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Biomedical subjects

M Berger

Publications and source records attributed to M Berger.

At least 937 records · Page 52Linked to original sources
PubMed1980

[Shulman's syndrome. A variant of scleroderma? Two cases (author's transl)].

Observations of two patients illustrating the problem of Shulman syndroma. The first had presented an oedema of the four limbs, without injury of the trunk, but with myalgias, histological fasciitis, eosinophilia and hypergammaglobulinemia. In spite of corticotherapy, evolution toward a generalized morphea. The second has presented the same oedema of the four limbs, with myalgias, but also Raynaud syndroma, histological fasciitis and eosinophilia. Evolution toward acrosclerosis in spite of corticotherapy. For the authors, Shulman's syndroma is apprehended as a particular clinical form of scleroderma.

Aged↗
PubMed1980

[Milroy's disease and primary lymphoedema. Exploration methods, therapeutic aspects (author's transl)].

The most early outset, the usually bilateral type, the eventual association with abnormalities of extremities distinguish Milroy-Meige-Nonne' disease and congenital not familial lymphedema. Two cases illustrate this problem. The simplicity of realization, the topographic informations and the possibility of repetition are arguments for isotope lymphangiography with colloidal sulfur of rhenium.

Adult↗
PubMed1980

[Sexual organogenesis and circulating androgens in the rabbit fetus. Study after active immunization of mothers against testosterone (author's transl)].

The circulating level of free androgens (testosterone and dihydrotestosterone) in fetal rabbit was reduced by active immunization of mothers against testosterone. The level of testosterone and dihydrotestosterone binding to circulating proteins was about 100% in immunized fetuses and newborns. The testosterone and dihydrotestosterone binding capacities were higher than their circulating concentrations. Macroscopically, all newborns exhibited feminine external genitalia. Histological examinations showed the presence of complete wolffian ducts differentiated in epididymis, deferent ducts and seminal vesicles with normal structure. Prostatic development was strongly inhibited; anterior prostates were present but lateral and posterior prostates were frequently absent. In most animals the masculinization of the genital tubercle was prevented: 60% of males exhibited feminine external genitalia, 40% severe hypospadias. These results suggest: 1 degrees that fetal free circulating androgens (testosterone and/or dihydrotestosterone) induced masculinization of urogenital sinus and genital tubercle; 2 degrees that testicular testosterone was responsible for stabilization and differentiation of the wolffian duct.

Androgens↗
PubMed1979

[Massive obesity with disturbance of glucose tolerance (author's transl)].

A long-term study of 63 extremely obese persons with disturbed glucose tolerance showed a further deterioration of glucose tolerance over 10 years. In 9 out of 23 patients manifest diabetes mellitus developed despite partial weight reduction (greater than or equal to 10% of the initial weight excess). Out of 14 patients who did not lose weight during this time even 11 developed manifestations of diabetes. All patients who were in different weight groups at the 5- and 10-year follow-up showed a deterioration in glucose tolerance after 10 years. In the individual groups there were only minimal differences in other characteristics apart from the different weight behaviour.

Adult↗
PubMed1979

[The course of diabetes and clinical findings in glucagonoma].

A 66-year-old male patient with non-insulin-dependent diabetes of probably 20 years' duration presented with necrolytic migratory erythema, stomatitis, anemia and weight loss. Plasma-glucagon concentration measured with Unger's antibody 30-K was 8500 pg/ml, representing a hundredfold elevation. Two thirds consisted of high molecular glucagon fractions (10 000--40 000 Dalton). This may be an important index for detection of glucagonoma with endocrine activity. After excision of the glucagonoma the clinical syndrome was reversed and the patient recovered completely. Histological and histochemical investigation confirmed that the tumor was a glucagonoma. Despite complete removal of the tumor and a normal plasma glucagon concentration, the diabetes remained unchanged. Excessive hyperglucagonemia does not appear to play a primary role in the pathogenesis of this patient's diabetes.

Aged↗
PubMed1979

[Radicular and pseudoradicular symptoms of the middle and lower cervical vertebral column (author's transl)].

The differential diagnostic classification of the "shoulder-hand-syndrome" according to etiology and pathophysiological principles is of major importance. The radicular syndrome, subsumed as the shoulder-hand syndrome following a local lesion, must be exactly defined. The pseudoradicular syndrome, which frequently appears clinically in the cervical region under the guise of middle and lower cervical syndrome, has its cause in disturbed function of the vertebral joints. But it can also arise as a mixed syndrome, radicular and pseudoradicular, through a substantial root lesion. The diagnosis of a referred pain in a "shoulder-hand syndrome" can lead to the discovery of internal organic lesions or lesions of the locomotor apparatus of the extremities.

Brachial Plexus Neuritis↗
PubMed1979

Inhibition of degradation of insulin by ophthalamic acid and by a bovine pancreatic proteinase inhibitor.

We have previously observed that, on subcutaneous administration, a significant proportion of insulin is degraded at the site of injection. The present paper reports that the degradative activity of slices of rat adipose tissue can be inhibited in vitro by ophthalmic acid, a natural analogue of glutathione, and by bovine pancreatic proteinase inhibitor, whereas it is increased by the addition of reduced glutathione.

Adipose Tissue↗
PubMed1979

[Fractional distribution of anti-glucagon immunoreactivity (GIR) and amino acid concentration in the plasma in duodenopancreatectomized patients; preliminary report].

Glucagon immunoreactivity (IRG) was measured in plasma of 8 duodenopancreatectomized patients with antiserum 30-K. Arginine infusions failed to raise plasma IRG, whereas in control subjects IRG rose 3-fold. Column chromatography revealed that the basal IRG measured in these plasmas was not due to glucagon (molecular weight 3485) but to other plasma factors, mainly of high molecular weight. This suggests that diabetes mellitus does not require the presence of glucagon to produce the clinical picture, as suggested by other authors. Plasma levels of the amino acids alanine, serine, ornithine, and arginine were significantly (p less than 0.05) elevated, the former two being gluconeogenic substrates and the latter two constituents of the urea cycle. This amino acid abnormality may be a consequence of glucagon deficiency.

Amino Acids↗
PubMed1979

Glucose metabolism in perfused skeletal muscle. Demonstration of insulin resistance in the obese Zucker rat.

1. The effect of insulin (0.5, 10 and 50 munits/ml of perfusate) on glucose uptake and disposal in skeletal muscle was studied in the isolated perfused hindquarter of obese (fa/fa) and lean (Fa/Fa) Zucker rats and Osborne-Mendel rats. 2. A concentration of 0.5 munit of insulin/ml induced a significant increase in glucose uptake (approx. 2.5 mumol/min per 30 g of muscle) in lean Zucker rats and in Osborne-Mendel rats, and 10 munits of insulin/ml caused a further increase to approx. 6 mumol/min per 30 g of muscle; but 50 munits of insulin/ml had no additional stimulatory effect. In contrast, in obese Zucker rats only 10 and 50 munits of insulin/ml had a stimulatory effect on glucose uptake, the magnitude of which was decreased by 50-70% when compared with either lean control group. Since under no experimental condition tested was an accumulation of free glucose in muscle-cell water observed, the data suggest an impairment of insulin-stimulated glucose transport across the muscle-cell membrane in obese Zucker rats. 3. The intracellular disposal of glucose in skeletal muscle of obese Zucker rats was also insulin-insensitive: even at insulin concentrations that clearly stimulated glucose uptake, no effect of insulin on lactate oxidation (nor an inhibitory effect on alanine release) was observed; [14C]glucose incorporation into skeletal-muscle lipids was stimulated by 50 munits of insulin/ml, but the rate was still only 10% of that observed in lean Zucker rats. 4. The data indicate that the skeletal muscle of obese Zucker rats is insulin-resistant with respect to both glucose-transport mechanisms and intracellular pathways of glucose metabolism, such as lactate oxidation. The excessive degree of insulin-insensitivity in skeletal muscle of obese Zucker rats may represent a causal factor in the development of the glucose intolerance in this species.

Adipose Tissue↗