@inproceedings{ScharhagHotzkowKopinskietal.2012,
  author    = {Scharhag, J{\"u}rgen and Hotzkow, Kristin and Kopinski, Stephan and Barche, Martin and Mayer, Frank},
  title     = {Echocardiographic 3d speckle tracking values on cardiac wall motion in elite adult, adolescent and pediatric athletes},
  series = {Medicine and science in sports and exercise : official journal of the American College of Sports Medicine},
  volume    = {44},
  booktitle = {Medicine and science in sports and exercise : official journal of the American College of Sports Medicine},
  publisher = {Lippincott Williams \& Wilkins},
  address   = {Philadelphia},
  issn      = {0195-9131},
  pages     = {241 -- 241},
  year      = {2012},
  language  = {en}
}
@inproceedings{IntziegianniCasselMuelleretal.2012,
  author    = {Intziegianni, Konstantina and Cassel, Michael and M{\"u}ller, Steffen and Mayer, Frank},
  title     = {Ultrasound evaluation of the patellar tendon cross-sectional area and its relation to maximum force},
  series = {Medicine and science in sports and exercise : official journal of the American College of Sports Medicine},
  volume    = {44},
  booktitle = {Medicine and science in sports and exercise : official journal of the American College of Sports Medicine},
  publisher = {Lippincott Williams \& Wilkins},
  address   = {Philadelphia},
  issn      = {0195-9131},
  pages     = {714 -- 714},
  year      = {2012},
  language  = {en}
}
@article{DorenkampBonaventuraSohnsetal.2012,
  author    = {Dorenkamp, Marc and Bonaventura, Klaus and Sohns, Christian and Becker, Christoph R. and Leber, Alexander W.},
  title     = {Direct costs and cost-effectiveness of dual-source computed tomography and invasive coronary angiography in patients with an intermediate pretest likelihood for coronary artery disease},
  series = {Heart},
  volume    = {98},
  journal   = {Heart},
  number    = {6},
  publisher = {BMJ Publ. Group},
  address   = {London},
  issn      = {1355-6037},
  doi       = {10.1136/heartjnl-2011-300149},
  pages     = {460 -- 467},
  year      = {2012},
  abstract  = {Aims The study aims to determine the direct costs and comparative cost-effectiveness of latest-generation dual-source computed tomography (DSCT) and invasive coronary angiography for diagnosing coronary artery disease (CAD) in patients suspected of having this disease. Methods The study was based on a previously elaborated cohort with an intermediate pretest likelihood for CAD and on complementary clinical data. Cost calculations were based on a detailed analysis of direct costs, and generally accepted accounting principles were applied. Based on Bayes' theorem, a mathematical model was used to compare the cost-effectiveness of both diagnostic approaches. Total costs included direct costs, induced costs and costs of complications. Effectiveness was defined as the ability of a diagnostic test to accurately identify a patient with CAD. Results Direct costs amounted to (sic)98.60 for DSCT and to (sic)317.75 for invasive coronary angiography. Analysis of model calculations indicated that cost-effectiveness grew hyperbolically with increasing prevalence of CAD. Given the prevalence of CAD in the study cohort (24\%), DSCT was found to be more cost-effective than invasive coronary angiography ((sic)970 vs (sic)1354 for one patient correctly diagnosed as having CAD). At a disease prevalence of 49\%, DSCT and invasive angiography were equally effective with costs of (sic)633. Above a threshold value of disease prevalence of 55\%, proceeding directly to invasive coronary angiography was more cost-effective than DSCT. Conclusions With proper patient selection and consideration of disease prevalence, DSCT coronary angiography is cost-effective for diagnosing CAD in patients with an intermediate pretest likelihood for it. However, the range of eligible patients may be smaller than previously reported.},
  language  = {en}
}
@article{LuethNeuberKleuser2012,
  author    = {L{\"u}th, Anja and Neuber, Corinna and Kleuser, Burkhard},
  title     = {Novel methods for the quantification of (2E)-hexadecenal by liquid chromatography with detection by either ESI QTOF tandem mass spectrometry or fluorescence measurement},
  series = {Analytica chimica acta : an international journal devoted to all branches of analytical chemistry},
  volume    = {722},
  journal   = {Analytica chimica acta : an international journal devoted to all branches of analytical chemistry},
  publisher = {Elsevier},
  address   = {Amsterdam},
  issn      = {0003-2670},
  doi       = {10.1016/j.aca.2012.01.063},
  pages     = {70 -- 79},
  year      = {2012},
  abstract  = {Sphingosine-1-phosphate lyase (SPL) is the only known enzyme that irreversibly cleaves sphingosine-1-phosphate (S1P) into phosphoethanolamine and (2E)-hexadecenal during the final step of sphingolipid catabolism. Because S1P is involved in a wide range of physiological and diseased processes, determining the activity of the degrading enzyme is of great interest. Therefore, we developed two procedures based on liquid chromatography (LC) for analysing (2E)-hexadecenal, which is one of the two S1P degradation products. After separation, two different quantification methods were performed, tandem mass spectrometry (MS) and fluorescence detection. However, (2E)-hexadecenal as a long-chain aldehyde is not ionisable by electrospray ionisation (ESI) for MS quantification and has an insufficient number of corresponding double bonds for fluorescence detection. Therefore, we investigated 2-diphenylacetyl-1,3-indandione-1-hydrazone (DAIH) as a derivatisation reagent. DAIH transforms the aldehyde into an ionisable and fluorescent analogue for quantitative analysis. Our conditions were optimised to obtain the outstanding limit of detection (LOD) of 1 fmol per sample (30 mu L) for LC-MS/MS and 0.75 pmol per sample (200 mu l) for LC determination with fluorescence detection. We developed an extraction procedure to separate and concentrate (2E)-hexadecenal from biological samples for these measurements. To confirm our new methods, we analysed the (2E)-hexadecenal level of different cell lines and human plasma for the first time ever. Furthermore, we treated HT-29 cells with different concentrations of 4-deoxypyridoxine (DOP), which competitively inhibits pyridoxal-5-phosphate (P5P), an essential cofactor for SPL activity, and observed a significant decrease in (2E)-hexadecenal relative to the untreated cells.},
  language  = {en}
}
@article{HenkelFredeSchanzeetal.2012,
  author    = {Henkel, Janin and Frede, Katja and Schanze, Nancy and Vogel, Heike and Sch{\"u}rmann, Annette and Spruß, Astrid and Bergheim, Ina and P{\"u}schel, Gerhard Paul},
  title     = {Stimulation of fat accumulation in hepatocytes by PGE(2)-dependent repression of hepatic lipolysis, beta-oxidation and VLDL-synthesis},
  series = {Laboratory investigation : the basic and translational pathology research journal ; an official journal of the United States and Canadian Academy of Pathology},
  volume    = {92},
  journal   = {Laboratory investigation : the basic and translational pathology research journal ; an official journal of the United States and Canadian Academy of Pathology},
  number    = {11},
  publisher = {Nature Publ. Group},
  address   = {New York},
  issn      = {0023-6837},
  doi       = {10.1038/labinvest.2012.128},
  pages     = {1597 -- 1606},
  year      = {2012},
  abstract  = {Hepatic steatosis is recognized as hepatic presentation of the metabolic syndrome. Hyperinsulinaemia, which shifts fatty acid oxidation to de novo lipogenesis and lipid storage in the liver, appears to be a principal elicitor particularly in the early stages of disease development. The impact of PGE(2), which has previously been shown to attenuate insulin signaling and hence might reduce insulin-dependent lipid accumulation, on insulin-induced steatosis of hepatocytes was studied. The PGE(2)-generating capacity was enhanced in various obese mouse models by the induction of cyclooxygenase 2 and microsomal prostaglandin E-synthases (mPGES1, mPGES2). PGE(2) attenuated the insulin-dependent induction of SREBP-1c and its target genes glucokinase and fatty acid synthase. Nevertheless, PGE(2) enhanced incorporation of glucose into hepatic triglycerides synergistically with insulin. This was most likely due to a combination of a PGE(2)-dependent repression of (1) the key lipolytic enzyme adipose triglyceride lipase, (2) carnitine-palmitoyltransferase 1, a key regulator of mitochondrial beta-oxidation, and (3) microsomal transfer protein, as well as (4) apolipoprotein B, key components of the VLDL synthesis. Repression of PGC1 alpha, a common upstream regulator of these genes, was identified as a possible cause. In support of this hypothesis, overexpression of PGC1 alpha completely blunted the PGE(2)-dependent fat accumulation. PGE(2) enhanced lipid accumulation synergistically with insulin, despite attenuating insulin signaling and might thus contribute to the development of hepatic steatosis. Induction of enzymes involved in PGE(2) synthesis in in vivo models of obesity imply a potential role of prostanoids in the development of NAFLD and NASH. Laboratory Investigation (2012) 92, 1597-1606; doi:10.1038/labinvest.2012.128; published online 10 September 2012},
  language  = {en}
}
@article{HesseJaschkeKanzleiteretal.2012,
  author    = {Hesse, Deike and Jaschke, Alexander and Kanzleiter, Timo and Witte, Nicole and Augustin, Robert and Hommel, Angela and P{\"u}schel, Gerhard Paul and Petzke, Klaus-J{\"u}rgen and Joost, Hans-Georg and Schupp, Michael and Sch{\"u}rmann, Annette},
  title     = {GTPase ARFRP1 is essential for normal hepatic glycogen storage and insulin-like growth factor 1 secretion},
  series = {Molecular and cellular biology},
  volume    = {32},
  journal   = {Molecular and cellular biology},
  number    = {21},
  publisher = {American Society for Microbiology},
  address   = {Washington},
  issn      = {0270-7306},
  doi       = {10.1128/MCB.00522-12},
  pages     = {4363 -- 4374},
  year      = {2012},
  abstract  = {The GTPase ADP-ribosylation factor-related protein 1 (ARFRP1) is located at the trans-Golgi compartment and regulates the recruitment of Arf-like 1 (ARL1) and its effector golgin-245 to this compartment. Here, we show that liver-specific knockout of Arfrp1 in the mouse (Arfrp1(liv-/-)) resulted in early growth retardation, which was associated with reduced hepatic insulin-like growth factor 1 (IGF1) secretion. Accordingly, suppression of Arfrp1 in primary hepatocytes resulted in a significant reduction of IGF1 release. However, the hepatic secretion of IGF-binding protein 2 (IGFBP2) was not affected in the absence of ARFRP1. In addition, Arfrp1(liv-/-) mice exhibited decreased glucose transport into the liver, leading to a 50\% reduction of glycogen stores as well as a marked retardation of glycogen storage after fasting and refeeding. These abnormalities in glucose metabolism were attributable to reduced protein levels and intracellular retention of the glucose transporter GLUT2 in Arfrp1(liv-/-) livers. As a consequence of impaired glucose uptake into the liver, the expression levels of carbohydrate response element binding protein (ChREBP), a transcription factor regulated by glucose concentration, and its target genes (glucokinase and pyruvate kinase) were markedly reduced. Our data indicate that ARFRP1 in the liver is involved in the regulation of IGF1 secretion and GLUT2 sorting and is thereby essential for normal growth and glycogen storage.},
  language  = {en}
}
@article{IkramFornageSmithetal.2012,
  author    = {Ikram, M. Arfan and Fornage, Myriam and Smith, Albert V. and Seshadri, Sudha and Schmidt, Reinhold and Debette, Stephanie and Vrooman, Henri A. and Sigurdsson, Sigurdur and Ropele, Stefan and Taal, H. Rob and Mook-Kanamori, Dennis O. and Coker, Laura H. and Longstreth, W. T. and Niessen, Wiro J. and DeStefano, Anita L. and Beiser, Alexa and Zijdenbos, Alex P. and Struchalin, Maksim and Jack, Clifford R. and Rivadeneira, Fernando and Uitterlinden, Andre G. and Knopman, David S. and Hartikainen, Anna-Liisa and Pennell, Craig E. and Thiering, Elisabeth and Steegers, Eric A. P. and Hakonarson, Hakon and Heinrich, Joachim and Palmer, Lyle J. and Jarvelin, Marjo-Riitta and McCarthy, Mark I. and Grant, Struan F. A. and St Pourcain, Beate and Timpson, Nicholas J. and Smith, George Davey and Sovio, Ulla and Nalls, Mike A. and Au, Rhoda and Hofman, Albert and Gudnason, Haukur and van der Lugt, Aad and Harris, Tamara B. and Meeks, William M. and Vernooij, Meike W. and van Buchem, Mark A. and Catellier, Diane and Jaddoe, Vincent W. V. and Gudnason, Vilmundur and Windham, B. Gwen and Wolf, Philip A. and van Duijn, Cornelia M. and Mosley, Thomas H. and Schmidt, Helena and Launer, Lenore J. and Breteler, Monique M. B. and DeCarli, Charles and Adair, Linda S. and Ang, Wei and Atalay, Mustafa and vanBeijsterveldt, Toos and Bergen, Nienke and Benke, Kelly and Berry, Diane J. and Coin, Lachlan and Davis, Oliver S. P. and Elliott, Paul and Flexeder, Claudia and Frayling, Tim and Gaillard, Romy and Groen-Blokhuis, Maria and Goh, Liang-Kee and Haworth, Claire M. A. and Hadley, Dexter and Hebebrand, Johannes and Hinney, Anke and Hirschhorn, Joel N. and Holloway, John W. and Holst, Claus and Hottenga, Jouke Jan and Horikoshi, Momoko and Huikari, Ville and Hypponen, Elina and Kilpelainen, Tuomas O. and Kirin, Mirna and Kowgier, Matthew and Lakka, Hanna-Maaria and Lange, Leslie A. and Lawlor, Debbie A. and Lehtimaki, Terho and Lewin, Alex and Lindgren, Cecilia and Lindi, Virpi and Maggi, Reedik and Marsh, Julie and Middeldorp, Christel and Millwood, Iona and Murray, Jeffrey C. and Nivard, Michel and Nohr, Ellen Aagaard and Ntalla, Ioanna and Oken, Emily and Panoutsopoulou, Kalliope and Pararajasingham, Jennifer and Rodriguez, Alina and Salem, Rany M. and Sebert, Sylvain and Siitonen, Niina and Strachan, David P. and Teo, Yik-Ying and Valcarcel, Beatriz and Willemsen, Gonneke and Zeggini, Eleftheria and Boomsma, Dorret I. and Cooper, Cyrus and Gillman, Matthew and Hocher, Berthold and Lakka, Timo A. and Mohlke, Karen L. and Dedoussis, George V. and Ong, Ken K. and Pearson, Ewan R. and Price, Thomas S. and Power, Chris and Raitakari, Olli T. and Saw, Seang-Mei and Scherag, Andre and Simell, Olli and Sorensen, Thorkild I. A. and Wilson, James F.},
  title     = {Common variants at 6q22 and 17q21 are associated with intracranial volume},
  series = {Nature genetics},
  volume    = {44},
  journal   = {Nature genetics},
  number    = {5},
  publisher = {Nature Publ. Group},
  address   = {New York},
  organization    = {Early Growth Genetics EGG Consorti, Cohorts Heart Aging Res Genomic Ep},
  issn      = {1061-4036},
  doi       = {10.1038/ng.2245},
  pages     = {539 -- +},
  year      = {2012},
  abstract  = {During aging, intracranial volume remains unchanged and represents maximally attained brain size, while various interacting biological phenomena lead to brain volume loss. Consequently, intracranial volume and brain volume in late life reflect different genetic influences. Our genome-wide association study (GWAS) in 8,175 community-dwelling elderly persons did not reveal any associations at genome-wide significance (P < 5 x 10(-8)) for brain volume. In contrast, intracranial volume was significantly associated with two loci: rs4273712 (P = 3.4 x 10(-11)), a known height-associated locus on chromosome 6q22, and rs9915547 (P = 1.5 x 10(-12)), localized to the inversion on chromosome 17q21. We replicated the associations of these loci with intracranial volume in a separate sample of 1,752 elderly persons (P = 1.1 x 10(-3) for 6q22 and 1.2 x 10(-3) for 17q21). Furthermore, we also found suggestive associations of the 17q21 locus with head circumference in 10,768 children (mean age of 14.5 months). Our data identify two loci associated with head size, with the inversion at 17q21 also likely to be involved in attaining maximal brain size.},
  language  = {en}
}
@article{LiWangChenetal.2012,
  author    = {Li, Jian and Wang, Zi-Neng and Chen, You-Peng and Dong, Yun-Peng and Shuai, Han-Lin and Xiao, Xiao-Min and Reichetzeder, Christoph and Hocher, Berthold},
  title     = {Late gestational maternal serum cortisol is inversely associated with fetal brain growth},
  series = {Neuroscience \& biobehavioral reviews : official journal of the International Behavioral Neuroscience Society},
  volume    = {36},
  journal   = {Neuroscience \& biobehavioral reviews : official journal of the International Behavioral Neuroscience Society},
  number    = {3},
  publisher = {Elsevier},
  address   = {Oxford},
  issn      = {0149-7634},
  doi       = {10.1016/j.neubiorev.2011.12.006},
  pages     = {1085 -- 1092},
  year      = {2012},
  abstract  = {To analyze the association between fetal brain growth and late gestational blood serum cortisol in normal pregnancy.Blood total cortisol was quantified at delivery in 432 Chinese mother/child pairs. Key inclusion criteria of the cohort were: no structural anomalies of the newborn, singleton pregnancy, no alcohol abuse, no drug abuse or history of smoking no hypertensive disorders and no impairment of glucose tolerance and no use of steroid medication during pregnancy. Differential ultrasound examination of the fetal body was done in early (gestational day 89.95 +/- 7.31), middle (gestational day 160.17 16.12) and late pregnancy (gestational day 268.89 +/- 12.42). Newborn's cortisol was not correlated with any of the ultrasound measurements during pregnancy nor with birth weight. Multivariable regression analysis, considering timing of the ultrasound examination, the child's sex, maternal BMI, maternal age, maternal body weight at delivery, the timing of cortisol measurement and maternal uterine contraction states, revealed that maternal serum total cortisol was significantly negative correlated with ultrasound parameters describing the fetal brain: late biparietal diameter (R-2 =0.512, p =0.009), late head circumference (R-2 = 0.498, p= 0.001), middle biparietal diameter (R-2= 0.819, p = 0.013), middle cerebellum transverse diameter R-2 = 0.76, p= 0.014) and early biparietal diameter(R-2 = 0.819, p = 0.013). The same analysis revealed that birth weight as well as ultrasound parameters such as abdominal circumference and femur length were not correlated to maternal cortisol levels. In conclusion, our study demonstrates that maternal cortisol secretion within physiological ranges may be inversely correlated to fetal brain growth but not to birth weight. It remains to be demonstrated whether maternal cortisol secretion negatively influencing fetal brain growth translates to adverse neurological outcomes in later life.},
  language  = {en}
}
@article{RailaEnjalbertMothesetal.2012,
  author    = {Raila, Jens and Enjalbert, Francis and Mothes, Ralf and Hurtienne, Andrea and Schweigert, Florian J.},
  title     = {Validation of a new point-of-care assay for determination of ss-carotene concentration in bovine whole blood and plasma},
  series = {Veterinary clinical pathology},
  volume    = {41},
  journal   = {Veterinary clinical pathology},
  number    = {1},
  publisher = {Wiley-Blackwell},
  address   = {Malden},
  issn      = {0275-6382},
  doi       = {10.1111/j.1939-165X.2012.00400.x},
  pages     = {119 -- 122},
  year      = {2012},
  abstract  = {Background: beta-Carotene is an important precursor of vitamin A, and is associated with bovine fertility. beta-Carotene concentrations in plasma are used to optimize beta-carotene supplementation in cattle, but measurement requires specialized equipment to separate plasma and extract and measure beta-carotene, either using spectrophotometry or high performance liquid chromatography (HPLC). Objective: The objective of this study was to validate a new 2-step point-of-care (POC) assay for measuring beta-carotene in whole blood and plasma. Methods: beta-carotene concentrations in plasma from 166 cows were measured using HPLC and compared with results obtained using a POC assay, the iCheck-iEx-Carotene test kit. Whole blood samples from 23 of these cattle were also evaluated using the POC assay and compared with HPLC-plasma results from the same 23 animals. The POC assay includes an extraction vial (iEx Carotene) and hand-held photometer (iCheck Carotene). Results: Concentrations of beta-carotene in plasma measured using the POC assay ranged from 0.40 to 15.84 mg/L (n = 166). No differences were observed between methods for assay of plasma (mean +/- SD; n = 166): HPLC-plasma 4.23 +/- 2.35 mg/L; POC-plasma 4.49 +/- 2.36 mg/L. Similar good agreement was found when plasma analyzed using HPLC was compared with whole blood analyzed using the POC system (n = 23): HPLC-plasma 3.46 +/- 2.12 mg/L; POC-whole blood 3.67 +/- 2.29 mg/L. Conclusions: Concentrations of beta-carotene can be measured in blood and plasma from cattle easily and rapidly using a POC assay, and results are comparable to those obtained by the highly sophisticated HPLC method. Immediate feedback regarding beta-carotene deficiency facilitates rapid and appropriate optimization of beta-carotene supplementation in feed.},
  language  = {en}
}
@article{Schneider2012,
  author    = {Schneider, Birgit},
  title     = {Climate model simulation visualization from a visual studies perspective},
  series = {Wiley interdisciplinary reviews : Climate change},
  volume    = {3},
  journal   = {Wiley interdisciplinary reviews : Climate change},
  number    = {2},
  publisher = {Wiley},
  address   = {Malden},
  issn      = {1757-7780},
  doi       = {10.1002/wcc.162},
  pages     = {185 -- 193},
  year      = {2012},
  abstract  = {The article gives an overview on the visualization of climate model data simulation from a visual studies perspective. On one hand the question is raised of what it means culturally when global images are used to communicate scenarios of a changing climate future beyond the field of climate research itself. The product of this process is one of the most widespread icons of climate change, the image of the blue planet that has turned red. On the other hand insights into how these visualizations are designed in the studio of a computer designer are given. The focus here is on the way in which specific visualization software shapes images of a changing global climate. The article takes as its starting point the perspective of visual and media studies, because images have become so crucial in communicating research results of climate science and convincing policy agents and the public. What is special about scientific images depicting climate change is that they have implicitly also become political images. As today various actors and recipient groups are making use of pictures depicting climate change, the article concerns climate science, media studies, computer visualization, cultural studies, and politics alike.},
  language  = {en}
}