Hypoxanthin,ein Zusatzwachstumsfaktor für Mucorineen

Summary In case ofAbsidia coerulea, Mucor mucedo, Rhizopus nodosus, Rhizopus oryzae andRhizopus suinus (auxoautotroph), Hypoxanthine effects, as well as in case ofPhycomyces Blakesleeanus (auxo-heterotroph), by acceleration of the germinating of the spores a temporary increased growth in contrary to controls without this additional growth factor.     

Über die Ursache des gegensätzlichen geotropischen Verhaltens von Sproß und Wurzel

Ohne Zusammenfassung     

静态电流变链组的导电性质

研究了微小玻璃球以矩形或立方结构在硅油中加直流电场后形成的“链组”的静态导电行为。发现流过静态（无应变）单链的电流密度随外加电场强度的增加而增大，它与组成链的玻璃球数无关，但随组成“链组”的链数（１￣４个链）的增加而增大。由４个相互接近的单链组成的链组的电流密度约是单链电流密度的２倍。     

Specificity in Toll-like receptor signalling through distinct effector functions of TRAF3 and TRAF6

Toll-like receptors (TLRs) are activated by pathogen-associated molecular patterns to induce innate immune responses and production of pro-inflammatory cytokines, interferons and anti-inflammatory cytokines. TLRs activate downstream effectors through adaptors that contain Toll/interleukin-1 receptor (TIR) domains, but the mechanisms accounting for diversification of TLR effector functions are unclear. To dissect biochemically TLR signalling, we established a system for isolating signalling complexes assembled by dimerized adaptors. Using MyD88 as a prototypical adaptor, we identified TNF receptor-associated factor 3 (TRAF3) as a new component of TIR signalling complexes that is recruited along with TRAF6. Using myeloid cells from TRAF3- and TRAF6-deficient mice, we show that TRAF3 is essential for the induction of type I interferons (IFN) and the anti-inflammatory cytokine interleukin-10 (IL-10), but is dispensable for expression of pro-inflammatory cytokines. In fact, TRAF3-deficient cells overproduce pro-inflammatory cytokines owing to defective IL-10 production. Despite their structural similarity, the functions of TRAF3 and TRAF6 are largely distinct. TRAF3 is also recruited to the adaptor TRIF (Toll/IL-1 receptor domain-containing adaptor-inducing IFN-beta) and is required for marshalling the protein kinase TBK1 (also called NAK) into TIR signalling complexes, thereby explaining its unique role in activation of the IFN response.     

The DNA helicase BRIP1 is defective in Fanconi anemia complementation group J

The protein predicted to be defective in individuals with Fanconi anemia complementation group J (FA-J), FANCJ, is a missing component in the Fanconi anemia pathway of genome maintenance. Here we identify pathogenic mutations in eight individuals with FA-J in the gene encoding the DEAH-box DNA helicase BRIP1, also called FANCJ. This finding is compelling evidence that the Fanconi anemia pathway functions through a direct physical interaction with DNA.