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Biomedical subjects

S S Baker

Publications and source records attributed to S S Baker.

At least 19 recordsLinked to original sources
PubMed2000

Randomized, double-blind, placebo-controlled pilot trial of megestrol acetate in malnourished children with cystic fibrosis.

BACKGROUND: Undernutrition is common in patients with cystic fibrosis (CF). Nutritional rehabilitation has been shown to improve linear growth, pulmonary function, well-being, and resistance to infection in this population. The purpose of this study was to determine whether the administration of megestrol acetate (MA) induces weight gain in malnourished patients with CF, and to assess the composition of weight gain. METHODS: In a randomized, placebo-controlled, double-blind, crossover study, 12 children with CF received MA (10 mg/kg/d) or placebo for 12 weeks, followed by a 12-week washout period, then the alternative treatment. Anthropometrics, caloric intake, and clinical assessment were obtained every 6 weeks; pulmonary function tests, biochemistry, hematology, cortisol, growth hormone, insulin, C-peptide, insulin-like growth factor-1, insulin-like growth factor binding protein-3, and dual-energy x-ray absorptiometry scans were obtained every 12 weeks. RESULTS: Six children did not complete the study, three for reasons unrelated to the study, two because they developed diabetes while receiving MA, and one who had glucose intolerance while receiving the placebo. Average weight gain was 3.05 kg in the MA group and 0.3 kg in the placebo group. The change in weight z score was +0.76 in the MA group and -0.05 in the placebo group. The change in height z score was -0.06 in the MA group and +0.06 in the placebo group. Lean body mass and body fat increased by 1507 g and 1192 g respectively in the MA group. Pulmonary function tests improved in the MA group; serum cortisol levels decreased. Side effects included glucosuria, insomnia, hyperactivity, and irritability. CONCLUSIONS: Weight, body fat, and lean body mass increased and pulmonary function improved in the children with CF given MA. Adrenal suppression, glucose intolerance, and diabetes are side effects.

Adolescent↗
PubMed2000

Glutathione oxidation and PTPase inhibition by hydrogen peroxide in Caco-2 cell monolayer.

The role of H(2)O(2) and protein thiol oxidation in oxidative stress-induced epithelial paracellular permeability was investigated in Caco-2 cell monolayers. Treatment with a H(2)O(2) generating system (xanthine oxidase + xanthine) or H(2)O(2) (20 microM) increased the paracellular permeability. Xanthine oxidase-induced permeability was potentiated by superoxide dismutase and prevented by catalase. H(2)O(2)-induced permeability was prevented by ferrous sulfate and potentiated by deferoxamine and 1,10-phenanthroline. GSH, N-acetyl-L-cysteine, dithiothreitol, mercaptosuccinate, and diethylmaleate inhibited H(2)O(2)-induced permeability, but it was potentiated by 1,3-bis(2-chloroethyl)-1-nitrosourea. H(2)O(2) reduced cellular GSH and protein thiols and increased GSSG. H(2)O(2)-mediated reduction of GSH-to-GSSG ratio was prevented by ferrous sulfate, GSH, N-acetyl-L-cysteine, diethylmaleate, and mercaptosuccinate and potentiated by 1,10-phenanthroline and 1, 3-bis(2-chloroethyl)-1-nitrosourea. Incubation of soluble fraction of cells with GSSG reduced protein tyrosine phosphatase (PTPase) activity, which was prevented by coincubation with GSH. PTPase activity was also lower in H(2)O(2)-treated cells. This study indicates that H(2)O(2), but not O(2)(-). or.OH, increases paracellular permeability of Caco-2 cell monolayer by a mechanism that involves oxidation of GSH and inhibition of PTPases.

Acetylcysteine↗
PubMed1999

Inhibition of oxidant-induced barrier disruption and protein tyrosine phosphorylation in Caco-2 cell monolayers by epidermal growth factor.

The effect of epidermal growth factor (EGF) on the H202-induced increase in paracellular permeability in Caco-2 and T-84 cell monolayers was evaluated to examine the role of EGF in intestinal mucosal protection from oxidative stress. Oxidative stress was induced by exposing cell monolayers to H2O2 or a mixture of xanthine oxidase + xanthine (XO + X). Paracellular permeability was assessed by measuring transepithelial electrical resistance (TER), sodium chloride dilution potential, and unidirectional flux of [3H]mannitol. H2O2 (0.1 to 5.0 mM) reduced TER and dilution potential and increased mannitol flux. Administration of EGF delayed H2O2 and XO + X-induced changes in TER, dilution potential, and [3H]mannitol flux. This protective effect of apically or basally administered EGF was concentration-related, with A50 (95% confidence limits) values of 2.1 (1.17 to 4.34) and 6.0 (4.37 to 8.34) nM, respectively. The EGF-mediated protection was prevented by treatment of cell monolayers with genistein (10 microM), a tyrosine kinase inhibitor. H2O2 and XO + X also induced tyrosine phosphorylation of a number of proteins in Caco-2 and T-84 cell monolayers. EGF treatment inhibited the oxidant-induced tyrosine phosphorylation of proteins, particularly those with a molecular mass of 110-220 kDa. Treatment of Caco-2 cells with anti-transforming growth factor-alpha antibodies potentiated the H2O2-induced changes in TER, dilution potential, and mannitol flux. These studies demonstrated that an EGF receptor-mediated mechanism delays oxidant-induced disruption of the epithelial barrier function, possibly by suppressing the oxidant-induced tyrosine phosphorylation of proteins.

Antibodies, Monoclonal↗
PubMed1999

Constipation in infants and children: evaluation and treatment. A medical position statement of the North American Society for Pediatric Gastroenterology and Nutrition.

BACKGROUND: Constipation, defined as a delay or difficulty in defecation, present for 2 or more weeks, is a common pediatric problem encountered by both primary and specialty medical providers. METHODS: The Constipation Subcommittee of the Clinical Guidelines Committee of the North American Society for Pediatric Gastroenterology and Nutrition has formulated clinical practice guidelines for the management of pediatric constipation. The Constipation Subcommittee, consisting of two primary care pediatricians, a clinical epidemiologist, and pediatric gastroenterologists, based its recommendations on an integration of a comprehensive and systematic review of the medical literature combined with expert opinion. Consensus was achieved through Nominal Group Technique, a structured quantitative method. RESULTS: The Subcommittee developed two algorithms to assist with medical management, one for older infants and children and the second for infants less than 1 year of age. The guidelines provide recommendations for management by the primary care provider, including evaluation, initial treatment, follow-up management, and indications for consultation by a specialist. The Constipation Subcommittee also provided recommendations for management by the pediatric gastroenterologist. CONCLUSIONS: This report, which has been endorsed by the Executive Council of the North American Society for Pediatric Gastroenterology and Nutrition, has been prepared as a general guideline to assist providers of medical care in the evaluation and treatment of constipation in children. It is not intended as a substitute for clinical judgment or as a protocol for the management of all patients with this problem.

Child↗
PubMed1999

American Academy of Pediatrics. Committee on Nutrition. Calcium requirements of infants, children, and adolescents.

This statement is intended to provide pediatric caregivers with advice about the nutritional needs of calcium of infants, children, and adolescents. It will review the physiology of calcium metabolism and provide a review of the data about the relationship between calcium intake and bone growth and metabolism. In particular, it will focus on the large number of recent studies that have identified a relationship between childhood calcium intake and bone mineralization and the potential relationship of these data to fractures in adolescents and the development of osteoporosis in adulthood. The specific needs of children and adolescents with eating disorders are not considered.

Adolescent↗
PubMed1998

Bovine milk inhibits proteolytic degradation of epidermal growth factor in human gastric and duodenal lumen.

Degradation of epidermal growth factor (EGF) in human gastric and duodenal lumen was analyzed by incubating 125I-labeled or unlabeled human recombinant EGF with human gastric or duodenal luminal fluids in vitro. Degradation of EGF was assessed by measuring the generation of acid soluble radioactivity or by reversed-phase high-performance liquid chromatography (HPLC). Incubation with gastric luminal fluids resulted in a time- and dose-dependent degradation of labeled and unlabeled EGF at pH 2.5 but not at pH 7.5. Duodenal luminal fluids, on the other hand, degraded EGF at pH 7.5 but not at pH 2.5. The rate of degradation of unlabeled EGF in gastric luminal fluids was nearly 12-fold higher than the rate of degradation of labeled EGF, whereas only a slight difference in rates of degradation of labeled and unlabeled EGF was observed in duodenal luminal fluids. High-performance liquid chromatography analysis detected three major degradation products that eluted with retention time of 17.5 min, 20.0 min, and 22.5 min that was associated with a reduction of intact EGF (retention time 23.5 min). Defatted and decaseinated supernatant of bovine milk effectively inhibited the degradation of EGF in both gastric and duodenal luminal fluids. Dietary derived protease inhibitors, such as soya bean trypsin inhibitor, lima bean trypsin inhibitor, egg white protease inhibitor, and Bowman-Birk protease inhibitor prevented EGF degradation in duodenal luminal fluids but failed to inhibit EGF degradation in gastric luminal fluids. These results suggest that bovine milk may contain specific inhibitors that protect EGF from proteolytic degradation in human gastric lumen.

Adolescent↗
PubMed1998

Hypocaloric oral therapy during an episode of diarrhea and vomiting can lead to severe malnutrition.

BACKGROUND: Malnutrition associated with diarrhea and vomiting can be prevented if the focus of treatment is on nutritional requirements. Some pediatricians inappropriately continue to recommend clear liquids followed by dilute feedings or hypocaloric diets until the diarrhea clears. METHODS: Medical records were retrospectively reviewed, and the literature was reviewed. RESULTS: Severe malnutrition occurred in two children with diarrhea and vomiting who were treated with clear liquids followed by restricted nutrient intake. CONCLUSION: Severe malnutrition associated with diarrhea and vomiting can occur when the prescribed treatment is bowel rest followed by hypocaloric diets until diarrhea clears. Malnutrition can be prevented if the focus of treatment is on nutritional requirements. Current American Academy of Pediatrics recommendations for treatment of diarrhea and vomiting are discussed.

Child, Preschool↗
PubMed1998

Selenium deficiency in tissue culture: implications for oxidative metabolism.

BACKGROUND: Selenium is located at the catalytic site of the enzyme glutathione peroxidase, and with selenium deficiency the activity of glutathione peroxidase is decreased. Cell culture is an important tool for studying oxidative processes-that is generation and metabolism of oxygen-derived metabolites in the gastrointestinal system. Cell culture is also used to understand the mechanisms of cell injury by oxygen-derived metabolites. METHODS: To assess the importance of the selenium content of cell culture media, Caco-2 cells and the hepatoma-derived cell lines, Hep3B and HepG2, were grown to confluence and placed in media with various concentrations of selenium. After 7 to 14 days, cells were harvested and assayed for glutathione peroxidase, lactate dehydrogenase, and protein content. RESULTS: Cells maintained in media unsupplemented with selenium demonstrated a progressive decrease in glutathione peroxidase activity. Cells maintained in media supplemented with various concentrations of selenium demonstrated a dose-dependent increase in glutathione peroxidase until a plateau was reached. The plateau was reached at approximately 400 times the selenium concentration routinely used in cell culture. In the Caco-2 and hepatoma cells, no toxicity was observed at selenium supplementation five times the lowest concentration needed to reach a plateau. CONCLUSIONS: Cell culture media are routinely deficient in selenium, and cells that are cultured in this medium are deficient in glutathione peroxidase activity. Studies of oxidative metabolism based on cultures deficient in selenium may yield results that could be falsely interpreted. The addition of 1 nM selenium is sufficient for these cell lines to reach a plateau for intracellular glutathione peroxidase activity. These observations may have important ramifications for the study of reactive oxygen metabolite injury in cell culture.

Caco-2 Cells↗
PubMed1998

Enteral nutrition in the pediatric population.

Enteral feeding, the provision of liquid nutrients into the gastrointestinal tract, is an important component of pediatric care. For the infant or child with a functioning or even a partially-functioning GI tract, the use of the enteral route provides a safe and efficient means of delivering nutrition at a time of life when requirements are extremely high. In addition to high nutrient requirements in the early years of life, there are a number of specific pediatric conditions, such as failure to thrive, short bowel syndrome, and congenital heart disease, which place further demands on the growing child. These demands can be met through the careful use of enteral feeds. This article reviews the physiology and practical application of enteral feeding to the pediatric age group.

Adolescent↗
PubMed1997

Oxidant-induced disruption of intestinal epithelial barrier function: role of protein tyrosine phosphorylation.

The effect of hydrogen peroxide (H2O2) on intestinal epithelial barrier function was examined in Caco-2 and T84 cell monolayers. H2O2 reduced transepithelial electrical resistance (TER) of Caco-2 and T84 cell monolayers. This decrease in TER was associated with a decrease in dilution potential and an increase in [3H]mannitol permeability, suggesting an H2O2-induced disruption of the paracellular junctional complexes. H2O2 administration also induced tyrosine phosphorylation of several proteins (at the molecular mass ranges of 50-90, 100-130, and 150-180 kDa) in Caco-2 cell monolayers. Phenylarsine oxide and sodium orthovanadate, inhibitors of protein tyrosine phosphatase, decreased TER and increased mannitol permeability and protein tyrosine phosphorylation (PTP). A low concentration of sodium orthovanadate also potentiated the effect of H2O2 on TER, dilution potential, mannitol permeability, and PTP. Pretreatment with genistein (30-300 microM) and tyrphostin (100 microM) inhibited the effect of H2O2 on TER, dilution potential, mannitol permeability, and PTP. These studies show that H2O2 increases the epithelial permeability by disrupting paracellular junctional complexes, most likely by a PTP-dependent mechanism.

Arsenicals↗
PubMed1996

Carbon dioxide laser transconjunctival lower lid blepharoplasty complications.

Lower eye lid blepharoplasty is a frequent cosmetic procedure. The carbon dioxide laser transconjunctival approach is a popular alternative to conventional techniques. Eight hundred eighty-nine consecutive cases were studied retrospectively to determine the occurrence of complications. All cases were included. Complications were divided into intraoperative, immediate postoperative (days 1-7) and late postoperative (greater than 7 days). Complications encountered in this study of carbon dioxide laser conjunctival blepharoplasty were uncommon and not severe.

Adult↗
PubMed1995

Polarized Caco-2 cells. Effect of reactive oxygen metabolites on enterocyte barrier function.

Reactive oxygen metabolites are implicated in gastrointestinal disease and enterocyte injury associated with ischemia-reperfusion, bacterial translocation, inflammatory bowel disease, and necrotizing enterocolitis. The ileal-like, human colon carcinoma cell line, Caco-2, was used to investigate oxidative damage. After challenging Caco-2 cells with reactive oxygen metabolites, the permeability, viability, and energy charge of Caco-2 cells were assessed. Permeability was determined by transepithelial electrical potential and flux of small molecules. Viability was determined by release of 51Cr. Cell energy was evaluated by determining adenylate energy charge. The source of reactive oxygen metabolites, with the exception of menadione, did not affect viability of Caco-2 cells; cell permeability was increased. The increased varied with the source and location of the reactive oxygen metabolite. There was no change in energy charge. This study suggests that reactive oxygen metabolites could cause enterocyte damage and that the source of the reactive oxygen metabolite is an important variable in determining the extent of damage. Antioxidants might prevent injury.

Adenosine Triphosphate↗