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Biomedical subjects

M Schweizer

Publications and source records attributed to M Schweizer.

At least 109 records · Page 6Linked to original sources
PubMed1994

Absence of foamy virus DNA in Graves' disease.

A report on the high prevalence of foamy virus DNA in lymphocytes from French patients with Graves' disease prompted us to investigate a similar cohort of 41 German patients. Using PCR amplification and Southern blot hybridization, we detected foamy virus DNA only in lymphocytes of two accidentally infected humans and five naturally infected monkeys, as well as in DNA samples from four Graves' disease patients investigated in the French study. However, we failed to detect foamy virus DNA in peripheral blood lymphocytes from any of the 41 Graves' disease patients of the German cohort. Thus, a causative role of foamy viruses in this thyroid disease is highly improbable.

Adult↗
PubMed1994

Cardiac late potentials for diagnosis in heart disease.

In recent years abundant information has been obtained about the relationship of heart disease and cardiac late potentials. Non-invasive recordings of ventricular late potentials are useful in risk stratification of various clinical conditions, in particular, in patients following myocardial infarction. Here a close correlation has been established between cardiac late potentials and spontaneous or induced sustained ventricular tachycardias using programmed electrical stimulation. Cardiac late potentials also appear to be associated with arrhythmic events in patients with cardiomyopathies, and following unsuccessful antitachycardia surgery. Furthermore, recording of abnormal late potentials are associated both with acute rejection after cardiac transplantation and unsuccessful thrombolytic therapy after myocardial infarction. Interestingly, antiarrhythmic drugs have no clear effect on cardiac late potentials.

Arrhythmias, Cardiac↗
PubMed1994

[The implantable cardioverter/defibrillator (ICD). Developments up to the present time and future perspectives].

The implantable cardioverter/defibrillator is gaining increasing significance in the therapy of life-threatening ventricular arrhythmias. Independently, the team of Mirowski and the team of Schuder started to develop experimental automatic implantable defibrillators in the seventies. In 1980, the first human implant of an automatic defibrillator was done by Levi Watkins together with the team of Mirowski in Baltimore, USA. Since 1989 implantable cardioverter/defibrillators exhibit multiple functions among which are high energy defibrillation therapy, low energy cardioversion, antitachycardia pacing, permanent and post therapy antibradycardia pacing, diagnostic counters, and device status parameters. This offers a markedly improved technical device to the patients. Evaluation of the patient's diagnostic counters provide a detailed overview about the patient's arrhythmia history and information for optimizing antitachycardia pacing therapy and additional antiarrhythmic drug therapy. The availability of non-thoractomy transvenous lead systems and biphasic shock forms allows the insertion of the device without open chest surgery and even without subcutaneous leads resulting in low mortality rates and an exclusively transvenous system. Single-lead unipolar devices are currently investigated in clinical trials. Future development of atrial sensing lead systems may further reduce inappropriate shock therapy triggered by sinus tachycardia or atrial tachyarrhythmias, e.g. atrial fibrillation, and may be used for dual chamber stimulation. Hemodynamic sensors for determining the severity of the arrhythmia are currently under experimental evaluation. Possible prognostic indications of ICD therapy in patients without a history of malignant arrhythmias are currently studied in several prospective trials. All new directions hold promise to expand and improve the use of ICDs in patients at risk for sudden cardiac death.

Death, Sudden, Cardiac↗
PubMed1993

Postnatal development and localization of an N-acetylgalactosamine containing glycoconjugate associated with nonpyramidal neurons in cat visual cortex.

We have analyzed the appearance of N-acetylgalactosamine containing glycoconjugates by staining sections of fixed cat visual cortex with the lectins from Vicia villosa (VVA) and Glycine max (SBA) conjugated to fluorescent labels, horseradish peroxidase, or biotin. The appearance of lectin staining during postnatal development followed an inside-out gradient starting in the deep cortical layers at the fourth postnatal week, successively including more of the superficial layers during the first three postnatal months until labelled cells were present throughout layers II-VI at the seventh postnatal month. Staining was associated with the soma and proximal dendrites of bipolar and multipolar nonpyramidal neurons. Outside layer IV large neurons with basket cell and neurogliaform morphology predominated, whereas small multipolar cells were stained in layer IV. High power observation revealed a lattice-like staining on neuronal surfaces. In the cortical white matter staining was found at the nodes of Ranvier. The ultrastructural localization of lectin binding sites was assessed by a pre-embedding histochemical procedure with biotinylated lectin visualized with HRP-conjugated avidin and diaminobenzidine as the chromogen. The reaction product was found exclusively in close association with synaptic terminals on somata and proximal dendrites of nonpyramidal neurons. There was no preference with respect to the morphology of the synaptic structure, i.e., symmetric synapses with ovoid or asymmetric synapses with round vesicles. In the vicinity of synaptic contacts the staining was associated with membranes of astrocytic processes ensheathing the synapses. In the cortical white matter astrocytic processes running along myelinated axons were strongly labelled at the nodes of Ranvier. Comparison of Western blots from 4-week-old and adult cat cortex membranes revealed one lectin-positive protein band with an apparent molecular weight of about 24 kD in conjunction with the histochemical expression of perisynaptic staining in the adult tissue. It is concluded that the employed lectins selectively visualize distal astroglial processes ensheathing synapses on a subpopulation of cortical interneurons and nodes of Ranvier. On the basis of the developmental appearance and localization we consider and discuss the possibility that the N-acetylgalactosamine containing glycoconjugate is involved in the stabilization of synaptic contacts on GABA-ergic interneurons.

Acetylgalactosamine↗
PubMed1993

Sensitivity of mitochondrial peptidyl-prolyl cis-trans isomerase, pyridine nucleotide hydrolysis and Ca2+ release to cyclosporine A and related compounds.

Prooxidants activate a specific Ca2+ release pathway from mitochondria. Here we investigate the inhibitory potency of cyclosporine A and six related compounds with respect to peptidyl-prolyl cis-trans isomerase (PPIase), pyridine nucleotide hydrolysis and Ca2+ release. Whereas the absolute inhibitory potency of the compounds varies by about three orders of magnitude, a given compound is always most effective on PPIase, followed by pyridine nucleotide hydrolysis, and least effective in Ca2+ release inhibition. The data show that pyridine nucleotide hydrolysis is a prerequisite but not a consequence of Ca2+ release. They also strongly suggest that PPIase participates in the Ca2+ release mechanism from intact mitochondria by regulating the intramitochondrial NAD+ glycohydrolase, and thereby ascribe a physiological function to the protein. Furthermore, a complete lack of correlation between the inhibitory potencies described here and the reported immunosuppressive activities of the drugs is evident.

Amino Acid Isomerases↗
PubMed1993

Simian foamy virus type 3 (SFV-3) in latently infected Vero cells: reactivation by demethylation of proviral DNA.

Cell cultures latently infected with simian foamy virus type 3 (SFV-3) were established by suppressing lytic infection in Vero cells with 3'-azido-3'-deoxythymidine (AZT) and homologous antibodies (African green monkey serum immune to SFV-3). The resulting cell line, designated Vero-L, was shown to contain at least one copy per cell of SFV-3 DNA stably integrated at a defined site of the host cell genome. Sequencing of 669 bp at the integration site did not identify a coding region and revealed a 4-bp imperfect repeat in host cell DNA due to SFV-3 integration. Over 2 years of subcultivation, no spontaneous expression of proviral genes could be detected. However, the demethylating agent 5'-azacytidine reactivated lytic infection, proving conservation of the complete viral genome. Comparison of proviral DNA from latently and lytically infected cells supports the notion that methylation is instrumental in keeping SFV-3 infection in latency.

Animals↗
PubMed1993

Pancreaticobiliary long common channel syndrome and congenital anomalous dilatation of the choledochal duct--study of 46 patients.

Retrospectively evaluated clinical, radiological and anatomical findings of 46 patients with tubular or cystic dilated choledochal ducts indicate the following conclusion: Pathological stricture of the sphincter of Oddi system, including a hypertrophic and spastic portion of the sphincter choledochus inferior, called "narrow segment", raises the pressure in the choledochal duct to pathological levels and consequently causes a dilatation of the duct during a specific embryonic phase. Such a pathological sphincter of Oddi system develops if a long common channel persists as the result of a disturbance in the development of the distal choledochal and pancreatic duct. This statement contradicts the classical conception which assumes that a reflux of pancreatic juice into the choledochal duct causes ductal dilatation. Authors who are in favor of this conception propose that pancreatic juice causes weakness of the ductal wall, which may be dilated in the embryonic period. However, the findings of the series evaluated here show that dilatation of the duct may also originate without any reflux of pancreatic juice into the choledochal duct if a "narrow segment" exists above the junction of the pancreatic and choledochal ducts. For this reason, pancreatic juice reflux cannot be the condition sine qua non in the development of choledochal duct dilatation. Similarly the pathologic junction angulation can only be an optional factor in this autogenetic anomaly. With regard to a pathological sphincter of Oddi system the question arises whether a partial or complete myotomy of the muscular sphincter may be able to remedy the dilatation and avoid resection of the choledochal duct.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1993

Foamy viruses.

Foamy viruses share complex genome organization with lentiviruses and certain oncoviruses. The open reading frame 3' of env encodes a transcriptional transactivator. Distinct responsive sequences were identified in the long terminal repeats (LTRs) of simian (SFV-1 and SFV-3) and human foamy viruses (HFV). Transactivation of heterologous LTRs was described including those of simian and human immunodeficiency viruses. Foamy viruses persist for the whole lifetime in infected hosts (primates, cats, hamsters, cattle, and probably other mammals). The virus may be orally shed and transmitted, while being latent in various internal organs. Selective viral gene expression in the brains of mice transgenic for HFV has suggested a particular relationship to neural tissue. In latently SFV-3-infected cultured cells, methylation of proviral DNA is apparently involved in the control of latency. Demethylation as well as transfection with the transactivator were shown to be instrumental in viral reactivation. Natural infections with foamy viruses are common, elicit strong immune responses, and seem to be asymptomatic in nonhuman primates. Detection of such infections, however, may not be a triviality in man. While accidental transmission of foamy viruses to man is well documented, reported seroprevalence in human populations and the association of HFV with specific pathology (e.g. thyroiditis de Quervain, amyotrophic lateral sclerosis, and Graves' disease) are controversial and remain to be proven.

Animals↗
PubMed1992

Prooxidant-induced Ca2+ release from liver mitochondria. Specific versus nonspecific pathways.

Ca2+ release from mitochondria can be induced by a variety of chemically different prooxidants. Release induced by these compounds is possibly regulated by protein mono(ADP)ribosylation, and leaves mitochondria initially intact. Excessive "cycling" (continuous release and uptake) of Ca2+ by mitochondria leads to their damage, as shown by a decreased membrane potential, fast Ca2+ release, and impairment of ATP synthesis. When cycling is prevented by Ca2+ chelators or by inhibition of the uptake route with ruthenium red, prooxidants still induce Ca2+ release but mitochondria remain intact. It has recently been suggested that formation of a "pore" in the inner mitochondrial membrane participates in the Ca2+ release mechanism. We find that the prooxidant-induced Ca2+ release is not paralleled by sucrose entry into, or K+ release from, or swelling of mitochondria, provided Ca2+ cycling is prevented. Thus, the prooxidant-induced Ca2+ release does not require formation of a "pore." We conclude that the release occurs via a specific pathway.

Animals↗
PubMed1992

'Pore' formation is not required for the hydroperoxide-induced Ca2+ release from rat liver mitochondria.

It has recently been suggested by several investigators that the hydroperoxide- and phosphate-induced Ca2+ release from mitochondria occurs through a non-specific 'pore' formed in the mitochondrial inner membrane. The aim of the present study was to investigate whether 'pore' formation actually is required for Ca2+ release. We find that the t-butyl hydroperoxide (tbh)-induced release is not accompanied by stimulation of sucrose entry into, K+ release from, and swelling of mitochondria provided re-uptake of the released Ca2+ ('Ca2+ cycling') is prevented. We conclude that (i) the tbh-induced Ca2+ release from rat liver mitochondria does not require 'pore' formation in the mitochondrial inner membrane, (ii) this release occurs via a specific pathway from intact mitochondria, and (iii) a non-specific permeability transition ('pore' formation) is likely to be secondary to Ca2+ cycling by mitochondria.

Animals↗
PubMed1992

Genomic organization and expression of simian foamy virus type 3 (SFV-3).

The complete nucleotide sequence of simian foamy virus type 3 (SFV-3) strain LK-3, isolated from an African green monkey, was determined. In addition to translation frames representing the gag, pol, and env genes, two open reading frames are located in the region between the env gene and the 3' long terminal repeat (LTR). Both SFV-3 and SFV-1 encode two open reading frames between env and the 3' LTR, whereas HFV encodes three open reading frames in this region. Northern blot analysis of cell cultures infected with SFV-3 revealed subgenomic RNAs for these open reading frames. The protease of SFV-3 is encoded by the pol gene in contrast to HFV which encodes the protease in the gag gene. Notably, the pol gene of SFV-3 in the +1 translational frame relative to the gag gene; this observation is in agreement with SFV-1, but differs for HFV and all other retrovirus genomes reported. Thus, gag-pol precursors of the SFVs appear to be expressed by a +1 frameshift. Nucleotide and deduced amino acid alignments of SFV-3, SFV-1, and HFV revealed an unexpected homology pattern; highest homologies are observed in the pol and env genes but low homologies are noted in the gag genes and the additional open reading frames. Analysis of phylogenetic trees confirms the classification of foamy viruses as a subfamily of retroviruses, distinct from the lentiviruses and oncoviruses.

Amino Acid Sequence↗
PubMed1992

The fatty acid synthase (FAS) gene and its promoter in Rattus norvegicus.

Screening of rat liver genomic libraries yielded 5 overlapping clones for rat fatty acid synthase (FAS). From these clones we determined the 18,170 bp sequence of the rat FAS together with 5,028 bp of the 5'-flanking region and 515 bp of the 3'-adjacent genomic sequence. The two FAS transcripts which differ only in the positions of their polyadenylation/termination sites consist of one untranslated and 42 translated exons. Surprisingly, the substrate binding site for enoyl reductase, one of the FAS component functions, is interrupted by an intron. The sizes and the boundaries of the individual domains could be mapped in relation to the exon/intron structure of the gene. These eight partial functions coincide with discrete units of exons. The acyl carrier protein with its prosthetic 4'-phosphopantetheine group is located within a single exon supporting the idea that rat FAS has evolved by gene fusion. Using primer extension the main transcription start site of the FAS mRNA in both hepatic and mammary gland tissues was located at 5,028 bp in the sequence determined. As expected of a gene which is pretranslationally regulated the 5'-flanking region contains, in addition to TATA and CAAT boxes, consensus sequences for several DNA binding proteins.

Amino Acid Sequence↗
PubMed1992

Electrophysiologic and antiarrhythmic effects of D-sotalol.

There is extensive experimental and clinical experience concerning the antiarrhythmic potency of DL-sotalol, a beta-adrenergic antagonist that lengthens the cardiac action potential duration. More recently, its dextrorotatory isomer, D-sotalol, has been evaluated in experimental studies and preliminary clinical trials. Whereas the isomer is almost free of beta-blocking activity, both experimental and clinical data demonstrate that potent class III activity of D-sotalol. Further investigations, particularly in patients with life-threatening arrhythmias, are needed to delineate the clinical usefulness of this compound.

Action Potentials↗
PubMed1992

[Extrahepatic bile duct atresia. Comparison of surgical and non-surgical therapy].

In recent years hepatoportoenterostomy according to Kasai undoubtedly was the only successful therapy for extrahepatic biliary atresia. Since liver-transplantation becomes more successful than previously, the question arises if the Kasai procedure is still justified. From this point of view a prospective study was started based on the following findings in 15 EHBA-children after hepatoportoenterostomy compared to those in 15 patients without the Kasai procedure: the survival rate at the end of two years of life; the development of ascites until the end of the first year of life; the weight and length percentiles at the end of the first year of life; and the activity of serum cholinesterase. In order to calculate significant differences in weight and length percentiles, the exact Fisher test was used. Serum cholinesterase activities of both the above mentioned groups were compared with each other, as well as with the normal values of a third group of 50 healthy children, by analyzing variances and then comparing one by one with adjustment for multiple comparisons. There was a significant difference between the operated and not-operated group, and in addition between the non-operated and the healthy group. In contrast, no significant difference was detected between the operated and the healthy group. These differences were best demonstrated by the findings of weight and length percentiles and the activity of serum cholinesterase. From this we conclude sofar hepatoportoenterostomy undoubtedly is standard procedure in the treatment of EHGA. However, if the Kasai procedure fails or the liver disease progresses to a greater extent, liver transplantation will become the method of choice.

Biliary Atresia↗
PubMed1991

Differential regulation of the two mRNA species of the rodent negative acute phase protein alpha 1-inhibitor 3.

Screening of two rat liver cDNA libraries, one of which was constructed using an alpha 1-inhibitor 3 (alpha 1-13) specific primer, yielded overlapping cDNA clones which correspond to the full length cDNA for alpha 1-13 mRNA. On the basis of sequence microheterogeneity existing throughout the cDNA sequence we identified two alpha 1-13 mRNA species whose sequences are so grossly different in their bait regions that the amino acid homology therein is only 30%. Using oligonucleotide probes derived from their respective bait regions we investigated the regulation of the two alpha 1 I3 mRNA species and demonstrated that only one of them, alpha 1-I3 variant I, is regulated pretranslationally following experimentally induced inflammation.

Acute-Phase Proteins↗