Int J Med Sci
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Spinal cord injury (SCI) results in acute inflammatory responses and secondary damages, including neuronal and glial cell death, axonal damage and demyelination, and blood-brain barrier (BBB) damage, eventually leading to neuronal dysfunction and other complications. C-X-C motif Chemokine Ligand 10 (CXCL10) is expressed after the injury, playing multiple roles in the development and progression of SCI. Moreover, the CXCL10 antagonist can restrict inflammatory immune responses and promote neuronal regeneration and functional recovery. In this review, we summarize the structure and biological functions of CXCL10, and the roles of the CXCL10 / CXCR3 axis in acute inflammatory responses, secondary damages, and complications during SCI, thus providing a potential theoretical basis by highlighting CXCL10 as a new potential drug target for the treatment of SCI.
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Randomized Controlled Trial
Comparison of the effects of dexmedetomidine and propofol on hypothermia in patients under spinal anesthesia: a prospective, randomized, and controlled trial.
Background: Redistribution hypothermia caused by vasodilation during anesthesia is the primary cause of perioperative hypothermia. Propofol exerts a dose-dependent vasodilatory effect, whereas dexmedetomidine induces peripheral vasoconstriction at high plasma concentrations. This study compared the effects of dexmedetomidine and propofol on core temperature in patients undergoing surgery under spinal anesthesia. ⋯ Results: Core temperature at the end of surgery did not differ significantly between the groups (36.4 ± 0.4 and 36.1 ± 0.7°C in the dexmedetomidine and propofol groups, respectively; P = 0.118). The lowest perioperative temperature, incidence and severity of perioperative hypothermia, thermal comfort score, and shivering grade did not differ significantly between the groups (all P > 0.05). Conclusions: In patients undergoing spinal anesthesia with moderate sedation, the effect of dexmedetomidine on patients' core temperature was similar to that of propofol.
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Glial cell line-derived neurotrophic factor family receptor alpha (GFRα) members have been widely connected to the mechanisms contributing to cell growth, differentiation, cell migration and tissue maturation. Here we review GFRα biological functions and discussed the evidence indicating whether GFRα signaling complex present novel opportunities for oncogenic intervention and treatment resistance. Thus, our work systematically reviewed the emerging role of GFRα family members in cancers, and provided novel insights for further researches.
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Breast cancer remains a worldwide public health issue. LncRNA and autophagy respectively or simultaneously, get involved in cellular and molecular processes of many different cancers, including genesis, metastasis, and deterioration of breast cancer and other malignant tumors. ⋯ Abnormal expression of LncRNA may lead to dysregulation of autophagy, resulting in tumor genesis, expansion, and resistance to anti-tumor therapy. Targeting specific lncRNAs for autophagy regulation may conduct as a bio-marker for reliable diagnosis and prognosis treatment of breast cancer or provide a promising therapeutic strategy.
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Acute myeloid leukemia (AML) is a quickly progressive and devastated hematological malignancy with large rate of relapse and the appearance of chemotherapy resistance. Therefore, the identification of new therapeutic targets is urgent. ZFP91 is a hidden oncogene. ⋯ This research demonstrates that ZFP91 boosts AML cell proliferation and stops AML cell apoptosis. Mechanistically, experimental results showed the interaction between ZFP91 and RIP1 and inhibitory effect of ZFP91 on the K48-linked ubiquitination of endogenous RIP1, which is an important molecule in AML. Taken together, our results provide the evidence that targeted inhibition of ZFP91 could be a hopeful measure to treat AML.