The consumption of high-fat and high-sugar diets, in the form of junk food, and binge eating are now common. Increasing evidence suggests that a high-fat diet (HFD) can induce neuroinflammation and alter behavior. I aimed to study the effects of diets of differing fat content on neuroinflammation and spatial memory using an object-place (OP) task. Thirty-two adult male rats were allocated to four groups and fed a regular diet (Regular diet), a control diet (Control diet), an HFD (60% of calories from lard), or a high-coconut oil diet (HCOD; 60% of calories from coconut oil) for 3 days. Their water intake, food consumption, body mass, and metabolic variables were measured.  https://www.selleckchem.com/products/YM155.html  HFD-fed rats showed significantly poorer performance on the OP task, as assessed using the discrimination index (- 0.208 ± 0.094), than the Regular (0.462 ± 0.078; P  less then  0.0001) and Control (0.379 ± 0.081; P = 0.0003) groups. However, no significant difference was observed in spatial memory between the HCOD and Regular groups. The concentrations of neuroinflammatory markers (interleukin [IL]-1β, IL-6, tumor necrosis factor α, and nuclear factor κB) were also measured in the hippocampus and prefrontal cortex. HFD-fed rats showed significantly higher levels of neuroinflammatory markers than the Regular and Control diet-fed groups. HCOD feeding did not induce neuroinflammation in the hippocampus and prefrontal cortex compared with the Regular and Control groups.Lung cancer is a leading cause of cancer-associated deaths worldwide. Lung cancer may lead to circadian disruption, which could contribute to the development of lung cancer. Recently, several studies using animal models indicated that tumors influence systemic circadian homeostasis in remote tissues. However, it is unclear whether carcinoma of the lungs influences remote circadian rhythm, whether this effect exists in humans, and whether signals from the tumor travel through the blood. In this study, we used a cell-based assay to determine whether serum from patients with lung adenocarcinoma could modulate the molecular clock. We found that the daily oscillation period of Bmal1 was significantly lengthened following treatment with serum from untreated lung adenocarcinoma patients. In addition, heat inactivation of this serum abolished the effect, suggesting that a heat-sensitive circulating factor(s) is present in the serum of untreated lung adenocarcinoma patients. Using real-time PCR, we also examined the mRNA abundance of Bmal1, Cry1, and Per1 in human osteosarcoma u2os cell line, HUVECs and A549 cell lines. The expression of Bmal1 was changed in A549 cells in the presence of sera from lung adenocarcinoma patients. Our study revealed a direct effect of serum from lung adenocarcinoma patients on the molecular clock.
  To identify novel miRNAs implicated in prostate cancer metastasis.
 
  Sixty-five prostate cancer tissues and paired pan-cancer tissues were sequenced. Novel miRNAs were re-analyzed by MIREAP program. Biological functions of miR-N5 were transwell experiment and colony formation. Target genes of miR-N5 were analyzed by bioinformatic analysis. Downstream of target gene was analyzed by The Cancer Genome Atlas (TCGA) and Memorial Sloan Kettering Cancer Center (MSKCC) databases and confirmed by CHIP experiment.
 
  We identified a novel miRNA-miR-N5, which was downregulated in PCa cells, PCa tissue, and in the serum of patients with PCa. Knockout of miR-N5 enhanced migration and invasiveness in vitro. miR-N5 specified targeted CREBBP 3'-UTR and inhibited CREBBP expression, which mediated H3K56 acetylation at the promoter of EGFR,β-catenin and CDH1.
 
  This study may shed the light on miR-N5 which influences metastasis via histone acetylation.
 This study may shed the light on miR-N5 which influences metastasis via histone acetylation.
  Malignant rhabdoid tumor (MRT) is a rare, highly aggressive sarcoma with an uncertain cell of origin. Despite the existing standard of intensive multimodal therapy, the prognosis of patients with MRT is very poor. Novel antitumor agents are needed for MRT patients. Forkhead box transcription factor 1 (FOXM1) is overexpressed and is correlated with the pathogenesis in several human malignancies. In this study, we identified the clinicopathological and prognostic values of the expression of FOXM1 and its roles in the progression of MRT.
 
  We investigated the FOXM1 expression levels and their clinical significance in 23 MRT specimens using immunohistochemistry and performed clinicopathologic and prognostic analyses. We also demonstrated correlations between the downregulation of FOXM1 and oncological characteristics using small interfering RNA (siRNA) and FOXM1 inhibitor in MRT cell lines.
 
  Histopathological analyses revealed that primary renal MRTs showed significantly low FOXM1 protein expression levels (p = 0.032); however, there were no significant differences in other clinicopathological characteristics or the survival rate. FOXM1 siRNA and FOXM1 inhibitor (thiostrepton) successfully downregulated the mRNA and protein expression of FOXM1 in vitro and the downregulation of FOXM1 inhibited cell proliferation, drug resistance to chemotherapeutic agents, migration, invasion, and caused the cell cycle arrest and apoptosis of MRT cell lines. A cDNA microarray analysis showed that FOXM1 regulated FANCD2 and NBS1, which are key genes for DNA damage repair.
 
  This study demonstrates that FOXM1 may serve as a promising therapeutic target for MRT.
 This study demonstrates that FOXM1 may serve as a promising therapeutic target for MRT.N-butanol is an important chemical and can be naturally synthesized by Clostridium species; however, the poor n-butanol tolerance of Clostridium impedes the further improvement in titer. In this study, Lactobacillus brevis, which possesses a higher butanol tolerance, was selected as host for heterologous butanol production. The Clostridium acetobutylicum genes thl, hbd, and crt which encode thiolase, β-hydroxybutyryl-CoA dehydrogenase, and crotonase, and the Treponema denticola gene ter, which encodes trans-enoyl-CoA reductase were cloned into a single plasmid to express the butanol synthesis pathway in L. brevis. A titer of 40 mg/L n-butanol was initially achieved with plasmid pLY15-opt, in which all pathway genes are codon-optimized. A titer of 450 mg/L of n-butanol was then synthesized when ter was further overexpressed in this pathway. The role of metabolic flux was reinforced with pLY15, in which only the ter gene was codon-optimized, which greatly increased the n-butanol titer to 817 mg/L. Our strategy significantly improved n-butanol synthesis in L.