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Institution

University of Tübingen

EducationTübingen, Germany
About: University of Tübingen is a education organization based out in Tübingen, Germany. It is known for research contribution in the topics: Population & Immune system. The organization has 40555 authors who have published 84108 publications receiving 3015320 citations. The organization is also known as: Eberhard Karls University & Eberhard-Karls-Universität Tübingen.


Papers
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Journal ArticleDOI
TL;DR: The data suggest that both adipocytokines are associated with central body fat distribution, and serum adiponectin concentrations are determined predominantly by the visceral fat compartment.
Abstract: Objective: We investigated whether serum concentrations of adiponectin are determined by body fat distribution and compared the findings with leptin. Research Methods and Procedures: Serum concentrations of adiponectin and leptin were measured by radioimmunoassay (n = 394) and analyzed for correlation with sex, age, and body fat distribution, i.e., waist-to-hip ratio, waist and hip circumference, and subcutaneous adipose tissue area of the lower leg as assessed by magnetic resonance imaging. Results: After adjusting for sex and percentage of body fat, adiponectin was negatively (r = −0.17, p < 0.001) and leptin was positively (r = 0.22, p < 0.001) correlated with waist-to-hip ratio. Leptin, but not adiponectin, correlated with both waist (r = 0.49, p < 0.001) and hip circumference (r = 0.46, p < 0.001). Furthermore, leptin, but not adiponectin, correlated with the proportion of subcutaneous fat of the lower leg cross-sectional area (r = 0.37, p < 0.001). Discussion: These data suggest that both adipocytokines are associated with central body fat distribution, and serum adiponectin concentrations are determined predominantly by the visceral fat compartment.

427 citations

Journal ArticleDOI
01 Nov 2003-Blood
TL;DR: Together, amoeboid shape change and contact guidance provide constitutive protease-independent mechanisms for leukocyte trafficking through interstitial tissues that are insensitive toward pharmacologic protease inhibitors.

425 citations

Journal ArticleDOI
TL;DR: The data suggest that Apx2 is a novel heat shock gene and that the enzymatic activity of APX2/APXS is required to compensate heat stress-dependent decline ofAPX1 activity in the cytosol.
Abstract: To find evidence for a connection between heat stress response, oxidative stress, and common stress tolerance, we studied the effects of elevated growth temperatures and heat stress on the activity and expression of ascorbate peroxidase (APX). We compared wild-type Arabidopsis with transgenic plants overexpressing heat shock transcription factor 3 (HSF3), which synthesize heat shock proteins and are improved in basal thermotolerance. Following heat stress, APX activity was positively affected in transgenic plants and correlated with a new thermostable isoform, APX(S). This enzyme was present in addition to thermolabile cytosolic APX1, the prevalent isoform in unstressed cells. In HSF3-transgenic plants, APX(S) activity was detectable at normal temperature and persisted after severe heat stress at 44 degrees C. In nontransgenic plants, APX(S) was undetectable at normal temperature, but could be induced by moderate heat stress. The mRNA expression profiles of known and three new Apx genes were determined using real-time PCR. Apx1 and Apx2 genes encoding cytosolic APX were heat stress and HSF dependently expressed, but only the representations of Apx2 mRNA met the criteria that suggest identity between APX(S) and APX2: not expressed at normal temperature in wild type, strong induction by heat stress, and HSF3-dependent expression in transgenic plants. Our data suggest that Apx2 is a novel heat shock gene and that the enzymatic activity of APX2/APX(S) is required to compensate heat stress-dependent decline of APX1 activity in the cytosol. The functional roles of modulations of APX expression and the interdependence of heat stress and oxidative stress response and signaling mechanisms are discussed.

425 citations

Journal ArticleDOI
28 Jan 2011-Science
TL;DR: The tool kit found at Jebel Faya has affinities to the late Middle Stone Age in northeast Africa, indicating that technological innovation was not necessary to facilitate migration into Arabia, and implies that AMH may have been present in South Asia before the Toba eruption.
Abstract: The timing of the dispersal of anatomically modern humans (AMH) out of Africa is a fundamental question in human evolutionary studies. Existing data suggest a rapid coastal exodus via the Indian Ocean rim around 60,000 years ago. We present evidence from Jebel Faya, United Arab Emirates, demonstrating human presence in eastern Arabia during the last interglacial. The tool kit found at Jebel Faya has affinities to the late Middle Stone Age in northeast Africa, indicating that technological innovation was not necessary to facilitate migration into Arabia. Instead, we propose that low eustatic sea level and increased rainfall during the transition between marine isotope stages 6 and 5 allowed humans to populate Arabia. This evidence implies that AMH may have been present in South Asia before the Toba eruption (1).

425 citations

Journal ArticleDOI
TL;DR: Knowing the biochemistry of this enzyme has potential implications for the treatment of various diseases and the understanding of the regulatory mechanisms underlying the expression and control of 5-LO activity is expanded.

425 citations


Authors

Showing all 41039 results

NameH-indexPapersCitations
John Q. Trojanowski2261467213948
Lily Yeh Jan16246773655
Monique M.B. Breteler15954693762
Wolfgang Wagner1562342123391
Thomas Meitinger155716108491
Hermann Brenner1511765145655
Amartya Sen149689141907
Bernhard Schölkopf1481092149492
Niels Birbaumer14283577853
Detlef Weigel14251684670
Peter Lang140113698592
Marco Colonna13951271166
António Amorim136147796519
Alexis Brice13587083466
Elias Campo13576185160
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Performance
Metrics
No. of papers from the Institution in previous years
YearPapers
2023206
2022854
20214,701
20204,480
20194,045
20183,634