Ecological innovation for environmental sustainability and human capital development: the role of environmental regulations and renewable energy in advanced economies

This study examines the trends in environmental sustainability and human well-being through green technologies, clean energy, and environmental taxes using panel data for the top eight advanced economies from 1990 to 2018. The study applies an advanced panel technique, cross-sectionally augmented distributed lags (CS-ARDL), to find long-run and short-run associations between these variables. Moreover, the role of foreign investment is added as a control variable. The CS-ARDL estimation confirms the productive impact of green technologies on environmental and human well-being, providing that it helps to reduce haze pollution while promoting human development. Moreover, clean energy and environmental taxes contribute toa sustainable environment and human development. Moreover, foreign investment is a direct source of haze pollution because of more industrialization and economic activities. The study finally recommends strengthening the promotion of green technology and clean energy to achieve both environmental and human well-being in the long run

Dendritic release of neurotransmitters

Release of neuroactive substances by exocytosis from dendrites is surprisingly widespread and is not confined to a particular class of transmitters: it occurs in multiple brain regions, and includes a range of neuropeptides, classical neurotransmitters and signaling molecules such as nitric oxide, carbon monoxide, ATP and arachidonic acid. This review is focused on hypothalamic neuroendocrine cells that release vasopressin and oxytocin and midbrain neurons that release dopamine. For these two model systems, the stimuli, mechanisms and physiological functions of dendritic release have been explored in greater detail than is yet available for other neurons and neuroactive substances

Fatty acid metabolism: target for metabolic syndrome

Fatty acids are a major energy source and important constituents of membrane lipids, and they serve as cellular signaling molecules that play an important role in the etiology of the metabolic syndrome. Acetyl-CoA carboxylases 1 and 2 (ACC1 and ACC2) catalyze the synthesis of malonyl-CoA, the substrate for fatty acid synthesis and the regulator of fatty acid oxidation. They are highly regulated and play important roles in the energy metabolism of fatty acids in animals, including humans. They are presently considered as an attractive target to regulate the human diseases of obesity, diabetes, cancer, and cardiovascular complications. In this review we discuss the role of fatty acid metabolism and its key players, ACC1 and ACC2, in animal evolution and physiology, as related to health and disease

Mutant mice lacking acetyl-CoA carboxylase 1 are embryonically lethal

Acetyl-CoA carboxylases (ACC1 and ACC2) catalyze the carboxylation of acetyl-CoA to form malonyl-CoA, an intermediate metabolite that plays a pivotal role in the regulation of fatty acid metabolism. We previously reported that ACC2 null mice are viable, and that ACC2 plays an important role in the regulation of fatty acid oxidation through the inhibition of carnitine palmitoyltransferase I, a mitochondrial component of the fatty-acyl shuttle system. Herein, we used gene targeting to knock out the ACC1 gene. The heterozygous mutant mice (Acc1(+/–)) had normal fertility and lifespans and maintained a similar body weight to that of their wild-type cohorts. The mRNA level of ACC1 in the tissues of Acc1(+/–) mice was half that of the wild type; however, the protein level of ACC1 and the total malonyl-CoA level were similar. In addition, there was no difference in the acetate incorporation into fatty acids nor in the fatty acid oxidation between the hepatocytes of Acc1(+/–) mice and those of the wild type. In contrast to Acc2(–/–) mice, Acc1(–/–) mice were not detected after mating. Timed pregnancies of heterozygotes revealed that Acc(–/–) embryos are already undeveloped at embryonic day (E)7.5, they die by E8.5, and are completely resorbed at E11.5. Our previous results of the ACC2 knockout mice and current studies of ACC1 knockout mice further confirm our hypotheses that malonyl-CoA exists in two independent pools, and that ACC1 and ACC2 have distinct roles in fatty acid metabolism