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Search Results: 1 - 10 of 1324 matches for " Dietrich Matern "
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Carnitine Deficiency in OCTN2?/? Newborn Mice Leads to a Severe Gut and Immune Phenotype with Widespread Atrophy, Apoptosis and a Pro-Inflammatory Response
Srinivas Sonne, Prem S. Shekhawat, Dietrich Matern, Vadivel Ganapathy, Leszek Ignatowicz
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0047729
Abstract: We have investigated the gross, microscopic and molecular effects of carnitine deficiency in the neonatal gut using a mouse model with a loss-of-function mutation in the OCTN2 (SLC22A5) carnitine transporter. The tissue carnitine content of neonatal homozygous (OCTN2?/?) mouse small intestine was markedly reduced; the intestine displayed signs of stunted villous growth, early signs of inflammation, lymphocytic and macrophage infiltration and villous structure breakdown. Mitochondrial β-oxidation was active throughout the GI tract in wild type newborn mice as seen by expression of 6 key enzymes involved in β-oxidation of fatty acids and genes for these 6 enzymes were up-regulated in OCTN2?/? mice. There was increased apoptosis in gut samples from OCTN2?/? mice. OCTN2?/? mice developed a severe immune phenotype, where the thymus, spleen and lymph nodes became atrophied secondary to increased apoptosis. Carnitine deficiency led to increased expression of CD45-B220+ lymphocytes with increased production of basal and anti-CD3-stimulated pro-inflammatory cytokines in immune cells. Real-time PCR array analysis in OCTN2?/? mouse gut epithelium demonstrated down-regulation of TGF-β/BMP pathway genes. We conclude that carnitine plays a major role in neonatal OCTN2?/? mouse gut development and differentiation, and that severe carnitine deficiency leads to increased apoptosis of enterocytes, villous atrophy, inflammation and gut injury.
UGT1A1 sequence variants and bilirubin levels in early postnatal life: a quantitative approach
Neil A Hanchard, Jennifer Skierka, Amy Weaver, Brad S Karon, Dietrich Matern, Walter Cook, Dennis J O'Kane
BMC Medical Genetics , 2011, DOI: 10.1186/1471-2350-12-57
Abstract: We sequenced the exons, PBREM, 5'-, and 3'- regions of the UGT1A1 gene in 80 otherwise healthy term neonates who had repeat bilirubin levels measured within the first five days of life.Three novel coding variants were observed, but there was no clear relationship between rare coding variants and bilirubin rise. Adjusted linear regression models fit to evaluate the relationship between changing bilirubin levels and common UGT1A1variants found that among 39 neonates whose bilirubin was resampled within 33 hours, individuals homozygous for the mutant allele of a 3'UTR SNP had significantly smaller changes in bilirubin (P = 0.003) than individuals carrying the wild-type allele.Collectively, rare UGT1A1 coding variants do not appear to play a prominent role in determining early bilirubin levels; however common variants in the 3' UTR of UGT1A1 may modulate the early bilirubin rise. A quantitative approach to evaluating early bilirubin kinetics provides a more robust framework in which to better understand the genetics of neonatal hyperbilirubinemia.Neonatal hyperbilirubinemia affects 60% of full-term newborns and remains a significant cause of hospital re-admission in the first week of life [1,2]. With most newborns being discharged from hospital at 48 hours of life - a time when serum unconjugated bilirubin levels are still rising - the American Academy of Pediatrics has placed more emphasis on identifying infants at increased risk of developing significant hyperbilirubinemia [3]. These infants require closer follow-up to stave off the potentially devastating neurological effects of bilirubin encephalopathy.In practice, an otherwise healthy term newborn's risk for developing severe 'physiological' hyperbilirubinemia is largely a function of their bilirubin level at discharge. Bilirubin, when plotted on an hour-specific nomogram, often directs the need for future evaluation [4-6]. Among those identified as being at high or high-intermediate risk at discharge, however, onl
The presence of non-organ-specific autoantibodies is associated with a negative response to combination therapy with interferon and ribavirin for chronic hepatitis C
Hermann E Wasmuth, Christian Stolte, Andreas Geier, Christoph G Dietrich, Carsten Gartung, Johann Lorenzen, Siegfried Matern, Frank Lammert
BMC Infectious Diseases , 2004, DOI: 10.1186/1471-2334-4-4
Abstract: Anti-nuclear, anti-smooth muscle, anti-mitochondrial, anti-neutrophil-cytoplasmatic and anti-liver/kidney microsomal antibodies were determined in 78 consecutive anti-HCV positive patients by indirect immunofluorescence. The presence of these antibodies was related to demographic variables and to the outcome of antiviral combination therapy with interferon-α and ribavirin in 65 patients.In our study, positivity for autoantibodies was associated with higher alanine aminotransferase levels and higher mean values for HCV-RNA (p < 0.01). Furthermore, negativity for non-organ-specific autoantibodies was associated with a favourable treatment outcome of combination therapy with at least one negative RT-PCR for HCV-RNA during treatment (OR 4.65, 95% CI 1.31 to 16.48, p = 0.02). ANA and SMA staining patterns and titers were not correlated to treatment response. With multiple logistic regression analysis, positivity for autoantibodies and HCV genotype were independently associated with outcome of antiviral combination therapy (p = 0.02).The absence of non-organ-specific autoantibodies might indicate a significantly higher chance for viral clearance in response to combination therapy for chronic hepatitis C infection. Therefore, despite of an overall higher treatment response, the addition of the immunomodulatory drug ribavirin could accentuate immunological differences that affect treatment outcome and might have been less obvious in earlier studies analysing interferon monotherapy.Various immunological phenomena have been described in patients being exposed to the hepatitis C virus (HCV) [1]. Organ-specific and non-organ-specific autoantibodies are found in a considerable number of patients with acute and chronic hepatitis C [2]. Especially the high percentage of non-organ-specific autoantibodies (NOSA) in chronic infection has led to further investigation of the potential biological relevance of these findings. In recent studies the prevalence of different NOSA, including
L. Jaspers, C. Stevens, Arbeid en tewerkstelling in Oost-Vlaanderen op het einde van het ancien régime. Een socio-proffessionele en demografische analyse
J. Materné
BMGN : Low Countries Historical Review , 1988,
Medium-Chain Acyl-CoA Dehydrogenase Deficiency in Gene-Targeted Mice
Ravi J Tolwani,Doug A Hamm,Liqun Tian,J. Daniel Sharer,Jerry Vockley,Piero Rinaldo,Dietrich Matern,Trenton R Schoeb,Philip A Wood
PLOS Genetics , 2005, DOI: 10.1371/journal.pgen.0010023
Abstract: Medium-chain acyl-CoA dehydrogenase (MCAD) deficiency is the most common inherited disorder of mitochondrial fatty acid β-oxidation in humans. To better understand the pathogenesis of this disease, we developed a mouse model for MCAD deficiency (MCAD?/?) by gene targeting in embryonic stem (ES) cells. The MCAD?/? mice developed an organic aciduria and fatty liver, and showed profound cold intolerance at 4 °C with prior fasting. The sporadic cardiac lesions seen in MCAD?/? mice have not been reported in human MCAD patients. There was significant neonatal mortality of MCAD?/? pups demonstrating similarities to patterns of clinical episodes and mortality in MCAD-deficient patients. The MCAD-deficient mouse reproduced important aspects of human MCAD deficiency and is a valuable model for further analysis of the roles of fatty acid oxidation and pathogenesis of human diseases involving fatty acid oxidation.
Some Properties of Glutamate Dehydrogenase from the Marine Red Alga Gracilaria sordida (Harv.) W. Nelson
Matern SP Mtolera
Western Indian Ocean Journal of Marine Science , 2003,
TATN-1 Mutations Reveal a Novel Role for Tyrosine as a Metabolic Signal That Influences Developmental Decisions and Longevity in Caenorhabditis elegans
Annabel A. Ferguson,Sudipa Roy equal contributor,Kaitlyn N. Kormanik equal contributor,Yongsoon Kim equal contributor,Kathleen J. Dumas,Vladimir B. Ritov,Dietrich Matern,Patrick J. Hu,Alfred L. Fisher
PLOS Genetics , 2013, DOI: 10.1371/journal.pgen.1004020
Abstract: Recent work has identified changes in the metabolism of the aromatic amino acid tyrosine as a risk factor for diabetes and a contributor to the development of liver cancer. While these findings could suggest a role for tyrosine as a direct regulator of the behavior of cells and tissues, evidence for this model is currently lacking. Through the use of RNAi and genetic mutants, we identify tatn-1, which is the worm ortholog of tyrosine aminotransferase and catalyzes the first step of the conserved tyrosine degradation pathway, as a novel regulator of the dauer decision and modulator of the daf-2 insulin/IGF-1-like (IGFR) signaling pathway in Caenorhabditis elegans. Mutations affecting tatn-1 elevate tyrosine levels in the animal, and enhance the effects of mutations in genes that lie within the daf-2/insulin signaling pathway or are otherwise upstream of daf-16/FOXO on both dauer formation and worm longevity. These effects are mediated by elevated tyrosine levels as supplemental dietary tyrosine mimics the phenotypes produced by a tatn-1 mutation, and the effects still occur when the enzymes needed to convert tyrosine into catecholamine neurotransmitters are missing. The effects on dauer formation and lifespan require the aak-2/AMPK gene, and tatn-1 mutations increase phospho-AAK-2 levels. In contrast, the daf-16/FOXO transcription factor is only partially required for the effects on dauer formation and not required for increased longevity. We also find that the controlled metabolism of tyrosine by tatn-1 may function normally in dauer formation because the expression of the TATN-1 protein is regulated both by daf-2/IGFR signaling and also by the same dietary and environmental cues which influence dauer formation. Our findings point to a novel role for tyrosine as a developmental regulator and modulator of longevity, and support a model where elevated tyrosine levels play a causal role in the development of diabetes and cancer in people.
The marimba: musical and secret language of the political violence in Guatemala La marimba: lenguaje musical y secreto de la violencia política en Guatemala
América Latina Hoy , 2010,
Abstract: The author reflects the construction of national music while the arise of the nation State in Guatemala. This development begins formally while the first decades of the nineteenth century and has not finished yet. For the myth of the Nation state and those who use it for their project of domination it is crucial that national music can be distinguished externally from musics generated by other nations while it can be applied internally for the aim of national homogenisation. Since the middle of the nineteenth century the music is used in Guatemala for the dissemination of ideologies that help to construct this myth. The vernacular music of the Maya people does not follow this logic. Hence it is considered inferior or incorrect . For the myth of the nation State only the totality of the people as an abstract concept can understand and appreciate the national music, but not the concrete or individual group. Assuming this the music is converted into an important tool of a repressive mechanism and deculturation. The marimba thus is the symbol of the nation State in Guatemala. The dictatorships of the army, who were the main responsible of the genocide of the Maya people, declared the chromatic marimba symbol of the nation. After a long history of violence the marimba desindianizada and therefore ladinizada reached the status of the national instrument. While the period of violence the chromatic marimba never ceased to sound in the nightclubs and the elegant restaurants of the Capital. In the meanwhile the Mayas of the highlands hided their K’ojomes in caves and ca ons to protect them from the army. Therefore the anarchic and rebellious diversity of the k’ojom’s tuning continues to be the vernacular and secret language of groups and individuals who do not belong to the national reality of the chromatic marimba. El autor refleja la construcción de la música nacional en el proceso del devenir del Estado nacional guatemalteco. Este proceso comienza formalmente a principios del siglo XIX, pero no ha concluido aún. Para el mito del Estado nación y para aquellos que lo utilizan para su proyecto de dominación, es de importancia d
PpiD is a player in the network of periplasmic chaperones in Escherichia coli
Yvonne Matern, Birgitta Barion, Susanne Behrens-Kneip
BMC Microbiology , 2010, DOI: 10.1186/1471-2180-10-251
Abstract: The analysis of the effects of both deletion and overexpression of ppiD on cell envelope phenotypes revealed that PpiD in contrast to prior observations plays only a minor role, if any, in the maturation of OMPs and cannot compensate for the lack of SurA in the periplasm. On the other hand, our results show that overproduction of PpiD rescues a surA skp double mutant from lethality. In the presence of increased PpiD levels surA skp cells show reduced activities of both the SigmaE-dependent and the Cpx envelope stress responses, and contain increased amounts of folded species of the major OMP OmpA. These effects require the anchoring of PpiD in the inner membrane but are independent of its parvulin-like PPIase domain. Moreover, a PpiD protein lacking the PPIase domain also complements the growth defects of an fkpA ppiD surA triple PPIase mutant and exhibits chaperone activity in vitro. In addition, PpiD appears to collaborate with DegP, as deletion of ppiD confers a temperature-dependent conditional synthetic phenotype in a degP mutant.This study provides first direct evidence that PpiD functions as a chaperone and contributes to the network of periplasmic chaperone activities without being specifically involved in OMP maturation. Consistent with previous work, our data support a model in which the chaperone function of PpiD is used to aid in the early periplasmic folding of many newly translocated proteins.It is well established that numerous chaperones, folding catalysts and proteases exist in the periplasm of E. coli and cooperate in protein folding and protein quality control in this cellular compartment of the cell. At least three of these factors, SurA, Skp and DegP, assist in the maturation of integral β-barrel outer membrane proteins (OMPs), a major class of proteins in the E. coli outer membrane, and are thought to be responsible for the transport of OMP folding intermediates through the periplasm to the OMP assembly site, a multi-protein complex in the oute
Chirurgisches Geschicklichkeitstraining in der Medizinischen Basisausbildung []
Schneider, Joachim H.,Kowalsky, Dominik,K?nigsrainer, Alfred,Matern, Ulrich
GMS Zeitschrift für Medizinische Ausbildung , 2007,
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