Analytical Study on Junction Temperatures of GaInN and AlGaN Ultraviolet Light Emitting Diodes.

Junction temperatures of GaInN and AlGaN UV LEDs are analytically investigated in this paper. GaInN and AlGaN UV LEDs have a wide variety of applications such as lighting, displays, spectrofluometry, photocatalytic processes, and high resolution optics. An analytical method is employed to analyze the junction temperature variations of GaInN and AlGaN UV LEDs with injection currents. The junction temperature is related to material properties, quantum efficiency, thermal resistance, and series resistance of LEDs. The results of GaInN and AlGaN UV LEDs predicted by this study agree with these obtained from emission peak shift method and forward voltage method.

Folate supplementation modifies CCAAT/enhancer-binding protein α methylation to mediate differentiation of preadipocytes in chickens.

Folate, an essential vitamin participating in 1-carbon metabolism leading to a methyl donor function, is a key factor inducing epigenetic changes. This study sought to determine if folate influences the methylation level of cytosine-guanine (CpG) islands in the promoters of critical adipogenic genes in chickens, and how this might affect gene expression and differentiation of preadipocytes in vitro. Preadipocytes were treated with 0 to 16 mg/L of folate during the induction of differentiation, and cell proliferation and lipid accumulation were assessed. The folate supplementation resulted in enhanced cell proliferation and decreased content of lipid per adipocyte at d 6 of differentiation. The effects of folate on relative expression of genes critical for adipocyte differentiation and 1-carbon metabolism were measured by quantitative reverse-transcription PCR. Folate caused a dose-dependent decrease in transcript abundance of peroxisome proliferator-activated receptor γ (PPARγ), CCAAT/enhancer-binding protein α (C/EBPα) gene expression, and the downstream enzyme fatty acid synthase; in contrast, expression of DNA (cytosine-5)-methyltransferase and methylenetetrahydrofolate reductase was obviously upregulated at d 6 of differentiation (P < 0.05). The DNA methylation was examined with the bisulfite sequencing PCR method. Overall CpG methylation in the C/EBPα gene promoter region was 21.8% lower (P < 0.05) and the gene's expression was 2.7-fold higher in the absence of folate, compared with cells treated with 16 mg/L of folate, whereas methylation of the PPARγ promoter was not affected. Overall, the results show that folate increased the proliferation of adipocytes but reduced per-cell lipid accumulation, thereby influencing differentiation; it increased expression of genes involved in 1-carbon metabolism resulting in greater methylation of the C/EBPα promoter during differentiation and decreased that gene's expression, perhaps accounting for decreased expression of PPARγ.

Transient Increases in Inflammation and Proapoptotic Potential Are Associated with the HESN Phenotype Observed in a Subgroup of Kenyan Female Sex Workers.

Interferon (IFN) -stimulated genes (ISGs) are critical effectors of IFN response to viral infection, but whether ISG expression is a correlate of protection against HIV infection remains elusive. A well-characterized subcohort of Kenyan female sex workers, who, despite being repeatedly exposed to HIV-1 remain seronegative (HESN), exhibit reduced baseline systemic and mucosal immune activation. This study tested the hypothesis that regulation of ISGs in the cells of HESN potentiates a robust antiviral response against HIV. Transcriptional profile of a panel of ISGs with antiviral function in PBMC and isolated CD4+ T cells from HESN and non-HESN sex worker controls were defined following exogenous IFN-stimulation using relative RT-qPCR. This study identified a unique profile of proinflammatory and proapoptotic ISGs with robust but transient responses to exogenous IFN-γ and IFN-α2 in HESN cells. In contrast, the non-HESN cells had a strong and prolonged proinflammatory ISG profile at baseline and following IFN challenge. Potential mechanisms may include augmented bystander apoptosis due to increased TRAIL expression (16-fold), in non-HESN cells. The study also identified two negative regulators of ISG induction associated with the HESN phenotype. Robust upregulation of SOCS-1 and IRF-1, in addition to HDM2, could contribute to the strict regulation of proinflammatory and proapoptotic ISGs in HESN cells. As reducing IRF-1 in the non-HESN cells resulted in the identified HESN ISG profile, and decreased HIV susceptibility, the unique HESN ISG profile could be a correlate of protection against HIV infection.

Genome-Wide Linkage Analysis Identifies Loci for Physical Appearance Traits in Chickens.

Physical appearance traits, such as feather-crested head, comb size and type, beard, wattles size, and feathered feet, are used to distinguish between breeds of chicken and also may be associated with economic traits. In this study, a genome-wide linkage analysis was used to identify candidate regions and genes for physical appearance traits and to potentially provide further knowledge of the molecular mechanisms that underlie these traits. The linkage analysis was conducted with an F2 population derived from Beijing-You chickens and a commercial broiler line. Single-nucleotide polymorphisms were analyzed using the Illumina 60K Chicken SNP Beadchip. The data were used to map quantitative trait loci and genes for six physical appearance traits. A 10-cM/0.51-Mb region (0.0-10.0 cM/0.00-0.51 Mb) with 1% genome-wide significant level on LGE22C19W28_E50C23 linkage group (LGE22) for crest trait was identified, which is likely very closely linked to the HOXC8. A QTL with 5% chromosome-wide significant level for comb weight, which partly overlaps with a region identified in a previous study, was identified at 74 cM/25.55 Mb on chicken (Gallus gallus; GG) chromosome 3 (i.e., GGA3). For beard and wattles traits, an identical region 11 cM/2.23 Mb (0.0-11.0 cM/0.00-2.23 Mb) including WNT3 and GH genes on GGA27 was identified. Two QTL with 1% genome-wide significant level for feathered feet trait, one 9-cM/2.80-Mb (48.0-57.0/13.40-16.20 Mb) region on GGA13, and another 12-cM/1.45-Mb (41.0-53.0 cM/11.37-12.82 Mb) region on GGA15 were identified. These candidate regions and genes provide important genetic information for the physical appearance traits in chicken.

Genome-wide linkage analysis and association study identifies loci for polydactyly in chickens.

Polydactyly occurs in some chicken breeds, but the molecular mechanism remains incompletely understood. Combined genome-wide linkage analysis and association study (GWAS) for chicken polydactyly helps identify loci or candidate genes for the trait and potentially provides further mechanistic understanding of this phenotype in chickens and perhaps other species. The linkage analysis and GWAS for polydactyly was conducted using an F2 population derived from Beijing-You chickens and commercial broilers. The results identified two QTLs through linkage analysis and seven single-nucleotide polymorphisms (SNPs) through GWAS, associated with the polydactyly trait. One QTL located at 35 cM on the GGA2 was significant at the 1% genome-wise level and another QTL at the 1% chromosome-wide significance level was detected at 39 cM on GGA19. A total of seven SNPs, four of 5% genome-wide significance (P < 2.98 × 10(-6)) and three of suggestive significance (5.96 × 10(-5)) were identified, including two SNPs (GGaluGA132178 and Gga_rs14135036) in the QTL on GGA2. Of the identified SNPs, the eight nearest genes were sonic hedgehog (SHH), limb region 1 homolog (mouse) (LMBR1), dipeptidyl-peptidase 6, transcript variant 3 (DPP6), thyroid-stimulating hormone, beta (TSHB), sal-like 4 (Drosophila) (SALL4), par-6 partitioning defective 6 homolog beta (Caenorhabditis elegans) (PARD6B), coenzyme Q5 (COQ5), and tyrosine 3-monooxygenase/tryptophan 5-monooxygenase activation protein, etapolypeptide (YWHAH). The GWAS supports earlier reports of the importance of SHH and LMBR1 as regulating genes for polydactyly in chickens and other species, and identified others, most of which have not previously been associated with limb development. The genes and associated SNPs revealed here provide detailed information for further exploring the molecular and developmental mechanisms underlying polydactyly.