Naturally brown-rotted lignin was structurally characterized by various chemical and spectroscopic techniques. Our results of extensively decayed Douglas-fir indicate that modification of lignin by brownrot fungi is mainly oxidative. In addition to modification of aromatic ring structures by demethylation, advanced decay by brown-rot fungi proceeds in the direction of partial depolymerization, perhaps involving aryl ether interunit bond cleavage, and oxidation and cleavage of the lignin side chain structures. Ring and side chain modification results in a significant increase in both phenolic and aliphatic hydroxyl and carboxyl groups, which makes this lignin chemically more reactive. Our results also suggest that aromatic hydroxylation is not involved in the softwood lignin modification by brown-rot fungi. In the course of this work various Isolation procedures for fractionating the lignin into different molecular weight ranges were examined, and it was found that refluxing with hol NaOH is a simple method that may have potential industrial uses.
The direct synthesis of nitrile from N2 under mild conditions is of great importance and has attracted much interest. Herein, we report a direct conversion of N2 into nitrile via a nitrile–alkyne cross‐metathesis (NACM) process involving a N2‐derived Mo nitride. Treatment of the Mo nitride with alkyne in the presence of KOTf afforded an alkyne‐coordinated nitride, which was then transformed into MoV carbyne and the corresponding nitrile upon 1 e− oxidation. Both aryl‐ and alkyl‐substituted alkynes underwent this process smoothly. Experiments and DFT calculations have proved that the oxidation state of the Mo center plays a crucial role. This method does not rely on the nucleophilicity of the N2‐derived metal nitride, offering a novel strategy for N2 fixation chemistry.
In this study, we determined the neuroprotective effect of aucubin on diabetes and diabetic encephalopathy. With the exception of the control group, all rats received intraperitoneal injections of streptozotocin (STZ; 60 mg/kg) to induce type 1 diabetes mellitus (DM). Aucubin (1, 5, 10 mg/kg ip) was used after induction of DM (immediately) and diabetic encephalopathy (65 days after the induction of diabetes). The diabetic encephalopathy treatment groups were divided into short-term and long-term treatment groups. Treatment responses to all parameters were examined (body weight, plasma glucose, Y-maze error rates and proportion of apoptotic cells). In diabetic rats, aucubin controlled blood glucose levels effectively, prevented complications, and improved the quality of life of diabetic rats. In diabetic encephalopathy, aucubin significantly rescued neurons in the hippocampal CA1 subfield and reduced working errors during behavioral testing. The significant neuroprotective effect of aucubin could be seen not only in the short term (15 days) but also in the long term (45 days), which was a highly encouraging finding. These data suggest that aucubin may be a potential neuroprotective agent.
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