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Biomedical subjects

H Vogel

Publications and source records attributed to H Vogel.

At least 163 records · Page 9Linked to original sources
PubMed1996

[Psychological contributions to rehabilitation in ambulatory health care].

Concepts and theories of psychology are represented which are suitable to enrich rehabilitation medicine in the outpatient medical attendance. First, the understanding of rehabilitation medicine is discribed as a comprehensive care to ensure handicapped persons remain incorporated in family, society and occupation. Second, special fields of psychology sciences are explained, which contribute to reach these aims of rehabilitation, especially pedagogics and health psychology, medical and clinical psychology and behavioural medicine as well as behavior therapy. Third, there are chances discussed to comprise psychologists in a comprehensive rehabilitative treatment.

Behavior Therapy↗
PubMed1995

Probing the binding domain of the NK2 receptor with fluorescent ligands: evidence that heptapeptide agonists and antagonists bind differently.

We have investigated the interaction of fluorescent peptide ligands with the G protein-coupled receptor NK2 using novel spectrofluorometric approaches. Several heptapeptide antagonists of structure PhCO-Xaa-Ala-D-Trp-Phe-D-Pro-Pro-Nle-NH2 were labelled on position 1 (Xaa) with the environment-sensitive nitrobenzoxadiazole (NBD) probe, differing only in the length of the spacer between the NBD group and the peptide. Upon binding of the labelled antagonist to NK2 receptors stably expressed in Chinese hamster ovary (CHO) cells, an increase in NBD fluorescence was observed when the spacer length was less than 10 A. Collisional quenching experiments using iodide and Co2+ ions were performed to define the accessibility of the NBD group on bound ligands to the solvent. By comparing ligands with spacer arms of varying lengths, we found that the binding pocket is buried at a depth of 5-10 A. In contrast, N-terminally NBD-labelled agonists, decapeptide neurokinin A (NKA) or heptapeptide Nle10-NKA[4-10], bound to the NK2 receptor were accessible to the solvent. Binding of fluorescent ligands to the NK2 receptor was accompanied by an enhancement in the fluorescence anisotropy. The changes in fluorescence properties were used to determine the kinetic parameters of antagonist binding and dissociation. These results indicate that the binding site on the NK2 receptor for the amino-terminal end of the heptapeptide antagonists is buried in the hydrophobic pocket of the receptor protein and clearly distinct from the binding site for the amino-terminal end of agonists, which is accessible to the solvent.(ABSTRACT TRUNCATED AT 250 WORDS)

4-Chloro-7-nitrobenzofurazan↗
PubMed1995

Multiple defects and perinatal death in mice deficient in follistatin.

Follistatin, an activin-binding protein and activin antagonist in vitro, can bind to heparan sulphate proteoglycans and may function in vivo to present activins to their receptors. In the mouse, follistatin messenger RNA is first detected in the deciduum (on embryonic day 5.5), and later in the developing hindbrain, somites, vibrissae, teeth, epidermis and muscle. In Xenopus laevis, overexpression of follistatin leads to induction of neural tissue. Here we use loss-of-function mutant mice to investigate the function of follistatin in mammals. We find that follistatin-deficient mice are retarded in their growth, have decreased mass of the diaphragm and intercostal muscles, shiny taut skin, skeletal defects of the hard palate and the thirteenth pair of ribs, their whisker and tooth development is abnormal, they fail to breathe, and die within hours of birth. These defects are more widespread than those seen in activin-deficient mutant mice, indicating that follistatin may modulate the actions of several members of the transforming growth factor-beta family.

Animals↗
PubMed1995

Mice deficient in both p53 and Rb develop tumors primarily of endocrine origin.

To examine whether a cooperative role exists between inherited Rb and p53 deficiency in tumorigenesis, crosses were made between p53- and Rb-deficient mice and were monitored for subsequent tumor incidence and spectrum. Parental mice containing either Rb or p53 mutant alleles showed a predisposition for pituitary adenomas or lymphomas and sarcomas, respectively. Mice heterozygous for both Rb and p53 mutant alleles developed tumors of endocrine origin (medullary thyroid carcinomas, pancreatic islet cell carcinomas, and pituitary adenomas) in addition to lymphomas and sarcomas. Except for pituitary adenomas, these endocrine tumors were rarely seen in the parental p53 or Rb mutant mice. Mice deficient for both Rb and p53 showed a faster rate of tumor development than mice deficient only in Rb or p53. These results indicate that p53 and Rb do cooperate in the acceleration of tumorigenesis and in the development of endocrine tumor types.

Adenocarcinoma↗
PubMed1995

[The value of selenotherapy in patients with mucoviscidosis].

In cystic fibrosis (CF) patients the antioxidative-oxidative balance is chronically disturbed. Free radicals were generated by bronchial-pulmonal infection and additional exist a deficiency of antioxidative substances by enteral malabsorption especially vitamin E and selenium. Because selenium is an essential content of glutathione peroxidase, which is acting in cytosol and cell membranes, for the present we tested a selenium therapy (peroral sodium selenite 155 micrograms (Se/m2 BSA/d i. e. 4 micrograms Se/kg/d; 4 fold of recommended supply) in 32 CF patients. After three months of this therapy we have seen positive metabolic (normalized content of plasma-selenium, -glutathione peroxidase), endocrine (enhanced efficacy of thyroid hormones, mild increased IgF-I reduced LDL-chol) and clinical consequences (enhanced left ventricular cardiac output), but in three patients side effects (anorexia, nausea, mild hair loss) were observed. Longtime sodium selenite therapy only with 60 micrograms Se/m2 BSA/d over 1 year, stabilized the favourable influences without side effects. For CF patients therefore we recommend a sodium selenite substitution therapy, the best in combination with vitamin E.

Administration, Oral↗
PubMed1995

Effects of genetic background on tumorigenesis in p53-deficient mice.

Mice with disrupted germline p53 alleles have been engineered by us and others and have been shown to have enhanced susceptibility to spontaneous tumors of various types. We monitored a large number of p53-deficient mice (p53+/- and p53-/-) and their wild-type littermates (p53+/+) of two different genetic backgrounds (129/Sv and mixed C57BL/6 x 129/Sv) up to 2 yr of age. p53+/- and p53-/- 129/Sv mice show accelerated tumorigenesis rates compared with their p53-deficient counterparts of mixed C57BL/6 x 129/Sv genetic background. The tumor spectra of the two strains of mice are similar except that almost half of 129/Sv p53-/- males develop malignant teratomas, whereas these tumors are rarely observed in C57BL/6 x 129/Sv mice and never in 129/Sv p53+/- males. In the study reported here, we further characterized the lymphomas that arose in the p53-nullizygous mice and found that over three-quarters of the lymphomas were of thymic origin and contained primarily immature (CD4+/CD8+) T-cells, whereas the remainder originated in the spleen and peripheral lymph nodes and were of B-cell type. The high incidence of early-onset lymphomas in the nullizygous mice makes these animals a good lymphoma model, whereas the heterozygous mice may be a useful model for Li-Fraumeni syndrome, a human inherited cancer predisposition.

Alleles↗
PubMed1995

Metabolism of the Fusarium mycotoxins zearalenone and deoxynivalenol by yeast strains of technological relevance.

The Fusarium mycotoxin zearalenone (ZEA), added at a level of 2 micrograms/ml, was reduced stereoselectively by cultures of Candida tropicalis, Torulaspora delbrückii, Zygosaccharomyces rouxii, and 7 Saccharomyces strains to both alpha- and beta-zearalenol. In contrast, only alpha-zearalenol was produced from ZEA by Pichia fermentans and several yeast strains of the genera Candida, Hansenula, Brettanomyces, Schizosaccharomyces, and Saccharomycopsis. No glucose conjugates of ZEA (zearalenone-4-beta-D-glucopyranoside) were detected. The trichothecene mycotoxin deoxynivalenol (DON) was not metabolized by any of the yeast strains that were used for analysis.

Beer↗
PubMed1995

Covalent attachment of functionalized lipid bilayers to planar waveguides for measuring protein binding to biomimetic membranes.

A new method is presented for measuring sensitively the interactions between ligands and their membrane-bound receptors in situ using integrated optics, thus avoiding the need for additional labels. Phospholipid bilayers were attached covalently to waveguides by a novel protocol, which can in principle be used with any glass-like surface. In a first step, phospholipids carrying head-group thiols were covalently immobilized onto SiO2-TiO2 waveguide surfaces. This was accomplished by acylation of aminated waveguides with the heterobifunctional crosslinker N-succinimidyl-3-maleimidopropionate, followed by the formation of thioethers between the surface-grafted maleimides and the synthetic thiolipids. The surface-attached thiolipids served as hydrophobic templates and anchors for the deposition of a complete lipid bilayer either by fusion of lipid vesicles or by lipid self-assembly from mixed lipid/detergent micelles. The step-by-step lipid bilayer formation on the waveguide surface was monitored in situ by an integrated optics technique, allowing the simultaneous determination of optical thickness and one of the two refractive indices of the adsorbed organic layers. Surface coverages of 50-60% were calculated for thiolipid layers. Subsequent deposition of POPC resulted in an overall lipid layer thickness of 45-50 A, which corresponds to the thickness of a fluid bilayer membrane. Specific recognition reactions occurring at cell membrane surfaces were modeled by the incorporation of lipid-anchored receptor molecules into the supported bilayer membranes. (1) The outer POPC layer was doped with biotinylated phosphatidylethanolamine. Subsequent specific binding of streptavidin was optically monitored. (2) A lipopeptide was incorporated in the outer POPC monolayer. Membrane binding of monoclonal antibodies, which were directed against the peptide moiety of the lipopeptide, was optically detected. The specific antibody binding correlated well with the lipopepitde concentration in the outer monolayer.

Acylation↗
PubMed1995

Neuronal pentraxin, a secreted protein with homology to acute phase proteins of the immune system.

We have identified, by affinity chromatography, a binding protein for the snake venom toxin taipoxin. The sequence of this 47 kDa protein is unique, is characteristic of a secreted protein, and has homology to the acute phase proteins serum amyloid P protein and C-reactive protein of the pentraxin family. We have named this protein neuronal pentraxin (NP), as Northern analysis and in situ hybridization demonstrate high message levels in neurons of cerebellum, hippocampus, and cerebral cortex. Because NP may be released synaptically and has homology to immune proteins potentially involved in uptake of lipidic, toxic, or other antigenic material, we suggest that NP may be involved in a general uptake of synaptic macromolecules.

Amino Acid Sequence↗
PubMed1995

A mutant p53 transgene accelerates tumour development in heterozygous but not nullizygous p53-deficient mice.

To test the behaviour of a mutant form of p53 in the presence and absence of wild-type p53 in vivo, we mated p53-deficient mice containing a p53 null allele to transgenic mice containing multiple copies of a mutant p53 gene (Val 135). Animals hemizygous for the endogenous wild-type p53 gene with the mutant transgene exhibited accelerated tumour development and an altered tumour spectrum compared to their non-transgenic counterparts. In contrast, transgenic and non-transgenic animals nullizygous for endogenous p53 developed tumours at the same rate. Thus, the mutant Val-135 p53 allele may act in vivo in a dominant negative manner in the presence of wild-type p53 but does not display gain of function activity in the absence of wild-type p53.

Animals↗
PubMed1995

Presumed central nervous system Whipple's disease in a child: case report.

Whipple's disease is a rare, chronic, multisystem illness that is pathologically characterized by the accumulation of macrophages in the involved tissue that have a positive periodic acid-Schiff reaction. It is typically seen in middle-aged white men, and only four cases involving persons younger than 15 years of age have been reported. CNS Whipple's disease without intestinal manifestations is rare; only six cases have been reported in the literature, all involving adults. We report the case of a young boy with clinical, laboratory, radiographic, and pathological signs and symptoms consistent with CNS Whipple's disease who responded to therapy with trimethoprimsulfamethoxazole.

Brain Diseases↗
PubMed1995

Propafenone-induced peripheral neuropathy.

Propafenone hydrochloride, a class IC antiarrhythmic drug, is used in the treatment of ventricular and supraventricular arrhythmias. Herein we describe a patient with episodic jabbing and crushing pain in his hands and feet, aching in his forearms, and hyperesthesias of his extremities. He had been taking propafenone for 1 year because of ventricular arrhythmias. Results of a nerve conduction velocity test were abnormal. Electron microscopic findings on a sural nerve biopsy specimen represented distal small fiber neuropathy. Findings on a thermoregulatory sweat test and on autonomic tests were abnormal, compatible with a distal small fiber neuropathy. To our knowledge, peripheral neuropathy has not previously been reported to occur with use of propafenone. In this patient, propafenone seemed to be responsible for the development of peripheral neuropathy, which resolved after use of the drug had been discontinued.

Adult↗
PubMed1995

[Recommendations for changing microbiological examination parameters in filling bottled water to comply with the mineral and drinking water regulation].

Microbiological Pollutions in Mineral, Spring and Table Waters have different potency according to health hazards or to noncompliance with good manufacturing practices. Therefore, the microbiological parameters of mineral water and table water directives should be reexamined for their suitability. Only Escherichia coli is an indicator of faecal pollution and therefore an indicator of health hazards. Enterobacteriaceae (coliform and noncoliform), Pseudomonas aeruginosa and elevated colony counts mainly suggest noncompliance with good manufacturing practices. Sulphite-reducing clostridia and faecal streptococci are worthless indicators at the moment because of inadequate analytical methods. In addition, investigations on Staphylococcus aureus are recommended at least for bottled waters which are declared to be suitable for the preparation of infant food. From this point of view, different procedures for penalty and marketing are also discussed.

Colony Count, Microbial↗
PubMed1994

Combined deficiencies of Src, Fyn, and Yes tyrosine kinases in mutant mice.

Three members of the Src family of tyrosine kinases, src, fyn, and yes, are broadly expressed throughout mouse development. Mutations in the c-src and fyn genes were shown previously to lead to restricted nonoverlapping phenotypes only in a subset of cells in which these kinases are expressed. In this work we show that a mutation in the yes gene does not lead to an overt phenotype. Except for brain, the level or distribution of related kinases is not altered in major tissues. To gain further insight into the possibility that these kinases compensate for each other, animals deficient in multiple src-kinases were generated. Whereas most of the src/fyn or src/yes double mutants die perinatally, a substantial proportion of fyn/yes double mutants are viable but undergo degenerative renal changes leading to diffuse segmental glomerulosclerosis. Taken together, these data are consistent with the hypothesis that, at least in some cells, these kinases are able to compensate for the loss of the other related kinases.

Animals↗
PubMed1994

Pf3 coat protein forms voltage-gated ion channels in planar lipid bilayers.

The coat protein of bacteriophage Pf3 forms discrete and stable ion channels of uniform size in planar bilayers of asolectin. Its primary sequence suggests a channel formed by a bundle of transmembrane helices. Since the apparent transmembrane region only consists of strongly hydrophobic residues, it represents a new class of channel-forming proteins. The channel activity is strongly voltage-dependent. The single-channel conductance of 60 pS (at 100 mV) in 0.2 M NaCl is slightly voltage-dependent, indicating conformational changes of the pore upon variation of the transmembrane electric field. The channel is unselective which suggests that the pore is of aqueous character. For the observed conductance, a channel diameter of 3.6 A is consistent with a tetrameric alpha-helix bundle, as calculated from a barrel-stave model. A pronounced dependence of the gating kinetics with increasing voltage arises from two opposing effects: an increase in the number of open channel structures, and a simultaneous, more than 3-fold decrease in the channel lifetime. Thus, a maximum activity is reached around 100 mV, a range which corresponds well with physiological membrane potentials. The channels activate only upon application of a positive voltage on the side of the membrane to which the protein had been added. The slow relaxation of the mean current upon application of sudden voltage jumps indicates a strong activation barrier in the channel gating process, which may result from the membrane translocation of the charged residues of the peptide ends. A channel-mediated import mechanism is suggested for the bacterial infection by phage DNA.

Amino Acid Sequence↗