The synthesis and characterization of a series of Ni, Co, and Fe complexes bearing a tridentate bis(phosphino)silyl ligand (κ 3 -(2-Ph 2 PC 6 H 4 ) 2 SiMeH, [PSiP]-H, 1) are reported. 1 reacted with Ni(PMe 3 ) 4 to afford the mononuclear nickel(0) complex [η 2 (Si−H)-PSiP]Ni(PMe 3 ) (2). The halogeno nickel complexes [PSiP]Ni(X)(PMe 3 ) (X = Cl (3), Br (4), I (5)) were synthesized in the reactions of 2 with Me 3 SiCl or MeHSiCl 2 , EtBr, and MeI. Complex 2 underwent ligand substitution of PMe 3 by CO to give [η 2 (Si−H)-PSiP]Ni(CO) (6). Complex 3 reacted with NaOMe to deliver [PSiP]Ni-(OMe)(PMe 3 ) (7) through anionic ligand substitution, while the neutral ligand replacement of PMe 3 by CO in 3 afforded the rare hexacoordinate 20-electron nickel(II) complex [PSiP]Ni(Cl)(CO) 2 (8). Unexpectedly, reaction of 1 with NiMe 2 (PMe 3 ) 3 produced the tetracoordinate nickel(0) complex [Me 2 PSiP] 2 Ni (9). The complex [Me 2 PSiP]Ni(CO) 2 (10) was acquired from 9 after the substitution of one [PSiP] ligand by two carbonyl ligands. 1 reacted with Co(PMe 3 ) 4 or CoCl(PMe 3 ) 3 to afford the hydrido cobalt(II) complex [PSiP]CoH(PMe 3 ) (11) or hydrido cobalt(III) complex [PSiP]Co(H)(Cl)(PMe 3 ) (13). Complex 12, [PSiP]Co(H)(I)(PMe 3 ), could be obtained from the reaction of MeI with 11 or 13. Treatment of 13 with 1 equiv of MeLi or n-BuMgBr in THF resulted in the clean formation of cobalt(I) complex [PSiP]Co(PMe 3 ) 2 ( 14) via reductive elimination. The simple anhydrous inorganic salt NiCl 2 or CoCl 2 could also react with 1 in the presence of PMe 3 to form the corresponding silyl complexes 3 and [PSiP]Co(Cl)(PMe 3 ) (15) via Si−H bond cleavage. 1 reacted with Fe(PMe 3 ) 4 to form the hexacoordinate octahedral hydrido iron(II) complex [PSiP]Fe(H)(PMe 3 ) 2 ( 16). The molecular structures of complexes 2−5, 10, 12, 13, 15, and 16 were determined by X-ray single crystal diffraction. 16 has excellent catalytic reactivity for the reduction of aldehydes and ketones.

Epilepsy is a common and refractory neurological disorder, but the neuronal regulatory mechanisms of epileptogenesis remain largely unclear. Activity-dependent transcription of genes for neurotrophins such as brain-derived neurotrophic factor (BDNF) has been shown to promote epileptogenesis; however, little is known about factors that may act as intrinsic, homeostatic or counterbalancing mechanisms. Using rodent models, here we show that limbic seizure activity upregulated NRG1-ErbB4 signaling and that epileptogenesis was inhibited by infusing NRG1 intracerebrally but exacerbated by neutralizing endogenous NRG1 with soluble ErbB4 extracellular domain, by inhibiting ErbB4 activation or by deleting the Erbb4 gene. Furthermore, specific depletion of ErbB4 in parvalbumin-expressing interneurons abolished NRG1-mediated inhibition of epileptogenesis and promoted kindling progression, resulting in increased spontaneous seizures and exuberant mossy fiber sprouting. In contrast, depleting ErbB4 in CaMKIIα-positive pyramidal neurons had no effect. Thus, NRG1-induced activation of ErbB4 in parvalbumin-expressing inhibitory interneurons may serve as a critical endogenous negative-feedback mechanism to suppress limbic epileptogenesis.

Chronic high-salt diet-associated renal injury is a key risk factor for the development of hypertension. However, the mechanism by which salt triggers kidney damage is poorly understood. Our study investigated how high salt (HS) intake triggers early renal injury by considering the ‘gut-kidney axis’. We fed mice 2% NaCl in drinking water continuously for 8 weeks to induce early renal injury. We found that the ‘quantitative’ and ‘qualitative’ levels of the intestinal microflora were significantly altered after chronic HS feeding, which indicated the occurrence of enteric dysbiosis. In addition, intestinal immunological gene expression was impaired in mice with HS intake. Gut permeability elevation and enteric bacterial translocation into the kidney were detected after chronic HS feeding. Gut bacteria depletion by non-absorbable antibiotic administration restored HS loading-induced gut leakiness, renal injury and systolic blood pressure elevation. The fecal microbiota from mice fed chronic HS could independently cause gut leakiness and renal injury. Our current work provides a novel insight into the mechanism of HS-induced renal injury by investigating the role of the intestine with enteric bacteria and gut permeability and clearly illustrates that chronic HS loading elicited renal injury and dysfunction that was dependent on the intestine.

Background:The roles of Rictor/mTORC2 in folliculogenesis and follicle survival are unknown. Results: Loss of Rictor in oocytes causes excessive follicular atresia and the mutant mice demonstrate progressive POF phenotype. Conclusion: Rictor/mTORC2 plays key roles in folliculogenesis, follicle survival, and female fertility. Significance: This study establishes a novel function of mTORC2 in folliculogenesis and a potential link between mTORC2 and POF.