Different windows on executive functions.
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Biomedical subjects
Publications and source records attributed to R Schubotz.
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Event-related potentials (ERPs) were recorded while subjects monitored a visually presented sequence of stimuli that provided information about both a temporal pattern (rhythm) and a spatial pattern, and responded to rhythmical or spatial deviants. A third task, which required the monitoring of the same sequence for screen flickers served as a perceptual baseline condition and controlled for response preparation effects. The monitoring of temporal and spatial sequential information elicited negative slow potentials (SPs) over distinct topographical areas. Thus, attention to the temporal and to the spatial domain of one and the same stimulus sequence are reflected by distinct ERP components, providing evidence for distinct cortical sources.
In order to study the neurophysiological correlates of working memory for different types of information, event-related brain potentials (ERPs) were recorded during a visual spatial and visual as well as auditory duration memory tasks. From stimulus onset to 500 ms ERPs were distinguishable by allocation to visual or auditory modality. From 500 to 2000 ms after stimulus onset, the spatial task generated a parieto-occipital focused negative slow wave, while corresponding ERPs of the temporal task showed a negative slow wave with frontolateral focus. From 1200 to 5500 ms a large positivity was found for the auditory temporal task and for good performers of the visual temporal task. The data suggest a distinction of three processing phases: modality-specific encoding, information-specific encoding and retention in conjunction with modality-specific inhibition processes.
A 70-year-old woman developed increasing dyspnoea and hoarseness without stridor. Bronchoscopy revealed the characteristic picture of a "rock-garden" with multiple whitish irregularly shaped nodules in the distal two third of the trachea, except the pars membranacea, involving the right-sided bronchial system to the origin of the lower-lobe bronchus, and the left main bronchus. The diagnosis of tracheobronchopathia osteochondroplastica was confirmed histologically: primary tracheobronchial amyloidosis was excluded. Tomography of the tracheobronchial tree demonstrated the findings, but a plain chest X-ray did not. The symptoms in this patient were not, however, caused by tracheobronchopathia osteochondroplastica but by concomitant pulmonary emphysema and acute laryngitis and were improved after symptomatic treatment of the laryngitis.
Roentgenograms and gallium-67 scans and gallium-67 counts of BAL fluid samples, together with differential cell counts, have proved to be useful in assessing activity and lung involvement in sarcoidosis. In active pulmonary sarcoidosis gallium-67 scans are usually positive. Quantitation of gallium-67 uptake in lung scans, however, may be difficult. Because gallium-67 uptake and cell counts in BAL fluid may be correlated, we set out to investigate gallium-67 activity in BAL fluid recovered from patient of different groups. Sixteen patients with recently diagnosed and untreated sarcoidosis, nine patients with healthy lungs, and five patients with CFA were studied. Gallium-67 uptake of the lung, gallium-67 activity in the lavage fluid, SACE and LACE levels, and alpha 1-AT activity were measured. Significantly more gallium-67 activity was found in BAL fluid from sarcoidosis patients than in that from CFA patients (alpha = .001) or patients with healthy lungs (alpha = .001). Gallium-67 activity in BAL fluid could be well correlated with the number of lymphocytes in BAL fluid, but poorly with the number of macrophages. Subjects with increased levels of SACE or serum alpha 1-AT showed higher lavage gallium-67 activity than did normals, but no correlation could be established. High gallium-67 activity in lavage fluid may be correlated with acute sarcoidosis or physiological deterioration; low activity denotes change for the better. The results show that gallium-67 counts in BAL fluid reflects the intensity of gallium-67 uptake and thus of activity of pulmonary sarcoidosis.
In short-term experiments, healthy fasting persons were given a basic dose of 0.5 g of ethanol/kg body weight, followed by hourly maintenance doses of 0.15 g of ethanol/kg body weight. After 10 h there was a significant increase of triglycerides in the VLDL, LDL, and HDL, the main rise (from 42 to 92 mg/dl) being found in the VLDL triglycerides. Other subjects, who received nourishment isocaloric with ethanol, likewise showed a significant rise of triglycerides in all lipoprotein fractions. Chylomicron triglycerides increased from 9.3 to 35.5 mg/dl. There was no significant change in postheparin HTGL, but postheparin LPL activity decreased after 10 h from 17.9 to 12.2 mmol FFA/ml/h in the fasting subjects, and from 28.5 to 10.2 mmol/FFA/ml/h in the persons receiving food. In long-term experiments after 4 weeks of 70 - 80 g of ethanol and isocaloric food daily, triglycerides increased, especially in the VLDL (from 50 to 82 mg/dl). The increase in the HDL, however, was also significant. After 4 weeks of ethanol, the chylomicron triglycerides in the plasma of the fasting subjects reached a value of 29.3 mg/100 ml, LDL cholesterol decreased, and HDL cholesterol increased. After 4 weeks of ethanol there was an increase in the lipoprotein lipase of the adipose tissue.
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The long term effect of 400 mg cimetidine ingested at various times on ulcer recurrence and drug compliance was investigated in 66 patients with severe course of duodenal ulcer, now healed. Patients were randomised in 3 treatment groups: group A (n = 29) received 400 mg cimetidine in the evening, group B (n = 23) 200 mg both morning and evening, group C (n = 14) no treatment. Follow up examinations were at 3 month intervals. Ulcer recurrence was observed in 10 out of 14 patients in group C and in 12 out of 52 patients of groups A and B within the first 6 months. Due to the highly significant difference between the treated and untreated groups (P less than 0.001) the control group was discontinued. The recurrence rate after 12 months was identical in groups A and B (51 and 52%). Comparison of patients with and without recurrences showed no differences as regards length of history, maximal acid secretion, cimetidine compliance or endoscopic findings such as duodenitis, circular constriction of the bulbus or antral erosions. However, it was noticeable that smokers with 63% recurrent ulceration had a worse prognosis than the non-smokers with 37% (P = 0.06).
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The stabilization parameters of patients under routine care are differentiated. 20 hyperlipoproteinemic patients (types IIa, IIb and IV) who were difficult to stabilize were treated with 0.9 g etofibrate daily. In addition to the cholesterold and triglyceride levels, we followed up the laboratory control parameters in the serum, fasting blood sugar and differential blood count. During the treatment period the cholesterol levels fell to 18%, triglycerides to 50%. Tachyphylaxis was never seen. The good tolerance of etofibrate shows that the substance is suitable as a potent hypolipidemic agent for longterm treatment of hyperlipoproteinemia.
We investigated the changes in serum lipid concentrations of patients treated with Etofibrate as part of their routine management in the metabolic ambulatory care unit of the Medical Policlinic at the University of Marburg. In our study, 26 patients who had not responded well to prior treatment for Types IIa, IIb, III and IV hyperlipoproteinemia were given a daily dose of 900 mg Etofibrate for up to 48 months. As a result to this treatment, serum total cholesterol levels fell by up to 17,6% and triglyceride levels by up to 47,8%. We observed no tachyphylaxis toward Etofibrate. The results of standard laboratory parameters measured in parallel with drug treatment reflect a good tolerance for Etofibrate. This substance is highly suited as a potent lipid-lowering agent.
Efficacy and tolerance of 1-(theophyllin-7-yl)-ethyl-2-[2-(p-chlorophenoxy)-2-methylpropionate] (etofylline clofibrate, Duolip) was investigated in 54 out-patients, 18 of whom were of Fredrickson-Types IIa, IIb and IV, over a therapeutical period of 4 months, in comparison to initial and final placebo phases of 4 weeks each. In type IIa etofylline clofibrate shows a good effect on total cholesterol and on the cholesterol fractions, both with regard to the collective treated and to the low dosage of 750 mg/d etofylline clofibrate compared to the usual dosage of 1500 mg clofibrate. The activity of etofyllineclofibrate on type IIb is inconsistent. Decreases of total cholesterol, i.e., of VLDL cholesterol along with high decreases of triglycerides in VLDL and LDL are measurable, but not significant. In type IV total cholesterol is distinctly decreased, along with high decreases of VLDL cholesterol and particularly so of the relevant VLDL triglycerides. Subjective and objective tolerability of etofylline clofibrate was most favourable.
We report on 41 patients with primary hyperlipoproteinemia (type IIa, IIb and IV) treated with 450 to 600 mg of bezafibrate for 12 months. Placebo periods of 8 weeks surrounded the treatment period. In types IIa and IIb total cholesterol decreased by up to 18,7%, triglycerides to 34,6%. In type IV serum triglycerides decreased up to 48,2 and cholesterol by 12,2%. In a second investigation we differentiated the cholesterol- and triglyceride-values of 16 patients regularly controlled. We found a significant decrease during the treatment period. Bezafibrate is a potent lipid-lowering agent of the new generation.
In a double-blind, randomised, cross-over trial clofibrate and a combination of polyenyl phosphatidyl choline (PPC) plus clofibrate were tested in 67 patients with hyperlipoproteinemia. Each treatment lasted for 4 weeks and was separated by a 4 week placebo period. The daily doses were clofibrate 1.2 g and PPC 1.8 g + clofibrate 1.2 g. respectively. The results revealed that polypenyl phosphatidyl choline prevented the elevation of LDL-cholesterol induced by clofibrate treatment, and that the lipid-lowering potency of the combination did not differ significantly from that of clofibrate. Since elevation of LDL-cholesterol is considered to increase the risk of coronary heart disease, the combination appears to offer a therapeutic advantage. Despite the significance of this clinical observation, a final decision may only be obtained from a prospective, long term investigation in patients with coronary heart diseases and hyperlipoproteinemia.
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