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Biomedical subjects

R Reshef

Publications and source records attributed to R Reshef.

18 recordsLinked to original sources
PubMed1990

Effect of a calcium-enriched diet on the colonic epithelial hyperproliferation induced by N-methyl-N'-nitro-N-nitrosoguanidine in rats on a low calcium and fat diet.

We examined whether hyperproliferation of colonic crypt epithelium during cancer induction by N-methyl-N-nitro-N-nitrosoguanidine (MNNG), in rats on a low fat and calcium diet could be reduced by added calcium p.o. From the age of 4 weeks, 104 male Sprague-Dawley rats received a low fat (3.5%), low calcium (0.05% calcium ion), and low vitamin D (0.4 IU/g) diet. Sixty-four also had calcium salts, derived from either calcium lactate or solubilized calcium carbonate, added to their drinking water; therefore their total calcium intake was about 1% of daily diet. At age 12 weeks the rats were divided into 4 treatment groups: 8 rats, not receiving added calcium, had rectal saline instillations weekly (saline control group) and were sacrificed after a further 28 weeks; 3 groups of 32 rats each received intrarectal MNNG (1.5 mg) weekly. One group, not receiving added calcium, was the MNNG control group; while the second group also received added calcium lactate, and the third group received calcium carbonate. Groups of 24 were sacrificed periodically until 28 weeks of treatment. Rats were sacrificed and epithelial proliferation was estimated, 1 week after the last intrarectal instillation, by in vivo labeling with tritiated thymidine and measuring the ratio of labeled to total colonic crypt epithelial cells. The mean labeling index of the MNNG treated and added calcium groups were significantly higher (8.7-9.5%) than that of the saline controls (2.8%) only at week 28; however, it was then still significantly less than that of the MNNG controls not having added calcium (17.9%). Hyperproliferation, during induction of colonic cancer by MNNG in rats on a low calcium diet, can be reduced by a calcium enriched diet even in the presence of a low fat intake.

Animals↗
PubMed1988

Colon cancer bearing rats produce a lymphokine which induces macrophage migration inhibition (MIF) in vitro.

We studied a series of 40 rats at various stages of colorectal carcinoma, as induced by N-methyl-N-nitro-Nitrosoguanidine. Lymphokine containing supernatants were obtained simultaneously from splenic and peripheral lymphocytes, after exposure to rat colon cancer antigen in vitro. The lymphokine was found capable of performing Macrophage Migration Inhibition (MIF) when obtained from rats with: carcinoma through serosa, carcinoma of submucosa, carcinoma of the mucosa and carcinoma in situ. All control rats were free of cancer and were MIF negative. The MIF response in this study was evaluated as a marker of chemically induced colorectal carcinoma in rats in order to better understand the lymphocyte response to tumor progression from atypia to adenocarcinoma of the colon.

Adenocarcinoma↗
PubMed1988

Recurrent acute pancreatitis associated with pancreas divisum.

Described is the case of a 24-yr-old patient in whom recurrent attacks of acute pancreatitis following a cholecystectomy were found to be associated with anomaly of the pancreas--the so-called pancreas divisum. An examination by endoscopic retrograde cholangiopancreatography showed typical findings of a short duct of Wirsung. Cannulation of the secondary duct of Santorini revealed a grossly dilated and strictured duct full of stones. After drainage of the duct by a pancreaticojejunostomy (Puestow procedure), the patient has not had any further episodes of acute pancreatitis during a follow-up period of 4 yr.

Acute Disease↗
PubMed1987

The macrophage migration inhibition (MIF) assay as a marker of colorectal cancer. Studies in patients with colorectal cancer, noncolonic neoplasms, and conditions predisposing to colorectal cancer.

A specific macrophage migration inhibition assay, using patient lymphocytes incubated with a human colonic cancer extract, was studied in 92 patients with proven colorectal cancer and in 134 other individuals (20 normal controls, 80 patients with various nonmalignant gastrointestinal diseases, and 34 patients with extracolonic malignancies). A positive response was obtained in 78 of 92 colorectal cancer patients, but in none of the 20 normal controls. A positive response occurred in four of 34 patients with extracolonic malignancies and in approximately half of patients with colonic adenomas and in one third of patients with ulcerative colitis. The significance of positive results in these patients (with diseases considered premalignant) is unclear, and is being studied further. In patients with previous resection of colorectal cancers, positive responses were frequent during the first year following resection, and rare thereafter. The results suggest that this method may be useful as a clinical marker for colorectal cancer, and warrants further technical refinement and study of specific patient populations.

Antigens, Neoplasm↗
PubMed1987

Comparison of two lymphokines (macrophage migration inhibition, leukocyte adherence inhibition factors) and carcinoembryonic antigen, in colorectal cancer and colonic premalignant lesions.

Previous studies in our laboratory on 92 patients with colonic cancer have suggested a promising degree of specificity and sensitivity for a macrophage migration inhibition factor (MIF) test using patient's lymphocytes incubated with a human colon cancer extract. This study compares the results of the MIF technique with serum carcinoembryonic antigen (CEA) levels and with the lymphocyte adherence inhibition (LAI) test in 18 colon cancer patients and 27 patients with conditions considered to predispose to colon cancer (colonic adenomas, ulcerative colitis, and Crohn's disease). Among colonic cancer patients, MIF and LAI were positive in 17 out of 18, but CEA was elevated in eight. MIF and CEA were negative in all 16 normal control subjects; LAI was negative in 13. Among patients with colonic adenomas, MIF and LAI were positive in three of five; CEA was negative in all. In the ulcerative colitis and Crohn's disease group, MIF was positive in seven of 22, LAI was positive in 11, and CEA was negative in all 22. Thus, MIF and LAI appear to be sensitive marker's for human colonic cancer. More extensive studies and precise characterization of these groups are warranted.

Carcinoembryonic Antigen↗
PubMed1987

Malignant tumor masquerading as eosinophilic gastroenteritis.

A 49-year-old patient presented with urticaria, vomiting, diarrhea and peripheral eosinophilia. A histological diagnosis of eosinophilic gastroenteritis was made. Within 3 weeks of admission a highly papillary adenocarcinoma of the right ovary was diagnosed. The gastrointestinal symptoms and the eosinophilia disappeared after partial resection of the tumor and chemotherapy. A possible relationship between cancer, eosinophilia and eosinophilic gastroenteritis is discussed.

Adenocarcinoma, Papillary↗
PubMed1984

Impaired oxidation of debrisoquine in patients with perhexiline liver injury.

Perhexiline maleate is an antianginal agent which depends on hepatic oxidation for its elimination. Its use may be complicated by the development of peripheral neuropathy and liver damage. The majority of patients with perhexiline neuropathy have an impaired ability to effect metabolic drug oxidation which is genetically determined. Information has not been available on drug oxidation capacity in patients with perhexiline liver injury. Drug oxidation was measured using an oxidation phenotyping procedure in four patients with perhexiline liver injury and in 70 patients with chronic liver disease serving as a control group. All four patients with perhexiline liver damage showed a substantial metabolic defect; three of the four patients (75%) showed a genetically determined impairment of oxidation capacity. The incidence of severely impaired oxidation capacity in the perhexiline group was significantly greater than in the patients with chronic liver disease (6/70; 8.6%) and in the healthy population (9%) (F = 0.0048). A clear association exists between perhexiline liver injury and diminished drug metabolic activity, suggesting that the propensity to develop perhexiline liver injury is, at least in part, genetically determined.

Adolescent↗
PubMed1978

Cardiac involvement and superior vena caval obstruction in Behçet's disease.

A patient with Behçet's disease developed the rare complications of pericarditis and, two months later, superior vena caval obstruction. The latter complication was investigated by angiography to exclude other causes. As a result of this investigation the caval obstruction was managed conservatively, the symptoms and signs improving spontaneously.

Adult↗
PubMed1977

Myocardial infarction association with the Riley-Day syndrome.

The "sudden death" of a 23-year-old Ashkenazy Jew, suffering from "familial dysautonomia" was probably caused by an arrhythmia accompanying a myocardial infarction. Such a report is unique. Diffuse coronary atherosclerosis and direct myocardial "catecholamine cardiomyopathy" seem responsible for the myocardial damage. However, diversion of the endocardial blood flow toward dpicardium and a "coronary steal" phenomenon, both the result of a sudden catecholamine discharge, could aggravate the ischemic injury.

Adult↗
PubMedDate not supplied

Oxidation phenotyping in alcoholics with liver disease of varying severity.

The propensity to develop alcoholic cirrhosis is probably, at least in part, genetically determined. A striking similarity exists histologically between perhexiline and alcohol-related hepatitis and both are potentially precirrhotic lesions. Liver damage due to perhexiline is associated with impaired drug oxidation capacity which is genetically determined and tested by use of debrisoquine. Oxidation phenotyping might be used to predict susceptibility to perhexiline liver damage; it might also predict the potential to develop alcoholic cirrhosis. Oxidation phenotyping was therefore undertaken, using debrisoquine in 100 alcoholic patients, 30 of whom had only fatty liver despite prolonged alcohol abuse, while the remaining 70 had alcoholic hepatitis and/or cirrhosis. One hundred patients with nonalcoholic chronic liver disease served as controls. The number of patients with severely impaired drug oxidation capacity (poor metabolizer phenotype) was similar in the alcoholic group (8%) and the nonalcoholic control group (7%). In particular, the incidence of the poor metabolizer phenotype was similar in alcoholics with severe liver disease (10%) and in those with only fatty change (3%). There appears to be no association between the susceptibility to develop alcoholic cirrhosis and drug oxidizing capacity.

Adult↗