Objective To detecte the changes of nephrin in adriamycin nephropathy rats, study the effects of mycophenolate mofetil on minimal change nephrotic syndrome, investigate its possible mechanism. Methods 18 SD rats were randomly divided into three groups: control group(CG, n=6), adriamycin model group(AG, n=6), MMF treated group(TG, n=6). Rats in MG and TG were given adriamycin 7.5mg/kg through vena caudalis. At the same time, an equal volume of normal saline was given to the rats in CG by the same method. The rats in TG received MMF 20mg/(kg?d) by daily gastric gavage from the second day. Urinary protein excretion of each rat were measured at the day before adriamycin injection,and the 14th day and the 28th day after adriamycin injection. Six rats of each group were killed at the 28th day. Serum urea nitrogen, creatinine, cholesterol, triglyceride and albumin were measured at the end of the study. Immunohistochemistry and western blot were used to examine the expression of nephrin. Results The urinary protein excretion of AG at 28th day was the highest. Serum albumin decreased markedly at the 14th day(p

Objective To explore the value of gastroendoscopy check-up early after non-surgical treatment of patients with gastroduodenal perfolation.Methods The patients suspected of perforated gastroduodenal ulcer on hospital admission underwent non-surgical treatment were enrolled.After cured clinically,performed gastroendoscopy at different time periods.Results Among 133 patients underwent gastrointestinal endoscopy,129 cases(97.0%)were diagnosed gastroduodenal ulcer,3 cases(2.3%)were diagnosed gastric carcinoma,1 case (0.8%)Was confirmed duodenal diverticulum,no compilcations occurred due to endoscopy.The 6 cases that had surgical indications had be implemented the early surgical treatment. Conclusions After non-surgical treatment of patient with gastroduodenal perforation,timely gsstroendoscopy can truly show pathologic changes with gastroduodenal perforation.So endoscopy is beneficial under condition appropriate time seleetion for confirmed the eliology of PGD,treatment promptly targeted etiology and understanding the mechanism healing the perforation as non-surgical treatment.

Endometrial Neoplasms ; drug therapy ; pathology ; Female ; Humans ; Precancerous Conditions ; drug therapy ; pathology ; Progestins ; therapeutic use

China ; Humans ; Speech-Language Pathology

Objective To investigate the role of intestinal immune dysfunction in the pathogenesis of irritable bowel syndrome(IBS) and to study the effects of Clostridium butylicum on the regulation of intestinal immune disorders.Methods A total of 50 male 6-week-old C57BL/6 mice were randomly divided into three groups,including the experimental group (n =20),the control group (n =20) and the Clostridium butylicum group(n =10).A mouse model of constipation-predominant IBS (C-IBS) was established by perfusing sodium butyrate solution(200 μl,concentration of 500 mmol/L) into the mouse colon twice a day for three consecutive days.The mice in control group were intrarectally perfused with normal saline enema (200 μl).Two hours before the perfusion of sodium butyrate into colon,the mice in Clostridium butylicum group were given Clostridium butylicum 500 μl(viable cell concentration of 1×109 CFU/ml) by oral gavage once a day for six days.The colorectal distention test(CRD) was carried out for evaluation of clinical parameters.HE staining of intestinal tissue section was performed for histopathological assessment of colonic mucosal inflammation.Intestinal intraepithelial lymphocytes (IELs) and lamina propria mononuclear cells (LPMCs) were isolated and analyzed by flow cytometry to evaluate the correlation between IBS and intestinal immune dysfunction/abnormal activation of intestinal immune cells in mouse model of C-IBS,and to assess the regulatory effects of Clostridium butylicum on the intestinal immune disorder.Results (1) Compared with the control group,the mice in experimental group showed a significant change in physiological parameters,histological structure of colon,inflammatory cells infiltration and low-grade inflammatory state.There was a significant increase in scores of CRD and a decrease in lowest sensory threshold (t=8.926 and t=6.103,both P＜0.001) ; (2) There was a decrease in the numbers of DC in IELs (t =2.878 and t =3.086,both P＜0.05),but an increase in the numbers of macrophage (t=3.191,P＜0.05) and the memory T cells in mice with IBS (t=3.071,P＜0.05) as compared with that in control group; (3)DCs were decreased (t=2.880 and t=2.664,both P＜0.05),but memory T cells were increased (t =3.732 and 2.682,P＜0.01 and P＜0.05) in the LPMCs of mice in experimental group; (4)There was no significant difference in the physiological index between the mice in control group and the Clostridium butylicum group.Levels of memory T cells,macrophages and DCs in the IELs were close to the normal level (6 d,t =1.103,0.0213,0.418,all P＞0.05),and levels of macrophages and DCs in the LPMCs of mice in the Clostridium butylicum group were also similar to that in the control group (6 d,t =0.782,0.347,both P＞0.05) ; (5) Compared with the mice in experimental group,the level of memory T cells in LPMCs of mice treated with Clostridium butylicum was dramatically declined (6 d,t=2.346,P=0.0470,P＜0.05),however,which was still higher than that of mice in control group (6 d,t =2.233,P =0.0476,P＜0.05).The intestinal immune function was restored to normal level with Clostridium butylicum intervention.Conclusion The pathophysiologic mechanism of IBS might be closely related to the abnormal activation of intestinal immune cellsand disordered functional state in the intestinal mucosa.Clostridium butylicum could regulate the intestinal immune homeostasis and restore the physiological function of gastrointestinal tract.

A new fluorimetric method was developed for the determi nation of ethanol in alcoholic beverage. The method is based on the principle that tetrasubstituted sulphonated aluminum phthalocyanine (AlS4Pc), a red-r egion fluorescent reagent, is induced to associate in the presence of cationic s urfactant, cetyltrimethylammonium bromide (CTMAB), thus its fluorescence is quen ched, and then the aggregate is disaggregated by the a ddition of ethanol and the fluorescence is recovered. This method has a linear determination range of 0.5%～90.0%(V/V), the detection limit is 0.48%(V /V). The method has been used to determine real alcoholic beverage samples w ith satisfactory results.

AIM: To investigate the effects of rosiglitazone on fibroblast-like synoviocyte ( FLS )-induced osteoclastogenesis in rheumatoid arthritis ( RA) and the related mechanism.METHODS: RA-FLS were cocultured with peripheral blood monocytes from healthy volunteers in the presence of macrophage colony-stimulating factor ( M-CSF) and rosiglitazone.Osteoclasts were assayed by tartrate-resistant acid phosphatase ( TRAP) staining.Resorption lacunae area was identified by toluidine blue staining and quantified by image analysis software.The mRNA expression of RANKL and OPG was evaluated by real-time PCR, and the protein levels of RANKL, OPG, p-ERK, p-p38 and p-JNK were measured by Western blot.RESULTS:Compared with control group ( without rosiglitazone treatment) , rosiglitazone at concentration of 15 μmol/L significantly decreased the number of osteoclasts (P<0.01) and resorption lacunae area (P<0.05).The expression of RANKL at mRNA and protein levels was significantly down-regulated by rosiglitazone at concentration of 15μmol/L, while the mRNA and protein expression of OPG was up-regulated (P<0.01).Rosiglitazone (15 μmol/L) sig-nificantly decreased the protein level of p-ERK ( P<0.05 ) , but not the protein level of p-p38 or p-JNK ( P>0.05 ) . CONCLUSION:Rosiglitazone inhibits RA-FLS-induced osteoclast formation and its resorption activity by down-regulating RANKL expression and ERK phosphorylation, suggesting that rosiglitazone may inhibit RA osteoclastogenesis and bone re-sorption.

Objective To investigate the mechanism of the permeability of intestinal mucosa in the pathogenesis of irritable bowel syndrome (IBS) and the interventional effects of Clostridium butyricum combined with glutamine.Methods According to random number method,fifty BALB/c mice were divided into control group,experimental control group,glutamine group,Clostridium butyricum group and combination group.IBS mice model was established by water-avoidance stress (WAS) experiment.The defecating time of mice and fecal water content were detected by dyed stool after mice gavaged with methylcellulose (1.5％).The pathological injury of intestine was assessed by hematoxylin and eosin staining.The visceral sensitivity was evaluated by colorectal distention test (CRD).The changes of the permeability of intestine was evaluated by detecting the changes of serum D-lactic acid (D-LA),level of diamine oxidase (DAO),expressions of intestinal epithelial cells (IEC) cell tight junction protein (TJ) (occludin-1,claudin-1,zonula occludens-1 (ZOL-1)) at protein level.The interventional effects of Clostridium butyricum combined with glutamine were evaluated.t test was performed for comparison between groups,and analysis of variance was used for comparison among multi-groups.Results Compared with the control group,the defecating time of experimental control group was significantly shorten ((100.40±14.80) min vs (75.88±12.20) min and water content of fecal significantly increased ((54.76±9.98)％ vs (74.95±7.15)％,t =3.692 and 4.023; P=0.002 and 0.002).The lowest threshold of visceral sensitivity significantly decreased ((40.87 ± 4.82) mmHg (1 mmHg=0.133 kPa) vs (27.80±3.18) mmHg; t=8.761,P＜0.01),while the mucosal pathological injury score significantly increased (0.50±0.15 vs2.60±0.97; t＝6.034,P＜0.01).The level of D-LA ((1 476±246.8) ng/L vs (913.6±90.1) ng/L)) and DAO ((3 391.0±256.9) vs (5 096.0±725.2) ng/L) significantly increased (t=40.920 and 29.810; both P＜0.05),and the expression of tight junction protein ZOL-1 (0.165±0.005 vs0.119±0.003),occludin-1 (0.104±0.016 vs 0.022±0.006) significantly decreased (t=19.830 and 19.830; both P＜0.01).Compared with the experimental control group,after intragastric intervention the defecating time of glutamine group,Clostridium butyricum group and combination group increased ((90.50±3.78),(97.56±8.79) and (99.89±11.90) min and water content of fecal decreased ((69.33±6.71)％,(58.07±8.97)％ and (56.74±8.12)％) and the differences were statistically significant (F=10.020 and 8.740; both P＜0.01).The results of Clostridium butyricum group and combination group were good (F=2.481 and 4.874; both P＜0.05).And the lowest threshold of visceral sensitivity significantly increased ((31.80±2.69),(36.04±5.06) and (38.93±3.30) mmHg; F=2.420,P＜0.05),the result of combination group was the best (F=3.550,P＜0.01).Jejunal mucosal injury was significantly reduced (2.00 ± 0.94,1.30 ± 0.68 and 1.30±0.48; F＝11.350,P＜0.01).After intragastric intervention,serum levels of D-LA ((1 370.0± 78.9),(1 066.0±155.5) and (1 039.0±129.0) ng/L) and DAO ((4 808.0±477.4),(3 713.0± 595.0) and (3 725.0±615.9) ng/L) of glutamine group,Clostridium butyricum group and combination group significantly decreased (F＝37.480 and 27.670; both P＜0.01).The level of ZOL-1(0.126± 0.014,0.125±0.006,0.138±0.004) and occludin 1 (0.037±0.013,0.073±0.028,0.078±0.027) of glutamine group,Clostridium butyricum group and combination group significantly increased,and the differences were statistically significant (F=5.867 and 10.630; both P＜0.05).The change of ZOL-1 of combination group was more than that of Clostridium butyricum group (t =5.457,P ＜ 0.05).Conclusions WAS experiment can induce visceral hypersensitivity,increase the permeability of intestine and reduce the function of intestinal epithelial barrier.Clostridium butyricum and glutamine are effective in the recovery of visceral hypersensitivity and the permeability of mucosal epithelia cells.

Objective To investigate the effects of Bifidobacterium infatn ison the expression of in -testinal corticotropin releasing factor ( CRF) receptors and how the peripheral CRF receptors activate mast cells in a murine model of irritable bowel syndrome (IBS).Methods Thirty BALB/c male mice were ran-domly divided into three groups including control group , model group and Bifidobacterium infantis group. The mouse model of IBS was established by using chronic restraint stress .Mice in Bifidobacterium infantis group received daily intragastrical administration of Bifidobacterium infantis for 14 days.Mice in control and model groups were treated with equal volume of saline .Then all mice were killed after the assessment of weight and abdominal withdrawal reflex ( AWR) .The levels of histamine , tryptase and tumor necrosis fac-tor-α( TNF-α) in serum samples were detected by ELISA .The expression of CRF in colonic mucosa was analyzed by immunohistochemistry .The expression of CRF-R1 and CRF-R2 in mast cells and the number of mast cells in colonic mucosa were detected by double immunofluorescence staining assay .The expression of CRF-R1 and CRF-R2 at mRNA level in colon were detected by reverse transcription polymerase chain reac-tion ( RT-PCR) .Results Compared with control group , the levels of histamine , tryptase and TNF-αin pe-ripheral blood samples , the expression of CRF-R1 and CRF-R2 at mRNA level , and the number of mast cells, CRF-R1+mast cells and CRF-R2+mast cells in colonic mucosa were increased significantly in model group (P<0.05), but were remarkably down-regulated with the treatment ofB ifidobacterium infantis (P<0.05).Conclusion Bifidobacterium infantis could reduce the activation of mast cells in a murine model of IBS by inhibiting the expression of CRF-R1 and CRF-R2 in intestinal mast cells .

Objective To detect the dynamic Th17 cells in a murine model of irritable bowel syn-drome ( IBS) and to study the effect of aryl hydrocarbon receptor ( Ahr) on Th17 cells activation .Methods Thirty BALB/c male mice were randomly divided into three groups including experiment group ,control group and Ahr antagonist group .A murine model of IBS was established by perfusing three nitrobenzene sulfonic acid (TNBS) into the colon of mice.Equal volume of saline was used to set up the control .The mice in Ahr antagonist group were intraperitoneally injected with 10 μg Ahr antagonist for four consecutive days .All mice were evaluated for visceral hypersensitivity and colonic mucosal inflammation .Mesenteric lymph nodes (MLNs) and peripheral blood mononuclear cells (PBMCs) were detected by flow cytometry through staining Th17 cells.The distribution of Ahr and IL-17A in colon and the number of Th17 cells activated by Ahr (Ahr and IL-17A double positive ) were detected by double immunofluorescence staining .Results ( 1 ) The percentage of Th17 cells in MLNs was significantly increased in experiment group followed by those in Ahr antagonist group and control group (P<0.05).(2)Compared with control group,the number of Th17 cells in peripheral blood samples was significantly increased in experiment group and Ahr antagonist group ( both P<0.05 ) ,but there was no difference between Ahr antagonist group and experiment group ( P=0.642 ) .( 3 ) The number of Ahr-activated Th17 cells ( Ahr+IL-17A+) was significantly increased in experiment group (10.00±1.58) as in comparison with that in control group (3.80±0.83,P<0.05),but the number was de-creased with Ahr antagonist intervention ( 5.80 ±0.83 , P<0.05 ) .Conclusion The number of activated Th17 cells was increased in MLNs and peripheral blood samples from mice with IBS .Ahr played an important role in the activation of Th17 cells in intestines.However,the number of Ahr-activated Th17 cells in intestinal mucosa and the proportion of Th 17 cells in MLNs could be down-regulated through blocking Ahr .