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Biomedical subjects

L Lazarus

Publications and source records attributed to L Lazarus.

At least 91 records · Page 5Linked to original sources
PubMed1976

Hormonal regulation of fetal brain cell proliferation: presence in serum of a trophin responsive to pituitary growth hormone stimulation.

Previous studies led us to hypothesize that brain growth was regulated by a growth hormone-dependent brain trophin. An in vitro bioassay system to assess this proposal was developed. Serum was shown to stimulate the uptake of tritiated thymidine into fetal brain cell DNA. This action could not be attributed to any nutrient contribution but was due to a non-dialyzable, heat-stable serum growth factor. The levels of the growth factor in serum were reduced after pituitary removal. When added in physiological concentration, growth hormone, prolactin, placental lactogen, insulin, nerve growth factor, thyroid and steroid hormones failed to stimulate the action of serum or to act synergistically with a serum component to stimulate DNA synthesis. Thyroxine, estradiol-17beta, and corticosterone inhibited serum activity. Administration of growth hormone to hypophysectomized rats restored serum levels to normal demonstrating that the serum growth factors was a mediating trophin responsive to pituitary growth hormone stimulation. The relationship of the brain trophin to other serum growth factors and its specificity of action remain to be defined. The present findings were in accordance with in vivo studies of hormonal influence on brain growth and support the proposal that fetal brain cell proliferation is stimulated by a serum trophin responsive to pituitary growth hormone.

Animals↗
PubMed1976

Prolactin secretion by metoclopramide in man.

Six men and nine women were given intravenous injections of 2.5 mg of metoclopramide to assess its potential as a stimulus to prolactin release. Following the administration of metoclopramide, there was prompt increase in serum prolactin to a peak response of 38.2 +/- 3.9 ng/ml in men and 103 +/- 10.2 ng/ml in women. The prolactin response to metoclopramide in men was compared with the response to 400 mug of TRH in 10 men. The peak response after TRH was 22.4 +/- 2.2 ng/ml, which was significantly less than that observed after metoclopramide. Pretreatment with 500 mg of L-dopa suppressed the prolactin response to metoclopramide in 6 men to a mean response of 16.3 +/- 4.3 ng/ml. We have concluded that metoclopramide is a safe, reliable, and potent stimulus of prolactin secretion and exerts this effect by blocking dopamine receptors in the hypothalamus and decreasing prolactin inhibiting factor. It is free of side effects and is a useful alternative to chlorpromazine.

Adolescent↗
PubMed1975

Carrier solutions for low-level intravenous insulin infusion.

In the use of low-level intravenous insulin infusion for treating diabetic hyperglycaemia and ketoacidosis adsorption of insulin to containers or plastic infusion apparatus results in significant losses of 60-80% of insulin in dilute physiological saline solution (40 U/l). It is therefore necessary to add protein to the carrier solution to minimize losses and maintain a constant delivery rate. Recovery studies showed that 3.5% w/v polygeline solution (polymer of degraded gelatin) was a suitable medium for this purpose, offering some advantages over human serum albumin. A minimum concentration of 0.5% polygeline was required to ensure adequate delivery of insulin to the patient.

Biological Availability↗
PubMed1975

Somatomedins.

An intact pituitary gland capable of secreting growth hormone has long been considered the prime requirement for the achievement of skeletal growth potential in man. Recent studies have revealed that the growth-promoting action of growth hormone is an in-vivo phenomenon which cannot be mimicked by the addition of the hormone to skeletal tissue in vitro. The humoral agent responsible for skeletal growth has now been identified as somatomedin, a peptide produced in the liver under the stimulus of pituitary growth hormone. Serum levels of somatomedin are measured in a bioassay system by monitoring the stimulation of uptake of labelled sulphate by cartilage. Low levels of somatomedin activity are detected in the serum of children with growth hormone deficiency and short stature; the levels are high in acromegalics and low in patients with cirrhosis of the liver or chronic renal failure. Undernourished children also have low levels despite reaised serum levels of growth hormone; this suggests the presence of an inhibitor which lowers the growth-promoting activity of the somatomedin molecule. Adequate nutrition in these children results in the restoration of serum somatomedin levels to normal. Attempts to isolate and purify somatomedin have led to the identification of a group of substances sharing similar actions on skeletal tissue. Insulin has also been demonstrated to share some of these growth-promoting activities but varies in its organ specificity. Nerve growth factor, epidermal growth factor and proinsulin are other molecules which form a large group of growth promoting peptides which may all be related to the somatomedins.

Acromegaly↗
PubMed1975

Maternal growth hormone and growth and function.

Factors regulating somatic growth postnatally have been proposed to affect brain growth and subsequent function when applied prior to birth. This study pertains to the role of growth hormone administered to pregnant rats and the subsequent growth of the progeny. The results showed a significant increase in brain weight and cortical neurone number as determined by the incorporation of labelled thymidine into DNA and subsequent autoradiography. At maturity, learning performance on a series of conditional discrimination tasks was found to be enhanced.

Animals↗
PubMed1975

Identification of IgG antibody as a carrier of reaginic activity in asthmatic patients.

In a previous study it was reported that a group of asthmatic patients, in whom cromolyn sodium did not inhibit bronchial immediate allergic reactions, had reaginic antibodies that did not appear to belong to the IgE class. This study was designed to extend these observations, and it was shown that the IgG fractions from these patients' sera, purified by ion exchange chromatography and specific immunosorbents, had skin-sensitizing activity to the antigen studied, while the IgE fractions did not. The skin-sensitizing activity in the IgG fractions was not removed by anti-IgE antiserum and was not inactivated by heating at 56 degrees C or by reduction/alkylation. It is proposed that IgG antibodies may mediate immediate allergic reactions in some asthmatic patients, that these patients can be detected by means of serum total IgE and allergen-specific IgE estimation, and that cromolyn sodium is not an effective inhibitor of bronchial immediate allergic reactions in these patients.

Adult↗
PubMed1975

The correlation between skin tests, bronchial provocation tests and the serum level of IgE specific for common allergens in patients with asthma.

Cutaneous and bronchial immediate allergic reactivity and the serum level of IgE specific for each of four common inhalant allergens were determined for 153 asthmatic patients. Positive bronchial reactivity to an extract was not detected in any of the patients with a negative prick test reaction to that extract but did occur in 9% of the patients in whom the serum tests results for IgE specific to that allergen fell within the range regarded as negative. Highly significant correlation coefficients between the degree of bronchial and cutaneous allergic reactivity to the allergen extracts were found and these were slightly but significantly less than the correlation between the serum level of allergen specific IgE and the degree of bronchial allergic reactivity to the allergen extracts. These findings indicate that the results both of prick testing with appropriate extracts and estimation of the serum level of allergen specific IgE can be used to predict not only the presence of detectable bronchial reactivity to inhalant allergens but also the degree of this reactivity. However, for the routine investigation of asthmatic patients measurement of the serum level of allergen specific. IgE would appear to have little advantage over properly performed prick tests.

Aerosols↗
PubMed1975

Rational therapy for thyroid storm.

An approach to the management of patients with thyroid storm is described. The treatment regimen, which is directed against the abnormalities as they are presently understood, incorporates: (a) Propranolol to inhibit the catecholamine-mediated peripheral effects of the circulating thyronines; (b) Propylthiouracil to inhibit thyroid hormone synthesis and to inhibit peripheral conversion of thyroxine to triiodothyronine (T3), the predominant source of T3 production; (c) Iodine to block the glandular release of thyroid hormones; (d) Dexamethasone along with general supportive therapy. The regimen has been used for a 13 year old schoolgirl with thyroid storm, and the induced rapid fall in serum T3 levels is illustrated. It has also been used in patients with florid thyrotoxicosis undergoing emergency surgery and has resulted in marked clinical improvement associated with rapid decreases in serum T3 levels. It is a simple and efficient regimen, rendering cumbersome forms of therapy such as plasmapheresis and peritoneal dialysis unnecessary.

Adolescent↗
PubMed1975

Serotoninergic control of rat growth hormone secretion.

The ability of 5-hydroxyl-L-tryptophan (5-HTP) or pentobarbital anesthesia to elevate rat serum GH levels is completely blocked by the simultaneous administration of the serotonin antagonist cyprophepatidine, as well as by the pineal gland principles melatonin and 5-methoxytryptamine (5-MT), and by the 0-methylated dopamine derivative 3,4-dimethoxyphenylethylamine (DMPEA). Small doses of 5-MT cause paradoxical elevations in serum rat GH but at the same time inhibit the action of 5-HTP. Blockade of dopaminergic pathways by treatment with either DMPEA or chlorpromazine causes a slight, nonsignificant suppression of serum GH in normal rats while serum prolactin levels are increased greater than tenfold showing that, unlike prolactin, rat GH is not subject to tonic inhibitory control by dopamine. The data presented support the recently advanced hypothesis that rat GH is under serotoninergic CONTROL AND DEMONSTRATE THAT GH secretion can be significantly suppressed by serotoninergic blockade. It is suggested that the results presented here for monoamine control of rat GH release are not a variance with those reported for man.

5-Methoxytryptamine↗
PubMed1975

The stimulation of human prolactin secretion by 3-Iodo-L-tyrosine.

Oral administration of a single 1 g dose of MIT to 10 normal male and female subjects resulted in a rise in serum prolactin in each subject. The mean peak level of serum prolactin attained by the 10 subjects was 36.3 plus or minus 7.9 ng/ml which was highly significantly elevated (P smaller than 0.0005) above the mean basal level of 5.3 plus or minus 1.0 ng/ml. While there was no significant difference between the basal serum prolactin levels of male and female subjects, the mean peak level attained by male subjects following MIT (18.8 plus or minus 3.3 ng/ml) was significantly less (P smaller than 0.0025) than that recorded for the female group (62.5 plus or minus 9.1). Serum levels of growth hormone (GH), thyroid-stimulating hormone (TSH), luteinizing hormone (LH), triiodothyronine (T3), thyroxine (T4) and cortisol were not significantly altered following MIT administration. The complete absence of side effects due to MIT make it a suitable drug for the acute clinical assessment of pituitary prolactin reserve.

Adult↗
PubMed1975

The influence of protein restriction imposed at various stages of pregnancy on fetal and placental development.

The effect of protein restriction on fetal and placental growth was investigated. Pregnant rats were maintained on an isocaloric diet containing either 23% or 5% protein. The diet was imposed either from days 1-21 of gestation or from days 7-21 of gestation. Fetal body development was assessed. Fetal brain and placental growth were determined by both analysis of organ DNA, RNA and protein and differential radiochemical labelling procedures. Maternal protein restriction inhibited fetal growth. Brain weight was reduced due to a significant decrease in cellular content. Brain cell size was significantly increased and may have accounted for the reduction in cell concentration. Placental growth was similarly impaired. These data demonstrate impaired fetal and placental growth following decreased maternal dietary protein intake. Severity of growth retardation increased with the duration of malnutrition. The results also suggest that malnutrition may affect the rate of development, causing premature cessation of cell division and early cell differentiation.

Animals↗
PubMed1974

Fetal brain growth: selective action by growth hormone.

Growth hormone was administered to pregnant rats maintained under dietary control, and fetal and placental growth and nutrition were examined. Growth hormone had a selective action on brain growth that could not be attributed to nutrient mobilization but suggested a trophic factor which is unique to the brain.

Animals↗