Streptococcus anginosus in the development and treatment of precancerous lesions of gastric cancer

The microbiota is strongly association with cancer.Studies have shown significant differences in the gastric microbiota between patients with gastric cancer(GC)patients and noncancer patients,suggesting that the microbiota may play a role in the development of GC.Although Helicobacter pylori(H.pylori)infection is widely recognized as a primary risk factor for GC,recent studies based on microbiota sequencing technology have revealed that non-H.pylori microbes also have a significant impact on GC.A recent study discovered that Streptococcus anginosus(S.anginosus)is more prevalent in the gastric mucosa of patients with GC than in that of those without GC.S.anginosus infection can spontaneously induce chronic gastritis,mural cell atrophy,mucoid chemotaxis,and heterotrophic hyperplasia,which promote the development of precancerous lesions of GC(PLGC).S.anginosus also disrupts the gastric barrier function,promotes the proliferation of GC cells,and inhibits apoptosis.However,S.anginosus is underrepresented in the literature.Recent reports suggest that it may cause precancerous lesions,indicating its emerging pathogenicity.Modern novel molecular diagnostic techniques,such as polymerase chain reaction,genetic testing,and Ultrasensitive Chromosomal Aneuploidy Detection,can be used to gastric precancerous lesions via microbial markers.Therefore,we present a concise summary of the relationship between S.anginosus and PLGC.Our aim was to further investigate new methods of preventing and treating PLGC by exploring the pathogenicity of S.anginosus on PLGC.

Prospects in the application of ultrasensitive chromosomal aneuploidy detection in precancerous lesions of gastric cancer

Gastric cancer(GC)is a prevalent malignant tumor within the digestive system,with over 40%of new cases and deaths related to GC globally occurring in China.Despite advancements in treatment modalities,such as surgery supplemented by adjuvant radiotherapy or chemotherapeutic agents,the prognosis for GC remains poor.New targeted therapies and immunotherapies are currently under invest-igation,but no significant breakthroughs have been achieved.Studies have indicated that GC is a heterogeneous disease,encompassing multiple subtypes with distinct biological characteristics and roles.Consequently,personalized treatment based on clinical features,pathologic typing,and molecular typing is crucial for the diagnosis and management of precancerous lesions of gastric cancer(PLGC).Current research has categorized GC into four subtypes:Epstein-Barr virus-positive,microsatellite instability,genome stability,and chromosome instability(CIN).Technologies such as multi-omics analysis and gene sequencing are being employed to identify more suitable novel testing methods in these areas.Among these,ultrasensitive chromosomal aneuploidy detection(UCAD)can detect CIN at a genome-wide level in subjects using low-depth whole genome sequencing technology,in conjunction with bioinformatics analysis,to achieve qualitative and quantitative detection of chromosomal stability.This editorial reviews recent research advancements in UCAD technology for the diagnosis and management of PLGC.

Differential diagnosis of gastric submucosal masses and external pressure lesions

Lesions of the left triangular ligament of the liver are rare,and there are even fewer cases of vascular tumors misdiagnosed as gastrointestinal stromal tumors.We comment on the two cases reported in the article.The article did not include pictures of laparoscopic surgery,making it unconvincing.For gastric submucosal lesions,enhanced computed tomography venous phase imaging may be beneficial for differential diagnosis.Although endoscopic ultrasound is an effective tool for diagnosing submucosal lesions of the stomach,due to various factors,it cannot achieve an accurate diagnosis.During endoscopic examination,a more accurate diagnosis can be made depending on the personal experience of the operators.

Research of Helicobacter pylori infection in precancerous gastric lesions

INTRODUCTION Helicobacter pylori(Hp)infection has beenconsidered to play significant roles in pathogenesisof peptic ulcer.Additionally Hp is associated withthe development of gastric epithelial hyperplasiaand lymphoid malignancies.The InternationalAgency for Research on Cancer has classified lip asa class Ⅰ carcinogen and a definite cause of gastriccancer in humans.Hp infection first causes chronicactive gastritis and may slowly lead to infection ofwhole stomach.In the late stages of infection,mucosal atrophy and intestinal metaplasia(IM),

Factors affecting occurrence of gastric varioliform lesions: A case-control study

AIM: To investigate the factors influencing the occurrence of gastric varioliform lesions(GVLs) and their possible link with gastric cancer.METHODS: A 1:1 matched case-control study was performed to retrospectively analyze data from 1638 chronic gastritis patients who had undergone gastroscopy at one of two Chinese hospitals between 2009 and 2014. Patients with GVLs(cases) were compared to those without such lesions(controls). Endoscopic and pathological findings were recorded, along with interview information on Helicobacter pylori(H. pylori) infection, medical, drug and family histories, lifestyle and eating habits. The association between each factor and the occurrence of GVLs was estimated, and then multivariate conditional logistic regression was used to evaluate the independent factors.RESULTS: The frequency and severity of glandular atrophy, intestinal metaplasia(IM) and low-grade intraepithelial neoplasia were significantly increased in the GVL group(P < 0.01). Overall analysis showed that H. pylori infection [3.051(2.157, 4.317), P <0.001], allergic respiratory diseases [3.636(2.183, 6.055), P < 0.001], work-related stress [2.019(1.568, 2.600), P < 0.001], irregular meals [2.300(1.462, 3.619), P < 0.001], high intake of spicy food [1.754(1.227, 2.507), P = 0.002] and high intake of fresh fruit [0.231(0.101, 0.529), P = 0.001] were significantly correlated with the occurrence of GVLs(positively, except for the latter). Stratified analyses indicated that pickled food consumption in patients over 50 years old [7.224(2.360, 22.115), P = 0.001] and excessive smoking in men [2.013(1.282, 3.163), P = 0.002] were also positively correlated, and that, for antral GVLs, vegetable consumption [0.491(0.311, 0.776), P = 0.002] was negatively correlated. CONCLUSION: Seven risk factors and two protective factors are determined for GVLs, which were found to be associated with premalignant abnormalities.

Expression and significance of Musashi-1 in gastric cancer and precancerous lesions

AIM:To investigate expression of stem cell marker Musashi-1(Msi-1)in relationship to tumorigenesis and progression of intestinal-type gastric cancer(GC).METHODS:Endoscopic biopsy specimens and surgical specimens were obtained,including 54 cases of intestinal-type GC,41 high-grade intraepithelial neoplasia,57low-grade intraepithelial neoplasia,31 intestinal metaplasia,and 36 normal gastric mucosa.Specimens were fixed in 10%paraformaldehyde,conventionally dehydrated,embedded in paraffin,and sliced in 4-μm-thick serial sections.Two-step immunohistochemical staining was used to detect Msi-1 and proliferating cell nuclear antigen(PCNA)expression.Correlation analysis was conducted between Msi-1 and PCNA expression.The relationship between Msi-1 expression and clinicopathological parameters of GC was analyzed statistically.RESULTS:There were significant differences in Msi-1and PCNA expression in different pathological tissues(χ2=15.37,P<0.01;χ2=115.36,P<0.01).Msi-1and PCNA-positive cells were restricted to the isthmus of normal gastric glands.Expression levels of Msi-1and PCNA in intestinal metaplasia were significantly higher than in normal mucosa(U=392.0,P<0.05;U=40.50,P<0.01),whereas there was no significant difference compared to low or high-grade intraepithelial neoplasia.Msi-1 and PCNA expression in intestinaltype GC was higher than in high-grade intraepithelial neoplasia(U=798.0,P<0.05;U=688.0,P<0.01).There was a significantly positive correlation between Msi-1 and PCNA expression(rs=0.20,P<0.01).Msi-1expression in GC tissues was correlated with their lymph node metastasis and tumor node metastasis stage(χ2=12.62,P<0.01;χ2=11.24,P<0.05),but not with depth of invasion and the presence of distant metastasis.CONCLUSION:Msi-1-positive cells may play a key role in the early events of gastric carcinogenesis and may be involved in invasion and metastasis of GC.

Significance and relationship between Cripto-1 and p-STAT3 expression in gastric cancer and precancerous lesions

AIM:To explore the relationship between Cripto-1 (CR-1) and tyrosine phosphorylation STAT3 (p-STAT3) expressions in gastric cancer (GC) and gastric carcinogensis and metastasis.METHODS: The PV9000 immunohistochemical method was used to detect the expression of CR-1 and p-STAT3 in 178 cases of GC, 95 matched normal gastric mucosa, 40 chronic atrophic gastritis (CAG), 48 intestinal meta-plasia (IM) and 25 dysplasia (DYS). RESULTS: The positive rates of CR-1 and p-STAT3 expression were significantly higher in CAG (65.0% and 60.0%), in IM (83.3% and 77.1%), DYS (80.0% and 68%) and GC (71.3% and 60.1%) than in normal gastric mucosa (43.2% and 41.1%, P < 0.05), respectively. The expressions of CR-1 and p-STAT3 (78.3% and 66.7%) were signifi cantly higher in GC with lymphnode metastasis than in those without metastasis (53.1% and 42.9%, P < 0.05). CR-1 expression was also related to histological and Lauren's types of GC (P < 0.001). Furthermore, there was positive relation-ship between CR-1 and p-STAT3 expressions in GC (rk = 0.189, P = 0.002).CONCLUSION: The up-regulation of CR-1 and p-STAT3 may play important roles in gastric carcinogenesis and lymph node metastasis. CR-1 and p-STAT3 expression in GC was positively correlated, and the relevant molecular mechanism requires further investigations.

Gastric subepithelial lesion complicated with abscess: Case report and literature review

Gastric abscess is a localized pyogenic inflammation of the gastric wall, which is a rare form of suppurative gastritis. The rarity of gastric abscess may be associated with the difficulty of early diagnosis and high mortality as a result. In general, subepithelial lesions (SELs) of the stomach are incidentally detected during the course of upper endoscopy without specific clinical symptoms and signs. However, some gastric SELs present rarely as a form of hemorrhage, obstruction, perforation, and abscess. Here we report a 45-year-old man with gastric SEL presenting as a gastric abscess, which was diagnosed as an ectopic pancreas of the stomach, along with a review of the literature. Although gastric SEL presenting as an abscess is known as a serious and life-threatening lesion, the patient made a complete recovery through surgical resection as well as medical treatment.

Loss of heterozygosity on 10q23.3 and mutation of tumor suppressor gene PTEN in gastric cancer and precancerous lesions

AIM: To investigate the loss of heterozygosity (LOH) and mutation of tumor suppressor gene PTEN in gastric cancer and precancerous lesions. METHODS: Thirty cases of normal gastric mucosa, advanced and early stage gastric cancer, intestinal metaplasia, atrophic gastritis, and atypical hyperplasia were analyzed for PTEN LOH and mutations within the entire coding region of PTEN gene by PCR-SSCP denaturing PAGE gel electrophoresis, and PTEN mutation was detected by PCR-SSCP sequencing followed by silver staining. RESULTS: LOH rate found in respectively atrophic gastritis was 10% (3/30), intestinal metaplasia 10% (3/30), atypical hyperplasia 13.3% (4/30), early stage gastric cancer 20% (6/30), and advanced stage gastric cancer 33.3% (9/30), None of the precancerous lesions and early stage gastric cancer showed PTEN mutations, but 10% (3/30) of the advanced stage gastric cancers, which were all positive for LOH, showed PTEN mutation. CONCLUSION: LOH of PTEN gene appears in precancerous lesions, and PTEN mutations are restricted to advanced gastric cancer, LOH and mutation of PTEN gene are closely related to the infiltration and metastasis of gastric cancer.

Clinical and endoscopic analysis of gastric Dieulafoy’s lesion

AIM:To investigate the incidence,location,clinical presentation,diagnosis and effectiveness of endoscopic treatment of gastric Dieulafoy's lesion(DL)in China. METHODS:All patients who received emergency upper gastrointestinal(GI)endoscopy due to gastric DL from February 2000 to August 2008 at GI endoscopy center of Renmin Hospital of Wuhan University were included in this study.The clinical presentation,medical history,location and characteristics of DL methods and effectiveness of therapy of patients with DL were retrospectively analysed by chart reviews.Long-term follow-up data were collected at outpatient clinics or telephone interviews. RESULTS:Fifteen patients were diagnosized with DL,which account for 1.04%of the source of bleed- ing in acute non-variceal upper GI bleeding.Common comorbidities were found in one patient with hypertension and diabetic mellitus.Hemoclip or combined therapy with hemoclip produced primary hemostasis in 92.8%(13/14) of patients. CONCLUSION:DL is uncommon but life-threatening in China.Hemoclip proved to be safe and effective in controlling bleeding from DL.

Effect of transplantation of BMMSCs on pathological change of gastric precancerous lesions of rats

Objective:To build the rat model of gastric precancerous lesions and discuss the effect of transplantation of mesenchymal stem cells(BMMSCs) on the pathological change.Methods:The rat model of gastric precancerous lesions was built using N-methyl-N-nitro-N-nitrosoguanidine.After the intravenous transplantation of BMMSCs,the migration and colonization location was then observed,as well as its effect on the related factors of gastric precancerous lesions,including VEGF,IL-10 and IFN-γ.Results:BMMSCs were mainly colonized in the gastric body and gastric antrum,which could be differentiated into the epithelial and interstitial cells.The expression of VEGF in the transplantation group and non-transplantation group was significantly higher than that in the control group(P<0.05);while the expression of VEGF in the transplantation group was significantly higher than that in the non-transplantation group(t=3.88,P<0.001).The expression of serum IL-10 and IFN- y in the transplantation group and non-transplantation group was significantly higher than that in the control group(P<0.05).while the expression of IL-10 and IFN-γ in the transplantation group was significantly lower than that in the non-transplantation group(t=3.03,P=0.004;t=3.80.P<0.001).Conclusions:BMMSCs can be directionally differentiated into the epithelial and interstitial cells and can also regulate the related growth factors and inflammatory factors to reduce the injury of inflammation,relieve or reverse the process of gastric precancerous lesions.

Anti-Helicobacter pylori therapy followed by celecoxib on progression of gastric precancerous lesions

AIM： To evaluate whether celecoxib, a selective cyclooxygenase 2 （COX-2） inhibitor, could reduce the severity of gastric precancerous lesions following Hel/cobacter pylori （H pylorl） eradication. METHODS： H pylori-eradicated patients with gastric precancerous lesions randomly received either celecoxib （n = 30） or placebo （n = 30） for up to 3 mo. COX-2 expression and activity was determined by immunostaining and prostaglandin E2 （PGE2） assay, cell proliferation by Ki-67 immunostaining, apoptosis by TUNEL staining and angiogenesis by microvascular density （MVD） assay using CD31 staining.RESULTS： COX-2 protein expression was significantly increased in gastric precancerous lesions （atrophy, intestinal metaplasia and dysplasia, respectively） compared with chronic gastritis, and was concomitant with an increase in cell proliferation and angiogenesis. A significant improvement in precancerous lesions was observed in patients who received celecoxib compared with those who received placebo （P 〈 0.001）. Of these three changes, 84.6% of sites with dysplasia regressed in patients treated with celecoxib （P = 0.002） compared with 60% in the placebo group, suggesting that celecoxib was effective on the regression of dysplasia. COX-2 protein expression （P 〈 0.001） and COX-2 activity （P 〈 0.001） in the gastric tissues were consistently lower in celecoxib-treated patients compared with the placebo-treated subjects. Moreover, it was also shown that celecoxib suppressed cell proliferation （P 〈 0.01）, induced cell apoptosis （P 〈 0.01） and inhibited angiogenesis with decreased MVD （P 〈 0.001）. However, all of these effects were not seen in placebo-treated subjects. Furthermore, COX-2 inhibition resulted in the up-regulation of PPARy expression, a protective molecule with anti-neoplastic effects. CONCLUSION： H pylori eradication therapy followed by celecoxib treatment improves gastric precancerous lesions by inhibiting COX-2 activity, inducing apoptosis, and suppressing cell proliferation and angiogenesis.

Gastric precancerous lesions are associated with gene variants in Helicobacter pylori -susceptible ethnic Malays

AIM: To identify genes associated with gastric pre-cancerous lesions in Helicobacter pylori (H. pylori )susceptible ethnic Malays. METHODS: Twenty-three Malay subjects with H. pylori infection and gastric precancerous lesions identified during endoscopy were included as "cases". Thirtyseven Malay subjects who were H. pylori negative and had no precancerous lesions were included as "controls". Venous blood was collected for genotyping with Affymetrix 50K Xba1 kit. Genotypes with call rates < 90% for autosomal single nucleotide polymorphisms (SNPs) were excluded. For each precancerous lesion, associated SNPs were identified from Manhattan plots, and only SNPs with a χ2 P value < 0.05 and Hardy Weinberg Equilibrium P value > 0.5 was considered as significant markers. RESULTS: Of the 23 H. pylori -positive subjects recruited, one sample was excluded from further analysis due to a low genotyping call rate. Of the 22 H. pylori positive samples, atrophic gastritis only was present in 50.0%, complete intestinal metaplasia was present in 18.25%, both incomplete intestinal metaplasia and dysplasia was present in 22.7%, and dysplasia only was present in 9.1%. SNPs rs9315542 (UFM1 gene), rs6878265 (THBS4 gene), rs1042194 (CYP2C19 gene) and rs10505799 (MGST1 gene) were significantly associated with atrophic gastritis, complete intestinal metaplasia, incomplete metaplasia with foci of dysplasia and dysplasia, respectively. Allele frequencies in "cases" vs "controls" for rs9315542, rs6878265, rs1042194 and rs10505799 were 0.4 vs 0.06, 0.6 vs 0.01, 0.6 vs 0.01 and 0.5 vs 0.02, respectively. CONCLUSION: Genetic variants possibly related to gastric precancerous lesions in ethnic Malays susceptible to H. pylori infection were identified for testing in subsequent trials.

Risk Factors of Precancerous Gastric Lesions in A Population at High Risk of Gastric Cancer

Objective： In cancer prevention, the targeting of precancerous lesions has been recognized as the most promising method. However, little attention has been paid to the risk factors of precancerous gastric lesions, especially in rural China where there is high prevalence of precancerous gastric lesions. We therefore conducted a cross-sectional study in Liaoning province, China, to investigate the potential risk and protective factors of these precancerous gastric lesions. Methods： A total of 1,179 subjects with high risk of gastric cancer from Zhuanghe County were included in this study. Standard questionnaires were used in collecting epidemiological factors and the data were then analyzed by the unconditional logistic regression model. Results： Smoking and drinking were the risk factors for the precancerous gastric lesions among rural subjects, and the association of smoking or drinking and the precancerous gastric lesions increased in strength with the daily consumption and duration. As the factors such as age, gender, smoking, alcohol were controlled, a multivariable analysis revealed that there was a significant correlation between the deep-fry food intake and the gastric epithelial dysplasia with the odds ratio （OR） of 1.78 [95% confidence interval （CI）： 1.01-3.12]. Garlic eating was shown to confer protection against the development of gastric ulcer （OR=0.55, 95% CI： 0.33-0.92）. Conclusion： Smoking and drinking were the risk factors for the precancerous gastric lesions among rural subjects. Deep-fry food intake might be one of the risk factors for the precancerous gastric lesions and garlic eating was shown to confer protection against the development of gastric ulcer among rural Chinese population.

Role of gene polymorphisms in gastric cancer and its precursor lesions:Current knowledge and perspectives in Latin American countries

Latin America shows one of the highest incidence rates of gastric cancer in the world,with variations in mortality rates among nations or even within countries belonging to this region.Gastric cancer is the result of a multifactorial complex process,for which a multistep model of carcinogenesis is currently accepted.Additionally to the infection with Helicobacter pylori,that plays a major role,environmental factors as well as genetic susceptibility factors are significant players at different stages in the gastric cancer process.The differences in population origin,demographic structure,socio-economic development,and the impact of globalization lifestyles experienced in Latin America in the last decades,all together offer opportunities for studying in this context the influence of genetic polymorphisms in the susceptibility to gastric cancer.The aim of this article is to discuss current trends on gastric cancer in Latin American countries and to review the available published information about studies of association of gene polymorphisms involved in gastric cancer susceptibility from this region of the world.A total of 40 genes or genomic regions and69 genetic variants,58%representing markers involved in inflammatory response,have been used in a number of studies in which predominates a low number of individuals(cases and controls)included.Polymorphisms of IL-1B(-511 C/T,14 studies;-31 T/C,10 studies)and IL-1RN(variable number of tandem repeats,17 studies)are the most represented ones in the reviewed studies.Other genetic variants recently evaluated in large metaanalyses and associated with gastric cancer risk were also analyzed in a few studies[e.g.,prostate stem cell antigen(PSCA),CDH1,Survivin].Further and better analysis centered in gene polymorphisms linked to other covariates,epidemiological studies and the information provided by meta-analyses and genome-wide association studies should help to improve our understanding of gastric cancer etiology in order to develop appropriate health programs in Latin America.

Role of the nucleus tractus solitarii in the protection of pre-moxibustion on gastric mucosal lesions

Previous studies have shown that somatic sensation by acupuncture and visceral nociceptive stimulation can converge in the nucleus tractus solitarii where neurons integrate signals impact- ing on the function of organs. To explore the role of the nucleus tractus solitarii in the protective mechanism of pre-moxibustion on gastric mucosa, nucleus tractus solitarii were damaged in rats and pre-moxibustion treatment at the Zusanli （ST36） point followed. The gastric mucosa was then damaged by the anhydrous ethanol lavage method. Morphological observations, enzyme linked immunosorbent assays, and western immunoblot analyses showed that gastric mucosa surface lesion and the infiltration of inflammatory cells were significantly ameliorated after pre-moxibustion treatment. Furthermore, the gastric mucosal damage index and somatostatin level were reduced, and epidermal growth factor content in the gastric mucosa and heat-shock protein-70 expression were increased. These results were reversed by damage to the nucleus tractus solitarii. These findings suggest that moxibustion pretreatment at the Zusanli point is protective against acute gastric mucosa injury, and nucleus tractus solitarii damage inhibits these responses. Therefore, the nucleus tractus solitarii may be an important area for regulating the signal transduction of the protective effect of pre-moxibustion on gastric mucosa.

Experimental study on model establishment, mechanism of production, and reverse therapy of gastric mucosal precancerous lesions in rats

This study was designed to establish an animal model of gastric mucosal precancerous lesions in Wistar rats and on this model, the mechanism to produce the precancerous lesions and their reverse therapy were studied. Ranitidine (R) 0.03% in the diet, N-methyl-N'-nitro-N-nitrosoguanidine(MNNG)50 μg/ml in drinking water, or both of them were administered to Wistar rats for 20 weeks. The iats were maintained without the drugs for additional 23 weeks. A control group of rats without any treatment of drugs were kept for 43 weeks Intestinal metaplasia (IM) was found in 86.5% of the rats in MNNG group, 22.5% in R groupand 100% in MNNG+R while only 7.5% in the control. The incidence of IM was significantly different between MNNG+R group and R group or MNNG group. The number of metaplastic glands was also the highest in the MNNG+R group. The therapeutic effects of retinoic acid (RA) and sodium butyrate (SB) on the iNduced precancerousous lesions of the glandular gastric mucosa were observed. It was found that the incidence of IM, moderate and severe dysplasia, and gastric cancer and the number of metaplastic glands in the pylorus and fundus were significantly lower in RA treated group (72.0%, 24.0%, 0%, 130.2±93.9 and 51.5±39.1) and SB treated gioup (60.0%,20.0%, 0%, 70.3±46.8, and 39.8±29.6) than in the RA untreated group (100%, 52.2%, 16.0%, 442.4±230.0 and 247.4±112.07) and the SB untreated group (88.0%, 48.0%. 16.0%, 241.4±113.9 and 146.4±66.3)(P<0.01 to 0.05). A mucosal flap with vascular pedicle from the gastric wall of the Wistar rats was transplanted to the duodenum, jejunum and colon respectively and the rats were killed in the 3td, 6th, 9th and 12th month after operation. IM was found in all the gastric grafts to the intestines with optical and electron microscopy. It is concluded on the basis of the findings that the concomitant administration of MNNG and R is a reliable method to induce IM of gastric mucosa in rats; RA and SB are efficient agents for the reverse thevapy of the precancerous lesions of gastric glandular mucosa in rats; and the formation of IM of gastric mucosa might be a pH-related process. The possible mechanism of the development of IM was discussed.

Reduced gastric acid production in burn shock period and its significance in the prevention and treatment of acute gastric mucosal lesions

AIM To investigate the changes of gastric acidproduction and its mechanism in shock period ofsevere burn in rats.METHODS A rat model with 30% TBSA full-thickness burn injury was employed and thegastric acid production,together with gastricmucosal blood flow(GMBF)and energy charge(EC)were measured serially within 48hpostburn.RESULTS The gastric acid production in theacute shock period was markedly inhibited aftersevere burn injury.At the 3rd h postburn,thegastric juice volume,total acidity and acidoutput were already significantly decreased(P【0.01),and reached the lowest point,0.63mL/L±0.20mL/L,10.81mmol/L±2.58mmol/L and 2.23mmol/h±0.73mmol/hrespectively,at the 12th h postburn.Althoughrestored to some degree 24 h after thermalinjury,the variables above were stillstatistically lower,compared with those ofcontrol animals at the 48th h postburn.TheGMBF and EC were also significantly reducedafter severe burns,consistent with the trend ofgastric acid production changes.CONCLUSION Gastric acid production,as wellas GMBF and EC was predominantly decreased in the early postburn stage,suggesting that gastricmucosal ischemia and hypoxia with resultantdisturbance in energy metabolism,but notgastric acid proper,might be the decisive factorin the pathogenesis of AGML after thermalinjury,and that the preventive use of anti-aciddrugs during burn shock period wasunreasonable in some respects.Therefore,taking effective measures to improve gastricmucosal blood perfusion as early as possiblepostburn might be more preferable for the AGMLprevention and treatment.

Expression of p-STAT3 and vascular endothelial growth factor in MNNG-induced precancerous lesions and gastric tumors in rats

AIM: To investigate the dynamic expression of p-signal transducer and activator of transcription 3 (STAT3) and vascular endothelial growth factor (VEGF) in the formation of gastric tumors induced by drinking water containing N-methyl-N’-nitro-N-nitrosoguanidine (MNNG) in Wistar rats. METHODS: One hundred and twenty Wistar rats were randomly divided into two groups (60 in each group): Control group and Model group. The rats in each group were then randomly divided into three groups (20 in each group): C/M15, C/M25 and C/M40 (15, 25 and 40 represent the number of feeding weeks from termination). Rats in the control group received normal drinking water and rats in the model group received drinking water containing 100 μg/mL MNNG. Stomach tissues were collected at the end of the 15th, 25th and 40th week, respectively, for microscopic measurement using hematoxylin and eosin staining. The expression of p-STAT3 and VEGF in different pathological types of gastric tissue, including normal, inflammation, atrophy, hyperplasia and gastric stromal tumor, was observed by immunohistochemistry and Western blot, and the corelation between p-STAT3 and VEGF was analyzed. RESULTS: (1) The expression of p-STAT3 in tissue with gastritis, atrophy, dysplasia and gastric stromal tumor were significantly increased in the model group compared with the control group (2.5 ± 1.0, 2.75 ± 0.36, 6.2 ± 0.45, 5.67 ± 0.55 vs 0.75 ± 0.36, P = 0.026, 0.035, 0.001, 0.002, respectively); the expression of p-STAT3 in tissue with dysplasia was higher than that in samples with gastritis or atrophy (6.2 ± 0.45 vs 2.5 ± 1.0, P = 0.006; 6.2 ± 0.45 vs 2.75 ± 0.36, P = 0.005, respectively); however, the expression of p-STAT3 in gastritis and atrophy was not significantly different (P > 0.05); (2) the expression of VEGF in tissue with gastritis, atrophy, dysplasia and gastric stromal tumor was significantly increased in the model group compared with normal gastric mucosa; and the expression of VEGF in tissue with dysplasia was higher than that in tissue with inflammation and atrophy (10.8 ± 1.96 vs 7.62 ± 0.25, P = 0.029; 10.8 ± 1.96 vs 6.26 ± 0.76, P = 0.033, respectively); similarly, the expression of VEGF in tissue with gastritis and atrophy was not significantly different (P > 0.05); and (3) the expression of VEGF was positively correlated with p-STAT3. CONCLUSION: p-STAT3 plays an important role in gastric cancer formation by regulating the expression of VEGF to promote the progression of gastric tumor from gastritis.

Treatment of gastric precancerous lesions with Weiansan

AIM： To observe the curative effect of Weiansan （WAS） on gastric precancerous lesions （GPL） and H pylori elimination. METHODS： Seventy-six patients with GPL were randomly divided into two groups： WAS group （n = 42） and Weifuchun （WFC） group （n = 34）. The patients in the WAS group were administered 5 g WAS 3 times a day, and the patients in the WFC group took WFC （4 tablets） 3 times a day. To monitor inflammation of gastric mucosa, degree of glandular atrophy （GA）, intestinal metaplasia （IM） and dysplasia, and H pylori infection, all patients underwent gastroscopy and biopsy with pathological examination before and after treatment. Fifty male Sprague-Dawley （SD） rats were used in animal experiments. Of these, 10 served as the control group （n = 10）, 40 were given ranitidine combined with N-methyl- N^1-nitro-N-nitrosoguanidine （MNNG） for 12 wk and divided into 4 groups randomly： model group （n = 10）, high-dose WAS group （n = 10）, low-close WAS group （n = 10） and WFC group （n = 10）. Twelve weeks later, all rats were killed and a 2 cm ×1 cm tissue was taken from the lesser curvature of the gastric antrum. H pylori infection was determined by the fast urease method. RESULTS： The curative effect in WAS groups was similar to that in WFC groups. There was no statistical difference in degree of GA, IM and dysplasia between WAS and WFC groups. The rate of Hpylori infection in the model group （positive/negative： 9/1） was significantly higher than that in the control group （positive/negative： 1/9） （P 〈 0.01）. H pylori elimination in the high-dose WAS group （positive/negative： 4/6） and low-dose WAS group （positive/negative： 6/4） was similar to that in the WFC group （positive/negative： 4/6） （P 〉 0.05）.CONCLUSION： WAS improves clinical symptoms by suppressing GA, IM and dysplasia and eliminating H pylori.