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mRNA vaccines are leading a medical revolution. mRNA technologies utilize the host's own cells as bio-factories to produce proteins that serve as antigens. This revolutionary approach circumvents the complicated processes involved in traditional vaccine production and empowers vaccines with the ability to respond to emerging or mutated infectious diseases rapidly. Additionally, the robust cellular immune response elicited by mRNA vaccines has shown significant promise in cancer treatment. However, the inherent instability of mRNA and the complexity of tumor immunity have limited its broader application. Although the emergence of pseudouridine and ionizable cationic lipid nanoparticles (LNPs) made the clinical application of mRNA possible, there remains substantial potential for further improvement of the immunogenicity of delivered antigens and preventive or therapeutic effects of mRNA technology. Here, we review the latest advancements in mRNA vaccines, including but not limited to target selection and delivery systems. This review offers a multifaceted perspective on this rapidly evolving field. [ABSTRACT FROM AUTHOR]

Parkinson's disease (PD), a neurodegenerative disorder characterized by impaired motor function, is typically treated with medications and surgery. However, recent studies have validated physical exercise as an effective adjunct therapy, significantly improving both motor and non-motor symptoms in PD patients. Irisin, a myokine, has garnered increasing attention for its beneficial effects on the nervous system. Research has shown that irisin plays a crucial role in regulating metabolic balance, optimizing autophagy, maintaining mitochondrial quality, alleviating oxidative stress and neuroinflammation, and regulating cell death-all processes intricately linked to the pathogenesis of PD. This review examines the mechanisms through which irisin may counteract PD, provides insights into its biological effects, and considers its potential as a target for therapeutic strategies., Competing Interests: Declaration of competing interest There are no financial or personal relationships with any commercial entities or organizations that could be perceived as influencing the study's content, results, interpretation, or conclusions., (Copyright © 2024 The Authors. Published by Elsevier Inc. All rights reserved.)

Objective: To investigate the safety and efficacy of intravenous Tirofiban infusion after mechanical thrombectomy in patients with acute ischemic stroke., Methods: A consecutive series of patients with acute ischemic stroke who underwent mechanical thrombectomy were included. The patients were categorized into two groups according to whether they received intravenous Tirofiban infusion after mechanical thrombectomy. Intracranial hemorrhage (ICH) and all-cause mortality were studied as safety outcomes; recanalization of target vessel evaluated by thrombolysis in cerebral infarct (TICI) scale, and neurological improvement evaluated by Institutes of Health Stroke Scale (NIHSS) and modified Rankin scale (mRS) were studied as efficacy outcomes., Results: A total of 31 patients who underwent mechanical thrombectomy were enrolled, among which 8 (25.81%) received a standard dose of intravenous Tirofiban infusion after mechanical thrombectomy. There was no significant difference in baseline characteristics between the two groups (all P>0.05). None (0.00%) of the patients suffered ICH in the Tirofiban group, while 3 (13.04%) suffered ICH in the control group (P=0.550); similar all-cause mortality rates were found in both groups (25.00% versus 17.39%, P=0.634). In the Tirofiban group, all patients achieved successful recanalization defined by TICI groups (25.00% versus 17.39%, P=0.634). In the und in both groups (25.00% versus 17.39%, P=0.634). In th4). In thle, and neurological improvement evaluated so, 'et al' is notned by 3-month mRS≤2, which were not statistically significant when compared to the control group (all P>0.05)., Conclusion: Intravenous Tirofiban infusion after mechanical thrombectomy is safe and effective in patients with acute ischemic stroke., Competing Interests: None., (AJTR Copyright © 2021.)

Objective To clarify the regulation role of tumor necrosis factor-related apoptosis inducing ligand-death receptor 5 (TRAIL-DR5) in cell autophagy induced by suberoylanilidehydroxamic acid (SAHA) in ER-positive breast cancer cell MCF-7. Methods The logarithmic growth phase of MCF-7 cells were divided into control group, SAHA treatment group, TRAIL-DR5 siRNA group and SAHA combined with TRAIL-DR5 siRNA treatment group. Western blotting was used to verify the results of TRAIL-DR5 gene silencing. Real-time quantitative PCR was performed to detect the mRNA levels of autophagy-related gene 9B (ATG9B), microtubule-associated protein 1 light chain 3A (LC3A) and LC3B in the different groups. The expressions of beclin-1, ATG3, ATG5, ATG7, ATG12, ATG16, ATG4A, ATG4B, ATG9B, LC3II, cathepsin B (CTSB) in the breast cancer cells were detected by Western blotting. The level of CTSB in the breast cancer cell culture supernatant was analyzed by ELISA. Immunofluorescence cytochemical staining was used to determine the expression and distribution of LC3II in the breast cancer cells. Results TRAIL-DR5 siRNA transfection significantly decreased the levels of TRAIL-DR5 in MCF-7 cells. After the knock-down of TRAIL-DR5 gene in MCF-7, the mRNA and protein levels of the autophagy-related factors in breast cancer cells markedly decreased, and the protein level of CTSB also decreased. After SAHA treatment of MCF-7 cells, the level of LC3II increased; when knockdown of TRAIL-DR5 receptor, LC3II level was significantly lower than that in the SAHA-alone-treated cells. Conclusion Down-regulating the TRAIL-DR5 gene can inhibit cell autophagy induced by SAHA in ER-positive MCF-7 breast cancer cells.