Marek's disease: resistance of Turkey herpesvirus-infected chicks against lethal JM-V agent.
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Biomedical subjects
Publications and source records attributed to R J Mason.
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Duodenogastric reflux has been implicated in the pathogenesis of complicated Barrett's esophagus and gastric ulceration. A group of 123 Barrett's patients were followed for a mean of 41 months; 9 (7%) developed gastric ulceration (GU). Of the Barrett's patients treated by antireflux surgery, 14% developed GU. We reviewed the gastric histology on 54 Barrett's patients (34 men, 20 women; average age 64 years) at presentation and classified the gastritis according to the Sydney system. A normal histologic pattern was present in seven patients; 15 patients had chronic pangastritis, 9 chronic antral gastritis, and 18 chronic gastritis of the corpus. Five patients had acute gastritis only, and in 74% there was reactive chronic gastritis. Of the patients with chronic gastritis, 45% (19 of 42) had histologic evidence of duodenogastric reflux, established by the bile reflux index. The presence of reactive chronic gastritis in Barrett's patients may have important pathophysiologic and therapeutic implications.
4-Aminopyridine (4-AP) was administered to two groups of patients with multiple sclerosis (MS). The first group consisted of 5 patients with labile visual symptoms, 2 of whom had arcuate scotomata. 4-AP improved visual performance of most patients in this group and reduced the size of scotomata. The second group consisted of 5 patients with the spinal form of MS who were in a stable state; in this group 4-AP had little effect clinically or on tests of visual function.
Gastroeosphageal reflux disease has been associated with long segments of Barrett's esophagus </=3 cm), but little is known about its association with shorter segments. The aim of this study was to evaluate anatomic and physiologic alterations of the cardia and esophageal exposure to gastric and duodenal juice in patients with short and long segments of Barrett's esophagus. Furthermore, these patients were compared to each other and to patients with erosive esophagitis and those with no mucosal injury. Two hundred sixty-two consecutive patients with foregut symptoms were divided into the following four groups based on endoscopic and histologic findings: group 1, no mucosal injury; group 2, erosive esophagitis; group 3, short-segment Barrett's esophagus; and group 4, long-segment Barrett's esophagus. Esophageal exposure time to acid and bilirubin, lower esophageal sphincter characteristics, and endoscopic anatomy of the cardia were compared between the groups. Patients with short-segment Barrett's esophagus had elevated esophageal acid and bilirubin exposure, decreased lower esophageal sphincter pressure and length, and a high incidence of hiatal hernia. These abnormalities were similar to those in patients with esophagitis and in general less profound than those found in patients with long-segment Barrett's esophagus. The length of intestinal metaplasia was higher in patients with a defective lower esophageal sphincter. Short-segment Barrett's esophagus is a complication of severe gastroesophageal reflux disease and is associated with the reflux of both gastric and duodenal juice similar to that seen in patients with long-segment Barrett's esophagus.
With the advent of laparoscopic surgery and the recognition that gastroesophageal reflux disease often requires lifelong medication, patients with normal resting sphincter characteristics are now being considered for surgery. The outcome of these patients after fundoplication is unknown and formed the basis of this study. The study population consisted of 123 patients undergoing laparoscopic Nissen fundoplication between 1992 and 1996. All patients had increased esophageal acid exposure on 24-hour esophageal pH monitoring. Patients were divided into those with a normal (n = 36) and those with a structurally defective (n = 87) lower esophageal sphincter (LES), based on LES resting pressure (normal >6 mm Hg), overall length (normal >2 cm), and abdominal length (normal >1 cm), and their outcomes were assessed. Each group was subsequently divided into patients presenting with a primary symptom that was "typical" (heartburn, regurgitation, or dysphagia) or "atypical" (gastric, respiratory, or chest pain) of gastro-esophageal reflux, and outcome was assessed. Median duration of follow-up was 18 months after surgery. Overall, laparoscopic fundoplication was successful in relieving symptoms of gastroesophageal reflux in 90% of patients. Patients with a typical primary symptom had an excellent outcome irrespective of the resting status of the LES (95% and 97%, respectively). Atypical primary symptoms were significantly more common in patients with a normal LES (29%) than in those with a structurally defective LES (10%; P <0.05), and these symptoms were less likely (50%) to be relieved by antireflux surgery. Laparoscopic antireflux surgery is highly successful and not dependent on the status of the resting LES in patients with increased esophageal acid exposure and primary symptoms "typical" of gastroesophageal reflux. Antireflux surgery should be applied cautiously in patients with atypical primary symptoms.
A structurally intact and competent lower esophageal sphincter in the experimental model shortens and becomes incompetent during gastric distention. The aim of this study was to evaluate postprandial reflux as an indirect measure of this volume-induced sphincter shortening and incompetency. Reflux (pH <4) in the 2-hour period following a meal was retrospectively analyzed from the 24-hour esophageal pH recordings of 94 healthy volunteers and 609 symptomatic patients. Forty-six percent of patients had pathologic postprandial reflux (>95th percentile of normal). The prevalence was lower in patients with a structurally intact compared to a defective lower esophageal sphincter (32% vs. 58%; P <0.001). Pathologic postprandial reflux was greater in patients with abnormal compared to normal findings on 24-hour pH study (76% vs. 21%; P <0.001). Patients with a normal 24-hour pH study and postprandial reflux had shorter sphincter lengths (2.33 vs. 2.82 cm; P <0.001) and lower pressures (10.78 vs. 14.24 mm Hg; P <0.005). A hiatal hernia increased the prevalence of postprandial reflux (P <0.001) in all patients (67% vs. 38%) and in the subgroup with a structurally intact sphincter (75% vs. 27%, P <0.001). Postprandial reflux is a dynamic indicator of sphincter competency, and increases as the structural sphincter characteristics deteriorate and is augmented by a hiatal hernia.
Tumor necrosis factor (TNF)-alpha, a cytokine present in inflammed lungs, is known to mediate some of the adverse effects of ozone and inhaled particles. The authors evaluated transgenic mice with constitutive pulmonary expression of TNF-alpha under transcriptional regulation of the surfactant protein-C promoter as an animal model of biological susceptibility to air pollutants. To simulate a repeated, episodic exposure to air pollutants, wild-type and TNF mice inhaled air or a mixture of ozone (0.4 ppm) and urban particles (EHC-93, 4.8 mg/m3) for 4 h, once per week, for 12 consecutive weeks and were sacrificed 20 h after last exposure. TNF mice exhibited chronic lung inflammation with septal thickening, alveolar enlargement, and elevated protein and cellularity in bronchoalveolar lavage fluid (genotype main effect, p < .001). Repeated exposure to pollutants did not result in measurable inflammatory changes in wild-type mice and did not exacerbate the inflammation in TNF mice. The pollutants decreased recovery of alveolar macrophages in tavage fluid of both wild-type and TNF mice (exposure main effect, p < .001). Exacerbation of the rate of protein nitration reactions specifically in the lungs of TNF mice was revealed by the high ratio of 3-nitrotyrosine to L-DOPA after exposure to the air pollutants (Genotype x Exposure factor interaction, p = .014). Serum creatine kinase-MM isoform increased in TNF mice exposed to pollutants (Genotype X Exposure factor interaction, p = .043). The marked pollutant-related nitration in the lungs of the TNF mice reveals basic differences in free radical generation and scavenging in the inflamed lungs in response to pollutants. Furthermore, elevation of circulating creatine kinase-MM isoform specifically in TNF mice exposed to pollutants suggests systemic adverse impacts from lung inflammatory mediators, possibly on muscles and the cardiovascular system.
To the surgeon, the importance of duodeno-gastro-esophageal reflux is related firstly to the injurious effects it has on the mucosa of the stomach and the esophagus, and secondly to the underlying pathophysiology causing the regulation of duodenal contents into the stomach and subsequently into the esophagus. Normally, the reflux of duodenal contents into the stomach rarely causes symptoms and consequently is usually not a primary disease. The symptoms develop after operations that distort or remove the pylorus. Consequently, in most situations the disease is iatrogenic in etiology. In contrast, the reflux of duodenal and gastric contents into the esophagus occurs very commonly as a primary disease entity. In such patients, a dysfunctional lower esophageal sphincter is the cause of the increased esophageal exposure and is of key importance to the surgeon. Surgery is the only treatment modality, which is able to specifically address and correct a structurally defective and dysfunctional lower esophageal sphincter. For patients with excessive duodenal reflux into the stomach, surgical diversion of the offending refluxate by means of a Roux-en-Y procedure is the only truly effective modality of treatment.