Mitochondrial protein prohibitin promotes learning memory recovery in mice following intracerebral hemorrhage via CAMKII/CRMP signaling pathway.

Prohibitin (PHB) is a mitochondrial inner membrane protein with neuroprotective, antioxidant, and apoptosis-reducing effects. This study aimed to explore the role of PHB in pathological symptoms, behavioral deficits, and cognitive impairment in a collagenase-IV-induced intracerebral hemorrhage (ICH) murine model. In this study, mice that received collagenase IV injection were pretreated with PHB or saline 21 days prior to modeling. The role of PHB in memory and learning ability was monitored using the Morris water maze, Y-maze, and rotarod, social, startle, and nest-building tests. The effect of PHB on depression-like symptoms was examined using the forced swimming, tail suspension, and sucrose preference tests. Subsequently, mouse samples were analyzed using immunohistochemistry, western blotting, Perls staining, Nissl staining, and gene sequencing. Results showed that collagenase IV significantly induced behavioral deficits, brain edema, cognitive impairment, and depressive symptoms. PHB overexpression effectively alleviated memory, learning, and motor deficits in mice with ICH. PHB markedly inhibited the number of terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick-end labeling-positive cells and protein levels of ionized calcium-binding adapter molecule 1, glial fibrillary acidic protein, and interleukin-1ß in the perihematomal region of ICH mice. PHB overexpression also remarkably promoted production of neurologin1 (NLGL1), and upregulated levels of Ca2+-calmodulin-dependent kinase II (CaMKII) and collapsin response mediator protein-1 (CRMP1) proteins. In conclusion, PHB overexpression can effectively alleviate the neurological deficits and neurodegeneration around the hematoma region. This may play a protective role by upregulating the expression of NLGL1 and promoting expression of CaMKII and CRMP1.

New Insight into Temperature Effects on Low-Rank Coal Flotation Using Diesel as a Collector.

Efficient flotation of low-rank coal is of great significance for the development of green and low-carbon cycles. Temperature is a crucial parameter of flotation, but the mechanism of its effect on flotation lacks understanding. In this paper, the mechanism was studied by kinetic flotation, scanning electron microscopy (SEM), Fourier transform infrared spectroscopy, low-temperature liquid-nitrogen adsorption (LP-N2A), X-ray photoelectron spectroscopy (XPS), and molecular dynamics simulation. The flotation combustible recovery gradually decreases as temperature rises. Compared with 60 °C, the combustible recovery at 5 °C increases by 18.13%. The desorption energy for oil droplets decreases as the temperature rises. As a result, the oil droplets are easier to desorb at high temperatures. The SEM and LP-N2A results demonstrate that the pores and fractures of the coal sample are well developed. Also, the oil-water interfacial tension and viscosity of oil droplets decrease as the temperature rises, while the diffusion ability increases. These increase the volume of oil droplets that penetrate into the pores, resulting in poor spreadability of oil droplets on the coal surface. The average volume of bubbles gradually increases as temperature rises, which renders the flotation foam unstable and worsens the flotation. Therefore, the flotation performance is better at low temperatures.