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S Klee

Publications and source records attributed to S Klee.

9 recordsLinked to original sources
PubMed1995

Effects of the tachykinin NK1 receptor antagonist, RP 67580, on central cardiovascular and behavioural effects of substance P, neurokinin A and neurokinin B.

1. We have investigated the effects of the non-peptide NK1 tachykinin receptor antagonist, RP 67580, and its inactive enantiomer, RP 68651, on the cardiovascular and behavioural responses to substance P (SP), neurokinin A (NKA) and neurokinin B (NKB) injected intracerebroventricularly (i.c.v.) in conscious rats. 2. The SP and NKA (25 pmol)-induced increases in blood pressure (BP) and heart rate (HR) were of the same magnitude. The cardiovascular responses to both peptides were associated with excessive grooming behaviour and wet dog shakes (WDS). Relative to SP, NKA was weaker in inducing hindquarter grooming (HG), but more effective in eliciting WDS. The cardiovascular response to NKB (50 pmol) comprised an increase in BP and HR, while the behavioural response was weak. 3. RP 67580 (100 pmol), injected 10 or 30 min prior to SP, effectively inhibited the cardiovascular and behavioural responses to the peptide whereas lower doses were ineffective. Pretreatment with 500 pmol of RP 67580, 10 or 30 min prior to SP, reduced the BP response. Of the behavioural manifestations, only face washing was attenuated when the antagonist was injected 10 min before SP. At 2500 pmol, the antagonist exaggerated the BP response to the peptide without affecting the behavioural response. RP 68651 (100 or 2500 pmol) did not modify the central responses to SP. 4. Neither RP 67580 nor RP 68651 (100 pmol), affected the cardiovascular and behavioural responses to NKA or NKB. 5. Our results indicate that RP 67580 is a selective and high affinity antagonist at central NK1 tachykinin receptors in the rat.

Animals↗
PubMed1995

Expression of Shigella dysenteriae serotype 1 O-antigenic polysaccharide by Shigella flexneri aroD vaccine candidates and different S. flexneri serotypes.

The potential utility of Shigella flexneri aroD vaccine candidates for the development of bi- or multivalent vaccines has been explored by the introduction of the genetic determinants rfp and rfb for heterologous O antigen polysaccharide from Shigella dysenteriae serotype 1. The serotype Y vaccine strain SFL124 expressed the heterologous antigen qualitatively and quantitatively well, qualitatively in the sense of the O antigen polysaccharide being correctly linked to the S. flexneri lipopolysaccharide R3 core oligosaccharide and quantitatively in the sense that typical yields were obtained, with ratios of homologous to heterologous O antigen being 4:1 for one construct and 1:1 for another. Moreover, both polysaccharide chains were shown to be linked to position O-4 of the subterminal D-glucose residue of the R3 core. In contrast to the hybrid serotype Y SFL124 derivatives, analogous derivatives of serotype 2a vaccine strain SFL1070 did not elaborate a complete heterologous O antigen. Such derivatives, and analogous derivatives of rough, O antigen-negative mutants of SFL1070, formed instead a hybrid lipopolysaccharide molecule consisting of the S. flexneri lipid A R3 core with a single repeat unit of the S. dysenteriae type 1 O antigen. Introduction of the determinants for the S. dysenteriae type 1 O antigen into a second serotype 2a strain and into strains representing other serotypes of S. flexneri, revealed the following for the expression of the heterologous O antigen: serotypes 1a, 1b, 2a, and 5a did not produce the heterologous O antigen, whereas serotypes 2b, 3a, 3b, 4a, 4b, 5b, and X did.

Bacterial Proteins↗
PubMed1994

The consequences of nitrofurantoin-induced oxidative stress in isolated rat hepatocytes: evaluation of pathobiochemical alterations.

Oxidative stress was induced in isolated rat hepatocytes by incubation with nitrofurantoin in the absence and presence of the GSSG reductase inhibitor BCNU. In both cases nitrofurantoin markedly reduced glutathione but exerted cytotoxicity as measured by LDH release and loss of intracellular potassium only in BCNU pretreated cells. The onset of cytotoxicity was accompanied by an increase of lipid peroxidation. Oxidation of protein thiols, however, could not be detected in the early phase of cell damage. The cytoprotective activity of N-acetyl-cysteine > dithiothreitol = deferoxamine revealed the substantial importance of glutathione for cellular defence and the sensitivity of not yet identified thiol-dependent targets of oxidative stress.

Acetylcysteine↗
PubMed1994

The role of glutathione and protein thiols in CBrCl3-induced cytotoxicity in isolated rat hepatocytes.

The role of glutathione (GSH) and protein thiols in the pathobiochemical process of CBrCl3 cytotoxicity was investigated in isolated hepatocytes. Administration of 0.5, 1.0 and 1.5 mmol/l CBrCl3 affected cellular viability as assessed by trypan blue exclusion, release of lactate dehydrogenase and loss of intracellular potassium in a dose-dependent manner. Intracellular glutathione and the capacity to reduce 3-(4,5-dimethylthiazolyl-2-)-2,5-diphenyltetrazolium bromide (MTT, thiazolyl blue) decreased almost independently of the CBrCl3 concentration. Protein thiols were not markedly oxidized in the presence of CBrCl3. However, compromising cellular defence mechanisms by either inhibition of glutathione regeneration or depletion of glutathione enhanced the cytotoxicity of CBrCl3 and induced a loss of protein thiols in the late phase of cellular injury. Under these conditions the thiol-dependent Na+,K+ATPase revealed high sensitivity towards CBrCl3. Thus, glutathione proved to exert effective cytoprotection, and sulfhydryl groups of particular proteins were supposed to be an important target of radical attack.

Animals↗
PubMed1993

Trichlorobromomethane-induced changes of purine nucleotides in hepatocytes.

The changes in nucleotide content during CBrCl3 treatment were investigated. In the first 5-10 minutes a significant ATP decrease was detected. The GTP loss leading to 57% of the initial level after 10 min surpasses the ATP loss which leads to 70% of the initial value after 10 min. The increase in uric acid is not only the result of CBrCl3 induced reaction, because of no significant changes in adenine and hypoxanthine values. The uric acid pool reflected different influx and efflux processes. These changes were compared with nucleotide degradation and accumulation of nucleotide degradation products during anoxia.

Adenosine Triphosphate↗
PubMed1992

[In vitro studies of intestinal absorption and biotransformation of furazolidone].

The intestinal biotransformation and absorption of the nitrofuran furazolidone were investigated in isolated gut cells and in the isolated perfused gut. In case of inhibiting furazolidone metabolism by high oxygen tension almost equal concentrations of the parent compound were measured on the mucosal and serosal side of the perfused gut segments. Lowering oxygen supply in order to adjust it to physiological conditions caused a complete degradation of furazolidone in isolated gut cells. Accordingly, hardly any unchanged furazolidone was detected on the serosal side of the isolated perfused gut. An open-chain cyanometabolite was formed in both systems indicating a reductive metabolic process which induces highly reactive intermediates. This metabolite also reached the serosal side of the gut representing the systemic circuit. Thus, the low systemic bioavailability is due to the considerable intestinal metabolism rather than a limited absorption. Unknown metabolites will reach the systemic circuit, the toxic potential of which is still obscure. Independent of its metabolic degradation, thus probably due to its redox cycle furazolidone inhibited intestinal functions as e. g. the flow of water and the transport of sodium.

Animals↗
PubMed1981

Alleviation of performance deficits of depression through thermal biofeedback training.

Explored thermal biofeedback as a method of reducing performance deficits associated with depression. A depressed and nondepressed control group and a depressed group given pretreatment with biofeedback were (N = 30) compared on their performance on an escape/avoidance task. As predicted by the learned helplessness model of depression, depressed controls showed significantly poorer performance than both other groups. The depressed biofeedback and nondepressed control groups did not differ from one another. Implications for alleviation of depression are discussed.

Achievement↗