Requirements for leukocyte transmigration via the transmembrane chemokine CX3CL1

The surface-expressed transmembrane CX3C chemokine ligand 1 (CX3CL1/fractalkine) induces firm adhesion of leukocytes expressing its receptor CX3CR1. After shedding by the disintegrins and metalloproteinases (ADAM) 10 and 17, CX3CL1 also acts as soluble leukocyte chemoattractant. Here, we demonstrate that transmembrane CX3CL1 expressed on both endothelial and epithelial cells induces leukocyte transmigration. To investigate the underlying mechanism, we generated CX3CR1 variants lacking the intracellular aspartate-arginine-tyrosine (DRY) motif or the intracellular C-terminus which led to a defect in intracellular calcium response and impaired ligand uptake, respectively. While both variants effectively mediated firm cell adhesion, they failed to induce transmigration and rather mediated retention of leukocytes on the CX3CL1-expressing cell layer. Targeting of ADAM10 led to increased adhesion but reduced transmigration in response to transmembrane CX3CL1, while transmigration towards soluble CX3CL1 was not affected. Thus, transmembrane CX3CL1 mediates leukocyte transmigration via the DRY motif and C-terminus of CX3CR1 and the activity of ADAM10.     

Na+,K+-ATPase as a docking station: protein–protein complexes of the Na+,K+-ATPase

The Na⁺,K⁺-ATPase, or sodium pump, is well known for its role in ion transport across the plasma membrane of animal cells. It carries out the transport of Na⁺ ions out of the cell and of K⁺ ions into the cell and thus maintains electrolyte and fluid balance. In addition to the fundamental ion-pumping function of the Na⁺,K⁺-ATPase, recent work has suggested additional roles for Na⁺,K⁺-ATPase in signal transduction and biomembrane structure. Several signaling pathways have been found to involve Na⁺,K⁺-ATPase, which serves as a docking station for a fast-growing number of protein interaction partners. In this review, we focus on Na⁺,K⁺-ATPase as a signal transducer, but also briefly discuss other Na⁺,K⁺-ATPase protein–protein interactions, providing a comprehensive overview of the diverse signaling functions ascribed to this well-known enzyme.     

水玻璃旧砂中的Na_2O

水玻璃砂铸型因受不同温度的作用，其断面浇注后变成７种不同的颜色．通过对７种不同色层旧砂的再生处理、化学分析和电性能测试，揭示了水玻璃砂型中的Ｎａ２Ｏ经高温浇注后的行为、在旧砂中的分布及其对水玻璃砂再生和再生砂性能的影响     

Probability in 1919/20: the von Mises-Pólya-Controversy

The correspondence between Richard von Mises and George Pólya of 1919/20 contains reflections on two well-known articles by von Mises on the foundations of probability in the Mathematische Zeitschrift of 1919, and one paper from the Physikalische Zeitschrift of 1918. The topics touched on in the correspondence are: the proof of the central limit theorem of probability theory, von Mises' notion of randomness, and a statistical criterion for integer-valuedness of physical data. The investigation will hint at both the fruitfulness and the limits of several of von Mises' notions such as ``collective', ``distribution' and ``complex adjuncts' (characteristic functions) for further developments in probability theory and in ``directional statistics'. By pointing to the selectiveness of Pólya's criticism, the historical analysis shows the differing expectations of the two men with respect to the further development of the theory of probability and its applications. The paper thus gives a glimpse of the provisional state of the theory around 1920, before others such as P. Lévy (1886–1971) and A. N. Kolmogorov (1903–1987) stepped in and created a new paradigm for probability theory.     

Analysis of nucleotides bound to the ATP synthetase from spinach chloroplasts isolated under different conditions

Summary The total amount of bound adenine nucleotides in the coupling factor isolated from spinach chloroplasts and its distribution on AMP, ADP and ATP was analyzed after various incubation conditions. During purification of the coupling factor, the distribution of AMP, ADP and ATP is not altered. The coupling factor from deenergized membranes contains approximately 1 ADP, less than 1 ATP, and small amounts of AMP. During phosphorylation the pattern is changed and ATP becomes the dominant species. When exogenous ADP is lacking, phosphate is readily incorporated into ATP. Inhibition of adenylate kinase by AP₅A does not change the distribution pattern of the adenine nucleotides. The distribution pattern shows no integer numbers for the different nucleotides, suggesting that the coupling factor is present in different states in a statistical distribution.Acknowledgment: We thank the Swiss National Foundation for Scientific Research (grant 3.582.79) for generous support.     

Versuche zum enzymatischen Abbau der «gebundenen» gibberelline vonPharbitis purpurea

Summary Seeds and fruit walls ofPharbitis purpurea contain in addition to the free gibberellins A₈, A₃, A₅, more polar gibberellin-like substances, so-called bound gibberellins tentatively namedPharbitis and. After purification by thin layer chromatography, these 2 substances were treated with both Ficin and Emulsin in buffered solutions of pH 6.2. After treatment with Emulsin, the free gibberellins A₈ and A₅, after treatment with Ficin the gibberellins A₃ and A₅, were detectable in thin layer chromatograms.     

Exome sequencing identifies ACAD9 mutations as a cause of complex I deficiency

An isolated defect of respiratory chain complex I activity is a frequent biochemical abnormality in mitochondrial disorders. Despite intensive investigation in recent years, in most instances, the molecular basis underpinning complex I defects remains unknown. We report whole-exome sequencing of a single individual with severe, isolated complex I deficiency. This analysis, followed by filtering with a prioritization of mitochondrial proteins, led us to identify compound heterozygous mutations in ACAD9, which encodes a poorly understood member of the mitochondrial acyl-CoA dehydrogenase protein family. We demonstrated the pathogenic role of the ACAD9 variants by the correction of the complex I defect on expression of the wildtype ACAD9 protein in fibroblasts derived from affected individuals. ACAD9 screening of 120 additional complex I-defective index cases led us to identify two additional unrelated cases and a total of five pathogenic ACAD9 alleles.