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Biomedical subjects

W Schreiber

Publications and source records attributed to W Schreiber.

At least 73 records · Page 4Linked to original sources
PubMed1995

gamma-Glutamylglutamine and taurine concentrations are decreased in the cerebrospinal fluid of drug-naive patients with schizophrenic disorders.

HPLC and gas chromatography-mass spectrometry analyses of 18 amino acids, N-acetylaspartate, N-acetylaspartylglutamate, and 5-hydroxyindoleacetic acid, derived from serotonin, and homovanillic acid, derived from dopamine, were performed in CSF collected from a group of patients with schizophrenia who either had been drug free for at least 1 year (n = 5) or were drug naive for psychotropic drugs (n = 21) and in 15 control subjects. Significant differences were found only for taurine (15% lower in the patients) and isoleucine (7% higher). A number of unidentified substances were detected, one of which proved to be markedly reduced (16%) among the schizophrenic patients. Liquid chromatography-mass spectrometry with continuous flow-fast atom bombardment interface allowed us to identify this substance as gamma-glutamylglutamine. The decreased level of gamma-glutamylglutamine may reflect a deficiency in the gamma-glutamyltransferase system, a system probably involved in glutamate uptake, or a deficiency in glutamine, an important precursor of releasable glutamate. Although glutamate was nonsignificantly reduced in the patients, it was one of the five substances (including gamma-glutamylglutamine) that were necessary for the best discrimination between the schizophrenic patients and the controls. These findings support the notion that the glutamatergic system is affected in schizophrenic disorders. In addition, they underscore the need to apply rigid bioanalytical techniques and use drug-naive patients to gain in-depth information on the pathophysiology of brain disorders such as schizophrenia.

Adult↗
PubMed1995

Solventogenic enzymes of Clostridium acetobutylicum: catalytic properties, genetic organization, and transcriptional regulation.

The enzymes acetoacetate decarboxylase and coenzyme A transferase catalyse acetone production from acetoacetyl-CoA in Clostridium acetobutylicum. The adc gene encoding the former enzyme is organized in a monocistronic operon, while the ctf genes form a common transcription unit with the gene (adhE) encoding a probable polyfunctional aldehyde/alcohol dehydrogenase. This genetic arrangement could reflect physiological requirements at the onset of solventogenesis. In addition to AdhE, two butanol dehydrogenase isozymes and a thiolase are involved in butanol synthesis. RNA analyses showed a sequential order of induction for the different butanol dehydrogenase genes, indicating an in vivo function of BdhI in low level butanol formation. The physiological roles of AdhE and BdhII most likely involve high level butanol formation, with AdhE being responsible for the onset of solventogenesis and BdhII ensuring continued butanol production. Addition of methyl viologen results in artificially induced butanol synthesis which seems to be mediated by a still unknown set of enzymes. Although the signal that triggers the shift to solventogenesis has not yet been elucidated, recent investigations suggest a possible function of DNA supercoiling as a transcriptional sensor of the respective environmental stimuli.

Base Sequence↗
PubMed1995

Altered hypothalamic-pituitary-adrenocortical regulation in healthy subjects at high familial risk for affective disorders.

Altered negative feedback control of the hypothalamic-pituitary-adrenocortical (HPA) system is a frequent laboratory sign of major depression. It coincides with depressive episodes and partially reverses after recovery from psychopathology. Such an HPA disturbance in feedback control can be acquired as a result of stressful life experiences and be compounded by age or it can be genetically predetermined at all levels involved in fine-tuned neuroendocrine regulation. Major psychiatric disorders run in families and a high familial load for an affective illness therefore increases an individual's risk of becoming affected. We investigated whether the HPA feedback disturbance observed among patients with depression is present in otherwise healthy individuals who are at high risk for psychiatric disorders because they have a first-degree relative with an affective illness. Using rigid psychodiagnostic techniques, we screened 431 consecutively admitted patients with depression and identified 35 families with one or more high-risk probands (HRPs). The results of a combined dexamethasone/human corticotropin-releasing hormone (DEX-CRH) test showed that the group of dexamethasone-pretreated (1.5 mg; 23.00 h) HRPs released more cortisol after stimulation with human CRH (100 micrograms; 15.00 h the next day) than a control group (CPs), but less than a group of patients with an acute major depressive episode (DPs). The peak cortisol values were 146.1 +/- 147.7 nmol/l (mean +/- SD) (HRPs), 75.3 +/- 47.9 nmol/l (CPs) and 278.2 +/- 199.2 nmol/l (DPs), yielding significant (F = 9.66, p < 0.001) group differences, with values for HRPs vs. CPs and HRPs vs. DPs being significant at the 1% level (t test).(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1994

[Neuropsychiatric symptoms in primary hyperparathyroidism].

Over a period of 3 months a 51-year-old woman developed a depressive syndrome with loss of memory, inability to find words, impaired fine movements and phases of spacial disorientation. Biochemical tests demonstrated occasional slight rises in serum calcium (2.8-2.9 mmol/l) and parathormone (4.6-5.2 pmol/l). She had a grade II nodular goitre with normal thyroid function. Ultrasonography of the thyroid suggested a right cranial parathyroid adenoma, confirmed at a right thyroidectomy with resection of the right upper parathyroid, while the other parathyroid glands were grossly normal. Calcium and parathormone levels returned to normal after the operation, as did the neuropsychiatric symptoms (within two months). This typical case illustrates that even in seemingly isolated neuropsychiatric changes an organic disease, like primary hyperparathyroidism, needs to be thought of.

Adenoma↗
PubMed1994

Adenosine for the management of patients with tachycardias--a new protocol.

We developed a new protocol for diagnosis and treatment of patients with sustained tachycardias (heart rate > 150 beats.min-1). The patients first underwent vagal manoeuvres; if those remained unsuccessful, i.v. adenosine in increasing doses of 6, 12, and 18 mg was administered until sinus rhythm (SR) or transient atrioventricular (AV) block, unmasking the underlying rhythm, was recorded. In the latter and in the non-responding cases other antiarrhythmics were applied. Ninety-three episodes of tachycardia in 46 patients were treated according to this protocol. Six episodes (6%) were terminated by carotid massage, 64 of the remaining 87 episodes (74%) responded to adenosine with return to SR. Conversion to SR occurred more often in episodes with narrow- than in wide-complex tachycardia (81 vs. 59%, P < 0.05). To achieve SR, the mean adenosine dose was lower in narrow- than in wide-complex tachycardia (13 +/- 8 vs 21 +/- 10 mg; P < 0.01). The duration of asystole after adenosine did not differ between these two groups, whereas the duration of arrhythmia after adenosine differed significantly (8.5 +/- 5.8 vs 18.6 +/- 22.9 s; P < 0.05). Side effects of adenosine such as flush, dyspnoea, and chest pain did not seem to be dose dependent and occurred in about 20%. According to our protocol, in more than 75% SR was achieved in patients with sustained tachycardias after vagal manoeuvres and adenosine.

Adenosine↗
PubMed1994

Endotoxin enhances EEG alpha and beta power in human sleep.

Endotoxin, a lipopolysaccharide (0.4 or 0.8 ng/kg body weight), was injected at 1900 hours in 17 healthy men in a single-blind, placebo-controlled experiment. The administration was followed by a 4-hour period of quiet wakefulness in bed (light intensity < 200 lux). Unlimited sleep was allowed after 2300 hours (lights off) until the next morning. The electroencephalogram (EEG), electromyogram, electrooculogram, electrocardiogram and rectal temperature were recorded throughout the experimental session. Standard sleep stages were assessed, and the EEG was submitted to a state-specific, serial spectral analysis. Endotoxin administration induced a rise of body temperature and heart rate, which started approximately 2 hours after the injection and persisted through most of the sleep period. Sleep latency remained unchanged, whereas rapid eye movement (REM) sleep latency increased from 60.3 to 89.0 minutes (paired t test; p = 0.06) compared to control values. Stage 2 sleep was elevated from 45.5 to 49.0% of time in bed (p < 0.05), and total nonrapid eye movement (NREM) sleep from 64.2 to 69.1% (p < 0.05). No significant change could be observed in slow-wave sleep (SWS, stages 3 and 4). During the first 4 hours of the sleep period, NREM sleep EEG spectral power was distinctly and markedly increased between 8 and 12 Hz (alpha) and 15 and 20 Hz (beta) (p < 0.05), whereas at the same time EEG power between 1 and 8 Hz (delta, theta) was not significantly changed. We conclude that in humans the primary host response induced by endotoxin initially suppresses REM sleep and increases stage 2 NREM sleep, but does not affect SWS. No clear modification of sleep EEG delta activity could be observed after endotoxin injection, despite marked endocrinological and physiological changes such as the elevation of body temperature. Numerous factors related to the human primary host response may be responsible for the EEG intensification of the alpha and beta range.

Adult↗
PubMed1994

[Thrombolysis of acute myocardial infarct: modifying factors of "door-to-needle time"].

Effect of thrombolytic treatment in acute myocardial infarction depends on several factors, most importantly on time to treatment. The door-to-needle time, the interval between admission and thrombolytic therapy initiation, may be one important factor. In a retrospective study, we analysed 151 patients who were admitted to our emergency department with acute myocardial infarction and who received thrombolytic treatment. We analysed door-to-needle time with respect to the factors age, gender, clinical symptoms, presence of prehospital ECG, presence of prehospital complications, day of admission, hour of admission, duration of pain and infarct site. We observed that the door-to-needle time is significantly shorter in those cases with a prehospital ECG (p < 0.001) or no prehospital complications (p < 0.001) as well as inferior infarction (p < 0.02). There was a trend towards a shorter interval in cases with typical chest pain plus autonomic symptoms (p = 0.05). No statistical significance was seen in respect to age, gender, day and hour of admission, and duration of pain. Door-to-needle time with respect to thrombolytic treatment seems to depend on several factors in the preclinical field. Improvement of prehospital diagnosis and prevention of preclinical complications might result in faster thrombolytic treatment of the patient after arrival at the emergency department.

Adult↗
PubMed1994

[Concomitant perforated ulcer and acute myocardial infarct--a diagnostic challenge in emergency medicine].

Clinical differentiation between acute myocardial infarction and peptic ulcer perforation may sometimes be difficult. We report on a sixty-five year-old patient who presented at the Emergency Department with upper abdominal pain and local tenderness suggestive of acute perforation of a gastric ulcer. However, the initial electrocardiogram (ECG) showed acute inferior wall myocardial infarction. Although abdominal pain is a major symptom of acute inferior wall myocardial infarction the history of gastritis and abdominal findings on admission of our patient required further exploration. The first plain abdominal radiograph was inconspicuous, therefore we performed a gastroscopy, which showed a prepyloric gastric ulcer. The second plain abdominal radiograph revealed air in the peritoneal cavity as sign of perforation. Echocardiography, ECG and the increase of heart enzymes confirmed acute inferior wall infarction. After successful surgical treatment of the perforated ulcer the patient recovered and progressed satisfactorily at the intensive care unit. He was discharged after three weeks and remains in good health. This case shows that rapid diagnosis and good interdisciplinary therapeutic management prevented a fatal outcome of acute myocardial infarction and concomitant gastric ulcer perforation in an elderly patient.

Aged↗
PubMed1993

Effect of morning and afternoon naps on mood after total sleep deprivation in patients with major depression.

In 30 depressed patients who had responded to total sleep deprivation therapy, morning naps led more frequently to relapses into depression than did afternoon naps. Longer naps were less detrimental than shorter ones, and there was no significant relationship between the effect of a nap on mood and its content of slow-wave-sleep. The amount of the rapid eye-movement sleep, too, was unrelated to clinical nap effects. Thus, some of the current theories on the relationship between sleep and depressive symptomatology are not supported by the data. Our results demonstrate the importance of nap timing, suggesting a circadian variation of propensity to relapse into depression.

Adult↗
PubMed1993

Influence of endotoxin on nocturnal sleep in humans.

Sleepiness is a common complaint during infectious diseases, but the interaction between sleep and host defense mechanisms has been poorly explored in humans. We therefore studied the effect of endotoxin, a major pathophysiological factor in gram-negative bacterial infections, on sleep and on parameters of the primary host response in men. In a single-blind counterbalanced trial, 15 healthy volunteers received either placebo or Salmonella abortus equi endotoxin (0.4 ng/kg body wt) intravenously on two separate occasions. Nocturnal sleep was recorded, and rectal temperature and the plasma levels of tumor necrosis factor-alpha, interleukin-6, adrenocorticotropic hormone, and cortisol were monitored for 12 h. Endotoxin reduced the relative amounts of wakefulness (P < 0.05) and rapid-eye-movement (REM) sleep (P < 0.05) and increased the relative amount of non-REM sleep (P < 0.01). Electroencephalogram delta power during non-REM sleep, as measured by spectral analysis, was not altered by endotoxin. The endotoxin-induced changes in sleep structure were related temporally and quantitatively to the increases in rectal temperature and to the release of cytokines and neurohormones. It is concluded that cytokines and neurohormones mediate the effects of endotoxin upon sleep. The ensuing increase in non-REM sleep may be part of the adaptive host response to bacterial infections in humans.

Adrenocorticotropic Hormone↗
PubMed1993

Endotoxin- and corticotropin-releasing hormone-induced release of ACTH and cortisol. A comparative study in men.

The present study compares the effects of endotoxin, a key factor in gram-negative bacterial infection, and of corticotropin-releasing hormone (CRH) on ACTH and cortisol secretion in healthy male volunteers in a placebo-controlled design. Endotoxin (isolated from Salmonella abortus equi; 0.4 ng/kg body weight) induced a significantly delayed and prolonged increase of ACTH and cortisol secretion as compared to CRH (100 micrograms), supporting the hypothesis that different intermediate mechanisms are involved (baseline/peak: ACTHEndotoxin vs. ACTHCRH: 140 +/- 40 min vs. 44 +/- 17 min (p < 0.001); CortisolEndotoxin vs. CortisolCRH: 113 +/- 51 min vs. 66 +/- 31 min (p < 0.05); peak/baseline: ACTHEndotoxin vs. ACTHCRH: 244 +/- 79 min vs. 200 +/- 25 min (p < 0.05); CortisolEndotoxin vs. CortisolCRH: 278 +/- 76 min vs. 182 +/- 16 min (p < 0.001)). Activation of the hypothalamo-pituitary-adrenocortical (HPA) system by endotoxin in men is associated with increased interleukin-6 (peak value: 124 +/- 109 pg/ml) and tumor necrosis factor-alpha (peak value: 69 +/- 53 pg/ml) plasma levels which, probably together with locally produced interleukin-1, stimulate the HPA system both at the hypothalamic and (to a lesser degree) at the pituitary site. Provided that strictly controlled laboratory conditions are applied, the endotoxin challenge test presented here may serve as an appropriate and safe tool to explore an individual's capacity for neuroendocrine adaptation to a bacterial stressor, thus providing information complementary to the CRH test.

Adrenocorticotropic Hormone↗
PubMed1992

Cholinergic REM sleep induction test in subjects at high risk for psychiatric disorders.

The influence of the cholinergic agonist RS 86 on electroencephalographic (EEG) sleep was investigated in 21 healthy members of families identified as being at high risk for psychiatric disorders and in 17 healthy control subjects without any personal or family history of a psychiatric illness. In comparison to the placebo night, the administration of RS 86 led to a shortening of rapid eye movement (REM) latency in both groups. This effect, however, was much more pronounced in the high-risk group, whereas in the control subjects the arousal system and the slow-wave sleep during the first nonREM period were more affected. These observations suggest that the cholinergic action on sleep regulating mechanisms has differing preferential targets in high-risk probands and in control subjects.

Adult↗
PubMed1992

Nocturnal plasma levels of cytokines in healthy men.

Nocturnal cytokine levels were measured serially in 12 healthy male volunteers for 12 h, including 8 h of polygraphically monitored nocturnal sleep. Plasma concentrations of interleukin-1 beta (IL-1 beta), interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-alpha) were determined in 30-min intervals by enzyme-linked immunoadsorbent assays. In some subjects cytokines were not detectable at all. In the remaining volunteers (27% for IL-1 beta, 58% for IL-6 and TNF-alpha, respectively) occasional values near to the detection limits (DL) of the assays could be measured. With respect to IL-1 beta and IL-6, plasma levels above the DL were significantly more frequent during sleep than during the preceding time of wakefulness. No temporal association with NREM or REM episodes could be shown. TNF-alpha values above the DL were randomly distributed across the 12-h period investigated. It is concluded that in a considerable percentage of healthy subjects small amounts of cytokines are released at night. Release of IL-1 beta and IL-6 is temporally associated with sleep, whereas the release of TNF-alpha is not. It remains to be established whether nocturnal cytokine release reflects either an interaction between sleep and host defense mechanisms or a sleep-independent circadian rhythmicity.

Adult↗
PubMed1992

Phenotype of human T cells expressing CD31, a molecule of the immunoglobulin supergene family.

The CD31 molecule is a leucocyte-surface glycoprotein of 130 kDa with homology to the immunoglobulin gene superfamily. In this study we report on the expression of CD31 on human T cells and demonstrate that it subdivides peripheral blood T lymphocytes into two novel subsets. CD31 is expressed by 38% of CD3+ lymphocytes. About 85% of CD31+ T cells display the CD45RA phenotype, 35% the CD45RO phenotype, 24% the CD4 phenotype and 72% the CD8 phenotype. There is also a correlation between CD31 expression and CD45RA expression in cord blood T cells; 89% of CD3+ cord blood cells express CD31, and most of them have the CD45RA phenotype. A discrepancy was found with thymocytes, which are positive for CD31 but negative for CD45RA. Stimulation of human T cells leads to down-regulation of CD45RA, while CD31 continues to be expressed. In functional studies, CD31 antibody binding to T lymphocytes does not lead to mobilization of intracellular calcium, proliferation or modulation of T-cell proliferation.

Antibodies, Monoclonal↗
PubMed1991

Nocturnal sleep in Huntington's disease.

Nocturnal sleep was studied in 16 inpatients with Huntington's disease. In comparison with healthy controls, patients exhibited a disturbed sleep pattern with increased sleep onset latency, reduced sleep efficiency, frequent nocturnal awakenings, more time spent awake and less slow wave sleep. These abnormalities correlated in part with duration of illness, severity of clinical symptoms, and degree of atrophy of the caudate nucleus. Patients showed an increased density of sleep spindles.

Adult↗
PubMed1991

Brain morphology and sleep EEG in patients with Huntington's disease.

In 12 patients with Huntington's disease, the relationship between brain morphology, nocturnal sleep EEG, and clinical variables was studied. Global cerebral atrophy did not significantly correlate with sleep parameters, whereas atrophy of the caudate nuclei was associated with reduced slow wave sleep and increased time spent awake. Several clinical parameters (e.g., anergia and thought disturbance scores of the Brief Psychiatric Rating Scale, illness duration and global clinical assessment) showed significant correlations with global cerebral atrophy. Similar studies in other neuropsychiatric disorders demonstrate associations between sleep alterations and brain morphological changes of different localizations, thus pointing to a complex relationship between both. It can be hypothesized that the caudate nuclei may be involved in sleep regulation; indirect evidence from studies with positron emission tomography (PET) point in the same direction.

Adult↗
PubMed1991

Nocturnal sleep EEG in patients with HIV infection.

Nocturnal sleep was studied in 14 human immunodeficiency virus (HIV)-positive patients without opportunistic infections of the central nervous system. Seven patients had no bodily complaints at the time of the investigation. Patients exhibited an impaired nocturnal sleep with longer sleep onset latency, reduced total sleep time, reduced sleep efficiency, and more time spent awake and in stage 1. Stage 2 sleep was significantly decreased; in 2 cases, sleep spindle density was extremely low. REM latency was reduced and correlated negatively with depressive symptomatology, while the percentages of REM and slow wave sleep were normal. No significant differences in sleep parameters were present among patients in different stages of the illness, or between patients with and without bodily complaints. Ventricular size and sulcal width on computed tomography scans correlated with sleep variables indicating reduced sleep quality, and with REM density. Decreased tryptophan plasma levels were associated with shorter and less efficient sleep, and with reduced stage 2 sleep. The findings demonstrate that sleep EEG investigations can be valuable for detecting and monitoring central nervous system affection in HIV-positive individuals.

AIDS Dementia Complex↗