[Supplemental views to the original contributions: Schreiner, W.: Data assessment by analog/digital conversion on personal computers. I, II and III].
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Biomedical subjects
Publications and source records attributed to K Weiss.
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Percutaneous transluminal angioplasty (PTA) takes its stable position in the therapy of obliterating arterial diseases. Its indication areas considerably extend. The authors present a survey of their experience and the results of PTA of arteries supplying the brain and upper extremities. This surgery was made in 29 patients on 31 arteries. The authors consider PTA on a. subclavia as a method of choice. In the angioplasty on a. vertebralis there is a very low risk in correctly indicated cases. An atherosclerotic stricture of a. carotis interna is not considered suitable for PTA for the risk of embolism from the exulcerated plaques. However, the method may be used with advantage in the stenosis based on fibromuscular dysplasia and in some cases of early restenoses in a. carotis interna after previous endarterectomy. The authors arrive at the conclusion that PTA, if correctly indicated, is a safe method even in arteries supplying the brain and upper extremities. No complication was observed in the reported group.
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Prostacyclin (PGI2) mediates like TSH its cellular effects through the interaction with specific binding sites associated with the adenylate cyclase-cAMP-system. Binding of PGI2 and the generation of cAMP induced by PGI2 was evaluated in thyroid tissue obtained intraoperatively from euthyroid and hyperthyroid patients with diffuse normofollicular colloid struma. Transformation of the binding data according to Scatchard revealed heterogeneity of the PGI2 binding sites in the tissue of euthyroid patients: the high-affinity binding sites were calculated to be 0.68 +/- 0.18 pmol/mg protein (Ka = 16.2 +/- 9.1 nM) and the low-affinity binding sites to be 5.4 +/- 1.6 pmol/mg protein (Ka = 151 +/- 43.1 nM). In contrast, in the hyperthyroid patients the low-affinity binding sites were not demonstrable and the high-affinity sites were significantly (p less than 0.001) reduced (0.17 +/- 0.05 pmol/mg protein, Ka = 83.5 +/- 19.6 nM). The competition of the agonist for the PGI2 sites in hyperthyroid patients was significantly (p less than 0.005) diminished (IC-50-values: 0.98 +/- 3.1 vs 46.9 +/- 12.1 microM). PGI2 stimulated cAMP-production in a dose-dependent manner. However, the basal value was significantly lower also in the hyperthyroid patients (p less than 0.001). The evidence of reduced PGI2 sites as well as reduced PGI2-induced cAMP production in the thyroid gland of patients with Graves' disease may indicate an important role for PGI2 to play in the modulation of thyroid cell function.
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The aim of the study was to investigate the influence of calcium blockers on the prostaglandin system of blood platelets and the vessel wall with respect to a possible beneficial effect on atherosclerosis. The influence of diltiazem, isradipine, nifedipine and verapamil was examined on ADP- and collagen-induced in vitro platelet aggregation, platelet malondialdehyde formation and other platelet function tests. All the calcium blockers investigated inhibited platelet activation in a dose-dependent manner, isradipine being the most effective. Malondialdehyde formation (measured photometrically) and thromboxane (TX) B2 production were decreased too. Vascular tissue PG12 formation was investigated in rat aortic rings (6-oxo-PGF1 alpha-RIA). PG12 formation was enhanced by all the calcium blockers investigated (p less than 0.01), isradipine again having the most pronounced effect. Platelet adenylate cyclase was stimulated by diltiazem only (RIA, HPLC). Ex vivo ADP-, collagen- and epinephrine-induced platelet aggregation and serum TX were studied 90 minutes after ingestion to diltiazem (60 mg), nifedipine (20 mg) and verapamil (40 mg). ADP- and epinephrine-induced platelet aggregation (19-36%) and serum TX were reduced significantly (p less than 0.01), but collagen-induced aggregation was not significantly affected. These results suggest a possibly beneficial effect of calcium blockers on atherosclerosis via the prostaglandin system.
Radionuclide scintigraphy can give a specific diagnosis when a hypervascular "cold" defect on colloid scans "fills in" with gallium scanning. The majority of hepatocellular carcinomas will also accumulate hepatobiliary agents especially in delayed images. Magnetic resonance imaging is superior to other modalities in providing anatomic detail, such as location and relation to vessels, needed by the surgeon in operative planning.
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Leigh's disease, or subacute necrotizing encephalomyelopathy (SNE), in adults is rare, and its diagnosis has depended on the postmortem identification of characteristic lesions in a typical distribution. We observed an autopsy-proved case of SNE in which the diagnosis was established by the distribution and evolution of lesions documented by serial magnetic resonance imaging (MRI). A 21-year-old woman insidiously developed diplopia and gait disturbance, and subsequently deteriorated to a vegetative state over seven months. An initial MRI obtained one month after presentation showed increased signal intensity that surrounded the aqueduct of Sylvius and involved the tectum of the midbrain. Serial MRI scans showed these lesions to extend and symmetrically involve the tectum of the midbrain, caudate, putamen, globus pallidus, and substantia nigra, while sparing the mammillary bodies and red nuclei. Despite treatment with 2 g of thiamine administered intravenously daily, she continued to deteriorate and died. Results of an autopsy established the diagnosis of SNE and confirmed the MRI-identified distribution of lesions. To our knowledge, this case is the first report of MRI findings in an adult with autopsy-proved SNE, suggesting that MRI can be valuable in the early diagnosis of this disease.
Thirty-two patients with clinically definite multiple sclerosis were evaluated with neuropsychological procedures and magnetic resonance imaging (MRI). Neuropsychological evaluation included assessment of language, memory, cognition, visuospatial skills, and depression. Significant impairment in any three areas, compatible with diagnosis of a dementia syndrome, was observed in 28% of these patients, and lesser or no cognitive impairment characterized the remaining patients. Magnetic resonance imaging was used to evaluate the number and distribution of lesions as well as the presence of cerebral atrophy and atrophy of specific anatomic structures such as the corpus callosum. Results suggest that neither the number of lesions, the distribution of lesions, nor the extent of generalized cerebral atrophy was significantly greater in demented compared with non-demented patients. The primary finding was that atrophy of the corpus callosum was significantly more extensive on MRI scans in demented patients. Although the callosum itself may not be implicated directly in the pathogenesis of dementia, the presence of callosal atrophy on MRI scans should alert the physician to the possible occurrence of dementia in patients with multiple sclerosis.
Thirteen patients with clinically definite multiple sclerosis (MS) were studied with electroencephalogram (EEG), magnetic resonance imaging (MRI), evoked potentials and cerebrospinal fluid (CSF) analysis. We attempted to correlate the findings with physical disability as defined by Kurtzke score and presence of dementia or seizures. More severe plaque disease on MRI and increased physical disability correlated significantly with abnormality on brain-stem auditory evoked potentials (BAEPs) while visual evoked potential (VEP) abnormality correlated only with MRI findings. No such correlation was found with the EEG. The close relationship between BAEP and MRI abnormalities probably reflects frequent involvement of brain-stem corticospinal pathways.
The clinical and cell growth characteristics of 11 children with monosomy 7 presenting as preleukemia (eight cases) or acute nonlymphoblastic leukemia (three cases) were studied. Anemia was common to all patients, with nine showing leukocytosis, seven thrombocytopenia, and one thrombocytosis. There was a striking predominance of males (M/F ratio, 10:1) and a young median age (3 years). Preleukemia evolved to acute nonlymphoblastic leukemia in five patients and to myelofibrosis in one. In vitro studies of bone marrow progenitor cells cultured in leukocyte feeder-stimulated agar revealed abnormal cell proliferative patterns, most often an increased number of small clusters, for all 11 subjects. The cells of some preleukemic patients showed increased growth even in the absence of an exogenous source of colony-stimulating factor, suggesting autonomous growth or possibly autocrine stimulation. Combination chemotherapy or bone marrow transplantation failed to induce complete remission in the seven patients who were treated. Our findings in these 11 cases confirm the poor prognosis of monosomy 7 presenting as preleukemia in children. The in vitro studies suggest an association between altered cell growth in vitro and clinical evolution to frank leukemia.
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A high frequency of conversion from L1 to L2 morphology in ALL at relapse has been reported in studies made without benefit of the French-American-British (FAB) scoring system. We compared the lymphoblast morphology at presentation and first hematologic relapse for 50 consecutive children with acute lymphoblastic leukemia using the FAB scoring system to determine the frequency of morphologic conversion. Forty-eight patients presented with L1 morphology, 42 of whom (88%) relapsed with L1 blasts, four (8%) with L2 blasts, and two (4%) with blasts intermediate between L1 and L2. Two presented with L2 morphology, both relapsing with L2 blasts. These data do not support previous findings of a high frequency of conversion from L1 to L2 at relapse. They suggest, instead, that L2 morphology is not a common morphologic expression of initial treatment failure.
Time sequences of low-exposure images from the enzyme molecules of glutamine synthetase have been recorded digitally using an on-line recording system. Processing the images results in a time sequence of averaged molecule images, which, in the very beginning, exhibit the molecule structure still undamaged by electron irradiation. Different sources of the noise which obscures structural details, such as shot noise, stain embedding and radiation damage, are investigated.