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Biomedical subjects

H Andersen

Publications and source records attributed to H Andersen.

At least 91 records · Page 5Linked to original sources

Combined test of hypothalamic-pituitary function in growth retarded children treated with growth hormone. I. Secretion of growth hormone and somatomedin before and after treatment.

In 23 growth retarded children two consecutive insulin tolerance tests (ITT) were performed to establish a diagnosis of growth hormone (GH) deficiency. Nine children did not respond (GH peak value less than 8 mU/1), whereas 14 were classified as having partial GH deficiency (GH peak value less than 20 mU/1). All were treated for an average period of 40 months with human growth hormone (HGH). In a combined stimulation test at the end of the treatment period 9 children demonstrated a persistent GH deficiency, whereas a normal response was found in 14 of the previous partial GH deficient children. During treatment the monthly growth rate rose from 0.21 cm 0.58 cm in the GH deficient children and from 0.31 cm to 0.70 cm in the partial deficient children, in most of whom spontaneous pubertal development occurred during treatment. Somatomedin (SM) values were decreased in the GH deficient children before and after treatment but increased to normal levels during treatment. Growth velocity in these children during treatment was correlated to SM values before treatment. In the partial GH deficient children SM values were subnormal before but normal after treatment. This supports the assumption that in some children with constitutional delay in puberty a reversible functional hypopituitarism exists, which is normalized after the onset of puberty, due to androgens sensitizing growth hormone releasing mechanisms. Treatment with HGH may induce increased growth velocity in some of these patients.

Body Height↗

Succinate dehydrogenase activity in the wall of rabbit aorta. The histochemical use of PMS and exogenous coenzyme Q10 as intermediate carriers.

An investigation of succinate dehydrogenase activity in the wall of rabbit aorta was carried out. The level of succinate dehydrogenase per se in the smooth muscle cells was found to be fairly high, while the mitochondrial level of carrier CoQ was low. The latter may explain the low level or lack of activity of succinate dehydrogenase in these cells as noticed by previous authors. A reliable image of the actual level of succinate dehydrogenase was obtained only by adding CoQ10 to the incubation system. PMS should be avoided, as it induced a "Nothing dehydrogenase" reaction even at low concentrations.

Animals↗

Methodological aspects of the histochemical localization and activity of some cerebellar dehydrogenases.

In a detailed study focused on the methodological problems in dehydrogenase histochemistry [e.g., fixation, diffusion of enzymes and of reduced inermediates, conversion of NADPH and NADP to NADH and NAD, respectively, penetration of tetrazolium salt and formazan substantivity, 'nothing dehydrogenase' reaction, use of exogenous CoQ10 and of flavoprotein substitute (PMS)], the distribution and activity of succinate dehydrogenase, NAD(P)H-tetrazolium reductase, glucose-6-phosphate dehydrogenase, lactate dehydrogenase (H and M types), and of L-glutamate dehydrogenase (E.C.1.4.1.2 and E.C.1.4.1.3) have been investigated in the rat cerebellum. It was evident from the study that reliable results could only be obtained if all the aforementioned factors had been considered. The image of actual concentration of SDH in the neuropil of the molecular layer could only be recorded by adding CoQ10, while other structures exhibited greater balance between SDH and endogenous mitochondrial CoQ. Contrary to previous studies, a reversed localization of the activity of G-6-PDH and LDH was noticed. The elements of molecular and Purkinje layers were rich in G-6-PDH, while the granular layer was nearly depleted. The actual level of LDH could only be recorded if NADH-tetrazolium reductase was bypassed with PMS. The H and M types of LDH coexisted in the three cortical layers, the H type being prevalent and the M type attaining its highest level in synaptic glomeruli followed by the structures of the molecular layer and the Purkinje cells. High activity of GDH was noticed in Bergmann glia followed by synaptic glomeruli, while most other structures showed weak to moderate activity. The two GDH types coexisted in all structures showing activity, except for Bergmann cells, which only showed presence of the E.C. 1.4.1.3 type. Furthermore, Bergmann glia was exceptional by showing no activity of SDH and LDH, but strong activity of G-6-PDH and NADPH-tetrazolium reductase. The granular cells were exceptional by showing weak or no activity of all enzymes in question.

Animals↗

Pituitary-thyroid responsiveness to thyrotropin-releasing hormone in preterm and small-for-gestational age newborns.

A dose of 40 microgram TRH was injected intravenously in 12 preterm (PT) and 15 small-for-gestational age (SGA) babies (with advanced gestational ages) between 5 and 167 hours after birth. Serum-thyrotropin (TSH) was measured prior to and 30 and 180 min after TRH; serum-thyroxine (T4) and serum-triiodothyronine (T3) were measured prior to and 180 min after TRH. The percentage increase in serum-TSH in PT and SGA babies was comparable to that of fullterm newborns. The serum-TSH 30 min after TRH in SGA newborns was significantly correlated to basal TSH values, such a correlation could not be shown in the preterms. One SGA and four PT babies had a repeat TRH-test performed later in infancy: In all but one PT with a gestational age of 27 weeks the TSH rise was lower than in the neonatal period. The thyroid hormone responses after TRH were similar in the two groups of babies. The percentage increase above basal levels were: Median serum-T3 increase about 46% and median serum-T4 increase about 14%. It is concluded that in low-birth-weight newborn babies the pituitary TSH response to exogenous TRH was like that detected in fullterm newborns and more pronounced that later in infancy. The effect of endogenous TSH as measured by thyroid hormone increases was of the same magnitude as observed in fullterms and in adults.

Female↗

Changes in serum levels of thyroxine and thyroxine-binding proteins (TBG, TBPA, ALBUMIN) induced by venous stasis.

Serum concentrations of thyroxine (T4), thyroxine-binding globulin (TBG), thyroxine-binding pre-albumin (TBPA) and albumin were determined in 21 healthy, young subjects before and after a brief venous stasis in two experiments: 1) 3 min stasis induced by a sphygmomanometer with constant pressure 20 mmHg above the diastolic blood pressure and 2) 2 min stasis induced by an arm tourniquet of rubber. In both experiments the serum T4 level was significantly rised (mean 9%) after venous compression. Increases of the same magnitude were observed for serum TBG, serum TBPA and serum albumin. The serum concentrations of the free constituents--sodium and creatinine--remained unchanged, whereas the haemoglobin concentration increased (mean 8%). This haemoconcentrating effect of venous stasis seemed to be more pronounced in females than in males. Our data emphasize the need for protein correction procedures when total serum T4 is measured.

Adult↗

Mass fragmentographic demonstration of low amounts of beta-phenylethylamine in human urine.

beta-Phenylethylamine (PEA) is determined with a simple, rapid and highly specific assay, 5 ml human urine, using GLC combined with mass fragmentography. The 24 h urinary excretion of PEA in ten healthy male subjects ranged from 28 to 131 nmol/24 h with a mean (+/- SD) of 66 (+/- 9) nmol/24 h. It is concluded that reinvestigation of PEA-excretion in psychiatric patients is needed, since earlier less specific methods have measured much higher levels of PEA in human urine.

Chromatography, Gas↗

Thyrotropin response to thyrotropin-releasing hormone in fullterm, euthyroid and hypothyroid newborns.

The serum concentration of thyrotropin (TSH) and the TSH response following thyrotropin-releasing hormone (TRH) were studied in 16 euthyroid babies from 16 to 172 hours after birth and in 2 primary hypothyroid babies, 3 and 28 days of age. Serum-TSH was measured before an intravenous injection of 40 mug TRH and after 30 and 180 min. In the euthyroid babies increased basal levels of TSH were seen shortly after birth, followed by a pronounced decline. The extent of TSH increase after TRH could be correlated with the basal levels, and the relative increase was comparable to that which occurs in adults. In the hypothyroid babies very high basal levels of serum-TSH were seen, 125 and 400 muU/ml respectively, with no further increase following TRH stimulation. It was concluded that in euthyroid fullterm newborn, the relative response of serum-TSH to TRH was equal to that of adults, in spite of elevated thyroid hormone concentrations. In the hypothyroid newborn very high levels of serum-TSH were seen and a supplementary TRH-test seems without diagnostic value in congenital hypothyroidism.

Congenital Hypothyroidism↗

The diagnostic value of liver scanning. A retrospective study.

Among 650 consecutive radioisotope liver scans there were selected 180 representing all cases in which a pathoanatomical evaluation of the liver was available. The scanning data, the clinical information, and the pathoanatomical diagnosis were reviewed independently, and the results achieved in each group were classified as evidence of normal liver, focal hepatic disease, or diffuse hepatic disease. Using pathology for verification scanning had a sensitivity of 97% and a specificity of 90% regarding detection of unspecified liver disease, which was significantly better than clinical setting alone. In diffuse hepatic disease scanning had a sensitivity of 100% and a specificity of 81%, whereas in the focal hepatic disease the corresponding figures were 78 and 97%, respectively. Passive hepatic congestion was recognized as a diffuse hepatic disease by scanning, thus representing a source of error in screening for liver disease sensu stricto. It is concluded that scanning, apart from being a rapid and simple procedure without significant inconvenenience to the patient, is a very accurate diagnostic tool that deserves more recognition in clinical departments.

Biopsy, Needle↗

The monoamine oxidase B inhibitor deprenyl potentiates phenylethylamine behaviour in rats without inhibition of catecholamine metabolite formation.

The drug l-deprenyl has been reported to have antidepressant properties, and in the present study three possible mechanisms of action were investigated in animal experiments. l-Deprenyl, which is a type B monoamine oxidase (MAO) inhibitor, was compared to clorgyline, an MAO A inhibitor with regard to its inhibitory effect on the formation of three major catecholamine metabolites, homovanillic acid (HVA), dihydroxyphenylacetic acid (DOPAC) and 3-methoxy-4-hydroxyphenylglycol (MOPEG) in the rat brain in vivo. Apart from a difference in dose levels the two drugs showed no difference in the dose--response pattern of all three metabolites. Clorgyline inhibited the formation of HVA, DOPAC and MOPEG with an ED50 of about 0.2 mg/kg s.c. and l-deprenyldopamine and noradrenaline are formed by the same type of monoamine oxidase(s), probably type A, in the rat brain in vivo. Antidepressant properties of l-deprenyl therefore seem to be independent of catecholamine deamination. l-Deprenyl but not clorgyline (2 or 8 mg/kg s.c.) potentiated the stereotyped sniffing behaviour induced by beta-phenylethylamine, a specific substrate for type B monoamine oxidase. This result is discussed in relation to a new hypothesis of phenylethylamine and dopamine involvement in depression. l-Deprenyl was 10,000 times less potent than DMI as inhibitor of noradrenaline uptake in crude synaptosomes from the occipital cortex of rat brain. Inhibition of noradrenaline uptake was therefore excluded as a possible mechanism for the antidepressant action of l-deprenyl.

Animals↗

Oxygen affinity of haemoglobin and red cell 2,3-diphosphoglycerate in childhood diabetes.

Red cell 2,3-diphosphoglycerate (2,3-DPG) and the oxygen haemoglobin dissociation curve (ODC) were determined in 32 ambulatory, non-acidotic diabetic children and in 49 healthy children. Despite the fact that the diabetic children had, on average, an increased haemoglobin concentration, their erythrocytes contained significantly more 2,3-DPG than normal. Both in diabetic and in healthy children a negative relationship was found between the content of 2,3-DPG and the haemoglobin concentrations. No relationship was present between the plasma glucose and the 2,3-DPG concentration. The concentration of plasma inorganic phosphate (Pi) in the diabetic children was significantly higher than in the control children, and for all children there was a significant relationship between the 2,3-DPG and the Pi. In the diabetics 2,3-DPG was positively correlated to the P50 (7.40) and to the P50 (in vivo ph) of the ODC. However, despite the significant increase in 2,3-DPG among the diabetic children the average P50 (7.40) and P50 (in vivo pH) was not increased as compared with the control children. The inhibitory factor preventing the oxygen affinity from decreasing among the diabetics was strongly correlated to an increase in the mean corpuscular haemoglobin concentration. The result of this study suggests the presence of an increased amount of haemoglobin fraction with high oxygen affinity (haemoglobin Alc) in the red cells of juvenile diabetics.

Adolescent↗

Increased immunoreactive plasma and urinary growth hormone in growth retardation with defective generation of somatomedin a (Laron's Syndrome).

In a boy 4 years old with clinical hypopituitary dwarfism, high plasma and urinary levels of immunoreactive growth hormone were found. Somatomedin A levels in serum were low and failed to respond after short-term treatment with human growth hormone. The parents were first cousins. In the arginine and insulin tolerance tests the initially high immunoreactive growth hormone levels were later followed by a decrease to high normal values. Insulinopenic response was present during the arginine and glucose tolerance tests. As a growth hormone molecule defect is not found in these patients and no growth or other metabolic response to exogenous HGH can be demonstrated, it is concluded that a defective somatomedin generation may be present, probably in conjunction with a generalized receptor defect and deficient feedback system with abnormal release of HGH. The lack of somatomedin A is responsible for the severe growth retardation and the disturbance in carbohydrate metabolism is probably caused by sustained high growth hormone levels.

Carbohydrate Metabolism, Inborn Errors↗

Quantitative determination of immunoglobulins, lysozyme, and certain electrolytes in breast milk during the entire period of lactation, during a 24-hour period, and in milk from the individual mammary gland.

During a period commencing at birth and lasting for up to 27 months 193 milk samples have been collected from 29 mothers. The IgA globulin content was high immediately after birth, averaging 2.7 arb.U, decreasing to 0.3 arb.U within the first 2 to 3 weeks after birth, then remaining almost constant for the rest of the lactational period. In the case of IgG globulin, similar results were obtained, but the quantity was much smaller. IgM globulin was demonstrated in small quantities during the first 3 weeks of lactation. The lysozyme content varied considerably during the whole lactational period. Individual variations were found for all the immunoglobulins, while the concentration in the individual woman varied only slightly from day to day following in other respects the pattern described above. In 19 mothers IgA, IgG, IgM, lysozyme and electrolyte content were determined in serum and in milk from the right and the left breast on the same day. No difference in content was found between milk from the left and the right mammary gland. A positive correlation was found between the concentrations of IgA and sodium chloride in milk, between those of IgG in milk and serum, and between those of lysozyme in milk and serum. No variations were registered during the individual breast feeding, nor for the 24-hour period as a whole.

Adult↗