Hoffmannfoss4467

Hyperglycemia activates innate leukocytes such as monocytes and induces pro-inflammatory cytokine expression, resulting in increased monocyte adhesion to aortic endothelial cells. In this study, we investigated whether high glucose and/or tumor necrosis factor (TNF) would enhance pro-inflammatory cytokine expression of tumor necrosis factor (TNF) and interleukin (IL)-1β (IL1B) by altering histone modifications in U937, a juvenile macrophage cell line. The mRNA levels of TNF and IL1B in U937 cells were significantly affected by glucose concentration and TNF treatment. Mono-methylated histone H3K4 signals around TNF and IL1B were lower in cells treated with high glucose compared with low glucose. Conversely, tri-methylated histone H3K4 and H3K36 signals were higher in cells treated with high glucose compared with low glucose. TNF treatment of U937 cells cultured in high glucose enhanced histone H3K36 tri-methylation, particularly around the gene regions of TNF and IL1B. Histone acetylation was induced by treatment with TNF in high-glucose medium. The induction of acetylation and tri-methylation of K4 and K36 of histone H3 around TNF and IL1B by treatment with high glucose and/or TNF was positively associated with the induction of these genes in juvenile macrophage U937 cells.Dehydrins (DHNs) play critical roles in plant adaptation to abiotic stresses. The objective of this study was to characterize DHNs in bermudagrass (Cynodon spp.). CdDHN4 gene was cloned from bermudagrass 'Tifway'. Two CdDHN4 transcripts were detected due to alternative splicing (the nonspliced CdDHN4-L and the spliced CdDHN4-S) and both the CdDHN4-S and CdDHN4-L proteins are YSK2-type DHNs, the Φ-segment is present in CdDHN4-L and absent in CdDHN4-S. Transgenic Arabidopsis thaliana expressing CdDHN4-L or CdDHN4-S exhibited improved tolerance to salt, osmotic, low temperature and drought stress compared to the wild type (WT). The two transgenic lines did not differ in salt or drought tolerance, while plants expressing CdDHN4-S grew better under osmotic stress than those expressing CdDHN4-L. Both transgenic lines exhibited reduced content of malondialdehyde (MDA) and reactive oxygen species (ROS); and higher antioxidant enzymatic activities than the wild type plants under salt or drought stress. CdDHN4-S exhibited a higher ROS-scavenging capacity than CdDHN4-L.Mouse Ptchd3 (patched domain containing 3) was previously identified as a male germ-cell specific gene. The protein product of this gene has been found on the surface of mouse, rat and human sperm. Since Ptchd3 contains a conserved patched domain, we hypothesize that it functions as a membrane receptor for the hedgehog ligand. Herein, we used a Ptchd3 knockout mouse model to study its function in mouse development and spermatogenesis. We found that Ptchd3 knockout mice were born and lived normally. The fertility and sperm production of knockout males were not changed. Moreover, our data indicated that the expression levels of several hedgehog signaling genes were not affected in mutant testis. Taken together, these findings demonstrate that Ptchd3 is a non-essential gene in mouse development and spermatogenesis.Background Human mesenchymal stromal cells (MSCs) phenotypically share their positive expression of the International Society for Cell and Gene Therapy (ISCT) markers CD73, CD90 and CD105 with fibroblasts. Fibroblasts are often co-isolated as an unwanted by-product from biopsy and they can rapidly overgrow the MSCs in culture. Indeed, many other surface markers have been proposed, though no unique MSC specific marker has been identified yet. Quantitative PCR (qPCR) is a precise, efficient and rapid method for gene expression analysis. To identify a marker suitable for accurate MSC characterisation, qPCR was exploited. Methods and results Two commercially obtained bone marrow (BM) derived MSCs and an hTERT immortalised BM-MSC line (MSC-TERT) have been cultured for different days and at different oxygen levels before RNA extraction. Together with RNA samples previous extracted from umbilical cord derived MSCs and MSC-TERT cells cultured in 2D or 3D, this heterogeneous sample set was quantitatively analysed for the expression levels of 18 candidate MSC marker genes. The expression levels in MSCs were compared with the expression levels in fibroblasts to verify the differentiation capability of these genes between MSCs and fibroblasts. None of the ISCT markers could differentiate between fibroblasts and MSCs. A total of six other genes (ALCAM, CLIC1, EDIL3, EPHA2, NECTIN2, and TMEM47) were identified as possible biomarkers for accurate identification of MSCs. GS-4997 mouse Conclusion Justified by considerations on expression level, reliability and specificity, Activated-Leukocyte Cell Adhesion Molecule (ALCAM) was the best candidate for improving the biomarker set of MSC identification.Black/African-American (B/AA) breast cancer patients tend to have more aggressive tumor biology compared to White/Caucasians. In this study, a variety of breast tumor molecular expression profiles of patients derived from the two racial groupings were investigated. Breast invasive carcinoma sample data (RNASeq version 2, Reverse Phase Protein Array, mutation, and miRSeq data) from the Cancer Genome Atlas were examined. The results affirm that B/AA patients are more likely than Caucasian patients to harbor the aggressive basal-like or the poor prognosis-associated HER2-enriched molecular subtypes of breast cancer. There is also a higher incidence of the triple-negative breast cancer (TNBC) among B/AA patients than the general population, a fact reflected in the mutation patterns of genes such as PIK3CA and TP53. Furthermore, an immortalization signature gene set, is enriched in samples from B/AA patients. Among stage III patients, TERT, DRAP1, and PQBP1, all members of the immortalization gene signature set, a of stage II patients 50 years of age or younger at diagnosis, was distinctly poorer in B/AA patients. Also associated with this subset of B/AA patients are missense mutations in HUWE1 and PTEN expression loss. Relative to Caucasian non-responders to endocrine therapy, B/AA non-responders show suppressed expression of a signature gene set on which biological processes including signaling by interleukins, circadian clock, regulation of lipid metabolism by PPARα, FOXO-mediated transcription, and regulation of TP53 degradation are over-represented. Thus, we identify molecular expression patterns suggesting diminished response to oxidative stress, changes in regulation of tumor suppressors/facilitators, and enhanced immortalization in B/AA patients are likely important in defining the more aggressive molecular tumor phenotype reported in B/AA patients.