H. A. Fennerty, O. T. Harrington to Mississippi Alpha Phi Delta Theta Fraternity, 25 September 1962

Fraternity members in Louisiana urge the Mississipi chapter to rush James Meredith. They cite several reasons and feel [he] will be compatible with members of Mississippi Alpha whom [they] have met.https://egrove.olemiss.edu/west_union_um/1059/thumbnail.jp

Rapid Development of Intestinal Type Gastric Adenocarcinoma

Intestinal type gastric adenocarcinoma is felt to develop over a protracted time period through a series of defined steps. Several potential risk factors for the development of gastric cancer have been identified, including a family history of gastric cancer and Helicobacter pylori infection. We present the case of a patient with neither risk factor who progressed in a 14 month time frame from histologically normal gastric mucosa to early stage intestinal type gastric adenocarcinoma in the setting of diffuse gastric intestinal metaplasia and atrophic gastritis. This patient's presentation conflicts with our current understanding of the development of intestinal type gastric adenocarcinoma

The diagnostic value of endoscopy and Helicobacter pylori tests for peptic ulcer patients in late post-treatment setting

BACKGROUND: Guidelines for management of peptic ulcer patients after the treatment are largely directed to detection of H. pylori infection using only non-invasive tests. We compared the diagnostic value of non-invasive and endoscopy based H. pylori tests in a late post-treatment setting. METHODS: Altogether 34 patients with dyspeptic complaints were referred for gastroscopy 5 years after the treatment of peptic ulcer using a one-week triple therapy scheme. The endoscopic and histologic findings were evaluated according to the Sydney classification. Bacteriological, PCR and cytological investigations and (13)C-UBT tests were performed. RESULTS: Seventeen patients were defined H. pylori positive by (13)C-UBT test, PCR and histological examination. On endoscopy, peptic ulcer persisted in 4 H. pylori positive cases. Among the 6 cases with erosions of the gastric mucosa, only two patients were H. pylori positive. Mucosal atrophy and intestinal metaplasia were revealed both in the H. pylori positive and H. pylori negative cases. Bacteriological examination revealed three clarithromycin resistant H. pylori strains. Cytology failed to prove validity for diagnosing H. pylori in a post-treatment setting. CONCLUSIONS: In a late post-treatment setting, patients with dyspepsia should not be monitored only by non-invasive investigation methods; it is also justified to use the classical histological evaluation of H. pylori colonisation, PCR and bacteriology as they have shown good concordance with (13)C-UBT. Moreover, endoscopy and histological investigation of a gastric biopsy have proved to be the methods with an additional diagnostic value, providing the physician with information about inflammatory, atrophic and metaplastic lesions of the stomach in dyspeptic H. pylori positive and negative patients. Bacteriological methods are suggested for detecting the putative antimicrobial resistance of H. pylori, aimed at successful eradication of infection in persistent peptic ulcer cases

Esophagitis in a High H. pylori Prevalence Area: Severe Disease Is Rare but Concomitant Peptic Ulcer Is Frequent

Background: Few data are available on the prevalence of erosive and severe esophagitis in Western countries. Objective: To retrospectively determine the prevalence and the factors predicting erosive esophagitis and severe esophagitis in a large series of endoscopies in Spain. Design: Retrospective observational study. A multivariate analysis was performed to determine variables predicting severe esophagitis. Setting: Databases of 29 Spanish endoscopy units. Patients: Patients submitted to a diagnostic endoscopy during the year 2005. Interventions: Retrospective review of the databases. Main Outcome Measurements: Esophagitis severity (graded according to the Los Angeles classification) and associated endoscopic findings. Results: Esophagitis was observed in 8.7% of the 93,699 endoscopies reviewed. Severe esophagitis (LA grade C or D) accounted for 22.5% of cases of the disease and was found in 1.9% of all endoscopies. Incidences of esophagitis and those of severe esophagitis were 86.2 and 18.7 cases per 100,000 inhabitants per year respectively. Male sex (OR 1.89) and advanced age (OR 4.2 for patients in the fourth age quartile) were the only variables associated with severe esophagitis. Associated peptic ulcer was present in 8.8% of cases. Limitations: Retrospective study, no data on individual proton pump inhibitors use. Conclusions: Severe esophagitis is an infrequent finding in Spain. It occurs predominantly in males and in older individuals. Peptic ulcer disease is frequently associated with erosive esophagitis

Prevalence of non Helicobacter pylori species in patients presenting with dyspepsia

<p>Abstract</p> <p>Background</p> <p>Helicobacter species associated with human infection include <it>Helicobacter pylori, Helicobacter heilmannii </it>and <it>Helicobacter felis </it>among others. In this study we determined the prevalence of <it>H. pylori </it>and non-<it>Helicobacter pylori </it>organisms <it>H. felis and H. heilmannii </it>and analyzed the association between coinfection with these organisms and gastric pathology in patients presenting with dyspepsia. Biopsy specimens were obtained from patients with dyspepsia on esophagogastroduodenoscopy (EGD) for rapid urease test, histology and PCR examination for Helicobacter genus specific 16S rDNA, <it>H. pylori </it>phosphoglucosamine mutase (<it>glmM</it>) and urease B (<it>ureB</it>) gene of <it>H. heilmannii </it>and <it>H. felis</it>. Sequencing of PCR products of <it>H. heilmannii </it>and <it>H. felis </it>was done.</p> <p>Results</p> <p>Two hundred-fifty patients with dyspepsia were enrolled in the study. The mean age was 39 ± 12 years with males 162(65%). Twenty-six percent (66 out of 250) were exposed to cats or dogs. PCR for Helicobacter genus specific 16S rDNA was positive in 167/250 (67%), <it>H. pylori glmM </it>in 142/250 (57%), <it>H. heilmannii </it>in 17/250 (6%) and <it>H. felis </it>in 10/250 (4%), respectively. All the <it>H. heilmannii </it>and <it>H. felis </it>PCR positive patients were also positive for <it>H. pylori </it>PCR amplification. The occurrence of coinfection of <it>H. pylori </it>and <it>H. heilmannii </it>was 17(6%) and with <it>H. felis </it>was 10(4%), respectively. Only one out of 66 exposed to pets were positive for <it>H. heilmannii </it>and two for <it>H. felis</it>. Histopathology was carried out in 160(64%) of 250 cases. Chronic active inflammation was observed in 53(56%) (p = 0.001) of the patients with <it>H. pylori </it>infection alone as compared to 3(37%) (p = 0.73) coinfected with <it>H. heilmannii </it>and <it>H. pylori </it>and 3(60%) coinfected with <it>H. felis </it>and <it>H. pylori </it>(p = 0.66). Intestinal metaplasia was observed in 3(3%)(p = 1.0) of the patients with <it>H. pylori </it>infection alone as compared to 2(25%) (p = 0.02) coinfected with <it>H. heilmannii </it>and <it>H. pylori </it>and 1(20%) coinfected with <it>H. felis </it>and <it>H. pylori </it>(p = 0.15).</p> <p>Conclusion</p> <p>The prevalence of <it>H. heilmannii </it>and <it>H. felis </it>was low in our patients with dyspepsia. Exposure to pets did not increase the risk of <it>H. heilmannii </it>or <it>H. felis </it>infection. The coinfection of <it>H. pylori </it>with <it>H. heilmannii </it>was seen associated with intestinal metaplasia, however this need further confirmation.</p

Primary uncleansed 2D versus primary electronically cleansed 3D in limited bowel preparation CT-colonography. Is there a difference for novices and experienced readers?

The purpose of this study was to compare a primary uncleansed 2D and a primary electronically cleansed 3D reading strategy in CTC in limited prepped patients. Seventy-two patients received a low-fibre diet with oral iodine before CT-colonography. Six novices and two experienced observers reviewed both cleansed and uncleansed examinations in randomized order. Mean per-polyp sensitivity was compared between the methods by using generalized estimating equations. Mean per-patient sensitivity, and specificity were compared using the McNemar test. Results were stratified for experience (experienced observers versus novice observers). Mean per-polyp sensitivity for polyps 6 mm or larger was significantly higher for novices using cleansed 3D (65%; 95%CI 57–73%) compared with uncleansed 2D (51%; 95%CI 44–59%). For experienced observers there was no significant difference. Mean per-patient sensitivity for polyps 6 mm or larger was significantly higher for novices as well: respectively 75% (95%CI 70–80%) versus 64% (95%CI 59–70%). For experienced observers there was no statistically significant difference. Specificity for both novices and experienced observers was not significantly different. For novices primary electronically cleansed 3D is better for polyp detection than primary uncleansed 2D

A systematic review of the safety of topical therapies for atopic dermatitis

Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/75613/1/j.1365-2133.2006.07538.x.pd

NSAIDs Modulate CDKN2A, TP53, and DNA Content Risk for Progression to Esophageal Adenocarcinoma

BACKGROUND: Somatic genetic CDKN2A, TP53, and DNA content abnormalities are common in many human cancers and their precursors, including esophageal adenocarcinoma (EA) and Barrett's esophagus (BE), conditions for which aspirin and other nonsteroidal anti-inflammatory drugs (NSAIDs) have been proposed as possible chemopreventive agents; however, little is known about the ability of a biomarker panel to predict progression to cancer nor how NSAID use may modulate progression. We aimed to evaluate somatic genetic abnormalities with NSAIDs as predictors of EA in a prospective cohort study of patients with BE. METHODS AND FINDINGS: Esophageal biopsies from 243 patients with BE were evaluated at baseline for TP53 and CDKN2A (p16) alterations, tetraploidy, and aneuploidy using sequencing; loss of heterozygosity (LOH); methylation-specific PCR; and flow cytometry. At 10 y, all abnormalities, except CDKN2A mutation and methylation, contributed to EA risk significantly by univariate analysis, ranging from 17p LOH (relative risk [RR] = 10.6; 95% confidence interval [CI] 5.2–21.3, p < 0.001) to 9p LOH (RR = 2.6; 95% CI 1.1–6.0, p = 0.03). A panel of abnormalities including 17p LOH, DNA content tetraploidy and aneuploidy, and 9p LOH was the best predictor of EA (RR = 38.7; 95% CI 10.8–138.5, p < 0.001). Patients with no baseline abnormality had a 12% 10-y cumulative EA incidence, whereas patients with 17p LOH, DNA content abnormalities, and 9p LOH had at least a 79.1% 10-y EA incidence. In patients with zero, one, two, or three baseline panel abnormalities, there was a significant trend toward EA risk reduction among NSAID users compared to nonusers (p = 0.01). The strongest protective effect was seen in participants with multiple genetic abnormalities, with NSAID nonusers having an observed 10-y EA risk of 79%, compared to 30% for NSAID users (p < 0.001). CONCLUSIONS: A combination of 17p LOH, 9p LOH, and DNA content abnormalities provided better EA risk prediction than any single TP53, CDKN2A, or DNA content lesion alone. NSAIDs are associated with reduced EA risk, especially in patients with multiple high-risk molecular abnormalities