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Biomedical subjects

J Weis

Publications and source records attributed to J Weis.

At least 73 records · Page 4Linked to original sources
PubMed1999

The influence of sound stimulation during hatching on the mortality of ducks.

In the work the influence of the artificial sound stimulation during incubation on the speed of the Pekin duck breed hatching as well as on their mortality during that period was observed. The set eggs were hatched in four hatcheries. The eggs of the first two hatcheries (control groups Ka and Kb) were not sound stimulated. In the other two groups the set eggs were, from the very first hour of hatching, stimulated by the "knocking" sound from an electronic sound generator (experimental groups "a" and "b"). For the stimulation, the acoustic signal with intensity of 25 dB and frequency 5.68 Hz was applied. The fastest hatching process was recorded in the groups with sound stimulation. The "a" experimental group was the fastest, the ducks were hatched after 640.75+/-10.15 hours, in the "b" experimental group the ducks were hatched after 656.50+/-1.70 hours of incubation. In both sound stimulated experimental groups (a, b) the increased embryonic mortality resulted in the decrease of the percentage of hatchability--to 68.09+/-1.77% and 76.44+/-2.68%, respectively. This is statistically evident (P<0.01) when compared with the respective control groups which reached the 88.81+/-1.86% and 89.35+/-0.81% hatchability.

Acoustic Stimulation↗
PubMed1998

GDNF expression is increased in denervated human skeletal muscle.

Glial cell line derived neurotrophic factor (GDNF) is a potent trophic factor for several subpopulations of neurons including motor neurons. Two different transcripts of the GDNF gene (GDNF633 and GDNF555) have been detected in various tissues, including skeletal muscle. Denervation leads to an upregulation of GDNF633 in rat skeletal muscle, indicating that GDNF is involved in the response of skeletal muscle to denervation and possibly in reinnervation. To determine the role of GDNF in human neuromuscular disease, we investigated the expression of both transcripts in normal and denervated muscle and in muscle biopsies from Duchenne muscular dystrophy patients. GDNF expression levels were analyzed by competitive RT-PCR in 38 muscle specimens. Levels of both transcripts were significantly elevated in denervated muscle compared to normal and dystrophic muscle. Morphometric analysis of muscle-fiber calibers and its correlation to GDNF expression revealed that higher levels of GDNF were expressed in rapidly-progressive neurogenic atrophy, including four amyotrophic lateral sclerosis (ALS) cases, compared to cases of chronic atrophy. In dystrophic muscle, transcript levels were not significantly altered compared to normal controls. These data indicate that denervation, but not dystrophy, enhances GDNF expression in human skeletal muscle. Thus, the increase of GDNF expression is part of the reaction of human skeletal muscle to denervation caused by motor nerve lesion. GDNF might act on regenerating nerve fibers during muscle fiber reinnervation.

Cells, Cultured↗
PubMed1998

Phrenic nerves and diaphragms in sudden infant death syndrome.

Disturbances of the respiratory system may be an important factor in the cascade of events leading to sudden infant death syndrome (SIDS). Even though the diaphragm is the major respiratory muscle in infants, little is known about alterations of this muscle and of the phrenic nerve in SIDS. In the present study, diaphragms and phrenic nerves of 24 SIDS infants and seven controls were analyzed. Morphometric analysis revealed only slightly larger cross sectional areas of phrenic nerve axons but no increase in myelin sheath thickness in SIDS cases. However, in one SIDS case, myelinated nerve fibre density was severely reduced. Using electron microscopy, several nerve fibres of SIDS infants showed focal accumulations of neurofilaments. Muscle fibre diameters in SIDS diaphragms were significantly larger compared to controls (P < 0.0001). However, in almost all SIDS and control cases, axons and myelin sheaths were artificially swollen, and acute segmental muscle fibre ruptures and contracture bands were found. These prominent nonspecific ultrastructural alterations should advise caution in the interpretation of morphometric data. Thus, in some cases exemplified by one case of the present series, decreased density of phrenic nerve myelinated axons might contribute to SIDS. Still, the present results indicate that development of phrenic nerves and diaphragms is not delayed in most SIDS infants.

Autopsy↗
PubMed1998

Distribution of B-50(GAP-43) mRNA and protein in the normal adult human spinal cord.

B-50(GAP-43) is a phosphoprotein mainly found in the nervous system which plays a major role in neurite growth during development and regeneration as well as in synaptic remodelling. In the mature intact central nervous system, intense B-50 immunoreactivity (B-50-IR) can still be detected in regions which maintain residual capacity for structural re-organization. B-50 expression has been studied extensively in laboratory animals; however, its distribution and regulation in the human spinal cord is largely unknown. As a first step to analyze lesion-induced structural alterations, we investigated the distribution of B-50 protein and mRNA in the normal adult human spinal cord and dorsal root ganglia. Intense B-50-IR was localized to the superficial laminae of the dorsal horn at all segmental levels, the intermediolateral nucleus at thoracic levels and Onuf's nucleus at sacral levels. Scattered neurons, particularly in the ventral horn of lumbar and sacral segmental levels (and occasionally also in Clarke's nucleus) displayed intense B-50-IR in close apposition to the perikaryal and proximal dendritic surfaces. Nonradioactive in situ hybridization indicated that B-50 mRNA could also be detected in neurons of the ventral horn and also in the intermediolateral nucleus. The distribution of B-50 mRNA and protein in the normal human spinal cord shows a marked similarity to that reported in experimental animals, including the selective labelling of Onuf's nucleus. However, the strong B-50-IR on the surface of some large anterior horn motor neurons has not been observed in other mammals. This finding might reflect a particular state of readiness for synaptic plasticity.

Aged↗
PubMed1998

Endovascular coil embolization of microsurgically produced experimental bifurcation aneurysms in rabbits.

BACKGROUND: Endovascular treatment of cerebral aneurysms is a relatively new method, since only a few animal models and data are available. The present experimental study was performed in order to establish an appropriate aneurysm animal model, to determine the rate of permanent occlusion, and to correlate radiologic and morphologic findings. METHODS: End-to-side anastomoses of both common carotid arteries were performed microsurgically in 53 chinchilla rabbits. Venous pouches were adapted into the newly created bifurcation, resulting in berry-shaped aneurysms comparable to those in humans with regard to size and hemodynamics. Platinum and tungsten coils were used for endovascular embolization. The embolized aneurysms were investigated radiologically and morphologically. RESULTS: Twenty-three carotid bifurcation aneurysms remained for testing endovascular therapeutic approaches. The morphologic examinations of 13 embolized aneurysms revealed in no instance a complete obliteration, even in the three cases that were considered completely embolized according to angiographic criteria. CONCLUSIONS: The present animal model is an optimal tool for endovascular research. Analysis of the results of coil obliteration revealed a considerable discrepancy between radiologic and pathologic findings. The radiologic degree of aneurysm occlusion was overestimated.

Animals↗
PubMed1998

Chemical shift artifact-free imaging: a new option in MRI?

A high-speed proton spectroscopic imaging method with high spatial resolution was used for obtaining water, fat, and chemical shift artifact-free images on a 1.5 T MR scanner. The technique is based on a fast radiofrequency (RF) spoiled gradient-echo sequence. The chemical shift information is encoded by incrementing the echo time in a series of image records. Suppression of water or fat signals is not used. The technique does not require a highly homogeneous magnetic field. Spectroscopic images of a human volunteer were compared with corresponding conventional images obtained using the short inversion time inversion recovery (STIR) and the selective partial inversion recovery (SPIR) methods. The results demonstrate that it is possible to produce images entirely free from chemical shift artifacts using only a few chemical shift encoding steps. The technique also produces pure water and fat images which are significantly better than those produced by using the conventional methods STIR and selective partial inversion recovery. The described method appears to be promising for routine clinical applications because it can be fully automated.

Adipose Tissue↗
PubMed1998

Magnetic resonance spectroscopic imaging for visualization and correction of distortions in MRI: high precision applications in neurosurgery.

We present a method for the quantification and correction of geometrical/intensity distortions of magnetic resonance images predominantly caused by bulk magnetic susceptibility shifts due to susceptibility heterogeneities of measured biologic tissues and shape of the object under investigation. The method includes precise and fast measurements of the static magnetic-field distribution inside the measured object and automated data processing. Magnetic-field deviations in the range (-2.4; 2.6) ppm were found in the human brain at B0 = 1.5 T. For routinely used imaging parameters, with a read gradient strength of about approximately 1 mT/m, the magnetic-field perturbations in the human brain can cause geometrical distortions up to +/-4 mm and intensity changes up to +/-50%. MR images corrected by the described method are suitable for planning high precision applications in neurosurgery.

Artifacts↗
PubMed1998

A case of primary progressive aphasia. A 14-year follow-up study with neuropathological findings.

Primary progressive aphasia has been clinically defined as a progressive language deficit leading to the dissolution of almost all language functions with relative preservation of other cognitive functions until late in the course of the disease. Two types of language impairment have been described for primary progressive aphasia, which differ with respect to the degree of fluency of spontaneous speech. Whereas some authors have emphasized non-fluency as a defining characteristic of primary progressive aphasia, others have proposed that phonemic rather than semantic paraphasias in naming, both in the fluent and the non-fluent subtype, should be used as a criterion to distinguish primary progressive aphasia from slowly progressive aphasia in other forms of degenerative brain disease. Patients with fluent speech and semantic dementia, as typically seen in Alzheimer's disease, produce semantic paraphasias and circumlocutions rather than phonemic errors in naming. This paper reports the long-term follow-up of a patient with fluent aphasic speech, whose language profile over a decade was similar to that of patients with semantic dementia. Neuropathological examination revealed no evidence of Alzheimer's disease. Pick's disease or Pick variant, but showed spongiform changes of cortical layers (II and III) in temporal and, less severely, in frontal gyri. The present case indicates that semantic dementia is not a reliable indicator of probable Alzheimer's disease and supports the notion that there are different subtypes of primary progressive aphasia which cannot be defined by fluency or by the presence of phonemic paraphasia. Progress in identifying the neuropathological correlates of these subtypes in cases with lobar atrophy and spongiform changes should be expected from hereditary variants of progressive disorder.

Aphasia, Primary Progressive↗
PubMed1998

Increased expression of CNTF receptor alpha in denervated human skeletal muscle.

The functional receptor for ciliary neurotrophic factor (CNTF) is comprised of a CNTF binding entity termed CNTF receptor alpha (CNTFRalpha), and 2 signaling molecules called LIF receptor beta and gp130. CNTFRalpha can be released from the cell surface; the soluble form can confer CNTF responsiveness to cells. CNTFRalpha has recently been localized to several nonneuronal cell types including rat skeletal muscle fibers. In this study we examined the expression pattern of CNTFRalpha in normal, denervated and dystrophic human muscle. In muscle biopsies from 12 normal subjects, 16 cases of neurogenic muscular atrophy, 4 cases of Duchenne muscular dystrophy, and 4 cases of limb girdle dystrophy, CNTFRalpha mRNA levels were determined by Northern blotting. Transcript levels were significantly increased in cases of neurogenic atrophy compared to normal controls and dystrophic muscle. By nonradioactive in situ hybridization, CNTFRalpha transcripts were detected in the sarcoplasm of both normal sized and atrophic muscle fibers. In addition, soluble CNTFRalpha was elevated 4.4-fold in the urine of ALS patients compared to normal adults. These results suggest that the expression of CNTFRalpha in human skeletal muscle fibers is regulated by innervation. This regulation appears to be selective, because CNTFRalpha mRNA was not increased in dystrophic human muscle. Increased CNTFRalpha could confer higher sensitivity to CNTF during neurodegeneration or nerve fiber regeneration.

Adult↗
PubMed1997

Enhanced apoptotic cell death of renal epithelial cells in mice lacking transcription factor AP-2beta.

Expression of AP-2 transcription factors has been detected previously in embryonic renal tissues. We show here that AP-2beta -/- mice complete embryonic development and die at postnatal days 1 and 2 because of polycystic kidney disease. Analyses of kidney development revealed that induction of epithelial conversion, mesenchyme condensation, and further glomerular and tubular differentiation occur normally in AP-2beta-deficient mice. At the end of embryonic development expression of bcl-X(L), bcl-w, and bcl-2 is down-regulated in parallel to massive apoptotic death of collecting duct and distal tubular epithelia. Addressing the molecular mechanism we show that transfection of AP-2 into cell lines in vitro strongly suppresses c-myc-induced apoptosis pointing to a function of AP-2 in programming cell survival during embryogenesis. The position of the human AP-2beta gene was identified at chromosome 6p12-p21.1, within a region that has been mapped for autosomal recessive polycystic kidney disease (ARPKD). Sequence analyses of ARPKD patients and linkage analyses using intragenic polymorphic markers indicate that the AP-2beta gene is located in close proximity to but distinct from the ARPKD gene.

Animals↗
PubMed1997

Cytogenetic analysis of gliomas by in situ hybridization of stereotactic biopsy material.

Chromosome analysis of brain tumours can provide important pathobiological data; however, cytogenetic tools are so far not routinely applied for diagnosis. In the present study 25 paraffin embedded stereotactic biopsies from 19 glioma patients were studied using in situ hybridization of chromosome #10 and #15 using biotinylated pericentromeric probes. Numerical changes of chromosome #10 are frequent alterations in glioblastoma. Quantification of chromosome #15 served as a control in order to exclude artificial monosomies or nonspecific changes. The number of chromosomes in at least 200 cells were counted for each specimen. 18 of 25 biopsies could be evaluated quantitatively. The small volume of probes was not a limiting factor for analysis. Quantification of "nonspecific" chromosome #15 revealed single spots in 22-41% of all cells in the 18 biopsies. Chromosome #10 showed single spots in a range between 34 and 44% of counted nuclei in 13/18 biopsies. In 5 out of 18 biopsies 51-60% monosomies were found: in this subgroup were 4 high grade gliomas. These cases were interpreted as monosomy of chromosome #10. The results demonstrate feasibility and quantitative evaluability of cytogenetic analysis in stereotactic biopsy material using in situ hybridization.

Adolescent↗
PubMed1997

1H-spectroscopic imaging with read gradient during acquisition in inhomogeneous fields: analysis, measurement strategy, and data processing.

The proton magnetic resonance spectroscopic imaging techniques that use read gradient during acquisition produce proton spectra with high spatial and moderately high spectroscopic resolution in a reasonable time for in vivo applications. These techniques suffer mainly from the spatial and spectral distortions caused by the convolution of spectral/spatial information (chemical-shift artifacts) and from the spectral shifts caused by static magnetic field inhomogeneities. The investigators analyze the chemical-shift artifacts in the presence of nonnegligible static magnetic field inhomogeneities and propose a postdetection processing scheme to correct for such effects. Spectral artifacts caused by chemical shifts, spectral line overlapping, streak broadening, and magnetic field inhomogeneities are discussed. The postdetection data processing scheme is demonstrated on measurements of a phantom as well as a human leg.

Artifacts↗
PubMed1997

29Si chemical shift tensors of silyl silicate cages.

Static and 29Si CP MAS spectra (spinning rates of 2000 and 500 Hz) of six silyl silicate cages are analyzed by deconvolution and simulation. The principal values of the various 29Si chemical shift tensors provide information about the point symmetry of the Si sites. The intensities of the signals correspond sufficiently well with the stoichiometries.

Isotopes↗
PubMed1997

Endovascular occlusion of experimental aneurysms with detachable coils: influence of packing density and perioperative anticoagulation.

OBJECTIVE: This study was designed to assess the intraluminal biological changes after endovascular coil occlusion of arterial aneurysms with detachable coils, to analyze the relationship between histological occlusion and mechanical packing density, and to evaluate the influence of perioperative anticoagulation on the occlusion rate. METHODS: In rabbits, 30 microsurgically produced arterial bifurcation aneurysms were occluded with coils (18 with platinum coils, electrically detached; 12 with tungsten coils, mechanically detached). Coils were placed until no further coils fit into the aneurysmal lumen and it was no longer filled with radiographic contrast material. The individual degree of occlusion was then determined by the "packing density" on the angiograms. Complete occlusion was considered only if no neck remnant was visible on the films. Anticoagulation during and 2 days after the treatment was performed in 11 cases. After an observation period ranging from 3 to 6 months, angiographic and histological analyses were performed to obtain control data. RESULTS: Complete occlusion was achieved in 9 cases, subtotal occlusion (i.e., > 95% occlusion, residual filling at the neck of the aneurysm) in 10 cases, and partial occlusion in 11 cases. Angiographically documented recanalization was detected in 14 aneurysms. In the remaining 16 aneurysms, the initially documented angiographic results were unchanged. A discrepancy between angiographic and pathological findings was frequently observed. Five of nine angiographically completely occluded aneurysms were recanalized. Endothelial-like tissue at the orifice of the aneurysm was able to be observed in only four of the nine initially completely occluded aneurysms. CONCLUSION: The results suggest that even dense packing does not always guarantee permanent occlusion, although there was a positive relationship between packing density and occlusion rate. Anticoagulation did not have any negative effect on the results.

Animals↗
PubMed1997

Ventricular dilatation in experimental intraventricular hemorrhage in pigs. Characterization of cerebrospinal fluid dynamics and the effects of fibrinolytic treatment.

BACKGROUND AND PURPOSE: Hemorrhagic ventricular dilatation (HVD) is a prominent feature of human intraventricular hemorrhage (IVH) and a strong indicator for poor outcome. We developed an IVH model to define the mechanisms responsible for HVD and to test the efficacy of intraventricular administration of tissue plasminogen activator (TPA) in the treatment of HVD. METHODS: Isolated IVH was produced in pigs by injecting 10 mL of blood simultaneously with thrombin into the right lateral ventricle. The treatment group received 1.5 mg of TPA after induction of IVH. Intraventricular blood volume and the volume of the lateral ventricles were assessed by CT after 90 minutes, 7 days, and 42 days. Intracranial pressure, the pressure-volume index, and the resistance to outflow of cerebrospinal fluid (R(out)) were measured 30 minutes and 7 days after IVH. RESULTS: After IVH, the volume of the lateral ventricles increased from 1.98 +/- 0.69 to 6.43 +/- 1.23 mL (P < .001). There was a linear relationship between ventricular and clot volume (P = .014). Initially, R(out) increased from 24.34 +/- 7.13 to 63.56 +/- 64.91 mm Hg/mL per minute (P < .001). After 7 days, restoration of normal cerebrospinal fluid circulation occurred, but the ventricles were still significantly enlarged (5.24 +/- 1.76 mL, P < .001) and filled with blood. Within 6 weeks, ventricular volume had returned to normal values, paralleled by complete clot resolution. Intraventricular administration of TPA significantly accelerated clot clearance and restoration of normal ventricle volume. CONCLUSIONS: These results suggest that intraventricular bleeding may cause impairment of cerebrospinal fluid circulation but that the mass effect of clots distending the ventricle walls is the most important mechanism responsible for HVD. This model closely imitates several prominent features of human IVH and may therefore be a useful tool for preclinical assessment of the efficacy and safety of treatment with TPA.

Animals↗