Beckerchristensen6108

"Societies unveil their entrails during a crisis and hide or conceal them in normal situations" is the premise of this essay that offers a propositional critique of the foundations of civilization by characterizing some revelations from the COVID-19 pandemic that seriously compromises the globalized world. Especially the neoliberal myth as the only way of human progress, and technological development as the essence of social progress and main reason for scientific research. Among the significant revelations is the dismantling of the Welfare state and public health services, which render the population's vulnerability in the face of pandemics. Planetary devastation favors its emergence, and the correlation between the despondency of human activities and the (fleeting) improvement of planetary life, which denotes the radical incompatibility between the permanence of neoliberal capitalism that degrades everything and preservation and care of life in its infinite diversity, including human life! Another notion of human progress is proposed the rise of values involved in the coexistence, and the spiritual, intellectual, and moral growth of the human condition in harmony with the planetary ecosystem. Regarding the deep reasons for the catastrophe, it is argued that it is humanity itself by its way of being, thinking, acting, living together and relating to the planet. Therefore, the conclusion reached is the urgent need to undertake an alternative path in the search for another possible world, hospitable and dignifying for all forms of life.

Promoting angiogenesis is a critical treatment strategy for ischemic cardiovascular diseases. Shexiang Baoxin Pill (SBP), a traditional Chinese medicine, has been reported to be capable of relieving angina and improve heart function by promoting angiogenesis. The aim of this study was to determine the role of mitochondrial aldehyde dehydrogenase 2 (ALDH2) in SBP-induced angiogenesis. Left femoral artery ligation was performed in wild-type mice (WT) and ALDH2 knockout mice, which were administrated with SBP (20 mg/kg/d) or equal volume saline per day by gastric gavage for 2 weeks. Perfusion recovery, angiogenesis in chronic hind limb ischemia, was significantly improved in the WT + SBP group than in the WT group. However, these beneficial effects were absent in ALDH2 knockout mice. In vitro, hypoxia impaired the ability of proliferation, migration and tube formation, sprouting angiogenesis, and promoted apoptosis in cardiovascular microvascular endothelial cells, whereas the hypoxia damage was restored by SBper day by gastric gavage for 2 weeks. Perfusion recovery, angiogenesis in chronic hind limb ischemia, was significantly improved in the WT + SBP group than in the WT group. However, these beneficial effects were absent in ALDH2 knockout mice. In vitro, hypoxia impaired the ability of proliferation, migration and tube formation, sprouting angiogenesis, and promoted apoptosis in cardiovascular microvascular endothelial cells, whereas the hypoxia damage was restored by SBP. The protective effect of SBP was remarkably weakened by ALDH2 knockdown. Furthermore, SBP suppressed hypoxia-induced ALDH2/protein kinase B (AKT)/mammalian target of rapamycin pathways. In conclusion, this study demonstrated that SBP protected lower limb from ischemia injury through the ALDH2-dependent pathway. read more The protective mechanism of SBP in cardiovascular microvascular endothelial cells was partly mediated through ALDH2/AKT/mammalian target of rapamycin pathways.

The calcium sensitizer levosimendan is indicated for the hemodynamic stabilization of patients with acutely decompensated heart failure and has been shown to be protective against reperfusion injury after myocardial infarction. However, affected forms of cell death and underlying signaling pathways remain controversial. Therefore, the aim of this study was to examine the influence of levosimendan preconditioning and postconditioning on anoxia/reoxygenation-induced apoptosis, necrosis, and autophagy in H9c2 myoblasts. To mimic conditions of myocardial ischemia/reperfusion, rat cardiac H9c2 myoblasts were exposed to anoxia/starvation, followed by reoxygenation/refeeding. Apoptosis, necrosis, autophagy, cell viability, survival signaling, and mitochondrial permeability transition pore (mPTP) opening were measured. Both, pharmacological preconditioning and postconditioning with levosimendan were capable to reduce apoptosis as well as necrosis in stressed H9c2 cells. However, preconditioning showed to have the sting enhanced repair processes initiated by the early presence of the drug. Underlying mechanisms differ between both interventions Although both are associated with PI3/Akt activation and reduced mPTP opening, only postconditioning but not preconditioning depended on mKATP activation. This variation might indicate that a pharmacological treatment after the onset of reoxygenation at least in part directly addresses mitochondrial structures for protection. In conclusion, we demonstrate that both pharmacological preconditioning and postconditioning with levosimendan protect anoxia/reoxygenation-stressed cells but differ in the underlying mechanisms. These results are decisive to obtain more insights into the beneficial effects of levosimendan in the treatment of reperfusion-mediated damage.

Chinese people have used the root of Salvia miltiorrhiza Bunge (called "Danshen" in Chinese) for centuries as an anticancer agent, anti-inflammatory agent, antioxidant, and cardiovascular disease drug. In addition, Danshen is considered to be a drug that can improve ischemia/reperfusion (I/R)-induced myocardium injury in traditional Chinese medicine. However, Danshen is a mixture that includes various bioactive substances. In this study, we aimed to identify the protective component and mechanism of Danshen on myocardium through network pharmacology and molecular simulation methods. First, cryptotanshinone (CTS) was identified as a potential active compound from Danshen that was associated with apoptosis by a network pharmacology approach. Subsequently, biological experiments validated that CTS inhibited ischemia/reperfusion-induced cardiomyocyte apoptosis in vivo and in vitro. Molecular docking techniques were used to screen key target information. Based on the simulative results, MAPKs were verified as well-connected molecules of CTS.