging finding may occur in some cases. However, the appearance of a separation of clinical symptoms and signs and imaging examination in patients may be caused by a variety of reasons in clinic. The exact mechanism involved in the interaction among nucleus pulposus tissue, dural sac and nerve root, secondary changes of pathophysiology and biomechanics around the nucleus pulposus, the determination of lesioned responsible segments, and how to overcome the limitations of imaging all need the further researches.
Humans ; Intervertebral Disc Displacement ; complications ; diagnosis ; Lumbar Vertebrae ; Nerve Compression Syndromes ; etiology

Objective To understand the isolation and change of drug resistance of mucoid Pseudomonas aeruginosa in sputum from 2013 to 2015 so as to provide a scientific basis for reasonable clinical use of antibacterial drugs.Methods The isolation,culture and identification were carried out according to the fourth edition of National Clinical Laboratory Operation Rules.The drug susceptibility testing was performed with the use of Kindy-Bauer.The drug susceptibility testing results were judged according to the standards of CLSI 2014.The clinical data were analyzed by software WHONET 5.6.Results Among 1 653 strains of Pseudomonas aeruginosa isolated in the clinical sputum specimens from 2013 to 2015,including 255(15.4%)strains of mucoid Pseudomonas aeruginosa;during the three years,the drugs of highest drug resistance rate was piperacillin,which was 29.0%;the drug resistance rate less than 10.0% had amikacin and piperacillin/tazobactam;the drugs with larger increase range of resistance rate included imipenem,levofloxacin,ciprofloxacin and ciprofloxacin,their resistance rates were increased from 12.5%,9.7%,8.3% and 9.7% in 2013 to 20.5%,17.0%,19.3% and 15.9% in 2015.Conclusion The isolating rate of mucoid Pseudomonas aeruginosa in sputm is gradually increased year by year from 2013 to 2015.At the same time,the drug resistance rates show an increasing trend in recent three years.It is necessary to strengthen the surveillance of drug resistance of mucoid Pseudomonas aeruginosa.

Purpose:To explore the preventive effect of hepatic arterial infusion (DDS) against recurrence of hepato- cellular carcinoma (HCC) after radical resection.Methods:From Jan,1996 to May,1998,287 patients of HCC after radical resection were randomly divided into four groups:intra-hepatic arterial infusion(97),intra-portal vein(80),intra-hepatic artery and portal vein (60),control (50).All patients received chemotherapy for two years and observed for postoperative recurrence of HCC.Results:The postoperative recurrence rate of HCC with intra-hepatic arterial infusion was significantly lower than that of intra-portal vein (P0.05).The 1～、2～ and 3～year survival rate of intra-hepatic arterial infusion was significantly higher than any of the other groups.Conclusions:Intra-hepatic arterial infusion (DDS) through gastro-duodenal artery can effectively pro- long the postoperative survival and decrease the post-operative recurrence rate of HCC.The preventive method of DDS through gastro-duodenal artery was safer and effective.

AIM:To investigate the effects of MG132,one of the proteasomal peptide aldehydes inhibitors,on lipopolysaccharide(LPS)-induced nuclear transcription factor-kappa B(NF-?B) activation,the production of nitric oxide(NO) and tumor necrosis factor-alpha(TNF-?),as well as the expression of inducible nitric oxide synthase(iNOS) in murine macrophage line RAW264.7.METHODS:Reporter gene assay was used to examine the activity of NF-?B by pNiFty-SEAP/HEK293 cells,which were transfected with the pNiFty reporter plasmid into human embryo kidney cells(HEK293).Fluorescence substrate DAF-2DA was used to testify NO level in Raw264.7 cell line induced by LPS.Furthermore,the secretion of TNF-? was examined by ELISA.Western blotting was used to reveal the expression of iNOS and I?B-?.RESULTS:MG132 significantly decreased the secretion of TNF-? induced by LPS,with the inhibitory rates of 36.7% and 60.4% to 5 ?mol/L and 10 ?mol/L MG132,respectively.The pro-inflammatory mediator NO production was decreased in a dose-dependent manner with the inhibitory rates increasing from 29.5%(2 ?mol/L) to 55.9%(10 ?mol/L).Pretreatment with MG132 reduced the expression of iNOS,but restored the I?B restrain caused by LPS treatment.Observed by a reporter gene assay,TNF-?-induced NF-?B activity was decreased gradually by addition of increasing concentration of MG132(2.5-10 ?mol/L).CONCLUSION:Our results suggest an anti-inflammation effect of MG132 by the suppression of LPS-induced the production of pro-inflammatory mediators including NO and TNF-?,and the expression of iNOS,which probably mediates the blockage of I?B degradation and NF-?B activation.

Objective To investigate the mechanism of a dipeptidyl-peptidase-4 (DPP-4) inhibitor, saxagliptin, pro?moting the regeneration of islet beta cells in diabetic rats. Methods The male SD rats were randomly divided into three groups including control group (NC, n=10), diabetes group (DM, n=10) and diabetes treated with saxagliptin group (DM-S, n=10). DM-S group was treated with saxagliptin 1 mg/(kg·d) for twelve weeks. The pancreaticβcell function was analysed by hyperglycemic clamps. Immunohistochemistry with anti-PCNA was performed to observe the proliferation rate of pancreaticβcells. Immunofluorescence double staining with anti-insulin, anti-glucagon, anti-DPP-4 and anti-SDF-1 were performed to observe the expression of insulin, glucagon, DPP-4 and SDF-1 in pancreatic tissue. Western blot assay was performed to test the expression of Akt, p-Akt,β-catenin and free-β-catenin protein, and RT-PCR was performed to test the expressionlevels of c-myc and cyclinD1 mRNA in pancreatic tissue. Results Compared with NC group, there were significantly in?creased blood glucose, decreased islet function andβcell mass in DM group. Compared with DM rats, saxagliptin treatment significantly inhibited the expression of DPP-4, decreased the degradation of SDF-1, stimulated the proliferation ofβcells, and ultimately improved the islet function and histopathological changes of pancreas. Conclusion DPP-4 inhibitor saxa?gliptin can significantly improve islet function, which involved in the inhibition of the expression of DPP-4, the decreased degradation of SDF-1 and the stimulation of the proliferation ofβcells.

OBJECTIVE:To study the in vitro antioxidant activity of chitosan(CTS)degradation derivatives and its preventive effects on drug-induced liver injury fibosis. METHODS:Acid hydrolysis method was used to prepare the CTS degradation deriva-tives CTS-3,CTS-6,CTS-8,CTS-10 for different hydrolysis time(3,6,8,10 h). The viscosity-average relative molecular mass and deacetylation degree of CTS and its degradation derivatives were determined,and its antioxidant activity was evaluated by de-tecting its in vitro scavenging ability on 1,1-diphenyl-2-trinitrophenylhydrazine (DPPH) and superoxide anion (O2-) radicals. Us-ing CTS-10 for in vivo liver injury fibosis prevention test,mice were randomly divided into normal control group(water),model group(water),CTS-10 high-dose,medium-dose,low-dose groups(100,50,25 mg/mL),8 in each group. Mice were intragastri-cally administrated 0.2 mL,then withdrawal after continuous 24 d. Then levofloxacin hydrochloride was intragastrically given for 7 d to establish drug-induced liver injury model(except for normal control group). Western blot method was used to detect the expres-sions of tumor necrosis factor α(TNF-α),transforming growth factor β1(TGF-β1)and Decorin protein in liver tissue of mice. RE-SULTS:The viscosity-average relative molecular mass of CTS,CTS-3,CTS-6,CTS-8,CTS-10 were 21.70×104,6.70×104,6.30× 104,5.01×104,4.87×104;and deacetylation degree were 83.44％,74.62％,67.28％,64.83％,54.23％,respectively. All of them had certain scavenging ability on DPPH and O2-,in which,CTS-10 was the strongest(25.47％ and 56.31％). Compared with nor-mal control group,expressions of TNF-α,TGF-β1 and Decorin protein in liver tissue in model group were enhanced (P<0.05). Compared with model group,expressions of TNF-α,TGF-β1 and Decorin protein in liver tissue in CTS-10 medium-dose and high-dose groups were weakened(P<0.01). CONCLUSIONS:The viscosity-average relative molecular mass and deacetylation de-gree of CTS-10 in CTS degradation derivatives are lower with stronger antioxidant activity,and show certain preventive effects on drug-induced liver injury fibosis in mice.

Objective To investigate the possible mechanisms of glucagon-like peptide 1 receptor agonists (GLP-1Ra) induced weight loss. Methods High fat diet induced obese c57BL/6 mice were divided into normal control group (N, n=8), high fat feeding group (HF, n=32) and GLP-1Ra group treated with GLP-1Ra (liraglutide 200μg/(kg·d) or 400μg/(kg·d) for 8 weeks). Changes of body weight, blood glucose and three acyl glycosides (TG) levels were observed in three groups. HE staining was used to observe the morphological changes. Immunofluorescence staining and real-time PCR were used to mea?sure the expression of UCP-1. Furthermore, the expression of PGC-1αin protein level was observed to explore the possible mechanism of GLP-1Ra induced browning in white fat (WAT). Results After 8-week liraglutide (Lira) administration, the body weights were significantly reduced in obese mice (P<0.05). The levels of blood glucose and TG were significantly high?er in HF group than those in N group, which reduced significantly in Lira (200μg·kg-1) and Lira (400μg·kg-1) administra?tion groups (P<0.05). HE staining showed adipocytes in perirenal and inguinal subcutaneous adipose tissue partly acquired brown-like morphological characteristics. The expression levels of UCP-1 protein and mRNA and PGC-1αprotein were ele?vated in adipse tissues, which increased more in Lira (400) than those in Lira (200, P<0.05). Conclusion GLP-1Ra can induce weight loss through white fat browning by activation of UCP-1.

Objective To investigate the protective effects of 1-hydroxy-2, 3, 5-trimethoxyxanthone (QGS) on acute lung injury of mice induced by ip lipopolysaccharide (LPS). Methods Mice were pretreated with QGS for 7 d. Murine models of acute lung injury were duplicated by injection of LPS 20 mg/kg intraperitoneally. In 12 h, the lung weight index was observed and the NO level in the bronchoalveolar lavage fluid (BALF) was measured with kits. The lung was also assessd for the expression of I-?B, inducible nitric oxide synthase (iNOS), and cyclooxygenase-Ⅱ (COX-2) using Western blotting analysis. Lung pathological changes were also observed by HE in each group. Results The lung weight index of injury lung in mice induced by LPS was decreased in 500 mg/kg QGS group (P

It has been well known that apoptosis induction and cell cycle arrest are typical biological effects observed in cancer cells after proteasome inhibition. TH2 is a new natural xanthone analogue isolated from the resin of Garcinia hurburyi tree. Here, the cell growth inhibition of TH2 on human hepatocellular carcinoma cell line (Bel-7402) was evaluated in vitro using SRB assay. The treatment of 10 ?mol/L TH2 reduced the surviving fraction from 86% (12 h) to 17.2% (48 h). To assess whether TH2 induce apoptosis, the appearance of sub-G1 peak, a specific fraction for apoptosis was detected by flow cytometry analysis. Progressive increase in the percentage of apoptotic population was observed in a dose-and time-dependent manner. Furthermore, a cleavage of poly (ADP-ribose) polymerase (PARP), a marker of early apoptosis, was observed clearly when the cells exposed to 10 ?mol/L of TH2 for 24 h by immunoblotting analysis. In vitro activities of 20 S proteasome purified from human erythrocytes on fluorogenic peptide substrates revealed that TH2 inhibited the trypsin-like, chymotrypsin-like and peptidylglutamyl peptide hydrolyzing activities in dose-dependent manner. Moreover, the turnover of tumor suppressor p53, a sign of deregulation of cell cycle progression and apoptosis induction by classical proteasome inhibitors, was disrupted in Bel-7402 cells. All these data indicate that TH2 had inhibitory effect on the proliferation of Bel-7402 cells and induction of apoptosis, which might be related to its inhibition of proteasome.