ABSTRACT
Alzheimer's disease (AD) represents the most widespread neurodegenerative disorder, distinguished by a gradual onset and slow progression, presenting a substantial challenge to global public health. The mitochondrial-associated membrane (MAMs) functions as a crucial center for signal transduction and material transport between mitochondria and the endoplasmic reticulum, playing a pivotal role in various pathological mechanisms of AD. The dysregulation of mitochondrial quality control systems is considered a fundamental factor in the development of AD, leading to mitochondrial dysfunction and subsequent neurodegenerative events. Recent studies have emphasized the role of MAMs in regulating mitochondrial quality control. This review will delve into the molecular mechanisms underlying the imbalance in mitochondrial quality control in AD and provide a comprehensive overview of the role of MAMs in regulating mitochondrial quality control.
ABSTRACT
Several cobalt complexes supported by 2,6-bis(arylimino)phenoxyl/phenthioxyl ligands κ2N,X-Ar[NXN]CoCl(THF) (1a, X = O, Ar = 2,6-Me2C6H3; 1b, X = O, Ar = 2,6-iPr2C6H3; 2a, X = S, Ar = 2,6-Me2C6H3; 2b, X = S, Ar = 2,6-iPr2C6H3) were synthesized by direct oxygen(sulfur) insertion into the C-Co bond of the mixed-valence cobalt complexes {κ2C,N,η6-Ar[NCN]Co-κN-CoCl(µ-Cl)}2. Crystallization of 1b in the presence of water gave the hydrolysis product 1b'. Treatment of Ar[NCN]Li with dioxygen followed by the addition of CoCl2 afforded the heteroatomic complexes {κ2N,O-Ar[NON]Co(µ-Cl)2Li}2 (3a, Ar = 2,6-Me2C6H3; 3b, Ar = 2,6-iPr2C6H3) or κ2N,O-Ar[NON]Co2Cl2(µ-Cl)2Li(THF)2 (4a, Ar = 2,6-Me2C6H3; 4b, Ar = 2,6-iPr2C6H3) depending on the amount of CoCl2 used. The Co(iii)/Li heterometallic complex 3b' with imino-phenoxyl-amino ligands was formed probably via a redox reaction of 3b. The reactions of Ar[NCN]Li with elemental sulfur and CoCl2 gave κ2N,S-Ar[NSN]Co2Cl2(µ-Cl)2Li(THF)2 (5a, Ar = 2,6-Me2C6H3; 5b, Ar = 2,6-iPr2C6H3) respectively. These complexes were well characterized by FT-IR and elemental analyses, and the molecular structures of 1b', 3b', 4a, and 4b were confirmed by X-ray crystallography. Upon activation with Al2Et3Cl3 in toluene, these complexes showed high activities in isoprene polymerization affording cis-1,4 enriched polymers with a moderate molecular weight (0.85-4.72 × 104 Da).
ABSTRACT
California methane (CH4) emissions are quantified for three years from two tower networks and one aircraft campaign. We used backward trajectory simulations and a mesoscale Bayesian inverse model, initialized by three inventories, to achieve the emission quantification. Results show total statewide CH4 emissions of 2.05 ± 0.26 (at 95% confidence) Tg/yr, which is 1.14 to 1.47 times greater than the anthropogenic emission estimates by California Air Resource Board (CARB). Some of differences could be biogenic emissions, superemitter point sources, and other episodic emissions which may not be completely included in the CARB inventory. San Joaquin Valley (SJV) has the largest CH4 emissions (0.94 ± 0.18 Tg/yr), followed by the South Coast Air Basin, the Sacramento Valley, and the San Francisco Bay Area at 0.39 ± 0.18, 0.21 ± 0.04, and 0.16 ± 0.05 Tg/yr, respectively. The dairy and oil/gas production sources in the SJV contribute 0.44 ± 0.36 and 0.22 ± 0.23 Tg CH4/yr, respectively. This study has important policy implications for regulatory programs, as it provides a thorough multiyear evaluation of the emissions inventory using independent atmospheric measurements and investigates the utility of a complementary multiplatform approach in understanding the spatial and temporal patterns of CH4 emissions in the state and identifies opportunities for the expansion and applications of the monitoring network.
