Final bound-state formation effect on dark matter annihilation

If the annihilation products of dark matter (DM) are non-relativistic and couples directly to a light force mediator, the non-perturbation effect like final state bound state (FBS) formation and final state Sommerfeld (FSS) effect must be considered. Non-relativistic region of final particles will appear when there is small mass split between DM and products, so we study those effects in the degenerate region of mass (including kinematics forbidden case) using two specific models. We demonstrate that FBS effect will significantly modify the DM relic abundance comparing to the standard perturbation calculation in some mass split region. We emphasize that FBS effect is comparable to the FSS effect in those mass split. The conservation angular momentum are subtle considering FBS formation, in some cases there may be not $s$-wave, so we use two models exhibit the different partial wave FBS effect contribution. We also show that the FBS formation with vector boson emission process also contributes in DM relic abundance, and first calculate the $p$-wave FSS effect in the specific model.Comment: 23 pages, 13 figure

Performance investigation of a micro-channel flat separated loop heat pipe system for data centre cooling

This paper investigates a novel micro-channel flat separated loop heat pipe system for cooling the information technology equipment in the data centres through theoretical and experimental analysis and by assessing the impact of the inlet water temperature on system performance. A computer model is developed to simulate the steady-state performance of the micro-channel flat separated loop heat pipe system. After comparing the experimental and modelling results, the new and conventional system under the same working conditions, the model is validated yielding high accuracy in predicting the performance of the micro-channel flat separated loop heat pipe system with recorded error being limited to 2.16–8.97%. The new system has better performance than the conventional system. Under the operating conditions of heat load intensity of 1,000 W/m2, water flow rate of 0.28 m3/h, refrigerant filling rate of 30%, ambient air temperature of 26°C, and evaporator and condenser height difference of 0.8 m, the performance of the system has been explored at inlet temperature from 15 to 24°C with increments of 3°C. The system’s averaged heat transfer efficiency was found to decrease with the increase in inlet temperature. This research provides valuable insight into the data centre information technology equipment cooling, which is of great significance for energy saving and environmentally friendly operation of data centres

Differential Role of p53 in Oligodendrocyte Survival in Response to Various Stresses: Experimental Autoimmune Encephalomyelitis, Cuprizone Intoxication or White Matter Stroke

Promoting oligodendrocyte viability has been proposed as a therapeutic strategy for alleviating many neuronal diseases, such as multiple sclerosis and stroke. However, molecular pathways critical for oligodendrocyte survival under various stresses are still not well known. p53 is a strong tumor suppressor and regulates cell cycle, DNA repair and cell death. Our previous studies have shown that p53 plays an important role in promoting neuronal survival after insults, but its specific role in oligodendrocyte survival is not known. Here, we constructed the mice with oligodendrocyte-specific p53 loss by crossing TRP53flox/flox mice and CNP-cre mice, and found that p53 was dispensable for oligodendrocyte differentiation and myelin formation under physiological condition. In the experimental autoimmune encephalomyelitis (EAE) model, p53 loss of function, specifically in oligodendrocytes, did not affect the EAE disease severity and had no effect on demyelination in the spinal cord of the mice. Interestingly, p53 deficiency in oligodendrocytes significantly attenuated the demyelination of corpus callosum and alleviated the functional impairment of motor coordination and spatial memory in the cuprizone demyelination model. Moreover, the oligodendrocyte-specific loss of p53 provided protection against subcortical white matter damage and mitigated recognition memory impairment in mice in the white matter stroke model. These results suggest that p53 plays different roles in the brain and spinal cord or in response to various stresses. Thus, p53 may be a therapeutic target for oligodendrocyte prevention in specific brain injuries, such as white matter stroke and multiple sclerosis

Differential Role of p53 in Oligodendrocyte Survival in Response to Various Stresses: Experimental Autoimmune Encephalomyelitis, Cuprizone Intoxication or White Matter Stroke

Promoting oligodendrocyte viability has been proposed as a therapeutic strategy for alleviating many neuronal diseases, such as multiple sclerosis and stroke. However, molecular pathways critical for oligodendrocyte survival under various stresses are still not well known. p53 is a strong tumor suppressor and regulates cell cycle, DNA repair and cell death. Our previous studies have shown that p53 plays an important role in promoting neuronal survival after insults, but its specific role in oligodendrocyte survival is not known. Here, we constructed the mice with oligodendrocyte-specific p53 loss by crossing TRP53flox/flox mice and CNP-cre mice, and found that p53 was dispensable for oligodendrocyte differentiation and myelin formation under physiological condition. In the experimental autoimmune encephalomyelitis (EAE) model, p53 loss of function, specifically in oligodendrocytes, did not affect the EAE disease severity and had no effect on demyelination in the spinal cord of the mice. Interestingly, p53 deficiency in oligodendrocytes significantly attenuated the demyelination of corpus callosum and alleviated the functional impairment of motor coordination and spatial memory in the cuprizone demyelination model. Moreover, the oligodendrocyte-specific loss of p53 provided protection against subcortical white matter damage and mitigated recognition memory impairment in mice in the white matter stroke model. These results suggest that p53 plays different roles in the brain and spinal cord or in response to various stresses. Thus, p53 may be a therapeutic target for oligodendrocyte prevention in specific brain injuries, such as white matter stroke and multiple sclerosis

The Activators of Cyclin-Dependent Kinase 5 p35 and p39 Are Essential for Oligodendrocyte Maturation, Process Formation, and Myelination.

The regulation of oligodendrocyte development and myelin formation in the CNS is poorly defined. Multiple signals influence the rate and extent of CNS myelination, including the noncanonical cyclin-dependent kinase 5 (Cdk5) whose functions are regulated by its activators p35 and p39. Here we show that selective loss of either p35 or p39 perturbed specific aspects of oligodendrocyte development, whereas loss of both p35 and p39 completely inhibited the development of mature oligodendrocytes and myelination. In the absence of p35, oligodendrocyte differentiation was delayed, process outgrowth was truncated in vitro, and the patterning and extent of myelination were perturbed in the CNS of p35(−/−) mice. In the absence of p39, oligodendrocyte maturation was transiently affected both in vitro and in vivo. However, loss of both p35 and p39 in oligodendrocyte lineage cells completely inhibited oligodendrocyte progenitor cell differentiation and myelination both in vitro and after transplantation into shiverer slice cultures. Loss of p35 and p39 had a more profound effect on oligodendrocyte development than simply the loss of Cdk5 and could not be rescued by Cdk5 overexpression. These data suggest p35 and p39 have specific and overlapping roles in oligodendrocyte development, some of which may be independent of Cdk5 activation. SIGNIFICANCE STATEMENT The development of oligodendrocytes and myelination is essential for normal CNS function and cyclin-dependent kinase 5 (Cdk5) activity is critical for oligodendrocyte maturation, but how Cdk5 activity is controlled is unclear. Here we show that the coactivators of Cdk5, p35 and p39, regulate distinct stages of oligodendrocyte development and myelination. Loss of p35 perturbs oligodendrocyte progenitor cell differentiation, whereas loss of p39 delays oligodendrocyte maturation. Loss of both completely inhibits oligodendrogenesis and myelination. Disruption of oligodendrocyte development was more pronounced in p35(−/−);p39 shRNA cells than loss of Cdk5 alone and could not be rescued by Cdk5 overexpression, suggesting that p35 and p39 have Cdk5-independent roles during oligodendrocyte development. These studies provide novel targets for therapeutic intervention in conditions in which myelination is perturbed