Vibration analysis of size dependent micro FML cylindrical shell reinforced by CNTs based on modified couple stress theory

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“…This difference was demonstrated when comparing the laser-treated group with the laser-plus-HANPs group and the laser-plus-IONPs group with the laser-treated group. It is possible that the additive effect of the two agents, which elevated microhardness values more than either agent could have done on its own, contributed to the statistically significant difference that was observed between the groups treated with laser and HANPs and those treated with IONPs [33][34][35][36][37][38][39][40]. There were statistically significant differences between the groups when comparing the laser + HANPs group to the IONPs + laser group, as well as when comparing the laser + IONPs group to the IONPs group and the IONPs + laser group.…”

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“…The current study finding of the lower level of cTn-I in the levosimendan group may be attributed to its anti-inflammatory action is linked to its ability to inhibit the Rho-kinase signaling cascade, which may contribute to its cardioprotection against sepsis-induced cardiotoxicity [23]. Another proposed pathway can explain levosimendan cardioprotective effects and lower level of cTn-I by its effect as an inodilator via its work as a calcium sensitizer and activator of ATP-sensitive K channel within the vascular smooth muscle and cardiac mitochondria hence protecting the cardiomyocytes against [13,14].…”

“…It is widely used to relieve the symptoms of acute heart failure, consequently to its effect on both systemic and pulmonary hemodynamics [12,13]. Additionally, it is indicated in the case of decompensated heart failure due to its inodilator effect, which the following mechanisms can obtained: the first mechanism is by increasing the troponin C sensitivity to calcium within the cardiomyocytes, thereby positively modulating the cAMP-independent inotropic impact, the second mechanism is by its effect as a vasodilator through activating of ATP sensitive K channel within the vascular smooth muscle, the third mechanism is by the stimulation of ATP sensitive K channel within cardiac mitochondria hence protect the cardiomyocytes against IR injury [13,14]. As far as we know, there is little information on the involvement of levosimendan in attenuating sepsis-induced cardiotoxicity.…”

Reprogramming the tumor microenvironment to improve the efficacy of cancer immunotherapies

“…1c). Hypoxia, nutrient deprivation, and increased cytokines in TME lead to the recruitment of distinct MSC subpopulations with immune-modulating capacity [52]. MSCs-supporting tumorigenesis secret GRO-y (growth-regulated oncogene) chemokine that mediates the differentiation of monocyte-derived dendritic cells toward MDSCs [53].…”