281 research outputs found
bruder · C · von Hakenberch / Maiſter datz Meurperg - 1293 September 27.
No full textBruder C[onrad] von Hakenberg, Meister des Johanniterhauses in Meuerberg, beurkundet, daß er für das Haus Meuerberg eine Hofstätte in Radendorf aus dem Besitz des Klosters Ebersberg als Burgrecht gekauft hat. Meuerberg muß daraus an das Kloster alljährlich 60 Pfennige, als Vogtrecht 9 Pfennige und für einen Schnitter 3 Pfennige abführen. Versäumt Meuerberg diese Abgaben, so soll das Kloster ihm gegenüber rechtlich genauso verfügen können wie über ihren anderen Besitz, der ebensoviel in Radendorf zinst. --{'name': 'BAdW', 'uri': 'badw.png'
Levosimendan improves diastolic and systolic function in failing human myocardium
No full textCa2+-sensitizers increase myocardial contractility, but may worsen diastolic dysfunction. Levosimendan, through its unique troponin-C interaction, may preserve diastolic function. We investigated the effects of levosimendan (10(-7)-10(-5) M) on diastolic and systolic function in multicellular cardiac muscle preparations from end-stage failing human hearts (1 and 2.5 Hz, 37 degrees C, 1.25 mM [Ca2+], pH 7.4). Levosimendan improved systolic function: at 1 Hz, developed force (F-dev) increased from 13.84 +/- 3.27 to 16.40 +/- 3.57 (10(-7) M, P < 0.05), while diastolic force (F-dia) decreased from 5.32 +/- 0.67 to 4.94 +/- 0.61 mN/mm(2) (P < 0.05). Under control conditions, the increase in stimulation frequency from 1 to 2.5 Hz resulted in a decrease in F-dev of - 0.51 +/- 1.80 mN/mm(2) (negative force-frequency relationship). Levosimendan improved this relationship: at 10-7 M, this change became positive (+1.81 +/- 2.06 mN/mm(2), P < 0.05). Diastolic function was markedly improved in the presence of levosimendan; the increase in F-dia of 1.56 +/- 0.41 mN/mm(2) (control) was attenuated to 0.70 +/- 0.19 nN/mm(2) (P < 0.05). To allow for a more derailed analysis, preparations were sometimes divided into two groups, based on their force-frequency behavior. Twitch timing parameters were accelerated by levosimendan in preparations with a negative force-frequency relationship. Levosimendan improves both systolic and diastolic function in failing human myocardium. Effects are even more pronounced at higher heart rates and under prevailing diastolic dysfunction. (C) 2000 Elsevier Science B.V. All rights reserved
Microsomal triglyceride transfer protein polymorphism (-493G/T) is associated with hepatic steatosis in patients with chronic hepatitis C
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Liver microsomal triglyceride transfer protein is involved in hepatitis C liver steatosis
No full textBACKGROUND & AIMS: Hepatic steatosis is frequent in chronic hepatitis C. Several mechanisms might be implicated, including metabolic cofactors and direct viral effects on intracellular lipid pathways. In a transgenic mouse model, hepatitis C virus (HCV) was shown to inhibit microsomal triglyceride transfer protein (MTP) activity, which is essential for hepatic lipoprotein assembly and secretion. No data are available on liver MTP activity in HCV-infected patients. We therefore investigated liver MTP gene expression and its lipid transfer activity in untreated cases infected with the major HCV genotypes showing variable degrees of hepatic steatosis.
METHODS: MTP messenger RNA (mRNA) levels were measured by real-time polymerase chain reaction, and MTP activity was assessed by fluorescent assay in liver biopsy specimens of 58 HCV-positive patients. A set of metabolic and serum lipid markers was also measured at the time of liver biopsies.
RESULTS: MTP mRNA levels showed a statistically significant (P = .001) inverse correlation with the degree of steatosis, independently of the HCV genotype. MTP mRNA levels also had an inverse correlation with serum insulin (P = .0002), homeostasis model assessment-insulin resistance (HOMA-IR) (P = .005), and body mass index (P = .02) in patients with HCV-1 and HCV-2 and with serum HCV-RNA (P = .02) in HCV-3 patients. Liver MTP-specific activity was significantly reduced in HCV-3 patients compared with those with other HCV genotypes (P = .004) and correlated with reduced serum cholesterol, apo B, and low-density lipoproteins.
CONCLUSIONS: MTP may play a central role in HCV-related steatosis, being modulated by different genotype-specific mechanisms, mainly hyperinsulinemia in non-HCV-3 patients, and more profound and direct virus-related effects in HCV-3-infected individuals
Liver microsomal triglyceride transfer protein is involved in hepatitis C related liver steatosis
No full textGenealogy of the Van Winkle Family, Account of its Origin and Settlement in this Country, with Data 1630-1913: Van Winkle Record
No full text300 page genealogical listing of Van Winkle family in America, with name index, compiled by Jersey City historian David Van Winkle. Entries list only birth, death and marriage information, without locations, but narrative sections suggest bulk of entries are in Hudson and Bergen Counties, NJ, and later in Kentucky.
Introductory sections describe history of Dutch settlement in America, and homes and customs in Bergen, the Dutch village that became a part of Jersey City. Narrative of Jacob Wallingen and his life in the village of Winkel, Netherlands and his settlement in New Netherlands where he married Trintje Jacobs. Their descendants make up the subsequent list
Influence of pyruvate on economy of contraction in isolated rabbit myocardium
No full textBackground: Treatment of acute heart failure frequently requires positive-inotropic stimulation. However, there is still no inotropic agent available, which combines a favourable haemodynamic profile with low expenditure for energy metabolism. Pyruvate exhibits positive inotropic effects in vitro and in patients with heart failure. The effect on myocardial energy metabolism however remains unclear, but is meaningful in light of a clinical application. Aims and methods: We investigated the influence of pyruvate on contractility and oxygen consumption in isolated isometric contracting rabbit myocardium compared to P-adrenergic stimulation with isoproterenol. Results: Pyruvate (30 mM) increased developed force from 18.7 +/- 4.1 to50.8 +/- 12.1 mN/mm(2) (n= 10,p < 0.01). Force-time integral (FTI) increased by 329%, oxygen consumption assessed by diffusion-microclectrode technique increased from 2.86 +/- 0.30 mlO(2)/min 100 g to 6.28 +/- 1.28 mlO(2)/ min 100g(n=7,p < 0.05). Economy of myocardial contraction calculated as the ratio of total FTI to oxygen consumption remained unchanged. In contrast, while isoproterenol (10 mu M) produced a comparable increase in developed force from 21.4 +/- 8.3 to 67.3 +/- 15 mN/mm(2) (n=7,p < 0.01),FTI increased only by 260% and MVO2 increased from 2.96 +/- 0.43 to 6.12 +/- 1.01 mlO(2)/min 100 g (n=7,p < 0.01); thus, economy decreased by 23% (n=7,p < 0.05). Conclusion: Pyruvate does not impair economy of myocardial contraction while isoproterenol decreases economy. Regarding energy expenditure, pyruvate appears superior to isoproterenol for the purpose of positive inotropic stimulation. (c) 2007 European Society of Cardiology. Published by Elsevier B.V. All rights reserved
DEPDC5 variants increase fibrosis progression in Europeans with chronic hepatitis C virus infection
No full textChronic hepatitis C virus (HCV) infection may progress to cirrhosis and hepatocellular carcinoma (HCC). Recently, two genetic variants, DEPDC5 rs1012068 and MICA rs2596542, were associated with the onset of HCC in Asian subjects with chronic HCV infection. The aim of the present study was to analyze whether DEPDC5 and MICA genetic variants were associated with liver disease progression in European subjects with chronic HCV infection. In a Northern Italian discovery cohort (n = 477), neither DEPDC5 rs1012068 nor MICA rs2596542 were associated with HCC (n = 150). However, DEPDC5 rs1012068 was independently associated with cirrhosis (n = 300; P = 0.049). The association of rs1012068 with moderate to severe fibrosis was confirmed in an independent cross-sectional German cohort (n = 415; P = 0.006). Furthermore, DEPDC5 rs1012068 predicted faster fibrosis progression in a prospective cohort (n = 247; P = 0.027). Next, we examined the distribution of nonsynonymous DEPDC5 variants in the overall cross-sectional cohort (n = 912). The presence of at least one variant increased the risk of moderate/severe fibrosis by 54% (P = 0.040). To understand the molecular mechanism underlying the genetic association of DEPDC5 variants with fibrosis progression, we performed in vitro studies on immortalized hepatic stellate cells (LX-2). In these cells, down-regulation of DEPDC5 resulted in increased expression of β-catenin and production of its target matrix metallopeptidase 2 (MMP2), a secreted enzyme involved in fibrosis progression. Conclusion: DEPDC5 variants increase fibrosis progression in European subjects with chronic HCV infection. Our findings suggest that DEPDC5 down-regulation may contribute to HCV-related fibrosis by increasing MMP2 synthesis through the β-catenin pathway
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