Biomedical subjects
Publications and source records attributed to K L Cox.
A Mallory-Weiss tear of the gastroesophageal mucosa is reported as an unusual cause of upper gastrointestinal bleeding in a 3-week-old infant. The lesion, documented by endoscopy, appeared to follow hiccups. The bleeding responded to conservative medical management and resolved without surgical intervention.
To develop a simple test for pancreatic exocrine function in patients with cystic fibrosis, we compared serum pancreatic amylase isoenzyme (P isoamylase) activity with the more complex standard tests of pancreatic function. Twenty-seven patients with cystic fibrosis, newborn to 46 years of age, were studied. All patients over 17 months old with evidence of pancreatic exocrine insufficiency, as manifested by abnormal duodenal secretions and/or abnormal 72-hour fecal fat absorption, had serum P isoamylase activity below the age-matched normal range; patients with adequate pancreatic function (aged 2 to 46 years) had P isoamylase activity in or above the normal range. Although both normal neonates and neonates with cystic fibrosis have very low levels of serum P isoamylase activity, in patients over 1 1/2 years of age serum P isoamylase activity may serve as a simple and useful discriminator of pancreatic exocrine function in patients with cystic fibrosis.
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Several Streptomyces species that produce restriction endonucleases were characterized for their ability to propagate 10 different broad host range bacteriophages. Each species displayed a different pattern of plaque formation. A restrictionless mutant of S. albus G allowed plaque formation by all 10 phages, whereas the wild-type strain showed plaques with only 2 phages. DNA isolated from three of the phages was analyzed for the presence of restriction sites for Streptomyces species-encoded enzymes, and a very strong correlation was established between the failure to form plaques on Streptomyces species that produced particular restriction enzymes and the presence of the corresponding restriction sites in the phage DNA. Also, the phages that lacked restriction sites in their DNA generally formed plaques on the corresponding restriction endonuclease-producing hosts at high efficiency. The DNAs from the three phages analyzed also generally contained either many or no restriction sites for the Streptomyces species-produced enzymes, suggesting a strong evolutionary trend to either eliminate all or tolerate many restriction sites. The data indicate that restriction plays a major role in host range determination for Streptomyces phages. Analysis of bacteriophage host ranges of many other uncharacterized Streptomyces hosts has identified four relatively nonrestricting hosts, at least two of which may be suitable hosts for gene cloning. The data also suggest that several restriction systems remain to be identified in the genus Streptomyces.
Seven of 10 patients with anorexia nervosa had ultrasonic and/or biochemical abnormalities of the pancreas. Seven patients had elevated amylase creatinine clearance ratios (greater than 4%), three patients had elevated serum amylase values (greater than 90 units/liter), and three patients had reduced echogenicity of the pancreas. There was no consistent association between presenting abdominal symptoms and abnormal ultrasonic and biochemical studies of the pancreas. After nutritional repletion, all studies reverted to normal. An eleventh patient, who was initially diagnosed as having anorexia nervosa but later found to have an astrocytoma of the medulla, had reduced echogenicity of the pancreas, suggesting malnutrition as the cause of these abnormal pancreatic studies. Pancreatic abnormalities due to protein-calorie malnutrition may be common in anorexia nervosa and must be differentiated from primary pancreatitis.
Human mucosal glycoconjugates were examined in normal small intestinal biopsies from five control subjects using six different fluorescein-conjugated lectins: Triticum vulgare agglutinin (WGA), Ulex europaeus agglutinin I (UEA1), Ricinus communis agglutinin I (RCA1), glycin max-soy bean agglutinin (SBA), Dolichus biflorus agglutinin (DBA), and Arachis hypogaea peanut agglutinin (PNA). These plant agglutinins bind to specific nonreducing end-terminal carbohydrate residues. Only the lectins derived from WGA, which produced the strongest staining, and UEA1 consistently bound to both intestinal goblet cell mucin and epithelial cell microvillar membranes. The intensity of lectin binding was greatest in the upper villus and diminished down towards the crypt, being weakest in the crypt base. Similar histochemical studies carried out on small bowel biopsies from five patients with cystic fibrosis revealed no major qualitative differences between the intestinal glycoconjugates in normal subjects and those with cystic fibrosis. These results suggest that glycoconjugate biosynthesis of human intestinal goblet cell mucin and epithelial cell membranes may be complete and hence full differentiation achieved only when these cells have migrated out of the crypt and onto the villus.
Twenty-nine patients underwent courses of home parenteral nutrition therapy ranging from 1.5 to 52 months (mean 14.5 months). The primary diagnoses responsible for the requirement of home parenteral nutrition were radiation enteritis in seven patients, short bowel syndrome secondary to resection in seven, Crohn's disease in two, malabsorption states in six, and other reasons in seven. Seventeen patients (57 percent) had at least one complication. Nine patients had intravenous catheter complications and nine had metabolic complications. Nine patients have died, 11 have been successfully weaned from home parenteral nutrition, and 9 continue to receive home parenteral nutrition. Home parenteral nutrition is useful in a variety of catastrophic clinical situations, including preparation for subsequent operative therapy, temporary malabsorption, and permanent disability of the gastrointestinal tract. Complications are frequent and may be life-threatening.
Eight children with cystic fibrosis and exocrine pancreatic insufficiency were voluntarily hospitalized in a clinical research setting so that diet and enzyme supplements could be well controlled for consecutive 72-h balance studies. We previously reported on these patients, as part of a larger study group, because they showed significantly reduced fecal losses of fat and nitrogen at the highest dose of cimetidine added to the otherwise constant regimen. Analysis of specimens from this same study shows a cimetidine-related reduction in fecal bile acid loss. Numerous variables thought to influence fecal bile acid loss were closely controlled and/or measured in this clinical study setting. In order to potentially learn more about this complex phenomenon, we carried out a stepwise regression analysis of the data which indicated that half of the variance in fecal bile acid loss is still unaccounted for by the five "independent" variables tested in the regression. However, in this variance analysis system cimetidine assumes a larger relative role in modulating bile acid loss than it does in fecal losses of fat and nitrogen.
In fasting human serum, cholecystokinin (CCK) is not the principal substance which causes in vitro rabbit gallbladder contraction. Removal of CCK by affinity chromatography from fasting sera from 8 healthy adults reduced bioactivity only by 18 +/- 4% (SEM). Unlike CCK, the bioactivity of serum was enhanced by 30 to 57% rather than destroyed by pronase and chymotrypsin respectively and was not inhibited by dibutyryl cGMP. Reduction of serum bioactivity by carboxypeptidase Y indicated that the bioactive substances in serum are peptides. On Sephadex G-50, bioactive substances eluted in positions different from any known form of CCK. Thus, the principal substances in fasting human serum causing in vitro gallbladder contraction are not CCK but are most likely small peptides which act at receptors different from the receptors for CCK.
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The capacities of normal and cystic fibrosis (CF) sera to bind to exogenous human [125I]trypsin were compared. Sera from eight older CF patients bound significantly more exogenous human [125I]trypsin than did sera from eight normal subjects (p less than 0.001). Disregarding the increased trypsin-binding (TB) of CF sera, serum immunoreactive trypsinogen (SIRT) levels were not detectable in these eight older CF patients. However, when SIRT levels were corrected for TB, four CF patients had normal SIRT concentrations and four had low but detectable SIRT levels. As compared to five normal newborns' sera, serum from a newborn with CF had normal TB and the SIRT levels were very high. In conclusion, increased TB in CF serum lowers results of SIRT assays. Therefore, unless SIRT levels are corrected for TB, results obtained from currently available SIRT kits may be invalid.
Increased basal and/or pentagastrin-stimulated gastric acid secretion was observed in 31 of 40 cystic fibrosis (CF) patients as compared to 13 age-matched control volunteers. Fasting serum gastrin level for 20 CF patients of 67.7 +/- 11.1 pg/ml (ranging from 10 to 145 pg/ml) was normal. Meal-stimulated serum gastrin concentrations were not significantly higher for seven CF patients as compared to nine normal subjects. In a rat bioassay, serum extracts from six CF patients produced gastric acid secretion comparable to 250 ng/ml of pentagastrin; significantly (p less than 0.01) greater than the responses produced by serum extracts from six normal subjects. There was no significant correlation of severity of pulmonary disease or steatorrhea with acid secretory results. Fourteen of 16 CF patients biopsied had evidence of proximal small intestinal injury which correlated with basal acid output elevation. Gastric acid hypersecretion in CF patients is due to nongastrin secretagogues and is a cause of proximal small intestinal injury.
Fifty-one pediatric patients (range, 1 mo. to 16 yr.), all of whom had normal clinical findings and laboratory data pertaining to the gallbladder and biliary tract, were examined by ultrasound. Scans showed a gradual increase in the size of the gallbladder with age; only one patient had a gallbladder diameter greater than 3.5 cm or a length greater than 7.5 cm. Wall thickness could be measured in 45 patients and was never more than 3 mm. The lumen of the common hepatic duct gradually increased with age but was never greater than 4 mm. The right portal vein also showed a gradual increase with age.
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Explore the source record for details and available documents.