Heidelberg University

About: Heidelberg University is a education organization based out in Heidelberg, Germany. It is known for research contribution in the topics: Population & Transplantation. The organization has 62066 authors who have published 119109 publications receiving 4678423 citations. The organization is also known as: Ruprecht-Karls-Universität Heidelberg & University of Heidelberg.

Nongenomic actions of steroid hormones

Abstract: Steroid hormones modulate many physiological processes. The effects of steroids that are mediated by the modulation of gene expression are known to occur with a time lag of hours or even days. Research that has been carried out mainly in the past decade has identified other responses to steroids that are much more rapid and take place in seconds or minutes. These responses follow nongenomic pathways, and they are not rare.

The neurobiology of itch

Abstract: Itch and pain are distinct sensations processed by different but overlapping neural pathways. Ikomaet al. review recent evidence on the molecular mechanisms that underlie itch sensation, highlighting the complex interaction with pain processing, and discuss the therapeutic implications. The neurobiology of itch, which is formally known as pruritus, and its interaction with pain have been illustrated by the complexity of specific mediators, itch-related neuronal pathways and the central processing of itch. Scratch-induced pain can abolish itch, and analgesic opioids can generate itch, which indicates an antagonistic interaction. However, recent data suggest that there is a broad overlap between pain- and itch-related peripheral mediators and/or receptors, and there are astonishingly similar mechanisms of neuronal sensitization in the PNS and the CNS. The antagonistic interaction between pain and itch is already exploited in pruritus therapy, and current research concentrates on the identification of common targets for future analgesic and antipruritic therapy.

Multi-component syntheses of heterocycles by transition-metal catalysis

Abstract: For a long time multi-component syntheses of heterocycles have undeniably been a domain of classical carbonyl condensation chemistry. However, the advent of transition-metal catalysis not only has fertilized strategies in heterocyclic synthesis by uni- and bimolecular transformations but the past decade has also witnessed a rapid development of transition-metal catalysis in new multi-component reactions (MCR). Expectedly, palladium catalyzed processes have received a dominant position, yet, other transition-metal complexes are catching up implying organometallic elementary steps that reach even further than cross-coupling and carbometallation. Besides domino MCRs that are purely based upon organometallic catalysis the sequential and consecutive combination with condensation, addition and cycloaddition steps opens a vast playground for the invention of new sequences in heterocyclic synthesis. This tutorial review outlines the underlying reaction based principles of transition-metal catalysis in multi-component syntheses of heterocycles, summarizes recent developments of palladium catalyzed MCR, and highlights the more recent contributions to MCR based heterocyclic synthesis by virtue of rhodium, ruthenium, and copper catalysis.

MPI-DING reference glasses for in situ microanalysis: New reference values for element concentrations and isotope ratios

Abstract: We present new analytical data of major and trace elements for the geological MPI-DING glasses KL2-G, ML3B-G, StHs6/80-G, GOR128-G, GOR132-G, BM90/21-G, T1-G, and ATHO-G. Different analytical methods were used to obtain a large spectrum of major and trace element data, in particular, EPMA, SIMS, LA-ICPMS, and isotope dilution by TIMS and ICPMS. Altogether, more than 60 qualified geochemical laboratories worldwide contributed to the analyses, allowing us to present new reference and information values and their uncertainties (at 95% confidence level) for up to 74 elements. We complied with the recommendations for the certification of geological reference materials by the International Association of Geoanalysts (IAG). The reference values were derived from the results of 16 independent techniques, including definitive (isotope dilution) and comparative bulk (e.g., INAA, ICPMS, SSMS) and microanalytical (e.g., LA-ICPMS, SIMS, EPMA) methods. Agreement between two or more independent methods and the use of definitive methods provided traceability to the fullest extent possible. We also present new and recently published data for the isotopic compositions of H, B, Li, O, Ca, Sr, Nd, Hf, and Pb. The results were mainly obtained by high-precision bulk techniques, such as TIMS and MC-ICPMS. In addition, LA-ICPMS and SIMS isotope data of B, Li, and Pb are presented.

Regulatory T cells are key cerebroprotective immunomodulators in acute experimental stroke

Abstract: Systemic and local inflammatory processes have a key, mainly detrimental role in the pathophysiology of ischemic stroke. Currently, little is known about endogenous counterregulatory immune mechanisms. We examined the role of the key immunomodulators CD4(+)CD25(+) forkhead box P3 (Foxp3)(+) regulatory T lymphocytes (T(reg) cells), after experimental brain ischemia. Depletion of T(reg) cells profoundly increased delayed brain damage and deteriorated functional outcome. Absence of T(reg) cells augmented postischemic activation of resident and invading inflammatory cells including microglia and T cells, the main sources of deleterious cerebral tumor necrosis factor-alpha (TNF-alpha) and interferon-gamma (IFN-gamma), respectively. Early antagonization of TNF-alpha and delayed neutralization of IFN-gamma prevented infarct growth in T(reg) cell-depleted mice. Intracerebral interleukin-10 (IL-10) substitution abrogated the cytokine overexpression after T(reg) cell depletion and prevented secondary infarct growth, whereas transfer of IL-10-deficient T(reg) cells in an adoptive transfer model was ineffective. In conclusion, T(reg) cells are major cerebroprotective modulators of postischemic inflammatory brain damage targeting multiple inflammatory pathways. IL-10 signaling is essential for their immunomodulatory effect.