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Durch natürliche und anthropogene Säureeinträge sind vor
allem auf naturnahen Standorten Mineleuropas, insbeson-
dere bei Waldböden, schwerwiegende und langfristig wirk-
same negative Veränderungen der Bodeneigenschaften, der
Bodenvegetation und teilweise auch der Qualität des Si-
ckerwassers und der Oberflächengewässer eingetreten
(Veerhoff et al. 1996). Die weitere Bodenentwicklung auf
solchen Standorten wird ganz wesentlich von der SNK und
den H'-Pufferraten der (noch) vorhandenen Bodenminerale
bestimmt. Um Prognosen über die zukünftige Entwicklung
machen zu können, wurden neun für Böden typische Mine-
rale auf ihr Pufferverhalten untersucht.
Chloritesare found in igneous rocks, and more commonly
in sediments and low grade metamorphic rocks (BrinJiey &
Brown 1980). Because chlorites are less stable than most of
the other clay minerals when placed into an acidic
environment (Barnhisel & Bertsch 1989), they play
significant roles in the solution chemistry and may be an
important source of magnesium and micronutrients in soils
(Ross 1975). The objective of the present study was to
compare the weathering behavior of different chlorites in
different chemical environments.
Mobilität und Bindungsformen von Cd, Cr, As und V in urbanen Böden unterschiedlicher Belastung
(1995)
Striated muscle contraction is regulated by the translocation of troponin-tropomyosin strands over the thin filament surface. Relaxation relies partly on highly-favorable, conformation-dependent electrostatic contacts between actin and tropomyosin, which position tropomyosin such that it impedes actomyosin associations. Impaired relaxation and hypercontractile properties are hallmarks of various muscle disorders. The α-cardiac actin M305L hypertrophic cardiomyopathy-causing mutation lies near residues that help confine tropomyosin to an inhibitory position along thin filaments. Here, we investigate M305L actin in vivo, in vitro, and in silico to resolve emergent pathological properties and disease mechanisms. Our data suggest the mutation reduces actin flexibility and distorts the actin-tropomyosin electrostatic energy landscape that, in muscle, result in aberrant contractile inhibition and excessive force. Thus, actin flexibility may be required to establish and maintain interfacial contacts with tropomyosin as well as facilitate its movement over distinct actin surface features and is, therefore, likely necessary for proper regulation of contraction.
RELA haploinsufficiency is a recently described autoinflammatory condition presenting with intermittent fevers and mucocutaneous ulcerations. The RELA gene encodes the p65 protein, one of five NF-κB family transcription factors. As RELA is an essential regulator of mucosal homeostasis, haploinsufficiency leads to decreased NF-κB signaling which promotes TNF-driven mucosal apoptosis with impaired epithelial recovery. Thus far, only eight cases have been reported in the literature. Here, we report four families with three novel and one previously described pathogenic variant in RELA. These four families included 23 affected individuals for which genetic testing was available in 16. Almost half of these patients had been previously diagnosed with more common rheumatologic entities (such as Behcet's Disease; BD) prior to the discovery of their pathogenic RELA variants. The most common clinical features were orogenital ulcers, rash, joint inflammation, and fever. The least common were conjunctivitis and recurrent infections. Clinical variability was remarkable even among familial cases, and incomplete penetrance was observed. Patients in our series were treated with a variety of medications, and benefit was observed with glucocorticoids, colchicine, and TNF inhibitors. Altogether, our work adds to the current literature and doubles the number of reported cases with RELA-Associated Inflammatory Disease (RAID). It reaffirms the central importance of the NF-κB pathway in immunity and inflammation, as well as the important regulatory role of RELA in mucosal homeostasis. RELA associated inflammatory disease should be considered in all patients with BD, particularly those with early onset and/or with a strong family history.