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Biomedical subjects

D I Mehta

Publications and source records attributed to D I Mehta.

24 records · Page 2Linked to original sources

Diagnosis of Helicobacter pylori.

In view of its potential risk for the development of gastrointestinal disease or even gastric cancer at a later age, the study of Helicobacter pylori infection in childhood is gaining increasing importance and H. pylori infection is being considered a major issue of public health. H. pylori infection can be detected by a variety of methods. Because of its easy use, affordability, and overall availability, serology is the preferred diagnostic test, especially for large epidemiological studies. Based on our results, one might consider treating a child with recurrent abdominal pain and positive serology for H. pylori without further work-up, and only perform additional investigations when an anti-H. pylori therapy fails to resolve the complaints. According to this proposition, endoscopy of the upper gastrointestinal tract remains indicated in children if the noninvasive tests for Helicobacter pylori are negative in the absence of a diagnosis, or if symptomatology persists despite treatment.

Breath Tests↗

Pediatric gastritis and peptic ulcer disease.

Inflammation of the gastric and duodenal mucosa is the end result of an imbalance between mucosal defensive and aggressive factors. The degree of inflammation and imbalance between defensive and aggressive factors can then result in varying degrees of gastritis and/or mucosal ulceration. Gastritis and ulcers of the duodenum or stomach can be classified as primary or secondary. The majority of children with chronic gastritis and ulcers in the stomach or duodenum have secondary inflammation or mucosal ulceration. These secondary ulcers generally occur due to a systemic condition like head trauma or overwhelming sepsis, or as sequelae to drug ingestion (i.e. non-steroidal anti-inflammatory agents), but secondary gastroduodenal ulcers can also occur in specific disease conditions such as Zollinger-Ellison syndrome or Crohn's disease. In almost all children with primary duodenal or gastric ulcers mucosal inflammation and, less frequently, ulceration is caused by a spiral shaped, gram-negative, microaerobic rod Helicobacter pylori. Recent epidemiological evidence has linked chronic H. pylori infection with the development of gastric carcinomas.

Child↗

Modified food starches in baby foods.

Modified food starches were developed as a stabilizer, providing desirable consistency, texture, and storage ability. They are used primarily in strained and junior foods and, to a minor extent, in infant formulas. However, despite the fact that there is an increasing tendency to introduce solid foods to infants at a very early age, there is few long-term studies to delineate the effect of starch feeding on the growth of young infants. Modified food starches used by the food industry for infants and young children are of concern and there is an urgent need for additional data regarding their bioavailability, effect on nutrient absorption, intestinal changes, and toxic, mutagenic, and carcinogenic effects. Therefore, the inclusion of modified food starches should be used prudently and sparingly.

Animals↗

Presentation and management of Helicobacter pylori infection in childhood.

Helicobacter pylori is responsible for one of the most frequently encountered infectious diseases worldwide. Helicobacter pylori infection can lead to the development of gastritis and peptic ulcer disease. The presence of Helicobacter pylori in the human stomach also represents an increased risk of gastric cancer and gastric lymphoma. Epidemiological data obtained in adults suggest that the actual colonization with Helicobacter pylori is in fact determined by childhood factors. Therefore, the pediatric age group represents the ideal target population for studies concerning the pathogenesis and epidemiology of Helicobacter pylori infection. The present work reflects our experience with regard to the diagnosis, epidemiology and pathogenesis of Helicobacter pylori infection in childhood.

Adolescent↗

Chronic diarrhea: causes, presentation, and management.

Important inroads are being made into understanding the pathophysiology of diarrhea. Clear understanding of key mechanisms should suggest new approaches to combat disease. Exciting developments are occurring in terms of super-ORS solutions, particularly with the promise of short chained glucose polymers and glutamine. Perhaps the most important development is the prospect of a good rotavirus vaccine being available before the end of the decade. Chronic diarrhea seems to be on the increase globally, probably because of the success of ORS. The mechanisms that lead to mucosal injury are elusive, and therapy still largely supportive and empiric. Celiac disease continues to be a puzzle, because of the uncomfortable feeling that a majority of cases may be missed because of atypical presentations. The successful use of long term parenteral nutrition has allowed survival and better characterization of cases that otherwise would have perished as 'lethal protracted diarrhea'. Microvillus inclusion disease may be the commonest congenital secretory diarrhea. The role of the recently reported high prevalence of glucoamlase deficiency may be important. Lastly, attention to micronutrients, particularly low vitamin A and probably zinc may prove to be important in prevention and amelioration of diarrhea and growth failure.

Child↗

Epidermal growth factor up-regulates sodium-glucose cotransport in enterocyte models in the presence of cholera toxin.

BACKGROUND: Sodium-glucose cotransport by enterocytes is key to the successful implementation of oral rehydration in diarrhea. Confluent, differentiated Caco-2 cells have enterocyte-like characteristics. We have previously shown that short-term incubation of isolated rat jejunal enterocytes with epidermal growth factor (EGF) results in the up-regulation of sodium-glucose cotransport. The aim of this study was to examine the effect of EGF on Caco-2 cells in the presence of cholera toxin. METHODS: Caco-2 cells grown on tissue culture dishes were used for glucose and sodium uptake studies and cells were grown on polycarbonate membranes for transport examinations. Effects of EGF on the kinetic parameters of sodium-glucose contransporter, thymidine transport, and on the activity of Na+/K(+)-ATPase were examined. The efficacy of basolateral vs apical EGF on sodium and glucose transport was compared after incubation of the monolayers with 10 nmol/L of cholera toxin. RESULTS: EGF increased both glucose and sodium uptake and transport, and we observed a simultaneous increase in the activity of Na+/K(+)-adenosine triphosphatase (ATPase). Kinetic studies performed on brush-border membrane vesicles prepared from EGF-incubated confluent monolayers and on intact cells showed an increase in the maximum velocity but not the Michaelis constant, suggesting increased availability of transporters rather than conformational change. This effect was seen within minutes in both of the two putative transporters, high-affinity, low-capacity and low-affinity, high-capacity. There was no acute effect on thymidine uptake. Studies in the presence of cholera toxin demonstrated a significant up-regulation in sodium-glucose cotransport when EGF was applied from the basolateral side; the increase was smaller but significant with apical application. CONCLUSIONS: Differentiated Caco-2 cells have two kinetically distinct sodium-glucose cotransporters. Short-term incubation of Caco-2 cells with EGF resulted in an up-regulation of sodium-glucose cotransport and subsequent increase in Na+/K(+)-ATPase activity. The effect of basolaterally applied EGF was more significant with or without incubation with cholera toxin. The early effect of EGF on glucose and sodium cotransport may have important therapeutic implications in diarrhea and dehydration states. The in vitro model described here uses a homogeneous cell population and provides a versatile system for uptake and transport studies.

Biological Transport↗