Biomedical subjects

R Staudt

Publications and source records attributed to R Staudt.

10 recordsLinked to original sources

PubMed2005

Chronic excessive erythrocytosis induces endothelial activation and damage in mouse brain.

Excessive erythrocytosis results in severely increased blood viscosity, which may have significant detrimental effects on endothelial cells and, ultimately, function of the vascular endothelium. Because blood-brain barrier stability is crucial for normal physiological function, we used our previously characterized erythropoietin-overexpressing transgenic (tg6) mouse line (which has a hematocrit of 0.8-0.9) to investigate the effect of excessive erythrocytosis on vessel number, structure, and integrity in vivo. These mice have abnormally high levels of nitric oxide (NO), a potent proinflammatory molecule, suggesting altered vascular permeability and function. In this study, we observed that brain vessel density of tg6 mice was significantly reduced (16%) and vessel diameter was significantly increased (15%) compared with wild-type mice. Although no significant increases in vascular permeability under normoxic or acute hypoxic conditions (8% O2 for 4 h) were detected, electron-microscopic analysis revealed altered morphological characteristics of the tg6 endothelium. Tg6 brain vascular endothelial cells appeared to be activated, with increased luminal protrusions reminiscent of ongoing inflammatory processes. Consistent with this observation, we detected increased levels of intercellular adhesion molecule-1 and von Willebrand factor, markers of endothelial activation and damage, in brain tissue. We propose that chronic excessive erythrocytosis and sustained high hematocrit cause endothelial damage, which may, ultimately, increase susceptibility to vascular disease.

Animals↗

PubMed2004

Multicomponent adsorption on activated carbons under supercritical conditions.

Adsorption of binary mixtures onto activated carbon Norit R1 for the system nitrogen-methane-carbon dioxide was investigated over the pressure range up to 15 MPa. A new model is proposed to describe the experimental data. It is based on the assumption that an activated carbon can be characterized by the distribution function of elements of adsorption volume (EAV) over the solid-fluid potential. This function may be evaluated from pure component isotherms using the equality of the chemical potentials in the adsorbed phase and in the bulk phase for each EAV. In the case of mixture adsorption a simple combining rule is proposed, which allows determining the adsorbed phase density and its composition in the EAV at given pressure and compositions of the bulk phase. The adsorbed concentration of each adsorbate is the integral of its density over the set of EAV. The comparison with experimental data on binary mixtures has shown that the approach works reasonably well. In the case of high-pressure binary mixture adsorption, when only total amount adsorbed was measured, the proposed model allows reliably determining partial amounts of the adsorbed components.

Journal Article↗

PubMed2002

Modeling of gas adsorption equilibrium over a wide range of pressure: a thermodynamic approach based on equation of state.

A thermodynamic approach based on the Bender equation of state is suggested for the analysis of supercritical gas adsorption on activated carbons at high pressure. The approach accounts for the equality of the chemical potential in the adsorbed phase and that in the corresponding bulk phase and the distribution of elements of the adsorption volume (EAV) over the potential energy for gas-solid interaction. This scheme is extended to subcritical fluid adsorption and takes into account the phase transition in EAV. The method is adapted to gravimetric measurements of mass excess adsorption and has been applied to the adsorption of argon, nitrogen, methane, ethane, carbon dioxide, and helium on activated carbon Norit R1 in the temperature range from 25 to 70 degrees C. The distribution function of adsorption volume elements over potentials exhibits overlapping peaks and is consistently reproduced for different gases. It was found that the distribution function changes weakly with temperature, which was confirmed by its comparison with the distribution function obtained by the same method using nitrogen adsorption isotherm at 77 K. It was shown that parameters such as pore volume and skeleton density can be determined directly from adsorption measurements, while the conventional approach of helium expansion at room temperature can lead to erroneous results due to the adsorption of helium in small pores of activated carbon. The approach is a convenient tool for analysis and correlation of excess adsorption isotherms over a wide range of pressure and temperature. This approach can be readily extended to the analysis of multicomponent adsorption systems.

Journal Article↗

PubMed2001

Correlation between local glucose transporter densities and local 3-O-methylglucose transport in rat brain.

The present study addresses the question whether local glucose transport kinetics are correlated with local glucose transporter densities in the brain. In 47 brain structures the local rate constants for 3-O-[(14)C]methylglucose (3-O-MG) transport, K(1) and k(2,) were quantified, and local glucose Glut1 and Glut3 transporter densities were determined by immuno-autoradiographic methods. Statistically significant correlations were found between the rate constants for glucose transport and the transporter densities. The correlations were tighter for Glut1 than for Glut3. Inasmuch as 3-O-MG is transported by the same transporter as glucose, these results indicate that the local densities of glucose transporters determine local glucose transport rates in the brain.

3-O-Methylglucose↗

PubMed2000

Increased cerebral glucose utilization and decreased glucose transporter Glut1 during chronic hyperglycemia in rat brain.

Whereas acute hyperglycemia has been shown to result in an unchanged local cerebral glucose utilization (LCGU) the changes of LCGU during chronic hyperglycemia are a matter of dispute. The present study had three aims: (1) To compare the effects of acute and chronic hyperglycemia on LCGU and to investigate in vivo the lactate level as a potential indicator of glycolytic flux. (2) To investigate local changes in brain Glut1 and/or Glut3 glucose transporter densities during chronic hyperglycemia. (3) To analyze the relationship between LCGU and local Glut densities during chronic hyperglycemia. To induce chronic hyperglycemia in rats steptozotocin was given i.p. and experiments were performed 3 weeks later. LCGU was measured by the 2-[14C]deoxyglucose method and intraparenchymal lactate concentration by MR-spectroscopy. Local densities of the glucose transport proteins were determined by immunoautoradiographic methods. During chronic hyperglycemia weighted average of LCGU increased by 13.9% whereas it remained unchanged during acute hyperglycemia. The cerebral lactate/choline ratio was increased by 143% during chronic hyperglycemia. The average density of glucose transporters Glut1 decreased by 7.5%. Local densities of Glut1 were decreased in 12 of 28 brain structures. Glut3 remained unchanged. Positive correlations were found between LCGU and local Glut densities during control conditions and during chronic hyperglycemia. It was concluded that (1) Chronic, but not acute hyperglycemia is followed by an increased LCGU. (2) The capacity to transport glucose is decreased during chronic hyperglycemia. (3) Increased LCGU and decreased densities of Glut1 are matched on a local level.

Animals↗

PubMed1999

Increase in glucose transporter densities of Glut3 and decrease of glucose utilization in rat brain after one week of hypoglycemia.

The present study addresses the question whether a chronic decrease of plasma glucose concentration for 1 week induces a global or local increase in glucose transporter densities Glut1 and Glut3 in the brain. To induce chronic hypoglycemia insulin was infused into rats by osmotic minipumps for 1 week resulting in a mean plasma glucose concentration of 3.1+/-0.5 mmol/l (control group: 8.1+/-0.5 mmol/l). Global and local densities of Glut1 and Glut3 glucose transporters were measured by immunoautoradiographic methods. The mean density of glucose transporters Glut1 remained unchanged, whereas the mean density of Glut3 increased slightly, although significantly. To determine whether the increased density of Glut3 is related to a change in glucose metabolism, the local cerebral metabolic rate of glucose (lCMR(glc)) was quantified by the 2-deoxyglucose method. Mean glucose utilization was decreased by 15%. Local analysis of transporter densities (Glut1 and Glut3) and glucose utilization showed a significant correlation between local glucose transporter densities (Glut1 and Glut3) and lCMR(glc) during hypoglycemia as already previously observed during normoglycemia. It is concluded that 1 week of hypoglycemia is a stimulus for the induction of additional glucose transporters Glut3 in the brain. These additional neuronal glucose transporters may support the maintenance of glucose utilization which is not completely maintained under these conditions.

Acute Disease↗

PubMed1998

Increase of glucose transporter densities (Glut1 and Glut3) during chronic administration of nicotine in rat brain.

Chronic infusion of nicotine is known to result in a distinct pattern of increases in local cerebral glucose utilization (LCGU). The present study addresses the question whether this increase in LCGU is paralleled by (1) a local increase in Glut1 and/or Glut3 glucose transporter densities and (2) a local increase in capillary density in the brain. Nicotine was infused by osmotic minipumps for one week. In cryosections of rat brains local densities of Glut1 (vascular) and Glut3 (neuronal) glucose transporters were measured by immunoautoradiographic methods whereas local capillary densities were determined by an immunofluorescent method. Densities of glucose transporters Glut1 and Glut3 were increased in 12 of the 27 structures investigated. Glut1 was elevated in four additional structures and Glut3 in two more structures. Comparison of the changes in transporter densities with the changes of LCGU measured in a previous study during chronic nicotine infusion showed that LCGU was also elevated in most of these structures. In contrast, capillary density remained unchanged in all structures investigated. It is concluded that one week of nicotine infusion is sufficient to raise the densities of Glut1 and Glut3 glucose transporters predominantly in those structures in which LCGU is elevated. The unchanged capillary density under these conditions indicates an increased density of Glut1 transporters per capillary.

Animals↗

PubMed1998

Local transport kinetics of glucose during acute and chronic nicotine infusion in rat brains.

Acute and chronic infusion of nicotine is known to result in a distinct increase in local cerebral glucose utilization (LCGU) in several brain structures. The present study addresses the question whether this increase in LCGU is paralleled by a local change in glucose transport in rat brain. Nicotine was infused either acutely for 3 hours or chronically by osmotic minipumps for one week. Local rate constants for glucose transport were measured in brain cryosections using the 3-O-[14C]methylglucose method. Local rate constants K1 and k2 were lower in part of the brain structures during acute (-10% to -20%) and in nearly all structures during chronic (-39% to -41%) nicotine. The finding of a decreased glucose transport during chronic nicotine was confirmed by additional experiments of 3-O-[14C]methylglucose transfer in an epithelial cell culture. It is concluded that acute and chronic nicotine infusion results in decreased glucose transport although LCGU is either unchanged or increased.

3-O-Methylglucose↗

PubMed1978

Chondroectodermal dysplasia (Ellis--van Creveld syndrome) with dysplasia of renal medulla and bile ducts.

A case of a 28-month-old boy with chondroectodermal dysplasia (Ellis-van Creveld syndrome) is reported. Besides polydactyly, ectodermal dysplasia, acromelic dwarfism and congenital heart defect, which are characteristic morphologic features of the syndrome, additional dysplastic developmental defects were discovered in the kidneys, liver, and lungs. Detailed histopathologic studies of the growth plates of tibia, femur and ribs disclosed an irregular, partly hyperplastic, partly dystrophic appearance of the epiphyseal cartilage, which was not resorbed properly by the invading blood vessels. Focal areas of necrosis occurred and barriers of tongue-shaped cartilaginous peninsulas persisted. Regular enchondral ossification was hindered and compensatory membrane ossification was found in the fibrosing metaphyseal bone marrow adjacent to the cartilage. Dysplasia and fibrosis of the renal medulla plus interstitial fibrosing nephritis in the cortex resulted in kidney contraction and renal failure. Hepatomegaly, portal fibrosis and bile duct hyperplasia and dysplasia were detected at autopsy, but did not have any clinical significance. These findings once again emphasize that derivatives of all three germ layers are involved in the Ellis-van Creveld syndrome. The possibility that a single metabolic or structural abnormality of the mesenchymal tissues could be responsible for the various organ dysplasias is discussed.

Bile Ducts↗

PubMed1976

[Poliomyelitis epidemic in a district of Freiburg i. Br. in autumn 1975 (author's transl)].

In the autumn of 1975 five cases of poliomyelitis occurred within 6 weeks in German children of families of low socioeconomic class. They lived in two districts of Freiburg with close familial and occupational contacts. One child had been immunised against polio once orally several years ago and none of the others were immunised. The clinical course and results of investigations of the environment are reported. Included is the state of immunisation of 472 school beginners in Freiburg schools and the antibody levels of 284 children aged 1 to 10 years from Freiburg and the adjoining areas.

Adolescent↗