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Biomedical subjects

V Vetter

Publications and source records attributed to V Vetter.

14 recordsLinked to original sources
PubMed2004

Visual information processing in dyslexic children.

OBJECTIVE: Several studies presented evidence for magnocellular deficits in dyslexics both in behavioural as well as in electrophysiological data of local electrode sites. We investigated two well-known paradigms (motion-onset and random-dot-kinematogram) with regard to global electrophysiological parameters. METHODS: Twenty-one-channel event-related potentials (ERPs) of 16 dyslectic and 15 control children were analyzed with reference-independent methods. For each paradigm quasi stable microstates were identified by means of a data-driven segmentation procedure and compared between both groups. RESULTS: Differences in global ERP responses between dyslexic and control children could be found for rapid moving gratings but not for the dot coherence. CONCLUSIONS: Dyslexic children seem to have some highly specific visual deficits in processing moving stimuli. These deficits can be related to the magnocellular system.

Child↗
PubMed2000

Paravertebral and intraspinal malposition of transfemoral central venous catheters in newborns.

We report permanent tetraplegia in a newborn resulting from intraspinal malposition of a transfemoral catheter. In 2 other neonates paravertebral malposition of indwelling Silastic lines was detected. We suggest that left-sided transfemoral catheterization and conditions enhancing collateral flow through the vertebrolumbar pathway may predispose to inadvertent paravertebral catheter placement.

Catheterization, Central Venous↗
PubMed1995

Lens sorbitol dehydrogenase deficiency in a patient with congenital cataract.

UNLABELLED: Lens sorbitol dehydrogenase activity was assayed in patients with congenital cataracts, senile cataracts, without cataracts and in one fetal lens. In patients with congenital cataracts we did not observe any abnormality of galactose and sorbitol metabolising enzymes in erythrocytes. In one of these patients with inexplicable congenital cataracts lens sorbitol dehydrogenase deficiency was found. CONCLUSION: Determination of galactose metabolising enzymes, sorbitol dehydrogenase and polyols in lenses may help in understanding the mechanism of formation of inexplicable congenital cataracts.

Cataract↗
PubMed1995

Evidence for presence of Ca2+ channel-gated Ca2+ stores in neonatal human atrial myocytes.

The characteristics of Ca2+ signaling in fura 2-loaded whole cell-clamped myocytes obtained from samples of human atrial appendages of 3-day to 4-yr-old patients were examined. In isolated myocytes, activation of Ca2+ current (ICa) (2.47 +/- 0.23 pA/pF) at 0 mV elicited sizable intracellular Ca2+ (Cai) transients (240 +/- 45 nM), which were caused by the release of Ca2+ from intracellular stores as they were suppressed in the presence of ryanodine or caffeine. The voltage dependence of both Cai transients and ICa were similar and bell shaped. The rate of release of Ca2+, normalized for the maximal Ca2+ release, increased with age, indicating increased efficiency of Ca2+ signaling in more mature myocytes. The results suggest that ICa-gated release of Ca2+ from the sarcoplasmic reticulum is the primary mechanism regulating the signaling of contraction in early postnatal as well as older human atrial myocytes.

Atrial Function↗
PubMed1994

Avidities of IgG directed against viral capsid antigen or early antigen: useful markers for significant Epstein-Barr virus serology.

Classical Epstein-Barr virus (EBV) serology can be misleading in some cases due to the variability of the viral capsid antigen (VCA)-IgM response, persistent or reactivated VCA-IgM, or loss of anti-EBNA-1 during suppression of the cellular immune system. Therefore, we studied the usefulness and significance of avidity determinations of VCA-IgG and EA-IgG to achieve unequivocal interpretation of serological results. Avidities of EBV capsid antigen-specific IgG (VCA-IgG) and early antigen-specific IgG (EA-IgG) were determined by indirect immunofluorescence during and after acute EBV infection. Low-avidity antibodies were removed from antigen-antibody complexes by incubation with 6 M urea for 3 minutes. The analysis of 105 sera taken at defined time spans with regard to the onset of clinical symptoms allowed us to determine the kinetics of maturation of avidity of VCA-IgG. All sera had low-avidity antibodies at the onset of disease. More than 90% of the sera showed an avidity index below 0.25 during the first 10 days after the onset of disease. Fifty percent of the sera exhibited an avidity index of 0.25 or above 20-30 days after the onset of clinical symptoms. Sera from past infections uniformly exhibited avidity indices of 0.5 or 1. Avidity of EA-IgG may still be low when avidity of VCA-IgG is already borderline or high, thus allowing further differentiation of acute and recent infections. Avidity determination represents an important additional marker of serology in classical cases and allows diagnosis in aberrant cases, such as acute infections with low or undetectable VCA-IgM.(ABSTRACT TRUNCATED AT 250 WORDS)

Acute Disease↗
PubMed1994

Adhesin regulatory genes within large, unstable DNA regions of pathogenic Escherichia coli: cross-talk between different adhesin gene clusters.

The uropathogenic Escherichia coli strain 536 possesses two large, unstable DNA regions on its chromosome, which were termed pathogenicity islands (pais). Deletions of pais, which occur with relatively high frequency in vitro and in vivo, lead to avirulent mutants. The genetic determinants for production of haemolysin (Hly) and P-related fimbriae (Prf) are located in one of these islands. Deletion of this pathogenicity island (paill) not only removes the hly- and prf-specific genes, but also represses S fimbriae (Sfa), although the sfa genes of this virulence factor are not located on paill. We have identified two regulatory genes, prfB and prfl, of the prf gene cluster that are homologous to the sfa regulatory genes sfaB and sfaC, respectively. Mutations in sfaB and sfaC that inhibit transcription of the major fimbrial subunit gene sfaA were complemented by the homologous prf genes, suggesting communication between the two fimbrial gene clusters in the wild-type strain. Chromosomal mutagenesis of the two prf regulators in strain 536 repressed transcription of sfaA, detected by Northern hybridization and a chromosomal sfaA-lacZ fusion. In addition, haemagglutination assays measured a lower level of S fimbriae in these mutants. Expression of the cloned prf regulators in trans reversed the effect of the mutations; furthermore, constitutive expression of prfB or prfl could also over-come the repression of S fimbriae in a strain that had lost the pathogenicity islands. Virulence assays in mice established that the prf mutants were less virulent than the wild-type strain. The results demonstrate that cross-regulation of two unlinked virulence gene clusters together with the co-ordinate loss of large DNA regions significantly influences the virulence of an extraintestinal E. coli wild-type isolate.

Amino Acid Sequence↗
PubMed1993

Regulation and binding properties of S fimbriae cloned from E. coli strains causing urinary tract infection and meningitis.

S fimbriae are able to recognize receptor molecules containing sialic acid and are produced by pathogenic E. coli strains causing urinary tract infection and menigitis. In order to characterize the corresponding genetic determinant, termed S fimbrial adhesin (sfa) gene cluster, we have cloned the S-specific genes from a urinary pathogen and from a meningitis isolate. Nine genes are involved in the production of S fimbriae, two of these, sfaB and sfaC code for regulatory proteins being necessary for the expression of S fimbriae. Two promoters, PB and PC, are located in front of these genes. Transcription of the sfa determinant is influenced by activation of the promoters via SfaB and SfaC, the action of the H-NS protein and an RNaseE-specific mRNA processing. In addition, a third promoter, PA, located in front of the major subunit gene sfaA, can be activated under special circumstances. Four genes of the sfa determinant code for the subunit-specific proteins, SfaA (16 kda), SfaG (17 kda), SfaS (14 kda) and SfaH (29 kda). It was demonstrated that the protein SfaA is the major subunit protein while SfaS is identical to the sialic-acid-specific adhesin of S fimbriae. The introduction of specific mutations into sfaS revealed that a region of six amino acids of the adhesin which includes two lysine and one arginine residues is involved in the receptor specific interaction of S fimbriae. Additionally, it has been shown that SfaS is necessary for the induction of fimbriation while SfaH plays a role in the stringency of binding of S fimbriae to erythrocytes.

Adhesins, Escherichia coli↗
PubMed1993

The long QT syndrome in children. An international study of 287 patients.

BACKGROUND: The Pediatric Electrophysiology Society studied children with the long QT syndrome (LQTS) to describe the features of LQTS in patients less than 21 years old, define potential "low-risk" and "high-risk" subpopulations, and determine optimal treatment. METHODS AND RESULTS: Patients less than 21 years old were included if either QTc was more than 0.44; they had unexplained syncope, seizures, or cardiac arrest preceded by emotion or exercise; or family history of LQTS. We found 287 patients from 26 centers in seven countries. Mean +/- SD age at presentation was 6.8 +/- 5.6; 9% presented with cardiac arrest, 26% with syncope, and 10% with seizures. Of those with symptoms, 67% had symptoms related to exercise. Family history was positive for long QT interval in 39% and for sudden death in 31%. Hearing loss was present in 4.5%. A normal QTc was present in 6%, and QTc of more than 0.60 was in 13%. Atrioventricular block occurred in 5%, but 13 of 15 patients had second-degree atrioventricular block (2:1), and only two of 287 had complete atrioventricular block. Ventricular arrhythmias were found on 16% of initial routine ECGs: 4% uniform premature ventricular contractions, 5% multiform premature ventricular contractions, 1% monomorphic ventricular tachycardia, and 6% torsade de pointes. Overall, treatment was effective for symptoms in 76% and for ventricular arrhythmias in 60%. There was no difference between propranolol and other beta-blockers in effective treatment. Left stellectomy was performed in nine patients, and defibrillators were implanted in four; no sudden death occurred in these 13 patients. In follow-up (duration, 5.0 +/- 4 years; age, 10.9 +/- 6.3 years), 5% had cardiac arrest, 4% had syncope, and 1% had seizures. The two multivariate predictors of symptoms at follow-up were symptoms at presentation and propranolol failure. Sudden death occurred in 8%; multivariate predictors of sudden death were length of QTc at presentation of more than 0.60 and medication noncompliance. CONCLUSIONS: The appearance of 2:1 atrioventricular block, multiform premature ventricular contractions, and torsade de pointes are relatively more common in children with LQTS than other children and should raise the index of suspicion for LQTS. Because 9% of patients presented with cardiac arrest and no preceding symptoms, perhaps prophylactic treatment in asymptomatic children is indicated. Asymptomatic patients with normal QTc and positive family history may be a low-risk group. Patients with QTc of more than 0.60 are at particularly high risk for sudden death, and if treatment is not effective, consideration should be given to cardiac sympathetic denervation, pacemaker implantation, and perhaps implantation of a defibrillator.

Adrenergic beta-Antagonists↗
PubMed1977

Association of maternal systemic lupus erythematosus with congenital complete heart block.

Infants born to mothers with disseminated lupus erythematosus occasionally have transient manifestations of the maternal disease. In six infants with congenital heart block born to mothers with systemic lupus erythematosus we postulated a causative relation. In one of the infants a post-mortem study of the conduction system suggested faulty embryonic development of the atrioventricular node with an abnormally thick annulus fibrosus and the effects of early inflammatory changes. Two of the infants had a cardiomyopathy and three, associated congenital heart disease.

Adult↗