This study employs super-efficiency DEA model with desirable inputs and an undesirable output in calculating environmental efficiency values in different regions in Asia-Pacific from 1990 to 2018. The study compares environmental efficiency index in South East Asia, South Asia and East Asia. The study also evaluates the determinants of environmental efficiency using truncated regression. The mean environmental efficiency score demonstrates that East Asia region is highly efficient whereas South East Asia is the least efficient. Results from the truncated regression established an inverted U-shape relationship between environmental efficiency and Technological Innovation (TI) in the main panel, and the three regions. Also, economic growth shows an inverted "U" shape link with environmental efficiency in the panels except in South East Asia. Human capital promotes environmental efficiency in the main panel and the rest of the regions. Moreover, while FDI promotes environmental efficiency in the main panel and East Asia, it reduces environmental efficiency in both South East and South Asia regions within the Asia-Pacific. In addition, an interaction effect between technological innovation and renewable energy use, advances environmental efficiency within the entire study countries. Based on the findings the study proposes several policy recommendations.Thirty samples of sediments were taken from Bosumtwi Lake (also called Bosomtwe Lake) in Ghana and analyzed for the contents of Fe, As, Hg, Co, Cr, Ni, Cd, and Pb. Several pollution indices (enrichment factor (EF), contamination factor (CF), geoaccumulation (Igeo), and pollution load index (PLI)) were used to determine sedimentary pollution levels, and the risk of environmental exposure was calculated using Hakanson's potential ecological risk (PER) indices. The results from PER assessments have indicated that sediments from the Bosumtwi Lake present a moderate environmental risk. According to EF calculations, Hg in Bosumtwi lake sediments is the element of concern that is being severely enriched. Hg was the largest contributor to PER with a 97% risk contribution. Multivariate statistical analysis revealed that the main sources of Hg were agrochemicals and atmospheric deposition, whereas the sources of Fe, As, Co, Cr, and Ni to Bosumtwi Lake were natural processes and are derived from the local lithology. There was no strong significant correlation among the contents of the heavy metals, sediment grain sizes, and total organic carbon (TOC), suggesting their lack of control in the distribution of heavy metals, the source, and the transport pathway. Finally, it is strongly recommended to do a study on Hg bioavailability in Bosumtwi Lake sediments. These findings will be relevant to Bosumtwi Lake's profiling and historical development of heavy metal loads.Fibrosis is perpetuated by an autocrine, pro-adhesive signaling loop maintained by the synthetic and contractile abilities of myofibroblasts and the stiff, highly-crosslinked extracellular matrix. Transcriptional complexes that are exquisitely responsive to mechanotransduction include the co-activator YAP1, which regulates the expression of members of the CCN family of matricellular proteins such as CCN2 and CCN1. Although selective YAP1 inhibitors exist, the effect of these inhibitors on profibrotic gene expression in fibroblasts is largely unknown, and is the subject of our current study. Herein, we use genome-wide expression profiling, real-time polymerase chain reaction and Western blot analyses, cell migration and collagen gel contraction assays to assess the ability of a selective YAP inhibitor verteporfin (VP) to block fibrogenic activities in dermal fibroblasts from healthy individual human controls and those from isolated from fibrotic lesions of patients with diffuse cutaneous systemic sclerosis (dcSSc). In control fibroblasts, VP selectively reduced expression of fibrogenic genes and also blocked the ability of TGFbeta to induce actin stress fibers in dermal fibroblasts. VP also reduced the persistent profibrotic phenotype of dermal fibroblasts cultured from fibrotic lesions of patients with dcSSc. Our results are consistent with the notion that, in the future, YAP1 inhibitors may represent a novel, valuable method of treating fibrosis as seen in dcSSc.The role of autophagy and lysosomal degradation pathway in the regulation of skeletal muscle metabolism was previously studied. However, underlying molecular mechanisms are poorly understood. L-lactate which is utilized as an energetic substrate by skeletal muscle can also augment genes expression related to metabolism and up-regulate those being responsive to reactive oxygen species (ROS). Since ROS is the most important regulator of autophagy in skeletal muscle, we tested if there is a link between cellular lactate metabolism and autophagy in differentiated C2C12 myotubes and the gastrocnemius muscle of male wistar rats. https://www.selleckchem.com/products/cpi-0610.html C2C12 mouse skeletal muscle was exposed to 2, 6, 10, and 20 mM lactate and evaluated for lactate autophagic effects. Lactate dose-dependently increased autophagy and augmented ROS generation in differentiated C2C12 myotubes. The autophagic effect of lactate deterred in N-acetylcysteine presence (NAC, a ROS scavenger) indicated lactate regulates autophagy with ROS participation. Lactate-induced up-regulation of extracellular signal-regulated kinase 1/2 (ERK1/2) through ROS was required to regulate the autophagy by lactate. Further analysis about ERK1/2 up- and downstream indicated that lactate regulates autophagy through ROS-mediated the activation of ERK1/2/mTOR/p70S6K pathway in skeletal muscle. The in vitro effects of lactate on autophagy also occurred in the gastrocnemius muscle of male Wistar rats. In conclusion, we provided the lactate-associated regulation evidence of autophagy in skeletal muscle by activating ROS-mediated ERK1/2/mTOR/p70S6K pathway. Since the increase in cellular lactate concentration is a hallmark of energy deficiency, the results provide insight into a skeletal muscle mechanism to fulfill its enhanced energy requirement.Calcium (Ca2+) signaling has a major role in regulating a wide range of cellular mechanisms, including gene expression, proliferation, metabolism, cell death, muscle contraction, among others. Recent evidence suggests that ~ 1600 genes are related to the Ca2+ signaling. Some of these genes' expression is altered in several pathological conditions, including different cancer types, and epigenetic mechanisms are involved. However, their expression and regulation in hepatocellular carcinoma (HCC) and the liver are barely known. Here, we aimed to explore the expression of genes involved in the Ca2+-signaling in HCC, liver regeneration, and hepatocyte differentiation, and whether their expression is regulated by epigenetic mechanisms such as DNA methylation and histone posttranslational modifications (HPM). Results show that several Ca2+-signaling genes' expression is altered in HCC samples; among these, a subset of twenty-two correlate with patients' survival. DNA methylation correlates with eight of these genes' expression, and Guadecitabine, a hypomethylating agent, regulates the expression of seven down-regulated and three up-regulated genes in HepG2 cells.