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This study investigates the impact of financial development, economic growth, and foreign direct investment on enhancing industrial growth for a panel of selected Sub-Sahara African (SSA) countries from 1990—2017. However, the present study enriches our understanding of financial development by employing a new comprehensive index focused on the accessibility, scope, and productivity of capital systems and banking institutions and incorporated foreign direct investment and economic growth as significant industrial growth drivers in the selected countries. A more robust technique Augmented Mean Group (AMG) and Common Correlated Effect Mean Group (CCEMG), were employed to access the long-run relationship among the understudy variables. Further empirical results shows that financial development and economic growth enhance industrial development with finance exhibiting signifcance while foreign direct investment is seen as adverse. Moreover, a two-way causality was obtained between industrialization and financial development while both foreign direct investment and economic growth had a one-way causality relationship with industrialization. Thus, our study implies that the government officials within these countries must provide a suitable environment for the public, private partnerships, i.e. private sector, which is the backbone for industrial development. [ABSTRACT FROM AUTHOR]

Objective: Patients with systemic lupus erythematosus (SLE) often develop multi-organ damages including heart and kidney complications. We sought to better define the underlying mechanisms with a focus on the chemokine receptor CX3CR1. Methods: We generated Cx3cr1-deficient MRL/lpr lupus-prone mice through backcrossing. We then employed heterozygous intercross to generate MRL/lpr littermates that were either sufficient or deficient of CX3CR1. The mice were also treated with either Lactobacillus spp. or a high-fat diet (HFD) followed by assessments of the kidney and heart, respectively. Results: Cx3cr1–/– MRL/lpr mice exhibited a distinct phenotype of exacerbated glomerulonephritis compared to Cx3cr1+/+ littermates, which was associated with a decrease of spleen tolerogenic marginal zone macrophages and an increase of double-negative T cells. Interestingly, upon correction of the gut microbiota with Lactobacillus administration, the phenotype of exacerbated glomerulonephritis was reversed, suggesting that CX3CR1 controls glomerulonephritis in MRL/lpr mice through a gut microbiota-dependent mechanism. Upon treatment with HFD, Cx3cr1–/– MRL/lpr mice developed significantly more atherosclerotic plaques that were promoted by Ly6C+ monocytes. Activated monocytes expressed ICOS-L that interacted with ICOS-expressing follicular T-helper cells, which in turn facilitated a germinal center reaction to produce more autoantibodies. Through a positive feedback mechanism, the increased circulatory autoantibodies further promoted the activation of Ly6C+ monocytes and their display of ICOS-L. Conclusions: We uncovered novel, Cx3cr1 deficiency-mediated pathogenic mechanisms contributing to SLE-associated glomerulonephritis and cardiovascular disease. [ABSTRACT FROM AUTHOR]

The ability of integrins on the cell surface to mediate cell adhesion to the extracellular matrix ligands is regulated by intracellular signaling cascades. During this signaling process, the talin (TLN) recruited to integrin cytoplasmic tails plays the critical role of the major adaptor protein to trigger integrin activation. Thus, intracellular levels of TLN are thought to determine integrin-mediated cellular functions. However, the epigenetic regulation of TLN expression and consequent modulation of integrin activation remain to be elucidated. Bioinformatics analysis led us to consider miR-200c-3p as a TLN1-targeting miRNA. To test this, we have generated miR-200c-3p-overexpressing and miR-200c-3p-underexpressing cell lines, including HEK293T, HCT116, and LNCaP cells. Overexpression of miR-200c-3p resulted in a remarkable decrease in the expression of TLN1, which was associated with the suppression of integrin-mediated cell adhesion to fibronectin. In contrast, the reduction in endogenous miR-200c-3p levels led to increased expression of TLN1 and enhanced cell adhesion to fibronectin and focal adhesion plaques formation. Moreover, miR-200c-3p was found to target TLN1 by binding to its 3′-untranslated region (UTR). Taken together, our data indicate that miR-200c-3p contributes to the regulation of integrin activation and cell adhesion via the targeting of TLN1. [ABSTRACT FROM AUTHOR]

Over the past two decades, global CO2 emissions have dramatically increased. In this context, this research aims to investigate a novel interaction between energy use, industrialization, and CO2 emissions as well as examine the underlying causal pathways with the implementation of more robust econometric methods to achieve valid and reliable results. Using estimation methods of AMG, CCEMG, and DCCEMG, this study shows that in the long-term energy use, industrialization, urbanization, and fossil fuel consumption have a non-significant positive impact on CO2 emissions for SSA countries with the exception of energy use depicting a significant impact. The documented results and findings are robust as compared to other studies. Furthermore, the study portrays the causal front as a bi-directional causal pathway between CO2 emissions, energy use, industrialization, and fossil fuel consumption with a uni-directional causal route to urbanization. Many of the variables are held to be causative agents of one another. The study suggests that policies that promote energy conservation and reduce CO2 emissions can be useful in achieving a lower emission rate. Policymakers and corporations should also abide by the laws and regulations on emissions mitigation. Companies need to invest in R&D as much as governments encourage business growth and development to help minimize emissions and degrade the environment. Similarly, the government should empower industries and households to acquire emission-reduction machinery. [ABSTRACT FROM AUTHOR]

The growth-induced effects of financial development have been well-established in the empirical literature, as well as the significance of financial development to energy demand behavior. However, the empirical evidence on the relationship between financial development and energy intensity remains sparse in the literature. Given the multifaceted nature of the effects of financial development, the proposed relationship seems a complex one and warrants an empirical investigation. Using the case of Ghana, this study provides an empirical answer to the question: does financial development lower energy intensity? To provide solid grounds for either rejection or acceptance of the null hypothesis, this study performed several robustness checks. Generally, the evidence revealed that financial development lowers energy intensity. Further, the results revealed that the price of energy, trade liberalization and industry structure play significant roles. These results have important implications for the design of macro energy efficiency policies and the creation of a 'Green Bank'. [ABSTRACT FROM AUTHOR]