C720

F. Robert Henderson et al., Increasing Eastern Bluebirds in Kansas, Kansas State University, November 1990

Active-matrix GaN micro light-emitting diode display with unprecedented brightness

Displays based on microsized gallium nitride light-emitting diodes possess extraordinary brightness. It is demonstrated here both theoretically and experimentally that the layout of the n-contact in these devices is important for the best device performance. We highlight, in particular, the significance of a nonthermal increase of differential resistance upon multipixel operation. These findings underpin the realization of a blue microdisplay with a luminance of 10⁶ cd/m²

Nucleocapsid Protein Zinc-Finger Mutants of Simian Immunodeficiency Virus Strain Mne Produce Virions That Are Replication Defectivein Vitroandin Vivo

AbstractAll retroviruses (except the spumaretroviruses) contain a nucleocapsid (NC) protein that encodes one or two copies of the Zn2+-finger sequence -Cys-X2-Cys-X4-His-X4-Cys-. This region has been shown to be essential for recognition and packaging of the genomic RNA during virion particle assembly. Additionally, this region has been shown to be involved in early infection events in a wide spectrum of retroviruses, including mammalian type C [e.g., murine leukemia virus (MuLV)], human immunodeficiency virus type 1 (HIV-1),Rous sarcomavirus, and other retroviruses. Mutations in the two Zn2+-fingers of the NC protein of simian immunodeficiency virus strain Mne [SIV(Mne)] have been generated. The resulting virions contained the normal complement of processed viral proteins with densities indistinguishable from wild-type SIV(Mne). All of the mutants had electron micrograph morphologies similar to those of immature particles observed in wild-type preparations. RNA packaging was less affected by mutations in the NC protein of SIV(Mne) than has been observed for similar mutants in the MuLV and HIV-1 systems. Nevertheless,in vitroreplication of SIV(Mne) NC mutants was impaired to levels comparable to those observed for MuLV and HIV-1 NC mutants; replication defective NC mutants are typically 105- to 106-fold less infectious than similar levels of wild-type virus. One mutant, ΔCys33–Cys36, was also found to be noninfectiousin vivowhen mutant virus was administered intravenously to a pig-tailed macaque. NC mutations can therefore be used to generate replication defective virions for candidate vaccines in the SIV macaque model for primate lentiviral diseases

Copy Number Variation of <i>CCL3-</i>like Genes Affects Rate of Progression to Simian-AIDS in Rhesus Macaques (<i>Macaca mulatta</i>)

Variation in genes underlying host immunity can lead to marked differences in susceptibility to HIV infection among humans. Despite heavy reliance on non-human primates as models for HIV/AIDS, little is known about which host factors are shared and which are unique to a given primate lineage. Here, we investigate whether copy number variation (CNV) at CCL3-like genes (CCL3L), a key genetic host factor for HIV/AIDS susceptibility and cell-mediated immune response in humans, is also a determinant of time until onset of simian-AIDS in rhesus macaques. Using a retrospective study of 57 rhesus macaques experimentally infected with SIVmac, we find that CCL3L CNV explains approximately 18% of the variance in time to simian-AIDS (pCCL3L copy number associating with more rapid disease course. We also find that CCL3L copy number varies significantly (p−6) among rhesus subpopulations, with Indian-origin macaques having, on average, half as many CCL3L gene copies as Chinese-origin macaques. Lastly, we confirm that CCL3L shows variable copy number in humans and chimpanzees and report on CCL3L CNV within and among three additional primate species. On the basis of our findings we suggest that (1) the difference in population level copy number may explain previously reported observations of longer post-infection survivorship of Chinese-origin rhesus macaques, (2) stratification by CCL3L copy number in rhesus SIV vaccine trials will increase power and reduce noise due to non-vaccine-related differences in survival, and (3) CCL3L CNV is an ancestral component of the primate immune response and, therefore, copy number variation has not been driven by HIV or SIV per se.</p

The Influence of {sup 18} F Induced Reactions in the Hot CNO Cycle

The contribution of the {sup 18}F(p,{gamma}) reaction to the production of {sup 19}Ne, which is an important isotope in connection with the breakout from the hot CNO cycle, has been investigated in experiments with {sup 18}F beams. Measurements of the cross sections for the {sup 18}F(p,{alpha}){sup 15}O and {sup 18}F(p,{gamma}){sup 19 }Ne reactions indicate that the contribution of the {sup 18}F(p, {gamma}) route to the formation or {sup 19}Ne is small