Primary appendiceal adenocarcinoma with cecocolic intussusception.
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Adenocarcinoma↗
Biomedical subjects
Jaw-Town Lin
Publications and source records attributed to Jaw-Town Lin.
Jejunojejunal intussusception secondary to a jejunal lipoma in an adult.
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Aged, 80 and over↗
Factors determining post-colonoscopy abdominal pain: prospective study of screening colonoscopy in 1000 subjects.
BACKGROUND: Factors determining post-colonoscopy abdominal pain remain poorly understood. Accordingly, a prospective study was conducted to reveal the key determinants. METHODS: One thousand consecutive and asymptomatic patients (569 men, 431 women; mean age 51 years, range 19-84 years) undergoing total colonoscopy were evaluated to assess their abdominal pain. Their demographic data, psychological profiles (determined on the Brief Symptom Rating Scale and Maudsley Personality Inventory), and endoscopic findings were treated as independent variables in polytomous logistic regression in which pain severities were treated as outcome variables. Factors affecting the duration of pain were evaluated on multivariate linear regression. RESULTS: Colonoscopy duration (s; odds ratio [OR]: 1.001, 95% confidence interval [CI]: 1-1.002, P<0.01) and female sex (OR: 1.368, 95%CI: 1.02-1.853, P=0.03) were significantly associated with abdominal pain, but age, body mass index, psychological traits, conscious sedation, use of i.v. hyoscine butylbromide, and colonic preparation were not. Duration of the colonoscopy was longer in female than male subjects (P=0.04). On stepwise linear regression, irritable bowel syndrome (regression coefficient: 27.47, 95%CI: 6.99-47.67, P<0.01) and conscious sedation (regression coefficient: -22.17, 95%CI: -42.52 to -1.42, P = 0.036) were the best predictors of prolonged pain in 485 patients who had pain. CONCLUSIONS: Female sex and duration of colonoscopy increased the likelihood of post-procedural abdominal pain. Conscious sedation temporarily suppressed the pain but had no effect on its occurrence. Irritable bowel syndrome may have prolonged the discomfort.
Abdominal Pain↗
Circadian change of cardiac autonomic function in correlation with intra-esophageal pH.
BACKGROUND AND AIM: Although autonomic alterations are observed in patients with gastroesophageal reflux disease (GERD), the influence of visceral receptor responses on the dynamics of autonomic function remains unknown. The aim of this study was to investigate the autonomic functional changes in association with intra-esophageal pH under ambulation. METHODS: Thirty patients referred for 48 h ambulatory pH monitoring underwent simultaneous 24 h cardiac monitoring for heart rate variability (HRV). We used linear mixed-effects models to estimate the relationship between esophageal acid exposure and power spectral analysis of HRV, including low-frequency power (0.04 < LF < 0.15 Hz), high-frequency power (0.15 < or = HF < 0.4 Hz), and LF/HF power ratio. RESULTS: Over the 24-h period, patients with pathological reflux had lower average LF and HF powers than patients with functional heartburn, but the LF/HF power ratios were similar for the two patient groups. As we stratified the data according to waking and sleeping times, a significantly higher HF power but lower LF/HF power ratio was found during sleeping time regardless of diagnosis. In the regression analysis, esophageal pH was positively associated with change (not basal tone) of both LF and HF powers during waking, but only with change of HF power during sleeping time. The significant associations between pH values and changes in HRV decreased gradually with time. The LF/HF power ratio did not alter significantly with pH. CONCLUSION: Esophageal acid exposure is generally associated with decreases in autonomic tone. A predominant parasympathetic fluctuation during sleeping and a superimposed sympathetic interaction during waking dictate diurnal characteristics of autonomic regulation.
Adult↗
A community-based study of Helicobacter pylori therapy using the strategy of test, treat, retest, and re-treat initial treatment failures.
BACKGROUND: Although eradication of Helicobacter pylori infection can decrease the risk of gastric cancer, the optimal regimen for treating the general population remains unclear. We report the eradication rate (intention-to-treat and per protocol) of a community-based H. pylori therapy using the strategy of test, treat, retest, and re-treat initial treatment failures. MATERIALS AND METHODS: In 2004, a total of 2658 residents were recruited for 13C-urea breath testing. Participants with positive results for infection received a standard 7-day triple therapy (esomeprazole 40 mg once daily, amoxicillin 1 g twice daily, and clarithromycin 500 mg twice daily), and a 10-day re-treatment (esomeprazole 40 mg once daily, amoxicillin 1 g twice daily, and levofloxacin 500 mg once daily) if the follow-up tests remained positive. Both H. pylori status and side-effects were assessed 6 weeks after treatment. RESULTS: Among 886 valid reporters, eradication rates with initial therapy were 86.9% (95% confidence interval [CI]: 84.7-89.1%) and 88.7% (95%CI: 86.5-90.9%) by intention-to-treat and per protocol analysis, respectively. Re-treatment eradicated infection in 91.4% (95%CI: 86-96.8%) of 105 nonresponders. Adequate compliance was achieved in 798 (90.1%) of 886 subjects receiving the initial treatment and in all 105 re-treated subjects. Mild side-effects occurred in 24% of subjects. Overall intention-to-treat and per protocol eradication rates were 97.7% (95%CI: 96.7-98.7%) and 98.8% (95%CI: 98.5-99.3%), respectively, which were only affected by poor compliance (odds ratio, 3.3; 95%CI, 1.99-5.48; p < .0001). CONCLUSIONS: A comprehensive plan using drugs in which the resistance rate is low in a population combined with the strategy of test, treat, retest, and re-treat of needed can result in virtual eradication of H. pylori from a population. This provides a model for planning country- or region-wide eradication programs.
Anti-Bacterial Agents↗
Helicobacter pylori infection and CagA protein translocation in human primary gastric epithelial cell culture.
BACKGROUND: Increasing evidence has shown that Helicobacter pylori CagA protein translocation into gastric epithelial cells plays an important role in the development of gastric inflammation and malignancy. Translocated CagA undergoes tyrosine phosphorylation in gastric adenocarcinoma cell line cells, and CagA involves disruption of cellular apical-junction complex in Madin-Darby canine kidney cells. METHODS: To elucidate whether these events take place in normal human gastric epithelium, we infected human primary gastric epithelial cells with H. pylori. RESULTS: Our results demonstrate that CagA protein was translocated into primary gastric epithelial cells and tyrosine phosphorylated. The translocated CagA induces cytoskeletal rearrangement and the disruption of tight junctions in primary gastric epithelial cells. CONCLUSIONS: This study provides direct evidence of the modulation of gastric epithelial cells by CagA protein translocation, and advances our understanding of the pathogenesis of H. pylori infection.
3T3 Cells↗
The influence of Helicobacter pylori infection and corpus gastritis on the postoperative outcomes of laparoscopic vertical banded gastroplasty.
BACKGROUND: Helicobacter pylori (HP) infection is linked to weight control through gastric inflammation-induced deregulation of satiety-related hormone, and eradication of HP before a weight reduction operation has been advocated. We aimed to examine the impact of HP infection and corpus gastritis on preoperative patient characteristics, postoperative complications and weight loss following laparoscopic vertical banded gastroplasty (LVBG). METHODS: A prospective cohort of 152 patients undergoing LVBG was enrolled. Gastric specimens at the corpus were obtained during LVBG operation and scored histologically according to the Sydney classification of gastritis. Excess weight loss, and early and late complications following LVBG, were recorded and correlated. RESULTS: 63 and 89 patients were identified as HP positive and negative groups respectively. The prevalence of individual components of the metabolic syndrome was comparable in both groups except hypertension. The occurrence of early and late complications, either minor or major, in both groups was similar. The severity of gastritis was correlated positively with age and negatively with preoperative BMI and excess weight. Patients with higher neutrophil activity, chronic inflammation, and HP density experienced less excess weight loss at 24 to 48 months follow-up. The impact of gastritis on weight loss became less recognizable after 48 months follow-up. CONCLUSIONS: HP infection and gastric inflammation play a significant role in the amount of weight loss after LVBG. Further prospective studies should examine possible mechanisms and long-term effects on weight loss to determine the utility of preventive eradication of HP in different types of bariatric surgery.
Adolescent↗
The influence of Helicobacter pylori infection on the development of gastric ulcer in symptomatic patients after bariatric surgery.
BACKGROUND: There are few data relating to the role of H. pylori infection and surgical procedures on the occurrence of gastric ulcer following bariatric surgery. METHODS: Subjects with upper gastrointestinal symptoms after bariatric surgery and receiving gastroscopic examinations were prospectively enrolled. All clinical data including age, sex, BMI before surgery, and surgical method were recorded. IgG antibodies against H. pylori were measured in preoperative serum by enzyme-linked immunosorbent assay (ELISA). RESULTS: A cohort of 636 patients undergoing laparoscopic vertical banded gastroplasty (LVBG) or Roux-en-Y gastric bypass (LRYGBP) was recruited. The seropositivity of H. pylori in symptomatic and asymptomatic patients after surgery was 39% (32/82) and 39.7% (220/554) respectively. Endoscopic examinations revealed that 22 (26.8%) of 82 symptomatic patients had a gastric ulcer. Comparison of demographic characteristics between patients with ulcer (n=22) and patients without ulcer (n=60) showed no difference in distribution of gender, age, BMI, and seroprevalence of H. pylori (27.3%, 6/22 vs 43.3%, 26/60, P=0.212). Patients undergoing LRYGBP showed a higher rate of gastric ulcer (45.5%, 10/22) when compared to patients undergoing LVBG (20%, 12/60; P=0.027). CONCLUSION: Gastric ulcers in symptomatic patients following laparoscopic bariatric surgery are related to surgical procedures rather than exposure to H. pylori infection.
Adult↗
Spectrum of endoscopic findings and therapy in patients with upper gastrointestinal symptoms after laparoscopic bariatric surgery.
BACKGROUND: More should be known about the spectrum of endoscopic abnormalities and treatments in patients with upper gastrointestinal (UGI) symptoms after laparoscopic bariatric surgery. METHODS: Patients referred for endoscopic evaluation of UGI symptoms after laparoscopic bariatric surgery were studied. Clinical manifestations, endoscopic findings and therapy were recorded and correlated. RESULTS: 76 patients who had undergone laparoscopic vertical banded gastroplasty (LVBG) and 28 who had undergone laparoscopic Roux-en-Y gastric bypass (LRYGBP) underwent 160 instances of upper endoscopy. The symptoms included nausea or vomiting (n=47, 29.4%), epigastric discomfort (n=44, 27.5%), UGI bleeding (n=26, 16.3%), heartburn or acid regurgitation (n=26, 16.3%), dysphagia (n=10, 6.3%) and anemia with dizziness (n=7, 4.4%). The endoscopic diagnosis consisted of normal findings (n=57, 35.6%), marginal ulcer (n=39, 24.4%), erosive esophagitis or esophageal ulcer (n=21, 13.1%), food impaction (n=21, 13.1%), stenosis or stricture (n=14, 8.8%), gastric ulcer (n=7, 4.4%), and duodenal ulcer (n=1, 0.6%). Patients with UGI bleeding, dysphagia and LRYGBP tended to have endoscopic abnormalities (P<0.001, P=0.09 and P=0.021, respectively). Endoscopic therapy was successful in resolving the complications including stenosis, UGI bleeding and food impaction. CONCLUSIONS: Endoscopy is an essential method of combining relevant endoscopic findings and therapeutic intervention in symptomatic patients following laparoscopic bariatric surgery.
Adult↗
Multistate and multifactorial progression of gastric cancer: results from community-based mass screening for gastric cancer.
Although multistate progression models for gastric cancer have been proposed, estimation of quantitative parameters of such models is yet to be done. The present study was conducted to elucidate risk factors for gastric cancer and its precursors, and to model the progression rates from superficial gastritis to gastric cancer. Data were derived from a community-based screening programme for gastric cancer in the Matzu region of Taiwan. A total of 2184 residents participated in a two-stage screening project. Subjects testing positive for Helicobacter pylori infection or pepsinogen (PGI or PII/PGII ratio) and immunoglobulin G (IgG), and subjects with a history of peptic ulcer or other upper gastrointestinal disease or with a family history of gastric cancer were referred to endoscopy. We identified 325 biopsy-proven precursors and gastric cancers, including 148 superficial gastritis (SG), 42 atrophic gastritis (AG), 117 intestinal metaplasia (IM) and two gastric cancers. Three further cancers were diagnosed on endoscopy alone and 14 were later diagnosed in those who did not comply with referral to endoscopy. A Markov process model was used to estimate the progression rates from superficial gastritis through to gastric cancer, with exponential regression to assess the effect of covariates on progression rates. The annual progression rate from SG to AG was 0.0670 (95% confidence interval [CI] 0.0446-0.0895). Annual progression rates from AG to IM and from IM to gastric cancer were 0.2775 (0.1665-0.3884) and 0.2265 (0.1315-0.3214), respectively. This gives average dwelling times in AG and IM of 3.60 years and 4.42 years, respectively. Progression from no disease to SG was significantly accelerated in those testing positive for H. pylori, those testing positive for PGI and in subjects with a family history of gastric cancer or a personal history of upper gastrointestinal disease. Further progression to AG and IM was significantly accelerated in those testing positive for PGI and in those with a history of upper gastrointestinal disease.
Adult↗
Gene expression profiling of gastric cancer by microarray combined with laser capture microdissection.
AIM: To examine the gene expression profile of gastric cancer (GC) by combination of laser capture microdissection (LCM) and microarray and to correlate the profiling with histological subtypes. METHODS: Using LCM, pure cancer cells were procured from 45 cancerous tissues. After procurement of about 5000 cells, total RNA was extracted and the quality of RNA was determined before further amplification and hybridization. One microgram of amplified RNA was converted to cDNA and hybridized to cDNA microarray. RESULTS: Among 45 cases, only 21 were qualified for their RNAs. A total of 62 arrays were performed. These included 42 arrays for cancer (21 cases with dye-swab duplication) and 20 arrays for non-tumorous cells (10 cases with dye-swab duplication) with universal reference. Analyzed data showed 504 genes were differentially expressed and could distinguish cancerous and non-cancerous groups with more than 99% accuracy. Of the 504 genes, trefoil factors 1, 2, and 3 were in the list and their expression patterns were consistent with previous reports. Immunohistochemical staining of trefoil factor 1 was also consistent with the array data. Analyses of the tumor group with these 504 genes showed that there were 3 subgroups of GC that did not correspond to any current classification system, including Lauren's classification. CONCLUSION: By using LCM, linear amplification of RNA, and cDNA microarray, we have identified a panel of genes that have the power to discriminate between GC and non-cancer groups. The new molecular classification and the identified novel genes in gastric carcinogenesis deserve further investigations to elucidate their clinicopathological significance.
Gene Expression Profiling↗
Helicobacter pylori-Induced invasion and angiogenesis of gastric cells is mediated by cyclooxygenase-2 induction through TLR2/TLR9 and promoter regulation.
Cyclooxygenase-2 (COX-2) plays a crucial role in Helicobacter pylori-associated gastric cancer. In this study, we report that H. pylori-induced COX-2 expression enhances the cancer cell invasion and angiogenesis via TLR2 and TLR9, which can be attenuated by the specific COX-2 inhibitor NS398 or celecoxib. The cAMP response element (CRE) and AP1 sites, but not kappaB on the COX-2 promoter, are involved in MAPKs-regulated COX-2 expression. Differential bindings of the CREB-1, ATF-2, c-jun to the CRE site, and the c-fos, c-jun, ATF-2 to the AP1 site are demonstrated by DNA affinity protein-binding, supershift, and chromatin immunoprecipitation assays. Activations of these transcription factors were attenuated by different MAPKs inhibitors. The mutants of TLR2, TLR9, or MAPKs inhibited H. pylori-induced COX-2 promoter, CRE, and AP-1 activities. MAPKs inhibitors attenuated the H. pylori-induced COX-2 mRNA and protein expressions. These results indicate that H. pylori acts through TLR2 and TLR9 to activate MAPKs, especially p38, and their downstream transcription factors (CREB-1, ATF-2, c-jun, and c-fos), resulting in the activations of CRE and AP-1 on the COX-2 promoter. These intracellular networks drive the COX-2-dependent PGE2 release and contribute to cell invasion and angiogenesis.
Cell Line, Tumor↗
Long-term results of anti-Helicobacter pylori therapy in early-stage gastric high-grade transformed MALT lymphoma.
BACKGROUND: Several independent clinical studies have reported that Helicobacter pylori eradication therapy could achieve complete remission in some patients with H. pylori-positive early-stage gastric mucosa-associated lymphoid tissue (MALT) lymphoma. METHODS: To compare the long-term results of anti-H. pylori therapy in early-stage, gastric low-grade and high-grade transformed MALT lymphoma, two multicenter prospective studies of anti-H. pylori therapy for early-stage gastric lymphoma conducted in Taiwan, one for low-grade MALT lymphoma, with 34 patients enrolled from March 1996 through April 1999, and one for high-grade transformed tumors (diffuse large B-cell lymphoma with features of MALT, DLBCL[MALT] lymphoma), with 24 patients enrolled since June 1995, were directly compared. In both studies, patients generally received 2 weeks of antibiotics and had multiple sequential follow-up endoscopic examinations until complete histologic remission (CR) or disease progression; patients were monitored through January 31, 2004. CR was defined as regression of lymphoid infiltration to Wotherspoon's score of 2 or less on all pathologic sections of endoscopic biopsy specimens. All statistical tests were two-sided. RESULTS: The H. pylori-positive rate among the 34 low-grade patients was 94% (32 of 34). All 24 selected high-grade patients were H. pylori positive. H. pylori was eradicated in 97% (30 of 31) of evaluable H. pylori-positive low-grade patients and in 92% (22 of 24) of high-grade patients, which led to CR in 80% (24 of 30, 95% confidence interval [CI] = 65% to 95%) and 64% (14 of 22, 95% CI = 42% to 86%) of patients, respectively. None of the five patients who were either initially H. pylori negative or had persistent H. pylori infection after antibiotics achieved CR. After median follow-up of more than 5 years in complete responders, tumor recurrence was observed in three (13%) low-grade patients but not in high-grade patients. CONCLUSIONS: Anti-H. pylori therapy may be considered as one of the treatment options for early-stage H. pylori-positive gastric DLBCL(MALT), and large-scale prospective studies to validate its use as first-line therapy for such tumors should be undertaken.
Adult↗
Expression of CD86 and increased infiltration of NK cells are associated with Helicobacter pylori-dependent state of early stage high-grade gastric MALT lymphoma.
AIM: A high percentage of early-stage high-grade gastric mucosa-associated lymphoid tissue (MALT) lymphomas remain Helicobacter pylori (H pylori)-dependent. However, unlike their low-grade counterparts, high-grade gastric MALT lymphomas may progress rapidly if unresponsive to H pylori eradication. It is mandatory to identify markers that may predict the H pylori-dependent status of these tumors. Proliferation of MALT lymphoma cells depends on cognate help and cell-to-cell contact of H pylori-specific intratumoral T-cells. To examine whether the expression of co-stimulatory marker CD86 (B7.2) and the infiltration of CD56 (+) natural killer (NK) cells can be useful markers to predict H pylori-dependent status of high-grade gastric MALT lymphoma. METHODS: Lymphoma biopsies from 26 patients who had participated in a prospective study of H pylori-eradication for stage I(E) high-grade gastric MALT lymphomas were evaluated. Tumors that resolved to Wotherspoon grade II or less after H pylori eradication were classified as H pylori-dependent; others were classified as H pylori-independent. The infiltration of NK cells and the expression of CD86 in pre-treatment paraffin-embedded lymphoma tissues were determined by immunohistochemistry. RESULTS: There were 16 H pylori-dependent and 10 H pylori-independent cases. CD86 expression was detected in 11 (68.8%) of 16 H pylori-dependent cases but in none of 10 H pylori-independent cases (P = 0.001). H pylori-dependent high-grade gastric MALT lymphomas contained significantly higher numbers of CD56 (+) NK cells than H pylori-independent cases (2.8+/-1.4% vs 1.1+/-0.8%; P = 0.003). CD86 positive MALT lymphomas also showed significantly increased infiltration of CD56 (+) NK cells compared to CD86-negative cases (2.9+/-1.1% vs 1.4+/-1.3%; P = 0.005). CONCLUSION: These results suggest that the expression of co-stimulatory marker CD86 and the increased infiltration of NK cells are associated with H pylori-dependent state of early-stage high-grade gastric MALT lymphomas.
Adult↗
A case-control study of association of Helicobacter pylori infection with morbid obesity in Taiwan.
BACKGROUND: Obesity is an increasing health problem in developed countries, where the prevalence of Helicobacter pylori infection is decreasing. Recent studies suggested colonization of the stomach by H pylori might affect gastric expression of appetite- and satiety-related hormone and patients cured of H pylori infection gained weight. It was hypothesized that H pylori could be a contributing pathogenic factor in childhood and adult obesity. METHODS: To determine whether H pylori infection is linked to obesity, a case-control study composed of 414 patients with morbid obesity (a body mass index [calculated as weight in kilograms divided by the square of height in meters] of > or = 35 with serious comorbidity or a body mass index of > or = 40) and 683 control subjects (a body mass index of <25) with a comparable socioeconomic status was conducted. Immunoglobulin G antibodies against H pylori were measured from frozen serum samples by an enzyme-linked immunosorbent assay. Logistic regression was used to calculate the odds ratio (OR) and 95% confidence interval (CI). RESULTS: The overall seropositivity was significantly lower in obese patients (181 [43.7%] of 414) than controls (410 [60.0%] of 683) (OR, 0.50; 95% CI, 0.39-0.65; P<.001). Differences in the estimated risk of the presence of H pylori were more pronounced in younger age groups, with ORs of 0.32 (95% CI, 0.10-1.00; P = .05) in those aged 10 to 19 years, 0.55 (95% CI, 0.34-0.89; P = .01) in those aged 20 to 29 years, 0.49 (95% CI, 0.30-0.80; P = .007) in those aged 30 to 39 years, and 0.58 (95% CI, 0.33-1.00; P = .05) in those aged 40 years or older. CONCLUSIONS: Our data indicated an inverse relationship between morbid obesity and H pylori seropositivity. These findings raise the hypothesis that a lack of H pylori infection, especially during childhood, might enhance the risk of the development of morbid obesity.
Adult↗
Expression of macrophage migration inhibitory factor is associated with enhanced angiogenesis and advanced stage in gastric carcinomas.
AIM: Macrophage migration inhibitory factor (MIF) was reported to inactivate p53 and play an essential role in the growth and angiogenesis of tumors that arise at sites of chronic inflammation. Gastric inflammation is a prerequisite for the development of gastric carcinoma (GC), which has recently been linked to Helicobacter pylori (H pylori) infection. This study aimed to investigate clinicopathological significance of MIF expression in GCs. METHODS: We selected 90 consecutive patients with GCs for investigation of the relation among MIF status, clinicopathological parameters, p53 expression and angiogenesis. MIF and p53 expression was assessed by immunohistochemistry as positive and negative groups. Tumor vascularity was evaluated by counting microvessel density on anti-CD34 stained sections. Expression status of MIF was correlated with determined clinicopathological data, p53 immunoreactivity and microvessel counts. RESULTS: Strong immunostainings of MIF were observed in the cytoplasm of cancerous cells in 40% (36/90) of cases but not in normal or metaplastic epithelia. There was no statistically significant correlation between MIF expression and age, gender, H pylori infection, tumor location, histological subtypes, lymph node metastasis or p53 expression. Early GC less frequently overexpressed MIF as compared to advanced GCs (4/20 vs 32/70, P = 0.04). A remarkably increased microvessel count was noted in GCs with MIF expression than those without MIF expression (55.1+/-30.1 vs 31.3+/-28.8, P = 0.0001). CONCLUSION: Our results suggest that expression of MIF may contribute to the progression and enhanced angiogenesis in a substantial portion of GCs.
Adult↗
Helicobacter pylori promote gastric cancer cells invasion through a NF-kappaB and COX-2-mediated pathway.
AIM: To examine the effects of Helicobacter pylori (H pylori) infection on the invasiveness of gastric cancer cells, and to elucidate its mechanism. METHODS: Gastric carcinoma cells, MKN-45, were incubated with CagA-positive H pylori, and cell invasion was determined by Matrigel analysis. The expression of matrix metalloproteinase-9 (MMP-9), vascular endothelial growth factor (VEGF), and cyclooxygenase-2 (COX-2) were assessed by Western-blot analysis, and transcriptional activation of the COX-2 promoter was examined by measuring luciferase and beta-galactosidase activities. Lastly, the protein-DNA interaction was confirmed by an electrophoretic mobility shift assay. RESULTS: The current studies showed that: (1) incubation of CagA-positive H pylori with MKN-45 cells significantly promotes gastric cancer cells invasion, and this effect is attenuated by pre-treatment with NS-398, a COX-2 inhibitor, or PDTC, a nuclear factor kappaB (NF-kappaB) inhibitor; (2) the induction of MKN-45 cells invasion by H pylori is associated with increases in COX-2, MMP-9, and VEGF protein expression, and co-incubation of NS-398 or PDTC significantly reduces these effects; (3) H pylori infection transactivates COX-2 promoter activity and increases the binding of NF-kappaB to this promoter. CONCLUSION: Our data demonstrate that H pylori infection promotes gastric epithelial cells invasion by activating MMP-9 and VEGF expression. These effects appear to be mediated through a NF-kappaB and COX-2 mediated pathway, as COX-2 or NF-kappaB inhibitor significantly attenuate the invasiveness of gastric cancer cells and the expressions of MMP-9 and VEGF protein.
Cell Line, Tumor↗
Typhlitis associated with Candida albicans and Pseudomonas aeruginosa infection in a patient with herbal drug-induced neutropenia.
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Aged↗