Bilateral internal carotid artery dissection in cystathionine beta-synthase deficiency.
Explore the source record for details and available documents.
Biomedical subjects
Publications and source records attributed to N Weiss.
Explore the source record for details and available documents.
Imaging studies indicate that experimental pain is processed in multiple cortical areas which are often characterized as a network. However, the functional connectivity within the network and the other properties of the network is poorly understood. Substantial evidence demonstrates that synchronous oscillations between two cortical areas may indicate functional connectivity between those areas. We test the hypothesis that cortical areas with pain-related activity are functionally connected during attention to a painful stimulus. We stimulated with a painful, cutaneous, laser stimulus and recorded the response directly from the cortical surface (electrocorticography--ECoG) over primary somatosensory (SI), parasylvian (PS), and medial frontal (MF) cortex through subdural electrodes implanted for treatment of epilepsy. The results demonstrate synchrony of ECoGs between cortical structures receiving input from nociceptors, as indicated by the occurrence of laser-evoked potentials (LEPs) and/or event-related desynchronization (ERD). Prior to the stimulus, directed attention to the painful stimulus consistently increased the degree of synchrony between SI and PS regions, as the subject anticipated the stimulus. After the laser stimulus, directed attention to the painful stimulus consistently increased the degree of synchrony between SI and MF cortex, as the subject responded by counting the stimulus. Therefore, attention to painful stimuli always enhanced synchrony between cortical pain-related structures. The pattern of this synchrony changed as the patient switched tasks from anticipation of the stimulus to counting the stimulus. These results are the first compelling evidence of pain networks characterized by rapidly switching, task-specific functional connectivity.
AIM: The aim of this study was to analyze the intermediate results of selective stenting of superficial femoral artery (SFA) lesions after a suboptimal balloon angioplasty result. METHODS: We analyzed 70 consecutive patients with claudication or critical limb ischemia due to peripheral arterial occlusive disease who underwent stent implantation of the SFA after unsuccessful balloon-angioplasty. All patients were followed-up immediately after the procedure and 3, 6 and 12 months thereafter. Restenosis was defined as an increase of peak systolic velocity-index >2 as determined by duplex sonography. RESULTS: Primary patency rates at 3, 6 and 12 months were 83.4%, 66.2% and 59%, respectively. Successful reinterventions were performed for 17 reobstructions, resulting in a secondary patency rate at 3, 6 and 12 months of 91%, 89.3%, and 83.8%, respectively. At 12 months 68.6% of the patients were asymptomatic, 21.6% complained of mild (Fontaine class II a), 5.9% of severe (Fontaine class II b) claudication and 2.9% were in critical limb ischemia. CONCLUSIONS: Our data indicate that selective stenting of the SFA after suboptimal balloon angioplasty results in intermediate patency rates similar to that reported for primarily successful PTA, thereby supporting the widely accepted policy of selective stenting as a rescue procedure after unsuccessful balloon angioplasty.
We report on the magnetic properties of two-dimensional Co nanoparticles arranged in macroscopically phase-coherent superlattices created by self-assembly on Au(788). Our particles have a density of 26 Tera/in2 (1 Tera=10(12)), are monodomain, and have uniaxial out-of-plane anisotropy. The distribution of the magnetic anisotropy energies has a half width at half maximum of 17%, a factor of 2 more narrow than the best results reported for superlattices of three-dimensional nanoparticles. Our data show the absence of magnetic interactions between the particles. Co/Au(788) thus constitutes an ideal model system to explore the ultimate density limit of magnetic recording.
Elevated plasma levels of homocysteine are associated with an increased generation of reactive oxygen species in aortas of hyperhomocysteinemic animals and in endothelial cells. This may contribute to endothelial dysfunction observed in hyperhomocysteinemia, and promote atherosclerotic vascular disease. Homocysteine seems to promote the formation of reactive oxygen species primarily by a biochemical mechanism involving endothelial nitric oxide synthase, as increased endothelial lipid peroxidation and oxidation of the redox-sensitve dye 2',7'-dichlorofluoresceine could only be observed after incubation of endothelial cells with L-, but not with D-homocysteine, and could be prevented by inhibition of endothelial nitric oxide synthase. An increased oxidation rate of aminothiols in plasma, as observed in patients with hyperhomocysteinemia, further contributes to increased generation of reactive oxygen species. These effects are amplified by a homocysteine-specific inhibition of cellular antioxidant enzymes, like superoxide dismutase and the cellular isoform of gluthatione peroxidase. All mechanisms together result in increased levels of superoxide anion and peroxyl radicals in the vasculature that react with nitric oxide to form peroxnitrites. This abolishes nitric oxide's bioactivity and contributes to endothelial dysfunction. In addition, increased vascular oxidant stress in hyperhomocysteinemia has been shown to activate proinflammatory signaling pathways in endothelial cells, like the transcription factor NF-kappaB. This leads to increased endothelial expression of chemokines and adhesion molecules that promote the recruitment, adhesion and transmigration of circulating leukocytes to the vessel wall. All these mechamisms may contribute to the increased risk for cardiovascular diseases associated with hyperhomocysteinemia.
DNA-based vaccination has emerged as a promising method of immunisation since the first demonstration of this technology. Improving the antibody responses is desirable for the protective efficacy and hence broad application of these vaccines. We examined the immunogenicity of a Plasmodium-based DNA vaccine that was targeted to antigen presenting cells by fusion to CTLA4. Fusion proteins comprising the extra-cellular domain of CTLA4, the hinge, CH2 and CH3 domains of human IgG1 and MSP-1 gene fragments were expressed in COS-7 cells. Three of the secreted proteins containing the mouse homologue of CTLA4 were shown to bind differently to the human B7-1 molecule expressed on THP-1 cells. Competition binding assays for two fusion proteins showed that binding was specific. When C57BL/6 mice were immunized with plasmids encoding the fusion proteins, antibodies against two denatured and one non-denatured MSP-1 gene fragments were successfully induced. The usefulness of this strategy in future studies of immunisaton against human malaria is discussed.
OBJECTIVE: To test the hypothesis that attention to painful cutaneous laser stimuli enhances event-related desynchronization (ERD) in cortical regions receiving nociceptive input. METHODS: We used wavelet time-frequency analysis and bandpass filtering to measure ERD quantitatively in subdural electrocorticographic recordings while subjects either attended to, or were distracted from, a painful cutaneous laser stimulus. RESULTS: ERD were observed over primary somatosensory and parasylvian (PS) cortices in all 4 subjects, and over medial frontal cortex in 1 subject. Laser-evoked potentials were also observed in all 3 regions. In all subjects, ERD was more widespread and intense, particularly over PS, during attention to laser stimuli (counting stimuli) than during distraction from the stimuli (reading for comprehension). CONCLUSIONS: These findings suggest that pain-associated ERD is modulated by attention, particularly over PS. SIGNIFICANCE: This study suggests that thalamocortical circuits are involved in attentional modulation of pain because of the proposed role of these circuits in the mechanisms of ERD.
Intensity encoding of painful stimuli in many brain regions has been suggested by imaging studies which cannot measure electrical activity of the brain directly. We have now examined the effect of laser stimulus intensity (three energy levels) on laser evoked potentials (LEPs) recorded directly from the human primary somatosensory (SI), parasylvian, and medial frontal cortical surfaces through subdural electrodes implanted for surgical treatment of medically intractable epilepsy. LEP N2* (early exogenous/stimulus-related potential) and LEP P2** (later endogenous potential) amplitudes were significantly related to the laser energy levels in all regions, although differences between regions were not significant. Both LEP peaks were also significantly correlated with the pain intensity evoked by the laser stimulus, excepting N2* over the parasylvian region. Peak latencies of both LEP peaks were independent of laser energy levels. N2* and P2** amplitudes of the maxima in all regions showed significant positive linear correlations with laser energy, excepting N2* over the parasylvian region. The lack of correlation of parasylvian cortical N2* with laser energy and pain intensity may be due to the unique anatomy of this region, or the small sample, rather than the lack of activation by the laser. Differences in thresholds of the energy correlation with amplitudes were not significant between regions. These results suggest that both exogenous in endogenous potentials evoked by painful stimuli, and recorded over SI, parasylvian, and medial frontal cortex of awake humans, encode the intensity of painful stimuli and correlate with the pain evoked by painful stimuli.
Elevated plasma levels of homocysteine (hyperhomocysteinemia) are increasingly recognized as a potential risk for atherothrombotic vascular diseases by numerous epidemiological and clinical studies. There are increasing experimental data that indicate mechanisms by which homocysteine may alter the vasculature in a way that predisposes to atherosclerotic vascular disease. A key event in the vascular pathobiology of hyperhomocysteinemia seems to involve the induction of endothelial dysfunction due to a reduction of the endogenous antiatherothrombotic molecular nitric oxide. Elevated homocysteine levels can be efficiently and safely reduced in most of hyperhomocysteinemic patients by supplementation of folic acid and cobalamin. This reduction is associated with an improvement in endothelial function and other surrogate markers of atherothrombosis, like carotid plaque area and the rate of abnormal stress electrocardiograms. Whether or not this translates into clinical benefits, is still under investigation. The first clinical study on homocysteine-lowering vitamin supplementation in patients that had undergone coronary intervention showed a benefitial effect on the rate on restenosis and the need for revascularization which translated into a reduction of major coronary events. In contrast, in three larger scaled secondary intervention trials in patients with stable coronary disease or post non-disabling stroke, vitamin supplementation had no effect on future vascular events although baseline homocysteine levels were significantly associated with a worse prognosis. Until the results of more clinical trials are available, the clinical relevant question whether or not homocysteine is just a risk predictor or a modifiable risk factor can not definitely be answered.
Negative and positive laser evoked potential (LEP) peaks (N2*, P2**) were simultaneously recorded from the primary somatosensory (SI), parasylvian, and medial frontal (MF: anterior cingulate and supplementary motor area) cortical surfaces through subdural electrodes implanted for the surgical treatment of intractable epilepsy. Distribution of the LEP N2* and P2** peaks was estimated to be in cortical areas (SI, parasylvian, and MF) identified by anatomic criteria, by their response to innocuous vibratory stimulation of a finger (v-SEP), and to electrical stimulation of the median nerve (e-SEP). The maximum of the LEP N2* peak was located on the CS, medial (dorsal) to the finger motor area, as determined by cortical stimulation, and to the finger somatosensory area, as determined from the e-SEP and v-SEP. This finding suggests that the generator source of the LEP N2* peak in SI was different from that of e-SEP or v-SEP in Brodmann's areas 3b or 1. In parasylvian and MF, polarity reversal was often observed, indicating tangential current sources in these regions. In contrast to e-SEP and v-SEP, the LEP N2* latency over SI was not shorter than that over the parasylvian region. The amplitude of N2* was larger over SI than over MF and the latencies of the LEP peaks in those 2 regions were different. These findings provide evidence for a significant LEP generator in the postcentral gyrus, perhaps SI cortex, that is situated outside the tactile homunculus in SI and that receives its input arising from nociceptors simultaneously with parasylvian and MF cortex.
The original magnetic properties of nanometre-sized particles are due to the distinct contributions of volume, surface and step atoms. To disentangle these contributions is an ongoing challenge of materials science. Here we introduce a method enabling the identification of the remarkably different contributions of surface and perimeter atoms to the magnetic anisotropy energy of two-dimensional nanostructures. Our method uses the generally nonlinear relationship between perimeter length and surface area. Atomic-scale characterization of the morphology of ensembles of polydisperse nanostructures, combined with in situ measurements of their temperature-dependent magnetic susceptibility, gives access to the role played by the differently coordinated atoms. We show for Co nanostructures on a Pt(111) surface that their uniaxial out-of-plane magnetization is entirely caused by edge atoms having 20 times more anisotropy energy than their bulk and surface counterparts. Identification of the role of perimeter and surface atoms opens up unprecedented opportunities for materials engineering. As an example, we separately tune magnetic hardness and moment in bimetallic core-shell nanostructures.
A multicentre evaluation of the Brugia Rapid dipstick test was performed using 1263 serum samples in four international laboratories, i.e. T.D. Medical College (TDMC, India), National Institutes of Health (NIH, USA), Swiss Tropical Institute (STI, Switzerland) and Leiden University Medical Centre (LUMC, Netherlands). In comparison with microscopy, the dipstick demonstrated sensitivities of 97.2% (70 of 72) at TDMC, 91.6% (175 of 191) at LUMC and 100% (six of six) at STI. Sera of chronic patients showed a positivity rate of 11.3% (19 of 168) and 61.2% (71of 116) at TDMC and LUMC, respectively. All 266 sera of non-endemic normals from STI, NIH and LUMC tested negative with the dipstick. At LUMC, sera of 'endemic normals' (amicrofilaraemics with no clinical disease) from an area with approximately 35% microfilaria positivity showed 60.8% positive results (31 of 51), thus demonstrating the likelihood of many cryptic infections occurring in this population. Specificities of the test with Onchocerca volvulus sera were 98.8% (80 of 81) and 100% (10 of 10) at the NIH and STI, respectively; while specificity with Loa loa sera at the NIH was 84.6% (44 of 52). At the STI, the dipstick test also demonstrated 100% specificity when tested with 75 sera from various protozoan and helminthic infections.
An aerobic and heterotrophic isolate, designated IFAM EL-30T, was obtained from hypersaline Ekho Lake (Vestfold Hills, East Antarctica). The isolate consisted of Gram-positive cocci or short rods which occasionally exhibited branching. The organism was moderately halotolerant, required thiamin.HCI and was stimulated by biotin and nicotinic acid. It grew well with glucose, acetate, pyruvate, succinate, malate or glutamate, and hydrolysed DNA but not gelatin, starch or Tween 80. Nitrate was aerobically reduced to nitrite. Chemical analysis revealed diphosphatidylglycerol, phosphatidylglycerol, phosphatidylcholine and an unidentified glycolipid as the major polar lipids. The cellular fatty acids were predominantly of the anteiso and iso methyl-branched types, and the major menaquinone6 were MK-7 and MK-8. The peptidoglycan type was A4alpha, L-Lys-L-Glu. The DNA base ratio was 66.1 mol% G+C. Comparisons of 16S rRNA gene sequences showed that the unidentified organism was phylogenetically closely related to Nesterenkonia halobia, although a sequence divergence value of > 3% demonstrated that the organism represents a different species. On the basis of phenotypic and genotypic evidence, it is proposed that the unknown bacterium be designated as a new species of the genus Nesterenkonia, namely Nesterenkonia lacusekhoensis sp. nov., the type strain being IFAM EL-30T (= DSM 12544T = CIP 107030T). An emended description of the genus Nesterenkonia is given.
Homocyst(e)ine (Hcy) inhibits the expression of the antioxidant enzyme cellular glutathione peroxidase (GPx-1) in vitro and in vivo, which can lead to an increase in reactive oxygen species that inactivate NO and promote endothelial dysfunction. In this study, we tested the hypothesis that overexpression of GPx-1 can restore the normal endothelial phenotype in hyperhomocyst(e)inemic states. Heterozygous cystathionine beta-synthase-deficient (CBS((-/+))) mice and their wild-type littermates (CBS((+/+))) were crossbred with mice that overexpress GPx-1 [GPx-1((tg+)) mice]. GPx-1 activity was 28% lower in CBS((-/+))/GPx-1((tg-)) compared with CBS((+/+))/GPx-1((tg-)) mice (P < 0.05), and CBS((-/+)) and CBS((+/+)) mice overexpressing GPx-1 had 1.5-fold higher GPx-1 activity compared with GPx-1 nontransgenic mice (P < 0.05). Mesenteric arterioles of CBS((-/+))/GPx-1((tg-)) mice showed vasoconstriction to superfusion with beta-methacholine and bradykinin (P < 0.001 vs. all other groups), whereas nonhyperhomocyst(e)inemic mice [CBS((+/+))/GPx-1((tg-)) and CBS((+/+))/GPx-1((tg+)) mice] demonstrated dose-dependent vasodilation in response to both agonists. Overexpression of GPx-1 in hyperhomocyst(e)inemic mice restored the normal endothelium-dependent vasodilator response. Bovine aortic endothelial cells (BAEC) were transiently transfected with GPx-1 and incubated with dl-homocysteine (HcyH) or l-cysteine. HcyH incubation decreased GPx-1 activity in sham-transfected BAEC (P < 0.005) but not in GPx-1-transfected cells. Nitric oxide release from BAEC was significantly decreased by HcyH but not cysteine, and GPx-1 overexpression attenuated this decrease. These findings demonstrate that overexpression of GPx-1 can compensate for the adverse effects of Hcy on endothelial function and suggest that the adverse vascular effects of Hcy are at least partly mediated by oxidative inactivation of NO.
Two strains of a previously undescribed Arcanobacterium-like bacterium were isolated from a dead harbour porpoise and a dead sallow deer. Biochemical testing and PAGE analysis of whole-cell proteins indicated that the strains were phenotypically closely related to each other and distinct from previously described Actinomyces and Arcanobacterium species. Comparative 16S rRNA gene sequencing studies showed the bacterium to be a hitherto unknown subline within the genus Arcanobacterium. Based on phylogenetic and phenotypic evidence, it is proposed that the unknown bacterium be classified as Arcanobacterium pluranimalium sp. nov. The type strain of Arcanobacterium pluranimalium is CCUG 42575T (= CIP 106442T).
A Gram-positive bacterium originating from garden soil was taxonomically studied. Cells are non-motile, non-sporulating, irregular rods and cocci. The cell wall peptidoglycan contains L-ornithine as diagnostic diamino acid and an interpeptide bridge consisting of L-Orn<--L-Ala<--Gly<--D-Asp. The major menaquinone is MK-8(H4). 13-Methyl tetradecanoic acid and 14-methyl pentadecanoic acid are the predominant fatty acids. The polar lipids are phosphatidylinositol, phosphatidylglycerol, diphosphatidylglycerol, three unknown glycolipids and three unknown phospholipids. Mycolic acids are absent. The DNA G+C composition is 70 mol%. The acyl type of the glycan chain of peptidoglycan is acetyl. Glucose is the dominating whole cell sugar; arabinose, rhamnose and xylose are present in traces. Results of 16S rDNA sequence comparisons revealed that strain HKI 0124T represents a novel lineage within the suborder Micrococcineae of the order Actinomycetales adjacent to the recently described genus Ornithinicoccus. On the basis of the clearly pronounced morphological, physiological, chemotaxonomic and phylogenetic differences between strain HKI 0124T and all members of the suborder Micrococcineae, it is proposed to assign strain HKI 0124T to a new genus and species, Ornithinimicrobium humiphilum gen. nov., sp. nov. The type and only strain is HKI 0124T (= DSM 12362T = CIP 106634T).
A spore-forming, halophilic bacterium was isolated from surface sediment located on the beach of Palaeochori Bay near to a shallow water hydrothermal vent area, Milos, Greece. The bacterium, designated SH 714T, consisted of motile, strictly aerobic rods which contained an Orn-D-Glu type murein and a G+C content of 35 mol%. Thin sections showed a cell wall typical for Gram-positive bacteria; the peptidoglycan layer, however, was very thin. The Gram-reaction of the organism was negative. Comparative 16S rRNA gene sequencing demonstrated that the isolate represents a new line of descent within the spore-forming rods branching at the periphery of the rRNA group 1 Bacillus (Bacillus sensu stricto). The nearest phylogenetic neighbours of the unknown bacterium were Bacillus haloalkaliphilus, Marinococcus albus and Halobacillus species. Based on phylogenetic and phenotypic evidence it is proposed that the unknown bacterium be classified as Filobacillus milensis gen. nov., sp. nov. The type strain is SH 714T (= DSM 13259T = ATCC 700960T).
Phylogenetic analysis of 16S rDNA provides evidence that Cellulomonas cellulans branches outside the phylogenetic confines of the genus Cellulomonas. The distinct phylogenetic and chemotaxonomic status of Cellulomonas cellulans as a phylogenetic neighbour of the genus Promicromonospora, justifies the description of a new genus for which the name Cellulosimicrobium gen. nov. with the type species Cellulosimicrobium cellulans comb. nov. is proposed.