Laparoscopic hernia repair: a point of view.
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Biomedical subjects
Publications and source records attributed to L M Nyhus.
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Capsaicin (Sigma Chemical Co.) is a unique chemical agent that causes degeneration of afferent nerve fibers. Previous conclusions about Capsaicin effects on the gastric mucosal response to stress have not precisely defined which afferent nerves were affected. Therefore, the aim of the first portion of this study was to define the origin of afferent vagus nerves to the anterior gastric wall after injections of fluorogold (which is an axonal tracer) into the stomach. The second part of this study was to compare the stress effects on the gastric mucosa in rats with impaired afferent nerve function after Capsaicin treatment.
Rat brain protein kinase C (PKC) isozymes I, II and III were stimulated by fatty acids in the absence and presence of calcium. Ethyl oleate, which by itself has no effect on PKC activity, had a potentiating effect on fatty acid-induced activation of all 3 isozymes. Potentiation was observed predominantly in the presence of calcium. Interaction of ethyl oleate with a signalling mechanism involving PKC may underlie the cognitive disturbances noted after alcohol consumption.
To investigate the viscerotopic distribution of the cells of origin of preganglionic vagus nerve in rats, Fluoro-Gold was injected into various visceral tissues. After injections into the gastroesophageal junction and the gastric corpus, labelled cells were localized in the medial half of the dorsal motor nucleus of the vagus (dmnX). Cells in the nucleus ambiguous (nA) were also labelled after injections into the gastroesophageal junction. After injections into the pancreatic head and the celiac plexus, labelled cells were located bilaterally in the lateral part of the caudal dmnX. In the rostral dmnX, however, the pancreatic head was represented in the medial segment. After injections into the lung, duodenum, liver and ascending colon, no labelling was observed in the brainstem.
We have developed, as part of our resident applicant ranking process, a computerized weighted scoring system incorporating, among other variables, the interview score (IS). This study was undertaken to test the IS as a dependent variable when the applicant file is available during the interview. Over a 3-year period, each of two faculty members interviewed 133 candidates in a "blinded" fashion (file unavailable) or 290 candidates with an "open" file. The mean discrepancy between paired interviewers (1 to 10 scale) was 1.34 +/- 0.10 for the blinded group versus 0.93 +/- 0.06 for the open group (p less than 0.001). Individual and multiple regression analysis were used to test the IS as a dependent variable in the open group, with the blinded group as a control. In each instance (except clerkship grades), the IS correlated more closely with other parameters (p less than 0.05) in the open group. Correlation coefficients were 0.27 (blinded) and 0.64 (open) for weighted scores combining all parameters (p less than 0.001) and 0.39 (blinded) and 0.65 (open) for multiple linear regression analysis (p less than 0.001). We conclude that the IS is significantly influenced if other objective variables are at hand, thus deflating the actual weight of the interview. To accurately quantify the value of the interview, a correction factor must be applied, or, more appropriately, the interview must be conducted blindly.
Use of a diaphragmatic flap to buttress and help secure persistent intestinal fistula is described. The potential for the use of muscle flaps in the management of recurrent intestinal fistula is presented.
Altered gluconeogenesis is frequently observed in cancerous hosts. To define its derangements in the liver, we studied glucose and glycogen production in the perfused livers of tumor-bearing rats using 13C NMR spectroscopy. Nine Fischer 344 rats were inoculated with mammary adenocarcinoma. After 5 weeks, the livers were removed and perfused with Krebs buffer containing 8 mM L-[3-13C]alanine, and 13C NMR spectroscopy was performed. Nine pair-fed rats were studied as controls. The peak heights of glucose and glycogen in the 13C NMR spectra of the perfused livers and final perfusates of the two groups of rats were compared. We found comparable amounts of C1-labeled glucose and glycogen in the two groups, but C2- to C5-labeled and C6-labeled glucose and glycogen, as well as total 13C-labeled glucose and glycogen, appeared in smaller quantities in the tumor rats than in the pair-fed rats. These findings suggest that appreciable amounts of unlabeled glycerol were utilized by both groups, but less so by the tumor rats than the pair-fed rats. In addition, there was decreased production of oxaloacetate through pyruvate dehydrogenase and the Krebs cycle in the livers of the tumor rats, where the overall metabolism of alanine into glucose and glycogen was also reduced.
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Epidemiologic studies suggest that certain psychosocial factors increase the risk of cancer. Yet, animal studies suggest that psychosocial stress inhibits the development of chemically induced tumorigenesis. The purpose of this study was to examine the effect of three different chronic mild stressors on the development of dimethylhydrazine (DMH)-induced colorectal carcinoma in rats. Results of this study show that the development of DMH-induced colorectal carcinoma was not significantly inhibited or altered by each individual stress treatment. Additionally, results indicate that mild stressors can induce neurochemical changes commonly associated with stress, without the confounding effects of more aversive stressors that are likely to compromise the nutritional and physiological status of the animal and thereby alter tumor formation.
Endoscopic sclerosis of the gastric cardia (ESGC) prevents experimental gastroesophageal reflux (GER) without changes in lower esophageal sphincter (LES) pressure and length. This study was performed to define the histologic appearance of the esophagus and stomach one year after ESGC. Four dogs were studied one year after ESGC with morrhuate sodium; ESGC had been performed at six sites, 1-3 cm distal to the esophagogastric junction. All animals had stable weight and eating habits at sacrifice. Light microscopy of the cardia and LES included morphometry of wall thickness (mm) and assessment of fibrosis (- to ). The esophagus had minimal changes; the gastric cardia had focal fibrosis, maximal on the greater curve, without any change difference in wall thickness. ESGC results in fibrosis of the gastric cardia, without significant changes in the esophagus. These changes prevent GER, possibly by preventing the initiation of a reflux event.
Purified rat pancreas protein kinase C (PKC) is activated by unsaturated free fatty acids (oleic and arachidonic). The ethyl esters of these fatty acids are ineffective as enzyme activators. However, when the ethyl esters are added in combination with a free fatty acid, there is significant enhancement of enzyme activation. Nearly optimal PKC activation was obtained when non-activating ethyl oleate or ethyl arachidonate was added to sub-optimally activating concentrations of oleic or arachidonic acids. In addition to the ethyl esters, 1-monooleylglycerol also had a potentiating effect on PKC activation by oleic acid. However, the degree of activation observed in the presence of a free fatty acid and an acyl ester of the fatty acid quantitatively never surpassed that produced by sn-1,2-dioleylglycerol. Our findings indicate that significant PKC activation can be achieved by presenting the enzyme with an environment which we believe approximates the structural characteristics of the endogenous activator, sn-1,2-diacylglycerol.
Gastroesophageal reflux disease remains a disorder of unknown etiology associated with abnormal function of the lower esophageal sphincter (LES) and other physiological co-factors of the pathologic reflux. Effective operations for reflux are designed to reinforce the anti-reflux barrier and alter the tendency towards abnormal reflux. We have postulated that the most important component of these procedures is the prevention of distraction of the lowermost components of the LES at the onset of a potential reflux episode. Distraction of the LES causes shortening of the effective sphincter mechanism and can initiate experimental reflux events. In this study we used endoscopic sclerosis of the submucosal space at the cardia as a means of reducing distraction of the cardia in the hope that this would reduce abnormal reflux events. Canine gastroesophageal reflux was induced by intravenous atropine and monitored by continuous esophageal pH monitoring. Sclerosis of the cardia prevented gastroesophageal reflux, without measurable effect on the LES pressure or length. Endoscopic sclerosis of the cardia may be a useful technique in the control of human gastroesophageal reflux.
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If preganglionic vagus nerve fibers enter the stomach via all of its neurovascular bundles, then proximal gastric vagotomy that divides only the bundles along the lesser curvature of the stomach neglects a potential source of innervation to the parietal cells. To determine whether or not these bundles contained preganglionic efferent vagal nerve fibers, horseradish peroxidase was applied to the central cut end of selected neurovascular bundles along the greater curvature of the stomach in rats and ferrets. Cells in the dorsal motor nucleus of the vagus (dmnX) of the rat were labeled after horseradish peroxidase applications to the right gastroepiploic, the splenic, and the short gastric bundles. The ferrets had horseradish peroxidase applied to the right gastroepiploic bundle and they also had cellular labeling of the dmnX. The labeling in cells of the dorsal motor nucleus of the vagus had a distinct topographic, rostrocaudal distribution in both species, and was maximal in the vicinity of the obex. Cells of the bilateral dmnX were labeled after horseradish peroxidase applications at all bundles. This study showed (1) that the bundles along the greater curvature of the stomach contained preganglionic efferent vagus nerve fibers, (2) that the cells of origin of these fibers were represented in the localized rostrocaudal position of the dmnX, and (3) that these fibers had their origins in the bilateral dmnX. Such nerve fibers may account for incomplete vagal denervation of the parietal cells after proximal gastric vagotomy.
Nerve cells in the dorsal motor nucleus of the vagus (dmnX) were identified by retrograde axonal transport after injections of a fluorescent tracer, Fluoro-Gold, into the anterior gastric wall. The intramural injection resulted in labeling of cells in the medial half of the left dmnX. These observations were contrasted with the diffuse (mediolateral and rostrocaudal) and bilateral distribution of labeled cells after Fluoro-Gold solution was dripped onto the stomach. In comparison with other neurotracers, the advantages of Fluoro-Gold are that (1) it can be visualized without the chemical reaction with chromogen, thereby allowing better reproducibility, and (2) it does not fade up to one year.
Recent studies have demonstrated the location in the dorsal motor nucleus of the vagus nerve (dmnX) of nerve cells that project preganglionic efferent vagus nerve fibers to the greater curvature of the stomach. Although it is clear that these fibers are contained within the vagus nerve trunks, the intra-abdominal pathways of these fibers are unknown. When a neurotracer was applied to the right gastroepiploic pedicle, nerve cells in the bilateral dmnX were labeled. If a preliminary anterior or posterior pyloroplasty was performed before the application of the neurotracer, cellular labeling was seen on the right or left side of the dmnX, respectively. Furthermore, division of the anterior Latarjet nerve eliminated labeling in cells of the left dmnX. This study demonstrates that the preganglionic vagus nerve fibers within the right gastroepiploic pedicle traverse an intramural course across the pylorus and are contained in the Latarjet nerve.