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This article examines the quantitative interrelations between sectoral composition of public spending and equilibrium (in)determinacy in a two-sector real business cycle model with positive productive externalities in investment. When government purchases of consumption and investment goods are set as constant fractions of their respective sectoral output, we show that the public-consumption share plays no role in the model's local dynamics, and that a sufficiently high public-investment share can stabilize the economy against endogenous belief-driven cyclical fluctuations. When each type of government spending is postulated as a constant proportion of the economy's total output, we find that there exists a trade-off between public consumption versus investment expenditures to yield saddle-path stability and equilibrium uniqueness. © 2014 Western Economic Association International.

OBJECTIVE: Atherosclerosis is an inflammation-associated disease resulting in a huge health hazard. Abundance of researches showed that long non-coding RNAs (lncRNAs) played vital roles in atherosclerosis, but the molecular mechanism of nuclear-enriched abundant transcript (NEAT1) has not been fully elucidated yet. PATIENTS AND METHODS: Human umbilical vein endothelial cells (HUVECs) were treated with oxidized low-density lipoprotein (ox-LDL) for constructing the model of atherosclerosis. The detection of NEAT1, microRNA-30c-5p (miR30c-5p), and transcription factor 7 (TCF7) expression was implemented by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). Cell proliferation and apoptosis were measured by 3-(4, 5-dimethylthiazol-2-y1)-2, 5-diphenyl tetrazolium bromide (MTT) and flow cytometry, respectively. The levels of apoptosis-associated proteins were examined through Western blot and the concentrations of inflammatory cytokines were determined by enzyme-linked immunosorbent assay (ELISA). The targeted relationship was analyzed by Dual-Luciferase reporter assay. RESULTS: NEAT1 was upregulated in serum of patients with atherosclerosis and HUVECs treated with ox-LDL. Knockdown of NEAT1 exerted the promotion of proliferation but suppression of apoptosis and inflammation in oxLDL-treated HUVECs. Moreover, NEAT1 targeted miR-30c-5p and the overexpression of miR30c-5p reversed the ox-LDL-induced effects in HUVECs. Furthermore, miR-30c-5p directly refrained the TCF7 level, and NEAT1 repression decreased the expression of TCF7 by upregulating miR-30c-5p. The knockdown of NEAT1 afforded the protective effect for HUVECs treated with ox-LDL through miR-30c-5p/TCF7 axis. CONCLUSIONS: The knockdown of NEAT1 overtly motivated proliferation but alleviated the apoptosis and inflammation in ox-LDLtreated HUVECs by miR-30c-5p/TCF7 axis. NEAT1 accelerated the progression of atherosclerosis therapies, functioning as an indicative element. [ABSTRACT FROM AUTHOR]

OBJECTIVE: The aim of this study was to investigate the role of interleukin-1β (IL- 1β) in the apoptosis of synovial cells in rheumatoid arthritis (RA) rats, and to explore the underlying mechanism. MATERIALS AND METHODS: The apoptosis of the synovial cells in RA rats in the IL-1β group and the control group was analyzed by scoring under an electron microscope. The expressions of cleaved-poly (ADP-ribose) polymerase (PARP), PARP and anti-apoptosis gene products in synovial cells of IL-1β treated RA rats were explored as well. Meanwhile, the expressions of B-cell lymphoma 2 (Bcl- 2), Bcl-xL, and Active-Caspase3 in the synovial cells of RA rats with IL-1β treatment were evaluated by the Western blotting. To further clarify the relationship between IL-1β and the nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) pathway in the synovial cells of RA rats, the expressions of NF-κB regulated the gene products of matrix metalloproteinase-3 (MMP-3), MMP-9, cyclooxygenase- 2 (Cox-2), and vascular endothelial growth factor (VEGF) in synovial cells of RA rats after that we investigated the treatment with IL-1β (was investigated). In addition, the expression of NF-κB in the synovial cells of RA rats treated with IL-1β was determined. RESULTS: The results showed that, compared with the control group, IL-1β treatment significantly increased the number of apoptotic cells. This meant that IL-1β treatment could promote the apoptosis of the synovial cells (p<0.05). IL-1β treatment significantly promoted the expression level of cleaved-PARP (p<0.05). However, it remarkably reduced the expressions of Bcl-2 and Bcl-xL (p<0.05). Meanwhile, the level of the active-Caspase3 in the synovial cells of RA rats treated with IL-1β was significantly enhanced (p<0.01). In comparison with the control group, the IL-1β group exhibited significantly elevated expressions of NF-κB-regulated gene products in the synovial cells of RA rats (p<0.01). Besides, the positive markers of the activated NF-κB were detected in the synovial cells of RA rats in the IL-1β group and the control group. The results demonstrated that they were mainly located in the nucleus of the IL-1β group. CONCLUSIONS: IL-1β can promote the apoptosis of the synovial cells in RA rats via the NF- κB pathway. [ABSTRACT FROM AUTHOR]