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Docosahexaenoic acid (DHA) is reported to have the potential to ameliorate pulmonary arterial hypertension (PAH), while the specific mechanism is still obscure. This study aims to investigate the function of DHA in pulmonary artery smooth muscle cells (PASMCs) and explore the underlying mechanism. In our study, DHA was used to incubate PASMCs. Cytosolic‐free Ca2+ concentration ([Ca2+]cyt) was measured using Fluo‐3 AM method. Real‐time polymerase chain reaction was used to detect microRNA‐16 (miR‐16) and calcium‐sensing receptor (CaSR) messenger RNA expression levels. CCK‐8 assay, BrdU assay, and Transwell assay were employed to detect the effects of DHA on proliferation and migration of PASMCs. CaSR was confirmed as a direct target of miR‐16 using dual‐luciferase assay, polymerase chain reaction, and Western blot analysis. It was found that DHA significantly inhibited PASMC proliferation and migration and decreased [Ca2+]cyt. After transfection of miR‐16 mimics, proliferation and migration ability of PASMCs were significantly inhibited, whereas opposite effects were observed after miR‐16 inhibition. [Ca2+]cyt was also inhibited by miR‐16 transfection. DHA then promoted the expression of miR‐16, and the effects of DHA on PASMCs were annulled when miR‐16 was inhibited. CaSR was identified as a direct target of miR‐16. CaSR was inhibited directly by miR‐16 and indirectly by DHA. In conclusion, DHA inhibits the proliferation and migration of PASMCs, and probably ameliorates PAH via regulating miR‐16/CaSR axis. [ABSTRACT FROM AUTHOR]

Recent studies indicate that disturbed structure and function of microglia can cause depression and associated neurogenesis impairments. Our previous work has demonstrated that exogenous fibroblast growth factor 2 (FGF2) reverses the depressive-like behaviors and the impaired hippocampal neurogenesis in a neuroinflammatory model of depression. However, whether and how the antidepressant effects of FGF2 involve the modulation of microglia activation has not been elucidated. In this study, to examine the effects of FGF2 on microglia activation, exogenous FGF2 was supplemented to the lateral ventricle of rats during the neuroinflammatory state induced by central lipopolysaccharides (LPS) administrations. It was found that FGF2 infusions reversed the LPS-induced depressive-like behaviors and inhibited the hippocampal microglia activation. In LPS-treated rats, FGF2 decreased the level of pro-inflammatory cytokines including interlukin-1β (IL-1β), IL-6 and tumor necrosis factor (TNF)-α, increased the level of IL-10, the anti-inflammatory cytokine and reversed the decreased expression of CX3CL1, a chemokine mainly expressed by neurons and keeping microglia in surveillance. Further, we examined the effects of inhibited FGF2 signaling by administration of SU5402, an FGFR inhibitor. It was found that SU5402 itself evoked depressive-like behaviors, induced microglia activation, increased production of pro-inflammatory cytokines including IL-1β, IL-6 and TNF-α, and decreased the expression of CX3CL1. Two lines of results that FGF2 signaling and FGFR inhibitor can effectively but oppositely modulate the regulation of microglia and the generation of depressive-like behavior, suggesting that microglia-regulated mechanisms may underlie the antidepressant role of FGF2. The present data provide novel insights into the understanding of mechanism of neuroinflammation-associated depression and may serve as a novel mechanism-based target for the treatment of inflammation-related depression. [ABSTRACT FROM AUTHOR]

Abstract: A model for option pricing of fractional version of the Merton model with ‘Hurst exponent’ being in is established with transaction costs. In particular, for the minimal price of an option under transaction costs is obtained, which displays that the timestep and the ‘Hurst exponent’ play an important role in option pricing with transaction costs. [Copyright &y& Elsevier]

Abstract: This paper deals with the problem of discrete-time option pricing by the mixed Brownian–fractional Brownian model with transaction costs. By a mean-self-financing delta hedging argument in a discrete-time setting, a European call option pricing formula is obtained. In particular, the minimal pricing of an option under transaction costs is obtained, which shows that timestep and Hurst exponent play an important role in option pricing with transaction costs. In addition, we also show that there exists fundamental difference between the continuous-time trade and discrete-time trade and that continuous-time trade assumption will result in underestimating the value of a European call option. [Copyright &y& Elsevier]

Docosahexaenoic acid (DHA) is reported to have the potential to ameliorate pulmonary arterial hypertension (PAH), while the specific mechanism is still obscure. This study aims to investigate the function of DHA in pulmonary artery smooth muscle cells (PASMCs) and explore the underlying mechanism. In our study, DHA was used to incubate PASMCs. Cytosolic-free Ca 2+ concentration ([Ca 2+ ]cyt) was measured using Fluo-3 AM method. Real-time polymerase chain reaction was used to detect microRNA-16 (miR-16) and calcium-sensing receptor (CaSR) messenger RNA expression levels. CCK-8 assay, BrdU assay, and Transwell assay were employed to detect the effects of DHA on proliferation and migration of PASMCs. CaSR was confirmed as a direct target of miR-16 using dual-luciferase assay, polymerase chain reaction, and Western blot analysis. It was found that DHA significantly inhibited PASMC proliferation and migration and decreased [Ca 2+ ]cyt. After transfection of miR-16 mimics, proliferation and migration ability of PASMCs were significantly inhibited, whereas opposite effects were observed after miR-16 inhibition. [Ca 2+ ]cyt was also inhibited by miR-16 transfection. DHA then promoted the expression of miR-16, and the effects of DHA on PASMCs were annulled when miR-16 was inhibited. CaSR was identified as a direct target of miR-16. CaSR was inhibited directly by miR-16 and indirectly by DHA. In conclusion, DHA inhibits the proliferation and migration of PASMCs, and probably ameliorates PAH via regulating miR-16/CaSR axis., (© 2020 Wiley Periodicals LLC.)

Increasing evidence has demonstrated that neuroinflammation contributes to the development of depressive-like behaviors, in both animal models and human patients; however, the brain areas and signaling pathways involved are still elusive. Recent studies have suggested novel roles of the habenula in the onset of depression and other psychiatric disorders; however, there is no evidence for whether the habenula has a function in neuroinflammation-induced depression. Using an animal model of depression, which is induced by the repeated central administration of lipopolysaccharide (LPS), we examined whether cytokine expression and p38 signal activation in the habenula were involved in the depressive-like behaviors. Body weight, saccharin preference test, and tail suspension test were used to measure depressive-like behaviors. Immunohistochemistry, quantitative-polymerase chain reaction (q-PCR), and western blot were used to measure the expression of tumor necrosis factor-α (TNF-α), interleukin-10 (IL-10), and the phosphorylation of p38 in the habenula. The results showed that central LPS administration induced depressive-like behaviors, characterized by anhedonia in the saccharin preference test and increased immobility in the tail suspension test. Central LPS administration also significantly increased the p-p38 level in microglial cells and increased TNF-α expression in the habenula. Treatment with fluoxetine, a widely prescribed antidepressant, or SB203580, a p38-specific inhibitor, reversed the depressive-like behaviors, normalized the alterations in p-p38 and TNF-α levels and increased the levels of the anti-inflammatory cytokine IL-10 in the habenula. The present findings suggest that the habenula is involved in the pathophysiology of behavioral depression induced by neuroinflammation, and the p38 pathway may serve as a novel mechanism-based target for the treatment of inflammation-related depression.

Intercropping studies usually focus on yield advantage and interspecific interactions but few quantify temporal niche differentiation and its relationship with intercropping yield advantage. A field experiment conducted in northwest China in 2013 and 2014 examined four intercropping systems (oilseed rape/maize, oilseed rape/soybean, potato/maize, and soybean/potato) and the corresponding monocultures. Total dry matter data collected every 20 d after maize emergence were fitted to logistic models to investigate the temporal dynamics of crop growth and interspecific interactions. All four intercropping systems showed significant yield advantages. Temporal niche complementarity between intercropped species was due to differences in sowing and harvesting dates or the time taken to reach maximum daily growth rate or both. Interspecific interactions between intercropped species amplified temporal niche differentiation as indicated by postponement of the time taken to reach maximum daily growth rate of late-maturing crops (i.e. 21 to 41 days in maize associated with oilseed rape or potato). Growth trajectories of intercropped maize or soybean recovered after the oilseed rape harvest to the same values as in their monoculture on a per plant basis. Amplified niche differentiation between crop species depends on the identity of neighboring species whose relative growth rate is crucial in determining the differentiation.

Latent transforming growth factor (TGF)-beta binding protein 2 (LTBP2) belongs to the fibrillin/LTBP extracellular matrix glycoprotein superfamily. It plays vital roles in tumorigenesis through regulating TGFβ activity, elastogenesis and maintenance of the extracellular matrix (ECM) structure. In this study, we determined the expression levels of LTBP2 mRNA and protein in head and neck squamous cell carcinoma (HNSCC) tissues and adjacent normal tissues by quantitative reverse transcription PCR (qRT-PCR) and tissue microarray immunohistochemistry analysis (TMA-IHC) respectively. LTBP2 protein levels in cancer tissues were correlated with HNSCC patients' clinical characteristics and overall survival. Both LTBP2 mRNA and protein levels were significantly higher in HNSCC tissues than in adjacent normal tissues. High LTBP2 protein level was associated with lymph node metastasis and higher pTNM stages. High LTBP2 protein level is an independent prognostic marker in HNSCC. Our data suggest that LTBP2 acts as an oncogene in HNSCC development and progression. Detection of LTBP2 expression could be a useful prognosis marker and targeting LTBP2 may represent a novel strategy for cancer treatment through regulating activities of TGFβ., Competing Interests: The authors declared that they have no competing interests.