Diphosphene TerP = PTer (; Ter = 2,6-MesCH; Mes = 2,4,6-MeCH) and NHC (NHC = 1,3,4,5-tetramethylimidazol-2-ylidene) exist in an equilibrium mixture with the NHC -coordinated diphosphene . While uncoordinated is inert to hydrolysis, the NHC adduct readily undergoes hydrolysis to afford a phosphino-substituted phosphine oxide with the liberation of NHC . On this basis, conditions suitable for the catalytic use of NHC were identified. Similarly, while the hydrogenation of free diphosphene with HN·BH is very slow, reacts instantaneously with HN·BH at room temperature to afford a dihydrodiphosphane.
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http://dx.doi.org/10.1039/c8sc00348c | DOI Listing |
Gut Microbes
December 2025
MOE/NHC/CAMS Key Lab of Medical Molecular Virology, School of Basic Medical Sciences, & National Clinical Research Center for Aging and Medicine, Huashan Hospital, Shanghai Medical College, Fudan University, Shanghai, China.
The gut microbiota plays a pivotal role in anxiety regulation through pathways involving neurotransmitter production, immune signaling, and metabolic interactions. Among these, gut-derived serotonin (5-hydroxytryptamine, 5-HT), synthesized from tryptophan metabolism, has been identified as a key mediator. However, it remains unclear whether specific microbial factors regulate tryptophan metabolism to influence 5-HT production and anxiety regulation.
View Article and Find Full Text PDFInt J Biol Sci
January 2025
CAMS Key Laboratory of Antiviral Drug Research, Institute of Medicinal Biotechnology, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing, 100050, China.
Although therapies based on direct-acting antivirals (DAAs) effectively eradicate hepatitis C virus (HCV) in patients, there is still a high risk of liver fibrosis even after a sustained virological response. Therefore, it is of great clinical importance to understand the mechanism of potential factors that promote liver fibrosis after virological cure by treatment with DAAs. Here, we found that tubulointerstitial nephritis antigen-like 1 (TINAGL1) is significantly increased in HCV-infected hepatocytes and in the liver of patients with liver fibrosis, and that higher TINAGL1 expression persists in HCV-eradicated hepatocytes after treatment with DAAs.
View Article and Find Full Text PDFInt J Biol Sci
January 2025
Department of Respiratory and Critical Care Medicine, National Clinical Research Center of Respiratory Disease, Key Laboratory of Pulmonary Diseases of Health Ministry, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Hubei, China.
As a leading cause of morbidity and mortality, fibrosis is the common pathway of various chronic inflammatory diseases in organs and causes death in a large number of patients. It can destroy the structure and function of organs and ultimately lead to organ failure, which is a major cause of disability and death in many diseases. However, the regulatory mechanism of organ fibrosis is not well clear and the lack of effective drugs and treatments, which seriously endangers human health and safety.
View Article and Find Full Text PDFSheng Li Xue Bao
December 2024
Department of Cardiology and Institute of Vascular Medicine, Peking University Third Hospital; State Key Laboratory of Vascular Homeostasis and Remodeling, Peking University; Institute of Advanced Clinical Medicine, Peking University; NHC Key Laboratory of Cardiovascular Molecular Biology and Regulatory Peptides; Beijing Key Laboratory of Cardiovascular Receptors Research, Beijing 100191, China.
Heart failure is characterized by abnormal β-adrenergic receptor (β-AR) activation and mitochondrial dysfunction. In heart failure, overactivation of β-AR mediates key pathological processes in cardiomyocytes, including oxidative stress, calcium overload and metabolic abnormalities, which subsequently lead to inflammation, myocardial apoptosis and necrosis. Mitochondria are the core organelles for energy metabolism, and also play a vital role in calcium homeostasis, redox balance and signaling transduction.
View Article and Find Full Text PDFClin Genet
January 2025
School of Medicine, Yunnan University, Kunming, Yunnan, China.
Oligoasthenoteratozoospermia (OAT) is a frequent but severe type of male infertility. As one of the most multifaceted male infertility resulting from sperm problems, its genetic etiology remains unknown in most cases. In this review, we systematically sort out the latest literature on clinical reports and animal models leading to OAT, summarise the expression profiles of causative genes for OAT, and highlight the important role of the protein transport system during spermiogenesis, spermatid cell-specific genes, Golgi and acrosome-related genes, manchette-related genes, HTCA-related genes, and axoneme-related genes in OAT development.
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