Radiofrequency ablation for dysplasia in Barrett's esophagus restores ß-catenin activation within esophageal progenitor cells.

BACKGROUND AND AIMS: Endoscopic therapies for Barrett's esophagus (BE) associated dysplasia, particularly radiofrequency ablation (RFA), are popular alternatives to surgery. The effect of such therapies on dysplastic stem/progenitor cells (SPC) is unknown. Recent studies suggest that AKT phosphorylation of ß-Catenin occurs in SPCs and may be a marker of activated SPCs. We evaluate the effect of RFA in restoring AKT-mediated ß-Catenin signaling in regenerative epithelium. METHODS: Biopsies were taken from squamous, non-dysplastic BE, dysplastic BE and esophageal adenocarcinoma (EAC). Also, post-RFA, biopsies of endoscopically normal appearing neosquamous epithelium were taken at 3, 6, and 12 months after successful RFA. Immunohistochemistry and Western blot analysis was performed for Pß-Catenin(552) (Akt-mediated phosphorylation of ß-Catenin), Ki-67 and p53. RESULTS: There was no difference in Pß-Catenin552 in squamous, GERD, small bowel and non-dysplastic BE. There was a fivefold increase in Pß-Catenin(552) in dysplasia and EAC compared to non-dysplastic BE (P < 0.05). Also, there was a persistent threefold increase in Pß-Catenin(552) in neosquamous epithelium 3 months after RFA compared to native squamous epithelium (P < 0.05) that correlated with increased Ki-67. Six months after RFA, Pß-Catenin(552) and Ki-67 are similar to native squamous epithelium. CONCLUSIONS: Enhanced AKT-mediated ß-Catenin activation is seen in BE-associated carcinogenesis. Three months after RFA, squamous epithelial growth from SPC populations exhibited increased levels of Pß-Catenin(552). This epithelial response becomes quiescent at 6 months after RFA. These data suggest that elevated Pß-Catenin(552) after RFA denotes a repair response in the neosquamous epithelium 3 months post-RFA.

Depression in patients of myocardial infarction--a cross-sectional study in northern India.

OBJECTIVES: To assess the prevalence of major depressive disorder and subsyndromal depression in patients with first episode of myocardial infarction (MI) and to compare the socio-demographic, clinical and coronary risk factors in patients with and without depression. METHODS: Patients of acute MI (n = 101) attending OPD at 4 to 6 weeks after the index event were the subjects. Diagnoses of Major Depressive Disorder were established according to Diagnostic and Statistical Manual for Mental Disorders fourth edition Test Revision (DSN-IV-TR) criteria. Schedule for Affective Disorder and Schizophrenia changed version modified for Bipolar disorder (SADS-CB) was applied to detect cases with depressive symptoms not amounting to major depressive disorder (sub-syndromal). It was a single point cross sectional study. RESULTS: No depressive symptoms (Group-A) were found in 56 patients (55.4%). Major Depressive Disorder (Group-B) was found in 24 patients (23.8%) and subsyndromal symptoms (Group-C) in 21 patients (20.8%). Sociodemographic and clinical variables were similar amongst three groups except, more patients in Group-C were from nuclear family (p = 0.01) and were educated (p = 0.03). More patients in Group-B had hypertension (p = 0.001), diabetes (p = 0.03) or were overweight (p = 0.02) as compared to Group-A. Similarly higher number of Group-C patients had hypertension (p = 0.04), diabetes (p = 0.01) and were current smokers (p = 0.01) as compared to Group-A. CONCLUSION: Unrecognized and untreated major depressive disorder and sub-syndromal symptoms were frequent in patients of MI. Established coronary factors were more commonly present in these groups as compared to no depressive symptom group. This emphasizes the need for routine screening for depression in post MI phase in our population.