No abstract

Methyl tert-butyl ether (MTBE) is widely used as a gasoline additive with toxicity and carcinogenicity, and has caused environmental pollution worldwide. Biodegradation is a promising method for the removal of MTBE from contaminated sites. In this paper, three strains with high adaptability and different degrading characteristics to MTBE were cultured. The kinetic models were established to systematically simulate the biodegradation of MTBE by various strains at different concentrations. Moreover, the removal of MTBE in a synergistic system containing a mixture of three pure strains was studied. The mixed consortium enhanced MTBE removal at high concentrations (30–50 mg/L), and the degradation efficiency was increased by about 20% compared to pure strains at a concentration of 30 mg/L. Further, the mixed consortium degraded MTBE nearly three times faster than any of the individual, indicating that the co-cultures of three pure cultures improved both efficiency and the rate of MTBE biodegradation. In addition, it was found that the mixed consortium effectively removed MTBE in the presence of other gasoline components, and exhibited stronger adaptability, especially at low or high temperatures. This study supports the cultivation of a mixed consortium to remediate MTBE-contaminated environments, either as a single substrate or in environments containing other gasoline components.

Understanding the complex action mechanism of appetite regulation peptides can significantly impact therapeutic options in the treatment of obesity and other metabolic diseases. Hypothalamic α-melanocyte-stimulating hormone (α-MSH) is an anorexigenic peptide, closely related to the occurrence of obesity, playing a central role in food intake and energy expenditure. In the central nervous system (CNS), α-MSH is cleaved from proopiomelanocortin (POMC) and then released into different hypothalamic regions to act on melanocortin 3/4 receptor (MC3/4R)-expressing neurons, lowering food intake and raising energy expenditure via appetite suppression and sympathetic nervous system. Furthermore, it can increase the transmission of some anorexigenic hormones (e.g., dopamine) and interact with other orexigenic factors (e.g., agouti-related protein, neuropeptide Y) to influence food reward rather than merely feeding behavior. Therefore, α-MSH is a critical node of the hypothalamus in transmitting appetite suppression signals and is a key component of the central appetite-regulating circuits. Herein, we describe the role of α-MSH in appetite suppression in terms of specific receptors, effector neurons, sites of action, and the interaction with other appetite-relative peptides, respectively. We focus on the role of α-MSH in obesity. The status of research on α-MSH-related drugs is also discussed. With the intention of illuminating a new approach for targeting α-MSH in the hypothalamus as a strategy to manage obesity, we hope to further understand the direct or indirect mechanisms by which α-MSH exerts its appetite-regulating effects.