Palaeomagnetic results from the Gordon Subgroup of Tasmania: Further evidence for a late Cretaceous magnetic overprint in Southeastern Australia

A thermal demagnetization study of 48 limestone samples from the Ordovician Gordon Subgroup of Ida Bay (Tasmania), indicated complete remagnetization (D = 9 .4° I= - 81.4°, k = 137.5, a95 = l. 3o, N = 92 South pole position 59.8°5 1 41.1°E, dp = 2.4°, dm = 2.5°) during Late Cretaceous or less likely Early Tertiary time . This finding further supports a recently recognized Late Cretaceous remagnetization event in southeastern Australia , which is attributed to rift forming processes preceding the opening of t he Tasman Sea. Conodont colour indicates that the limestones studied have not been subjected to temperatures in excess of l00°c . This suggests a possible widespread occurrence of this magnetic overprint

An intensive study of LPCVD silicon morphology and texture for non volatile memory

Results of an intensive study by means of XRD, SEM, AFM and TEM of the microstructure (i.e. the texture and morphology) of LPCVD silicon layers as a function of different process parameters are described. The influence of different deposition parameters, like partial and total pressure, doping, deposition and anneal temperature is shown. In particular the roughness of the silicon surface is investigated. The relation of surface roughness to the electrical properties of dielectrics, grown on these silicon layers, is briefly discussed

A missense mutation in Ehd1 associated with defective spermatogenesis and male infertility

Normal function of the C-terminal Eps15 homology domain-containing protein 1 (EHD1) has previously been associated with endocytic vesicle trafficking, shaping of intracellular membranes, and ciliogenesis. We recently identified an autosomal recessive missense mutation c.1192C>T (p.R398W) of EHD1 in patients who had low molecular weight proteinuria (0.7–2.1 g/d) and high-frequency hearing loss. It was already known from Ehd1 knockout mice that inactivation of Ehd1 can lead to male infertility. However, the exact role of the EHD1 protein and its p.R398W mutant during spermatogenesis remained still unclear. Here, we report the testicular phenotype of a knockin mouse model carrying the p.R398W mutation in the EHD1 protein. Male homozygous knockin mice were infertile, whereas the mutation had no effect on female fertility. Testes and epididymes were significantly reduced in size and weight. The testicular epithelium appeared profoundly damaged and had a disorganized architecture. The composition of developing cell types was altered. Malformed acrosomes covered underdeveloped and misshaped sperm heads. In the sperm tail, midpieces were largely missing indicating disturbed assembly of the sperm tail. Defective structures, i.e., nuclei, acrosomes, and sperm tail midpieces, were observed in large vacuoles scattered throughout the epithelium. Interestingly, cilia formation itself did not appear to be affected, as the axoneme and other parts of the sperm tails except the midpieces appeared to be intact. In wildtype mice, EHD1 co-localized with acrosomal granules on round spermatids, suggesting a role of the EHD1 protein during acrosomal development. Wildtype EHD1 also co-localized with the VPS35 component of the retromer complex, whereas the p.R398W mutant did not. The testicular pathologies appeared very early during the first spermatogenic wave in young mice (starting at 14 dpp) and tubular destruction worsened with age. Taken together, EHD1 plays an important and probably multifaceted role in spermatogenesis in mice. Therefore, EHD1 may also be a hitherto underestimated infertility gene in humans

Unraveling the New England orocline, east Gondwana accretionary margin

The New England orocline lies within the Eastern Australian segment of the Terra Australis accretionary orogen and developed during the late Paleozoic to early Mesozoic Gondwanide Orogeny (310–230 Ma) that extended along the Pacific margin of the Gondwana supercontinent. The orocline deformed a pre-Permian arc assemblage consisting of a western magmatic arc, an adjoining forearc basin and an eastern subduction complex. The orocline is doubly vergent with the southern and northern segments displaying counter-clockwise and clockwise rotation, respectively, and this has led to contrasting models of formation. We resolve these conflicting models with one that involves buckling of the arc system about a vertical axis during progressive northward translation of the southern segment of the arc system against the northern segment, which is pinned relative to cratonic Gondwana. Paleomagnetic data are consistent with this model and show that an alternative model involving southward motion of the northern segment relative to the southern segment and cratonic Gondwana is not permissible. The timing of the final stage of orocline formation (~270–265 Ma) overlaps with a majorgap in magmatic activity along this segment of the Gondwana margin, suggesting that northward motion and orocline formation were driven by a change from orthogonal to oblique convergence and coupling between the Gondwana and Pacific plates

Spina bifida-predisposing heterozygous mutations in Planar Cell Polarity genes and Zic2 reduce bone mass in young mice

Fractures are a common comorbidity in children with the neural tube defect (NTD) spina bifida. Mutations in the Wnt/planar cell polarity (PCP) pathway contribute to NTDs in humans and mice, but whether this pathway independently determines bone mass is poorly understood. Here, we first confirmed that core Wnt/PCP components are expressed in osteoblasts and osteoclasts in vitro. In vivo, we performed detailed µCT comparisons of bone structure in tibiae from young male mice heterozygous for NTD-associated mutations versus WT littermates. PCP signalling disruption caused by Vangl2 (Vangl2Lp/+) or Celsr1 (Celsr1Crsh/+) mutations significantly reduced trabecular bone mass and distal tibial cortical thickness. NTD-associated mutations in non-PCP transcription factors were also investigated. Pax3 mutation (Pax3Sp2H/+) had minimal effects on bone mass. Zic2 mutation (Zic2Ku/+) significantly altered the position of the tibia/fibula junction and diminished cortical bone in the proximal tibia. Beyond these genes, we bioinformatically documented the known extent of shared genetic networks between NTDs and bone properties. 46 genes involved in neural tube closure are annotated with bone-related ontologies. These findings document shared genetic networks between spina bifida risk and bone structure, including PCP components and Zic2. Genetic variants which predispose to spina bifida may therefore independently diminish bone mass

When and where did India and Asia collide?

Timing of the collision between India and Asia is the key boundary condition in all models for the evolution of the Himalaya-Tibetan orogenic system. Thus it profoundly affects the interpretation of the rates of a multitude of associated geological processes ranging from Tibetan Plateau uplift through continental extrusion across eastern Asia, as well as our understanding of global climate change during the Cenozoic. Although an abrupt slowdown in the rate of convergence between India and Asia around 55 Ma is widely regarded as indicating the beginning of the collision, most of the effects attributed to this major tectonic episode do not occur until more than 20 Ma later. Refined estimates of the relative positions of India and Asia indicate that they were not close enough to one another to have collided at 55 Ma. On the basis of new field evidence from Tibet and a reassessment of published data we suggest that continent-continent collision began around the Eocene/Oligocene boundary (∼34 Ma) and propose an alternative explanation for events at 55 Ma. Copyright 2007 by the American Geophysical Union.published_or_final_versio

Molecular Phylogeny and Biogeography of the Native Rodents of Madagascar (Muridae: Nesomyinae): A Test of the Single-Origin Hypothesis

Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/72349/1/j.1096-0031.1999.tb00267.x.pd