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Biomedical subjects

J K Stephens

Publications and source records attributed to J K Stephens.

At least 37 records · Page 2Linked to original sources
PubMed1990

Endoscopic and histologic findings in the upper gastrointestinal tract of children with Crohn's disease.

In an attempt to define endoscopic and histologic changes suggestive of upper gastrointestinal Crohn's disease (CD), the medical histories, endoscopic reports, and biopsies were reviewed from 24 pediatric patients with CD and 28 age-matched patients without CD in whom esophagogastroduodenoscopies were performed because of upper GI symptoms. No differences in the overall frequency of endoscopic abnormalities were found between the two groups. However, gastric erosions and ulcerations were more frequent in CD patients. Histological abnormalities in the stomach and duodenum were also more frequent in CD patients. Noncaseating granulomas were found in five patients with CD and in one patient without clinical, radiologic, or endoscopic evidence of CD. Focal inflammation in the stomach and duodenum occurred more frequently in CD patients. Two patients with CD had focal and deep chronic inflammatory infiltrates in the esophagus, which reached the submucosa. Abnormal histology was often seen in CD patients with normal endoscopic appearances. We conclude that superficial ulcerations seen during endoscopy and the histological finding of focal inflammation may represent upper GI CD in pediatric patients. Histological changes can be missed if biopsies are not taken from normal-appearing mucosa during endoscopy.

Adolescent↗
PubMed1989

Correlation between automated karyometric measurements of squamous cell carcinoma of the esophagus and histopathologic and clinical features.

The clinical staging of esophageal carcinoma is unreliable currently, making it difficult to select patients for aggressive therapy. To further refine staging criteria, the nuclear characteristics of a series of 31 patients with squamous cell carcinoma of the esophagus were studied using a computerized image analysis system (MicroTICAS). Karyometric measurements, including total nuclear DNA content, nuclear area, and nuclear roundness were compared with various clinical and histologic variables. Nearly all tumors (30 of 31) were aneuploid. Tumors with nuclear areas greater than 70 microns2 were associated with transmural esophageal penetration (P less than 0.05) and to a lesser extent with poor survival (less than 6 months; P = 0.06). Surprisingly, nuclear ploidy did not correlate with either variable. These data support a role for nuclear analysis on preoperative biopsy specimens as an adjunct in clinical staging.

Aneuploidy↗
PubMed1989

Unusual urethral diverticulum lined by colonic epithelium with Paneth cell metaplasia.

Diverticulum of the female urethra has an incidence of 1.4% to 4.7%. It is generally agreed that the majority of these are acquired lesions. There is, however, evidence that some are of congenital origin. Documented cases of diverticula with colon-type tissue are rare. A case of urethral diverticulum with colonic epithelium and features of Paneth cell metaplasia is presented. Causes, symptoms, diagnostic methods, and treatment are discussed.

Adult↗
PubMed1989

A case report of three synchronous stage I malignant neoplasms.

A patient with three synchronous, Stage I neoplasms of the ovary, kidney, and lung, who underwent resection of all lesions at the same operative procedure, is presented. The incidence of multiple primary malignancies and the prognosis for Stage I cancers of the ovary, kidney, and lung are reviewed.

Adenocarcinoma↗
PubMed1988

Barrett's ulcer.

A case of an ulcer developing within previously documented Barrett's epithelium is reported. The patient had symptoms of gastroesophageal reflux for many years and Barrett's esophagus beginning 21 cm from the incisor teeth was documented by endoscopy one year earlier. Hospitalization was necessitated by an upper gastrointestinal bleed which was found to be due to an ulcer at 29 cm from the incisors. There was no inflammation of the surrounding columnar epithelium nor was there any esophagitis within the squamous epithelium. This case documents that ulcers in Barrett's esophagus can arise de novo within the columnar epithelium despite the hypothesis that this epithelium is present because it is more resistant to acid/peptic damage than squamous epithelium. This suggests that some ulcers in Barrett's epithelium may be due to spontaneous degeneration of the epithelium as this patient had no esophagitis, suggesting that gastroesophageal reflux was not causing diffuse damage.

Aged↗
PubMed1983

[3H]dopamine depletion from osmotically defined storage sites: effects of reserpine, 53 mM KCl, and d-amphetamine.

A crude synaptosome-containing fraction (P2') prepared from rat striatal slices incubated with [3H]dopamine was exposed to hypoosmotic conditions and rapidly subjected to Millipore filtration. P2'-associated [3H]dopamine trapped on the filters was defined as hypoosmotic resistant, whereas P2'-associated [3H]dopamine that washed through the filters was defined as hypoosmotic sensitive. Electron microscopic examination of sections prepared from a P2' pellet that had been exposed to hypoosmotic conditions revealed extensive synaptosomal lysis. [3H]Dopamine accumulation and retention by the hypoosmotic-resistant fraction were reduced by reserpine. The proportional distribution of [3H]dopamine between hypoosmotic-resistant and -sensitive fractions was measured following in vitro exposure of the preloaded P2' fraction to reserpine, 53 mM KCl, and d-amphetamine. Each of these treatments resulted in a time-dependent loss of [3H]dopamine from the loaded P2' fraction without eliciting an alteration in the proportional distribution of [3H]dopamine between hypoosmotic-resistant and -sensitive fractions. Release induced by reserpine and d-amphetamine was independent of extrasynaptosomal Ca2+, whereas 53 mM KCl-induced release was dependent on extrasynaptosomal Ca2+. These results suggest that dopamine may be rapidly equilibrated between osmotically defined storage compartments, and thus specific compartmental depletion of loaded [3H]dopamine cannot be identified on the basis of osmotic lability.

Animals↗
PubMed1981

Immunocytochemical localization of tyrosine hydroxylase in rat adrenal medulla by the peroxidase labeled antibody method: effects of enzyme activation on ultrastructural distribution of the enzyme.

A monospecific antibody against tyrosine hydroxylase (TH), purified from a transplantable rat pheochromocytoma, was produced in rabbits. Immunohistochemical techniques were employed in order to determine if a relationship exists between the subcellular distribution of TH and the level of activation of the enzyme in the rat adrenal medulla. Tyrosine hydroxylase activity in adrenals removed from non-stressed rats following pentobarbital anesthesia was found to be 12.9 +/- 1.0 nmol DOPA formed x mg protein-1. The use of ether anesthesia (17.9 +/- 2.0 nmol DOPA formed x mg protein-1), and the administration of electroconvulsive shock (ECS) followed by decapitation (35.9 +/- 2.0 nmol DOPA formed x mg protein-1) was associated with an acute activation of adrenal TH. The subcellular distribution of TH within the cytosol of chromaffin cells from animals subjected to anesthesia or ECS, as determined by immunocytochemical techniques, was similar. In all treatment groups chromaffin cells were found which had TH associated with some chromaffin granules. The percentage of chromaffin granules which appeared to contain TH was lower in animals subjected to ECS plus decapitation as compared with anesthetized animals. These observations suggest that the activation of adrenal medullary TH is not associated with a shift in the subcellular distribution of the enzyme from the cytosol to membranous structures.

Adrenal Medulla↗
PubMed1979

Hormonal effects on the regulation of hepatic heme biosynthesis.

Drug-induced porphyrin accumulation occurs in chick embryo liver cells maintained in serum-free Waymouth MD 705/1 medium. Addition of insulin and thyroxine to the medium results in a marked enhancement of porphyrin accumulation. The addition of hydrocortisone results in a further enhancement of porphyrine accumulation. Several agents which are reported to increase intracellular adenosine 3':5'-monophosphate (cAMP) levels, viz. glucagon, sodium fluoride, cAMP or its dibutyryl derivative, 3-isobutyl-1-methylxanthine and papaverine enhanced drug-induced porphyrin biosynthesis. On the other have, agents which are reported to decrease intra-cellular cAMP levels, viz. alloxan and imidazole, diminished drug-induced porphyrin accumulation. cAMP appears to enhance, but not to function as a "second messenger" in drug-induced porphyrin biosynthesis. Drug-induced porphyrin accumulation in chick embryo liver cells depend upon the insulin to glucagon ratio. A low level of porphyrin accumulation occurs at insulin to glucagon ratios similar to those found following glucose administration in vivo, suggesting a possible explanation for the therapeutic effect of glucose in hepatic porphyria. The 5 alpha A(A:B trans) and 5 beta H(A:Bcis) steroids are equipotent in inducing delta-aminolevulinic acid synthetase and porphyrin accumulation in chick embryo liver cells maintained in serum-free culture medium. Thus, there is no specific steric requirement for porphyrin-inducing activity in steroids.

1-Methyl-3-isobutylxanthine↗
PubMedDate not supplied

Defect in fatty acid oxidation: laboratory and pathologic findings in a patient.

The clinical, laboratory, and pathologic findings in a patient with a previously undescribed deficiency in fatty acid oxidation are summarized. The patient had a fatal defect in fatty acid metabolism profoundly affecting heart, skeletal muscle, liver, and kidney. Oxidation of palmitate was 38-51% of controls. Complementation assays demonstrated that the patient's fibroblasts complemented fibroblast lines from all known defects in fatty acid oxidation except long-chain acyl-CoA dehydrogenase deficiency. Urine and serum carnitine profiles also were indicative of a defect in the oxidation of long-chain substrate; however, the palmitoyl-CoA dehydrogenase activity was actually increased. This finding indicates that the patient had a defect that was distinct from, but possibly related to, long-chain acyl-CoA dehydrogenase deficiency. This patient demonstrates the laboratory and pathologic findings in defects in fatty acid oxidation and how they differ from those in Reye syndrome.

Acyl-CoA Dehydrogenase, Long-Chain↗