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Biomedical subjects

S M Borowitz

Publications and source records attributed to S M Borowitz.

36 records · Page 2Linked to original sources
PubMed1989

The role of phospholipase A2 in microsomal lipid peroxidation induced with t-butyl hydroperoxide.

The role of phospholipase A2 (PlA2) in lipid peroxidation induced with t-butyl hydroperoxide was examined in rat liver microsomes. Exposure of microsomes to t-butyl hydroperoxide was associated with activation of endogenous PlA2. When PlA2 was inhibited with chlorpromazine, mepacrine, or p-bromphenacyl bromide, the accumulation of thiobarbituric acid reactive substances (TBARS) was reduced in a dose dependent manner. In contrast, the accumulation of conjugated dienes was not affected by chlorpromazine, and was slightly increased by mepacrine. When endogenous PlA2 was activated with mellitin prior to induction of peroxidation, accumulation of both TBARS and dienes was reduced. Analogously, pretreatment with exogenous PlA2 reduced both dienes and TBARS. In contrast, addition of mellitin following the induction of peroxidation did not alter either TBARS or dienes.

Acetophenones↗
PubMed1989

Phosphate transport in human jejunal brush-border membrane vesicles.

Phosphate transport was studied in isolated brush-border membrane vesicles prepared from human jejunum. Transport consisted of two components: passive diffusion across the brush border, and sodium-dependent, carrier-mediated uptake. Both carrier-mediated transport and passive diffusion of phosphate were significantly greater at pH 6.1 than at pH 7.4. Sodium-dependent uptake was saturable at both pH values; the apparent Km was not affected by pH, whereas Vmax was significantly greater at pH 6.1 (179.3 vs. 118.4 pM/mg per 15 s). Phosphate uptake was half-maximally stimulated by a sodium concentration of 34 mM at pH 7.4, and a sodium concentration of 76 mM at pH 6.1. At both pH values, Hill coefficients were greater than 1 and were unaffected by pH. Moreover, sodium-dependent phosphate uptake was electroneutral at pH 7.4 and electrogenic at pH 6.1. These data suggest that at acid and neutral pH, both monovalent and divalent phosphate are transported across the human jejunal brush border membrane. The transport of each phosphate molecule is associated with the cotransport of two sodium ions.

Biological Transport↗
PubMed1989

Ulcerative esophagitis. A rare source of upper gastrointestinal bleeding in a neonate. Use of fiberoptic endoscopy for diagnosis.

A case of upper gastrointestinal hemorrhage in a newborn infant due to ulcerative esophagitis is described. This is a previously undescribed cause of upper gastrointestinal neonatal bleeding. This case further illustrates the safety and efficacy of fiberoptic endoscopy in elucidating the source of upper gastrointestinal bleeding in the immediate newborn period.

Cimetidine↗
PubMed1989

Effects of EGF and PMA on the growth and proliferation of IEC-6 cells.

Proliferation of an epithelial line (IEC-6) derived from the crypts of rat jejunum was induced with epidermal growth factor (EGF). EGF enhanced synthesis of protein, RNA, and DNA in a dose-dependent manner. Protein synthesis increased within 6-12 hours of exposure to EGF and remained elevated for 72 hours. Maximal 3H-thymidine incorporation occurred 48 hours after addition of EGF. The stimulatory effect of EGF on 3H-thymidine incorporation was two-fold greater in serum-free media than in media containing fetal calf serum (FCS). In contrast to EGF, phorbol-12-myristate-13-acetate (PMA) decreased 3H-thymidine uptake by IEC-6 cells and had no effect on either protein synthesis or RNA synthesis. EGF did not alter protein kinase-C activity in IEC-6 cells whereas PMA induced enzyme activity: activity was translocated from cytosol to membrane. Moreover, the EGF-associated increase in 3H-thymidine uptake was not altered by amiloride. These data suggest protein kinase-C activation may not be involved in the proliferation of IEC-6 cells.

Animals↗
PubMed1988

Effects of growth and differentiation inducing factors on protein kinase-C of cultured intestinal crypt cells.

To assess the role of protein kinase-C (PK-C) in the growth and differentiation of small intestinal enterocytes, IEC-6 cells (a cell line derived from the crypts of rat small intestine) were incubated with factors known to induce growth (insulin, epidermal growth factor, gastrin, somatostatin and transferrin) or differentiation (transforming growth factor-beta, retinoic acid and phorbol 12-myristate 13-acetate (PMA)). Cell proliferation (3H-thymidine incorporation) and PK-C activity (Ca++/phospholipid dependent) were measured. Among growth promoting factors only epidermal growth factor, insulin and transferrin were associated with increased 3H-thymidine incorporation, and none of these agents induced PK-C activation as measured by its translocation from cytosol to membrane fraction. Of the differentiation inducing factors, only PMA translocated PK-C from cytosol to membrane. PMA also inhibited 3H-thymidine incorporation in a dose dependent manner. These results suggest that growth and proliferation of enterocytes occur independent of PK-C signal transduction.

Animals↗
PubMed1988

Promotion of iron-induced rat liver microsomal lipid peroxidation by copper.

Although copper has been demonstrated to promote lipid peroxidation in a number of systems, the mechanisms involved have not been fully defined. In this study, the role of copper in modifying lipid peroxidation has been explored in rat hepatic microsomes. In an in vitro system containing reduced glutathione (GSH, 200 microM) and Tris buffer, pH 7.4, cupric sulfate (1-50 microM) potentiated lipid peroxidation induced by ferrous sulfate (10 microM) but was unable to elicit peroxidation in the absence of iron. Higher levels of cupric sulfate (100 microM or greater) were inhibitory. The nature as well as the extent of the peroxidative response of microsomes to cupric sulfate were dependent on glutathione levels in addition to those of iron. Cupric sulfate (100 microM) strongly potentiated ferrous ion-induced lipid peroxidation in the presence of 400-800 microM GSH, while it inhibited peroxidation at lower levels of GSH (0-200 microM) and did not affect ferrous ion-induced peroxidation with glutathione levels of 3-10 mM. The potentiating effect of copper on ferrous ion-induced lipid peroxidation was further explored by investigating: (1) potential GSH-mediated reduction of cupric ions; (2) potential copper/GSH-mediated reduction of ferric ions (formed by oxidation during incubation); and (3) possible promotion of propagation reactions by copper/GSH. Our results indicate that cupric ions are reduced by GSH and thus are converted from an inhibitor to an enhancer of iron-induced lipid peroxidation. Cuprous ions appear to potentiate lipid peroxidation by reduction of ferric ions, rather than by promoting propagation reactions. Iron (in a specific Fe+2/Fe+3 ratio) is then an effective promoter of initiation reactions.

Animals↗
PubMed1987

The role of phospholipase A activity in rat liver microsomal lipid peroxidation.

The involvement of phospholipase(s) A in lipid peroxidation of rat liver microsomes was investigated by: (a) determining the effects of phospholipase A inhibitors (p-bromophenylacyl bromide, chlorpromazine, mepacrine) on the accumulation of thiobarbituric acid reactivity or on levels of oxidized phospholipids in response to selected oxidative stimuli and (b) measurement of phospholipase A activities in response to these agents. Lipid peroxidation in response to various peroxidation systems was inhibited completely by exposure of microsomes to p-bromophenylacyl bromide (250 microM). The effectiveness of p-bromophenylacyl bromide was dependent on the presence of glutathione (200 microM) in preincubation mixtures. Chlorpromazine (100 microM) and mepacrine (100 microM) also effectively inhibited peroxidation, and their potency was independent of glutathione. The accumulation of oxidized phospholipids in response to the potent peroxidation stimulus alloxan/ferrous ion was similarly inhibited by p-bromophenylacyl bromide, although the level of oxidized phospholipid in response to the initiator ADP/ferrous ion was not affected. Microsomal phospholipase A1 activity, assessed using a liposomal substrate, was substantially enhanced by promoters of lipid peroxidation. Phospholipase A2 activity was not detected using a liposomal substrate but was evident using radiolabeled microsomes as endogenous substrate and was enhanced by oxidative stimuli. We conclude that phospholipase A activity may play an integral role in the microsomal lipid peroxidation mechanism. Based on this study, we hypothesize a role for phospholipases in facilitating propagation reactions.

Acetophenones↗
PubMed1986

Acute water intoxication in healthy infants.

We have described two infants with profound hyponatremia and seizures due to metabolic derangements resulting from inappropriate feeding of large volumes of solute-poor liquids. All of the 23 similar cases in the current literature described children with normal renal and neurologic function before and after the episode of hyponatremia. The chronic feeding of solute-poor fluids in these infants impaired their ability to excrete free water, and continued feeding of solute-poor fluids resulted in progressive hyponatremia and convulsions. Upon reinstitution of normal sodium intake, all metabolic abnormalities disappeared.

Acute Disease↗
PubMed1986

The effects of metabolic acidosis on jejunal phosphate and glucose transport in weanling rats.

To investigate the effects of metabolic acidosis on jejunal phosphate and glucose absorption, in vivo and in vitro transport studies were performed on weanling rats fed 1.5% NH4Cl for three days and on group pair-fed controls. Both in vivo and in vitro, acidosis significantly depressed phosphate transport without effecting glucose transport. In vitro, the decrease of phosphate transport was due to a depression of sodium-phosphate cotransport, but not of sodium independent phosphate transport. This corresponded to a significant increase of the Km of sodium-phosphate cotransport with no change of the Vmax. Treatment of the acidotic animals with intraperitoneal 1,25 dihydroxycholecalciferol did not restore phosphate transport to control levels. These studies indicate that in weanling rats, metabolic acidosis selectively suppresses jejunal phosphate transport independent of circulating levels of 1,25 dihydroxycholecalciferol.

Acidosis↗
PubMed1985

Maturation of jejunal phosphate transport by rat brush border membrane vesicles.

The transport of phosphate into jejunal brush border membrane vesicles isolated from 14- to 42-day-old rats was investigated using a rapid filtration technique. The presence of a sodium gradient enhanced phosphate uptake at all ages. Both sodium-dependent phosphate uptake and passive phosphate uptake declined with increasing age. The activity of the sodium/phosphate cotransporter was significantly greater in the 14-day-old suckling animals than in the 42-day-old animals. Experiments with valinomycin in 14- and 42-day-old animals showed that at pH 7.4, phosphate uptake is electroneutral at both ages. These findings demonstrate there are maturational changes in the jejunal transport of phosphate. Suckling animals transport significantly more phosphate than adult animals. The increased uptake in the younger animals is related to an increase in the active uptake of phosphate and an increase in the passive permeability to phosphate.

Age Factors↗
PubMedDate not supplied

Using the Internet to teach parents and children about constipation and encopresis.

Since 1995, we have maintained a tutorial about chronic childhood constipation and encopresis on our web site. The tutorial is directed at parents and older children and includes a feedback form comprised of six multiple-choice questions and a free-text comment field. Between 1 January 1998 and 30 April 2000, we received 1,142 completed feedback forms. The vast majority of respondents identified themselves as parents or guardians of a child with constipation or encopresis. All respondents felt the tutorial was clear and easy to understand. 98% of respondents felt the tutorial helped them understand why children develop constipation and/or encopresis and 91% of respondents felt the tutorial made them better able to take care of a child suffering from constipation and/or encopresis. More than 99% of respondents felt this type of tutorial was a good way to teach people about health problems. 74% of respondents sent us comments about the tutorial. Most often, the comments expressed thanks for having this information available in clear and understandable language, however a significant number of people inquired about a particular child's difficulties or asked a general question not clearly pertaining to a particular child. The results of this study indicate that many people are searching the Internet for information concerning childhood encopresis and that the World Wide Web can provide families with useful information about this common paediatric problem.

Adult↗
PubMedDate not supplied

Cornstarch therapy in a patient with type III glycogen storage disease.

A child with type III glycogen storage disease is described. The patient presented with growth failure and hepatic dysfunction, and no clinical or biochemical evidence of myopathy. Institution of high protein nocturnal intragastric feedings was associated with improved growth and less hepatic dysfunction. Compliance with tube feedings was sporadic necessitating another approach to the patient's management. The use of oral cornstarch supplements enabled the child to maintain normoglycemia and was associated with clinical and biochemical improvement. Our experience with this child suggests cornstarch therapy may be useful in those patients with type III glycogen storage disease who suffer primarily from hepatic dysfunction and growth failure.

Dietary Proteins↗
PubMedDate not supplied

Comparison of dietary therapy and portacaval shunt in the management of a patient with type Ib glycogen storage disease.

A patient with glycogen storage disease type IB (GSD-Ib) is described. Beginning at age 34 months, the patient was managed with dietary measures, including nocturnal intragastric feedings. Therapy caused substantial biochemical and clinical improvement while the patient remained hospitalized; chronic noncompliance at home, however, resulted in profound growth failure and biochemical abnormalities. Due to a previous case report describing clinical, biochemical, and hematological improvement following a portacaval shunt in a similar patient, portacaval shunt was performed in our patient at age 13 years. During the 12 months following surgery, there was no improvement of our patient's growth or of biochemical or hematological abnormalities. Due to the lack of improvement following surgery, 24-hour constant infusion intragastric feedings were instituted and have been associated with substantial benefit.

Adolescent↗
PubMedDate not supplied

Computer-based speech recognition as an alternative to medical transcription.

The purpose of this report is to describe the author's experience using computerized dictation during routine outpatient medical practice. During a six-month period, patients seen by the author in the Pediatric Gastroenterology Clinic at the University of Virginia were assigned to human or computer-based transcription. Of 1,129 notes, 580 were completed by a transcriptionist and 549 by computer. The total time spent dictating and editing notes was approximately one minute more for computerized dictation than for a human transcriptionist (379.81 +/- 132.69 sec vs. 326.14 +/- 126.02 sec; P: < 0.0001). Notes generated by computer were slightly longer than notes generated by a transcriptionist (52.42 +/- 16.45 lines vs. 50. 41 +/- 16.73 lines; P: = 0.0422). Of notes generated by a transcriptionist, 139 (24 percent) were completed within two days of the visit, whereas all notes generated by computer were completed on the day of the visit.

Documentation↗
PubMedDate not supplied

Alteration of normal gastric flora in neonates receiving ranitidine.

OBJECTIVES: To determine if the administration of ranitidine to neonates leads to an increase in gastric pH to > or = 4 and if this increase in gastric pH correlates with gastric colonization. STUDY DESIGN: 628 pH measurements and 276 gastric cultures were obtained from 86 neonates. Twenty-three patients received ranitidine and 63 patients served as controls. RESULTS: Treated patients had a mean gastric pH of 5.6 compared with a control mean pH of 4.4 (p < 0.0001). Gastric pH was significantly affected by feeding and postnatal age. 54 patients were colonized with pathogenic bacteria and/or yeast (n = 20 treated, n = 34 control). Length of hospitalization (p < 0.0001), increase in gastric pH (p < 0.01), days of antibiotics before culture (p < 0.0001), and ranitidine use (p < 0.0001) were associated with an increased rate of colonization. CONCLUSIONS: The use of ranitidine did lead to a significant increase in gastric pH and with this increase in gastric pH gastric colonization rates increased. No increased frequency of infection was found in ranitidine-treated infants.

Anti-Bacterial Agents↗