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Biomedical subjects

O Andersen

Publications and source records attributed to O Andersen.

At least 217 records · Page 12Linked to original sources
PubMed1986

Insulin receptor binding to monocytes and erythrocytes during normal human pregnancy.

In normal human pregnancy glucose tolerance deteriorates gradually in spite of a steady increase in plasma insulin levels. To see whether this change in insulin resistance is accompanied by changes in insulin receptor binding, insulin binding to monocytes and erythrocytes was measured serially during pregnancy and again post-partum in fifteen normal women. Insulin binding to monocytes increased from week 12 to week 24 of gestation (P less than 0.001) and it decreased from week 32 to week 36 (P less than 0.05). After delivery a new increase in insulin binding to monocytes was seen (P less than 0.05). Insulin binding to erythrocytes increased from week 30-32 to week 36 (P less than 0.05), decreased from week 36 to delivery (P less than 0.01) and decreased further post-partum (P less than 0.001). Insulin receptor binding was not significantly correlated to plasma insulin, estradiol, estriol, progesterone or cortisol. The insulin receptor binding to monocytes, but not to erythrocytes, paralleled the insulin resistance found in human pregnancy.

Adult↗
PubMed1986

Insulin receptors in normal pregnant women and women with gestational diabetes.

In a serial study of insulin receptor binding to monocytes from normal pregnant women, a significant increase in insulin binding in mid pregnancy followed by a significant decrease in late pregnancy at tracer insulin concentration was found. No changes in the insulin concentration necessary to reduce tracer binding by 50% (ID50) were observed. At delivery, binding to isolated adipocytes was significantly lower in normal pregnant women than in non-pregnant normal controls while no difference in ID50 was observed. No differences in insulin binding at tracer insulin concentration to monocytes and adipocytes between normal weight women with gestational diabetes and healthy non-diabetic pregnant controls were found, but the ID50 was significantly lower in women with gestational diabetes diagnosed in late pregnancy than in pregnant controls at the same weeks of gestation.

Adipose Tissue↗
PubMed1986

alpha-Methyldopa for climacteric hot flushes. A double-blind, randomized, cross-over study.

The effects of single evening doses of alpha-methyldopa and placebo have been compared in 40 women with climacteric hot flushes. The study was designed as a double-blind, randomized and cross-over investigation. Of the 24 patients who completed the study, 15 reported that they preferred the alpha-methyldopa treatment (p greater than 0.05). alpha-methyldopa seemed to affect both the severity (p less than 0.05) and the frequency of climacteric hot flushes (p greater than 0.05). It is concluded that alpha-methyldopa is efficacious against climacteric hot flushes when given as single evening doses, but further study is required to answer whether this dosage is as effective as a twice daily regimen.

Climacteric↗
PubMed1986

Choroideremia in interstitial deletion of the X chromosome.

An earlier reported family with a deletion of the proximal long arm of the X chromosome was reinvestigated with special attention to the presence of choroideremia. Two females were identified as carriers of choroideremia while a tapeto-retinal dystrophy was ascertained in a mentally retarded boy. RFLP analysis revealed that the interstitial deletion covered the locus DXYS1 and not DXS17. Chromosome studies indicated a deletion within the Xq21 area.

Abnormalities, Multiple↗
PubMed1985

Effects of liver damage induced by polychlorinated biphenyls (PCB) on cadmium metabolism in mice.

Polychlorinated biphenyls (PCB) were added to the diets of mice at different concentrations. Mice fed these diets were given a sc or oral doses of 109Cd. The uptake and excretion of Cd was followed by whole-body counting. The gastrointestinal absorption of Cd after an oral dose of 109Cd was less in animals fed on 66 ppm PCB diet, compared with a control group, and the body elimination of Cd was faster. In the liver, the amount of Cd was reduced by dietary PCB exposure, after both oral and sc administration of 109Cd, and the data suggest a faster transport of Cd from liver to kidneys in PCB-exposed animals than in controls. The mobilized liver Cd was not quantitatively recovered in the kidneys, thus increased urinary excretion due to PCB exposure may have taken place. Histological examination of the livers revealed a dose-dependent induction of liver changes characterized by centrilobular enlargement of liver cells and centrilobular focal necroses. In four of eight livers from animals fed 200 ppm PCB for 32 weeks there were five liver cell tumors with cytological signs of malignancy. In the control group and in groups fed lower doses of PCB (10-100 ppm) no such tumors were found among 28 animals. The results support observations made with agents inducing acute liver damage, that liver damage increases the rate of redistribution of cadmium from the liver to the kidney.

Animals↗
PubMed1985

Release of gastrointestinal hormones in cardiodepressive shock.

In previous studies increased plasma levels of vasoactive intestinal polypeptide (VIP), somatostatin and pancreatic polypeptide (PP) were demonstrated in a porcine endotoxin shock model. Unchanged levels of gastric inhibitory polypeptide (GIP) and secretin point to a specific shock reaction of peptide release and not to a diffuse mucosal leakage. A porcine model of cardiodepressive shock was developed to enable discrimination to be made between a general low-flow state and endotoxin reaction. Infusion of the tricyclic antidepressive agent nortriptyline 15 mg/kg bodyweight resulted in a grave shock state. Increased plasma levels of somatostatin, PP and insulin were found. No increase in VIP levels could be demonstrated. Endotoxin given after nortriptyline administration resulted in the increase of VIP levels regularly seen during endotoxinaemia. VIP release during endotoxin shock is related to endotoxin and not to a general low flow state.

Animals↗
PubMed1985

Influence of the maternal plasma glucose concentration at delivery on the risk of hypoglycaemia in infants of insulin-dependent diabetic mothers.

Plasma glucose concentrations at birth and at two hours of age were measured in 53 infants of insulin-dependent mothers (IDMs). The plasma glucose concentrations at delivery were measured in the mothers of 17 IDMs and in the remaining 36 mothers, glucose was estimated by interpolation from concentrations achieved just before and after delivery. Clinical and laboratory data from the two groups were otherwise similar, so the groups were combined for further analyses. The maternal plasma glucose at delivery correlated positively with the glucose concentration of the IDMs at birth (rho = 0.82, p less than 0.001) and negatively with the glucose concentration at two hours of age (rho = -0.46, p less than 0.001). Maternal plasma glucose concentration was higher in mothers delivered by caesarean section than in vaginally delivered mothers (p less than 0.05). Eleven IDMs became hypoglycaemic at two hours of life (plasma glucose less than or equal to 1.7 mmol/l). These infants had higher cord plasma glucose concentrations at birth than those who remained normoglycaemic; the maternal glucose concentration was also higher. None of the IDMs became hypoglycaemic if the maternal glucose concentration at delivery was less than 7.1 mmol/l. In 28 IDMs the simultaneous plasma concentrations of non-antibody bound immunoreactive insulin (IRI) were recorded. Cord plasma IRI correlated with glucose and IRI at two hours of age (rho = -0.73, p less than 0.001 and rho = 0.77, p less than 0.001, respectively). Cord plasma IRI was higher in IDMs who became hypoglycaemic than in the remaining infants.(ABSTRACT TRUNCATED AT 250 WORDS)

Blood Glucose↗
PubMed1985

Etiology and pathophysiology of gestational diabetes mellitus.

In pregnancy, several physiologic changes take place, the sum of which tends to reset the glucose homeostasis in the direction of diabetes. About 1-2% of all pregnant women develop an abnormal glucose tolerance in pregnancy, but most often glucose tolerance returns to normal postpartum. This condition is called gestational diabetes mellitus (GDM). The possibility that glucose tolerance deteriorates in pregnancy because of diabetes-like changes in the secretory function of the endocrine pancreas has been investigated in healthy controls and in normal-weight gestational diabetic subjects. The insulin responses to oral glucose and mixed meals are equally large in these two groups, but the insulin response per unit of glycemic stimulus is significantly lower in the gestational diabetic subjects than in the controls. Diabetes-like changes in glucagon secretion are not observed in either group. Insulin degradation is unaffected by human pregnancy and the proinsulin share of the total plasma insulin immunoreactivity does not increase in pregnancy. Insulin receptor binding to monocytes from normal pregnant women is increased in midpregnancy but is significantly decreased in late pregnancy. No difference in insulin binding (at tracer insulin concentration) to monocytes from healthy pregnant controls and gestational diabetic subjects is found. The insulin concentration necessary to reduce tracer insulin binding by 50% (ID50) is lower in the gestational diabetic subjects diagnosed in late pregnancy than in the pregnant controls. Together, these findings indicate that the number of insulin receptors on monocytes is decreased in GDM at this stage of pregnancy.(ABSTRACT TRUNCATED AT 250 WORDS)

Alanine↗
PubMed1985

Possible association of herpes simplex virus infection with demyelinating disease.

Administration of herpes simplex virus (HSV) in sublethal doses to experimental animals may cause a relapsing demyelination in the central nervous system (CNS) but will leave the peripheral myelin unimpaired. Demyelination will be followed by remyelination by oligodendroglial cells or by invading Schwann cells. Relapsing episodes of CNS demyelination seen in HSV latently infected animals may be caused either by reactivation of HSV residing in the CNS itself or virus transported to the CNS after reactivation of a latent infection in peripheral sensory or autonomic ganglia. Although HSV is not the only virus known to induce a demyelination in the CNS of experimental animals, the similarities of this HSV induced demyelination and multiple sclerosis (MS) are intriguing, albeit an association of HSV reactivation and MS has not as yet been reported. However, circumstantial evidence for HSV induction of restricted CNS demyelination in man has recently been obtained: Several laboratories have reported on association of HSV with acute idiopathic facial palsy (Bell's palsy). If HSV be the cause of this palsy, the site of a lesion giving the nerve dysfunction should be located in the brain stem of the CNS rather than in the extrapontine part of the facial nerve. Indeed, most of Bell's palsy patients studied had signs of a brain stem disorder revealed by either one or more of the following tests: auditory brain stem response test, trigeminal evoked potential test or extensive clinical neurological examination. Furthermore, 35% of patients with Bell's palsy had increased concentrations of myelin basic protein in the cerebrospinal fluid collected in the acute stage of the disease.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1985

Evaluation of the spindle-inhibiting effect of Ni++ by quantitation of chromosomal super-contraction.

In vitro exposure of human lymphocytes to spindle inhibitors reduce the average chromosome length (Andersen and Rønne, 1981, 1983. Andersen et al 1983). In this report chromosome length measurements were used for indirect but quantitative evaluation of the effects of Ni++ on spindle function. In two donors 4 h or 20 h exposure of phytohemagglutinin stimulated peripheral lymphocyte cultures to 10(-3) M but not 10(-4) M Ni++ induced statistically significant reductions in average chromosome length, indicating that Ni++ is a powerful spindle inhibitor in a narrow concentration range just below the lethal concentration. Although systemic effects are unlikely to occur, local effects induced by Ni++ released after pulmonary deposition of Ni containing dusts cannot be ruled out. Spindle dysfunction may result in aneuploidy. The significance of the finding reported here in relation to nickel carcinogenicity is presently unknown.

Chromosome Aberrations↗