Mirizzi syndrome type V complicated with both cholecystobiliary and cholecystocolic fistula: a case report.

Mirizzi syndrome (MS) is a common bile duct (CBD) obstruction caused by extrinsic compression from an impacted stone in the cystic duct or infundibulum of the gallbladder. Patients affected by MS may present abdominal pain and jaundice. A 37-year-old male with neurologic residuals post-encephalitis arrived at the emergency department reporting abdominal pain, jaundice and fever.

Endoscopic Treatment of Iatrogenic Perforation of Sigmoid Diverticulum: A Case Report of Multidisciplinary Management.

Iatrogenic perforations are severe complications of gastrointestinal endoscopy; therefore, their management should be adequately planned. A 77-year-old man with a history of diverticulosis underwent a colonoscopy for anemia. During the procedure, an iatrogenic perforation occurred suddenly in the sigmoid colon, near a severe angle among the numerous diverticula.

Mirizzi syndrome in a patient with partial gastrectomy with Billroth II anastomosis: A case report.

Introduction: Mirizzi Syndrome (MS) is a common bile duct (CBD) obstruction caused by extrinsic compression from an impacted stone in the cystic duct or infundibulum of the gallbladder. Radiological evaluation may mistake it for CBD stones in jaundiced patient, especially in those who have altered anatomy of upper gastrointestinal (e.g.

Retrospective analysis of management of ingested foreign bodies and food impactions in emergency endoscopic setting in adults.

Background: Ingestion of foreign bodies and food impaction represent the second most common endoscopic emergency after bleeding. The aim of this paper is to report the management and the outcomes in 67 patients admitted for suspected ingestion of foreign body between December 2012 and December 2014.

Methods: This retrospective study was conducted at Palermo University Hospitals, Italy, over a 2-year period.

Stump appendicitis. A case report.

Introduction: Today, the diagnosis of SA is usually not considered as the etiology for right lower quadrant pain in patient with history of appendectomy, resulting in delaying making the correct diagnosis and treatment. Obviously, other more common causes should be excluded first.

Discussion: Stump appendicitis (SA) was first described by Rose in 1945.

Detection of amyloid plaques in mouse models of Alzheimer's disease by magnetic resonance imaging.

We performed three-dimensional, high-resolution magnetic resonance imaging (MRI) of fixed mouse brains to determine whether MRI can detect amyloid plaques in transgenic mouse models of Alzheimer's disease. Plaque-like structures in the cortex and hippocampus could be clearly identified in T2-weighted images with an image resolution of 46 microm x 72 microm x 72 microm. The locations of plaques were confirmed in coregistration studies comparing MR images with Congo red-stained histological results.

Intracranially administered anti-Abeta antibodies reduce beta-amyloid deposition by mechanisms both independent of and associated with microglial activation.

Active immunization against the beta-amyloid peptide (Alphabeta) with vaccines or passive immunization with systemic monoclonal anti-Abeta antibodies reduces amyloid deposition and improves cognition in APP transgenic mice. In this report, intracranial administration of anti-Alphabeta antibodies into frontal cortex and hippocampus of Tg2576 transgenic APP mice is described. The antibody injection resulted initially in a broad distribution of staining for the antibody, which diminished over 7 d.

Increased fibrillar beta-amyloid in response to human clq injections into hippocampus and cortex of APP+PS1 transgenic mice.

Human C1q when injected directly into hippocampus and cortex of doubly transgenic APP+PS1 mice results in the increase of Congo red-positive fibrillar deposits. Although there was no significant change in overall area stained for Abeta total, qualitatively it appeared that there was less diffuse Abeta in C1q-treated mice versus vehicle. There was no apparent change in astroglial or microglial activation caused by injection of C1q with respect to vehicle injections.

Microglial activation and beta -amyloid deposit reduction caused by a nitric oxide-releasing nonsteroidal anti-inflammatory drug in amyloid precursor protein plus presenilin-1 transgenic mice.

3-4-(2-Fluoro-alpha-methyl-[1,1'-biphenyl]-4-acetyloxy)-3-methoxyphenyl]-2-propenoic acid 4-nitrooxy butyl ester (NCX-2216), a nitric oxide (NO)-releasing derivative of the cyclooxygenase-1-preferring nonsteroidal anti-inflammatory drug (NSAID) flurbiprofen, dramatically reduced both beta-amyloid (Abeta) loads and Congo red staining in doubly transgenic (Tg) amyloid precursor protein plus presenilin-1 mice when administered at 375 ppm in diet between 7 and 12 months of age. This reduction was associated with a dramatic increase in the number of microglia expressing major histocompatibility complex-II antigen, a marker for microglial activation. In contrast, ibuprofen at 375 ppm in diet caused modest reductions in Abeta load but not Congo red staining, suggesting that the effects of this nonselective NSAID were restricted primarily to nonfibrillar deposits.

Time course of the development of Alzheimer-like pathology in the doubly transgenic PS1+APP mouse.

Doubly transgenic mice expressing both a mutated amyloid precursor protein and a mutated presenilin-1 protein accumulate A(beta) deposits as they age. The early A(beta) deposits were found to be primarily composed of fibrillar A(beta) and resembled compact amyloid plaques. As the mice aged, nonfibrillar A(beta) deposits increased in number and spread to regions not typically associated with amyloid plaques in Alzheimer's disease.