Efficacy of artificial intelligence in reducing miss rates of GI adenomas, polyps, and sessile serrated lesions: a meta-analysis of randomized controlled trials.

BACKGROUND AND AIMS: The aim of this study was to determine if utilization of artificial intelligence (AI) in the course of endoscopic procedures can significantly diminish both the adenoma miss rate (AMR) and the polyp miss rate (PMR) compared with standard endoscopy. METHODS: We performed an extensive search of various databases, encompassing PubMed, Embase, Cochrane Library, Web of Science, and Scopus, until June 2023. The search terms used were artificial intelligence, machine learning, deep learning, transfer machine learning, computer-assisted diagnosis, convolutional neural networks, gastrointestinal (GI) endoscopy, endoscopic image analysis, polyp, adenoma, and neoplasms. The main study aim was to explore the impact of AI on the AMR, PMR, and sessile serrated lesion miss rate. RESULTS: A total of 7 randomized controlled trials were included in this meta-analysis. Pooled AMR was markedly lower in the AI group versus the non-AI group (pooled relative risk [RR], .46; 95% confidence interval [CI], .36-.59; P < .001). PMR was also reduced in the AI group in contrast with the non-AI control (pooled RR, .43; 95% CI, .27-.69; P < .001). The results showed that AI decreased the miss rate of sessile serrated lesions (pooled RR, .43; 95% CI, .20 to .92; P < .05) and diminutive adenomas (pooled RR, .49; 95% CI, .26-.93) during endoscopy, but no significant effect was observed for advanced adenomas (pooled RR, .48; 95% CI, .17-1.37; P = .17). The average number of polyps (Hedges' g = -.486; 95% CI, -.697 to -.274; P = .000) and adenomas (Hedges' g = -.312; 95% CI, -.551 to -.074; P = .01) detected during the second procedure also favored AI. However, AI implementation did not lead to a prolonged withdrawal time (P > .05). CONCLUSIONS: This meta-analysis suggests that AI technology leads to significant reduction of miss rates for GI adenomas, polyps, and sessile serrated lesions during endoscopic surveillance. These results underscore the potential of AI to improve the accuracy and efficiency of GI endoscopic procedures.

Drug-drug interaction of rabeprazole and clopidogrel in healthy Chinese volunteers.

PURPOSE: This study was aimed to determine the impact of rabeprazole (RBRZ) on the antiplatelet efficacy of clopidogrel (CPG) in healthy Chinese volunteers, and further to predict the effect of CYP2C19 genetic polymorphism on the efficacy of rabeprazole and clopidogrel. METHODS: The open-label, two period cross-over study was conducted in 20 healthy Chinese subjects with different CYP2C19 genotypes receiving clopidogrel, rabeprazole or the two drugs, respectively. All the volunteers were divided into two groups, poor metabolizers (PMs) and extensive metabolizers (EMs), depending on CYP2C19 genotypes. Blood samples were collected at baseline and at 0.5, 1, 2, 3, 4, 6, 8, 10, and 12 h after administration. The plasma concentrations of rabeprazole and clopidogrel were analyzed by LC-MS/MS and ADP-induced platelet aggregation was detected by the optical turbidimetric method. RESULTS: There were no significant differences in the mean plasma concentration-time curves of clopidogrel (CPG), the inactive metabolite clopidogrel carboxylic acid (CPG-CA), the active metabolite clopidogrel-MP-Derivative (MP-AM), and rabeprazole (RBRZ) according to the co-administration of CPG and RBRZ. There were no major changes in the pharmacokinetics of CPG and RBRZ. The maximal ADP-induced platelet aggregation (2 µmol/L) was decreased in EMs compared with PMs. CONCLUSION: Co-administration of rabeprazol and clopidogrel did not affect the antiplatelet efficacy of clopidogrel. The CYP2C19 genetic polymorphism may impact the efficacy of clopidogrel.

[Effect of metoclopramide on capsule endoscopy examination: a randomized study].

OBJECTIVE: To investigate the effect of metoclopramide on capsule endoscopy (CE) examination. METHODS: Total 116 patients referred for CE were randomized into two groups with 58 patients in each group. In treatment group patients received 10 mg metoclopramide intramuscular injection after swallowing the capsule and in control group no metoclopramide was administered. The gastric transit time, small bowel transit time, complete endoscopy rate were observed in both groups. RESULTS: The CE examination was completed in 51 patients of treatment group (87.9%) and 48 of control group (84.2%). Mean gastric transit time was (32.45 ± 29.63) min in treatment group and (45.81 ± 40.01)min in control group, there was significant difference between two groups (P<0.05). Mean small bowel transit time was (252.69 ± 113.29) min in treatment group and (258.75 ± 83.83) min in control group, there was no significant difference between two groups (P>0.05). CONCLUSION: Metoclopramide may reduces gastric transit time, but not effect small bowel transit time,which suggests that it might increase the likelihood of complete small-bowel examination in patients undergoing capsule endoscopy.

Nitroglycerin in the prevention of post-ERCP pancreatitis: a meta-analysis.

The objective of this research paper is to evaluate the effect of prophylactic nitroglycerin in the prevention of post-endoscopic retrograde cholangiopancreatography (ERCP) pancreatitis (PEP) by performing a meta-analysis of randomized controlled trials (RCTs). Electronic databases, including PubMed, EMBASE, the Cochrane library, and the Science Citation Index, were searched to retrieve relevant trials. Outcome measures were the incidence of PEP. Four RCTs, enrolling a total of 856 patients, were included. Meta-analysis of these trials indicated a significant association between the use of nitroglycerin and the reduction of PEP (RR 0.60; 95%CI: 0.39-0.92; P = 0.02). However, subsequent sensitive analysis failed to confirm that nitroglycerin was statistically superior to a placebo in reducing PEP (RR 0.68; 95%CI: 0.41-1.11; P = 0.12). Based on the limitations in this meta-analysis, prophylactic use of nitroglycerine for all patients who underwent ERCP is not recommended. Further clinical trials are required to confirm the effect of nitroglycerin in the prevention of PEP.

ADP-ribosylation factor like 7 (ARL7) interacts with alpha-tubulin and modulates intracellular vesicular transport.

ADP-ribosylation factor (ARF) like 7 (ARL7, also named ARL4C) is a member of ARL family and recent studies showed that it is involved in the AI-dependent cholesterol secretion process. Yet its biological function remains largely unknown. Using a MALDI-TOF/MS analysis, we identified alpha-tubulin interacted with ARL7. The interaction was confirmed by GST pull-down assay and co-immunoprecipitation in renal carcinoma cell 786-O in which we found the endogenous ARL7 is expressed. This is the second ARL member found interacting with tubulin after ARL8. In addition, ARL7Q72L, a GTP-binding form, promoted the transferrin transport from early endosome to recycling endosome significantly. The above data suggested that ARL7 might modulate the intracellular vesicular transport via interaction with microtubules.

Can wire-guided cannulation reduce the risk of post-endoscopic retrograde cholangiopancreatography pancreatitis? A meta-analysis of randomized controlled trials.

BACKGROUND AND AIM: The use of wire-guided cannulation (WGC) for prevention of post-endoscopic retrograde cholangiopancreatography (ERCP) pancreatitis (PEP) is controversial. The aim of the present study was to assess the overall effect of WGC for PEP compared with conventional contrast-assisted cannulation by carrying out a meta-analysis of all available randomized controlled trials (RCT). METHODS: Electronic databases, including PubMed, EMBASE, the Cochrane library and the Science Citation Index, were searched to retrieve relevant trials. In addition, meeting abstracts and the reference lists of retrieved articles were reviewed for further relevant studies. Outcome measures were the incidence of PEP. RESULTS: Four RCT, enrolling a total of 1413 patients, were included. The meta-analysis failed to indicate a significant association between the use of WGC and the reduction of PEP (RR 0.34; 95% CI: 0.10-1.17; P = 0.09). Subgroup analysis including trials without cross-over design showed a significant benefit with the use of WGC in reducing PEP (RR 0.20; 95% CI: 0.09-0.40; P < 0.00001) and trials without precut used failed to indicate a significant differences between the two group (RR 0.38; 95% CI: 0.01-11.73; P = 0.58). CONCLUSIONS: This meta-analysis showed only a non-significant reduction in the rate of PEP with the use of WGC. Further well-designed RCT are required to confirm the effect of WGC, especially in patients who were easier to cannulate.

Therapeutic effects of rectal administration of muscovite on experimental colitis in rats.

BACKGROUND AND AIMS: The aim of this study was to investigate whether rectal administration of muscovite can ameliorate colonic inflammation in a rat model of experimental colitis, and its possible mechanism. METHODS: Female Sprague-Dawley (SD) rats with trinitrobenzene sulfonic acid (TNBS)-induced colitis were treated with rectal administration of muscovite or 5-aminosalicylic acid (5-ASA) daily for 14 days. The changes in body weight, macroscopic damage and histologic scores were subsequently evaluated. Gene expression of tumor necrosis factor-alpha (TNF-alpha), interleukin-1beta (IL-1beta), mucin2 (MUC2) and trefoil factor 3 (TFF3) in the colonic tissues was assessed by semiquantitative reverse transcription polymerase chain reaction (RT-PCR) while protein levels of TNF-alpha and IL-1beta were detected by ELISA. Mucin2 expression in colonic mucosa was detected by immunohistochemistry. The capacity of muscovite to adsorb cytokines in vitro was determined by the changes in the amount of TNF-alpha, IL-1beta secreted by lipopolysaccharide (LPS)-stimulated THP-1 cells and IL-8 secreted by LPS-stimulated HT-29 cells. RESULTS: Rectal administration of muscovite improved the loss of body weight, macroscopic and histologic scores of TNBS-induced colitis in a dose-dependent manner. Trinitrobenzene sulfonic acid-induced expression of TNF-alpha and IL-1beta was reduced by muscovite and 5-ASA treatment. Reduction of MUC2 expression in colitis rats was reversed by muscovite and 5-ASA treatment. However, the expression of TFF3 mRNA in colonic mucosa was not affected. In addition, we found muscovite inhibited the expression of TNF-alpha, IL-1beta secreted by THP-1 and IL-8 secreted by HT-29 cells in a dose-dependent manner. CONCLUSIONS: Our study demonstrated for the first time that rectal administration of muscovite can ameliorate colonic inflammation of TNBS-induced colitis. Further confirmatory studies are needed to prove that muscovite might be a potential therapeutic agent for the treatment of ulcerative colitis.

Effect of H pylori infection and its eradication on hyperammo-nemia and hepatic encephalopathy in cirrhotic patients.

AIM: To investigate the relationship between H pylori infection, blood ammonia concentration and hepatic encephalopathy (HE), and the effect of H pylori eradication in cirrhotic patients. METHODS: From July 2003 to January 2005, 457 cirrhotic patients in five regions of Zhejiang Province were enrolled. Patients were evaluated for demographics, number connection test, H pylori infection, liver impairment, blood ammonia concentration and HE. Patients with H pylori infection were given 1 wk therapy with omeprazole plus clarithromycin and tinidazole. (14)C urea breath test was performed and mental symptoms and blood ammonia level were reassessed after bacterium eradication. RESULTS: Overall H pylori infection rate was 60.6%, and HE occurred in 47.5% of cirrhotic patients. Subclinical HE (SHE) was detected in 55 of 117 cirrhotic patients. Blood ammonia concentration in H pylori negative (n = 180) and positive (n = 277) cirrhotic patients was 53.8 +/- 51.4 and 78.4 +/- 63.6 mumol/L, respectively (P < 0.01), which was significantly reduced to 53.5 +/- 37.7 mumol/L after bacterium eradication (n = 126) (P < 0.01). Blood ammonia was 97.5 +/- 81.0 mumol/L in H pylori-positive cirrhotic patients, and this did not significantly change in those with persistent infection after H pylori eradication (n = 11). HE was more frequently observed in patients with H pylori infection than in those without (58.5% vs 30.6%, P < 0.01). HE rate significantly dropped to 34.1% after H pylori eradiation (P < 0.01). H pylori prevalence significantly differed among cirrhotic patients with HE (74.4%), SHE (69.1%), and those without HE (53.2%) (P < 0.05). Blood ammonia level was significantly different among cirrhotic patients with HE (94.5 +/- 75.6 mumol/L), SHE (59.9 +/- 49.2 mumol/L), and without HE (47.3 +/- 33.5 mumol/L) (P < 0.05). Logistic regression analysis showed that blood ammonia concentration, Child-Pugh stage, upper gastrointestinal bleeding, electrolyte disturbance, and urea nitrogen were risk factors for HE. CONCLUSION: H pylori infection is an important factor for inducing high blood ammonia concentration and HE in cirrhotic patients. H pylori eradication may be helpful for treatment and prevention of HE.

Anticancer activity of genistein on implanted tumor of human SG7901 cells in nude mice.

AIM: To investigate genistein-induced apoptosis of implanted tumors of SG7901 cells in nude mice, and the relationship between this apoptosis and expression of Bcl-2 and Bax. METHODS: Establishing a transplanted tumor model by injecting human SG7901 cells into subcutaneous tissue of nude mice. Genistein (0.5, 1 and 1.5 mg/kg) was directly injected adjacent to the tumor, six times at 2-d intervals. Then, changes in tumor volume were measured continuously and tumor inhibition rate of each group was calculated. We observed the morphological alterations by transmission electron microscopy (TEM), measured the apoptotic rate by the TUNEL staining method, and detected the expression of apoptosis-regulated gene Bcl-2 and bax by immunohistochemical staining and RT-PCR. RESULTS: Genistein 0.5, 1 and 1.5 mg/kg significantly inhibited carcinoma growth when it was injected near the tumor by 10.8%, 29.9% and 39.6%, respectively. Genistein induced implanted tumor cells to undergo apoptosis, with apoptotic characteristics seen by TEM. The apoptosis index was increased progressively with increasing genistein dose (28.9%+/-1.2%, 33.8%+/-1.6% and 37.7%+/-1.2%). The positive rate of Bcl-2 protein was decreased progressively (11.9%+/-0.9%, 5.9%+/-0.7% and 4.2%+/-0.6%), and the positive rate of bax protein was increased progressively (0.9%+/-1.7%, 24.9%+/-0.8% and 29.6%+/-1.7%) by immunohistochemical staining, with increasing dose of genistein. The density of Bcl-2 mRNA decreased progressively and the density of bax mRNA increased progressively with elongation of time by RT-PCR. CONCLUSION: Genistein was able to induce apoptosis of transplanted tumor cells. This apoptosis may be mediated by down-regulation of the apoptosis-regulated gene Bcl-2 and up-regulation of apoptosis-regulated gene bax.

Reliable experimental model of hepatic veno-occlusive disease caused by monocrotaline.

BACKGROUND: Hepatic veno-occlusive disease (HVOD) is a severe complication of chemotherapy before hematopoietic stem cell transplantation and dietary ingestion of pyrrolizidine alkaloids. Many experimental models were established to study its mechanisms or therapy, but few are ideal. This work aimed at evaluating a rat model of HVOD induced by monocrotaline to help advance research into this disease. METHODS: Thirty-two male rats were randomly classified into 5 groups, and PBS or monocrotaline was administered (100 mg/kg or 160 mg/kg). They were sacrificed on day 7 (groups A, B and D) or day 10 (groups C and E). Blood samples were collected to determine liver enzyme concentrations. The weight of the liver and body and the amount of ascites were measured. Histopathological changes of liver tissue on light microscopy were assessed by a modified Deleve scoring system. The positivity of proliferating cell nuclear antigen (PCNA) was estimated. RESULTS: The rats that were treated with 160 mg/kg monocrotaline presented with severe clinical symptoms (including two deaths) and the histopathological picture of HVOD. On the other hand, the rats that were fed with 100 mg/kg monocrotaline had milder and reversible manifestations. Comparison of the rats sacrificed on day 10 with those sacrificed on day 7 showed that the positivity of PCNA increased, especially that of hepatocytes. CONCLUSIONS: Monocrotaline induces acute, dose-dependent HVOD in rats. The model is potentially reversible with a low dose, but reliable and irreversible with a higher dose. The modified scoring system seems to be more accurate than the traditional one in reflecting the histopathology of HVOD. The enhancement of PCNA positivity may be associated with hepatic tissue undergoing recovery.

The associations among Helicobacter pylori infection, white blood cell count and nonalcoholic fatty liver disease in a large Chinese population.

Reported relationships among Helicobacter pylori infection, white blood cell (WBC) count and nonalcoholic fatty liver disease (NAFLD) are inconsistent and controversial. We, therefore, conducted a cross-sectional study to investigate the associations among the presence of NAFLD, WBC count and H pylori infection, as diagnosed using the C-urea breath test (UBT).This study included 20,389 subjects enrolled at the International Health Care Center of the Second Affiliated Hospital of the Zhejiang University School of Medicine from January 2015 to December 2015. All participants underwent a C-UBT for the diagnosis of H pylori infection and ultrasonography for NAFLD as well as a blood test to determine WBC count. Multivariate logistic regression was then performed to evaluate the relationship among H pylori infection, WBC count and NAFLD.H pylori infection was detected in 38.49% (7,848/20,389) of the subjects via the UBT, and NAFLD was present in 37.24% (7,592/20,389) of the subjects. The prevalence of H pylori infection was higher in the NAFLD group than in the control group (41.25% vs 36.85%, P <.001). Significant differences were found between various WBC quartiles and H pylori infection, age, gender, body mass index (BMI), systolic blood pressure (SBP), diastolic blood pressure (DBP), high-sensitivity C-reactive protein (HS-CRP), glycosylated hemoglobin (HbA1c), triglyceride (TG), low-density lipoprotein (LDL-C), fasting blood glucose (FPG), homeostasis model assessment of insulin resistance (HOMA-IR), and smoking. Multivariate logistic regression revealed that the combination of H pylori infection and WBC count (odds ratio [OR] = 1.067, 95% confidence interval [CI]: 1.014, 1.093; P = .007; OR = 1.165, 95% CI: 1.023, 1.488; P <.001; OR = 1.183, 95% CI: 1.085, 1.559; P <.001, respectively) was positively associated with NAFLD.H pylori infection and WBC count may contribute to the pathogenesis of NAFLD.

Downregulation of GEP100 Improved the Growth Inhibition Effect of Erlotinib Through Modulating Mesenchymal Epithelial Transition Process in Pancreatic Cancer.

OBJECTIVE: The epidermal growth factor receptor is overexpressed in the majority of pancreatic cancer. Epidermal growth factor receptor tyrosine kinase inhibitor erlotinib was approved to treat patients combining with gemcitabine. However, the sensitivity is low. Here, we try to reveal the regulatory role of guanine nucleotide exchange protein 100 (GEP100) in erlotinib sensitivity. METHODS: We investigated the correlation between GEP100 expression and sensitivity to erlotinib in different pancreatic cancer cell lines, followed by examination of the effect of GEP100 on erlotinib sensitivity by establishing the stable knocked-down cell line. The expression level of epithelial mesenchymal transition-related protein was examined by Western blot, and the regulatory mechanism was investigated by short hairpin RNA. Xenograft experiment was also performed in nude mice. RESULTS: We identified a significant correlation between sensitivity to erlotinib and expression of GEP100. GEP100 downregulation increased its sensitivity to erlotinib. E-cadherin short hairpin RNA treatment inhibited this sensitivity. Immunohistochemical staining showed a mutual exclusive expression pattern of GEP100 and E-cadherin in human pancreatic cancer tissues. Xenograft showed that downregulation of GEP100 enhanced the growth inhibition of erlotinib in nude mice. CONCLUSIONS: Our results suggested that GEP100 and E-cadherin have the predictive value for responsiveness to erlotinib in pancreatic cancer.

Effect of emodin on pancreatic fibrosis in rats.

AIM: To establish the rats model of chronic fibrosing pancreatitis and to prove the anti-fibrotic effect of emodin in chronic pancreatitis with fibrosis. METHODS: Fifty rats were randomly divided into five groups, 10 rats in each group. Trinitrobenzene sulfonic acid (TNBS) was infused into the pancreatic duct to induce chronic pancreatitis in rats (except for normal group). Emodin-treated rats were fed with different doses of emodin (20, 40 and 80 mg/kg body weight) for 28 d, while normal group and control group received 0.9% sodium chloride solution. Serum levels of hyaluronic acid (HA) and laminin (LN) were determined by radioimmunoassay. Histopathological alterations were studied by optical microscopy. Expression of collagen was also examined while transforming growth factor-beta-1 (TGF-beta(1)) was localized by immunochemistry. RESULTS: In emodin-treated rats, the serum levels of HA and LN were decreased significantly (HA, 62.2 +/- 19.3 microg/L vs 112.7 +/- 26.5 microg/L, P < 0.05; LN 44.3 +/- 10.4 microg/L vs 86.2 +/- 16.5 microg/L, P < 0.05); the degree of fibrosis was ameliorated observably; the expression of collagen in pancreatic tissue was reduced especially in high-dose emodin-treated group (36% +/- 5% vs 42% +/- 6%, P < 0.05); with the increased doses of emodin, the expression of TGF-beta(1) was declined, compared with those in control group. CONCLUSION: Emodin has an anti-fibrotic effect on pancreatic fibrosis in rats. Because of its anti-fibrotic effect, it could be a potential herb for the treatment of chronic pancreatitis.

Induction of experimental acute ulcerative colitis in rats by administration of dextran sulfate sodium at low concentration followed by intracolonic administration of 30% ethanol.

Several models of experimental ulcerative colitis have been reported previously. However, none of these models showed the optimum characteristics. Although dextran sulfate sodium-induced colitis results in inflammation resembling ulcerative colitis, an obvious obstacle is that dextran sulfate sodium is very expensive. The aim of this study was to develop an inexpensive model of colitis in rats. Sprague-Dawley rats were treated with 2% dextran sulfate sodium in drinking water for 3 d followed by an intracolonic administration of 30% ethanol. The administration of 2% dextran sulfate sodium followed by 30% ethanol induced significant weight loss, diarrhea and hematochezia in rats. Severe ulceration and inflammation of the distal part of rat colon were developed rapidly. Histological examination showed increased infiltration of polymorphonuclear leukocytes, lymphocytes and existence of cryptic abscesses and dysplasia. The model induced by dextran sulfate sodium at lower concentration followed by 30% ethanol is characterized by a clinical course, localization of the lesions and histopathological features similar to human ulcerative colitis and fulfills the criteria set out at the beginning of this study.

Expression of trefoil factors 1 and 2 in precancerous condition and gastric cancer.

AIM: To study the expression of trefoil factor 1 (TFF1) and TFF2 in precancerous condition and gastric cancer and to explore the relationship between TFFs and tumorigenesis, precancerous condition and gastric cancer. METHODS: The expression of TFF1 and TFF2 was immunohistochemically analyzed in paraffin-embedded samples from 140 patients including 35 cases of chronic superficial gastritis (CSG), 35 cases of gastric ulcer (GU), 35 cases of chronic atrophic gastritis (CAG) and 35 cases of gastric cancer (GC). RESULTS: TFF1 and TFF2 were located in cytoplasm of gastric mucous cells. In CSG, GU, CAG and GC, the level of TFF1 expression had a decreased tendency (P < 0.05). The expression of TFF2 was higher in GU than in CSG, but the difference was not significant. The expression of TFF2 also had a decreased tendency in GU, CAG, and GC (P < 0.05). CONCLUSION: The reduced expression of TFF1 and TFF2 in precancerous conditions and gastric cancer may be associated with the proliferation and malignant transformation of gastric mucosa. More investigations are needed to explore the mechanism of TFFs and the relationship between TFFs and gastric cancer.

[The effects of Helicobacter pylori infection on hyperammonaemia and hepatic encephalopathy in cirrhotic patients].

OBJECTIVE: To evaluate the relationship among Helicobacter pylori (Hp)infection, blood ammonia concentrations, and hepatic encephalopathy (HE) status, and to investigate the effect of Hp eradication on blood ammonia levels and hepatic encephalopathy status in cirrhotic patients. METHODS: From July 2003 to Jan 2005, cirrhotic patients in 5 regions of Zhejiang Province were enrolled. Patients were evaluated for the demographic checklists, number connection test, Hp infection, liver impairment level, blood ammonia concentrations and hepatic encephalopathy status. Patients with Hp infection were given one week therapy with omeprazole plus clarithromycin and tinidazole. (14)C urea breath test was performed and the mental symptoms and blood ammonia levels were reassessed after the eradication therapy. RESULTS: (1) 457 cirrhotics were enrolled, the overall Hp infection rate was 60.6%, and HE happened with 47.5%. Subclinical hepatic encephalopathy (SHE) were detected 55 in 47.0% of 117 cirrhotics. (2) Blood ammonia concentration in Hp (-) and Hp (+) cirrhotics was (53.8 +/- 51.4) micromol/L and (78.4 +/- 63.6) micromol/L respectively (P < 0.01), which was significantly reduced to (53.5 +/- 37.7) micromol/L after Hp eradication (P < 0.01). HE was more frequently observed in patients with Hp infection than without it (58.5% vs 30.6%, P < 0.01). HE rate were significantly dropped to 34.1% after Hp eradication (P < 0.01). (3) Hp prevalence significantly differed among cirrhotic with HE (74.4%), those with SHE (69.1%), or without HE (53.2%) (P < 0.05). The level of blood ammonia had significant difference among the cirrhotics with HE (94.5 +/- 75.6) micromol/L, those with SHE (59.9 +/- 49.2) micromol/L, or without HE (47.3 +/- 33.5) micromol/L (P < 0.05). CONCLUSIONS: Hp infection was an important factor of inducing with high blood ammonia concentration and hepatic encephalopathy in cirrhotic patients. Hp eradication may be helpful for treatment and prevention of HE.

Morphological and pathologic changes of experimental chronic atrophic gastritis (CAG) and the regulating mechanism of protein expression in rats.

OBJECTIVE: To study the pathologic change and molecular regulation in cell proliferation and apoptosis of gastric mucosa in rats with chronic atrophic gastritis (CAG), and evaluate the possible mechanisms. METHODS: Rats were administered with 60% alcohol or 2% salicylate sodium, 20 mmol/L deoxycholate sodium and 0.1% ammonia water to establish chronic atrophic gastritis (CAG) models. The gastric specimens were prepared for microscopic view with hematoxylin and eosin (H-E) and alcian blue (A-B) stain. The number of infiltrated inflammatory cells, the thickness of the mucosa gland layer (microm) and the number of gastric glands were calculated. The damage of barrier in mucosa with erosion or ulceration, and the thickness of mucin were examined by scanned electron microscope (SEM). The levels of PGE(2), EGF (epiderminal growth factor) and gastrin in the serum were measured with radioimmunoassay or ELISA method. The immunohistochemistry method was used to observe the number of G cells, the expression of protein of EGFR (EGF receptor), C-erbB-2, p53, p16 and bcl-2 in gastric tissue. RESULTS: Under SEM observation, the gastric mucosa was diffused erosion or ulceration and the thickness of mucin was decreased. Compared with normal rats, the grade of inflammatory cell infiltration in CAG rats was elevated, whereas the thickness and number of gastric gland were significantly lower (P<0.05). Compared with normal level of (0.61+/-0.28) microg/L, EGF in CAG (2.24+/-0.83) microg/L was significantly higher (P<0.05). The levels of PGE(2) and gastrin in serum were significantly lower in CAG rats than that in normal rats (P<0.05). Immunohistochemistry detection showed that the number of G cell in antrum was lower in CAG group (P<0.05). Immuno-stain showed EGFR protein expression in the basal and bilateral membrane, and the cytoplasma in atrophic gastric gland, while negative expression was observed in normal gastric epithelial cells. Positive staining of p53 and p16 protein was localized in the nucleus of epithelial cells. The former was higher positively expressed in atrophic gland, while the later was higher positively stained in normal gastric tissue. bcl-2 protein was positively stained in the cytoplasma in atrophic gastric gland, while very weakly stained in normal gastric tissue. CONCLUSION: The pathological findings in gastric gland accorded with the Houston diagnostic criteria of antrum-predominant CAG. CAG in rats was related with the damage of barrier in gastric mucosa and the misbalance of cell proliferation and apoptosis. There was high protein expression of oncogene, while inhibitor of suppressor gene in CAG rats indicated high trend of carcinogenesis.

[Effect of emodin on pancreatic fibrosis: experiment with rats].

OBJECTIVE: To study the effect of emodin on pancreatic fibrosis and potential mechanism thereof. METHODS: Fifty SD rats were randomly divided into 5 equal groups: normal control group, model control group, low-dose emodin-treated group, mediate-dose emodin-treated group, and high-dose emodin-treated group. The rats of the latter 4 groups underwent infusion of trinitrobenzene sulfonic acid (TNBS) into the pancreatic duct so as to establish models of pancreatic fibrosis. The emodin-treated rats were fed with different doses of emodin (20, 40, and 80 mg/kg body weight), while the normal and model control groups received 0.9% sodium chloride solution instead. Twenty-eight days later the rats were killed, blood samples were collected, and their pancreases were taken out. The serum levels of hyaluronic acid (HA) and laminin (LN) were determined by radioimmunoassay. The histopathological alterations were studied by optical microscopy. The expression of collagen was examined by Van Gieson staining. Western blotting was used to detect the protein expression of transforming growth factor-beta(1) (TGF-beta(1)). RESULTS: (1) The serum level of HA of the low-dose, mediate-dose, and high-dose emodin-treated groups were 87 microg/L +/- 22 microg/L, 78 microg/L +/- 25 microg/L, and 62 microg/L +/- 19 microg/L respectively, all significantly lower than that of the model control group (113 microg/L +/- 27 microg/L, P < 0.05 or < 0.01). The serum levels of laminin in the low-dose, mediate-dose, and high-dose emodin-treated groups were 67 microg/L +/- 14 microg/L, 57 microg/L +/- 12 microg/L, and 44 microg/L +/- 10 microg/L respectively, all significantly lower than that of the model control group (86 microg/L +/- 17 microg/L, P < 0.05 or P < 0.01); (2) The degrees of fibrosis of the emodin-treated groups were obviously ameliorated in comparison with the model control group, the higher the dose of emodin the more improved the pathological changes, especially in the high-dose emodin-treated group (P < 0.05). (3) The percentages of collagen positive cells of the low-dose, mediate-dose, and high-dose emodin-treated groups were 39% +/- 7%, 38% +/- 4%, and 36% +/- 5% respectively, all lower than that of the model control group (42% +/- 6%), with a significant difference between the high-dose emodin-treated group and the model control group (P < 0.05). (4) The protein content of TGF-beta(1) of the low-dose, mediate-dose, and high-dose emodin-treated groups were 44.3% +/- 2.1%, 39.2% +/- 1.8%, and 28.8% +/- 1.6% respectively, all significantly lower than that of the model control group (60.7% +/- 1.7%, all P < 0.05), and the protein content of TGF-beta(1) of the high-dose emodin-treated group was significantly lower than those of the other 2 emodin-treated groups (both P < 0.05). CONCLUSION: Emoidn has an anti-fibrosis effect on pancreatic fibrosis, which maybe related to the content of TGF-beta(1) protein.

Anticancer activity of resveratrol on implanted human primary gastric carcinoma cells in nude mice.

AIM: To investigate the apoptosis of implanted primary gastric cancer cells in nude mice induced by resveratrol and the relation between this apoptosis and expression of bcl-2 and bax. METHODS: A transplanted tumor model was established by injecting human primary gastric cancer cells into subcutaneous tissue of nude mice. Resveratrol (500 mg/kg, 1,000 mg/kg and 1,500 mg/kg) was directly injected beside tumor body 6 times at an interval of 2 d. Then changes of tumor volume were measured continuously and tumor inhibition rate of each group was calculated. We observed the morphologic alterations by electron microscope, measured the apoptotic rate by TUNEL staining method, detected the expression of apoptosis-regulated genes bcl-2 and bax by immunohistochemical staining and PT-PCR. RESULTS: Resveratrol could significantly inhibit carcinoma growth when it was injected near the carcinoma. An inhibitory effect was observed in all therapeutic groups and the inhibition rate of resveratrol at the dose of 500 mg/kg, 1,000 mg/kg and 1,500 mg/kg was 10.58%, 29.68% and 39.14%, respectively. Resveratrol induced implanted tumor cells to undergo apoptosis with apoptotic characteristics, including morphological changes of chromatin condensation, chromatin crescent formation, nucleus fragmentation. The inhibition rate of 0.2 mL of normal saline solution, 1,500 mg/kg DMSO, 500 mg/kg resveratrol, 1 000 mg/kg resveratrol, and 1 500 mg/kg resveratrol was 13.68+/-0.37%, 13.8+/-0.43%, 48.7+/-1.07%, 56.44+/-1.39% and 67+/-0.96%, respectively. The positive rate of bcl-2 protein of each group was 29.48+/-0.51%, 27.56+/-1.40%, 11.86+/-0.97%, 5.7+/-0.84% and 3.92+/-0.85%, respectively by immunohistochemical staining. The positive rate of bax protein of each group was 19.34+/-0.35%, 20.88+/-0.91%, 40.02+/-1.20%, 45.72+/-0.88% and 52.3+/-1.54%, respectively by immunohistochemical staining. The density of bcl-2 mRNA in 0.2 mL normal saline solution, 1,500 mg/kg DMSO, 500 mg/kg resveratrol, 1,000 mg/kg resveratrol, and 1,500 mg/kg resveratrol decreased progressively and the density of bax mRNA in 0.2 mL normal saline solution, 1,500 mg/kg DMSO, 500 mg/kg resveratrol, 1,000 mg/kg resveratrol, and 1,500 mg/kg increased progressively with elongation of time by RT-PCR. CONCLUSION: Resveratrol is able to induce apoptosis of transplanted tumor cells. This apoptosis may be mediated by down-regulating apoptosis-regulated gene bcl-2 and up-regulating the expression of apoptosis-regulated gene bax.