Sequential Structural Degradation of Red Perovskite Quantum Dots and Its Prevention by Introducing Iodide at a Stable Gradient Concentration into the Core–Shell Red Perovskite Quantum Dots

Perovskite quantum dots (QDs) have been extensively studied as emissive materials for next-generation optoelectronics due to their outstanding optical properties; however, their structural instabilities, specifically those of red perovskite QDs,...

The structure-activity relationship between precursor fine structure and cathodes performance in Ni-rich layered oxide

Cathode’s primary particle structure plays a key role in the performance of lithium ion batteries, which can be controlled by the precursor synthesis. Regretfully, the relevance between primary particle structure and cathode performance is not explicitly elucidated, that is, what is the discrepancy of cathode’s primary particle size on the structural degradation? In order to elaborate the structure-activity relationship between them, we have systematically investigated the regulation of primary particle size through an in-depth analysis of the precursor growth mechanism, ammonia-stirring coupling and hydrodynamics optimization. Structural and electrochemical characterizations of LiNi0.92Co0.04Mn0.04O2 with different primary sizes (336, 447, 565 and 675 nm) and a rounded analysis of structural degradation after cycling provide insight into the correlation between precursor fine structure and cathode performance, i.e. larger cathode’s primary particle size can effectively inhibit CEI film formation, structure decay, the intragranular/intergranular cracks formation owing to the alleviation of localized stress.

Structural Degradation in Midcingulate Cortex Is Associated with Pathological Aggression in Mice

Pathological aggression is a debilitating feature of many neuropsychiatric disorders, and cingulate cortex is one of the brain areas centrally implicated in its control. Here we explore the specific role of midcingulate cortex (MCC) in the development of pathological aggression. To this end, we investigated the structural and functional degeneration of MCC in the BALB/cJ strain, a mouse model for pathological aggression. Compared to control animals from the BALB/cByJ strain, BALB/cJ mice expressed consistently heightened levels of aggression, as assessed by the resident-intruder test. At the same time, immunohistochemistry demonstrated stark structural degradation in the MCC of aggressive BALB/cJ mice: Decreased neuron density and widespread neuron death were accompanied by increased microglia and astroglia concentrations and reactive astrogliosis. cFos staining indicated that this degradation had functional consequences: MCC activity did not differ between BALB/cJ and BALB/cByJ mice at baseline, but unlike BALB/cByJ mice, BALB/cJ mice failed to activate MCC during resident-intruder encounters. This suggests that structural and functional impairments of MCC, triggered by neuronal degeneration, may be one of the drivers of pathological aggression in mice, highlighting MCC as a potential key area for pathologies of aggression in humans.