Search PubMed⌕ Search

Biomedical subjects

S R Hamilton

Publications and source records attributed to S R Hamilton.

250 records · Page 14Linked to original sources
PubMed1980

Enhancement by cholera toxin of IgA secretion from intestinal crypt epithelium.

Studies of the effects of cholera toxin on the intestine have produced conflicting results regarding stimulation of IgA secretion. In the present study rabbit ileal loops were perfused with saline, and the IgA content of the perfusate was assessed by immunoradiometric assay. Crypt epithelial IgA content in biopsies was studied by immunofluorescence. Cumulative loop fluid IgA production 300 minutes after exposure to cholera toxin was 6216 +/- 993 microgram/cm compared with 4646 +/- 953 microgram/cm in controls (P < 0 . 20). However, rate of fluid IgA production above baseline at 300 minutes was 1742 +/- 181 microgram/h/cm in cholera loops and 1049 +/- 310 microgram/h/cm in controls, and the mean difference between the cholera and control loops was statistically significant (P < 0 . 05). In biopsies, mean rank of crypt epithelial IgA at 300 minutes was decreased compared with controls (P < 0 . 05). The findings of increased rate of fluid IgA production and decreased epithelial IgA suggest that a single dose of cholera toxin enhanced secretion of IgA from crypt epithelium into the intestinal lumen, although the magnitude of the enhancement was not great.

Animals↗
PubMed1980

Transient increase in serum creatine kinase isoenzyme BB activity after prostatectomy in a patient with massive benign prostatic hyperplasia.

The activity of creatine kinase isoenzyme BB (CK-BB) in serum is rarely abnormally high (i.e., detectable). An increase in immunoreactive CK-BB or CK-BB activity in patients with prostatic disease has been proposed as an indication of prostatic adenocarcinoma. Here we report the case of an elderly man with massive benign prostatic hyperplasia but no clinical or pathological evidence of prostatic adenocarcinoma, whose serum CK-BB activity was found by agarose gel electrophoresis to be 1 U/L (normal: 0%), 10% of his total CK activity. Serum CK-BB activity was further increased to 16 U/L (20% of total CK activity) 1 h after prostatectomy, but became undetectable by the second day after the operation. The findings suggest that: (a) the source of the serum CK-BB activity was the enlarged prostate gland; (b) abnormally high CK-BB activity in serum of men with prostatic disease does not necessarily indicate the presence of prostatic adenocarcinoma; and (c) myocardial injury could be erroneously diagnosed postoperatively in prostatectomy patients if CK isoenzyme methods are used that do not consistently separate "heart-specific" CK-MB from CK-BB.

Aged↗
PubMed1979

Serum creatine kinase isoenzyme MB activity: evaluation of a kit employing agarose-gel electrophoresis with overlay paper fluorescence scanning.

A commercial kit for determining serum creatine kinase isoenzyme MB activity was evaluated. The kit employed agarose-gel electrophoresis followed by incubation of overlay paper on the agarose and then fluorescnece scanning of the paper. Within-day coefficients of variation ranged from 24.9% for a specimen with no elevation of MB activity of 6.6% for a specimen with moderately elevated MB activity. The kit appeared to demonstrate MB in all sera and showed higher than expected values in recovery studies. The kit performed in a relatively linear fashion from 50 to 500 I.U./l total creatine kinase activity. Hemolysis appeared to lower measured MB. For comparison with another method, specimens were also analyzed by microcolumn chromatography, which was found to incompletely separate isoenzymes. The kit produced lower values than microchromatography for specimens with low MB activities and higher values for specimens with elevated MB activities. Patients without corroborative evidence of myocardial injury showed a somewhat hyperbolic relationship between per cent MB and total creatine kinase activity, but MB activity was generally 4 I.U./l or less. Although the kit had serious laboratory shortcomings, it may be as clinically useful as other methodologies.

Chromatography, Ion Exchange↗
PubMed1979

Comparison of microchromatography and electrophoresis with elution for hemoglobin A2 (Hb A2) quantitation.

Microcolumns prepared in the authors' laboratory, two commercial microchromatography kits, and electrophoresis with elution were compared for Hb A2 quantitation. Day-to-day imprecision of microchromatographic methods was similar (CV 4.7--6.6%) and somewhat less than electrophoresis with elution (CV 8.0--9.1%). Both commercial kits showed variable imprecision in different lots; one lot of Kit B gave erratic results due to resin leakage. From 49 patient specimens, Kit A microcolumns and those of the authors identified the same 14 patients with an elevated percentage of Hb A2 and showed good correlation (P = 0.90), although Kit A showed constant bias toward higher values. Electrophoresis with elution resulted in a false-positive and a false-negative value, did not correlate well with microcolumns (P = 0.78 and 0.76), and showed proportional bias toward lower values for an elevated percentage of Hb A2. Commercial kits were convenient, relatively quick, and cost-effective. Frozen, stabilized hemolysates performed well for quality control.

Blood Protein Electrophoresis↗
PubMed1979

Suppression of local intestinal immunoglobulin A immune response to cholera toxin by subcutaneous administration of cholera toxoids.

Cholera toxin has been shown to modulate immune responses, generally producing enhancement when administered simultaneously with antigen and suppression when administered a day or more earlier. In a previous study using chronically isolated ileal loops in rabbits, we found that two subcutaneous (s.c.) "priming" and "boosting" doses of biologically active cholera toxin suppressed the local intestinal immunoglobulin A response to intraloop doses of cholera toxin. In the study reported here, two different biologically inactive but antigenically intact cholera toxoids, glutaraldehyde toxoid and choleragenoid, where administered s.c. by the same immunization schedule as for toxin in the earlier experiment. Suppression of local immune response to intraloop cholera toxin as compared with animals receiving no s.c. inoculations was again found. The results suggest that in this model suppression was immunological (mediated by an immunological mechanism) rather than toxigenic (mediated by biological activity of cholera toxin). In addition, the occurrence of suppression of local intestinal immune response after systemic immunization suggests that suboptimal protection against enteric infections could occur after s.c. vaccination.

Antibody Formation↗
PubMed1979

Ileal adenomas after colectomy in nine patients with adenomatous polyposis coli/Gardner's syndrome.

Adenomas of the ileal mucosa are an uncommon finding in adenomatous polyposis coli/Gardner's syndrome. We report 9 patients who were found to have ileal adenomas 1 yr 11 mo to 25 yr 11 mo after colectomy. The ileal adenomas occurred proximal to an ileorectal anastomosis in 7 patients, both proximal to a cecoproctostomy and later proximal to an ileostomy in 1 patient, and in an ileostomy in 1 patient. The cases confirm that ileal mucosa is susceptible to adenoma formation in adenomatous polyposis coli/Gardner's syndrome and thus provide additional evidence that adenomas are not confined to the colon in these patients. In addition, the findings in the cases suggest that the ileal adenomas developed after colectomy. Thus, our cases suggest that the small intestine should be studied for the presence of adenomas after colectomy with either ileoproctostomy or ileostomy, as well as before resection. On the other hand, aggressive management does not seem warranted as carcinoma of the jejunum and ileum has been reported only rarely.

Adult↗
PubMed1978

Local (immunoglobulin A) immune response by the intestine to cholera toxin and its partial suppression with combined systemic and intra-intestinal immunization.

Chronically isolated Thiry-Vella (T-V) ileal loops in rabbits were used to study the local and systemic immune response to purified cholera toxin (CT). Immunization consisted of intraloop (i.l.), subcutaneous (s.c.), or combined i.l. and s.c. inoculation of CT. Fluid from the loops and sera were tested for neutralization of CT by the blueing test and for relative content of isotype-specific (immunoglobulins A [IgA] and G [IgG]) anti-CT. To demonstrate protection against CT, fluid production by the chronic T-V loops was measured after challenge with CT; an "acute" loop prepared from adjacent intestine at the time of challenge was also tested in some animals. The highest neutralizing titers in loop fluids were found in animals receiving i.l. or i.l. and s.c. inoculations, whereas titers in sera were highest in rabbits receiving s.c. or i.l. and s.c. inoculations. IgA anti-CT in fluids became greatest after i.l. inoculation alone and was lowest in s.c. animals. Combined s.c. and i.l. immunization was accompanied by reduced content of IgA anti-CT in fluids as compared with that obtained with i.l. inoculation alone. This finding strongly suggested a suppressive effect on local immunization by s.c. inoculation. While this suppression may have been due to a direct (toxigenic) effect of CT on lymphocytes, an immunogenic mechanism, probably mediated through suppressor T cells, is favored. Little IgG anti-CT was detected in any loop fluids, but high levels were found in sera after two s.c. inoculations or four i.l. inoculations. Neutralization titers for the fluid specimens showed much better correlation with IgA anti-CT values than with IgG anti-CT values. The chronic and acute T-V loops showed protection against fluid production after exposure to CT in systemically and locally immunized animals. However, IgG anti-CT usually appeared in both loops; leakage of serum antibodies because of surgical manipulation was felt, therefore, to invalidate these protection results as a demonstration of local immunity. In challenge studies in undisturbed chronic loops, only local immunization alone was found to result in definite protection.

Animals↗
PubMed1977

Regnerative of cardiac type mucosa and acquisition of Barrett mucosa after esophagogastrostomy.

The surgically created squamocolumnar junction in patients who have undergone an esophagogastrostomy after partial esophagogastrectomy provides a unique opportunity to study mucosal regeneration in the setting of gastroesophageal reflux. The pathological and clinical findings in 17 such patients are presented. In each patient the anastomosis had been performed between histologically documented squamous-lined esophagus and gastric fundus. Cardiac type mucosa had regenerated in the region of the anastomosis in 9 patients and was detected as early as 2 months after operation. In addition, 3 patients, 2 of whom had cardiac type mucosa, had acquired Barrett or Barrett-like mucosa on the distal esophagus by 76 to 119 months. Gastroesophageal reflux was prominent in all 3 of these patients. The findings strongly support the hypothesis that the distinctive mucosa of Barrett's esophagus develops after reflux-induced ulceration and subsequent mucosal regeneration by immature cells that are derived from cardiac and/or fundic mucosa, and which undergo specialized differentiation in the presence of reflux.

Adult↗
PubMedDate not supplied

Prevalence of ras gene mutations in human colorectal cancers.

A combination of DNA hybridization analyses and tissue sectioning techniques demonstrate that ras gene mutations occur in over a third of human colorectal cancers, that most of the mutations are at codon 12 of the c-Ki-ras gene and that the mutations usually precede the development of malignancy.

Adenoma↗
PubMedDate not supplied

Congenital diarrhea with intestinal inflammation and epithelial immaturity.

We report an interesting case of congenital inflammatory bowel disease and intestinal epithelial immaturity that presented as secretory diarrhea. No infectious, metabolic, or anatomical basis for these findings was identified. As differentiated from previous reports of neonatal enteropathies, this infant demonstrated involvement of both the small and large intestine with histopathologic findings of acute and chronic inflammation, extensive submucosal fibrosis, and "flat" small intestine mucosa. In addition, this patient had a polyamine deficiency (a primary or secondary phenomenon), which may have contributed to delayed epithelial maturation. These findings suggest that the inflammatory bowel disease and altered epithelial maturation contributed to a fatal intractable diarrhea.

Diarrhea, Infantile↗
PubMedDate not supplied

Molecular and phenotypic markers of hamartomatous polyposis syndromes in the gastrointestinal tract.

Hamartomatous gastrointestinal polyposis syndromes have always been considered as non-neoplastic. Nevertheless, an increased cancer risk both within and outside the gastrointestinal tract may exist in these syndromes. The hamartomatous polyps may sometimes harbor dysplasia, but their neoplastic potential is unknown. The genetic defects causing the hamartomatous syndromes are less well established than, for example, familial adenomatous polyposis (FAP) and hereditary non-polyposis colorectal cancer (HNPCC). The genetic studies on the Mendelian inherited syndromes FAP and HNPCC have made a major contribution to the identification of genes involved in colorectal tumorigenesis. The genes involved in colorectal cancer development may also contribute to cancer development in the hamartomatous polyposis syndromes, and are currently under investigation. Furthermore, new insights into the development of various cancers may be obtained by the isolation and characterization of genes involved in Mendelian inherited hamartomatous polyposis syndromes. This report summarizes the available literature on this subject, and describes the pheno- and genotypic features of the hamartomatous syndromes of juvenile polyposis, Peutz-Jeghers syndrome, and Cowden's disease.

Adenomatous Polyposis Coli↗
PubMedDate not supplied

Cerebrospinal fluid cytology in histiocytic proliferative disorders.

Morphologically atypical histiocytes were observed in the cerebrospinal fluid (CSF) of five patients with histiocytic proliferative disorders, including one each classified as Letterer-Siwe disease and Hand-Schüller-Christian disease and three as malignant histiocytosis. In all of these patients except the one with Letterer-Siwe disease, neurologic examination, CSF leukocyte count and protein and glucose concentrations were normal. Necropsy studies in the three fatal cases (one patient with Letterer-Siwe disease and two with malignant histiocytosis) demonstrated leptomeningeal involvement by atypical histiocytes in all three and brain involvement in the patient with Letterer-Siwe disease. These observations suggest that cytologic examination of CSF is warranted in patients with histiocytic proliferative disorders and may be reliable in documenting central nervous system, particularly leptomeningeal, involvement. The atypicality of the histiocytes in the CSF, however, was not indicative of the classification of the histiocytic proliferative disorder. Because the patient with Hand-Schüller-Christian disease continues to have a normal neurologic examination seven years after abnormal histiocytes were initially detected in his CSF, we believe that the clinical condition of the patient and classification of the histiocytic proliferative disorder are of primary importance for initiating aggressive therapy directed at the central nervous system.

Adolescent↗