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Biomedical subjects

B Rothe

Publications and source records attributed to B Rothe.

At least 19 recordsLinked to original sources
PubMed2001

Remote F-wave changes after local botulinum toxin application.

OBJECTIVE: Although the therapeutic effects of botulinum toxin A can be explained by its action at the neuromuscular junction, central or more proximal effects have also been discussed. METHODS: Eleven patients with torticollis spasmodicus and 3 patients with writer's cramp were studied before and 1 and 5 weeks after the first treatment with botulinum toxin. We measured compound muscle action potentials (CMAPs), motor conduction velocities (MCVs), the shortest (SFL) and the mean F-wave latencies (MFL) and F-wave persistence (30 trials) of untreated muscles for each side (ulnar nerve-abductor digiti minimi muscle, peroneal nerve-tibialis anterior muscle). RESULTS: CMAPs and MCVs showed no significant changes. For both nerves, however, SFL and MFL were prolonged slightly 1 week after treatment and returned to about baseline after 5 weeks (t test). The F-wave persistence was reduced 1 week after treatment for the right ulnar and both peroneal nerves (t test). CONCLUSIONS: These results are not likely due to an impairment of neuromuscular transmission. Instead, we propose a decreased excitability of alpha-motoneurons supplying non-treated muscles. A reduction of muscle spindle activity or changes of the recurrent inhibition are discussed as possible causes.

Action Potentials↗
PubMed2000

Neutropenia and anaemia due to carbimazole-dependent antibodies.

Carbimazole-dependent antibodies to erythrocytes were detected in the sera of three anaemic patients who had been treated with carbimazole for hyperthyroidism. By the use of Rhnull-typed erythrocytes, we could show that some of these were directed against the proteins of the Rh complex. Carbimazole-dependent antibodies eluted from erythrocytes showed no binding to other blood cells. One patient also presented with neutropenia and mild thrombocytopenia. Additional carbimazole-dependent antibodies against the neutrophil-specific Fcgamma receptor IIIb (FcgammaRIIIb, CD16b) and the broadly expressed platelet endothelial cell adhesion molecule 1 (PECAM-1; CD31) were detected in this patient's serum. Surprisingly, the PECAM-1-reactive drug-dependent antibodies were also detectable in the sera of the other two patients with normal leucocyte and platelet counts. We assume that carbimazole can induce cell lineage-specific drug-dependent antibodies that cause cytopenia and also drug-dependent antibodies against the broadly expressed PECAM-1 molecule that may cause mild but not severe cytopenia.

Aged↗
PubMed1998

Effects of thyrotropin-releasing hormone on the sleep EEG and nocturnal hormone secretion in male volunteers.

Various peptides including corticotropin-releasing hormone (CRH) exert selective effects on sleep structure and noctural secretions of cortisol and growth hormone (GH). In animal studies analeptic effects and sleep disturbances after thyrotropin-releasing hormone (TRH) administration have been observed; studies of endocrine function in depressed patients suggest a pathological activity of CRH and TRH as compared with that in healthy volunteers. As the role of TRH in the regulation of the sleep endocrine pattern in humans has not yet been clarified, we performed a study to examine the effects of pulsatile administration of TRH on the sleep EEG pattern and the nocturnal secretions of cortisol and GH in 7 healthy male subjects. The sleep EEG was recorded from 23.00 to 07.00 h, and blood samples were collected every 20 min from 20.00 to 07.00 h for the analysis of GH and cortisol concentrations during intravenous administration of placebo or 4 x 50 microgram TRH at 22.00, 23.00, 24. 00, and 01.00 h. In contrast to the well-known effects of CRH on the sleep endocrine pattern, TRH exerts only a weak effect on the sleep EEG which is reflected in a slight decrease in sleep efficiency associated with a trend to wakefulness during the night. Furthermore, after TRH administration, the cortisol rise appeared earlier, and a nonsignificant tendency to an increased secretion of cortisol during the first half of the night was found. The GH secretion did not differ significantly after application of TRH or placebo. The activating, albeit weak, effect of TRH on the sleep EEG and nocturnal cortisol secretion in healthy volunteers confirms and adds to the results previously observed in animals. On the basis of these findings, we surmise that TRH may contribute to the disturbed sleep continuity seen in depressed patients, probably acting as a cofactor of CRH in a synergistic manner.

Adult↗
PubMed1997

Characterization of three distinct extradiol dioxygenases involved in mineralization of dibenzofuran by Terrabacter sp. strain DPO360.

The dibenzofuran-degrading bacterial strain DPO360 represents a new species of the genus Terrabacter together with the previously described dibenzofuran-mineralizing bacterial strain DPO1361 (K.-H. Engesser, V. Strubel, K. Christoglou, P. Fischer, and H. G. Rast, FEMS Microbiol. Lett. 65:205-210, 1989; V. Strubel, Ph.D. thesis, University of Stuttgart, Stuttgart, Germany, 1991; V. Strubel, H. G. Rast, W. Fietz, H.-J. Knackmuss, and K.-H. Engesser, FEMS Microbiol. Lett. 58:233-238, 1989). Two 2,3-dihydroxybiphenyl-1,2-dioxygenases (BphC1 and BphC2) and one catechol-2,3-dioxygenase (C23O) were shown to be expressed in Terrabacter sp. strain DPO360 growing with dibenzofuran as a sole source of carbon and energy. These enzymes exhibited strong sensitivity to oxygen. They were purified to apparent homogeneity as homodimers (BphC and BphC2) and as a homotetrameric catechol-2,3-dioxygenase (C23O). According to their specificity constants kcat/Km, both BphC1 and BphC2 were shown to be responsible for the cleavage of 2,2',3-trihydroxybiphenyl, the first metabolite in dibenzofuran mineralization along the angular dioxygenation pathway. With this substrate, BphC2 exhibited a considerably higher kcat/Km, value (183 microM/min) than BphC1 (29 microM/min). Catechol-2,3-dioxygenase was recognized to be not involved in the ring cleavage of 2,2',3-trihydroxybiphenyl (kcat/Km, 1 microM/min). Analysis of deduced amino acid sequence data of bphC1 revealed 36% sequence identity to nahC from Pseudomonas putida PpG7 (S. Harayama and M. Rekik, J. Biol. Chem. 264:15328-15333, 1989) and about 40% sequence identity to various bphC genes from different Pseudomonas and Rhodococcus strains. In addition, another 2,3-dihydroxybiphenyl-1,2-dioxygenase gene (bphC3) was cloned from the genome of Terrabacter sp. strain DPO360. Expression of this gene, however, could not be detected in Terrabacter sp. strain DPO360 after growth with dibenzofuran.

Amino Acid Sequence↗
PubMed1996

Trimipramine and imipramine exert different effects on the sleep EEG and on nocturnal hormone secretion during treatment of major depression.

In a 4-week double-blind clinical trial we compared the effects of the tricyclic antidepressants trimipramine and imipramine on the sleep EEG and on nocturnal bormone secretion in 20 male inpatients with major depression. Both treatments produced rapid significant clinical improvement in depression without severe adverse effects. However, the two drugs had markedly different neurobiologic profiles. Trimipramine enhanced rapid eye movement (REM) sleep and slow wave sleep, whereas imipramine suppressed REM sleep and showed no effect on slow wave sleep. Total sleep time and the sleep efficiency index increased under trimipramine but not under imipramine. Nocturnal cortisol secretion decreased with trimipramine but remained unchanged with imipramine. In contrast to imipramine, trimipramine induced an increase in prolactin secretion compatible with its known antagonism at dopamine (D2) receptors. Imipramine induced a decrease in growth hormone secretion during the first half of the night. Neither of the drugs induced significant changes in plasma testosterone concentration. We conclude that trimipramine is an antidepressant with sleep-improving qualities that possibly acts through inhibition of hypothalamic-pituitary-adrenocortical system activity by a yet unknown mechanism.

Adult↗
PubMed1995

Bretazenil modulates sleep EEG and nocturnal hormone secretion in normal men.

Preclinical data suggest that the imidazodiazepinone derivative bretazenil (Ro 16-6028) has anxiolytic and anticonvulsant properties with only weak sedative effects. We examined the influence of oral administration of 1 mg bretazenil on the sleep EEG and the concomitant nocturnal secretion of cortisol, growth hormone and prolactin in ten healthy young men. After bretazenil we found a significant increase in stage 2 sleep and a significant reduction in stage 3 sleep. REM latency was prolonged. Spectral analysis of sleep-EEG power revealed a decrease in delta and in theta power and an increase in sigma power. We found no significant influence on sleep onset latency or on intermittent wakefulness. Bretazenil prompted a significant decrease in cortisol secretion and a significant increase in prolactin release. It had no major influence on growth hormone secretion.

Adult↗
PubMed1994

Effects of 5HT3 receptor antagonism by tropisetron on the sleep EEG and on nocturnal hormone secretion.

Two dosages (5 mg and 25 mg) of the selective 5HT3 receptor antagonist tropisetron (ICS 205-930) were administered to healthy male controls, and the effects on the sleep EEG and nocturnal secretory activity of growth hormone (GH) and cortisol were evaluated. The lower dosage was administered to four subjects and the higher dosage to eight on 5 consecutive days, preceded and followed by 2 days of placebo treatment. After 25 mg of tropisetron, there was a slight increase in REM sleep in the first part of the sleep period, and stage 2 was decreased during the total night. In addition, plasma cortisol levels increased earlier than under placebo, and plasma GH levels were reduced in the second part of the night. Thus, only discrete effects of tropisetron upon sleep-endocrine activity were noted, making it unlikely that serotoninergic neurotransmission exerts its well-documented effects upon sleep through 5HT3 receptors.

Adult↗
PubMed1994

Role of human chorionic gonadotropin in patients with pure seminoma.

Human chorionic gonadotropin (beta-hCG) and alpha-fetoprotein (AFP) are widely established specific and sensitive tumor markers for nonseminomatous testicular cancer. In 106 patients with pure seminoma, a highly sensitive method detected beta-hCG both before and repeatedly during therapy. The low detection limit of the test (0.3 IU/l) coincided with the 95 percentile of a group of 60 healthy blood donors. Its 100 percentile of < 1.0 IU/l was applied as the upper limit of the normal range. In 30.2% of our patients with pure seminoma, elevated beta-hCG levels were noted prior to orchiectomy. The levels returned to normal in 76% of these patients thereafter, and in 34% after additional irradiation or chemotherapy. During an observation period of 2-84 months, all beta-hCG-positive patients were in complete remission. Prior to semicastration, 1 patient showed extremely high beta-hCG levels, while in another patient, beta-hCG and AFP were elevated simultaneously. In both cases, tumor marker levels did not seem to agree with the histology of 'pure seminoma' and rather suggested the presence of nonseminomatous tumor cells. Increased AFP levels contradict the presence of a pure seminoma and indicate a nonseminomatous testicular tumor. The same holds true for strongly elevated beta-hCG levels, whereas levels of up to 200 IU/l correlate with the diagnosis of pure seminoma.

Adult↗
PubMed1993

Neurosteroid pregnenolone induces sleep-EEG changes in man compatible with inverse agonistic GABAA-receptor modulation.

The steroid pregnenolone (P) and its sulfate (PS) can accumulate in the central nervous system independent of peripheral sources. Pharmacologically, the sulphated form of P interacts with the GABAA receptor complex, and functional assays show that this steroid behaves as an allosteric GABAA receptor antagonist. The present study explored the effect of a single dose of P upon the sleep-EEG and concurrent secretion of growth hormone and cortisol in male volunteers. P increased the amount of time spent in slow wave sleep and depressed EEG sigma power. Sleep-associated nocturnal cortisol and growth hormone secretion remained unchanged, ruling out the possibility that P exerted its effect via altered regulation of these hormones. Furthermore, results from in vitro studies on the potency of P to activate gene transcription via corticosteroid receptors made a genomic action of P via hormone receptor-sensitive DNA sequences unlikely. We conclude that P acts in a non-genomic fashion at or in the vicinity of the benzodiazepine binding site, modulating allosterically the GABAA receptor like a partial inverse.

Adult↗
PubMed1993

The sleep EEG and nocturnal hormonal secretion studies on changes during the course of depression and on effects of CNS-active drugs.

1. The sleep EEG and nocturnal hormone secretion were studied simultaneously in normal male controls and in male patients with major endogenous depression before treatment with tricyclics and after recovery and drug cessation. 2. Several studies were performed in normal male controls to investigate the effect of antidepressants (brofaromine, moclobemide, amitriptyline, clomipramine and trimipramine) and of neuropeptides (CRH and the ACTH (4-9) fragment analog ebiratide) on the sleep EEG and sleep-associated hormone secretion. 3. Elevated cortisol and blunted testosterone secretion are state markers of acute depression, whereas sleep EEG, GH and prolactin variables do not show marked differences between acute depression and recovery. Except for trimipramine, all antidepressants investigated suppress REM sleep. No systematic relationship between the sleep EEG and endocrine effects of antidepressants is detectable. Pulsatile application of CRH in controls mimicks some of the neurobiological symptoms of acute depression. More shallow sleep occurs under ebiratide, whereas hormonal secretion remains unchanged. 4. Our data demonstrate that antidepressants exert distinct effects on sleep. However, these substances do not induce changes in sleep structure which persist after their withdrawal in remitted patients. Pulsatile application of neuropeptides leads to specific effects on CNS activity which are not mediated by changes of peripheral hormone secretion. The view that CRH plays a key role in the pathophysiology of affective disorders is corroborated.

Adult↗
PubMed1992

Effects of growth hormone-releasing hormone and somatostatin on sleep EEG and nocturnal hormone secretion in male controls.

When applied centrally to animals, growth hormone-releasing hormone (GHRH) stimulates slow-wave sleep (SWS), whereas somatostatin (SRIF) increases REM sleep. We investigated whether these peptides also affect the sleep EEG in humans when given intravenously by comparing polysomnographically the effects of four boluses of (1) placebo, (2) 50 micrograms GHRH or (3) 50 micrograms SRIF administered at 22.00, 23.00, 24.00 and 1.00 h to 7 male controls. In addition, we collected blood samples through a long catheter every 20 min from 22.00 to 7.00 h and measured plasma cortisol and growth hormone (GH) levels. In comparison with SRIF and placebo, GHRH produced a significant increase in plasma GH concentration throughout the night (mean +/- SD: 10.8 +/- 2.0 ng/ml after GHRH; 3.0 +/- 1.7 ng/ml after SRIF and 3.2 +/- 2.0 ng/ml after placebo). SRIF failed to substantially attenuate the nocturnal GH release. Nocturnal cortisol secretion was blunted after GHRH but remained unaffected by SRIF (61.4 +/- 12.9 ng/ml after placebo; 46.6 +/- 19.7 ng/ml after GHRH and 70.8 +/- 12.6 ng/ml after SRIF). Quantitative sleep EEG staging showed a significant increase in SWS after GHRH administration but no change after SRIF (percent spent in SWS per night: 14.0 +/- 5.6 after placebo, 20.2 +/- 6.6 after GHRH and 15.1 +/- 8.2 after SRIF). Application of SRIF was accompanied by a trend toward increased REM density. The effects of episodic GHRH administration upon SWS, GH and cortisol secretion were opposite to those previously reported for corticotropin-releasing hormone, which supports the view that neuroregulation of human sleep involves an interaction of central GHRH and corticotropin-releasing hormone.

Adult↗
PubMed1991

Application of sialidase antibodies for the diagnosis of clostridial infections.

Two immunological methods, a sialidase-inhibition test and an ELISA, had been developed for a species-specific detection of sialidases (EC 3.2.1.18) secreted by growing cells of Clostridium perfringens, C. septicum, and C. sordellii. These assays were applied to samples from the infected tissues and cotton wool plugs soaked with wound exudate from patients suspected to be suffering from gas gangrene. The results from 72 patients were compared with bacteriological investigations of 67 homologous samples. From these, 35 patients were found to be infected with one or two of the clostridial species: thirty patients contained C. perfringens, six samples showed an immunologically positive reaction for C. septicum and eight for C. sordellii. In the case of C. perfringens, a high degree of coincidence between the immunological and the bacteriological analyses was obtained. However, in infections with C. septicum or C. sordellii the bacteriological and immunological tests did not agree well. The simple and rapid sialidase inhibition test or the slightly more time-consuming ELISA, which even detects low quantities of sialidase, can be applied for the specific diagnosis of infections caused by C. perfringens, thus allowing a species-specific detection of this bacterial species in two or six hours, respectively, even at an early stage of infection. This early diagnosis is a prerequisite for a specific and life-saving therapy of this severe disease.

Bacterial Typing Techniques↗
PubMed1991

The sialidase gene from Clostridium septicum: cloning, sequencing, expression in Escherichia coli and identification of conserved sequences in sialidases and other proteins.

An oligonucleotide mixture corresponding to the codons for conserved and repeated amino acid sequences of bacterial sialidases (Roggentin et al. 1989) was used to clone a 4.3 kb PstI restriction fragment of Clostridium septicum DNA in Escherichia coli. The complete nucleotide sequence of the sialidase gene was determined from this fragment. The derived amino acid sequence corresponds to a protein of 110,000 Da. The ribosomal binding site and promoter-like consensus sequences were identified upstream from the putative ATG initiation codon. The molecular and immunological properties of the sialidase expressed by E. coli are similar to those of the sialidase as isolated from C. septicum. The newly synthesized protein is assumed to include a leader peptide of 26 amino acids. On sequence alignment, the sialidases from C. septicum, C. sordellii and C. perfringens show significant homologies. As in other bacterial sialidases, conserved amino acid sequences occur at four positions in the protein. Aside from the consensus sequences, only poor homology to other bacterial and viral sialidases was found. The consensus sequence could be identified even in other, non-sialidase proteins, indicating a common function or the evolutionary relatedness of these proteins.

Amino Acid Sequence↗
PubMed1989

Conserved sequences in bacterial and viral sialidases.

The genes of the bacterial sialidases from Clostridium sordellii G12, C. perfringens A99, Salmonella typhimurium LT-2 and Vibrio cholerae 395 sequenced so far were examined for homologies and were compared with sequences of viral sialidases. Each of the bacterial sialidases contains a short sequence of twelve amino-acids, which is repeated at four positions in the protein. All these sequences exhibit significant similarities. Comparing the repeated sequences of the four sialidases, five amino-acids were found to be highly conserved at defined positions: Ser-X-Asp-X-Gly-X-Thr-Trp. Additionally, most of the distances between the four repeated regions are also conserved among the different sialidases. The conserved bacterial sequences show similarity with sialidases of influenza A H7N1 and H13N9.

Amino Acid Sequence↗
PubMed1989

Cloning, sequencing and expression of a sialidase gene from Clostridium sordellii G12.

A 4.3 kb XbaI restriction fragment of DNA from Clostridium sordellii G12 hybridized with a synthetic oligonucleotide representing the N-terminus of the sialidase protein secreted by C. sordellii. This cloned fragment was shown to encode only part of the sialidase protein. The sialidase gene of C. sordellii was completed by a 0.7 kb RsaI restriction fragment overlapping one end of the XbaI fragment. After combining the two fragments and transformation of Escherichia coli, a clone that expressed sialidase was obtained. The nucleotide sequence of the sialidase gene of C. sordellii G12 was determined. The sequence of the 18 N-terminal amino acids of the purified extracellular enzyme perfectly matched the predicted amino acid sequence near the beginning of the structural gene. The amino acid sequence derived from the complete gene corresponds to a protein with a molecular mass of 44,735 Da. Upstream from the putative ATG initiation codon, ribosomal-binding site and promoter-like consensus sequences were found. The encoded protein has a leader sequence of 27 amino acids. The enzyme expressed in E. coli has similar properties to the enzyme isolated from C. sordellii, except for small differences in size and isoelectric point. Significant homology (70%) was found with a sialidase gene from C. perfringens.

Amino Acid Sequence↗
PubMed1988

Cloning and sequencing of a Clostridium perfringens sialidase gene.

Escherichia coli was transformed with pUC vectors containing Sau3A restriction fragments (RF) of Clostridium perfringens DNA. Two clones expressed sialidase activity when assayed with the fluorogenic substrate 4-methylumbelliferyl-alpha-D-N-acetylneuraminic acid. A synthetic oligonucleotide representing the N-terminus of the expressed enzyme hybridized with the clostridial insert and with a corresponding 2.1 kb Sau3A RF of the C. perfringens genome. The insert reduced to 1.4 kb, which still encoded active sialidase, has been sequenced. The structural gene encodes 382 amino acids representing an Mr of 42770. A hydrophobic leader sequence is absent. Upstream from the initiation codon ATG, a GA-rich region is found and considered as the Shine-Dalgarno sequence. Homology with the N-terminus of the Vibrio cholerae sialidase gene and with viral sialidase sequences was not found.

Amino Acid Sequence↗
PubMed1986

Immunoscintigraphy and radioimmunotherapy in patients with pancreatic carcinoma.

A new monoclonal antibody (BW 494/32) labeled with 131I or 111In was used for planar and tomographic immunoscintigraphy (IS) in patients with pancreatic carcinoma. It appears that IS for pancreatic carcinoma and its metastases remains a hopeful but still difficult procedure and labeling with 111In is of advantage and results in more convincing images in the case of tumor lesions distant from liver and spleen. Attempts at radioimmunotherapy with 131I-anti-CA 19-9 and with 131I-494/32 in a patient with local recurrence of a pancreatic cancer and with large liver metastases were without success because of extremely poor blood supply to the metastatic tumor masses. Intraarterial infusion of the tracer without or with blockade and perfusion of the common hepatic artery with saline solution could not enhance the tracer uptake compared to that after intravenous infusion. High intratumoral concentrations, however, as achieved e.g. by intratumoral instillation in animal studies, represent a necessary precondition for effective beta-irradiation of tumor lesions.

Adult↗