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Biomedical subjects

C Albrecht

Publications and source records attributed to C Albrecht.

At least 55 records · Page 3Linked to original sources
PubMed1998

Release and accumulation of neurotransmitters in the rat brain: acute effects of ethanol in vitro and effects of long-term voluntary ethanol intake.

Release from and accumulation in tissue slices of some neurotransmitters under acute ethanol in naive rats and in long-term voluntarily ethanol drinking rats were investigated. Slices of the rat caudatoputamen were prelabeled with [3H]choline and release of [3H]acetylcholine was stimulated through either N-methyl-D-aspartate (NMDA) receptors or strychnine-sensitive glycine receptors. Ethanol in vitro at 2 per thousand, 4 per thousand, and 6 per thousand (34 mM, 68 mM, and 102 mM, respectively) concentration-dependently depressed the maximum effect of the concentration-response curve of NMDA in naive rats. In contrast, voluntary ethanol consumption over months led to a significantly enhanced NMDA receptor response characterized by an increase in the maximum effect of the concentration-response curve. The glycine receptor-mediated release of [3H]acetylcholine, which is inhibited by acute ethanol in a competitive-like fashion, was not changed in animals that ingested ethanol over months. Electrically evoked release of [3H]noradrenaline ([3H]NA) and its presynaptic modulation by morphine through mu-opioid receptors in neocortical slices of the rat, preloaded with [3H]NA, was nearly identical in both ethanol-naive rats and in ethanol drinking rats. The accumulation of [3H]gamma-aminobutyric acid in rat cerebellum tissue was neither affected by acute ethanol in vitro nor after chronic ethanol consumption. In summary, long-term voluntary ethanol intake caused a significant increase in NMDA receptor function in the rat caudatoputamen, but did not result in changes in glycine-evoked [3H]acetylcholine release of electrically evoked [3H]NA release modulated by morphine or cerebellar [3H]gamma-aminobutyric acid accumulation.

Acetylcholine↗
PubMed1997

Provirus variants of the bovine leukemia virus and their relation to the serological status of naturally infected cattle.

Infection of cattle with the bovine leukemia virus (BLV) results in a strong permanent antibody response to the BLV antigens some weeks after infection. However, cattle may carry provirus and not have detectable antibody titers. To prove the occurrence of different BLV provirus variants in German cattle and to study the influence of special BLV variants on the immunoreaction, a 444-bp fragment of the env gene of 35 naturally BLV infected animals was analyzed. Seven different groups of BLV provirus variants were found on the basis of restriction fragment length polymorphism. Three BLV provirus variant groups and five additionally sequenced BLV isolates showed a high similarity to BLV provirus isolates from other geographical areas. The variation in nucleotide sequence of the five BLV isolates compared with nine previously sequenced BLV isolates ranged up to 5. 3%. While BLV provirus variant groups A, C, D, E, F, and G were clearly related to agar-gel immunodiffusion test (AGID)- and enzyme-linked immunosorbent assay (ELISA)-positive animals, BLV provirus variant group B was solely found in permanent AGID- and ELISA-negative or in transient ELISA-positive animals. Altogether, these results indicate that special BLV provirus variants may be responsible for atypical forms of BLV infection in cattle.

Amino Acid Sequence↗
PubMed1997

Targeting naproxen coupled to human serum albumin to nonparenchymal cells reduces endotoxin-induced mortality in rats with biliary cirrhosis.

Endotoxin is thought to play a major role in cirrhotic liver disease. Cyclo-oxygenase inhibitors were shown to be partially protective against endotoxin but cannot be used in cirrhotic patients because of renal side-effects. We argued that administration of naproxen (NAP) linked to human serum albumin (HSA), which results in specific delivery of NAP to endothelial cells (EC) and Kupffer cells (KC) and exhibited hepatoprotective effects against lipopolysaccharide (LPS) in vitro, could protect cirrhotic rats from LPS toxicity while preserving renal function. The studies were performed in rats rendered cirrhotic by bile duct ligation (BDL); animals received LPS (Escherichia coli, 800 microg/kg) intravenously. Five groups were studied: LPS alone, rats pretreated with a conventional dose of NAP (50 mg/kg), NAP-HSA (22 mg/kg), NAP equimolar to NAP-HSA (1.5 mg/kg), or the HSA carrier. LPS induced significant mortality (55%); this was not affected by equimolar NAP (57%) but accentuated by conventional NAP (88%). In contrast, NAP-HSA provided significant protection (9%; P < .05). After conventional NAP treatment, significant renal toxicity was observed as evidenced by a marked reduction in sodium excretion (LPS vs. NAP-HSA vs. NAP [50 mg/kg] 33 +/- 22 vs. 50 +/- 39 vs. 4 +/- 3 micromol/h; P < .05). Renal prostaglandin E2 (PGE2) excretion was reduced by NAP in all groups, but most markedly at the conventional dosage (LPS vs. NAP-HSA vs. NAP [50 mg/kg] 132 +/- 115 vs. 39 +/- 19 vs. 9 +/- 8 ng/mL; P < .05). Successful targeting was evidenced by a significant hepatic enrichment of NAP in the NAP-HSA group compared with the equimolar untargeted group (30.16 +/- 9.33 vs. 1.13 +/- 1.95 nmol/g liver). Thus, targeting NAP to EC/KC results in improved survival, higher efficacy, and sparing of renal function in cirrhotic rats.

Animals↗
PubMed1997

Differentiation between naproxen, naproxen-protein conjugates, and naproxen-lysine in plasma via micellar electrokinetic capillary chromatography--a new approach in the bioanalysis of drug targeting preparations.

Pharmacotherapy through the targeting of drugs is a promising new approach that requires adequate analytical methods capable of differentiating between the free drug, the drug carrier, and metabolites. Using micellar electrokinetic capillary chromatography (MECC), we report the separation of naproxen (NAP) from NAP covalently coupled to human serum albumin or to mannosylated serum albumin and the metabolite naproxen-lysine. An assay for selective analysis of the different forms of NAP by direct plasma injection was developed with salicylate as internal standard and solute detection by laser-induced fluorescence. Compared with previously applied techniques, including HPLC and total plasma fluorescence, MECC offers the advantage that free and covalently bound NAP can be differentiated in one run and can be accurately monitored in microliter quantities of plasma. Summation of all NAP equivalents determined by MECC revealed data that compare well with those produced by total plasma fluorescence and HPLC.

Animals↗
PubMed1996

Purified human peripheral blood basophils release interleukin-13 and preformed interleukin-4 following immunological activation.

Recent studies have shown that human basophils, like mast cells, generate interleukin (IL)-4 following immunological activation and may thus participate in late-phase allergic and inflammatory processes. Here, we report the capacity of human basophils to release IL-13 within 24 h following stimulation with anti-IgE. Additionally, in 14 out of 31 experiments, we observed that basophils rapidly release performed IL-4 within 5-10 min, as well as newly generated IL-4, which was released 4 h following stimulation of the cells with anti-IgE. In contrast to the biphasic release of IL-4 from the cells, no preformed IL-13 was detected at earlier times (5-30 min). Preformed IL-4 and IL-4 and IL-13 generated de novo were also released after stimulation of the cells with IL-3; an enhanced production of these cytokines was observed using a combination of IL-3 and anti-IgE. We conclude from these data that, by releasing performed IL-4 and IL-4 and IL-13 generated de novo, human basophils may be centrally involved in the orchestration of allergic inflammation by providing a trigger to IL-4-mediated T helper 2 lymphocyte activation, B cell IgE switching, and increased vascular adhesion molecule expression.

Antibodies, Anti-Idiotypic↗
PubMed1990

Effect of loxiglumide, a cholecystokinin antagonist, on pancreatic polypeptide release in humans.

The purpose of this study was to determine the role of cholecystokinin in the regulation of postprandial pancreatic polypeptide secretion in humans. The pancreatic polypeptide responses to modified sham feeding and gastric instillation of a test meal were first compared with the response to oral ingestion of the same meal. The experiments were repeated under cholinergic (atropine) and cholecystokinin (loxiglumide) blockade. Atropine completely abolished the pancreatic polypeptide response to sham feeding and caused significant reductions after gastric and oral food intake. Loxiglumide, on the other hand, significantly reduced pancreatic polypeptide release to oral food (51% inhibition) without affecting the response to sham feeding. In separate experiments using a duodenal perfusion system, the effects of atropine and loxiglumide on intestinal phase-stimulated pancreatic polypeptide release were examined, and both cholinergic and cholecystokinin blockade induced complete suppression. It was concluded (a) that cholecystokinin is involved in postprandial pancreatic polypeptide response, especially during the intestinal phase stimulation, and (b) that the cholinergic system is crucial and superimposed on cholecystokinin in stimulating pancreatic polypeptide release.

Adult↗
PubMed1990

Theoretical and experimental considerations linking an environmental stress to expression of endogenous retroviruses in a mammalian tumour.

CBA mice, containing the transplantable CaNT adenocarcinoma were exposed to magnetic fields of 0.5T. Doubling times of the tumours were found to increase significantly from 71 to 123 hours. Electron microscopy of these tumours revealed that the numbers of intracisternal A-type viral-like particles increased from a total of 127 in control mice (counted in 97 fields from 4 different tumours), to 459 in mice exposed to magnetic fields (counted in 95 fields from 5 different tumours). Similarly, intra-cytoplasmic A-type particle numbers increased from 98 to 184. In contrast the number of budding and extracellular C-type virus particles did not differ significantly in mice exposed to the magnetic field. To our knowledge this is the first report linking an environmental stress (magnetic field) to the visible expression of endogenous retro-viral-like type-A particles. We therefore propose the hypothesis that environmental stress may be relevant to the expression of endogenous retroviruses in mammalian cells. Such a mechanism could be relevant in the mechanisms of carcinogenesis and in the rapid evolution of species.

Animals↗
PubMed1987

Interferon-induced cytolysis correlates with the degree of transformation of epidermal cells.

The cytolytic activity of interferon (IFN) was evaluated for its ability to distinguish between paired sets of nontumorigenic/tumorigenic epidermal cells (JB-1/JB-8; D1/D11a) as well as a set consisting of nonpromotable, promotable, and tumorigenic epidermal cell lines (JB-6 clones 30, 21, and RT101). The viability of the cell types was measured in a microassay using histoplates. IFN-gamma and IFN-alpha/beta, when employed singly, demonstrated an equivalent and limited effect on the viability of all cell lines. Treatment of nontumorigenic and nonpromotable cell lines with the combination of IFN-gamma + IFN-alpha/beta also caused only a limited effect on cell viability, whereas treatment of tumorigenic and promotable cell lines with the combination of IFNs caused a marked decrease in cell viability. Thus, the cytolytic effect of IFNs employed in combination but not singly was discriminatory between tumorigenic and nontumorigenic cells as well as between promotable and nonpromotable cells. Addition of cytotoxic effector cells was found to have a relatively moderate effect on the survival of target cells that were treated with IFN-gamma or IFN-alpha/beta separately. Addition of cytotoxic effectors to target cells treated with the IFNs in combination had a discriminatory effect. Nontumorigenic and nonpromotable cells were moderately affected; the tumorigenic and the promotable cells, however, were markedly affected, resulting in their complete (or nearly complete) eradication. The results demonstrate that combination IFN treatment: has a discriminatory cytolytic effect on tumorigenic and promotable cells in contrast to their nontumorigenic and nonpromotable counterparts; and when added to cytotoxic effector cells can completely eradicate tumorigenic and promotable cells while having a significantly lesser effect on nontumorigenic and nonpromotable cells.

Animals↗
PubMed1978

Afrikander cattle congenital goiter: characteristics of its morphology and iodoprotein pattern.

The morphology and some properties of the complex iodoprotein pattern of the genetically determined congenital goiter in Afrikander cattle is described. The goiter contained irregularly shaped follicles which were devoid of colloid and the follicular epithelial cells were elongated, measuring about 20 micrometer in length compared to 10 micrometer for normal thyroid cells. The goiter cells contained apical clusters of larger and more numerous lysosomes than normal thyroid cells. Apical vesicles containing electron-dense material which were in contact with the plasma membrane could be seen in most normal thyroid cells, but were extremely scarce in the goiter. In 36 cell profiles studied none was found. The endoplasmic reticulum cisternae of the goiter differed significantly from normal thyroid cells. Fewer ribosomes were seen to be attached to the membranes of goiter cells. Furthermore, unlike normal thyroid cells, many free polysomes were seen in goiter cells. The characteristics of the unusual iodoprotein pattern of the goiter extract, resolved by gel chromatography and sucrose density gradient centrifugation, were qualitatively and quantitatively similar to that described previously (Endocrinology 91, 470, 1972). A relatively small amount of the total soluble protein was iodinated. Of these, only a 12S sedimenting species was precipitated by antithyroglobulin immunoglobulin. When separated on polyacrylamide gels containing sodium dodecyl sulfate and mercaptoethanol, this 12S species was resolved into at least 14 polypeptide components ranging in molecular weights from less than 66,000--330,000. Three of the bands, representing a small percentage of the total protein, seemed to comigrate with the major polypeptides of thyroglobulin and were also precipitated with rabbit antihyroglobulin immunoglobulin. The data indicate that glycosylation of iodoproteins was not affected although 19S thyroglobulin synthesis and subsequent storage were drastically impaired.

Animals↗
PubMedDate not supplied

delta 1-Opioid receptor-mediated control of acetylcholine (ACh) release in human neocortex slices.

In slices of human neocortex, prelabelled with [3H]-choline, the release of [3H]-acetylcholine reflects the evoked release of endogenous acetylcholine which was elicited by the same electrical stimulation paradigm. [3H]-Acetylcholine release was depressed by the delta-opioid receptor agonist D-Pen2-D-Pen5-enkephalin. When the nerve endings were depolarized by elevating extracellular potassium the evoked [3H]-acetylcholine release was similarly depressed by D-Pen2-D-Pen5-enkephalin in the absence, but not in the presence, of tetrodotoxin which blocks action potential propagation. Therefore, the delta-opioid receptor inhibiting [3H]-acetylcholine release should not be located to cholinergic nerve terminals, but rather to interneurons. The somatostatin2 receptor partial agonist octreotide per se did not influence action potential-evoked [3H]-acetylcholine release, but prevented the inhibition of release of [3H]-acetylcholine by D-Pen2-D-Pen5-enkephalin. Similarly, the delta 1-opioid receptor antagonist 7-benzylidenenaltrexon per se did not influence [3H]-acetylcholine release, but prevented of the inhibition of release by D-Pen2-D-Pen5-enkephalin. From the present findings we conclude: (1) The evoked release of [3H]-acetylcholine from human neocortex slices reflects the release of endogenous acetylcholine. (2) It is inhibited in an indirect manner by opioid receptors of the delta 1-subtype, which (3) are not localized on cholinergic axon terminals but on soma and dendrites of somatostatin-containing interneurons, where they inhibit somatostatin release. (4) These interneurons innervate cholinergic nerve endings in the human neocortex and appear to facilitate acetylcholine release via somatostatin2 receptors.

Acetylcholine↗