Objective To observe the adjuvant therapy efficacy of Saccharomyces boulardii sachets in liver cirrhosis patients with spontaneous bacterial peritonitis(SBP).Methods 72 liver cirrhosis patients with SBP were randomly divided into the observation group and control group.The patients in the control group (30 cases) were giv-en routine medical treatment such as anti-infection,correction of hypoproteinemia,liver protection,and diuresis,etc. At the base of the control group,the patients in the observation group (32 cases) were orally given Saccharomyces boulardii ( Baili Pharmaceutical Factory,French) 0.5g for one time,two times daily for 10 days.The changes of serum interleukin-6(IL-6),pmcalcitonin (PCT) and hypersensitive c-reactive protein (hs-CRP) levels in the two groups were observed and compared before and after treatment, and curative effect and safety were also observed. Results Before treatment,the serum IL-6,PCT and hs-CRP levels in the two groups had no obviously statistical difference(all P>0.05),but after treatment,the serum IL-6,PCT and hs-CRP levels of the observation group were much lower than those of the control group[(60.50 ±19.10) pg/mL vs (98.32 ±17.20) pg/mL,(1.80 ± 0.34)μg/L vs (6.38 ±3.56)μg/L,(6.20 ±4.15) mg/L vs (20.28 ±8.30) mg/L,t=8.147,7.246,8.529,all P<0.01].Meanwhile,the total effective rate of the observation group was significantly higher than that of the control group(93.75%vs 73.33%,χ2 =4.771,P<0.05).The incidence rate of DAR between the two groups had no obvi-ously statistical difference(9.38% vs 13.33%,χ2 =0.242,P>0.05).Conclusion Saccharomyces boulardii can significantly reduce serum IL-6,PCT and hs-CRP levels of liver cirrhosis patients with SBP,and reduce inflamma-tion reaction to control development of SBP.

Background:Currently,chronic atrophic gastritis( CAG)is diagnosed by endoscopy combined with pathological examination. Narrow-band imaging magnifying endoscopy( NBI-ME)has been widely applied to diagnose CAG. However, it is a issue how to optimize the examination technology. Aims:To investigate the clinical value of NBI-ME in diagnosis of CAG,intestinal metaplasia and intraepithelial neoplasia. Methods:One hundred CAG patients reexamined gastroscopy were enrolled,sequential examination was performd,i. e. the extent of disease was observed under convention white light endoscopy( C-WLI ) followed by NBI-ME mode to observe locally,morphological changes of gastric mucosa pit was analyzed,endoscopic findings and histological results was compared. Results:Sensitivity of sequential examination for the diagnosis of CAG was 89. 7%,specificity was 63. 3%;sensitivity and specificity for the diagnosis of intestinal metaplasia were 89. 4%,89. 3%,respectively,for intraepithelial neoplasia were 84. 2%,95. 9%,respectively. Conclusions:Sequential examination can significantly improve the diagnostic accuracies of CAG,intestinal metaplasia and intraepithelial neoplasia,and effectively guide targeted biopsy,and easily to operate.

Aged ; Antineoplastic Combined Chemotherapy Protocols ; therapeutic use ; Calbindin 2 ; metabolism ; Cholecystitis ; pathology ; Cisplatin ; administration & dosage ; Cystitis ; pathology ; Diagnosis, Differential ; Female ; Glutamates ; administration & dosage ; Guanine ; administration & dosage ; analogs & derivatives ; Humans ; Inflammation ; pathology ; Keratins ; metabolism ; Lung Neoplasms ; drug therapy ; metabolism ; pathology ; surgery ; Male ; Mesothelioma ; drug therapy ; metabolism ; pathology ; surgery ; Middle Aged ; Pemetrexed ; Peritoneal Neoplasms ; drug therapy ; metabolism ; pathology ; surgery ; Survival Rate ; Vimentin ; metabolism

Objective To study the role of IL-18 in the pathogenesis and treatment of ulcerative colitis (UC). Method An enzyme-linked immunosorbent assay (ELISA) was utilized to detect the serum IL-18 level of 58 UC patients. Results The serum IL-18 level in acute period of UC patients was significantly higher than that in control ones(P < 0.05 ). There was no significant difference between remisson period of UC and control ones (P> 0.05). The serum IL-18 level was closely related with the degree of UC (P < 0.05),the mean concentration of serum IL-18 was significantly higher in patients with severe ulcerative colitis [ (392.78 ± 50.17)pg/ml]than in patients with mild colitis ulcerative [ (138.92 ± 23.41 )pg/ml]and in control ones. Serum IL-18 in active ulcerative colitis were positively related to clinical disease severity and activity or laboratory parameters,including CAI,serum CRP,erythrocyte sedimentation rates,or total leukocyte counts (r = 0.775,0.705,0.662,0.625,P < 0.01 ). The level of IL-18 was declined after treatment with corticoids(P< 0.05). Conclusions IL-18 might play an important role in the pathogenesis of UC. The measurement of IL-18 is helpful to estimate the disease activity of UC and it may be considered as laboratory and activity criteria for UC.

Objective To investigate the clinical value of serum gastric function(pepsinogen I, II and PGR, gastrin-17), Helicobacter pylori (Hp) infection combined with narrow-band imaging magnifying endoscopy for the diagnosis of gastric ulcer. Methods From October 2015 to December 2016, we selected 113 patients diagnosed as gastric ulcer and gastric cancer by narrow-band imaging endoscopy (NBI-ME) and diagnosed by pathological examination. 65 patients were divided into gastric ulcer group. 48 patients were divided into gastric cancer group, 65 healthy subjects who had passed the physical examination were selected as the control group. Enzyme-linked immunosorbent assay was used to measure serum gastric function parameters such as serum pepsinogen I / Ⅱ, PGR, and gastrin-17, and C14 breath test was used to detect Hp. Results The Hp infection rate in the gastric ulcer group and the gastric cancer group was significantly higher than that in the control group, the difference was statistically significant (P＜0. 05). Compared with the control group, serum PG I and PGR levels in the gastric ulcer group were significantly increased (P＜0. 05); serum PG I and PGR levels in the gastric cancer group were lower than those in the control group(P＜0. 05). The PGI and PGR levels in the gastric ulcer group were significantly higher than those in the gastric cancer group, the difference was statistically significant (P＜0. 05). Compared with the control group, the serum G-17 concentration in the gastric ulcer group and the gastric cancer group was higher than that in the control group(P＜0. 05). Conclusion PG I, PG Ⅱ, G-17 and other serum gastric functional parameters combined with Hp indicators have been further measured by NBI-ME in gastric ulcer and gastric cancer diagnosis and prognosis has a high reference value.

Present study aimed to investigate the eff ect of curcumin-pretreatment on intestinal I/R injury and on intestinal mucosa barrier. Thirty Wistar rats were randomly divided into: sham, I/R, and curcumin groups (n=10). Animals in curcumin group were pretreated with curcumin by gastric gavage (200 mg/kg) for 2 days before I/R. Small intestine tissues were prepared for Haematoxylin & Eosin (H&E) staining. Serum diamine oxidase (DAO) and tumor necrosis factor (TNF)-alpha levels were measured. Expression of intestinal TNF-alpha and tight junction protein (ZO-1) proteins was detected by Western blot and/or immunohistochemistry. Serum DAO level and serum and intestinal TNF-alpha leves were signifi cantly increased after I/R, and the values were markedly reduced by curcumin pretreatment although still higher than that of sham group (p<0.05 or p<0.001). H&E staining showed the significant injury to intestinal mucosa following I/R, and curcumin pretreatment signifi cantly improved the histological structure of intestinal mucosa. I/R insult also induced significantly down-regulated expression of ZO-1, and the eff ect was dramatically attenuated by curcumin-pretreatment. Curcumin may protect the intestine from I/R injury through restoration of the epithelial structure, promotion of the recovery of intestinal permeability, as well as enhancement of ZO-1 protein expression, and this eff ect may be partly attributed to the TNF-alpha related pathway.
Amine Oxidase (Copper-Containing) ; Animals ; Blotting, Western ; Curcumin* ; Eosine Yellowish-(YS) ; Immunohistochemistry ; Intestinal Mucosa ; Intestine, Small ; Intestines ; Permeability ; Rats, Wistar ; Reperfusion Injury* ; Tight Junctions* ; Tumor Necrosis Factor-alpha* ; Zonula Occludens-1 Protein*

Renal interstitial fibrosis (RIF) is the crucial pathway in chronic kidney disease (CKD) leading to the end-stage renal failure. However, the underlying mechanism of Shen Qi Wan (SQW) on RIF is not fully understood. In the current study, we investigated the role of Aquaporin 1 (AQP1) in SQW on tubular epithelial-to-mesenchymal transition (EMT). A RIF mouse model induced by adenine and a TGF-β1-stimulated HK-2 cell model were etablished to explore the involvement of AQP 1 in the protective effect of SQW on EMT in vitro and in vivo. Subsequently, the molecular mechanism of SQW on EMT was explored in HK-2 cells with AQP1 knockdown. The results indicated that SQW alleviated kidney injury and renal collagen deposition in the kidneys of mice induced by adenine, increased the protein expression of E-cadherin and AQP1 expression, and decreased the expression of vimentin and α-smooth muscle actin (α-SMA). Similarly, treatmement with SQW-containing serum significantly halted EMT process in TGF-β1 stimulated HK-2 cells. The expression of snail and slug was significantly upregulated in HK-2 cells after knockdown of AQP1. AQP1 knockdown also increased the mRNA expression of vimentin and α-SMA, and decreased the expression of E-cadherin. The protein expression of vimentin increased, while the expression of E-cadherin and CK-18 significantly decreased after AQP1 knockdown in HK-2 cells. These results revealed that AQP1 knockdown promoted EMT. Furthermore, AQP1 knockdown abolished the protective effect of SQW-containing serum on EMT in HK-2 cells. In sum, SQW attentuates EMT process in RIF through upregulation of the expression of AQP1.
Drugs, Chinese Herbal/pharmacology* ; Humans ; Animals ; Mice ; Male ; Cell Line ; Rats ; Kidney/physiology* ; Fibrosis/drug therapy* ; Renal Insufficiency, Chronic/drug therapy* ; Adenine ; Epithelial-Mesenchymal Transition ; Aquaporin 1/metabolism*