Neutralizing antibodies against botulinum toxin a after a wasp sting.
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Antibodies, Blocking↗
Biomedical subjects
Sebastian Paus
Publications and source records attributed to Sebastian Paus.
Acute hebephrenia.
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Activated Protein C Resistance↗
Lack of association between the interleukin-1 alpha (-889) polymorphism and early-onset Parkinson's disease.
An increasing number of studies have shown that an inflammatory process is part of Parkinson's disease (PD) brain pathology. Interleukin-1 (IL-1) is a multifunctional cytokine and is considered to contribute to several inflammatory diseases. Recently, we detected an associated risk in a subgroup of PD patients with a disease onset < 50 years and a C to T transition in the IL-1alpha promoter (-889). One-hundred-seventy-six German PD patients (42.1 +/- 6.4 years; 42.4% male) and 170 unrelated age-matched control individuals (40.4 +/- 8.7 years; 57.6% male) were investigated for the presence of the IL-1alpha (-889C/T) polymorphism. No significant difference in the allelic distribution of the analyzed IL-1alpha polymorphism has been found between PD and controls. We conclude that the C/T polymorphism in the IL-1alpha promoter region at -889 does not increase the risk to develop PD.
Adult↗
Association study of dopamine D2, D3, D4 receptor and serotonin transporter gene polymorphisms with sleep attacks in Parkinson's disease.
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Alleles↗
Systematic screening for mutations in the human N-methyl-D-aspartate receptor 1 gene in schizophrenic patients from the German population.
Evidence for a dysfunction of the N-methyl-D-aspartate (NMDA) type of ionotropic glutamate receptors in schizophrenic patients, comes from neurochemical and clinical pharmacologic data. Therefore, the NMDAR1 gene can be regarded as an interesting candidate gene for schizophrenia. Several groups have tried to identify variants of this gene in schizophrenic patients in different, however not in German, populations. We sought to identify sequence changes of potential functional relevance in genomic DNA from 46 German unrelated schizophrenic patients by means of single-strand conformation analysis. No mutations of likely functional relevance were observed. We identified two synonymous coding Single Nucleotide Polymorphisms (cSNPs) in exons 6 and 7, and two SNPs in exon-flanking intronic sequences. Genotype distribution of these four SNPs was not significantly different between schizophrenic patients and controls. Our results suggest that the NMDAR1 subunit is not frequently involved in the development of schizophrenia in the German population.
DNA↗
Sleep attacks, daytime sleepiness, and dopamine agonists in Parkinson's disease.
To study the putative association of dopamine agonists with sleep attacks in patients with Parkinson's disease (PD) and their relation to daytime sleepiness, we performed a survey of 2,952 PD patients in two German counties. In 177 patients, sudden, unexpected, and irresistible sleep episodes while engaged in some activity were identified in a structured telephone interview. Ninety-one of these patients denied the occurrence of appropriate warning signs. A total of 133 patients (75%) had an Epworth Sleepiness Scale (ESS) score >10; 65 (37%) >15. Thirty-one patients (18%) had an ESS score < or =10 and yet experienced sleep attacks without warning signs. Thus, although a significant proportion of patients at risk for sleep attacks might be identified using the ESS, roughly 1% of the PD patient population seems to be at risk for sleep attacks without appropriate warning signs and without accompanying daytime sleepiness. Sleep attacks occurred with all dopamine agonists marketed in Germany (alpha-dihydroergocryptine, bromocriptine, cabergoline, lisuride, pergolide, pramipexole, ropinirole), and no significant difference between ergot and nonergot drugs was evident. Levodopa (L-dopa) monotherapy carried the lowest risk for sleep attacks (2.9%; 95% confidence interval [CI], 1.7-4.0%) followed by dopamine agonist monotherapy (5.3%; 95% CI, 1.5-9.2%) and combination of L-dopa and a dopamine agonist (7.3%; 95% CI, 6.1-8.5%). Neither selegeline nor amantadine or entacapone appeared to influence the occurrence of sleep attacks. A high ESS score, intake of dopamine agonists, and duration of PD were the main influencing factors for the occurrence of sleep attacks. The odds ratio for dopamine agonist therapy was 2.9 compared to 1.9 with L-dopa therapy and 1.05 for a 1-year-longer disease duration.
Activities of Daily Living↗
Thalamic involvement in sporadic Creutzfeldt-Jakob disease: a diffusion-weighted MR imaging study.
BACKGROUND AND PURPOSE: Recent neuropathologic research suggests thalamic involvement in sporadic Creutzfeldt-Jakob disease (sCJD), which has been disregarded in imaging studies. Diffusion-weighted (DW) MR imaging has the highest sensitivity for the detection of signal intensity (SI) abnormalities in CJD. We hypothesized that pathologic changes in the thalamus in sCJD can be detected by using a subtle analysis of DW MR imaging. METHODS: Six sCJD patients and nine healthy controls were examined with a 1.5-T system by using DW single-shot spin-echo echo planar (b = 0, 1000 s/mm(2)), T2-weighted turbo spin-echo, and fluid-attenuated inversion recovery sequences. One patient was examined serially (3, 4, and 8 months after onset of symptoms). MR images were reviewed for SI changes in the striatum, hippocampus, mediodorsal thalamic nucleus (MD), and pulvinar thalami. Apparent diffusion coefficients (ADCs) were measured in these areas. RESULTS: All sCJD patients showed increased SI on DW images in the striatum bilaterally. ADCs in these areas were significantly reduced. Four of six sCJD patients showed increased SI on DW images in the pulvinar thalami, whereas ADCs were significantly reduced in all patients (mean ADC +/- SEM: in patients with SI changes, 701 +/- 38; in patients without SI changes, 684 +/- 37; in controls, 853 +/- 15 [P <.0001]). No patient showed SI changes in the MD on DW images, whereas ADCs were significantly reduced in all (664 +/- 28 as compared with 800 +/- 24 in controls [P =.0011]). Serial measurements in one sCJD patient showed ADC reduction in the pulvinar thalami preceding the SI changes on DW images. CONCLUSION: A quantitative analysis of DW images with ADC measurements shows slight MR imaging changes in the thalamus in sCJD when abnormal SI may not be present.
Aged↗
Transcriptional profiling in human epilepsy: expression array and single cell real-time qRT-PCR analysis reveal distinct cellular gene regulation.
Highly parallel expression monitoring by microarrays is a powerful tool to study human brain disorders. In contrast to various nonneuronal tissues, the CNS is composed of a multitude of different cell types. Changed mRNA levels in neuropathological conditions may simply reflect altered tissue composition, rather than specific gene transcription regulation. Therefore, it is crucial, to supplement expression array data of histologically heterogeneous brain samples with a detailed analysis at the cellular level. Here, we have used a two-step approach to identify specific changes in hippocampal gene expression in patients with a hippocampal seizure focus (TLE) and marked neuronal damage. Using comparative expression array hybridization, 21 genes appeared to be differentially regulated. Expression alterations of a subset of these genes, i.e. (up-regulation of ataxin-3 and glial fibrillary acid protein (GFAP) as well as down-regulation of calmodulin) was confirmed in an extended series of individuals by real-time quantitative RT-PCR (qRT-PCR). In order to determine the cellular localization of these mRNAs, we performed real-time qRT-PCR of individual laser-microdissected neurons and glial cells. While ataxin-3 was expressed only in hippocampal neurons, GFAP was detected in reactive astrocytes. The differential calmodulin expression found on the tissue level was not observed in mRNA analyses from single neurons, suggesting that lower calmodulin mRNA levels are a consequence of segmental cell loss and do not indicate reduced cellular expression. Ataxin-3 has been related to neuronal maintenance. Its functional role for TLE has to be further evaluated.
Ataxin-3↗