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Biomedical subjects

J Roth

Publications and source records attributed to J Roth.

At least 685 records · Page 38Linked to original sources
PubMed1978

Extreme insulin resistance in ataxia telangiectasia: defect in affinity of insulin receptors.

The syndrome of ataxia telangiectasia is associated with glucose intolerance and insulin resistance. We examined the status of insulin receptors on circulating monocytes and on cultured fibroblasts from two siblings with ataxia telangiectasia and severe insulin resistance. 125I-insulin binding to monocytes of the two patients consistently demonstrated an 80 to 85 per cent decrease in receptor affinity. In contrast, the defect in receptor affinity was not expressed on the patients' cultured fibroblasts or on monocytes or fibroblasts obtained from unaffected family members. Whole plasma and immunoglobulin-enriched fractions of plasma from the patients inhibited the normal binding of insulin to its receptors on cultured human lymphocytes (IM -9 line) and on human placental membranes. We conclude that the insulin resistance in the two siblings with ataxia telangiectasia was associated with defects in the affinity of the receptors for insulin, probably caused by circulating inhibitors of insulin binding.

Acanthosis Nigricans↗
PubMed1978

[Electron microscopic observations in internal organs in morbus Fabry (author's transl)].

Electron microscopic findings are reported on the localization and fine structure of glycolipid inclusions in different organs (heart, kidney, lymph nodes, arterial blood vessels, pancreas) in Fabry's disease in a female. The intracellular and extracellular inclusions were made up of multilamellar membraneous systems in concentric, excentric, and parallel arrangement. This fine structure is characteristic of liquid-crystalline phases of phospholipid-water systems. The same type of inclusions are found in the internal organs of heterozygotic women as in homozygotic men. The relationship between the glycolipid inclusions and the lysosomes is discussed.

Adult↗
PubMed1978

[Genetic radiation burden of the population in the canton Basel-City due to nuclear medicine].

The genetically significant radiation dose is defined as the gonadal dose which, if received by every member of the population, would produce the same genetic hazard to the population as do the actual doses received by the individuals. PORETTI et al. published a value of 42.9 mrad for Switzerland as the result of X-ray diagnostic examinations in 1971. The contribution from nuclear medicine was determined with reference to special circumstances in the Canton of Basle City: the annual genetically significant dose amounted to 0.5 mrad in 1976. This value represents about 0.5% of the annual annual background radiation.

Body Burden↗
PubMed1978

Role of ultrasonography in the primary diagnosis of cholelithiasis: an analysis of fifty cases.

The use of ultrasonography to diagnose cholelithiasis has recently been recommended to supplement standard reinforced oral cholecystography or as an alternative to reinforced oral studies when a single dose fails to visualize the gallbladder. As yet the use of ultrasonography in the primary diagnosis of cholelithiasis is not generally accepted. To assess the specificity and sensitivity of this mode of diagnosis, fifty patients were reviewed retrospectively. The findings of ultrasonography are compared with standard oral cholecystography and with the pathologic findings. The results of this analysis suggest that diagnosis of cholelithiasis by ultrasonography has a high level of accuracy. Use of this mode of evaluating the gallbladder is suggested as a primary diagnostic test for jaundiced or pregnant patients.

Adult↗
PubMed1978

Cellular responses to surface binding and internalization of concanavalin A. An electron microscopic investigation on the problem of membrane cycling.

Monolayer cultures of normal and diethylnitrosamine-transformed rat liver cells were labeled in situ with Con A-HRP or ferritin-conjugated Con A. Ligand-induced redistribution with simultaneous internalization of labeled membrane areas occurred in normal as well as in transformed cells when they were reincubated with PBS at 37 degrees C for different periods of time (from 5 min up to 3 hrs). Compared to normal cells, these afore mentioned processes were accelerated in transformed cells. Internalization in normal and transformed cells resulted in a recycling of labeled plasma membrane areas in the Golgi region with the label being finally accumulated in elements which correspond mostly, but not exclusively, to GERL. Then formation of phagolysosomes and multivesiculated bodies occurred whose labeled content was exocytized after fusion with the plasma membrane. This suggested that the internalized plasma membrane areas were at least partly degraded. The relabeling of some parts of the plasma membrane by extruded lysosomal content indicates that at least some Con A molecules are still biological active. Membrane internalization by endocytosis after binding of Con A obviously causes an increased of membrane biogenesis and exocytosis, thus compensating for membrane removal. This is suggested by the vacuolization and enlargement of unlabeled (not in recycling involved) Golgi apparatus. It may indicate a differential functional role of the Golgi apparatus in membrane turnover in the same cell. The fusion of phagolysosomes with the plasma membrane and the insertion of phagolysosomal membrane into the plasma membrane might be another compensatory mechanism.

Animals↗
PubMed1978

Identification of insulin in rat brain.

Insulin concentrations in acid/ethanol extracts of the whole rat brain were on the average 25 times higher than plasma insulin levels. Brain insulin was indistinguishable from authentic pancreatic insulin, based on its behavior in radioimmunoassay, radioreceptor assay, and bioassay and its chromatographic pattern on Sephadex G-50 column chromatography. Insulin was found in all regions of the brain examined, but distribution was uneven. Some regions had insulin concentrations as much as 100 times higher than in plasma; levels at least 10 times higher were found in other regions. The role of insulin in the central nervous system is not clear at present but, because both insulin and insulin receptors are abundant in the central nervous system, an extensive physiological regulation of the central nervous system by insulin is proposed.

Adipose Tissue↗
PubMed1978

Regulation of the major proline permease gene of Salmonella typhimurium.

The structural gene for the major proline permease is located in a tight cluster with genes coding for the proline degradative enzymes, proline oxidase and pyrroline-5-carboxylic acid dehydrogenase. Expression of the permease is regulated in parallel with the two degradative enzymes, and all three functions are subject to catabolite repression. Regulatory mutants (putC) have constitutively high levels of all three activities, suggesting that all are regulated by a single mechanism.

Amino Acid Oxidoreductases↗
PubMed1978

Cluster of genes controlling proline degradation in Salmonella typhimurium.

A cluster of genes essential for degradation of proline to glutamate (put) is located between the pyrC and pyrD loci at min 22 of the Salmonella chromosome. A series of 25 deletion mutants of this region have been isolated and used to construct a fine-structure map of the put genes. The map includes mutations affecting the proline degradative activities, proline oxidase and pyrroline-5-carboxylic dehydrogenase. Also included are mutations affecting the major proline permease and a regulatory mutation that affects both enzyme and permease production. The two enzymatic activities appear to be encoded by a single gene (putA). The regulatory mutation maps between the putA gene and the proline permease gene (putP).

Amino Acid Oxidoreductases↗
PubMed1978

Demonstration of the insulin receptor in vivo in rabbits and its possible role as a reservoir for the plasma hormone.

Based on studies of the interaction of insulin with its receptors in vitro, we calculated that a receptor compartment should be measurable directly in vivo. For this purpose, rabbits were injected intravenously with a labeled insulin that has low affinity for receptors in combination with a radioiodinated insulin that has high affinity for receptors. Plasma concentrations of labeled insulins were measured at selected intervals after injection. Apparent volumes of distribution were calculated by extrapolation of plasma distribution were calculated by extrapolation of plasma disappearance curves; high affinity insulins consistently distributed into spaces that were two-three times greater than those of the low affinity insulins. Injections of unlabeled pork insulin before tracer insulins decreased the distribution space of the high affinity insulin in a dose-dependent manner while having little or no effect on the distribution space of the low affinity labeled insulin. When unlabeled insulin was injected after the tracer insulins, there was an immediate rise in the plasma concentration of the high affinity insulin with only a slight change in the plasma concentration of the low affinity insulin. These results demonstrate that high affinity insulins distribute into a body compartment which has many properties of the insulin receptor previously studied in vitro. This receptor compartment: (a) recognizes insulins based on their biological potencies; (b) is saturated by elevated concentrations of insulin; and (c) insulin bound to receptors is in equilibrium with free hormone in plasma. Further, the bound to free ratios for hormone, calculated from these data, suggest that in vivo greater than 50% of the extrapancreatic insulin is bound to receptors during normal physiological states.

Animals↗
PubMed1978

Ultrastructural localization of intracellular antigens by the use of protein A-gold complex.

An immunocytochemical technique for the demonstration of intracellular antigens (secretory proteins) on thin sections is reported. Staphylococcal protein A which reacts with the Fc fragment of IgG molecules was labeled with colloidal gold as a marker. The antigenic sites were visualized on aldehyde-fixed and Epon-embedded tissue in a two step procedure. The specific antisera were applied to thin sections for binding to the antigens and then visualized by the protein A-gold complex. By using this technique different secretory proteins of the exocrine and endocrine pancreas were localized. The protein A-gold technique is proposed as a general method for visualization of antigenic sites on thin sections.

Animals↗
PubMed1978

Coloidal gold, ferritin and peroxidase as markers for electron microscopic double labeling lectin techniques.

Three markers, colloidal gold, ferritin and peroxidase, were checked for usefulness in double labeling of lectin-binding sites. The amount of various lectins for the stabilization of good sols of a different particle size was evaluated. Several lectin-gold complexes were prepared for electron microscopic labeling purposes, and the optimal amount of various lectins needed for stabilization of gold solutions of a different particle size was determined. The following combinations were investigated for their usefulness in labeling two different lectin-binding sites: lectin-gold and lectin-gold (different particle size), lectin-gold and lectin-ferritin, as well as lectin-ferritin and lectin-peroxidase. Of these combinations the latter did not give satisfactory results for double labeling. In all single and double labeling techniques with the above mentioned markers the quantitative evaluation of the number of lectin-binding sites is not feasible, but these techniques will be of considerable value for the investigation of the dynamics of different lectin-binding sites on the cell surface.

Cell Line↗
PubMed1978

Insulin resistance, acanthosis nigricans, and normal insulin receptors in a young woman: evidence for a postreceptor defect.

We have previously described a group of young females with virilization, acanthosis nigricans, insulin resistance, and markedly decreased binding of insulin to its receptor (syndrome of insulin resistance and acanthosis nigricans type A). The present report concerns a 15-yr-old female with clinical features indistinguishable from the type A patients, including virilization, acanthosis nigricans, and extreme resistance to endogenous and exogenous insulin. Insulin levels were 400-650 microU/ml while fasting and were over 2200 microU/ml when stimulated. Proinsulin was less than 10% of the total immunoassayable insulin. In distinct contrast to the type A patients, insulin receptors on cells from this patient were entirely normal on the basis of specificity, negative cooperativity, affinity, concentration, and interaction with antiinsulin receptor antibodies. These findings suggest the presence of an intracellular defect as the cause of the observed insulin resistance.

Acanthosis Nigricans↗
PubMed1978

The evolving clinical course of patients with insulin receptor autoantibodies: spontaneous remission or receptor proliferation with hypoglycemia.

Three patients with insulin resistance caused by autoantibodies to the insulin receptor were investigated serially over a 3-yr period. Major changes in carbohydrate metabolism, insulin receptor status, and titer of antireceptor antibodies were observed in each case. In one patient, normalization of glucose tolerance, insulin sensitivity, and receptor binding were associated with a spontaneous fall in the titer of antireceptor antibody. A second, more severely affected patient had two entirely distinct phase to her illness. The first, or hyperglycemic phase, was characterized by insulin resistance, negligible insulin binding to receptors on circulating monocytes, and high titers of circulating antireceptor antibodies. The second phase was characterized by refractory hypoglycemia, in association with proliferation of membrance insulin receptors; these occurred despite persistence of high titers of antireceptor antibody. An unusual heptic lesion, diffuse adenomatosis, was observed during this phase. A third patient showed features of both of the other patients, with spontaneous fall in antibody titer as well as a later phase of receptor proliferation. These studies demonstrate that patients with antibodies to insulin receptors may have a fluctuating clinical course. There may be spontaneous changes in antibody titers as well as independent changes in receptor concentration. Hypoglycemia and hepatic proliferation are newly recognized clinical sequelae in patients with this syndrome.

Adult↗
PubMed1978

[The question of the possibility to reproduce field positions in high-voltage therapy (author's transl)].

In order to obtain informations about the possibility to reproduce field positions in high-voltage therapy, controls were made by therapy films on several patients during the irradiation with a linear accelerator and a telecobalt unit. An incorrect position of the fields and/or lead satellites was found in 51% of the controls. The authors discuss possible reasons and their consequences for the radiotherapeutic practice. It must be taken into consideration especially when therapy plans are elaborated, that their realization may cause difficulties in the daily practice.

Cobalt Radioisotopes↗
PubMed1978

[Brucella titers in subclinical infections due to Yersinia enterocolitica serotype O:9 in a pig-breeding farm (author's transl)].

According to the Federal German Veterinary Public Health Regulations part of the stock of a pig-breeding farm in Lower Franconia (South Germany) had to be destroyed due to the findings of positive serological titers against Brucella. B. suis was not isolated from various specimens examined by the local veterinary public health authorities, but the authors found Yersinia enterocolitica serotype O:9 in 15 of 117 pigs investigated (12.8%). The organisms were cultured from 6 out of 117 specimens of fecal material (5.1%), and from 10 out of 55 pharyngeal tonsils (18.2%). The examination of 45 mesenteric and 2 submandibular lymphnodes remained negative. In 9 out of 93 sera titers against B. abortus between 1:20 and 1:40 were detected in tube agglutination but not in complement fixation tests. These sera and an additional serum specimen gave simultaneous reactions against Y. enterocolitica serotype O:9 ranging from 1:40 to 1:640 (Table 2). By cross-absorption antibodies to Brucella were completely removed, but to Yersinia titers between 1:10 and 1:320 remained detectable in 7 sera. It may be concluded that the Brucella titers observed in the animals were caused by subclinical infections with Y. enterocolitica serotype O:9 which is known to give rise to marked serological cross-reactions with various Brucella antigens. The importance of the above findings will be discussed in view of the current veterinary public health regulations.

Animals↗