Effects of X-irradiation during hibernation on tissue catecholamine contents

Zusammenfassung 20 h nach Bestrahlung mit letaler Röntgenstrahlendosis (2000 r) zeigten winterschlafendeCitellus tridecemlineatus Herabsetzung der Konzentration von Catecholaminen in Leber und Niere. Werden Veränderungen des Wassergehaltes im Gewebe mitberücksichtigt, so erscheint der Gehalt an myokardialen Catecholaminen unverändert.

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Acknowledgments. This research was aided by Grants HE-06312, USPHS; and Ns G-271-62, NASA. The authors are grateful to DoctorD. E. Smith, Division of Biological and Medical Research, Argonne National Laboratory, for providing the ground squirrels and the facilities for their hibernation and radiation.     

Role of acoustic stress on the development of polyoma tumors in immunized golden hamsters]

An acoustic stress increases the metastatic spread of polyoma virus-induced tumors in syrian Hamsters. To try to elucidate the mechanism of this action, we studied the effect of stress on the protection afforded by the virus against tumour challenge. Exposure to ultrasonics during the immunization period markedly decreased the protective effect of the virus.     

Deafness and renal tubular acidosis in mice lacking the K-Cl co-transporter Kcc4

Hearing depends on a high K(+) concentration bathing the apical membranes of sensory hair cells. K(+) that has entered hair cells through apical mechanosensitive channels is transported to the stria vascularis for re-secretion into the scala media(). K(+) probably exits outer hair cells by KCNQ4 K(+) channels(), and is then transported by means of a gap junction system connecting supporting Deiters' cells and fibrocytes() back to the stria vascularis. We show here that mice lacking the K(+)/Cl(-) (K-Cl) co-transporter Kcc4 (coded for by Slc12a7) are deaf because their hair cells degenerate rapidly after the beginning of hearing. In the mature organ of Corti, Kcc4 is restricted to supporting cells of outer and inner hair cells. Our data suggest that Kcc4 is important for K(+) recycling() by siphoning K(+) ions after their exit from outer hair cells into supporting Deiters' cells, where K(+) enters the gap junction pathway. Similar to some human genetic syndromes(), deafness in Kcc4-deficient mice is associated with renal tubular acidosis. It probably results from an impairment of Cl(-) recycling across the basolateral membrane of acid-secreting alpha-intercalated cells of the distal nephron.     

Indium phosphide nanowires as building blocks for nanoscale electronic and optoelectronic devices

Nanowires and nanotubes carry charge and excitons efficiently, and are therefore potentially ideal building blocks for nanoscale electronics and optoelectronics. Carbon nanotubes have already been exploited in devices such as field-effect and single-electron transistors, but the practical utility of nanotube components for building electronic circuits is limited, as it is not yet possible to selectively grow semiconducting or metallic nanotubes. Here we report the assembly of functional nanoscale devices from indium phosphide nanowires, the electrical properties of which are controlled by selective doping. Gate-voltage-dependent transport measurements demonstrate that the nanowires can be predictably synthesized as either n- or p-type. These doped nanowires function as nanoscale field-effect transistors, and can be assembled into crossed-wire p-n junctions that exhibit rectifying behaviour. Significantly, the p-n junctions emit light strongly and are perhaps the smallest light-emitting diodes that have yet been made. Finally, we show that electric-field-directed assembly can be used to create highly integrated device arrays from nanowire building blocks.     

The lipid phosphatase SHIP2 controls insulin sensitivity

Insulin is the primary hormone involved in glucose homeostasis, and impairment of insulin action and/or secretion has a critical role in the pathogenesis of diabetes mellitus. Type-II SH2-domain-containing inositol 5-phosphatase, or 'SHIP2', is a member of the inositol polyphosphate 5-phosphatase family. In vitro studies have shown that SHIP2, in response to stimulation by numerous growth factors and insulin, is closely linked to signalling events mediated by both phosphoinositide-3-OH kinase and Ras/mitogen-activated protein kinase. Here we report the generation of mice lacking the SHIP2 gene. Loss of SHIP2 leads to increased sensitivity to insulin, which is characterized by severe neonatal hypoglycaemia, deregulated expression of the genes involved in gluconeogenesis, and perinatal death. Adult mice that are heterozygous for the SHIP2 mutation have increased glucose tolerance and insulin sensitivity associated with an increased recruitment of the GLUT4 glucose transporter and increased glycogen synthesis in skeletal muscles. Our results show that SHIP2 is a potent negative regulator of insulin signalling and insulin sensitivity in vivo.     

N-terminal acetylation in a third protein family of vertebrate alcohol dehydrogenase/retinal reductase found through a 'proteomics' approach in enzyme characterization

A recent finding of a novel class of retinol-active alcohol dehydrogenase (ADH) in frog prompted analysis of this activity in other vertebrate forms. Surprisingly, yet another and still more unrelated ADH was identified in chicken tissues. It was found to be a member of the aldo-keto reductase (AKR) enzyme family, not previously known as an ADH in vertebrates. Its terminal blocking group and the N-terminal segment, not assigned by protein and cDNA structure analysis, were determined by electrospray tandem mass spectrometry after protein isolation by two-dimensional gel electrophoresis. The N terminus is Acetyl-Ala- and the N-terminal segment contains two consecutive Asn residues. The results establish the new ADH enzyme of the AKR family and show the usefulness of combined gel separation and mass spectrometry in enzyme-characterization.     

Recent mass balance of polar ice sheets inferred from patterns of global sea-level change

Global sea level is an indicator of climate change, as it is sensitive to both thermal expansion of the oceans and a reduction of land-based glaciers. Global sea-level rise has been estimated by correcting observations from tide gauges for glacial isostatic adjustment--the continuing sea-level response due to melting of Late Pleistocene ice--and by computing the global mean of these residual trends. In such analyses, spatial patterns of sea-level rise are assumed to be signals that will average out over geographically distributed tide-gauge data. But a long history of modelling studies has demonstrated that non-uniform--that is, non-eustatic--sea-level redistributions can be produced by variations in the volume of the polar ice sheets. Here we present numerical predictions of gravitationally consistent patterns of sea-level change following variations in either the Antarctic or Greenland ice sheets or the melting of a suite of small mountain glaciers. These predictions are characterized by geometrically distinct patterns that reconcile spatial variations in previously published sea-level records. Under the--albeit coarse--assumption of a globally uniform thermal expansion of the oceans, our approach suggests melting of the Greenland ice complex over the last century equivalent to -0.6 mm yr(-1) of sea-level rise.