***TASK*** the task is to summarize an input biomedical literature in six sentences 
    ***INPUT*** the input is a biomedical literature 
    ***OUTPUT*** the output is the summary of an input biomedical literature in six sentences 
    ***DOCUMENTATION*** 
    ***EXAMPLES*** 
    Input: Previous studies have shown that the bisphosphonates ( BP ) vary in their damaging effect on the gastric mucosa , and endoscopy scores ( erosions or erosions plus ulcers ) after 1 and 2 weeks use of BP were significantly lower in H. pylori-positive versus -negative subjects . The mechanism of this damaging effect of BP and the interaction with H. pylori is unknown . As part of a separately reported study of the incidence of gastric damage after 2 weeks of treatment of healthy female postmenopausal volunteers with risedronate ( 5 mg/day ) or  alendronate  ( 10 mg/day ) , gastric aspirates were taken at the time of the baseline esophagogastroduodenoscopy ( EGD ) , and again at 1 and 2 weeks after daily intake of a BP . At the time of the third EGD , when the volunteers had been on risedronate or alendronate for 2 weeks , antral biopsies were taken from normal-appearing mucosa . Gastric juice and antral biopsies were assessed for their concentration of the cytokines interleukin-1α ( IL-1α ) , IL-8 , IL-13 , and epidermal growth factor ( EGF ) . H. pylori , the use of BP , and development of gastric mucosal lesions had no effect on gastric mucosal concentrations of IL-1α , IL-13 , or EGF . In contrast , the concentration of IL-8 in antral mucosal biopsies of volunteers given BP for 2 weeks was higher in the presence than in the absence of an H. pylori infection and was increased further in those who develop lesions associated with the use of BP . There was no correlation between gastric mucosal and gastric juice concentrations of IL-8 . Gastric juice concentrations of IL-8 and EGF were not affected by H. pylori status , the use of BP , or the development of lesions . However , gastric juice concentrations of IL-1α were numerically lower in those who were negative for H. pylori with no mucosal lesions ( Hp−L− ) , intermediate in those who were H. pylori-negative with lesions ( Hp−L+ ) , and highest in those who were positive for H. pylori and had lesions ( Hp+L+ ) . The gastric juice concentration of IL-13 was threefold higher in the absence than in the presence of H. pylori , and the relative abundance of IL-13 was : Hp−L− > Hp−L+ > Hp+L−1 > Hp+L+ . The prostagl and in E2 concentration in gastric antral biopsies was similar in the four groups and was unchanged with the in vitro biopsy incubation with celecoxib . We speculate that the higher gastric endoscopy scores observed with the use of BP in H. pylori negative as compared with H. pylori positive individuals is due to their lower mucosal concentration of IL-8 as well as the lower gastric juice concentration of IL-1α and higher concentration of IL-13 BACKGROUND This study characterized the phenotypic subsets of isolated gastric lymphocytes and the cellular immune response in cultured gastric biopsy specimens . METHODS Endoscopy specimens from 40 Helicobacter pylori-positive and 40 H. pylori-negative patients were studied . a ) Isolated gastric lymphocytes were analysed for CD4 + , CD8 + T-lymphocyte subsets , activated T cells , and natural killer cells on a fluorescence-activated cell sorter , using monoclonal antibodies . b ) The supernatant of cultured gastric biopsy specimens were assayed for interleukin (IL)-2 , IL-4 , and IL-6 levels . RESULTS In H. pylori-positive patients there was ( a ) a decrease in CD4+/CD8 + T cells , no change in activated T cells , and an increase in natural killer cells , and ( b ) no change in IL-2 levels and a significant increase in IL-4 and IL-6 levels . CONCLUSIONS There is an increase in CD8 + lymphocytes and natural killer cells , and the observed increase in IL-4 and IL-6 might be important in H. pylori-associated gastritis Objectives : In order to test the hypothesis that H. pylori infections in the gastric antrum increase pepsinogen I release , fasting serum pepsinogen I concentrations were compared in peptic ulcer patients with and without H. pylori infection . A r and omized prospect i ve study was performed to determine whether the increased serum pepsinogen I concentrations associated with H. pylori infection respond to treatment that eradicates H. pylori . Methods : Fasting serum pepsinogen I concentrations were measured by RIA in 736 patients with endoscopically and histologically confirmed benign peptic ulcer with and without H. pylori infection . Out of 511 patients with H. pylori infection , 110 patients ( group 1 ) were r and omly selected and were treated with metronidazole and tripotassium dicitrato bismuthate combined with ranitidine and antacid , and 97 patients ( group 2 ) were treated only with ranitidine and antacid . The third group , 54 patients free of H. pylori infection , was design ed to evaluate the influence of H2-receptor antagonist and antacid on the change of pepsinogen I. Fasting pepsinogen I concentration and H. pylori status were compared before and after the treatment . Results : Patients infected by H. pylori ( gastric ulcer 208 , duodenal ulcer 303 ; total 511 ) had significantly higher fasting serum pepsinogen I concentrations than H. pylori negative patients ( gastric ulcer 110 , duodenal ulcer 115 : total 225 ) . Mean pepsinogen I level of the former was 124.3±46.9 and that of the latter was 77.9±25.8 ng/ml . ( p<0.0001 ) The difference in serum pepsinogen I concentrations according to the location of ulcer crater was significant only in non-infected subjects e.g. , mean pepsinogen I level H. pylori-negative gastric ulcer was significantly lower than that of H. pylori-negative duodenal ulcer patients . H. pylori was eradicated in all the patients who had received antibacterial therapy for 4 weeks and serum pepsinogen I concentrations were significantly decreased from 129.8 + 43.0 to 82.4±24.0 ng/ml after eradication of the organism . ( p<0.0001 ) In contrast , H. pylori-positive patients who had not received antibacterial therapy were still infected at the completion of the study and there was no significant change in the serum pepsinogen I concentrations after the treatment ( 120.8±40.9 vs 126.3± 40.4 ng/ml ) . ( p>0.57 ) None of the patients who were initially H. pylori-negative has been reinfected during the period of the study and their serum pepsinogen I concentrations were not changed . ( pre-treatment value 75.1±8.0 ; post-treatment value 77.3±24.5 mg/ml)(p<0.75 ) Four-to six-week therapy of H2-receptor antagonist and antacid did not exert any influence on serum pepsinogen I concentrations . Conclusions : On the basis of our results , we have confirmed that the chronic infection of H. pylori of gastric antrum in peptic ulcer patients causes increased pepsinogen I release into the circulation , and eradication of the organism results in significant fall in serum pepsinogen I concentrations The aim of the present study was to determine the efficacy of a new combination regimen including antioxidant , proton pump inhibitor , and antibiotics against Helicobacter pylori and to document the changes of oxidative stress and cytokines involved in H. pylori-associated gastritis . From each of 57 patients with endoscopically diagnosed gastric and /or duodenal ulcers associated with H. pylori infection , five gastric antral biopsy specimens were taken for the diagnosis of H. pylori and for experimental measures . The patients were then treated either with lansoprozole 30 mg + amoxicillin 1.5 g ( LA group ; 21 patients ) or lansoprazole 30 mg + amoxicillin 1.5 g + rebamipide 300 mg ( LAM group ; 36 patients ) for two weeks . Four weeks after the initiation of treatment , the patients were endoscoped again and biopsy specimens were obtained . Mucosal malondialdehyde ( MDA ) levels ; myeloperoxidase ( MPO ) activities ; superoxide dismutase ; catalase ; glutathione peroxidase ; cytokines IL-1 , IL-6 , TNF-alpha ; and chemokines IL-8 , GRO-alpha , RANTES ( regulated on activation normal T expressed and secreted ) were measured . Using paraffin-embedded tissue sections , in situ terminal deoxyribonucleotide transferase ( TdT ) -mediated dUTP nick end labeling ( TUNEL ) for apoptosis and immunohistochemical staining for inducible nitric oxide synthase ( iNOS ) were performed . Two weeks of treatment with the LA regimen result ed in 57.4 % eradication rates of H. pylori , whereas two weeks of treatment with the LAM regimen result ed in 75.0 % eradication rates . Eradication rates between these two groups were statistically significantly different ( P < 0.05 ) . Mucosal MDA levels and MPO activities were significantly lower in the LAM group than the LA group . Mucosal levels of cytokines IL-1 , IL-6 , and TNF-alpha and of chemokines IL-8 , GRO-alpha , and RANTES were all significantly decreased after the treatment of H. pylori , especially in the LAM-treated group . The apoptotic index and iNOS score were significantly reduced after the eradication of H. pylori . The addition of the antioxidative drug rebamipide to the eradication regimen against H. pylori has quantitative and qualitative advantages such as either augmenting the eradication rates of H. pylori or decreasing oxidative stress and cytokines levels generated by H. pylori infection Helicobacter pylori ( H pylori ) raises serum gastrin but it is unclear whether this stimulates increased acid secretion . Gastrin mediated acid secretion and plasma gastrin after the intravenous infusion of gastrin releasing peptide was studied in nine H pylori negative and nine H pylori positive healthy volunteers , and in 11 duodenal ulcer patients . Nine of the last group were re-examined one month after eradication of H pylori . The median acid output ( mmol/h ) to gastrin releasing peptide ( 40 pmol/kg/h ) in the H pylori positive healthy volunteers was 15.1 ( range 3.3 - 38.3 ) , which was three times that of the H pylori negative healthy volunteers ( median = 5.5 , range 1.0 - 9.0 ) ( p < 0.02 ) . The median acid output in the duodenal ulcer patients with H pylori was 37 ( range 8.5 - 57 ) , which was > six times that of the H pylori negative healthy volunteers . Eradication of H pylori in the duodenal ulcer patients lowered their acid secretion by a median of 66 % ( range 30%-80 % ) ( p < 0.01 ) and to values equivalent to the H pylori positive healthy volunteers . The pepsin output in response to gastrin releasing peptide followed the same pattern as the acid output . The median plasma gastrin concentrations during gastrin releasing peptide were similar in the H pylori positive duodenal ulcer patients ( 150 ng/l , range 95 - 400 ) and H pylori positive healthy volunteers ( 129 ng/l , range 23 - 420 ) and both were appreciably higher than H pylori negative healthy volunteers ( 60 ng/l , range 28 - 135 ) ( p < 0.005 for each ) . Eradication of H pylori lowered the plasma gastrin in the duodenal ulcer patients to values equivalent to the H pylori negative healthy volunteers . These findings show a threefold increase in acid secretion in H pylori positive healthy volunteers that is explained by H pylori induced hypergastrinaemia and a sixfold increase in acid secretion in the duodenal ulcer patients that is explained by the combination of H pylori induced hypergastrinaemia and an exaggerated acid response to stimulation by gastrin . Eradicating H pylori lowers gastrin mediated acid secretion by 66 % in duodenal ulcer patients as a result of the resolution of the hypergastrinaemia . Increased gastrin mediated acid secretion seems to be the key factor in the pathophysiology of duodenal ulceration and explains the role of H pylori infection in the disorder Ascorbic acid , the reduced form of vitamin C , may protect against gastric cancer and is secreted by the normal stomach . Secretion is impaired in Helicobacter pylori ( H pylori ) associated chronic gastritis . This study examined if eradication of H pylori improves gastric juice ascorbate values . Fasting gastric juice and 
    Output:
    
Results : In addition to st and ard markers such as pepsinogens , we confirmed the close relationship between the levels of several biomarkers including gastrin , interleukin-8 , HLA class II molecules , reactive oxygen species , and the histological grade s. Conclusions : This review provides valuable information describing the clinical implication of these biomarkers for evaluating the static conditions or dynamic alterations of human gastric inflammation