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Biomedical subjects

D Bloom

Publications and source records attributed to D Bloom.

At least 55 records · Page 3Linked to original sources
PubMed1979

Bloom's syndrome. VII. Progress report for 1978.

The Bloom's Syndrome Registry was published in this journal in 1977. Now, in the first in a series of progress reports, recent accessions to the Registry are recorded, new instances of neoplasia are listed, and recent clinical observations and experimental results of general interest are cited.

Abnormalities, Multiple↗
PubMed1978

The interactive effects of locus of control and situational stress upon performance accuracy and time.

The present paper sought to clarify the conceptual relationship between expectancy for personal control, stress, and behavioral reactions to stress. Expectancy for control was assessed as a personality characteristic of internal control; stress was experienced as strong environmental interruptions, disturbances and unpredictable obstacles encountered during the performance of assigned tasks. Subjects were junior high school aged students who attempted to complete three academic type tasks during one of two levels of stress or a base line, no stress, condition. Analyses of the data included: (a) internal subjects were capable of sustaining task performance under high stress, but external students experienced performance decrements as stress increased; (b) time to complete the mathematics task reflected a facilitating effect of stress for internals but a debilitating effect for externals; (c) performance differences between internal and external students, in the absence of differences in reported anxiety, could be attributed to the stronger reward expectancies possessed by the internal individual. Interpretation of the data suggested an interactive relationship between type of stress (threat to ego vs. threat to instrumental performance) and expectancy for control in the influencing of behavior reactions to stress.

Achievement↗
PubMed1977

Bloom's syndrome. V. Surveillance for cancer in affected families.

The Bloom's Syndrome Registry comprises the 71 individuals in whom this rare genetic disorder has been recognized between the time it was described in 1954 and the end of 1976. The major objective of the Registry is surveillance for cancer in both affected homozygotes and heterozygotes. Of the 61 homozygotes known to have had Bloom's syndrome before cancer was diagnosed and for whom follow-up has been possible, one in nine has developed cancer. Thirteen cancers have been diagnosed, in 12 individuals. The mean age in 1976 of the living individuals with the syndrome was 16.4 years. The mean age at the time cancer was diagnosed was 20 years. Cancers have been of multiple types and have affected various sites.

Abnormalities, Multiple↗
PubMed1977

Bloom's syndrome. VI. The disorder in Israel and an estimation of the gene frequency in the Ashkenazim.

An effort was made to identify all individuals with Bloom's syndrome living in Israel between September 1971 and September 1972. Each of the eight individuals located were Jewish and could readily be classified Ashkenazic. The frequency of the Bloom's syndrome gene in Ashkenazim was estimated to be .0042 (minimum), implying a heterozygote frequency greater than 1 in 120. A striking distortion of the sex ratio (M/F = 7.0) may have been due to underascertainment of affected females. One of the affected individuals ascertained during the survey subsequently has died from cancer, which is in keeping with the recognized cancer proneness of this condition. Four of the affected have married, but no conception is known to have occurred, which suggests that sub- or infertility is a feature of the syndrome.

Adult↗
PubMed1975

The effects of jaundiced plasma and hypercholesterolaemic plasma on vascular sensitivity to injected noradrenaline.

Jaundiced plasma and plasma from hyperlipidaemic patients was perfused into an isolated artery or kidney preparation. The responses of the artery to doses of noradrenaline when Krebs solution was perfused were compared to the responses when the plasmas were perfused. It was found that both jaundiced and hyperlipidaemic plasmas potentiated the effects of noradrenaline on the isolated arteries and kidneys.

Animals↗
PubMed1975

Effects of jaundiced plasma on vascular sensitivity to noradrenalin.

Alterations in renal perfusion have been shown in a variety of liver diseases. We have examined the possibility that the syndrome is due to a renal vascular hypersensitivity to noradrenalin (NA). Isolated perfused kidneys and segments of rabbit femoral artery were used. Potentiation of the pressor effects of injected NA occurred in all (five artery and five kidney) preparations when jaundiced baboon plasma was perfused. These changes were significant (P less than 0.05) in nine out of the ten experiments. Controls to which normal baboon plasma was administered showed no such change. No correlation was found between the degree of NA potentiation and the plasma concentrations of bilirubin (total and conjugated), serum glutamic oxaloacetic transaminase, blood urea nitrogen, serum glutamic pyruvic transaminase, alkaline phosphatase, Na+ ions or K+ ions in the jaundiced plasma. Plasma renin levels were not significantly changed. When arteris were perfused with Krebtentiation of NA was found. Perfusion of sodium taurocholate or sodium deoxycholate (400 mug/ml) yielded no potentiation. Thus, the altered renal perfusion associated with jaundice may be attributed to a potentiated pressor response to NA which may be caused by an increased level of cholesterol carried on the beta-lipoprotein.

Animals↗
PubMed1975

The effects of hypercholesterolaemic plasma on vascular sensitivity to noradrenaline.

1. The pressor responses to injected noradrenaline (NA) of 42 isolated perfused femoral arteries of the rabbit were studied. 2. Potentiation of the responses was found when hypercholesterolaemic plasma was perfused through the arteries. No change was found with normal plasma. 3. Potentiation of the responses was found when isolated beta-lipoprotein in Krebs solution was perfused. No change was found with similar amounts of bovine-albumen. 4. Pure cholesterol dissolved directly into normal plasma, and dissolved via propanol into Krebs solution or plasma caused no potentiation. Propanol alone in Krebs or plasma had no effect. 5. Potentiation was caused by a decreased equilibrium coefficient (Keq) for the NA-adrenoceptor interaction and an increased maximal pressor response (Rmax). 6. It is concluded that cholesterol carried on its apoprotein is capable of potentiating the pressor effects of noradrenaline.

Animals↗