Browsing by Author "Becker, J."

Litterfall is one of the major pathways connecting above-and below-ground processes. The effects of climate and land-use change on carbon (C) and nutrient inputs by litterfall are poorly known. We quantified and analyzed annual patterns of C and nutrient deposition via litterfall in natural forests and agroforestry systems along the unique elevation gradient of Mt. Kilimanjaro. Tree litter in three natural (lower montane, Ocotea and Podocarpus forests), two sustainably used (homegardens) and one intensively managed (shaded coffee plantation) ecosystems was collected on a biweekly basis from May 2012 to July 2013. Leaves, branches and remaining residues were separated and analyzed for C and nutrient contents. The annual pattern of litterfall was closely related to rainfall seasonality, exhibiting a large peak towards the end of the dry season (August-October). This peak decreased at higher elevations with decreasing rainfall seasonality. Macronutrients (N, P, K) in leaf litter increased at mid elevation (2100ma. s. l.) and with land-use intensity. Carbon content and micronutrients (Al, Fe, Mn, Na) however, were unaffected or decreased with land-use intensity. While leaf litterfall decreased with elevation, total annual input was independent of climate. Compared to natural forests, the nutrient cycles in agroforestry ecosystems were accelerated by fertilization and the associated changes in dominant tree species.

In order to constrain the temporal relationship between granite (sensu lato) emplacement and metamorphism, isotope work was carried out on the minerals zircon and apatite (U-Pb), garnet (Pb-Pb) and hornblende (Ar-Ar) from wall rock samples in the Shamva area in Zimbabwe. The area, encompassing parts of the Chinamora and Murehwa batholiths and a wedge-shaped greenstone belt segment in between, is commonly quoted in the literature as an example illustrating pluton emplacement processes and deformational models for the Archean. New U-Pb dating of apatite from a boudinaged pegmatite within mafic schists in the batholith-greenstone contact zone has yielded an age of 2619 +28/-24 Ma. This age is interpreted as the best estimation of the intrusion age of this unit, depending on the assumed closure temperature, and provides an upper age limit for the syntectonic emplacement of the now gneissic granites. Pb-Pb dating of late kinematic garnets in cordierite-bearing rocks within the greenstone belt wall rocks gives an age of 2623+/-8 Ma. Together, this timing of relatively late, syntectonic plutonism and metamorphic mineral growth at ca. 2.62 Ga compares well with existing zircon crystallization ages for felsic volcanics (2645+/-4 Ma, 2643+/-8 Ma) and post-tectonic porphyritic monzogranites (2601+/-14 Ma). Ar-Ar hornblende ages for mafic schists from different areas within the greenstone belt wall rocks range between 2621 and 2498 Ma and have been interpreted to indicate mixing between metamorphic ages and cooling ages. The data support a geological model whereby volcanism and sedimentation are associated with an early phase of regional deformation at ca. 2.64 Ga, which may have started earlier and lasted longer, and evolves into the voluminous emplacement of granites (now gneissic granites) in the batholiths at approximately 2.62 Ga. Emplacement of post-tectonic tabular monzogranites takes place at ca. 2.60 Ga.

A 70-year-old former professional boxer suffered from severe dementia and died after food aspiration. Neuropathological examinations revealed chronic traumatic encephalopathy (CTE; stage III-IV), detectable by immunohistochemistry in formalin-fixed brain tissue and in stored formalin-fixed paraffin-embedded (FFPE) blocks. Whether this condition could have contributed to a suspected diminished responsibility regarding a serious crime he committed 27 years earlier can only be speculated.

Neuroblastoma is the most common extracranial childhood tumor. High expression of activin A is associated with a favorable prognosis, but the contributing mechanisms have remained unclear. Our previous demonstration of the activin A-mediated up-regulation of keratoepithelin led to the consideration that keratoepithelin could modulate neuroblastoma growth and/or progression. We report here that enhanced keratoepithelin expression in human neuroblastoma cells suppresses neuroblastoma cell cohesion and adhesion to various extracellular matrix proteins and that it inhibits neuroblastorna cell proliferation and invasion in vitro and in vivo. Using microarray analysis, we identified several keratoepithelin-regulated genes that may contribute to these biological changes. Together with the observation that keratoepithelin is expressed in human neuroblastomas in vivo, our data suggest that keratoepithelin could play a beneficial role in neuroblastoma development and/or progression.

Objectives: To compare clinical features and outcome, imaging characteristics, biopsy results and laboratory findings in a cohort of 69 patients with suspected or diagnosed primary central nervous system vasculitis (PCNSV) in adults; to identify risk factors and predictive features for PCNSV. Patients and methods: We performed a case-control-study including 69 patients referred with suspected PCNSV from whom 25 were confirmed by predetermined diagnostic criteria based on biopsy (72%) or angiography (28%). Forty-four patients turned out to have 15 distinct other diagnoses. Clinical and diagnostic data were compared between PCNSV and Non-PCNSV cohorts. Results: Clinical presentation was not able to discriminate between PCNSV and its differential diagnoses. However, a worse clinical outcome was associated with PCNSV (p = 0.005). Biopsy (p = 0.004), contrast enhancement (p = 0.000) or tumour-like mass lesion (p = 0.008) in magnetic resonance imaging (MRI), intrathecal IgG increase (p = 0.020), normal Duplex findings of cerebral arteries (p = 0.022) and conventional angiography (p 0.010) were able to distinguish between the two cohorts. Conclusion: In a cohort of 69 patients with suspected PCNSV, a large number (64%) was misdiagnosed and partly received treatment, since mimicking diseases are very difficult to discriminate. Clinical presentation at manifestation does not help to differentiate PCNSV from its mimicking diseases. MRI and cerebrospinal fluid analysis are unlikely to be normal in PCNSV, though unspecific if pathological. Cerebral angiography and biopsy must complement other diagnostics when establishing the diagnosis in order to avoid misdiagnosis and mistreatment. (C) 2017 Elsevier B.V. All rights reserved.

Coronary heart disease (CHD) is based on the development of atherosclerosis in coronary arteries. Shear stress-induced endothelial nitric oxide (NO) release not only contributes to local blood pressure control but also effectively helps to retard atherosclerosis. Therefore, functionally relevant polymorphisms in the endothelial NO synthase (NOS-3) gene may contribute to the development of CHD. NOS-3 expression was analyzed in endothelial cells isolated from umbilical cords genotyped for the C-786/T single nucleotide polymorphism (SNP) of the human nos-3 gene. Moreover, NO-dependent relaxation was examined in segments of saphenous vein isolated from genotyped patients undergoing aortocoronary bypass surgery, and patients subjected to quantitative coronary angiography were genotyped to verify an association between this SNP and CHD. Shear stress-induced NOS-3 mRNA and protein expression was present in TT and CT genotype cells but absent in cells with CC genotype. Pretreatment of these cells with a decoy oligonucleotide comprising position -800 to -779 of the C-type nos-3 promoter reconstituted shear stress-induced NOS-3 expression. These results were confirmed by reporter gene analysis with the corresponding nos-3 promoter luciferase constructs. In addition, the NO-mediated relaxant response of vein grafts from CC genotype patients was significantly attenuated as compared with the CT or TT genotype, and in CHD-positive patients, the CC genotype was significantly more frequent (19.0%) than in CHD-negative patients (4.4%). The C-786/T SNP of the nos-3 gene thus constitutes a genetic risk factor for CHD, presumably due to binding of an inhibitory transcription factor to the C-type promoter blocking shear stress-dependent maintenance of NOS-3 expression.