Zur Untersuchung lebender menschlicher Leukozytenin vitro

Summary A simple method of examining living Leucocytesin vitro is represented. This method renders possible the study of the effects of various drugs on Leucocytes. Moreover it permits, as a personal observation demonstrates, examining the resistance and the Leucocytes under different conditions of maladies.     

Nephrocystin-5, a ciliary IQ domain protein, is mutated in Senior-Loken syndrome and interacts with RPGR and calmodulin

Nephronophthisis (NPHP) is the most frequent genetic cause of chronic renal failure in children. Identification of four genes mutated in NPHP subtypes 1-4 (refs. 4-9) has linked the pathogenesis of NPHP to ciliary functions. Ten percent of affected individuals have retinitis pigmentosa, constituting the renal-retinal Senior-Loken syndrome (SLSN). Here we identify, by positional cloning, mutations in an evolutionarily conserved gene, IQCB1 (also called NPHP5), as the most frequent cause of SLSN. IQCB1 encodes an IQ-domain protein, nephrocystin-5. All individuals with IQCB1 mutations have retinitis pigmentosa. Hence, we examined the interaction of nephrocystin-5 with RPGR (retinitis pigmentosa GTPase regulator), which is expressed in photoreceptor cilia and associated with 10-20% of retinitis pigmentosa. We show that nephrocystin-5, RPGR and calmodulin can be coimmunoprecipitated from retinal extracts, and that these proteins localize to connecting cilia of photoreceptors and to primary cilia of renal epithelial cells. Our studies emphasize the central role of ciliary dysfunction in the pathogenesis of SLSN.     

Genomic buffering mitigates the effects of deleterious mutations in bacteria

The relationship between the number of randomly accumulated mutations in a genome and fitness is a key parameter in evolutionary biology. Mutations may interact such that their combined effect on fitness is additive (no epistasis), reinforced (synergistic epistasis) or mitigated (antagonistic epistasis). We measured the decrease in fitness caused by increasing mutation number in the bacterium Salmonella typhimurium using a regulated, error-prone DNA polymerase (polymerase IV, DinB). As mutations accumulated, fitness costs increased at a diminishing rate. This suggests that random mutations interact such that their combined effect on fitness is mitigated and that the genome is buffered against the fitness reduction caused by accumulated mutations. Levels of the heat shock chaperones DnaK and GroEL increased in lineages that had accumulated many mutations, and experimental overproduction of GroEL further increased the fitness of lineages containing deleterious mutations. These findings suggest that overexpression of chaperones contributes to antagonistic epistasis.     

Trefoil factors

Trefoil factor family (TFF) peptides have many in vivo and in vitro effects on restitution, wound healing, apoptosis, cell motility, adhesion and vectorial ion pumping, amongst others. (125)I-TFF peptides bind to cell membranes with classical saturable ability. It would be surprising if there were not TFF-protein interactions that would explain these actions, but to date no convincing TFF-binding partner has been shown which unambiguously takes part in any of these functions. Nevertheless, several TFF-binding proteins exist, including the small intestinal CRP-ductin (muclin), which binds TFF2, and the recently described gastric foveolar proteins TFIZ1 (TFF1-binding) and blottin (TFF2-binding), any of which may yet interact in novel ways to elicit TFF-mediated events. This review describes the expression and, where known, the functions of such proteins.     

Barttin is a Cl- channel beta-subunit crucial for renal Cl- reabsorption and inner ear K+ secretion.

Renal salt loss in Bartter's syndrome is caused by impaired transepithelial transport in the loop of Henle. Sodium chloride is taken up apically by the combined activity of NKCC2 (Na+-K--2Cl- cotransporters) and ROMK potassium channels. Chloride ions exit from the cell through basolateral ClC-Kb chloride channels. Mutations in the three corresponding genes have been identified that correspond to Bartter's syndrome types 1-3. The gene encoding the integral membrane protein barttin is mutated in a form of Bartter's syndrome that is associated with congenital deafness and renal failure. Here we show that barttin acts as an essential beta-subunit for ClC-Ka and ClC-Kb chloride channels, with which it colocalizes in basolateral membranes of renal tubules and of potassium-secreting epithelia of the inner ear. Disease-causing mutations in either ClC-Kb or barttin compromise currents through heteromeric channels. Currents can be stimulated further by mutating a proline-tyrosine (PY) motif on barttin. This work describes the first known beta-subunit for CLC chloride channels and reveals that heteromers formed by ClC-K and barttin are crucial for renal salt reabsorption and potassium recycling in the inner ear.     

Über das Problem der Welkekrankheiten bei Pflanzen

Summary Lycomarasmin is a plasma poison produced byFusarium lycopersici Sacc., the pathogen of tomato wilt. In a dilution of 10^–2 and 10^–3 mol it causes a pathological wilting of tomato plants and usually disturbs their water balance; in a dilution of 10^–4 mol it only disturbs the latter.In the present paper, we develop the theory that in sufficient concentration lycomariasmin damages or destroys thesemipermeability of the plasma boundary layer.In a dilution of 10^–2 and 10^–3 mol of lycomarasmin the semipermeability of the plasma membranes iscompletely destroyed. Thus on the one hand the conditions for osmotic pressure disappear and irreversible pathological wilting appears, and on the other hand cellular fluid passes into the transpiration current of the cell-membrane and leads to a momentary excess humidity, particularly in the leaf-tissues, and thus also to a momentaryexcess transpiration.The water-deficit regularly observed in wilt-literature is therefore not the cause of pathological wilting but, just as the wilting itself, a consequence of the distruction of the semipermeability of the plasma boundary layer.In a dilution of 10^–4 mol lycomarasmin apparently only affects the permeability of the exterior plasma boundary layer forwater, but not for sugars etc. Therefore it only produces an excess of fluid in the leaf tissues and thus an excess transpiration, but no definite inactivation of the plasma membrane and therefore also no pathological wilt.     

水平排列硅光二极管色传感器及其特性

简要介绍水平排列硅光二极管色传感器的制作工艺，该器件波长在５００ｎｍ到６５０ｎｍ范围内有一个单调的近于线性的光谱响应。入射光波长为６００ｎｍ时，入射光强度化五个数量级，测出的波长基本不变，器件波长分辨率、最低入射光强、长时间测量的波长漂移以及波长温漂系数等特性的测量结果表明：该类色传感器已达高性能实用要求。