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

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 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 .

Objective To study the influence and mechanism of hepatocyte growth factor (HGF) on myotube phenotype by myotube transdifferentiation induced by transforming growth factor-β1 (TGF-β1). Methods C2C12 cells were cultured in differentiation medium to induce myotubes formation. The cells were randomly devided into 3 groups. The control group without growth factor interruption. The induction group was supplemented with TGF-β1 (5 ng/mL) while the inhibition group was supplenmented with both TGF-β1 (5 ng/mL) and HGF (30 ng/mL). After 12 hours, the expressions of connective tissue growth factor (CTGF) protein in myotubes were detected by Western blot, the levels of CTGF mRNA were measured by RT-PCR. Results Compared to the control group, the protein and mRNA levels of CTGF significantly increased in TGF-β1 treated group , whereas the protein and mRNA levels of CTGF were significantly lower in inhibition group than those in induction group (P < 0.05). Conclusion HGF can inhibit the effect of TGF-β1 on the expression of CTGF in myotubes , which provides the evidences on the study of skeletal muscle cell transdifferentiation.

Objective To investigate the optimal technology of blind needle synovial biopsy.Methotis Blind needle synovial biopsy was performed on 81 knees with pain and swelling.Twenty patients with rheumatoid arthritis (RA) received uhrasonographic (US) examination before biopsies.Results Synovium were obtained in all patients and the successful rate was (71±21)%,while the area of synovium was (1.8±0.8)mm2.The time for accomplishing the procedure was (26±6) min and the depth of trocar insertion Was (3.1±0.7) cm.The successful rate in patients with RA (80±6)% was much higher than that in non-RA patients (54±10)%.The successful rate with US guidance (85±5)% was much higher than that without US guidance (78±6)%.The positive predictive value of synovium evaluation by naked eye Was 95.0%,while the negative predictive value was 81.1%.Conclusion Blind needle synovial biopsy should be spread because it is simple and safe to perfonn and it can obtain sufficient synovium for all purposes.

Objective To investigate the effect of hypoxia-inducible factor (HIF)-1α and vascular en-dothelial growth factor (VEGF) on the angioge-nesis of rheumatoid arthritis (RA). Methods The collagen-induced arthritis (CIA) model was set up in male Wistar rats. The pathological angiogenesis and expression of HIF-1α and VEGF in the synovia different time points were observed by H&E and immunohistochemistry staining. Results The expressions of HIF-1α and VEGF on CIA synovium were significantly elevated and their expression increased gradually with the prolonged disease course. Both synovial HIF-1α expression and VEGF expression were correlated significantly with the pathological angiogenesis score. Synovial lining and sublining HIF-1α expression were correlated significantly with VEGF expression respectively. Conclusion H1F-1α may play an important role in the pathogenesis of RA by upregulating the expression of VEGF and then promoting angiogenesis.