Olefin chemistry, through pericyclic reactions, polymerizations, oxidations, or reductions, plays an essential role in the foundation of how organic matter is manipulated.1 Despite its importance, olefin synthesis still largely relies upon chemistry invented more than three decades ago, with metathesis2 being the most recent addition. Here we describe a simple method to access olefins with any substitution pattern or geometry from one of the most ubiquitous and variegated building blocks of chemistry: alkyl carboxylic acids. The same activating principles used in amide-bond synthesis can thus be employed, under Ni- or Fe-based catalysis, to extract CO2 from a carboxylic acid and economically replace it with an organozinc-derived olefin on mole scale. Over sixty olefins across a range of substrate classes are prepared, and the ability to simplify retrosynthetic analysis is exemplified with the preparation of sixteen different natural products across a range of ten different families.

Turn you inside out: A novel method for performing in situ separation and recycling of submicrometer-sized solid catalysts is developed based on the pH-triggered inversion of Pickering emulsions (see scheme; o = oil, w = water). Solid catalysts can be recycled 36 times without significant loss of activity. The method differs from conventional methods in terms of speed, energy consumption, catalyst separation, and recycling effectiveness.

Summary• AtDjB1 belongs to the J-protein family in Arabidopsis thaliana. Its biological functions in plants are largely unknown.• In this study, we examined the roles of AtDjB1 in resisting heat and oxidative stresses in A. thaliana using reverse genetic analysis.• AtDjB1 knockout plants (atj1-1) were more sensitive to heat stress than wildtype plants, and displayed decreased concentrations of ascorbate (ASC), and increased concentrations of hydrogen peroxide (H 2 O 2 ) and oxidative products after heat shock. Application of H 2 O 2 accelerated cell death and decreased seedling viability in atj1-1. Exogenous ASC conferred much greater thermotolerance in atj1-1 than in wildtype plants, suggesting that a lower concentration of ASC in atj1-1 could be responsible for the increased concentration of H 2 O 2 and decreased thermotolerance. Furthermore, AtDjB1 was found to localize to mitochondria, directly interact with a mitochondrial heat-shock protein 70 (mtHSC70-1), and stimulate ATPase activity of mtHSC70-1. AtDjB1 knockout led to the accumulation of cellular ATP and decreased seedling respiration, indicating that AtDjB1 modulated the ASC concentration probably through affecting the function of mitochondria.• Taken together, these results suggest that AtDjB1 plays a crucial role in maintaining redox homeostasis, and facilitates thermotolerance by protecting cells against heat-induced oxidative damage.

Isoniazid (INH) continues to be a highly effective drug in the chemoprophylaxis and treatment of tuberculosis; however, its use is associated with hepatotoxicity (predominantly hepatic necrosis) in 1-2% of individuals. The INH metabolites, acetylhydrazine and hydrazine, have each been implicated as the causative hepatotoxin in INH-induced hepatotoxicity. Using a model of INH-induced hepatotoxicity in rabbits, in which INH-induced hepatotoxicity manifests as hepatic necrosis, hepatic steatosis (hepatic fat accumulation) and hypertriglyceridaemia (elevated plasma triglycerides), we compared the severity of these measures of toxicity with plasma levels of INH, acetylhydrazine and hydrazine. Plasma INH and acetylhydrazine were not correlated with markers of INH-induced hepatic necrosis or fatty changes. Plasma hydrazine at 32 h was correlated significantly with plasma argininosuccinic acid lyase (ASAL, a sensitive marker of hepatic necrosis) activity as area under the curve (r2 = 0.54, P < 0.002) and log plasma ASAL activity at 48 h after the first dose of INH (r2 = 0.53, p < 0.005), but not with fatty changes. These results show in this model of INH-induced hepatotoxicity in rabbits that hydrazine, and not INH or acetylhydrazine, is most likely involved in the pathogenic mechanism of hepatic necrosis.

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