Together, these results indicate that Arabidopsis JMJ28 functions as a CO activator by interacting with the FBH transcription factors to remove H3K9me2 from the CO locus.Over the past four decades, group-based microfinance programs have spread rapidly throughout south Asia, sub-Saharan Africa and Latin America. Recent evaluations of the programs have identified social capital as a common byproduct of frequent association by members, increasing trust, belonging and normative influence. Concurrently, social capital is increasingly recognized as an important health determinant. We present an overview of a program intervention operating in Kenya that utilizes a microfinance approach to produce social capital, and seeks to leverage that social capital to promote health at three levels-the village, group, and individual. A theory of change is presented for each of these three levels, demonstrating conceptually and with program examples how social capital can be applied to promote health. Related social theories and approaches, further research and program directions are given for each of the three levels. We identify potential to improve a broad range of health outcomes through this innovative model, which requires engagement with health promotion researchers and planners in low- and middle-income countries for further refinement and validation.The uptake of di/tripeptides is mediated by the proton-dependent oligopeptide transporter (POT) family. In this study, 3 POT family transporters, designated PotA, PotB, and PotC were identified in Aspergillus oryzae. Growth comparison of deletion mutants of these transporter genes suggested that PotB and PotC are responsible for di/tripeptide uptake. PotA, which had the highest sequence similarity to yeast POT (Ptr2), contributed little to the uptake. Nitrogen starvation induced potB and potC expression, but not potA expression. When 3 dipeptides were provided as nitrogen sources, the expression profiles of these genes were different. PrtR, a transcription factor that regulates proteolytic genes, was involved in regulation of potA and potB but not in potC expression. Only potC expression levels were dramatically reduced by disruption of ubrA, an orthologue of yeast ubiquitin ligase UBR1 responsible for PTR2 expression. Expression of individual POT genes is apparently controlled by different regulatory mechanisms.Pneumonia is a common respiratory disease worldwide. Long noncoding RNAs have been implicated in the pathogenesis of pneumonia.  https://www.selleckchem.com/products/gpr84-antagonist-8.html  However, the effect and mechanism of long intergenic nonprotein-coding RNA (LINC00707) on pneumonia pathogenesis were still unclear. Lipopolysaccharide (LPS) reduced cell viability and promoted apoptosis and inflammation in MRC-5 cells. LINC00707 was increased, and miR-223-5p was decreased in LPS-treated MRC-5 cells. LINC00707 knockdown relieved LPS-triggered injury in MRC-5 cells. LINC00707 directly interacted with miR-223-5p through acting as a miR-223-5p sponge. Moreover, miR-223-5p mediated the regulation of LINC00707 silencing on LPS-stimulated cytotoxicity in MRC-5 cells. p38 mitogen-activated protein kinases and nuclear factor-κB signaling pathways were modulated by the LINC00707/miR-223-5p axis in LPS-induced MRC-5 cells. Our present study indicated that LINC00707 depletion alleviated LPS-induced injury in MRC-5 cells at least partly by acting as a sponge of miR-223-5p, highlighting a new potential therapeutic avenue for pneumonia treatment.Neohesperidin (NEO) exerts antiviral, antioxidant, anti-inflammation, and antitumor effects in some diseases. The purpose of this study was to investigate the effect and mechanism of NEO on myocardial ischemia-reperfusion (I/R) injury. Results indicated that NEO suppressed the levels of serum inflammatory cytokines, myocardial damage markers, and oxidative stress markers, and increased the levels of antioxidant in myocardial I/R rats. NEO also inhibited cell apoptosis. Besides, NEO also inhibited the phosphorylation of c-Jun N-terminal kinases (JNK) and nuclear factor kappa B (NF-κB) p65. Furthermore, the protective effects of NEO on myocardial tissue damage, inflammatory cytokines, myocardial injury markers, oxidative stress markers, cell apoptosis, spleen, thymus and liver indices, and phagocytic indices were reversed by JNK activator and NF-κB activator, respectively. In conclusion, NEO alleviates myocardial damage, oxidative stress, cell apoptosis, and immunological imbalance in I/R injury via the inactivation of JNK and NF-κB, making NEO a potential agent for myocardial I/R therapy.APS001F is a strain of Bifidobacterium longum genetically engineered to express cytosine deaminase that converts 5-fluorocytosine (5-FC) to 5-fluorouracil. In the present study, antitumor effects of APS001F plus 5-FC (APS001F/5-FC) in combination with anti-PD-1 monoclonal antibody were investigated using a CT26 syngeneic mouse model. Both of dosing of APS001F/5-FC before and after anti-PD-1 mAb in the combination dosing exhibited antitumor effects as well as prolonged survival over the nontreated control. The survival rate in the combination therapy significantly increased over the monotherapy with APS001F/5-FC and that with anti-PD-1 mAb. Regulatory T cells among CD4+ T cells in tumor decreased in the combination therapy, while the ratio of CD8+ T cells was maintained in all groups. Taken these results together, APS001F/5-FC not only demonstrates a direct antitumor activity, but also immunomodulatory effects once localized in the hypoxic region of the tumor, which allows anti-PD-1 mAb to exert potentiated antitumor effects.Non-small cell lung cancer (NSCLC) accounts for ∼80-85% of all lung cancer cases, and the EML4-ALK fusion oncogene is a well-known contributor to NSCLC cases. Expensive methods such as FISH, IHC, and NGS have been used to detect the EML4-ALK fusion oncogene. Here, a cost-effective and facile method of detecting and differentiating an EML4-ALK fusion oncogene from the wild-type gene has been accomplished by DNA hybridization using the microfluidic biochip. First, oligonucleotide probes were confirmed for successful detection of immobilized sense strands. Second, capture of the sense PCR product strands (fusion and WT) and their subsequent detection and differentiation were accomplished. Our proof-of-concept study shows the ability to detect 1% fusion products, among WT ones.