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Biomedical subjects

M Beck

Publications and source records attributed to M Beck.

At least 343 records · Page 19Linked to original sources
PubMed1976

Sugar absorption by small bowel biopsy samples from patients with primary lactase deficiency and with adult celiac disease.

The present study was undertaken to compare the 3-O-methyl-D-glucose (3MG) absorption by jejunal biopsies from normal human subjects (N = 3) with that by the jejunum of the rat (N = 8) and of the hamster (N = 8), and to examine whether jejunal biopsies from normal subjects (N = 3), patients with primary lactase deficiency (N = 5) and from patients with celiac sprue (N = 5) follow the same pattern of sugar absorption as usually observed in vivo. The results indicate that under the conditions of our experiments the estimated affinity of carrier for 3MG (ie, apparent Km) in the biopsies from normal subjects did not differ significantly from that in rat or hamster jejunum. The estimated capacity of carriers for 3MG absorption (ie, Vmax) appeared to be similar in biopsies from normal subjects and in hamster jejunum, but significantly lower in rat jejunum. There was no difference in apparent Km between the biopsies from normal subjects and those from the patients with lactase deficiency. Although the Vmax for the lactase deficient patients was substantially higher than that for the normal subjects, the difference was not statistically significant. The absorption of 3MG by the biopsies from patients with celiac sprue did not follow Michaelis-Menten kinetics and was compatible with that of passive diffusion or low saturation conditions. Since the intracellular concentration of 3MG in all biopsies from celiac patients exceeded the concentration of the media, sugar transport could not have occurred by diffusion, and it is concluded that the absence of Michaelis-Menten kinetics was the result of low saturation conditions. This active transport with low saturation kinetics in patients with celiac disease suggests that in these patients not only the number of functioning carrier molecules is diminished but also the affinity of the existing carrier for sugar molecule is reduced. This situation, at least in some patients, seems to improve after treatment with gluten-free diet.

Adult↗
PubMed1975

Isoosmotic transport of fluid across the hamster small intestine in the presence of phlorizin-induced inhibition of sugar transport.

Experiments were performed to investigate whether the fluid transported across the small intestine is isoosmotic with the mucosal solution when the active transport of glucose is partially inhibited. Everted hamster mid small intestine was incubated in one of the following four mucosal solutions: (1) Isotonic control, Krebs-Ringer bicarbonate solution containing 10 mM glucose (KRBSG), (2) Isotonic with phlorizin, KRBSG + 5X10-5 M phlorizin, (3) Hypertonic control, KRBSG + 50 mM mannitol, (4) Hypertonic with phlorizin, KRBSG + 50 MM mannitol + 5x10-5 M phlorizin. The serosal surface of the intestine was not bathed. Results indicate that the transported fluid was always isoosmotic with any of the mucosal solutions used. When the mucosal solution was made hypertonic with mannitol, the concentration of glucose and electrolytes in the absorbate increased, and as a result, the absorbate became hypertonic and isoosmotic with the mucosal solution. The presence of phlorizin either in the isotonic or in the hypertonic mucosal solution decreased the glucose concentration of the absorbate, but the transported fluid became isoosmotic with the mucosal solution due to a higher concentration of Na, K, and their associated anions. Phlorizin caused a decrease in the transmural potential difference. In spite of this, the presence of this glucoside in the mucosal solution increased the transport of sodium in relation to glucose transport. It is suggested that, at the concentrations used, phlorizin inhibits sodium movement through the electrogenic pathway, but increases the transport of this ion through the non-electrogenic route. This increase in neutral sodium transport seems to compensate for the low concentration of glucose in the absorbate, so that the absorbate becomes isoosmotic with the mucosal solution whether the latter is isotonic or hypertonic. It is suggested further that isoosmotic transport of fluid is an inherent property of the small intestine and that there may be an osmoregulatory mechanism in the gut which controls this process.

Animals↗
PubMed1975

Effect of ethanol on sodium-dependent glucose transport in the small intestine of the hamster.

The objective of this study was to investigate the mechanism by which ethanol inhibits intestinal absorption of sugars. In vitro experiments on hamster jejunum have shown that the presence of ethanol in the mucosal solution caused an inhibition of the net transport of water and glucose. There was also a decrease in the intracellular water content and an increase in the intracellular sodium and potassium concentration of the gut tissue. In contrast, the intracellular glucose concentration decreased in the presence of ethanol. These ethanol-induced changes were directly related to the ethanol concentration of the mucosal solution. In the presence of 450 mM (2%) ethanol in the mucosal solution, there was also a significant inhibition of transmural potential difference, estimated glucose metabolism, and both unidirectional fluxes of sodium. The net flux of sodium to the serosal side however did not decrease significantly. These effects of ethanol cannot be fully explained by its osmotic action, and it is suggested that the ethanol-induced reduction in glucose transport could be mainly the result of an interference with the carrier-mediated coupled entrance of glucose and sodium across the brush border. A depression of cellular metabolism could also have played a role in this process.

Animals↗
PubMed1974

[Karyometric analysis of the supraoptic nucleus and the paraventricular nucleus before and after milking the cow].

With mathematical-statistical methods the reaction of the Nucleus supraopticus (N.S.O.) and Nucleus paraventricularis (N.P.V.) were investigated before and after the milking of the cows. The frequency-distributions of the tests of the nuclear volumes in the N.S.O. and N.P.V. show an increase of the mean values of the nuclear volumes from the unmilked cows to those studied 15 minutes after the milking. The mean values of the nuclei volumes of the cows studied 60 minutes after the milking fall off, but they are higher than the values of the unmilked cows. The results of the histological-histochemical investigations mainly coincided with the results obtained by caryometry. It is discussed, that the changes in the nuclear bolumes show an increased protein synthesis and that -- combined with the release of oxytocin -- the milk stimulus caused a secretory synthesis in the neurosecretory cells, mainly in the N.P.V.

Animals↗
PubMedDate not supplied

Heterogeneity of metatropic dysplasia.

Metatropic dysplasia is a neonatally manifest entity that is characterized clinically by a rapidly progressing kyphoscoliosis leading to severe shortening of the originally long trunk ("metatropism"). Major radiographic features include flattening and defective ossification of the vertebral bodies, a narrow thorax and a marked hypoplasia of the basilar portions of the ilia with crescent-shaped iliac crests. There is some evidence of genetic heterogeneity. From five personal observations and from a review of the literature we conclude that metatropic dysplasia comprises at least three genetic entities: (1) a nonlethal type with autosomal recessive transmission; (2) a nonlethal dominant type and (3) a lethal type with death before or shortly after birth and possibly autosomal recessive inheritance. A careful clinical and radiologic analysis permits their classification and differentiation from similar, not yet well-delineated disorders. Attention is also drawn to the possibility of atlanto-axial instability in metatropic dysplasia which may cause severe neurologic defects.

Adult↗
PubMedDate not supplied

Thalamic hyperdensity--is it a diagnostic marker for Sandhoff disease?

Sandhoff disease, also known as GM2-gangliosidoses variant 0, is caused by the deficient activity of both hexosaminidase A and hexosaminidase B. We report a 15-month-old boy diagnosed with Sandhoff disease by demonstrating the enzyme deficiency. The interesting finding was bilateral thalamic hyperdensity on the CT scan. The hyperdensity in all previously published cases was homogeneous and symmetric and limited to the thalamus; the cause still remains unknown. We suggest that the finding of dense thalami may be useful as a specific diagnostic criterion for the GM2-gangliosidoses and especially for Sandhoff disease.

Brain↗
PubMedDate not supplied

Long-term basal forebrain cholinergic-rich grafts derived from trisomy 16 mice do not develop beta-amyloid pathology and neurodegeneration but demonstrate neuroinflammatory responses.

Patients with Down syndrome (human trisomy 21) develop neuropathological and cholinergic functional defects characteristic of Alzheimer's disease, which has been attributed to the location of the Alzheimer beta-amyloid precursor protein on chromosome 21. Due to the partial genetic homology between mouse chromosome 16 and human chromosome 21, murine trisomy 16 was used as a model to study functional links between increased expression of the amyloid precursor protein, neurodegeneration and neuroinflammatory responses. Basal forebrain cholinergic-rich tissue derived from trisomy 16 mice at embryonic age of day 16 was transplanted into the lateral ventricle of adult normal mice. At 1, 3, 6, 9 and 12 months after transplantation, the grafts were characterized by immunocytochemistry, molecular biological analysis, and stereological methods. Grafts survived up to one year and still demonstrated immunoreactivity for cholinergic, GABAergic and astroglial cells. Though a 1.5-fold neuronal over-expression of amyloid precursor protein was detected in brains from trisomy 16 embryos by Northern analysis, beta-amyloid deposits were found neither in control nor trisomic grafts. Detailed stereological analysis of trisomic grafts did not reveal any neurodegeneration or morphological changes of cholinergic and GABAergic neurons during the course of graft maturation up to one year, as compared to grafts derived from euploid tissue. However, both euploid and trisomic grafts demonstrated a strong infiltration with T- and B-lymphocytes and a significant micro- and astroglial activation (hypertrophic astrocytes) within and around the grafts. These observations further suggest that the trisomy 16-induced neurodegeneration is seemingly due to a lack of neuron supporting factors which are provided by either the metabolic interaction of trisomic graft with surrounding healthy host tissue or by cells of the immune system infiltrating the graft.

Acetylcholine↗