Shear heating as the origin of the plumes and heat flux on Enceladus

Enceladus, a small icy satellite of Saturn, has active plumes jetting from localized fractures ('tiger stripes') within an area of high heat flux near the south pole. The plume characteristics and local high heat flux have been ascribed either to the presence of liquid water within a few tens of metres of the surface, or the decomposition of clathrates. Neither model addresses how delivery of internal heat to the near-surface is sustained. Here we show that the most likely explanation for the heat and vapour production is shear heating by tidally driven lateral (strike-slip) fault motion with displacement of approximately 0.5 m over a tidal period. Vapour produced by this heating may escape as plumes through cracks reopened by the tidal stresses. The ice shell thickness needed to produce the observed heat flux is at least 5 km. The tidal displacements required imply a Love number of h2 > 0.01, suggesting that the ice shell is decoupled from the silicate interior by a subsurface ocean. We predict that the tiger-stripe regions with highest relative temperatures will be the lower-latitude branch of Damascus, Cairo around 60 degrees W longitude and Alexandria around 150 degrees W longitude.     

Extracellular wildtype and mutant SOD1 induces ER–Golgi pathology characteristic of amyotrophic lateral sclerosis in neuronal cells

Amyotrophic lateral sclerosis (ALS) is a fatal and rapidly progressing neurodegenerative disorder and the majority of ALS is sporadic, where misfolding and aggregation of Cu/Zn-superoxide dismutase (SOD1) is a feature shared with familial mutant-SOD1 cases. ALS is characterized by progressive neurospatial spread of pathology among motor neurons, and recently the transfer of extracellular, aggregated mutant SOD1 between cells was demonstrated in culture. However, there is currently no evidence that uptake of SOD1 into cells initiates neurodegenerative pathways reminiscent of ALS pathology. Similarly, whilst dysfunction to the ER–Golgi compartments is increasingly implicated in the pathogenesis of both sporadic and familial ALS, it remains unclear whether misfolded, wildtype SOD1 triggers ER–Golgi dysfunction. In this study we show that both extracellular, native wildtype and mutant SOD1 are taken up by macropinocytosis into neuronal cells. Hence uptake does not depend on SOD1 mutation or misfolding. We also demonstrate that purified mutant SOD1 added exogenously to neuronal cells inhibits protein transport between the ER–Golgi apparatus, leading to Golgi fragmentation, induction of ER stress and apoptotic cell death. Furthermore, we show that extracellular, aggregated, wildtype SOD1 also induces ER–Golgi pathology similar to mutant SOD1, leading to apoptotic cell death. Hence extracellular misfolded wildtype or mutant SOD1 induce dysfunction to ER–Golgi compartments characteristic of ALS in neuronal cells, implicating extracellular SOD1 in the spread of pathology among motor neurons in both sporadic and familial ALS.     

Evidence for suppression of immune function by insulin-like growth factor-1 in dwarf rats in vivo

These studies were undertaken to investigate the effects of increasing or decreasing IGF-1 levels on aspects of immune function in rats. Female dwarf rats were treated with recombinant human IGF-1 or with a potent sheep anti-IGF-serum. Body weight, thymus weight and spleen weight increased with IGF-1 treatment (p<0.001), while there was no effect of anti-IGF-1 treatment when compared with the appropriate normal sheep serum (NSS) treated controls. IGF-1 treatment significantly decreased WBC and RBC counts, but increased the ratio of CD4⁺:CD8⁺ T-cells. Anti-IGF-1 serum had no effect on these parameters compared with NSS. However anti-IGF-1 was associated with increased T-cell numbers, decreased natural killer cells, and enhancement of the animals' ability to produce specific IgG in response to injection of keyhole limpet haemocyanin (KLH). These results indicate that IGF-1 may suppress immune function although increasing the size of immune organs such as spleen.These studies were part of an M.Sc. at the University of Waikato, Hamilton, New Zealand.     

隔震结构动力时程响应的一种工程实用算法

对非比例阻尼体系动力响应的时域一般解答做了简介,分析了非比例阻尼隔震体系在阻尼耦联及频域响应方面的特点,提出了任意多自由度体系时域动力响应的一种工程实用算法.并通过实际隔震工程算例的结果对比,表明本文算法与复振型分解法、双精度Fortran下的Wilson θ法及Matlab下的Simulink这3种方法几种算法的时程曲线完全重合.     

Sequences homologous to ZFY, a candidate human sex-determining gene, are autosomal in marsupials

Sexual differentiation in placental mammals results from the action of a testis-determining gene encoded by the Y chromosome. This gene causes the indifferent gonad to develop as a testis, thereby initiating a hormonal cascade which produces a male phenotype. Recently, a candidate for the testis-determining gene (ZFY, Y-borne zinc-finger protein) has been cloned. The ZFY probe detects a male-specific (Y-linked) sequence in DNA from a range of eutherian mammals, as well as an X-linked sequence (ZFX) which maps to the human X chromosome. In marsupials it is also the Y chromosome that seems to determine the fate of the gonad, but not all sexual dimorphisms. Using the ZFY probe we find, surprisingly, that the ZFY homologous sequences are not on either the X or the Y chromosome in marsupials, but map to the autosomes. This implies ZFY is not the primary sex-determining gene in marsupials. Either the genetic pathways of sex determination in marsupials and eutherians differ, or they are identical and ZFY is not the primary signal in human sex determination.     

Lipid polarity and sorting in epithelial cells

Lipid polarity and sorting in epithelial cells     

The biogenesis of helminthosporal

Zusammenfassung Die Biogenese des Pilzstoffes Helminthosporal wurde untersucht, indem der Pilz bei Anwesenheit von Mevalonsäure, mit C₂ mit Kohlenstoff-14 markiert, gezüchtet wurde. Es wird gezeigt, dass das Dialdehyd aus einem tricyclischen Vorläufer durch oxidative Spaltung entsteht.