[Lethal hemorrhagic syndrome after mithramycin. Lack of platelet aggregation and inhibitor of factor V].
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Blood Coagulation Disorders↗
Biomedical subjects
A Robert
Publications and source records attributed to A Robert.
Response to an editorial on gastric cytoprotection.
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Animals↗
Potentiation of aspirin-induced gastric lesions by exposure to cold in rats. Role of acid secretion, mucosal blood flow, and gastric mucosal prostanoid content.
We investigated the mechanism by which exposure to cold sensitizes rats to the formation of gastric lesions after a low dose of aspirin (50 mg/kg). Six times more lesions were produced by aspirin plus cold than by aspirin alone. Three hypotheses were studied to explain the synergism of aspirin plus cold on lesion formation: gastric acid hypersecretion, reduced gastric mucosal blood flow, and decreased prostanoid synthesis by the stomach. Cold, and cold plus aspirin, stimulated gastric acid secretion (to a similar extent), whereas aspirin had no effect. Gastric mucosal blood flow, measured by the hydrogen gas clearance method, was decreased by cold, aspirin, and aspirin plus cold, and the extent of decrease was similar. Prostanoid generation [prostaglandin E2 (PGE2), PGF2 alpha, 6-keto PGF1 alpha, and thromboxane B2] by the gastric corpus mucosa was not affected by cold, but was reduced equally (by at least 90%) in animals receiving aspirin alone or aspirin plus cold. After oral administration of aspirin, the plasma contained mostly salicylic acid (98%), whereas the gastric mucosa contained mostly aspirin (80%-85%). We conclude that the synergism of aspirin plus cold on the formation of gastric lesions probably results from the combined effects of three factors: increased secretion of acid (because of exposure to cold) that is in contact with a gastric mucosa in which blood flow is reduced (because of exposure to cold or to aspirin), and in which the synthesis of cytoprotective prostaglandins is inhibited (by aspirin). Such mucosa may be particularly vulnerable to the damaging effect of hyperacidity.
Animals↗
Hyperbilirubinemia does not interfere with hemoglobin saturation measured by pulse oximetry.
This prospective clinical study evaluated the influence of high bilirubin plasma levels on the Nellcor pulse oximeter readings (SpO2). Twenty-nine icteric patients (mean total bilirubin 19.2 mg/dl, range 2.3-84.3 mg/dl) were compared with 46 controls. The difference between SpO2 and oxyhemoglobin percentage of hemoglobin (HbO2corr) or fractional saturation as measured by a seven wavelengths Corning Co 2500 Co-oximeter and corrected for the spectral error induced by hyperbilirubinemia in that co-oximeter was greater in icteric patients (bias and precision: 2.9% +/- 2.2% vs. 1.7% +/- 2.7%, P less than 0.03). However, icteric patients had also higher corrected carboxyhemoglobin levels (CoHbcorr) (1.8% +/- 0.7% vs. 1.3% +/- 0.8%, P less than 0.005) due to production of carbon monoxide during the catabolism of hemoglobin. Pulse oximeters read most of CoHb as oxyhemoglobin. After correcting SpO2 for carboxyhemoglobin in both groups of patients, the 99% confidence limits from the obtained regression line were the same in icteric patients (-0.81%, 1.03%) as in controls (-0.89%, 1.08%). There was thus no demonstrable direct influence of high bilirubin plasma levels on SpO2 as measured by a Nellcor pulse oximeter.
Adolescent↗
Diet and opiate addiction: a quantitative assessment of the diet of non-institutionalized opiate addicts.
The diet, weight and height of 38 non-institutionalized chronic opiate addicts have been assessed and compared to those of a random sample of the 20-35 year old general population of Canton Geneva, Switzerland. A history questionnaire was administered by specially trained dietitians. Results show that, after adjustment for age and alcohol intake, male addicts have the same caloric intake as non-addicts. However, addicts tend to replace foods that are rich in fat and proteins with foods rich in sucrose and relatively poor in vitamins and minerals. Beer is the major component of their much larger alcohol consumption. On the other hand, the body mass index (kg/m2) of the male addicts is within the normal range, suggesting this may not be a good indicator of their unbalanced diet. This study gives a quantitative assessment, in terms of nutrient intake, of the typical craving for sweet described by opiate addicts.
Adult↗
Role of glutathione status in protection against ethanol-induced gastric lesions.
The role of glutathione status in gastric mucosal cytoprotection has been a subject of controversy. Cysteamine, an exogenous sulfhydryl agent and diethyl maleate (DEM), an endogenous glutathione (GSH) depletor both appear to protect rats from ethanol-induced gastric lesions. In this study, we used various agents to alter gastric mucosal GSH levels and assessed the effects on susceptibility to ethanol injury. We found that DEM and buthionine sulfoximine both depleted gastric GSH but only DEM protected against ethanol-induced gastric lesions. L-Oxothiazolidine-4-carboxylate (OXT) and N-acetyl-L-cysteine (NAC) both potentiated ethanol-induced gastric lesions even though only NAC significantly raised the GSH level. The depletion of GSH by DEM was reversed by supplying cysteine in the form of OXT or NAC so that the net result was a GSH level close to normal control. The potentiation of ethanol injury by NAC and OXT was still apparent. These experiments show no relation between gastric GSH levels and susceptibility to ethanol injury.
Acetylcysteine↗
Receptor-mediated endocytosis of insulin: inhibition of [125I]iodoinsulin internalization in insulin resistant diabetic states of man.
We have used electron microscopic autoradiography to quantitatively study receptor-mediated endocytosis of [125I]insulin in freshly isolated monocytes from patients with non-insulin-dependent diabetes mellitus. In obese, non-obese, and lipoatrophic patients with diabetes, internalization of [125I]insulin was impaired at 30 min of incubation at 37 degrees C. By 60 min of incubation, however, internalization was indistinguishable from that of normals. In obese non-diabetic controls, internalization at 30 min was slightly less than internalization in normals but greater than that of the diabetic group. Dieting was associated with normalization of internalization in the obese group. We conclude that the rate of [125I]insulin internalization is impaired in non-insulin-dependent diabetes and compare this to previously reported results in insulin-dependent diabetes mellitus.
Adult↗
Immunohistochemical detection of post-therapy residual testicular lymphoblasts in childhood acute lymphoblastic leukemia (ALL).
The aim of this study was to evaluate the diagnostic value of immunohistochemistry with monoclonal antibodies (MoAbs) in detecting residual blast cells in testicular biopsies from children with acute lymphoblastic leukemia (ALL). In a prospective study of 26 patients, testicular biopsies were performed after completion of therapy, and the average follow-up after biopsies was 29 months. After immunostaining, seven patients with negative biopsies on routine histology showed scattered, strongly calla-positive cells as well as cells reacting with anti-B (CD22) MoAb. Among these seven patients with residual blast cells, four had relapsed either in testes (n = 1), bone marrow and testes (n = 1), or in the bone marrow (n = 2). In contrast, among the 15 patients without residual blast cells, all but 1 remained in complete remission. In four other cases no definite conclusion was possible after immunohistochemical study. Four testicular biopsies from patients with occult infiltration were used as positive controls. Negative controls consisted of testicular biopsies from children with testicular ectopia and postmortem testicular tissue specimens. Results suggest that the risk of relapse is significantly higher in patients with positive immunohistochemical findings indicating persistent residual blast cells. However, the predictive value of these findings requires confirmation on a larger number of cases to have therapeutic implications.
Adolescent↗
Prevention by prostaglandins of caerulein-induced pancreatitis in rats.
Acute edematous pancreatitis was produced in rats by subcutaneous administration of caerulein. Pancreas weight, pancreas histology and plasma amylase were used as endpoints to quantitate the severity of the syndrome. A caerulein dose of 10 micrograms/kg.hour produced the most severe pancreatitis, whereas at 5 micrograms/kg.hour the values were half-maximal. The pancreatic lesions were characterized by edema, formation of cytoplasmic vacuoles, leukocytic infiltration, necrosis, and with time (12-hour caerulein infusion) dilated acini. Cholecystokinin octapeptide also produced pancreatitis when given at ten times the dose required for caerulein (50 micrograms/kg.hour instead of 5 micrograms/kg.hour). Carbachol did not induce pancreatitis. Two prostaglandins, 16,16-dimethyl prostaglandin E2 injected subcutaneously and prostaglandin E2 infused subcutaneously, dose dependently prevented caerulein-induced pancreatitis (pancreatic edema, leukocytic infiltration, and necrosis) and reduced the number and size of intracellular vacuoles. The ED50 were 15 to 25 micrograms/kg for 16,16-dimethyl prostaglandin E2 and 90 micrograms/kg.hour for prostaglandin E2. Neither prostaglandin, given at doses inhibiting the development of pancreatitis, prevented the retardation of gastric emptying caused by caerulein, a finding suggesting that the prostaglandins may act specifically on the effect of caerulein on the pancreas but not on caerulein receptors in gastric smooth muscle. Indomethacin, an inhibitor of prostaglandin synthesis, and methscopolamine bromide, an anticholinergic agent, had no effect on caerulein-induced pancreatitis. We concluded that prostaglandins of the E type prevent the development of caerulein-induced pancreatitis. The mechanism by which prostaglandins protect the pancreas may involve stabilization of lysosomes within the acinar cells and inhibition of intracellular activation of pancreatic digestive enzymes.
16,16-Dimethylprostaglandin E2↗
Patch tests demonstrating immune (antibody and cell-mediated) reactions to foods.
For decades food allergists have sought a simple, inexpensive test for food allergy. Intradermal tests of aqueous material have not proved reliable. When positive, they are probably only 10% accurate. The newer laboratory tests for food allergy are expensive and highly sophisticated. They are impractical for use in the laboratories of practicing allergists with whom individuals with a potential food allergy are most liable to consult. The RAST is capable of identifying only Type I of the Gell-Coombs' reaction classification. Since 1980, a patch test of individual foods suspended in dimethylsulfoxide has been used as a screen for sensitivity to foods. Controlled clinical studies suggest this might prove to be a valuable test for food allergy. Immune studies appear to confirm the accuracy and reliability of this inexpensive test. No systemic reactions have been observed in the 400 patients tested indicating it to be a safe procedure.
Antibody Formation↗
[Relation of alcohol consumption and blood lipids and apolipoproteins--a study of a population of 3,897 wage-earners from the Lyon region].
Between June 1982, and September 1984, a survey was conducted among 3,897 employees in the Region of Lyon to study the relationship between alcohol consumption and serum concentrations of total cholesterol and triglycerides. In 400 randomly selected men, the following data were also obtained: concentrations of the cholesterol of the high density lipoproteins (HDL) and of their subfractions, and concentrations of the apoproteins A-I, A-II and B. All these biochemical concentrations increased, more or less, with alcohol consumption. Relative to non drinkers, the concentrations increased among males who declared drinking more than 80 grams of alcohol per day: for total cholesterol, by 10.0%; for triglycerides, by 24.7%; for HDL-cholesterol, by 26.7%; for HDL2-cholesterol, by 76.0%; for HDL3-cholesterol, by 15.0%; for apoprotein A-I, by 30.0%; for apoprotein A-II, by 52.2%; for apoprotein B, by 5.1%. These results, with the limitations inherent in a cross-sectional study, suggest that regular consumption of alcohol raises the concentrations of blood lipid components, both atherogenic and non-atherogenic.
Adult↗
[Severe Epstein-Barr virus infection in an infant].
A 11 month-old boy, without any informative familial pedigree, was admitted for peritonitis after intestinal perforation, associated with signs of pseudolymphoma and histiocytic activation. He developed later unexplained gastrointestinal bleeding and interstitial pneumonitis, which spontaneously improved. All infectious and immunologic studies were negative. Epstein-Barr Virus was found in throat, lungs and blood, whereas the specific antibodies production was delayed. No abnormality was detected 18 months later, except for a disappearance of vaccinal antibodies.
Humans↗
[Hypoplasia of cartilage and hair with combined immune deficiency].
We report a case of cartilage-hair hypoplasia in a girl. The patient had short stature with short limbs and scalloped long bone metaphyses, sparse, poorly-pigmented hair, and increased susceptibility to infections. Several features of this case deserve attention: neutropenia, probably due to an autoimmune mechanism, was an initial manifestation; the immune deficiency (defective B and T cell immunity, autoimmune manifestations) was severe, and cytomegalovirus infection possibly aggravated the immune deficiency and hormone abnormalities. Whereas this patient's short stature is becoming more marked, prophylaxis of infections and administration of immune globulins have effectively prevented complications for the last two years.
Cartilage Diseases↗
Indomethacin-induced gastric antral ulcers in hamsters.
Antral ulcers account for about half of gastric ulcers in humans. An animal model was developed to produce such ulcers. Indomethacin given subcutaneously to normally fed hamsters produced antral ulcers within 1-5 h, dose dependently. These ulcers penetrated the muscularis mucosae. With repeated administration of indomethacin and longer duration of treatment, the lesions became more severe and most animals died with perforated antral ulcers after 2-5 days. Like indomethacin, aspirin given orally also produced antral ulcers in hamsters. Indomethacin reduced the formation of prostaglandin E2, prostaglandin F2 alpha, and 6-keto prostaglandin F1 alpha by the antral mucosa, and increased gastric acid output more than twofold. The ulcers were prevented by various antisecretory agents (cimetidine, methscopolamine bromide, and omeprazole), and the antiulcer dose of each of these agents corresponded to the antisecretory dose. By contrast, several prostaglandins prevented the ulcers at very low, nonantisecretory doses. 16,16-Dimethyl prostaglandin E2 prevented the ulcers at a dose nearly 3000 times lower than the gastric antisecretory ED50. The mechanism by which prostaglandins prevent formation of these ulcers is unknown, but the effect is consistent with cytoprotection, i.e., protection of the gastric mucosa by nonantisecretory doses. Indomethacin-induced antral ulcers appear to depend on two factors: a depletion of prostaglandin content of the antrum and gastric hyperacidity.
Administration, Oral↗
Non-invasive data provide independent prognostic information in patients with chest pain without previous myocardial infarction: findings in male patients who have had cardiac catheterization.
From 1978 to 1985, 470 consecutive male patients with complaints of chest pain underwent a maximal exercise test with a thallium scan and coronary angiography (CA). Patients with a history of myocardial infarction (MI) were excluded. During the follow-up (from 12 to 96 months), 32 patients died and 30 had a non-fatal MI. Survival (SR) and event-free rates (EFR) were estimated by actuarial methods; the influence of non-invasive and invasive variables were examined in univariate and multivariate models using Cox analysis. The five-year SR was 89% and EFR was 81%. Among historical data, age (less than 0.001), type of complaints (less than 0.01) and pretest likelihood of CAD (less than 0.01) were univariate predictors of EFR; by multivariate analysis, age was the only significant predictor (less than 0.001). Most of the maximal-exercise (MEX) test data were good univariate predictors; by multivariate analysis, workload (less than 0.001) and the maximal-exercise test score (less than 0.001) were the significant predictors. From history and maximal-exercise test data, multivariate analysis indicated that the prognostic information was given by age (less than 0.05) and maximal-exercise test score (less than 0.001). Among the invasive data, the number of diseased vessels (less than 0.001) and ejection fraction were the predictors. The combination of invasive and non-invasive data indicated that age, MEX score, number of diseased vessels and ejection fraction contributed significantly and independently to the estimation of prognosis. Among 242 patients with two or three diseased vessels, the prognosis was determined by the maximal workload (less than 0.01); ejection fraction (less than 0.07) was no longer significant.(ABSTRACT TRUNCATED AT 250 WORDS)
Adult↗
Assessment of thallium-201 redistribution versus glucose uptake as predictors of viability after coronary occlusion and reperfusion.
Both 201Tl redistribution and persistent glucose uptake have been proposed as markers of viability after reperfusion. In the present study, they have been compared in the same open-chest canine preparation of occlusion and reperfusion. Ten fasting dogs were subjected to 2 hr of left anterior descending coronary artery occlusion and 4 hr of reperfusion. Myocardial blood flow was determined by a microsphere technique 100 min after occlusion and 3 hr after reperfusion. 201Tl was injected intravenously 20 min before reperfusion. Serial biopsy samples were obtained from ischemic and normal areas. 18F-2-deoxyglucose, a tracer of exogenous glucose uptake, was injected 3 hr after reperfusion. Thirty minutes before the animals were killed, simultaneous blood samples were taken from the femoral artery and the regional coronary veins draining the reperfused and the remote areas. Dogs were killed 4 hr after reperfusion was established. Area at risk was assessed by dye injection in vivo and area of necrosis by triphenyl tetrazolium chloride (TTC) staining, with confirmation by electron microscopy. Immediately after death, endocardial and epicardial samples were taken from regions characterized as risk regions, areas of necrosis, areas of patchy necrosis, and normal areas. These samples were counted in a scintillation well counter. Four hours after reperfusion, in ischemic myocardium (TTC positive) the relative 201Tl gradient between ischemic and normal regions was 26 +/- 13%, whereas in necrotic samples, this gradient was 71 +/- 26%.(ABSTRACT TRUNCATED AT 250 WORDS)
Animals↗
Coexpression of epithelial membrane antigen (EMA), Ki-1, and interleukin-2 receptor by anaplastic large cell lymphomas. Diagnostic value in so-called malignant histiocytosis.
A group of 63 cases of anaplastic large cell lymphomas (variants of diffuse large cell lymphomas often diagnosed as "malignant histiocytosis") was characterized on both morphologic criteria and expression of epithelial membrane antigen (EMA) and Ki-1 antigen (CD30). On the basis of the reactivity of these tumors with anti-EMA and anti-Ki-1 antibodies, four subtypes could be distinguished. In the majority of cases (n = 49), neoplastic cells coexpressed EMA and Ki-1 antigens. Nineteen of these cases were tested for IL-2R, and all were positive (Type I, EMA+, Ki-1+, IL-2R+). In the second group (n = 5), the neoplastic cells expressed EMA but not the Ki-1 antigen. These cases were not tested for the presence of IL-2R (Type II, EMA+, Ki-1-, IL-2R?). There were tumors with similar morphology expressing only Ki-1 antigen (Type III, EMA-, Ki-1+, IL-2R-) or negative for both EMA and Ki-1 antigens (Type IV, EMA-, Ki-1-, IL-2R-). EMA appeared to occur predominantly on activated cells, as has been previously shown for Ki-1 antigen. Analysis using monoclonal antibodies to T-cell, B-cell, or macrophage-associated differentiation antigens showed that these tumors were heterogeneous in terms of cell lineage. Tumors coexpressing EMA, Ki-1, and IL-2R (Type I), were most commonly of T-cell origin (n = 12); the remainder in this type expressed B-cell markers (n = 4), a mixed B/T phenotype (n = 2), or no clear phenotype (n = 9). By contrast, tumors of Types II, III, and IV were mainly from B-cell origin (n = 6) or showed a mixed B/T phenotype (n = 1). Despite the fact that a significant proportion of these cases were initially classified morphologically as "malignant histiocytosis," only 3 of the 63 cases were possibly of histiocytic origin. These results confirm that true malignant histiocytosis is rare and that most tumors with histologic features currently regarded as being consistent with this diagnosis are lymphocytic in origin and express activation antigens such as EMA, Ki-1 antigen, and IL-2R.
Antibodies↗
[Initial antibacterial prophylaxis after bone marrow allograft. Pilot study with systemic vancomycin].
In 22 consecutive patients treated by allogenic bone marrow transplantation, the authors report their experience in complete gastrointestinal decontamination and prophylactic systemic vancomycin. Neither septicemia from the low digestive tract nor with Gram positive is noticed. A child developed septicemia with Capnocytophaga ochracea, resistant to vancomycin. There is no infectious death in this study and no significative toxicity is reported.
Adolescent↗