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Articles by G Klein
Total Records ( 3 ) for G Klein
  D Hilfiker Kleiner , P Shukla , G Klein , A Schaefer , B Stapel , M Hoch , W Muller , M Scherr , G Theilmeier , M Ernst , A Hilfiker and H. Drexler
 

Background— In patients with myocardial infarction, high serum levels of interleukin-6 cytokines predict a poor outcome. The common receptor of interleukin-6 cytokines, glycoprotein-130 (gp130), signals via janus kinase/signal transducer and activator of transcription (STAT), cytoplasmic protein tyrosine phosphatase/extracellular signal-regulated kinase, and phosphoinositide-3-kinase/Akt pathways, and the regulation of these pathways depends at least in part on the gp130 tyrosine-757 residue. By analyzing cardiomyocyte-specific gp130Y757F mutant mice, we investigated the effect of disturbed gp130 signaling after myocardial infarction.

Methods and Results— The cardiomyocyte-restricted -myosin heavy chain-Cre-recombinase-loxP system was used to generate mice with gp130Y757F mutant cardiomyocytes (MHC-Cretg/–;gp130fl/Y757F [Y757F]); all other cells carried at least 1 functional gp130 gene, ensuring normal gp130 signaling. Y757F mice displayed normal cardiac function and morphology at 3 months of age comparable to their nonmutant littermates. In response to myocardial infarction, Y757F mice displayed higher mortality associated with increased left ventricular rupture rate, sustained cardiac inflammation, and heart failure. These adverse effects were associated with prolonged and enhanced STAT3 activation and increased expression of interleukin-6 and of the complement-activating mannose-binding lectin C. Pharmacological inhibition of the complement system by cobra venom factor attenuated inflammation, prevented left ventricular rupture, and improved cardiac function in Y757F mice. Stronger effects were observed with a genetic reduction of STAT3 (STAT3flox/+) restricted to cardiomyocytes in Y757F mice, which prevented extensive upregulation of interleukin-6, complement activation, and sustained inflammation and lowered left ventricular rupture rate, heart failure, and mortality in subacute myocardial infarction.

Conclusion— Impaired downregulation of gp130-mediated STAT3 activation in subacute infarction promotes cardiac inflammation, adverse remodeling, and heart failure, suggesting a potential causative role of high interleukin-6 serum levels after myocardial infarction.

  R Cappato , H Calkins , S. A Chen , W Davies , Y Iesaka , J Kalman , Y. H Kim , G Klein , A Natale , D Packer , A Skanes , F Ambrogi and E. Biganzoli
 

Background— The purpose of this study was to provide an updated worldwide report on the methods, efficacy, and safety of catheter ablation of atrial fibrillation (AF).

Methods and Results— A questionnaire with 46 questions was sent to 521 centers from 24 countries in 4 continents. Complete interviews were collected from 182 centers, of which 85 reported to have performed 20 825 catheter ablation procedures on 16 309 patients with AF between 2003 and 2006. The median number of procedures per center was 245 (range, 2 to 2715). All centers included paroxysmal AF, 85.9% also included persistent and 47.1% also included long-lasting AF. Carto-guided left atrial circumferential ablation (48.2% of patients) and Lasso-guided ostial electric disconnection (27.4%) were the most commonly used techniques. Efficacy data were analyzed with centers representing the unit of analysis. Of 16 309 patients with full disclosure of outcome data, 10 488 (median, 70.0%; interquartile range, 57.7% to 75.4%) became asymptomatic without antiarrhythmic drugs and another 2047 (10.0%; 0.5% to 17.1%) became asymptomatic in the presence of previously ineffective antiarrhythmic drugs over 18 (range, 3 to 24) months of follow-up. Success rates free of antiarrhythmic drugs and overall success rates were significantly larger in 9590 patients with paroxysmal AF (74.9% and 83.2%) than in 2800 patients with persistent AF (64.8% and 75.0%) and 1108 patients with long-lasting AF (63.1% and 72.3%) (P<0.0001). Major complications were reported in 741 patients (4.5%).

Conclusions— When analyzed in a large number of electrophysiology laboratories worldwide, catheter ablation of AF shows to be effective in 80% of patients after 1.3 procedures per patient, with 70% of them not requiring further antiarrhythmic drugs during intermediate follow-up.

  G Klein , B Lindner , W Brabetz , H Brade and S. Raina
 

To elucidate the minimal lipopolysaccharide (LPS) structure needed for the viability of Escherichia coli, suppressor-free strains lacking either the 3-deoxy-d-manno-oct-2-ulosonic acid transferase waaA gene or derivatives of the heptosyltransferase I waaC deletion with lack of one or all late acyltransferases (lpxL/M/P) and/or various outer membrane biogenesis factors were constructed. (waaC lpxL lpxM lpxP) and waaA mutants exhibited highly attenuated growth, whereas simultaneous deletion of waaC and surA was lethal. Analyses of LPS of suppressor-free waaA mutants grown at 21 °C, besides showing accumulation of free lipid IVA precursor, also revealed the presence of its pentaacylated and hexaacylated derivatives, indicating in vivo late acylation can occur without Kdo. In contrast, LPS of (waaC lpxL lpxM lpxP) strains showed primarily Kdo2-lipid IVA, indicating that these minimal LPS structures are sufficient to support growth of E. coli under slow-growth conditions at 21/23 °C. These lipid IVA derivatives could be modified biosynthetically by phosphoethanolamine, but not by 4-amino-4-deoxy-l-arabinose, indicating export defects of such minimal LPS. waaA and (waaC lpxL lpxM lpxP) exhibited cell-division defects with a decrease in the levels of FtsZ and OMP-folding factor PpiD. These mutations led to strong constitutive additive induction of envelope responsive CpxR/A and E signal transduction pathways. (lpxL lpxM lpxP) mutant, with intact waaC, synthesized tetraacylated lipid A and constitutively incorporated a third Kdo in growth medium inducing synthesis of P-EtN and l-Ara4N. Overexpression of msbA restored growth of (lpxL lpxM lpxP) under fast-growing conditions, but only partially that of the (waaC lpxL lpxM lpxP) mutant. This suppression could be alleviated by overexpression of certain mutant msbA alleles or the single-copy chromosomal MsbA-498V variant in the vicinity of Walker-box II.

 
 
 
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