Int J Med Sci
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Background: Triggering receptor expressed in myeloid cells 2 (TREM2), a transmembrane receptor, has garnered extensive research attention due to its pivotal role in the diagnosis and treatment of various diseases. Despite the abundance of studies on its function, there is a gap in comprehensive analysis and summarization of the current state of this research field. Methods: Articles and reviews related to TREM2 were retrieved from the Web of Science Core Collection (WOSCC) on October 1, 2023. ⋯ Emerging directions such as metabolism and tumor microenvironment have recently gained attention in numerous studies. Conclusion: The current study utilizes bibliometric analysis software and visual graphics to intuitively highlight TREM2-related hotspots, trends, and prospects in human disease. Such insights are valuable for scholars seeking a deeper understanding of TREM2-related research progress, enabling a focused approach to its application in human disease.
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Uterine leiomyomas (ULM) are the most common benign tumors of the female genitalia, while uterine leiomyosarcomas (ULMS) are rare. The sarcoma is diffuse growth, prone to hematogenous metastasis, and has a poor prognosis. ⋯ This review searched and studied the published articles on ULM and ULMS, and summarized the potential markers for the differential diagnosis of ULMS. These markers will facilitate differential diagnosis and personalized treatment, providing timely diagnosis and potentially better prognosis for patients.
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Multicenter Study
Herpes Zoster Risk After Total Knee Replacement: a multicenter, propensity-score-matched cohort study in the United States.
Background: Total knee replacement (TKR) is a common surgical procedure for osteoarthritis (OA) patients. TKR may increase susceptibility to herpes zoster (HZ) by inducing immunosuppression, surgical stress, and nerve injury. However, limited data exist on the relationship between TKR and HZ. ⋯ The risk of HZ was statistically significant for females and older adults in the TKR cohort than in the control cohort. Conclusions: OA patients who underwent TKR had an increased risk of HZ compared to those who did not receive the procedure, especially females and older adults. These findings highlight the need for HZ monitoring/prevention protocols and further research on mitigating viral reactivation after major joint surgery.
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NLRC3, a negative regulator, exhibits considerable potential in the realm of lung cancer immunotherapy by virtue of its profound impact on the immune response intensity, primarily through its regulatory effects on the cGAS-STING pathway. The inhibition of NLRC3 has been found to augment the activity of the aforementioned pathway, thereby enhancing the anti-tumor immune response. This comprehensive review endeavors to elucidate the molecular and genetic structures of NLRC3, its role within the immune system, and its interaction with the cGAS-STING pathway, with a particular emphasis on its potential applications in lung cancer immunotherapy. ⋯ The development of pharmaceutical interventions and gene therapy strategies targeting NLRC3 presents a promising avenue for the creation of novel therapeutic options for individuals afflicted with lung cancer. Nonetheless, the clinical application of these therapies is confronted with both technical and biological challenges. This review aims to provide a theoretical foundation for related research endeavors and delineate future research directions in this field.
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Review
Enhancement of Mitochondrial Homeostasis: A Novel Approach to Attenuate Hypoxic Myocardial Injury.
Cardiomyocytes are highly oxygen-dependent cells, relying on oxygen-driven oxidative phosphorylation to maintain their function. During hypoxia, mitochondrial ATP production decreases, leading to calcium overload, acidosis, and oxidative stress, which collectively trigger myocardial injury. Ischemic heart disease, caused by coronary atherosclerosis, results in myocardial ischemia and hypoxia, leading to ischemia-reperfusion (I/R) injury. ⋯ In the early stages of ischemia and hypoxia, mitochondrial dysfunction disrupts mitochondrial homeostasis, causing the accumulation of unfolded or misfolded proteins in the mitochondria. This activates the mitochondrial unfolded protein response (mtUPR) and mitophagy, which work to clear damaged proteins and mitochondria, playing a key role during this period. This review focuses on mitochondrial mechanisms during the ischemic phase of ischemia-reperfusion injury, aiming to provide new theoretical foundations and potential therapeutic strategies to reduce myocardial damage.