A Eu(III)-based Metal Organic Framework: Selective Sensing of Picric Acid and Nursing Application Values On the Cerebral Edema Induced by Cerebral Hemorrhage Via Reducing the Coagulation Factor II Activity.

A new three-dimensional lanthanide metal-organic framework (Ln-MOF), [Eu4(L)4(H2O)8]·10H2O (1, H3L = biphenyl-3'-nitro-3,4',5-tricarboxylic acid), has been constructed via solvothermal technology and its framework has been detected by the single-crystal X-ray diffraction and elemental analyses. Complex 1 with typical emission of Eu3+ ion represents dramatic luminescence quenching affect for picric acid (PA) and the linear Stern-Volmer plot was surveyed in the consistence, ranging from 0.05 to 0.15 mM (Ksv = 98,074 M- 1). Its therapeutic effect of the compound on the cerebral edema caused by cerebral hemorrhage was estimated and the mechanism was explored. Possible binding interactions have been investigated by molecular docking simulations, from which the binding interactions are identified and the carboxyl oxygens are responsible for those identified interactions.

Identification of Parkinson's disease-related pathways and potential risk factors.

OBJECTIVE: To identify Parkinson's disease (PD)-associated deregulated pathways and genes, to further elucidate the pathogenesis of PD. METHODS: Dataset GSE100054 was downloaded from the Gene Expression Omnibus, and differentially expressed genes (DEGs) in PD samples were identified. Functional enrichment analyses were conducted for the DEGs. The top 10 hub genes in the protein-protein interaction (PPI) network were screened out and used to construct a support vector machine (SVM) model. The expression of the top 10 genes was then validated in another dataset, GSE46129, and a clinical patient cohort. RESULTS: A total of 333 DEGs were identified. The DEGs were clustered into two gene sets that were significantly enriched in 12 pathways, of which 8 were significantly deregulated in PD, including cytokine-cytokine receptor interaction, gap junction, and actin cytoskeleton regulation. The signature of the top 10 hub genes in the PPI network was used to construct the SVM model, which had high performance for predicting PD. Of the 10 genes, GP1BA, GP6, ITGB5, and P2RY12 were independent risk factors of PD. CONCLUSION: Genes such as GP1BA, GP6, P2RY12, and ITGB5 play critical roles in PD pathology through pathways including cytokine-cytokine receptor interaction, gap junctions, and actin cytoskeleton regulation.

PDGFRα Regulated by miR-34a and FoxO1 Promotes Adipogenesis in Porcine Intramuscular Preadipocytes through Erk Signaling Pathway.

Suitable intramuscular fat (IMF) content improves porcine meat quality. The vital genes regulating IMF deposition are necessary for the selection and breeding of an IMF trait. However, the effect and mechanism of PDGFRα on IMF deposition are still unclear. Here, PDGFRα is moderately expressed in porcine longissimus dorsi muscle (LD), whereas it highly expressed in white adipose tissue (WAT). Moreover, PDGFRα-positive cells were located in the gaps of LD fibers which there were IMF adipocytes. Compared with 180-day-old and lean-type pigs, the levels of PDGFRα were much higher in one-day-old and fat-type pigs. Meanwhile the levels of PDGFRα gradually decreased during IMF preadipocyte differentiation. Furthermore, PDGFRα promoted adipogenic differentiation through activating Erk signaling pathway. Based on PDGFRα upstream regulation analysis, we found that the knockdown of FoxO1 repressed lipogenesis by downregulating PDGFRα, and miR-34a inhibited adipogenesis through targeting PDGFRα. Collectively, PDGFRα is a positive regulator of IMF deposition. Therefore, we suggest that PDGFRα is a possible target to improve meat quality.

Fibroblast-derived CXCL12/SDF-1α promotes CXCL6 secretion and co-operatively enhances metastatic potential through the PI3K/Akt/mTOR pathway in colon cancer.

AIM: To investigate the underlying mechanism by which CXCL12 and CXCL6 influences the metastatic potential of colon cancer and internal relation of colon cancer and stromal cells. METHODS: Western blotting was used to detect the expression of CXCL12 and CXCL6 in colon cancer cells and stromal cells. The co-operative effects of CXCL12 and CXCL6 on proliferation and invasion of colon cancer cells and human umbilical vein endothelial cells (HUVECs) were determined by enzyme-linked immunosorbent assay, and proliferation and invasion assays. The angiogenesis of HUVECs through interaction with cancer cells and stromal cells was examined by angiogenesis assay. We eventually investigated activation of PI3K/Akt/mTOR signaling by CXCL12 involved in the metastatic process of colon cancer. RESULTS: CXCL12 was expressed in DLD-1 cancer cells and fibroblasts. The secretion level of CXCL6 by colon cancer cells and HUVECs were significantly promoted by fibroblasts derived from CXCL12. CXCL6 and CXCL2 could significantly enhance HUVEC proliferation and migration (P < 0.01). CXCL6 and CXCL2 enhanced angiogenesis by HUVECs when cultured with fibroblast cells and colon cancer cells (P < 0.01). CXCL12 also enhanced the invasion of colon cancer cells. Stromal cell-derived CXCL12 promoted the secretion level of CXCL6 and co-operatively promoted metastasis of colon carcinoma through activation of the PI3K/Akt/mTOR pathway. CONCLUSION: Fibroblast-derived CXCL12 enhanced the CXCL6 secretion of colon cancer cells, and both CXCL12 and CXCL6 co-operatively regulated the metastasis via the PI3K/Akt/mTOR signaling pathway. Blocking this pathway may be a potential anti-metastatic therapeutic target for patients with colon cancer.

Sirt1 AS lncRNA interacts with its mRNA to inhibit muscle formation by attenuating function of miR-34a.

Recent studies demonstrate the functions of long non-coding RNAs (lncRNAs) in mediating gene expression at the transcriptional or translational level. Our previous study identified a Sirt1 antisense (AS) lncRNA transcribed from the Sirt1 AS strand. However, its role and regulatory mechanism is still unknown in myogenesis. Here, functional analyses showed that Sirt1 AS lncRNA overexpression promoted myoblast proliferation, but inhibited differentiation. Mechanistically, Sirt1 AS lncRNA was found to activate its sense gene, Sirt1. The luciferase assay provided evidences that Sirt1 AS lncRNA interacted with Sirt1 3' UTR and rescued Sirt1 transcriptional suppression by competing with miR-34a. In addition, RNA stability assay showed that Sirt1 AS lncRNA prolonged Sirt1 mRNA half-life from 2 to 10 h. Ribonuclease protection assay further indicated that it fully bound to Sirt1 mRNA in the myoblast cytoplasm. Moreover, Sirt1 AS overexpression led to less mouse weight than the control because of less lean mass and greater levels of Sirt1, whereas the fat mass and levels of miR-34a were not altered. Based on the findings, a novel regulatory mechanism was found that Sirt1 AS lncRNA preferably interacted with Sirt1 mRNA forming RNA duplex to promote Sirt1 translation by competing with miR-34a, inhibiting muscle formation.

Mulberry 1-Deoxynojirimycin Inhibits Adipogenesis by Repression of the ERK/PPARγ Signaling Pathway in Porcine Intramuscular Adipocytes.

Intramuscular fat (IMF), which is modulated by adipogenensis of intramuscular adipocytes, plays a key role in pork quality associated with marbling, juiceness, and flavor. However, the regulatory mechanism of 1-deoxynojirimycin (DNJ) on adipogenesis is still unknown. Here, we found that both DNJ (2.0, 3.0, 4.0, 5.0, and 6.0 µM) and rosiglitazone (RSG; 0.1, 0.2, 0.3, 0.4, and 0.5 mM) had no effect on cell viability. Moreover, 4 µM DNJ significantly inhibited adipogenesis, whereas 0.4 mM RSG increased lipogenesis of porcine intramuscular adipocytes. Interestingly, DNJ sharply inhibited phosphorylation of extracellular regulated protein kinases 1/2 (ERK1/2), but did not change phosphorylation of AKT (protein kinase B) in intramuscular adipocytes. We further found that the inhibitory adipogenesis of DNJ was attenuated by RSG via up-regulation of PPARγ. On the basis of the above findings, we suggest that DNJ inhibited adipogenesis through the ERK/PPARγ signaling pathway in porcine intramuscular adipocytes.

Comment on "plasma oscillations and nonextensive statistics".

The paper authored by Lima et al. [Phys. Rev. E 61, 3260 (2000)] has discussed the dispersion relation and Landau damping of a Langmuir wave in the context of the nonextensive statistics proposed by Tsallis. However, the results obtained in this paper are not appropriate. In this comment on the paper we shall derive the correct analytic formulas for both the dispersion relation and Landau damping in the Tsallis formalism. We hope that this comment will be useful in providing the correct results.