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Biomedical subjects

S Schwarz

Publications and source records attributed to S Schwarz.

At least 109 records · Page 6Linked to original sources
PubMed2000

Acute disseminated encephalomyelitis after parenteral therapy with herbal extracts: a report of two cases.

Two patients with acute disseminated encephalomyelitis after repeated injection of extracts from several different plants are described. There was no evidence of prior infection or vaccination. Both patients recovered rapidly after treatment with methylprednisolone. Acute disseminated encephalomyelitis should be considered a rare complication of parenteral therapy with herbal extracts.

Adult↗
PubMed2000

Influence of positive airway pressure on the pressure gradient for venous return in humans.

To study the effect of positive airway pressure (Paw) on the pressure gradient for venous return [the difference between mean systemic filling pressure (Pms) and right atrial pressure (Pra)], we investigated 10 patients during general anesthesia for implantation of defibrillator devices. Paw was varied under apnea from 0 to 15 cmH(2)O, which increased Pra from 7.3 +/- 3.1 to 10.0 +/- 2.3 mmHg and decreased left ventricular stroke volume by 23 +/- 22%. Episodes of ventricular fibrillation, induced for defibrillator testing, were performed during 0- and 15-cmH(2)O Paw to measure Pms (value of Pra 7.5 s after onset of circulatory arrest). Positive Paw increased Pms from 10.2 +/- 3.5 to 12.7 +/- 3.2 mmHg, and thus the pressure gradient for venous return (Pms - Pra) remained unchanged. Echocardiography did not reveal signs of vascular collapse of the inferior and superior vena cava due to lung expansion. In conclusion, we demonstrated that positive Paw equally increases Pra and Pms in humans and alters venous return without changes in the pressure gradient (Pms - Pra).

Aged↗
PubMed2000

No association between dehydroepiandrosterone sulfate and development of atherosclerosis in a prospective population study (Bruneck Study).

Antiatherogenic properties of dehydroepiandrosterone (DHEA) have been postulated for >40 years. Large-scale epidemiological studies on this important issue, however, are still sparse, and those available have yielded contradictory results. The Bruneck Study involved a large random sample of men and women aged 40 to 79 years that were enrolled in 1990 and reevaluated 5 years later. Baseline DHEA sulfate (DHEAS) levels were measured in 867 subjects after an overnight fast. Development and progression of carotid atherosclerosis was monitored by high-resolution duplex ultrasound. DHEAS levels declined with advancing age (29% and 44% per decade in men and women) and showed a complex sex-specific association with various vascular risk attributes and factors conferring protection against atherosclerosis. Age- and sex-adjusted DHEAS baseline levels did not differ between subjects with or without incident/progressive atherosclerosis (geometric mean 1161 versus 1253 microg/L). After adjustment for vascular risk factors and potential confounders, the odds ratio of incident/progressive atherosclerosis comparing a 50% increase in DHEAS levels was 0.99 (95% CI 0.89 to 1.11). Lack of an association between DHEAS and atherogenesis was confirmed in sex-specific and a variety of supplementary analyses. Statistical power would be high enough to detect differences in DHEAS between outcome categories as low as 15% (alpha=0.05). This prospective community-based study does not support a role for endogenous DHEA(S) in the development of human atherosclerosis.

Adult↗
PubMed1999

[Time delays in admission to a Stroke Unit and emergency treatment of patients with ischemic stroke].

BACKGROUND AND OBJECTIVE: This observational study describes the time delays involved in the emergency treatment of acute strokes admitted for treatment in the acute stroke unit of the Landesnervenklinik Gugging, Austria. The aim was to define avoidable delays in the prehospital and intrahospital phase. PATIENTS AND METHODS: 261 stroke patients were included consecutively within the one-year study period (September 1996 until September 1997). Minute-by-minute reconstruction of events starting from the first symptoms to the first therapeutic application within the stroke unit was performed for every stroke patient by a neurologist during or immediately after treatment. RESULTS: Time delays are predominantly in the prehospital phase. Only 20.5% are admitted within 120 minutes after noticing first symptoms. Public registration time was 42 +/- 212 minutes. In the intrahospital phase, the mean door-to-drug-time was 50 +/- 28 minutes (including CT). In 25% of the patients, adequate treatment of acute stroke was started within 35 minutes after the patient's arriving at the hospital. In 92% cerebral computed tomography was performed before treatment was started. CONCLUSIONS: This study shows the necessity for continuing efforts to increase public awareness for immediate hospitalisation after stroke in order to achieve a higher rate of urgent and direct admission to a stroke unit.

Acute Disease↗
PubMed1999

Extensive electroporation abolishes experimentally induced shape transformations of erythrocytes: a consequence of phospholipid symmetrization?

As shown in earlier work (M.M. Henszen et al., Mol. Membr. Biol. 14 (1997) 195-204), exposure of erythrocytes to single brief electric field pulses (5-7 kV cm(-1)) enhances the transbilayer mobility of phospholipids and produces echinocytes which can subsequently be transformed into stomatocytes in an ATP-dependent process. These shape transformations arise from partly reversible changes of the transbilayer disposition of phospholipids, in agreement with the bilayer couple concept. Extensive membrane modification by repetitive (</=20) field pulses followed by 20 h incubation at 37 degrees C is now shown to produce discocytic cells which are resistant to many established shape-transforming treatments, including (A) single electric field pulses, Ca(2+) incorporation and exposure to membrane active amphiphiles, but also (B) metabolic depletion, binding of band 3 ligands, alkaline pH and contact with glass surfaces. The suppression of type A effects can readily be interpreted by a complete symmetrization of the phospholipids in extensively field pulse-modified cells which prevents shape transformations related to the asymmetric disposition of the phospholipids. This symmetrization could be further substantiated by more direct determinations of the transbilayer distribution of phospholipids. Suppression of shape transformations of type B may indicate an involvement of phospholipid asymmetry in these processes on a yet unknown mechanistic basis. Alternatively we discuss field pulse-induced alterations of the disposition of peripheral proteins or of the conformation of integral membrane proteins as mechanisms interfering with shape transformations of type B.

Cell Size↗
PubMed1999

A chicken embryo protein related to the mammalian DEAD box protein p68 is tightly associated with the highly purified protein-RNA complex of 5-MeC-DNA glycosylase.

We have shown previously that DNA demethylation by chick embryo 5-methylcytosine (5-MeC)-DNA glycosylase needs both protein and RNA. Amino acid sequences of nine peptides derived from a highly purified 5-MeC-DNA glycosylase complex were identified by Nanoelectrospray ionisation mass spectrometry to be identical to the mammalian nuclear DEAD box protein p68 RNA helicase. Antibodies directed against human p68 helicase cross-reacted with the purified 5-MeC-DNA glycosylase complex and immunoprecipitated the glycosylase activity. A 2690 bp cDNA coding for the chicken homologue of mammalian p68 was isolated and sequenced. Its derived amino acid sequence is almost identical to the human p68 DEAD box protein up to amino acid position 473 (from a total of 595). This sequence contains all the essential conserved motifs from the DEAD box proteins which are the ATPase, RNA unwinding and RNA binding motifs. The rest of the 122 amino acids in the C-terminal region rather diverge from the human p68 RNA helicase sequence. The recombinant chicken DEAD box protein expressed in Escherichia coli cross-reacts with the same p68 antibodies as the purified chicken embryo 5-MeC-DNA glycosylase complex. The recombinant protein has an RNA-dependent ATPase and an ATP-dependent helicase activity. However, in the presence or absence of RNA the recombinant protein had no 5-MeC-DNA glycosylase activity. In situ hybridisation of 5 day-old chicken embryos with antisense probes of the chicken DEAD box protein shows a high abundance of its transcripts in differentiating embryonic tissues.

Amino Acid Sequence↗
PubMed1999

Plasmid-encoded tetracycline resistance in Salmonella enterica subsp. enterica serovars choleraesuis and typhimurium: identification of complete and truncated Tn1721 elements.

During routine screening of Salmonella enterica subsp., S. enterica isolates of animal origin for plasmid-encoded tetracycline resistance, two tetracycline resistance plasmids, the 50 kbp plasmid pGFT3 of Salmonella choleraesuis and the 9.5 kbp plasmid pGFT4 of Salmonella typhimurium var. Copenhagen DT002, were detected. The respective tetracycline resistance genes (tet) were identified by hybridization and PCR analysis to belong to hybridization class A. Conjugation experiments identified plasmid pGFT3 as a conjugative plasmid. Molecular analysis of the tet(A) gene area and the flanking regions identified a complete Tn1721-like transposon on plasmid pGFT3 and a truncated Tn1721-like element on plasmid pGFT4. The complete Tn1721-like element was integrated into a transposase reading frame of a truncated Tn3 transposon also located on plasmid pGFT3. The truncated Tn1721-like element of plasmid pGFT4 lacked the entire transposase part. This Tn1721-relic was integrated in an unknown reading frame which on amino acid level showed homology to the Rop protein of Escherichia coli. A model for the deletion of the transposase part was developed on the basis of the sequences present at the termini of the truncated Tn1721-like element.

Animals↗
PubMed1999

Molecular subtyping of Staphylococcus aureus isolates from cases of bovine mastitis in Brazil.

Sixty-six isolates of Staphylococcus aureus obtained from milk samples of dairy cows suffering from subclinical mastitis in southern Brazil were analysed by five different molecular typing methods. These included the analysis of plasmid profiles, the analysis of coagulase (coa) gene polymorphisms by PCR amplification of the 3' terminal region of the coa gene, the PCR-based detection of polymorphisms in the X region of the protein A gene (spa), the PCR-directed analysis of variations in the spacer region between 16S and 23S rRNA, and the comparison of pulsed-field gel electrophoretically separated genomic SmaI fragment patterns. The molecular typing methods were supplemented with the biochemical characterization of the isolates and the determination of their in-vitro susceptibility to 14 different antibiotics. All genotypic and phenotypic typing methods were analyzed for their ability to discriminate between the isolates. Macrorestriction analysis proved to be the most discriminatory single method (D = 0.96) followed by rRNA spacer typing (D = 0.85), coa PCR (D = 0.82), and spa PCR (D = 0.80).

Animals↗
PubMed1999

Complement receptor 1 (CD35) on human reticulocytes: normal expression in systemic lupus erythematosus and HIV-infected patients.

The low levels of complement receptor 1 (CR1) on erythrocytes in autoimmune diseases and AIDS may be due to accelerated loss in the circulation, or to a diminished expression of CR1 on the red cell lineage. Therefore, we analyzed the expression of CR1 on reticulocytes (R) vs erythrocytes (E). Healthy subjects had a significant higher CR1 number per cell on R (919 +/- 99 CR1/cell) than on E (279 +/- 30 CR1/cell, n = 23), which corresponded to a 3. 5- +/- 1.3-fold loss of CR1. This intravascular loss was confirmed by FACS analysis, which showed that all R expressed CR1, whereas a large fraction of E was negative. The systemic lupus erythematosus (SLE), HIV-infected, and cold hemolytic Ab disease (CHAD) patients had a CR1 number on R identical to the healthy subjects, contrasting with a lower CR1 on their E. The data indicated a significantly higher loss of CR1 in the three diseases, i.e., 7.0- +/- 3.8-, 6.1- +/- 2.9-, and 9.6- +/- 5.6-fold, respectively. The intravascular loss was best exemplified in a patient with factor I deficiency whose CR1 dropped from 520 CR1/R to 28 CR1/E, i.e., 18.6-fold loss. In one SLE patient and in the factor I-deficient patient, the FACS data were consistent with a loss of CR1 already on some R. In conclusion, CR1 is lost progressively from normal E during in vivo aging so that old E are almost devoid of CR1. The low CR1 of RBC in autoimmune diseases and HIV-infection is due to a loss occurring in the circulation by an active process that remains to be defined.

Agglutinins↗
PubMed1999

A re-investigation of the ribonuclease sensitivity of a DNA demethylation reaction in chicken embryo and G8 mouse myoblasts.

Recently published results (Nucleic Acids Res. 26, 5573-5580, 1998) suggest that the ribonuclease sensitivity of the DNA demethylation reaction may be an experimental artifact due to the possible tight binding of the nucleases to the methylated DNA substrate. Using an improved protocol we show for two different systems that demethylation of hemimethylated DNA is indeed sensitive to micrococcal nuclease, requires RNA and is not an experimental artifact. The purified 5-MeC-DNA glycosylase from chicken embryos and G8 mouse myoblasts was first incubated for 5 min at 37 degrees C with micrococcal nuclease in the presence of Ca2+ in the absence of the DNA substrate. Upon blocking the nuclease activity by the addition of 25 mM EGTA, the DNA demethylation reaction was initiated by adding the labeled hemimethylated DNA substrate to the reaction mixture. Under these conditions the DNA demethylation reaction was abolished. In parallel controls, where the purified 5-MeC-DNA glycosylase was pre-incubated at 37 degrees C with the nuclease, Ca2+ and EGTA or with the nuclease and EGTA, RNA was not degraded and no inhibition of the demethylation reaction was obtained. As has already been shown for chicken embryos, the loss of 5-MeC-DNA glycosylase activity from G8 myoblasts following nuclease treatment can also be restored by the addition of synthetic RNA complementary to the methylated strand of the substrate DNA. No reactivation of 5-MeC-DNA glycosylase is obtained by complementation with a random RNA sequence, the RNA sequence complementary to the non-methylated strand or DNA, thus ruling out a non-specific competition of the RNA for the binding of the nuclease to the labeled DNA substrate.

Animals↗
PubMed1999

Metabolic characterization of AIDS dementia complex by spectroscopic imaging.

Prospective proton chemical shift imaging (CSI) of the brain was performed in 30 HIV- 1-seropositive patients and 11 healthy controls. Significant (P < 0.05) reductions in the N-acetyl-L-aspartate (NAA)/total creatine (Cr), and NAA/total choline (Cho) ratios and significant increases in Cho/Cr occurred in patients with 1) AIDS-defining diagnoses; 2) <200 CD4 lymphocyte counts/microl; 3) neurological evidence for an AIDS dementia complex (ADC); 4) magnetic resonance imaging (MRI) signs of cerebral atrophy. The basal ganglia and the insula were affected to approximately the same extent and without indications of spatial variations within these areas. Reduced NAA seems to indicate progressive neuronal injury or loss due to productive HIV infection in the brain and its clinical picture ADC. Spectroscopic abnormalities were, however, also observed in neurologically normal HIV patients or those with normal MRI results. Proton CSI may therefore serve as an early quantitative marker of central nervous system involvement in AIDS.

AIDS Dementia Complex↗
PubMed1999

Soluble complement receptor 1 is increased in patients with leukemia and after administration of granulocyte colony-stimulating factor.

Complement receptor type 1 is expressed by erythrocytes and most leukocytes. A soluble form is shed from the leukocytes and found in plasma (sCR1). sCR1 is a powerful inhibitor of complement. We report an increased sCR1 in the plasma of leukemia patients, up to levels producing measurable complement inhibition. Half of the 180 patients with acute myeloid leukemia (AML), acute lymphoblastic leukemia (ALL), and chronic lymphocytic leukemia (CLL) had sCR1 levels above the normal range. The highest levels were observed in T-ALL (17 patients). The complement function of a T-ALL serum was improved by blocking sCR1 with a specific mAb (3D9). Measurements in 16 peripheral stein cell donors before and after granulocyte colony-stimulating factor (G-CSF) administration showed an increase in sCR1 (before, 43.8+/-15.4; at day 5, 118.3+/-44.7 ng/mL; P < 0.0001). This increase paralleled the increase in total leukocyte counts and was concomitant with de novo leukocyte mRNA CR1 expression in all three individuals tested. Whether pharmacological intervention may be used to up-regulate sCR1 so as to inhibit complement in vivo should be further investigated.

Animals↗
PubMed1999

[Status epilepticus. Rational diagnosis and current therapeutic concepts].

Status epilepticus (SE) is defined as a seizure persisting over 10 min or repeated seizures without recovery between the attacks. SE is a frequent medical emergency with a high mortality, requiring aggressive and prompt treatment and a systematic, coordinated approach. A variety of new drugs has been introduced for the treatment of SE, including midazolam, propofol, fosphenytoin, and valproate. However, there are very few controlled clinical trials. Benzodiazepines are highly effective in terminating the SE in most patients and should be used as initial treatment. Phenytoin and Phenobarbital are employed if Benzodiazepines are not successful. The optimal therapeutic approach for the patient with refractory SE remains to be defined. Refractory SE has a poor prognosis and should be treated in a specialized ICU with EEG-monitoring. Barbiturates, propofol, and midazolam are substances that can be used alternatively.

Humans↗
PubMed1999

[Enzyme defects of the urea cycle in differential acute encephalopathy diagnosis in adulthood. Diagnosis and current therapy concepts].

Six enzyme defects of the urea cycle have been described. Ornithine transcarbamylase deficiency is the most frequent of these diseases. The cumulative frequency is 1:8000. Most patients become symptomatic in childhood, but onset of symptoms may occur later in childhood or even adulthood. The patients present with recurrent episodes of an unspecific acute encephalopathy, seizures and clouding of consciousness to a variable degree. Focal neurological signs such as hemiparesis, aphasia or ataxia may also occur. These episodes may be triggered by infection, protein overload or drugs. Diagnostic are increased blood ammonia levels. Characteristic patterns of plasma amino acids and the determination of orotic acid in the urine mostly discriminate the individual disorders. Further diagnostic steps include the allopurinol challenge test, liver or skin biopsy for measurement of enzyme activity and molecular genetic studies. Treatment requires restriction of protein intake, supplementation of arginine and activation of alternative pathways of nitrogen excretion with benzoate or phenylbutyrate. Untreated, the acute episode may be lethal. Long-term treatment improves the clinical outcome considerably. Urea cycle defects should be included in the differential diagnosis of any encephalopathy or coma of unclear origin, and blood ammonia should be determined early in the evaluation of such patients.

Adult↗
PubMed1999

[Fibrinolysis of intraventricular hematoma with rt-PA].

Intraventricular administration of recombinant tissue plasminogen activator (rt-PA) is an experimental therapy to hasten the lysis of intraventricular hemorrhages. We report nine patients (7 male, 2 female, mean age 64a) with intracerebral hematoma with ventricular extension who were treated with intraventricular infusion of rt-PA (2-32 mg, mean dose 17 mg). In two patients, clinically significant bleeding complications were associated with the fibrinolytic therapy. In one of these patients, fibrinolytic therapy was stopped. Other complications could not be observed. In eight of all nine patients, a rapid and extensive reduction of the amount of intraventricular blood occurred. A persistent shunt became necessary in two patients. We conclude, that intraventricular fibrinolysis probably leads to a faster clearance of intraventricular blood. Despite of fibrinolytic treatment, a permanent shunt becomes necessary in some cases. Intraventricular fibrinolysis is a potentially hazardous therapy with the risks of bleeding complications and infection.

Adult↗
PubMed1999

[Moderate hypothermia for the treatment of malignant middle cerebral artery infarct].

Moderate hypothermia was induced in 30 patients with malignant middle cerebral artery (MCA) territory infarction. Patients were kept at 33 degrees C body-core temperature for 48 to 72 h, and ICP, CPP, and brain temperature were monitored. Outcome at 4 weeks and at 3 months after the stroke as well as side effects of moderate hypothermia were analysed. Mortality of malignant MCA infarction could be reduced from 80% in historical controls, to 43% (13/30) under hypothermia. During hypothermia elevated ICP values could be significantly reduced. Herniation due to a secondary rise of ICP after rewarming was the cause of death in all 13 patients. The most frequent complication of moderate hypothermia was pneumonia in 12 of the 30 patients (40%). Other severe side effects of hypothermia could not be detected. Moderate hypothermia may improve clinical outcome in patients with malignant MCA infarction.

Adolescent↗