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Typhoid fever is usually a mild clinical disease. Typhoid fever with massive intestinal hemorrhage is rare in the antibiotic era. Acute acalculous cholecystitis (AAC) is also rare in adults. Here, we describe the first adult case of typhoid fever with both complications due to Vi-negative and fluoroquinolone-insensitive Salmonella enterica serovar Typhi (S. Typhi) infection. We aim to alert physicians to this rare condition.

The acquisition of rapid desiccation tolerance for the resurrection plant Boea hygrometrica requires a cycle of drought acclimation. Here, a gas chromatography-mass spectrometry based global untargeted metabolite profiling analysis was conducted on leaves of B. hygrometrica during dehydration and rehydration. Metabolic profiles between non-acclimated and drought acclimated plants were clearly distinguished in principal-component and hierarchical cluster analysis, indicating that drought acclimation response required the process in metabolic reprogramming. Accumulation of numerous metabolites involved in carbon and energy metabolism as well as amino acid and fatty acid biosynthesis was observed to be significantly changed upon drought acclimation and dehydration treatments. Using partial least-squares discriminant analysis, 25 known metabolites and 51 compounds with unknown structures were identified as putative biomarkers contributed to the discrimination between drought acclimated and non-acclimated plants. Remarkably, as revealed by transcriptome data analysis, some up-accumulated metabolites in acclimated plants, such as maltose, glutaric acid, L-tryptophan and α-tocopherol, which are in good correlation with the increased desiccation tolerance, and were precisely controlled by the transcript changes in multigene family members of related enzymes. Furthermore, genes positively correlated with the up-accumulated biomarkers in transcription abundances were enriched in multiple biological processes, such as “ubiquitin-dependent protein catabolism” and “abscisic acid-activated signaling pathway”. Taken together, our observations indicate that the accumulation of important metabolites correlates with the transcriptional activity of biosynthetic related enzymes and putative regulators involved in ubiquitination and ABA signal transduction during a short period of drought acclimation might contribute to the acquisition of rapid desiccation tolerance in B. hygrometrica.

The link between microbiota and gastric cancer (GC) has attracted widespread attention. However, the phylogenetic profiles of niche-specific microbiota in the tumor microenvironment is still unclear. Here, mucosa-associated microorganisms from 62 pairs of matched GC tissues and adjacent non-cancerous tissues were characterized by 16S rRNA gene sequencing. Functional profiles of the microbiota were predicted using PICRUSt, and a co-occurrence network was constructed to analyze interactions among gastric microbiota. Results demonstrated that mucosa-associated microbiota from cancerous and non-cancerous tissues established micro-ecological systems that differed in composition, structure, interaction networks, and functions. Microbial richness and diversity were increased in cancerous tissues, with the co-occurrence network exhibiting greater complexity compared with that in non-cancerous tissue. The bacterial taxa enriched in the cancer samples were predominantly represented by oral bacteria (such as Peptostreptococcus, Streptococcus, and Fusobacterium), while lactic acid-producing bacteria (such as Lactococcus lactis and Lactobacillus brevis) were more abundant in adjacent non-tumor tissues. Colonization by Helicobacter pylori, which is a GC risk factor, also impacted the structure of the microbiota. Enhanced bacterial purine metabolism, carbohydrate metabolism and denitrification functions were predicted in the cancer associated microbial communities, which was consistent with the increased energy metabolism and concentration of nitrogen-containing compounds in the tumor microenvironment. Furthermore, the microbial co-occurrence networks in cancerous and non-cancerous tissues of GC patients were described for the first time. And differential taxa and functions between the two groups were identified. Changes in the abundance of certain bacterial taxa, especially oral microbiota, may play a role in the maintenance of the local microenvironment, which is associated with the development or progression of GC.

There have been no reports on the relationship between virulence genes and gastric diseases based on the same bacterial colonization density. Our results indicated that Helicobacter pylori virulence genes were more relevant than colonization density as a pathogenic mechanism of gastric diseases, which helps elucidate the pathogenic mechanisms of bacteria and aids in the development of improved strategies for the treatment of gastric disease.

XN901 is a K-type three-line hybrid wheat with a high yield potential, and its leaves and stem remaining green during grain maturation, suggesting much assimilate stay in leaves and stem. The grain water content, grain volume, carbohydrate content, and enzyme activity of sucose metabolism in the grain, as well as source-sink relationship were studied in order to investigate the physiological reason of the assimilate remaining in leaves and stem at the late stage. The results showed that the hybrid grains had more water and soluble sugar, higher activities of acid invertase and sucrose synthase at the early stage that led to a faster expansion growth, greater grain volume and faster starch synthesis at the early to mid stage of grain development. Also it had a longer period for actively filling. As a result, the grain weight and yield of the hybrid were increased by 14 and 15% respectively compared to that of Shaan 229. Additionally, the biomass of XN901 was 41.7% more than that of control, but its harvest index was 9% lower than Shaan 229. However, its lower activity of sucrose synthase indicated a lower sink activity at the late stage, resulting in a slow rate of filling and starch synthesis. Also, the hybrid wheat XN901 had a large source-sink ratio. It is the main reason for much assimilate remaining in the straw at the late stage and lower harvest index. Strengthening the sink activity and raising the harvest index should be the key means of improving the yield of hybrid wheat.

Analyzed the relationship between 568 site A/G polymorphism in mucin 1(MUC1) gene in a population from Liaoning Province and susceptibility to gastric cancer. Sequence specific primers-polymerase chain reaction(PCR-SSPs) were performed to analyze the genotype of the A/G polymorphism in its 568 site of exon 2 for 138 gastric cancer cases and 131 normal ones tested, and ELISA was performed to test IgG antibody of H. pylori. We found that the distribution fre-quency of AA, AG, GG three genotypes were 73.3%, 22.1%, 4.6%, respectively. The frequency of AA genotype was statis-tically higher in the gastric cancer (GC) group compared to the control group(P=0.03), moreover, individuals with the MUC1 AA genotype increased 1.92 fold risk for gastric cancer. And compared with subjects carrying both AG+GG geno-type and H. pylori-IgG negative, there was an obviously increased risk of developing gastric cancer for those who carried both AA genotype and H. pylori-IgG negative, both AG+GG genotype and H. pylori-IgG positive, and both AG+GG geno-type and H. pylori-IgG negative, but there were no significantly differences between the every two of the latter three. Our results indicated that there was a relationship between MUC1 A/G polymorphism and susceptibility to gastric cancer. Andthere were probably no statistically interaction between the 568 site A/G polymorphism in MUC1 and H. pylori infection in the occurrence and development process of gastric cancer.

OBJECTIVE: To investigate the influence of gender, age, site of lesion, disease type and Helicobacter pylori (H. pylori) infection on the human serum gastrin-17 level and to study the diagnostic value of serum gastrin-17 in gastric precancerous lesions and gastric cancer. METHODS: Serum gastrin-17 and serum H. pylori IgG antibody were detected by the ELISA method. The different gastric disease groups were confirmed by endoscopy and histopathology. RESULTS: Among the 3906 serum samples according to the gender, age, site of lesion and the data of different gastric disease groups, the serum gastrin-17 level was markedly higher in people ≥60 years old than that in younger age groups. The serum gastrin-17 level increased progressively in the following order: healthy control group, nonatrophic gastritis group, gastric ulcer group, and the serum gastrin-17 level was higher in the atrophic gastritis with dysplasia group than that without it, the lowest level being in the gastric cancer group. Among the 2946 serum samples matched with the site of the lesion, the serum gastrin-17 level was higher in those with antral diseases than in those with gastric corpus diseases. Among the 3805 serum samples matched with the H. pylori infection data, the serum gastrin-17 level was higher in the H. pylori-positive group than in the H. pylori-negative group. CONCLUSIONS: In people over 60 years of age, the serum gastrin-17 level tends to increase. In subjects with precancerous gastric lesions, it may increase significantly with the progression of gastric disease, and ultimately decrease in gastric cancer. Serum gastrin-17 is a good biomarker to differentiate benign from malignant gastric diseases. The site of the gastric lesions is an important factor affecting the serum gastrin-17 level, whereas H. pylori infection is usually associated with its increment.

There have been no reports on the relationship between virulence genes and gastric diseases based on the same bacterial colonization density. Our results indicated that Helicobacter pylori virulence genes were more relevant than colonization density as a pathogenic mechanism of gastric diseases, which helps elucidate the pathogenic mechanisms of bacteria and aids in the development of improved strategies for the treatment of gastric disease.

The effect of high salt environments on biological characteristics of Helicobacter pylori is still unclear. In the present study, we therefore investigated biological characteristics of the bacterium exposed to high salt concentrations. H. pylori strain, L301, was cultured in media supplemented with different concentrations (3%, 15% and 30%) of sodium chloride (NaCl) under microaerophilic conditions for 48 h. Morphology was assessed by light microscopy, the ATP content was quantitated by single-tube fluorescent light-emission and the levels of CagA and UreB proteins were determined by Western blotting. After exposure to NaCl, H. pylori transformed from common spiral shape to U or even coccoid shapes. The ATP content was significantly higher in 30% NaCl group than in 15% and 3% NaCl group and the level of CagA protein increased with the salt concentration. The urease reaction was all strongly positive in H. pylori exposed to different salt concentrations. The level of 8-OHdG expression was significantly increased in GES-1 cells co-cultured with H. pylori exposed to high salt, compared with the level in uninfected cells. H. pylori survives under exposure to high salt concentrations up to 30%, exhibiting changes in mobility, morphology and CagA expression, associated with increased 8-OHdG in the gastric epithelial cells, indicative of DNA damage.

Helicobacter pylori, a microaerophilic Gram-negative bacterium, is known to cause chronic gastritis, peptic ulcer and gastric cancer. Genes that are present in certain isolates may determine strain-specific traits such as disease association and drug resistance. In order to understand the pathogenic mechanisms of gastric diseases, identify molecular markers of the diseases associated with H. pylori strains and provide clues for target treatment of H. pylori-related diseases, a subtracted DNA library was constructed from a gastric cancer-associated H. pylori strain and a superficial gastritis-associated H. pylori strain by suppression subtractive hybridization. The presence of gastric cancer-specific genes was identified by dot blot hybridization, DNA sequencing and PCR-based screening. Twelve gastric cancer-specific high-copy genes and nine low-copy genes were found in gastric cancer compared with the superficial gastritis strain. These genes were confirmed by PCR analysis of H. pylori isolates. Notably, peptidyl-prolyl cis-trans isomerase (PPIase) was detected positively in 11 out of 22 (50%) gastric cancer-associated H. pylori strains. In contrast,24% of the H. pylori strains from superficial gastritis showed positive results. Given the potential role of PPIases in cell growth, apoptosis and oncogenic transformation, our results suggest that PPIase may represent a novel marker and potential therapeutic target for gastric cancer.

Serum pepsinogen II (sPGII) is underutilized and considered an inconspicuous biomarker in clinical practice. We refocused on this neglected but novel biomarker and conducted the present study, aiming to elucidate the normal level of sPGII in healthy Chinese patients and to investigate the clinical utility of sPGII for gastric disease screening.In 2008-2009, a total of 2022 participants from northern China were selected and enrolled in the study. sPGII and Helicobacter pylori (H. pylori)-immunoglobulin G were measured with ELISA.sPGII showed a normal value of 6.6 microg/L in a total of 466 patients with endoscopically- and histologically-normal stomachs. A small sex difference was observed: the average value of sPGII was 7 microg/L and 6 microg/L in males and females, respectively (P0.001). In the differentiation between healthy and diseased (endoscopically-diseased stomach or gastritis/atrophic gastritis in endoscopic biopsies) stomach mucosae, the best sPGII cut-off value was 8.25 microg/L (sensitivity 70.6%, specificity 70.8%). In screening the H. pylori seropositivity, the optimum cut-off sPGII value was 10.25 microg/L (sensitivity 71.6%, specificity 70.1%).We demonstrated that the mean values of sPGII in a healthy Chinese population are 7 microg/L and 6 microg/L for males and females, respectively. sPGII significantly increases in diseased and H. pylori-infected stomach, and the best sPGII cut-off value is 8.25 microg/L in the differentiation between patients with healthy and diseased stomach mucosae. Furthermore, Chinese patients with sPGII greater than 10.25 microg/L are at greater risk of various H. pylori-related gastropathies, and are therefore prior candidates for gastro-protection therapy.

Epidemiologic studies have demonstrated that Helicobacter pylori infection is associated with increased risk for the development of gastric cancer. Animal studies have also shown that H. pylori infection leads to gastric carcinogenesis, especially intestinal phenotypes. However, no in vitro study has been carried out for cell transformation induced by H. pylori. The present study aimed to investigate whether 'chronic'H. pylori infection induces gastric epithelial cell transformation, and elucidate the underlying mechanisms of transformation induced by H. pylori. The immortalized 'normal' gastric epithelial cell line, GES-1, was co-cultured for 45 days with H. pylori strains B975 and L301. The cell proliferation was measured by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay, Ki-67 antigen, and colony formation assay. The cell transformation was determined by observing cell morphology and measuring the expression of E-cadherin, β-catenin, and transcription factor-4 (TCF-4) at both protein and mRNA levels. H. pylori induced morphologic changes in GES-1 cells and significantly increased the proliferation of GES-1 cells. Moreover, H. pylori up-regulated the expression of β-catenin and TCF-4, and also induced the nuclear accumulation of β-catenin. In addition, the diffusive gastric cancer-related gene, E-cadherin, was up-regulated at the protein level, but down-regulated at the mRNA level. H. pylori infection is capable of inducing GES-1 transformation to present with the characteristics of intestinal-type gastric cancers in vitro, likely through the β-catenin/TCF-4 signaling pathway.

Identifying the genetic variants that alter MUC I protein expression may further our understanding of the risk for development of gastric cancer (GC). We used PCR-SSPs to identify the genotype of MUC1 A/G polymorphism at its 568 site of exon 2 and immunohistochemistry to detect MUC1 protein expression in GC patients and non-cancer subjects and analyzed the association between this polymorphism and MUC1 protein expression. We found that the frequency of AA genotype was significantly high in the GC patients and the risk for GC in AA genotype carriers increased 1.81-fold. Moreover, we found a significant underexpression of MUC protein in GC as compared to non-cancer subjects, which was negatively correlated to AA genotype of MUCI (r=-0.1790, P=0.004). Furthermore, this study provides a possible mechanistic insight that the MUC1 A/G polymorphism at its 568 site disrupts the physiological functions of MUC1 which is important to the physiological protection of gastric mucosa. Thus we have provided evidence that may identify the MUCI A/G polymorphism at 568 site, as a potential genetic factor which leads to an increase in susceptibility for GC through alteration of MUCI gene and MUC1 expression in the population that carry the A allele.

To investigate the feasibility of detecting Helicobacter pylori (Hp) directly from gastric mucosa and the relationship of HP genotypes to gastric diseases.Specimens of gastric mucosa were collected by biopsy from 217 patients, 90 with superficial gastritis (GS), 70 with atrophic gastritis (GA), 28 with gastroesophageal erosions and ulcers (GEU), and 29 with gastric cancer (GC), to undergo pathological examination, culture of Hp, and DNA isolation from the gastric mucosa respectively. Routine phenol/chloroform method was used to isolate the DNA in the cultured Hp. PCR was conducted to detect the ureB, cagA, vacAs1, vacAm1, vacAm2, iceA1, iceA2, and baba2 genotypes in both the gastric mucosa-originated Hp-DNA and cultured Hp-DNA.The concordance rates of ureB, cagA, vacAs1, vacAm1, vacAm2, iceA1, iceA2, and baba2 genotypes between the gastric mucosa-originated Hp-DNA and cultured Hp-DNA were 74.23%, 73.39%, 93.69%, 62.16%, 78.16%, 89.13%, 88.37%, and 75% respectively (all P0.05). There were no significant differences in the distribution rates of ureB, cagA, vacAs1, vacAm1b, iceA1, iceA2, and baba2 genotypes among different gastric diseases (all P0.05). However, the distribution frequency of vacAs1m1 strain in the GA patients was 22.22%, significantly higher than that in the GA patients (5.71%, chi2 = 8.416, P = 0.004), and the distribution frequency of vacAs1m2 strains in the GA patients was 47.14%, significantly higher than that in GS patients (18.89%, chi2 = 13.336, P = 0.000).Rapid detection of Hp can be achieved by using DNA isolated directly from infected gastric mucosa. VacAs1 m1 is associated with GA and vacAs1m2 is associated with GA.

Analyzed the relationship between 568 site A/G polymorphism in mucin 1(MUC1) gene in a population from Liaoning Province and susceptibility to gastric cancer. Sequence specific primers-polymerase chain reaction(PCR-SSPs) were performed to analyze the genotype of the A/G polymorphism in its 568 site of exon 2 for 138 gastric cancer cases and 131 normal ones tested, and ELISA was performed to test IgG antibody of H. pylori. We found that the distribution frequency of AA, AG, GG three genotypes were 73.3%, 22.1%, 4.6%, respectively. The frequency of AA genotype was statistically higher in the gastric cancer (GC) group compared to the control group(P=0.03), moreover, individuals with the MUC1 AA genotype increased 1.92 fold risk for gastric cancer. And compared with subjects carrying both AG+GG genotype and H. pylori-IgG negative, there was an obviously increased risk of developing gastric cancer for those who carried both AA genotype and H. pylori-IgG negative, both AG+GG genotype and H. pylori-IgG positive, and both AG+GG genotype and H. pylori-IgG negative, but there were no significantly differences between the every two of the latter three. Our results indicated that there was a relationship between MUC1 A/G polymorphism and susceptibility to gastric cancer. And there were probably no statistically interaction between the 568 site A/G polymorphism in MUC1 and H. pylori infection in the occurrence and development process of gastric cancer.

To investigate the condition of Helicobacter pylori (Hp) colonization in different gastric diseases and the application of immunostaining technique in Hp density measurement.Biopsy specimens of gastric mucosa were obtained from 174 patients with different gastric diseases confirmed by pathological examination, 99 males and 75 females, aged 53.37 (19-87), 135 from Zhuanghe, a high risk area of gastric cancer, and 39 from Shenyang, a low risk area. Hematoxylin and eosin (HE) staining and immunohistochemistry were used to detect the Hp density in different parts of gastric mucosa.When the grade of Hp density in the gastric mucosa epithelium cell surface and lumen of gland1 there was a significant difference between HE stain and immunohistochemistry (chi(2) = 9.446, P0.01), however, when the grade of Hp density in the gastric mucosa epithelium cell surface and lumen of gland1 there was no significant difference between them (P0.05). The grade of Hp density of gastric mucosa epithelium cell surface and lumen of gland in superficial gastritis was1, significantly higher than those of atrophic gastritis group (23.8%) and gastric cancer group (16.7%) (chi(2) = 2.780, P0.05; chi(2) = 4.876, P0.05). The Hp colonization density in the gastric mucosa epithelium cell surface and lumen of the patients from Zhuanghe region was significantly lower than that of the patients from Shenyang region (chi(2) = 5.915, P = 0.015); and the Hp density in the gastric mucus in the patients from Zhuanghe was significantly higher than that of the patients from Shenyang region (chi(2) = 8.879, P = 0.003, chi(2) = 22.036, P = 0.000). The grades of Hp density within the surface mucous gel layer in atrophic gastritis and gastric cancer was significantly higher than that of the superficial gastritis group (53.7%, chi(2) = 11.002, P0.05; chi(2) = 19.401, P0.05).The density of Hp colonization in gastric mucosa epithelium cell surface and lumen of gland gradually decreases in the order of superficial gastritis-atrophic gastritis-gastric cancer, while the density of Hp within the surface mucous gel layer increases in the order of superficial gastritis- atrophic gastritis-gastric cancer.

Objective To explore the features and clinical significance of serum pepsinogen (PG) assay in a follow-up study on a high-risk gastric cancer (GC) population. Methods A total of 444 participants from a high-risk area of GC in north China were enrolled in this follow-up study from April 1997 to December 1999. Serum PG was measured by enzyme-linked immunosorbent assay (ELISA), and the percentage changes in PG were calculated with 'PG( follow-up)/PG (first test)' thrice from the beginning to the end of these 30 months. Stomach diseases were diagnosed by a gastroscopy with biopsy examination. Helicobacter pylori (H. pylori) status was assessed by histopathological examination and serum H. pylori-immunoglobulin (Ig)G antibody assay with ELISA. Results In all groups except for the 51-60-year olds no significant differences of percentage changes in PGII and the PGI/II ratio were observed during 30-month follow-up period. In the superficial gastritis (SG) group the percentage change in PGI of group A (after 6 months' follow up) was significantly lower than that of group B (after 12 months' follow up) (0.69 vs 0.97, P = 0.002) in SG-->SG; while in SG-->normal (NOR), it was significantly higher than that in SG-->atrophic gastritis (AG) (0.94 vs 0.79, P = 0.022). In the AG group the percentage change in the PGI/II ratio of group A was significantly higher than that of group C (after 30 months' follow up) (1.13 vs 0.75, P = 0.042) in AG-->AG; and the percentage changes in PGI and PGII in AG-->NOR were significantly lower than those in AG-->SG (0.43 vs 0.87, P = 0.000; 0.60 vs 1.11, P = 0.010, respectively). In the H. pylori(-) (Hp(-)) group, the percentage change in PG of Hp(-)-->Hp(+) was significantly higher than that of Hp(-)-->Hp(-) (0.94 vs 0.81, P = 0.026). Percentage changes in PGI and PGII of Hp(+)-->Hp(-) were significantly lower than those of Hp(+)-->Hp(+) (0.74 vs 0.93, P = 0.000; 0.86 vs 1.15, P = 0.000, respectively), while the percentage change in the PGI/II ratio was higher than that the group of Hp(+)-->Hp(-) (0.90 vs 0.70, P = 0.022). Conclusion The serum PG levels were influenced by the physiopathologic status of gastric mucosa and H. pylori infection, but they altered during the period of follow up. Serum PG assay might be a feasible and appropriate procedure to use in following up on a high-risk GC population.

To explore the value of combined assay of serum PG and OPN concentration for gastric cancer screening.Pepsinogen I , II and osteopontin (OPN) concentrations in fasting serum were measured by ELISA in 570 subjects, including 144 gastric cancer, 60 dysplasia, 113 atrophic gastritis, 70 erosion or ulcer, 92 superficial gastritis and 91 healthy control. The cut off point for PG and OPN was determined using receiver operator characteristics curves (ROC).Using a serum PG I concentrationor =80 ng/ml, I: II rationor =5.0 and OPN concentrationor =34 ng/ml oror =30.4 ng/ml (based on ROC) for gastric cancer screening,the specificity, positive and negative predictive values were superior to that obtained by PG concentration only. Using a serumPGI concentrationor =50 ng/ml, I : II ration C 5. 0 and OPN concentrationor =35.2 ng/ml oror =29. 2 ng/ml (based on ROC), the sensitivity, positive and negative predictive values were superior to that obtained by PG concentration only. Combining PG and OPN for gastric cancer screening, both sensitivity and specificity were more than 70% , while with OPN alone, only good specificity can be achieved.Combining different serum PG and OPN concentration for gastric cancer screening is superior to PG or OPN only. This may be used as a new method in gastric cancer mass screening.

To investigate the dynamic changes of serum pepsinogen (PG) among the high risk populations of gastric cancer.Peripheral blood samples were collected from 444 subjects in the high risk areas of gastric cancer in Zhuanghe county, Liaoning province, who underwent screening of gastric cancer, 225 males and 219 females, aged 48.31 (21 - 76). ELISA was used to measure the serum PG I and PG II. The PG I/II ratio was calculated. Gastroscopy was conducted to take 4 pieces of biopsy specimens from each subject to undergo pathological examination. Histological examination and serum Hp-IgG antibody determination by ELISA were performed to detect the infection of Helicobacter pylori (Hp). The above mentioned examinations were carried out at the first screening and 6, 12, and 30 months later during follow-up.(1) In the age group 51 - 60, the percentage change in PG II of 6-month follow-up was 0.84, significantly lower than those of the 12-month follow-up (1.22, P = 0.019) and 30-month follow-up (1.24, P = 0.004), and the percentage change in PG I/II of the 6-month follow-up was 1.09, significantly higher than those of the 12-month follow-up (0.75, P = 0.027) and 30-month follow-up (0.69, P = 0.001). However, there were no significant differences in serum PG I, serum PG II, and PG I/II ratio in other age groups. (2) The percentage change in serum PG I of the patients of superficial gastritis (SG) with mitigation of the 6-month follow-up was 0.69, significantly lower than that of the 12-month follow-up (0.97, P = 0.002). The percentage change in PG I/II of the patients of atrophic gastritis (AG) with mitigation of the 6-month follow-up was 1.13, significantly higher than that of the 12-month follow-up (0.75, P = 0.042). (3) The percentage change in PG I of the SG--NOR (normal) group was 0.94, significantly higher than that of the SG--AG group (0.79, P = 0.002). The percentage changes in PG I and PG II of the AG--NOR group were 0.43 and 0.60 respectively, both significantly lower than those of the AG--SG group (0.87, P = 0.000, and 1.11, P = 0.010). (4) The percentage change in PG I of the Hp negative--Hp positive group was 0.94, significantly higher than that of the Hp negative--Hp negative group (0.81, P = 0.026). The percentage changes in PG I and PG II of the Hp positive--Hp negative group were 0.74 and 0.86 respectively, both significantly lower than those of Hp positive--Hp positive group (0.93 and 1.15 respectively, both P = 0.000), and the percentage change in PG I/II of the Hp positive--Hp negative group was 0.90, significantly higher than that of the Hp positive--Hp positive group (0.70, P = 0.022).The percentage change of serum PG is correlated with time of follow-up, feature of stomach disease, and status of Hp infection. Dynamic detection of serum PG can be applied in monitoring the populations in high risk area of gastric cancer.

AIM: To compare the distribution of virulence-associated genotypes of Helicobacter pylori (H pylori) in two areas of north China with different gastric cancer risk and furthermore probe into the pathogenicity of the bacterium. METHODS: Gastric biopsies were taken from 355 subjects from Zhuanghe, a high risk area of gastric cancer, and 136 subjects from Shenyang, a low risk area of gastric cancer. A total of 149 H pylori strains isolated from these patients were studied by PCR for differences in the genotypes of cagA, vacA, and iceA. RESULTS: In patients with high risk for gastric cancer, higher frequencies of vacA s1 or s1m1b genotypes were found as compared to those from the low risk area. CONCLUSION: There is significantly different distribution of H pylori genotypes between Zhuanghe and Shenyang areas in north China.

To explore influence factors of DNA extraction, the protease and phenol-chloroform method was used to extract DNA in whole blood, fresh tissues, frozen tissues embedding with OCT and tissues embedding in paraffin. It results that 200-300 microg DNA was extracted from 1 ml whole blood or 0.2 g fresh tissues or frozen tissue embedding with OCT. DNA extracted from paraffin specimen can be directly used in PCR amplification. Purity DNA can be extracted from four kinds of different tissues. OCT hasn't harmful effect on tissue DNA extraction.

To study the relationship between Helicobacter pylori (H. pylori) and gastric carcinoma and its possible pathogenesis by H. pylori.DNEL technique and immunohistochemical technique were used to study the state of apoptosis, proliferation and p53 gene expression. A total of 100 gastric mucosal biopsy specimens, including 20 normal mucosa, 30 H. pylori-negative and 30 H. pylori-positive gastric precancerous lesions along with 20 gastric carcinomas were studied.There were several apoptotic cells in the superficial epithelium and a few proliferative cells within the neck of gastric glands, and no p53 protein expression in normal mucosa. In gastric carcinoma, there were few apoptotic cells, while there were a large number of proliferative cells, and expression of p53 protein significantly was increased. In the phase of metaplasia, the apoptotic index (AI, 4.36%+/-1.95%), proliferative index (PI, 19.11%+/-6.79%) and positivity of p53 expression (46.7%) in H. pylori-positive group were higher than those in normal mucosa (P0.01). AI in H. pylori-positive group was higher than that in H. pylori-negative group (3.81%+/-1.76%), PI in H. pylori-positive group was higher than that in H. pylori-negative group (12.25%+/-5.63%, P0.01). In the phase of dysplasia, AI (2.31%+/-1.10%) in H. pylori-positive group was lower (3.05%+/-1.29%) than that in H. pylori-negative group, but PI (33.89%+/-11.65%) was significantly higher (22.09+/-8018%, P0.01). In phases of metaplasia, dysplasia and gastric cancer in the H. pylori-positive group, AIs had an evidently graduall decreasing trend (P0.01), while PIs had an evidently gradual increasing trend (P0.05 or P0.01), and there was also a trend of gradual increase in the expression of p53 gene.In the course of the formation of gastric carcinoma, proliferation of gastric mucosa can be greatly increased by H. pylori, and H. pylori can induce apoptosis in the phase of metaplasia, but in the phase of dysplasia H. pylori can inhibit cellular apoptosis. And H. pylori infection can strengthen the expression of mutated p53 gene.