We examined cross-sectional associations between depression and both inflammatory markers and fractional exhaled nitric oxide (FeNO).
 
  This cross-sectional study is a secondary analysis of the data of the Iwaki Health Promotion Project 2016 (1,148 subjects). We analyzed the subjects' characteristics and laboratory data including plasma interleukin (IL)-6, high-sensitivity C-reactive protein (hs-CRP), and FeNO. The subjects with Center for Epidemiologic Studies Depression Scale scores ≥16 were assigned to the depression group. We performed a multivariate logistic regression analysis to determine whether inflammatory markers and FeNO were associated with depression.
 
  We assessed 1,099 subjects (430 males, 669 females). The depression group was 237 subjects (21.5%) [84 males (19.5%), 153 females (22.9%)]. The non-depression group was 862 subjects (346 males and 516 females). There were no significant differences in IL-6, hs-CRP, or FeNO between both groups. However, the multivariate logistic regression analysis indicated that lower FeNO was significantly associated with depression in males after adjusting for possible confounding factors (age, BMI, comorbidities, high-sensitivity troponin T, FEV
  %, asthma, antidepressant use, smoker and alcohol drinker) (per 1bpm increase, OR 0.982; 95%CI 0.967-0.998; p=0.032).
 
  Our findings indicate that lower FeNO may be associated with depression in males.
 Our findings indicate that lower FeNO may be associated with depression in males.Oxidative stress and inflammation lead to cell damage and are implicated in many disease states. High concentrations of hydrogen peroxide (H2O2) may mediate cells apoptosis by increasing intracellular reactive oxygen species (ROS) levels. In this study, we established a LYCK-PrxIV cell line (large yellow croaker head kidney cell line stably expressing peroxiredoxin IV). The level of nitric oxide (NO), superoxide anion and hydrogen peroxide (H2O2) in this LYCK-PrxIV cells were significantly lower than those in control cells of LYCK-pcDNA3.1 (LYCK cell line stably transfected by pcDNA3.1 vector). Additionally, when exposed to H2O2, cell apoptosis was significantly alleviated in LYCK-PrxIV than in control cells. Meanwhile, the ROS level and ATP content were maintained more stable in LYCK-PrxIV than in LYCK-pcDNA3.1. The over-expression of LcPrxIV in LYCK-PrxIV cells induced a declined mRNA expression of LcCXC, LcCC, LcIL-8 and LcTNF-α2, as well as an increase of LcIL-10 mRNA expression, when compared to LYCK-pcDNA3.1. On the other hand, the expression of chemokine LcCXC, LcCC and LcTNF-a2 increased in LYCK-pcDNA3.1 after H2O2 stimulation, while that of LcIL-8 and LcIL-10 decreased.  https://www.selleckchem.com/  The regualtion of gene expression in LYCK-PrxIV cells was almost the same as that in LYCK-pcDNA3.1, but the change fold was much more moderate. These results suggest that LcPrxIV may be an indispensable ROS scavenger protecting LYCK cells against oxidative damage as well as the subsequent apoptosis and inflammatory response, which provides a clue that LcPrxIV may be an assist in fish immune response.Sepsis-induced inflammatory damage is a crucial cause of acute kidney injury (AKI), and AKI is an ecumenical fearful complication in approximately half of patients with sepsis. CCAAT/enhancer-binding protein β (C/EBPβ) plays roles in regulating acute phase responses and inflammation. However, the role and mechanism of C/EBPβ in AKI are unclear. LPS combined with ATP-treated renal epithelial cells HK2 and cecal ligation-peferation (CLP)-mice were used as models of AKI in vitro and in vivo. Cell damage, the secretion of interleukin-1 beta (IL-1β), IL-18 and cysteinyl aspartate specific proteinase 1 (caspase-1) activity were tested by LDH, ELISA assay and flow cytometry analysis, respectively. The expression levels of TFAM, C/EBPβ, and pyroptosis-related molecules were tested by qRT-PCR and Western blotting. Chromatin immunoprecipitation (ChIP) assessed the interaction between C/EBPβ with TFAM. Hematoxylin-Eosin (H&E) staining detected pathological changes of kidney tissues, and immunohistochemistry measured TFAM and C/EBPβ in mice kidney tissues. C/EBPβ or TFAM were up-regulated in LPS combined with ATP -induced HK2 cells. Knockdown of C/EBPβ could suppress cell injury and the secretion of IL-1β and IL-18 induced by LPS combined with ATP. Furthermore, C/EBPβ up-regulated the expression levels of TFAM via directly binding to TFAM promoter. Overexpression of TFAM reversed the effects of C/EBPβ deficiency on pyroptosis. Knockdown of C/EBPβ could inhibit NLRP3 inflammasome-mediated caspase-1 signaling pathway by inactivating TFAM/RAGE pathway. It was further confirmed in the AKI mice that C/EBPβ and TFAM promoted AKI by activating NLRP3-mediated pyroptosis. The interaction of between C/EBPβ and TFAM facilitated pyroptosis by activating NLRP3/caspase-1 signal axis, thereby promoting the occurrence of AKI.The aim of this study was to determine the interaction of peripheral immunity vs. the CNS in the setting of AD pathogenesis at the transcriptomic level in a data driven manner. For this purpose, publicly available gene expression data from the GEO Datasets repository. We performed differential gene expression and functional enrichment analyses were performed on the five retrieved studies (a) three hippocampal cortex (HC) studies (b) one study of peripheral blood mononuclear cells (PBMC) and (c) one involving neurofibrillary tangle - containing neurons of the entorhinal cortex (NFT EC). Subsequently, BLAST was used to determine protein conservation between human proteins vs. microbial, whereas putative protein / oligopeptide antigenicity were determined via RANKPep. Gene ontology and pathway analyses revealed significantly enriched viral parasitism pathways in both PBMC and NFT - EC datasets, mediated by ribosomal protein families and epigenetic regulators. Among these, a salient viral pathway referred to Influenza A infection. NFT - EC annotations included leukocyte chemotaxis and immune response pathways. All datasets were significantly enriched for infectious pathways, as well as pathways involved in impaired proteostasis and non - phagocytic cell phagosomal cascades. In conclusion, our in silico analysis outlined an ad hoc model of AD pathophysiology in which double hit (PBMC and NFT-EC) viral parasitism is mediated by eukaryotic translational hijacking, and may be further implicated by impaired immune responses. Overall, our results overlap with the antimicrobial protection hypothesis of AD pathogenesis and support the notion of a pathogen - driven etiology.