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J Meyer

Publications and source records attributed to J Meyer.

At least 145 records · Page 8Linked to original sources
PubMed2000

Characterization of the gene encoding the [Fe]-hydrogenase from Megasphaera elsdenii.

The gene encoding the [Fe]-hydrogenase from the anaerobic bacterium Megasphaera elsdenii has been cloned and sequenced. The gene is monocistronic, in keeping with the protein being a monomer. The translated protein sequence (484 residues, M(r)=53 kDa) comprises a small 2[4Fe-4S] ferredoxin-like domain and a large domain containing the catalytic site. Comparisons with other [Fe]-hydrogenase sequences, including two of which the crystal structures are known, show that the M. elsdenii protein is among the smallest of these enzymes and provide useful indications regarding the basic structural core common to all [Fe]-hydrogenases. It is, nevertheless, to be noted that the genome of Thermotoga maritima encodes a putative [Fe]-hydrogenase that would consist of only 301 residues.

Amino Acid Sequence↗
PubMed2000

Ten-year outcome after coronary angioplasty in patients with single-vessel coronary artery disease and comparison with the results of the Coronary Artery Surgery Study (CASS).

The 10-year results of randomized trials comparing percutaneous transluminal coronary angioplasty (PTCA) in patients with single-vessel coronary artery disease (CAD) with coronary artery bypass grafting (CABG) and medical treatment are not available yet. The aim of this evaluation was to compare our 10-year follow-up results after PTCA in patients with single-vessel CAD with the 10-year follow-up results after CABG and medical treatment in the Coronary Artery Surgery Study (CASS) trial. We evaluated the clinical outcome of 509 patients with single-vessel CAD 10 years after coronary angioplasty. The data were compared with the results of 214 patients with single-vessel CAD after CABG or medical treatment from the CASS trial. End points were defined as death and myocardial infarction. Statistical evaluation was performed by life-table analysis and 2-sided Fisher's exact test. The rate of survival was 86% 10 years after PTCA compared with 85% after CABG and 82% after medical treatment in patients from the CASS trial (p = NS). Survival free from myocardial infarction was 77% after coronary angioplasty, 70% after CABG, and 72% after medical treatment (p = NS). Thus, in patients with single-vessel CAD, infarct-free survival 10 years after coronary angioplasty compared favorably with the results after bypass surgery or medical treatment from the CASS trial.

Adrenergic beta-Antagonists↗
PubMed2000

NO reduces PMN adhesion to human vascular endothelial cells due to downregulation of ICAM-1 mRNA and surface expression.

Reperfusion damage is largely due to the adherence of polymorphonuclear leukocytes to the endothelium initiated by adhesion molecule upregulation. The reduced endothelial nitric oxide release during ischemia may be involved in the upregulation of intercellular adhesion molecule 1. In this study, we tested if nitric oxide donors suppress polymorphonuclear leukocyte adherence to activated endothelial cells by inhibition of the intercellular adhesion molecule 1 surface expression. Confluent human umbilical vein endothelial cells were stimulated with tumor necrosis factor alpha (300 U/mL) after preincubation with increasing concentrations of the nitric oxide donors CAS 1609 (0.005-5 mM/L) and 3-(4-morpholinyl)-sydnonimine (0.01-1 mM/L). Intercellular adhesion molecule 1 surface expression was measured in a cell surface enzyme-linked immunosorbent assay, intercellular adhesion molecule 1 mRNA by Northern analysis. Human saphenous vein endothelial cells were transfected with the inducible nitric oxide synthase gene and stimulated with tumor necrosis factor alpha (300 U/mL). Fluorescein green-labeled polymorphonuclear leukocytes adhering to activated human umbilical vein endothelial cells/human saphenous vein endothelial cells were quantified by epifluorescent microscopy. The intercellular adhesion molecule 1 surface expression of activated human umbilical vein endothelial cells/human saphenous vein endothelial cells was significantly diminished to 40 to 60% of the maximum after treatment with CAS 1609, 3-(4-morpholinyl)-sydnonimine, or transfection with the inducible nitric oxide synthase gene. Intercellular adhesion molecule 1 mRNA was diminished by CAS 1609 and 3-(4-morpholinyl)-sydnonimine in the same manner. The functional relevance of our data was shown by reduction of polymorphonuclear leukocyte adherence to activated human umbilical vein endothelial cells/human saphenous vein endothelial cells following treatment with CAS 1609 and 3-(4-morpholinyl)-sydnonimine or transfection with inducible nitric oxide synthase. Tumor necrosis factor-induced polymorphonuclear leukocyte adherence was abolished by blocking antibody against intercellular adhesion molecule 1. Thus, exogenous or endogenous substitution of nitric oxide diminishes the expression of endothelial intercellular adhesion molecule 1 and its mRNA following tumor necrosis factor alpha stimulation. This results in a reduced polymorphonuclear leukocyte adherence to activated endothelium.

Adult↗
PubMed2000

Thermodynamic modulation of light chain amyloid fibril formation.

To obtain further insight into the pathogenesis of amyloidosis and develop therapeutic strategies to inhibit fibril formation we investigated: 1) the relationship between intrinsic physical properties (thermodynamic stability and hydrogen-deuterium (H-D) exchange rates) and the propensity of human immunoglobulin light chains to form amyloid fibrils in vitro; and 2) the effects of extrinsically modulating these properties on fibril formation. An amyloid-associated protein readily formed amyloid fibrils in vitro and had a lower free energy of unfolding than a homologous nonpathological protein, which did not form fibrils in vitro. H-D exchange was much faster for the pathological protein, suggesting it had a greater fraction of partially folded molecules. The thermodynamic stabilizer sucrose completely inhibited fibril formation by the pathological protein and shifted the values for its physical parameters to those measured for the nonpathological protein in buffer alone. Conversely, urea sufficiently destabilized the nonpathological protein such that its measured physical properties were equivalent to those of the pathological protein in buffer, and it formed fibrils. Thus, fibril formation by light chains is predominantly controlled by thermodynamic stability; and a rational strategy to inhibit amyloidosis is to design high affinity ligands that specifically increase the stability of the native protein.

Amino Acid Sequence↗
PubMed2000

Increased carbon monoxide in exhaled air of critically ill patients.

Heme oxygenase produces carbon monoxide (CO) during breakdown of heme molecules primarily in liver and spleen. Recent data suggest that CO is also produced in the lungs. CO is excreted by exhalation via the lungs. A number of inflammatory agents induce the expression of heme oxygenase, possibly leading to increased CO production. To investigate whether critical illness results in increased CO production we measured the CO concentration in exhaled air in 30 critically ill patients and in healthy controls (n = 6). Critically ill patients showed a significantly higher CO concentration in exhaled air (median 2.4 ppm, 95% CI 1.0-7.0 ppm vs median 1.55 ppm, 95% CI 1.2-1.7 ppm, P = 0.01) as well as total CO production (median 20 ml/min, 95% CI 8 to 90 ml/min vs median 13.5 ml/min, 95% CI 11 to 19 ml/min, P = 0.026) compared to healthy controls. No correlation was found between CO concentration in exhaled air and carboxyhemoglobin concentration in arterial and central venous blood (P > 0.05). The increase of CO concentration in exhaled air in critical illness suggests an induction of inducible heme oxygenase (HO-1) and might reflect the severity of illness.

Adult↗
PubMed2000

Brain serotonin1A receptor binding measured by positron emission tomography with [11C]WAY-100635: effects of depression and antidepressant treatment.

BACKGROUND: Pharmacological and postmortem investigations suggest that patients with major depressive disorder have alterations in function or density of brain serotonin1A (5-HT1A) receptors. The aim of the present study was to use positron emission tomography with the selective 5-HT1A receptor antagonist [11C]WAY-100635 to measure 5-HT1A receptor binding in depressed patients before and during treatment with selective serotonin reuptake inhibitors. METHODS: Positron emission tomographic scans with [11C]WAY-100635 were performed on 25 patients with major depressive disorder. These included 15 unmedicated depressed patients. Ten of these unmedicated patients were scanned again during selective serotonin reuptake inhibitor treatment. A further 10 patients with major depressive disorder were scanned on one occasion only while taking selective serotonin reuptake inhibitors. Comparisons were made with [11C]WAY-100635 positron emission tomographic scans in 18 healthy volunteer subjects. Region of interest analysis and statistical parametric mapping were performed on binding potential images generated using a reference tissue model. RESULTS: Binding potential values were reduced across many of the regions examined, including frontal, temporal, and limbic cortex in both unmedicated and medicated depressed patients compared with healthy volunteers. Binding potential values in medicated patients were similar to those in unmedicated patients. CONCLUSIONS: Major depressive disorder is associated with a widespread reduction in 5-HT1A receptor binding. This reduced 5-HT1A receptor binding was not changed by selective serotonin reuptake inhibitor treatment.

Adult↗
PubMed2000

Sources on the anterior and posterior banks of the central sulcus identified from magnetic somatosensory evoked responses using multistart spatio-temporal localization.

A Multi-Start Spatio-Temporal (MSST) multidipole localization algorithm was used to study sources on the anterior and posterior banks of the central sulcus localized from early somatosensory magnetoencephalography (MEG) responses. Electrical stimulation was applied to the right and left median nerves of 8 normal subjects. Two sources, one on the anterior and one on the posterior bank of the central sulcus, were localized from 16 data sets (8 subjects, 2 hemispheres). Compared with the more traditional practice of single-dipole fits to peak latencies, MSST provided more reliable source locations. The temporal dynamics of the anterior and posterior central sulcus sources, obtained using MSST, showed considerable temporal overlap. In some cases, the two sources appeared synchronous. On the other hand, in the traditional single-dipole peak-latency fit approach, there is no time course other than a focal dipole moment activated only at the selected peak latency. The same group of subjects also performed a motor task involving index-finger lifting; the anterior central sulcus source obtained from electrical median nerve stimulation localized to the same or similar region in the primary motor area identified from the finger-lift task. The physiological significance of the anterior central sulcus source is discussed. The findings suggest that one can test the integrity of cortical tissue in the region of primary motor cortex using electrical somatosensory stimulation.

Adult↗
PubMed2000

Articulatory/phonetic sequencing at the level of the anterior perisylvian cortex: a functional magnetic resonance imaging (fMRI) study.

Damage to the anterior peri-intrasylvian cortex of the dominant hemisphere may give rise to a fairly consistent syndrome of articulatory deficits in the absence of relevant paresis of orofacial or laryngeal muscles (apraxia of speech, aphemia, or phonetic disintegration). The available clinical data are ambiguous with respect to the relevant lesion site, indicating either dysfunction of the premotor aspect of the lower precentral gyrus or the anterior insula in the depth of the Sylvian fissure. In order to further specify the functional anatomic substratum of this syndrome, functional magnetic resonance imaging (fMRI) was performed during reiteration of syllables differing in their demands on articulatory/phonetic sequencing (CV versus CCCV versus CVCVCV). Horizontal tongue movements and a polysyllabic lexical item served as control conditions. Repetition of the CV and CCCV monosyllables elicited a rather bilateral symmetric hemodynamic response at the level of the anterior and posterior bank of the central sulcus (primary sensorimotor cortex), whereas a more limited area of neural activity arose within this domain during production of lexical and nonlexical polysyllables, significantly or exclusively lateralized toward the left hemisphere. There is neurophysiological evidence that primary sensorimotor cortex mediates the "fractionation" of movements. Assuming that the polysyllables considered are organized as coarticulated higher-order units, the observed restricted and lateralized cortical activation pattern, most presumably, reflects a mode of "nonindividualized" motor control posing fewer demands on "movement fractionation." These findings may explain the clinical observation of disproportionately worse repetition of trisyllabic items as compared to monosyllables in apraxia of speech. The various test materials failed to elicit significant activation of the anterior insula. If at all, only horizontal tongue movements yielded a hemodynamic reaction extending beyond the sensorimotor cortex to premotor areas. Since limbic projections target the inferior dorsolateral frontal lobe, the enlarged region of activation during horizontal tongue movements might reflect increased attentional requirements of this task.

Adult↗
PubMed2000

Plastic foil technique attenuates inflammation in mesenteric intravital microscopy.

BACKGROUND: Interpretation of intravital microscopic observations is complicated by the "inflammatory"-type response to the trauma inflicted on the tissue by the surgical preparation. The present study evaluates different experimental conditions for prolonged observations of the mesenteric microcirculation in the rat. METHODS: The mesentery was exteriorized through a median laparotomy and subjected to an organ bath or a modified plastic foil technique. Hemodynamic, metabolic, respiratory, and microcirculatory data were analyzed. RESULTS: In contrast to the plastic foil technique, which yielded stable baseline values over a 5-h observation period, venular velocity and wall shear rates decreased significantly in the organ bath technique, and leukocyte adhesion to the endothelium was significantly increased. Likewise, abdominal blood flow decreased significantly by 35% and base excess declined (-10.0+/-0.4 mmol/L) in the organ bath, with reduced pco(2) (26.4+/-2.5 mm Hg vs. 33.7+/-1.1 mm Hg in plastic foil technique) due to respiratory pH compensation. CONCLUSIONS: The plastic foil technique was found clearly superior to the organ bath technique for maintenance of stable baseline metabolic, hemodynamic, and microcirculatory conditions in mesenteric intravital microscopy.

Animals↗
PubMed2000

[Flow quantification in coronary and bypass vessels with MR phase contrast technique].

PURPOSE: To evaluate accuracy of velocity encoded cine MR imaging for determination of blood flow in coronary arteries and coronary bypass grafts. MATERIALS AND METHODS: 12 patients with 22 coronary bypass grafts underwent intraoperative flow quantification using the transit time ultrasound method. These values were compared to postoperative MR phase shift measurements. Flow measurements were performed preoperatively in 28 coronary arteries of 20 patients. For flow measurement, we used a velocity-encoded k-space segmented gradient echo sequence with a temporal resolution of 110 or 125 ms, respectively. 6-8 pase shift images could be acquired during one cardiac cycle. RESULTS: There was a significant correlation between intraoperative and flow measurements using velocity-encoded MR imaging (r = 0.74, p < 0.0001, t-test). Flow volumes determined by MR imaging were systematically larger than those determined by the transit time ultrasound method. Mean flow in coronary arteries was reduced in severely stenosed vessels (> 70%) compared to normal vessels. Intra- and interobserver variability were 10.5 and 15% (coronary bypass grafts), and 12.3 and 15.8% (coronary arteries), respectively. CONCLUSIONS: Velocity-encoded MR imaging enables determination of flow in coronary artery bypass grafts and coronary arteries. Future developments should aim at the improvement of spatial and temporal resolution of the method.

Adult↗
PubMed2000

Potential of a new laser target system for percutaneous CT-guided nerve blocks: technical note.

A prototype of a laser target device was used for CT-guided nerve blocks in a preliminary series of nine interventions. The system provides guidance from any possible approach. High accuracy of needle insertion was achieved; the average deviation of the planned from the actual angle was 1.4 degrees. The target device is valuable for facilitating minimally invasive therapy and can decrease the time required for the procedure.

Adult↗
PubMed2000

[Noninvasive evaluation of coronary bypass grafts by magnetic resonance imaging. Comparison of the Haste and Fisp-3-D sequences with the conventional coronary angiography].

The aim of the study was to evaluate the patency of coronary artery bypass grafts (CABG) with the 2D and 3D magnetic resonance (MR) imaging techniques. 29 patients with 74 bypass grafts and a total of 91 distal anastomoses were studied on a 1.5 Tesla scanner using a phased array body coil. A 2D T-2 weighted breathhold turbo spin echo sequence (Haste) and a 3D breath hold contrast enhanced MR angiography sequence (Fisp-3-D) were performed. With the Haste and Fisp-3-D sequences 55 of the 58 patent and 15 of the 16 occluded grafts were recognized; the sensitivity and specificity were 95% and 94%, respectively. With the Haste sequence 74% (47/63) and with the Fisp-3-D sequence 64% (40/63) of the distal anastomoses were seen in good image quality. Only 3 of 8 significant grafts stenoses were detected. The patency of CABGs can be evaluated non-invasively with the Haste and the Fisp-3-D angiography sequences. Better results can be expected with the development of a blood-pool contrast medium and the combination of MR flow measurements with imaging techniques.

Aged↗
PubMed2000

[A case report: suppurative pericardial effusion].

We present the case of a 67 year old woman who was resuscitated due to cardiac tamponade. Examination of the pus fluid showed a bacterial infection with streptococcus milleri. Four days before resuscitation the patient experienced weakness, dyspnoea, increased temperature (39 degrees C), swelling of the neck, and pain on swallowing. Using computed tomography, examination revealed an infection extending from the right tonsil to the mediastinum and into the pericardium. After surgery to remove the retropharyngeal abscess, the patient healed well. Therefore, on presentation of a cardiac tamponade, possible hematogenous or lymphogenous causes or per continuitatem infections should always be considered. In this case the germs in the fluid and the typical patient history indicated an oropharyngeal reason.

Aged↗
PubMed2000

hKCNN3 which maps to chromosome 1q21 is not the causative gene in periodic catatonia, a familial subtype of schizophrenia.

The human calcium-activated potassium channel gene (hKCNN3, hSKCa3) contains two tandemly arranged, multiallelic CAG repeats located in exon 1 which result in short to moderate polyglutamine stretches of unknown functional significance. Case-control and family-based association studies suggested an association of hKCNN3 repeats with susceptibility for schizophrenia. Twelve multiplex pedigrees with periodic catatonia, a schizophrenia subtype with major gene effect and patterns of anticipation, were genotyped using the multiallelic hKCNN3 repeat polymorphism. Using a dominant model of inheritance with sex- and age-dependent penetrance classes, cumulative results showed exclusion of linkage of hKCNN3 to periodic catatonia under the assumption of genetic homogeneity with lod score of -48.01 at zero recombination fraction. Our results provide evidence that hKCNN3 is not the causative gene in the familial schizophrenia subtype of periodic catatonia. By fluorescent in situ hybridization we confirmed the assignment of hKCNN3 to chromosome 1q21 near the heterochromatin region. Linkage mapping showed segregation with marker D1S498 (theta = 0.05) and placed hKCNN3 in the genetic linkage map in a cluster of genes near the centromeric region of chromosome 1.

Adult↗