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Biomedical subjects

S Nurko

Publications and source records attributed to S Nurko.

32 records · Page 2Linked to original sources

Benefit of uncooked cornstarch in the management of children with dumping syndrome fed exclusively by gastrostomy.

OBJECTIVES: Children with dumping syndrome fed exclusively by gastrostomy are difficult to manage because liquid diets are given directly into the antrum. The gastric contents are emptied rapidly into the small intestine, with consequent hyperglycemia followed by a delayed hypoglycemia and multiple, often debilitating, symptoms. Uncooked cornstarch is a complex carbohydrate that provides a slow and continuous glucose source and may delay gastric emptying. The objective of this study was to determine the efficacy of uncooked cornstarch in the treatment of these children. METHODS: The medical records of eight children with dumping syndrome fed exclusively by gastrostomy were reviewed. Dumping syndrome was diagnosed if there was consistent symptomatology, rapid gastric emptying, and abnormal glucose measurements after a glucose tolerance test. Enough uncooked cornstarch to match hepatic glucose production for 4 h was added to control hypoglycemia, and the feeding formula was modified to control hyperglycemia. RESULTS: All patients had debilitating symptoms. Weight z-score on admission was -2.31 +/- 0.29. Glucose shifts were controlled in all. There was a significant difference between the maximum (221.3 +/- 19.3 mg/dl vs 121.3 +/- 6.9 mg/dl; p < 0.008) and minimum serum glucose (47 +/- 7.8 mg/dl vs 65.6 +/- 4 mg/dl; p < 0.04) before and after uncooked cornstarch. Weight increased from 11.87 +/- 1.4 kg to 15.10 +/- 2.3 kg (p = 0.06). In seven patients, bolus feedings were successfully administered, and symptoms improved or resolved. CONCLUSIONS: Uncooked cornstarch controlled the glucose shifts, resolved most of the symptoms, allowed bolus feedings, and enhanced weight gain in these children.

Child, Preschool↗

Successful use of a chicken-based diet for the treatment of severely malnourished children with persistent diarrhea: a prospective, randomized study.

OBJECTIVE: To evaluate the efficacy of a chicken-based diet for the treatment of persistent diarrhea in severely malnourished children. STUDY DESIGN: Prospective, randomized, double-blind study that compared a chicken-based diet with elemental (Vivonex) and soy (Nursoy) diets. Hospitalized children with third-degree malnutrition and persistent diarrhea, aged 3 to 36 months, were included. Diets were isocaloric and given nasogastrically at 150 ml/kg per day in progressively increasing concentrations. RESULTS: Fifty-six children were included (18 received Vivonex, 19 Nursoy, 19 chicken). They had a mean age of 6.4 +/- 4.4 months, a mean weight of 3604 +/- 1232 gm, and a mean weight-for-age percentage of 51.4% +/- 7.2%. Sixty-four percent had associated conditions on admission to the hospital. Forty-one children (73.2%) were successfully treated (13 Vivonex, 13 Nursoy, 15 chicken). There were no differences in diarrheal outcomes, and all groups had significant weight gain. Failure was independent of the diet and was associated with the presence of infection on admission. There was a significantly higher nitrogen balance in the children from the chicken group (358.2 +/- 13 mg/kg per day) than in those receiving Vivonex (226.6 +/- 61) or Nursoy (291-4 +/- 111.6; p < 0.05) groups. CONCLUSIONS: The chicken-based diet was as effective as Vivonex or Nursoy. It is well tolerated, inexpensive, and widely available and thus represents an effective and inexpensive alternative to the treatment of severely malnourished children with persistent diarrhea.

Animals↗

Hyperhomocysteinemia: detection, risk assessment, and treatment.

Homocysteine is formed by the demethylation of methionine in the course of its normal metabolism. Hyperhomocysteinemia is an independent risk factor for vascular disease. It develops most commonly from folate deficiency, genetic abnormalities, and chronic renal failure. Current models favor direct angiotoxicity involving endothelial and vascular smooth muscle cells, and impaired thrombolysis. Folic acid reduces hyperhomocysteinemia and thus provides an opportunity for risk-factor modification.

Animals↗

Treatment of intractable constipation in children: experience with cisapride.

To establish whether cisapride is beneficial in children with intractable constipation, an open trial was performed. Chronically constipated children who had failed at least 12 weeks of medical therapy received cisapride at a dose of 0.2 mg/kg/dose TID for 12 weeks. Children with pelvic floor dyssynergia were excluded. Patients were followed prospectively for at least 12 months. Thirty children were initially enrolled, and 27 (14 boys, 13 girls) completed the study. At the end of 12 weeks of cisapride treatment, there was a significant increase in the number of bowel movements per week (1.43 +/- 0.52 to 6.48 +/- 4.16; p < 0.05) and significant decreases in the number of accidents per day (2.86 +/- 2.71 to 0.52 +/- 1.23; p < 0.05) and doses of laxatives used per week (14.33 +/- 5.84 to 3.37 +/- 7.10; p < 0.05). Encopresis disappeared in 65.2% of cases (p < 0.0001) and improved in 26%. Sixty-nine percent of the patients stopped using laxatives (p < 0.001). After 12 weeks 18 patients (66.6%) were asymptomatic, seven (25.9%) showed some improvement in bowel movement frequency and number of accidents, and two (7.4%) showed no improvement. The cisapride was well tolerated. After long-term follow-up (20 +/- 9.8 months), 37% of patients had recovered (asymptomatic and off laxatives and cisapride) and 29.6% were still asymptomatic but were using laxatives or cisapride. There were no differences in baseline characteristics between recovered and nonrecovered patients. We conclude that cisapride is effective in the treatment of some children with intractable constipation without pelvic floor dyssynergia.

Anal Canal↗

Contribution of actin cytoskeletal alterations to ATP depletion and calcium-induced proximal tubule cell injury.

The actin cytoskeleton of rabbit proximal tubules was assessed by deoxyribonuclease (DNase) binding, sedimentability of detergent-insoluble actin, laser-scanning confocal microscopy, and ultrastructure during exposure to hypoxia, antimycin, or antimycin plus ionomycin. One-third of total actin was DNase reactive in control cells prior to deliberate depolymerization, and a similar proportion was unsedimentable from detergent lysates during 2.5 h at 100,000 g. Tubules injured by hypoxia or antimycin alone, without glycine, showed Ca(2+)-dependent pathology of the cytoskeleton, consisting of increases in DNase-reactive actin, redistribution of pelletable actin, and loss of microvilli concurrent with lethal membrane damage. In contrast, tubules similarly depleted of ATP and incubated with glycine showed no significant changes of DNase-reactive actin or actin sedimentability for up to 60 min, but, nevertheless, developed substantial loss of basal membrane-associated actin within 15 min and disruption of actin cores and clubbing of microvilli at durations > 30 min. These structural changes that occurred in the presence of glycine were not prevented by limiting Ca2+ availability or pH 6.9. Very rapid and extensive cytoskeletal disruption followed antimycin-plus-ionomycin treatment. In this setting, glycine and pH 6.9 decreased lethal membrane damage but did not ameliorate pathology in the cytoskeleton or microvilli; limiting Ca2+ availability partially protected the cytoskeleton but did not prevent lethal membrane damage. The data suggest that both ATP depletion-dependent but Ca(2+)-independent, as well as Ca(2+)-mediated, processes can disrupt the actin cytoskeleton during acute proximal tubule cell injury; that both types of change occur, despite protection afforded by glycine and reduced pH against lethal membrane damage; and that Ca(2+)-independent processes primarily account for prelethal actin cytoskeletal alterations during simple ATP depletion of proximal tubule cells.

Actins↗

Calcium dependence of integrity of the actin cytoskeleton of proximal tubule cell microvilli.

To better define the role of Ca2+ in pathophysiological alterations of the proximal tubule microvillus actin cytoskeleton, we studied freshly isolated tubules in which intracellular free Ca2+ was equilibrated with highly buffered, precisely defined medium Ca2+ levels using a combination of the metabolic inhibitor, antimycin, and the ionophore, ionomycin, in the presence of glycine, to prevent lethal membrane damage and resulting nonspecific changes. Increases of Ca2+ to > or = 10 microM were sufficient to initiate concurrent actin depolymerization, fragmentation of F-actin into forms requiring high-speed centrifugation for recovery, redistribution of villin to sedimentable fractions, and structural microvillar damage consisting of severe swelling and fragmentation of actin cores. These observations implicate Ca(2+)-dependent, villin-mediated actin cytoskeletal disruption in tubule cell microvillar damage under conditions conceivably present during pathophysiological states. However, despite prior evidence for cytosolic free Ca2+ increases of the same order of magnitude and similar structural microvillar alterations, Ca(2+)- and villin-mediated events did not appear to account for the initial microvillar damage that occurs during ATP depletion induced by antimycin alone or hypoxia.

Actins↗

Anorectal function in children after ileoanal pull-through.

Mucosal proctectomy and ileoanal pull-through is increasingly used in children requiring total colectomy for ulcerative colitis or familial polyposis. Excellent continence can be achieved with this procedure, and it avoids proctocolectomy and permanent ileostomy. We have evaluated prospectively anorectal function in nine consecutively treated children who underwent ileoanal pull-through. Patients were 8 to 17.5 years of age (median, 11.3 years) at the time of surgery; seven had ulcerative colitis, and two had familial polyposis. Anorectal evaluation was performed before colectomy and ileoanal pull-through, following ileoanal pullthrough, after rectal training, and then at yearly intervals. A biofeedback "rectal training" program was instituted 6 weeks after ileoanal pull-through and a contrast study documenting integrity of the pouch. The program consisted of an initial biofeedback session with the motility unit, followed by daily instillations, through a catheter, of progressively larger volumes of water (from 1 to 6 oz, increasing 1 oz per week) into the ileal pouch. Patients were instructed to retain the water and participate in normal activities after the instillation. This protocol acclimated the patient to sensing distension of the pouch and using the sphincters. The follow-up period ranges from 1 to 4.5 years (median, 2.2 years). All patients are continent by day and night. One patient has nocturnal incontinence with episodes of pouchitis. Stool frequency is three to eight movements per day (median, four), with none at night. Preoperative resting rectal sphincter pressures averaged 74.3 +/- 23.1 mm Hg (mean +/- standard deviation), and a maximum squeeze pressure was 93.9 +/- 25.3 mm Hg.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenomatous Polyposis Coli↗

Role of neuropeptide Y in opossum internal anal sphincter.

The present investigation was undertaken to examine the effects and role of neuropeptide Y (NPY) on the internal anal sphincter (IAS). The studies were performed in alpha-chloralose-anesthetized opossums. Resting pressure in the IAS (IASP) was recorded using low-compliant continuously perfused catheters. The effect of NPY administered close intra-arterially on the resting IASP was examined before and after different neurohumoral antagonists and the neurotoxin tetrodotoxin (TTX). To examine the influence of sympathetic nerves, the ventral roots of lumbar sympathetic nerves were isolated in some experiments and stimulated electrically. The influence of NPY on the IAS relaxation in response to rectoanal reflex mimicked by rectal balloon distension (RD) was also examined. NPY caused dose-dependent rise in the IASP, which was not modified by different neurohumoral antagonists and TTX. The rise in IASP by electrical stimulation of ventral lumbar nerve root (L3) was suppressed but not abolished by phentolamine. However, guanethidine (which depletes both norepinephrine and NPY) caused complete obliteration of this response. The other effect of NPY on the IAS was significant antagonism of IAS relaxation caused by RD. From these results, we conclude that NPY exerts two different actions on the IAS. First, it causes a rise in IASP by its action directly at the IAS smooth muscle. Sympathetic nerve stimulation may cause a rise in IASP by its action directly at the IAS smooth muscle partially through release of NPY. Second, it inhibits IAS relaxation produced by rectoanal reflex. These findings would suggest an important regulatory role of NPY in rectoanal physiology.

Anal Canal↗

Peptide histidine isoleucine and vasoactive intestinal polypeptide cause relaxation of opossum internal anal sphincter via two distinct receptors.

The purpose of this investigation was to characterize the nature of peptide histidine isoleucine (PHI) and vasoactive intestinal polypeptide (VIP) receptors, and to examine the role of PHI in internal anal sphincter (IAS) relaxation. The studies were performed on opossums anesthetized with alpha-chloralose. The pressures in the IAS were recorded using continuously perfused catheters. The IAS responses to PHI analogues, PHI-27, PHM-27, PHI-(14-27)-NH2, PHI-(1-13), to VIP, to rectal balloon distention, sacral nerve stimulation, and local intramural stimulation were evaluated before and after PHI-(14-27)-NH2, PHI tachyphylaxis, and the VIP antagonists [4 Cl-D-Phe6, Leu17] VIP (VIP analogue) and (N-Ac-Tyr1, D-Phe2)-GRF(1-29)-NH2 (growth hormone releasing factor analogue). The inhibitory responses by all of the PHI analogues and VIP were not modified by tetrodotoxin. PHI-(14-27)-NH2 and PHI tachyphylaxis caused significant antagonism of the fall in internal anal sphincter pressure by PHI-27 and PHM-27 without modifying the IAS responses to VIP and rectal balloon distention, sacral nerve stimulation, and local intramural stimulation. On the other hand, VIP and growth hormone releasing factor analogues caused significant antagonism of VIP responses without modifying the responses to PHI-27. We conclude that distinct PHI and VIP receptors are present in the IAS smooth muscle and that PHI may not play a significant role in the IAS relaxation via the rectoanal reflex.

Anal Canal↗

Role of vasoactive intestinal polypeptide in the internal anal sphincter relaxation of the opossum.

The nature of the inhibitory neurotransmitter responsible for internal anal sphincter (IAS) relaxation in response to rectoanal reflex is not known. The objective of the present investigation was to examine the role of VIP in IAS relaxation in response to the rectoanal reflex in intact opossums with the use of VIP antagonists, [4CI-D-Phe6,Leu17] VIP and (N-AC-Tyr1,D-Phe2)-GRF (1-29)-NH2. Intraluminal pressures from the sphincter were monitored using low-compliance, continuously perfused catheters. VIP and the antagonists were administered close-intraarterially. The responses to VIP, rectoanal reflex, sacral nerve stimulation, and local intramural stimulation were examined before and after the VIP antagonists. The present studies in intact animals show: (a) VIP causes a dose-dependent fall in the IAS pressures by a direct action at the IAS smooth muscle; (b) VIP antagonists selectively and significantly antagonized the inhibitory action of VIP; and (c) VIP antagonists caused significant antagonism of the IAS relaxation caused by rectoanal reflex and the other neural stimuli. The antagonism of the IAS relaxation by the VIP antagonists, depending upon the volume of rectal distension used, ranged from 40% to 62% (P less than 0.05). From these results, we conclude that VIP acts as an inhibitory neurotransmitter for IAS relaxation during the rectoanal reflex.

Anal Canal↗

Pectus carinatum and pectus excavatum: are they the same disease?

Eighty cases of anterior chest wall deformities were reviewed. The group consisted of 47 patients with pectus carinatum and 33 patients with pectus excavatum. This 1.4:1 distribution has not been reported in the literature, where a 1:10 distribution is regularly cited. Important bronchopulmonary changes were found by chest x-rays in both groups. Formerly, alterations in pectus excavatum were attributed to the mechanical effect of the depressed sternum. The presence of the same symptoms and bronchopulmonary radiographic changes in patients with pectus carinatum suggests a primary pulmonary defect in both entities. However, bronchopulmonary changes were more prominent in patients with pectus excavatum than in patients with carinatum, which suggests that mechanical compression enhances the problem. Postoperative radiologic improvement was similar in both groups. The patients underwent a surgical procedure that included a sternal osteotomy and a complete removal of the costal cartilages. All patients survived. There were two recurrences. Considerable postoperative overgrowth of the unresected second costal cartilages was observed, hence our recommendation for routine removal of these structures. The habitus of prominent abdomen and stooped shoulders was not modified by the operation, but important symptomatic improvement and some radiologic improvement were observed in both groups.

Adolescent↗