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排序方式: 共有680条查询结果,搜索用时 15 毫秒
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Bianka Goetze Karl-Friedrich Schmidt Konrad Lehmann Wilko Detlev Altrock Eckart Dieter Gundelfinger Siegrid Löwel 《NeuroImage》2010,49(2):1622-1631
How little neurotransmission in the visual system is sufficient to promote decent visual capabilities? This question is of key importance for therapeutic approaches to restore vision in patients who suffer from degenerative retinal diseases. In the retinae of mice, mutant for the presynaptic scaffolding protein Bassoon (Bsn), signal transfer at photoreceptor ribbon synapses is severely disturbed due to impaired ribbon attachment to the active zone. We have used two different behavioural tasks and optical imaging of intrinsic signals to probe vision in young and adult Bsn?/? mice and their wild-type littermates. Here we show that while visual acuity was significantly reduced in mutants compared to controls, vision guided behavioural decisions and optical imaging revealed essentially unperturbed cortical signals and retinotopy in spite of the photoreceptor synaptopathy. In addition, both vision and visual cortical maps were adult-like at 4 weeks of age. These results show that (i) while Bassoon-dependent fast exocytosis is essential for normal vision surprisingly good visual performance can be achieved in the absence of synaptic ribbons, (ii) both the development and maintenance of visual cortical maps is independent of synaptic ribbons and (iii) visual development in the mutants is completed at 4 weeks of age indicating that later developing ectopic synapses do not affect vision. Thus, the central visual system can make use of slow and weak retinal signals to subserve surprisingly robust vision. 相似文献
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Hai-Ying Shen Theresa A Lusardi Rebecca L Williams-Karnesky Jing-Quan Lan David J Poulsen Detlev Boison 《Journal of cerebral blood flow and metabolism》2011,31(7):1648-1659
Adenosine kinase (ADK) is the major negative metabolic regulator of the endogenous neuroprotectant and homeostatic bioenergetic network regulator adenosine. We used three independent experimental approaches to determine the role of ADK as a molecular target for predicting the brain''s susceptibility to ischemic stroke. First, when subjected to a middle cerebral artery occlusion model of focal cerebral ischemia, transgenic fb-Adk-def mice, which have increased ADK expression in striatum (164%) and reduced ADK expression in cortical forebrain (65%), demonstrate increased striatal infarct volume (126%) but almost complete protection of cortex (27%) compared with wild-type (WT) controls, indicating that cerebral injury levels directly correlate to levels of ADK in the CNS. Second, we demonstrate abrogation of lipopolysaccharide (LPS)-induced ischemic preconditioning in transgenic mice with brain-wide ADK overexpression (Adk-tg), indicating that ADK activity negatively regulates LPS-induced tolerance to stroke. Third, using adeno-associated virus-based vectors that carry Adk-sense or -antisense constructs to overexpress or knockdown ADK in vivo, we demonstrate increased (126%) or decreased (51%) infarct volume, respectively, 4 weeks after injection into the striatum of WT mice. Together, our data define ADK as a possible therapeutic target for modulating the degree of stroke-induced brain injury. 相似文献
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Detlev Boison 《Epilepsy Currents》2011,11(5):155-156
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S2k Guidelines – Cutaneous Lymphomas Update 2016 – Part 1: Classification and Diagnosis (ICD10 C82 ‐ C86) 下载免费PDF全文
Edgar Dippel Chalid Assaf Jürgen C. Becker Michael von Bergwelt‐Baildon Marc Beyer Antonio Cozzio Hans Theodor Eich Markus Follmann Stephan Grabbe Uwe Hillen Wolfram Klapper Claus‐Detlev Klemke Cristina Lamos Carmen Loquai Frank Meiß Dominik Mestel Dorothee Nashan Jan P. Nicolay Ilske Oschlies Max Schlaak Christoph Stoll Tibor Vag Michael Weichenthal Marion Wobser Rudolf Stadler 《Journal der Deutschen Dermatologischen Gesellschaft》2017,15(12):1266-1273
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Lindner O Vogt J Baller D Kammeier A Wielepp P Holzinger J Lamp B Horstkotte D Burchert W 《European journal of heart failure》2005,7(2):225-230
OBJECTIVE: In patients with dilated cardiomyopathy (DCM), left bundle branch block (LBBB) is a common finding. The characteristic feature is an asynchronous septal wall motion and most frequently a delay of the lateral and/or posterior wall segments. With the onset of cardiac resynchronization therapy, there is a focus on the specific pathophysiology of a LBBB. However, quantitative data on regional myocardial oxygen consumption (MVO(2)) and blood flow (MBF) are missing. METHODS: We studied 31 patients with severe DCM and LBBB (ejection fraction 22.1+/-7.1%) and 14 patients with mild to moderate DCM without LBBB (ejection fraction 46.7+/-7.9%). Global and regional MVO(2) as well as MBF were determined from a dynamic (11)C-acetate positron emission tomography (PET) study. RESULTS: Global MVO(2) and MBF were lower in the DCM group with LBBB than in the control group (P<0.05). Regionally, the LBBB group revealed a higher (P<0.05) MVO(2) and MBF in the lateral wall than in the other walls. The control group did not show significant differences between the myocardial walls and demonstrated a smaller variability of the parameters. CONCLUSION: DCM patients with LBBB exhibit a more heterogeneous distribution of MVO(2) and MBF among the myocardial walls than DCM patients without LBBB. Due to the LBBB associated electromechanical alterations, the highest regional values of MVO(2) and MBF are found in the lateral wall. 相似文献
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Callén E Casado JA Tischkowitz MD Bueren JA Creus A Marcos R Dasí A Estella JM Muñoz A Ortega JJ de Winter J Joenje H Schindler D Hanenberg H Hodgson SV Mathew CG Surrallés J 《Blood》2005,105(5):1946-1949
Fanconi anemia (FA) is a genetic disease characterized by bone marrow failure and cancer predisposition. Here we have identified Spanish Gypsies as the ethnic group with the world's highest prevalence of FA (carrier frequency of 1/64-1/70). DNA sequencing of the FANCA gene in 8 unrelated Spanish Gypsy FA families after retroviral subtyping revealed a homozygous FANCA mutation (295C>T) leading to FANCA truncation and FA pathway disruption. This mutation appeared specific for Spanish Gypsies as it is not found in other Gypsy patients with FA from Hungary, Germany, Slovakia, and Ireland. Haplotype analysis showed that Spanish Gypsy patients all share the same haplotype. Our data thus suggest that the high incidence of FA among Spanish Gypsies is due to an ancestral founder mutation in FANCA that originated in Spain less than 600 years ago. The high carrier frequency makes the Spanish Gypsies a population model to study FA heterozygote mutations in cancer. 相似文献