Surgery for Peptic Ulcer in the Helicobacter pylori Era

OPERATIONS currently performed for peptic ulcer disease were designed prior to the identification of Helicobacter pylori as a major cofactor in ulcerogenesis. These operations decrease gastric acid secretion by eliminating vagal stimulation and gastrin production and/or by diminishing the parietal cell mass. The complications and ulcer recurrence rates for each antiulcer operation can be recited by most surgical residents. Most of these data were collected prior to the widespread use of fiberoptic endoscopy and therefore probably represent modest estimates.1 Prospective trials with almost complete endoscopic follow-up have identified ulcer recurrences in 30% to 95% of patients medically treated for peptic ulcer.2,3 Few, if any, patient populations have been systematically screened by endoscopy for recurrent ulcer after surgical therapy for peptic ulcer. In fact, most surgical series have used endoscopic follow-up only in patients with hematemesis, perforation, or persistent, severe dyspepsia.4,5Helicobacter pylori infection of the gastric mucos

Neutrophil recruitment to the gastrointestinal tract

The infiltration of an organ or tissue by neutrophils is the hallmark of acute inflammation. Recent work from many laboratories suggests that neutrophils may play a role in the development of tissue injury in a variety of disease states in the gastrointestinal tract. These diseases include gastritis, necrotizing enterocolitis, ileitis, ulcerative colitis, and ischemia reperfusion injuries. In view of this recent interest in the neutrophil and its relationship to GI diseases, it seems timely to review what is known about neutrophil recruitment to the gastrointestinal tract. This review will therefore focus on the sojourn of the neutrophil from the circulation to its destination in the GI tract

Editorial: Anti-infectives: Helicobacter pylori and peptic ulcer disease: Recent developments

In this day and age, it is rare to discover a medical breakthrough which defies decades of medical dogma. The concept of bacterial infection causing peptic ulcer represents such an event. After an explosion of scientific research during the 1980s, the 'ulcer causing bacteria' made it to popular news-stand magazines during the 1990s. Over this time span, Helicobacter pylori underwent two name changes, from Campylobacter pyloridis to Campylobacter pylori to its current moniker. This review covers our current understanding of the pathophysiology, diagnosis and treatment of Helicobacter pylori-associated gastroduodenal inflammatory states

Frank Hastings Hamilton: Medical educator and surgeon to president Garfield

Frank Hastings Hamilton was a pioneer in academic surgery. His career involved the development of several medical schools. At the request of Mrs. Garfield, Hamilton was consulted after the shooting of President James Garfield. Surgical thinking at that time did not favor operation for gunshot wounds. Garfield's death reflected the lack of understanding in trauma care during that era. Hamilton's many contributions to medical education shall be remembered

Prenatal Neuropathologies in Autism Spectrum Disorder and Intellectual Disability: The Gestation of a Comprehensive Zebrafish Model

Autism spectrum disorder (ASD) and intellectual disability (ID) are neurodevelopmental disorders with overlapping diagnostic behaviors and risk factors. These include embryonic exposure to teratogens and mutations in genes that have important functions prenatally. Animal models, including rodents and zebrafish, have been essential in delineating mechanisms of neuropathology and identifying developmental critical periods, when those mechanisms are most sensitive to disruption. This review focuses on how the developmentally accessible zebrafish is contributing to our understanding of prenatal pathologies that set the stage for later ASD-ID behavioral deficits. We discuss the known factors that contribute prenatally to ASD-ID and the recent use of zebrafish to model deficits in brain morphogenesis and circuit development. We conclude by suggesting that a future challenge in zebrafish ASD-ID modeling will be to bridge prenatal anatomical and physiological pathologies to behavioral deficits later in life

Drugs prescribed for Phelan-McDermid syndrome differentially impact sensory behaviors in shank3 zebrafish models. [version 1; peer review: 1 approved with reservations]

Background: Altered sensory processing is a pervasive symptom in individuals with Autism Spectrum Disorders (ASD); people with Phelan McDermid syndrome (PMS), in particular, show reduced responses to sensory stimuli. PMS is caused by deletions of the terminal end of chromosome 22 or point mutations in Shank3. People with PMS can present with an array of symptoms including ASD, epilepsy, gastrointestinal distress, and reduced responses to sensory stimuli. People with PMS are often medicated to manage behaviors like aggression and/or self-harm and/or epilepsy, and it remains unclear how these medications might impact perception/sensory processing. Here we test this using zebrafish mutant shank3ab PMS models that likewise show reduced sensory responses in a visual motor response (VMR) assay, in which increased locomotion is triggered by light to dark transitions. Methods: We screened three medications, risperidone, lithium chloride (LiCl), and carbamazepine (CBZ), prescribed to people with PMS and one drug, 2-methyl-6-(phenylethynyl) pyridine (MPEP) tested in rodent models of PMS, for their effects on a sensory-induced behavior in two zebrafish PMS models with frameshift mutations in either the N- or C- termini. To test how pharmacological treatments affect the VMR, we exposed larvae to selected drugs for 24 hours and then quantified their locomotion during four ten-minute cycles of lights on-to-off stimuli. Results: We found that risperidone normalized the VMR in shank3 models. LiCl and CBZ had no effect on the VMR in any of the three genotypes. MPEP reduced the VMR in wildtype (WT) to levels seen in shank3 models but caused no changes in either shank3 model. Finally, shank3 mutants showed resistance to the seizure-inducing drug pentylenetetrazol (PTZ), at a dosage that results in hyperactive swimming in WT zebrafish. Conclusions: Our work shows that the effects of drugs on sensory processing are varied in ways that can be highly genotype- and drug-dependent