Overcoming the fundamental light-extraction efficiency limitations of deep ultraviolet light-emitting diodes by utilizing transverse-magnetic-dominant emission

While the demand for deep ultraviolet (DUV) light sources is rapidly growing, the efficiency of current AlGaN-based DUV light-emitting diodes (LEDs) remains very low due to their fundamentally limited light-extraction efficiency (LEE), calling for a novel LEE-enhancing approach to deliver a real breakthrough. Here, we propose sidewall emission-enhanced (SEE) DUV LEDs having multiple light-emitting mesa stripes to utilize inherently strong transverse-magnetic polarized light from the AlGaN active region and three-dimensional reflectors between the stripes. The SEE DUV LEDs show much enhanced light output power with a strongly upward-directed emission due to the exposed sidewall of the active region and Al-coated selective-area-grown n-type GaN micro-reflectors. The devices also show reduced operating voltage due to better n-type ohmic contact formed on the regrown n-GaN stripes when compared with conventional LEDs. Accordingly, the proposed approach simultaneously improves optical and electrical properties. In addition, strategies to further enhance the LEE up to the theoretical optimum value and control emission directionality are discussed.ope

Role of Intraspecies Recombination in the Spread of Pathogenicity Islands within the Escherichia coli Species

Horizontal gene transfer is a key step in the evolution of bacterial pathogens. Besides phages and plasmids, pathogenicity islands (PAIs) are subjected to horizontal transfer. The transfer mechanisms of PAIs within a certain bacterial species or between different species are still not well understood. This study is focused on the High-Pathogenicity Island (HPI), which is a PAI widely spread among extraintestinal pathogenic Escherichia coli and serves as a model for horizontal transfer of PAIs in general. We applied a phylogenetic approach using multilocus sequence typing on HPI-positive and -negative natural E. coli isolates representative of the species diversity to infer the mechanism of horizontal HPI transfer within the E. coli species. In each strain, the partial nucleotide sequences of 6 HPI–encoded genes and 6 housekeeping genes of the genomic backbone, as well as DNA fragments immediately upstream and downstream of the HPI were compared. This revealed that the HPI is not solely vertically transmitted, but that recombination of large DNA fragments beyond the HPI plays a major role in the spread of the HPI within E. coli species. In support of the results of the phylogenetic analyses, we experimentally demonstrated that HPI can be transferred between different E. coli strains by F-plasmid mediated mobilization. Sequencing of the chromosomal DNA regions immediately upstream and downstream of the HPI in the recipient strain indicated that the HPI was transferred and integrated together with HPI–flanking DNA regions of the donor strain. The results of this study demonstrate for the first time that conjugative transfer and homologous DNA recombination play a major role in horizontal transfer of a pathogenicity island within the species E. coli

An elegant route to overcome fundamentally-limited light extraction in AlGaN deep-ultraviolet light-emitting diodes: Preferential outcoupling of strong in-plane emission

While there is an urgent need for semiconductor-based efficient deep ultraviolet (DUV) sources, the efficiency of AlGaN DUV light-emitting diodes (LEDs) remains very low because the extraction of DUV photons is significantly limited by intrinsic material properties of AlGaN. Here, we present an elegant approach based on a DUV LED having multiple mesa stripes whose inclined sidewalls are covered by a MgF2/Al omni-directional mirror to take advantage of the strongly anisotropic transverse-magnetic polarized emission pattern of AlGaN quantum wells. The sidewall-emission-enhanced DUV LED breaks through the fundamental limitations caused by the intrinsic properties of AlGaN, thus shows a remarkable improvement in light extraction as well as operating voltage. Furthermore, an analytic model is developed to understand and precisely estimate the extraction of DUV photons from AlGaN DUV LEDs, and hence to provide promising routes for maximizing the power conversion efficiency.open111812sciescopu

Improving "color rendering" of LED lighting for the growth of lettuce

Light plays a vital role on the growth and development of plant. On the base of white light with high color rendering to the benefit of human survival and life, we proposed to improve “color rendering” of LED lighting for accelerating the growth of lettuce. Seven spectral LED lights were adopted to irradiate the lettuces under 150 μmol·m−2·s−1 for a 16 hd−1 photoperiod. The leaf area and number profiles, plant biomass, and photosynthetic rate under the as-prepared LED light treatments were investigated. We let the absorption spectrum of fresh leaf be the emission spectrum of ideal light and then evaluate the “color rendering” of as-prepared LED lights by the Pearson product-moment correlation coefficient and CIE chromaticity coordinates. Under the irradiation of red-yellow-blue light with high correlation coefficient of 0.587, the dry weights and leaf growth rate are 2-3 times as high as the sharp red-blue light. The optimized LED light for lettuce growth can be presumed to be limited to the angle (about 75°) between the vectors passed through the ideal light in the CIE chromaticity coordinates. These findings open up a new idea to assess and find the optimized LED light for plant growth

HIV-1 Vpu Neutralizes the Antiviral Factor Tetherin/BST-2 by Binding It and Directing Its Beta-TrCP2-Dependent Degradation

Host cells impose a broad range of obstacles to the replication of retroviruses. Tetherin (also known as CD317, BST-2 or HM1.24) impedes viral release by retaining newly budded HIV-1 virions on the surface of cells. HIV-1 Vpu efficiently counteracts this restriction. Here, we show that HIV-1 Vpu induces the depletion of tetherin from cells. We demonstrate that this phenomenon correlates with the ability of Vpu to counteract the antiviral activity of both overexpressed and interferon-induced endogenous tetherin. In addition, we show that Vpu co-immunoprecipitates with tetherin and β-TrCP in a tri-molecular complex. This interaction leads to Vpu-mediated proteasomal degradation of tetherin in a β-TrCP2-dependent manner. Accordingly, in conditions where Vpu-β-TrCP2-tetherin interplay was not operative, including cells stably knocked down for β-TrCP2 expression or cells expressing a dominant negative form of β-TrCP, the ability of Vpu to antagonize the antiviral activity of tetherin was severely impaired. Nevertheless, tetherin degradation did not account for the totality of Vpu-mediated counteraction against the antiviral factor, as binding of Vpu to tetherin was sufficient for a partial relief of the restriction. Finally, we show that the mechanism used by Vpu to induce tetherin depletion implicates the cellular ER-associated degradation (ERAD) pathway, which mediates the dislocation of ER membrane proteins into the cytosol for subsequent proteasomal degradation. In conclusion, we show that Vpu interacts with tetherin to direct its β-TrCP2-dependent proteasomal degradation, thereby alleviating the blockade to the release of infectious virions. Identification of tetherin binding to Vpu provides a potential novel target for the development of drugs aimed at inhibiting HIV-1 replication

Antagonism of Tetherin Restriction of HIV-1 Release by Vpu Involves Binding and Sequestration of the Restriction Factor in a Perinuclear Compartment

The Vpu accessory protein promotes HIV-1 release by counteracting Tetherin/BST-2, an interferon-regulated restriction factor, which retains virions at the cell-surface. Recent reports proposed β-TrCP-dependent proteasomal and/or endo-lysosomal degradation of Tetherin as potential mechanisms by which Vpu could down-regulate Tetherin cell-surface expression and antagonize this restriction. In all of these studies, Tetherin degradation did not, however, entirely account for Vpu anti-Tetherin activity. Here, we show that Vpu can promote HIV-1 release without detectably affecting Tetherin steady-state levels or turnover, suggesting that Tetherin degradation may not be necessary and/or sufficient for Vpu anti-Tetherin activity. Even though Vpu did not enhance Tetherin internalization from the plasma membrane (PM), it did significantly slow-down the overall transport of the protein towards the cell-surface. Accordingly, Vpu expression caused a specific removal of cell-surface Tetherin and a re-localization of the residual pool of Tetherin in a perinuclear compartment that co-stained with the TGN marker TGN46 and Vpu itself. This re-localization of Tetherin was also observed with a Vpu mutant unable to recruit β-TrCP, suggesting that this activity is taking place independently from β-TrCP-mediated trafficking and/or degradation processes. We also show that Vpu co-immunoprecipitates with Tetherin and that this interaction involves the transmembrane domains of the two proteins. Importantly, this association was found to be critical for reducing cell-surface Tetherin expression, re-localizing the restriction factor in the TGN and promoting HIV-1 release. Overall, our results suggest that association of Vpu to Tetherin affects the outward trafficking and/or recycling of the restriction factor from the TGN and as a result promotes its sequestration away from the PM where productive HIV-1 assembly takes place. This mechanism of antagonism that results in TGN trapping is likely to be augmented by β-TrCP-dependent degradation, underlining the need for complementary and perhaps synergistic strategies to effectively counteract the powerful restrictive effects of human Tetherin

Walking ability during daily life in patients with osteoarthritis of the knee or the hip and lumbar spinal stenosis: a cross sectional study

<p>Abstract</p> <p>Background</p> <p>Degenerative musculoskeletal disorders are among the most frequent diseases occurring in adulthood, often impairing patients' functional mobility and physical activity. The aim of the present study was to investigate and compare the impact of three frequent degenerative musculoskeletal disorders -- knee osteoarthritis (knee OA), hip osteoarthritis (hip OA) and lumbar spinal stenosis (LSS) -- on patients' walking ability.</p> <p>Methods</p> <p>The study included 120 participants, with 30 in each patient group and 30 healthy control individuals. A uniaxial accelerometer, the StepWatch™ Activity Monitor (Orthocare Innovations, Seattle, Washington, USA), was used to determine the volume (number of gait cycles per day) and intensity (gait cycles per minute) of walking ability. Non-parametric testing was used for all statistical analyses.</p> <p>Results</p> <p>Both the volume and the intensity of walking ability were significantly lower among the patients in comparison with the healthy control individuals (p < 0.001). Patients with LSS spent 0.4 (IQR 2.8) min/day doing moderately intense walking (>50 gait cycles/min), which was significantly lower in comparison with patients with knee and hip OA at 2.5 (IQR 4.4) and 3.4 (IQR 16.1) min/day, respectively (p < 0.001). No correlations between demographic or anthropometric data and walking ability were found. No technical problems or measuring errors occurred with any of the measurements.</p> <p>Conclusions</p> <p>Patients with degenerative musculoskeletal disorders suffer limitations in their walking ability. Objective assessment of walking ability appeared to be an easy and feasible tool for measuring such limitations as it provides baseline data and objective information that are more precise than the patients' own subjective estimates. In everyday practice, objective activity assessment can provide feedback for clinicians regarding patients' performance during everyday life and the extent to which this confirms the results of clinical investigations. The method can also be used as a way of encouraging patients to develop a more active lifestyle.</p

Species-Specific Activity of HIV-1 Vpu and Positive Selection of Tetherin Transmembrane Domain Variants

Tetherin/BST-2/CD317 is a recently identified antiviral protein that blocks the release of nascent retrovirus, and other virus, particles from infected cells. An HIV-1 accessory protein, Vpu, acts as an antagonist of tetherin. Here, we show that positive selection is evident in primate tetherin sequences and that HIV-1 Vpu appears to have specifically adapted to antagonize variants of tetherin found in humans and chimpanzees. Tetherin variants found in rhesus macaques (rh), African green monkeys (agm) and mice were able to inhibit HIV-1 particle release, but were resistant to antagonism by HIV-1 Vpu. Notably, reciprocal exchange of transmembrane domains between human and monkey tetherins conferred sensitivity and resistance to Vpu, identifying this protein domain as a critical determinant of Vpu function. Indeed, differences between hu-tetherin and rh-tetherin at several positions in the transmembrane domain affected sensitivity to antagonism by Vpu. Two alterations in the hu-tetherin transmembrane domain, that correspond to differences found in rh- and agm-tetherin proteins, were sufficient to render hu-tetherin completely resistant to HIV-1 Vpu. Interestingly, transmembrane and cytoplasmic domain sequences in primate tetherins exhibit variation at numerous codons that is likely the result of positive selection, and some of these changes coincide with determinants of HIV-1 Vpu sensitivity. Overall, these data indicate that tetherin could impose a barrier to viral zoonosis as a consequence of positive selection that has been driven by ancient viral antagonists, and that the HIV-1 Vpu protein has specialized to target the transmembrane domains found in human/chimpanzee tetherin proteins