Risk of Sexually Transmitted Zika Virus in a Cohort of Economically Disadvantaged Urban Residents.

To understand the disease burden of sexually transmitted Zika virus (ZIKV), we prospectively followed a cohort of 359 adult and adolescent residents of an urban community in Salvador, Brazil, through the 2015 ZIKV epidemic. Later, in 2017, we used a retrospective survey to associate sexual behavior during the epidemic with ZIKV infection as defined by immunoglobulin G3 NS1 enzyme-linked immunosorbent assay. We found that males who engaged in casual sexual encounters during the epidemic were more likely (adjusted odds ratio, 6.2 [95% confidence interval, 1.2-64.1]) to be ZIKV positive, suggesting that specific groups may be at increased risk of sexually transmitted infections.

RNA ligation in neurons by RtcB inhibits axon regeneration.

Activity of the RNA ligase RtcB has only two known functions: tRNA ligation after intron removal and XBP1 mRNA ligation during activation of the unfolded protein response. Here, we show that RtcB acts in neurons to inhibit axon regeneration after nerve injury. This function of RtcB is independent of its basal activities in tRNA ligation and the unfolded protein response. Furthermore, inhibition of axon regeneration is independent of the RtcB cofactor archease. Finally, RtcB is enriched at axon termini after nerve injury. Our data indicate that neurons have co-opted an ancient RNA modification mechanism to regulate specific and dynamic functions and identify neuronal RtcB activity as a critical regulator of neuronal growth potential.

Preparation and Photoluminescence of Sm (3+) Doped YAlO 3 Phosphor.

YAlO3: Sm(3+) phosphor has been synthesized by the solid state reaction method with calcium flouride used as a flux. The resulting YAlO3: Sm(3+) phosphor was characterized by X-ray diffraction (XRD) technique, Fourier transmission infrared spectroscopy (FTIR), photoluminescence . . PL excitation spectrum was found at 254,332,380,400,407, 603 and 713 nm. Under excitation of UV(713 nm) YAlO3: Sm(3+) (0-3 %) broad band emission were observed from 400 to 790 nm with a maximum around 713 nm of YAlO3 host lattice accompanied by weak emission of Sm(3+) ((4)G5/2 - (6)H5/2, (6)H7/2,(6)H9/2) transitions. The results of the XRD show that obtained YAlO3: Sm(3+) phosphor has a orthorhombic structure. The study suggested that Sm(3+) doped phosphors are potential luminescence material for laser diode pumping and inorganic scintillators.

Synthesis and characterization of erbium-doped YAlO3 phosphor.

In the yttrium aluminium system, the YAlO3 phosphor is a prominent host because of the yttrium aluminium ratio (1:1). Phosphor was synthesized by the solid-state reaction method at variable concentrations of erbium (0.1-2.5 mol%). This method is suitable for large-scale production and is a less time-consuming method when compared with the soft synthesis method. The prepared sample was characterized by X-ray diffraction technique and the crystallite size was calculated by Scherer's formula. Vibrational and bending analysis of prepared phosphor for optimized concentration of erbium ion is described based on the Fourier transform infrared spectroscopic technique. The photoluminescence (PL) emission spectra of prepared phosphor for variable concentrations of erbium ion were recorded and the excitation spectrum was found to be at 291 nm with three shoulder peaks at 305, 270 and 242 nm. For 291 nm excitation, the emission spectrum was found at 546 nm and 552 nm. PL intensity increased with increasing concentrations of erbium and after 2 mol% emission intensity decreased due to concentration quenching. Spectrophotometric determination of YAlO3:Er(3+) is described by CIE co-ordinates and shows an intense emission in the green region such that the prepared phosphor can act as a single host for green light emission. Thermoluminescence glow curve analysis of the YAlO3:Er(3+) phosphor was recorded for different ultraviolet (UV) light exposures and gamma exposure. Different gamma doses 0.5-2 kGy show a linear response. Kinetic parameters were calculated by the peak shape method.

Mitochondria Localize to Injured Axons to Support Regeneration.

Axon regeneration is essential to restore the nervous system after axon injury. However, the neuronal cell biology that underlies axon regeneration is incompletely understood. Here we use in vivo, single-neuron analysis to investigate the relationship between nerve injury, mitochondrial localization, and axon regeneration. Mitochondria translocate into injured axons so that average mitochondria density increases after injury. Moreover, single-neuron analysis reveals that axons that fail to increase mitochondria have poor regeneration. Experimental alterations to axonal mitochondrial distribution or mitochondrial respiratory chain function result in corresponding changes to regeneration outcomes. Axonal mitochondria are specifically required for growth-cone migration, identifying a key energy challenge for injured neurons. Finally, mitochondrial localization to the axon after injury is regulated in part by dual-leucine zipper kinase 1 (DLK-1), a conserved regulator of axon regeneration. These data identify regulation of axonal mitochondria as a new cell-biological mechanism that helps determine the regenerative response of injured neurons.