Near-Infrared-II Imaging Revealed Hypothermia Regulates Neuroinflammation Following Brain Injury by Increasing the Glymphatic Influx.

Advanced in vivo imaging techniques have facilitated the comprehensive visual exploration of animal biological processes, leading to groundbreaking discoveries such as the glymphatic system. However, current limitations of macroscopic imaging techniques impede the precise investigation of physiological parameters regulating this specialized lymphatic transport system. While NIR-II fluorescence imaging has demonstrated advantages in peripheral lymphatic imaging, there are few reports regarding its utilization in the glymphatic system. To address this, a noninvasive transcranial macroscopic NIR-II fluorescence imaging model is developed using a cyanine dye-protein coupled nanoprobe. NIR-II imaging with high temporal and spatial resolution reveals that hypothermia can increase the glymphatic influx by reducing the flow rate of cerebrospinal fluid. In addition, respiratory rate, respiratory amplitude, and heart rate all play a role in regulating the glymphatic influx. Thus, targeting the glymphatic influx may alter the trajectory of immune inflammation following brain injury, providing therapeutic prospects for treating brain injury with mild hypothermia.

Traumatic Brain Injury Is Associated With Both Hemorrhagic Stroke and Ischemic Stroke: A Systematic Review and Meta-Analysis.

BACKGROUND: Traumatic brain injury (TBI) is considered a risk factor for the development of stroke (Hemorrhagic Stroke and Ischemic Stroke). We performed this systemic review and meta-analysis to determine the association of prior TBI with the subsequent diagnosis of stroke. METHODS: We systematically searched PubMed, EMBASE, and the Cochrane Library for cohort studies involving TBI patients who subsequently developed stroke. Study selection, data extraction, and quality assessment were performed by two separate researchers. Data were analyzed with random-effects models, and a secondary analysis stratified by the type of stroke was performed. RESULTS: Of the 741 identified studies, 6 studies were eligible for inclusion, with more than 2,200,000 participants. TBI predicted the occurrence of stroke in the random-effect model, with a relative risk of 2.14 (95% CI 1.97-2.32, P < 0.001). Furthermore, in the analysis of each type of stroke, TBI was associated with the incidence of ischemic stroke (RR 1.351 95% CI 1.212-1.506, P < 0.001), and TBI was associated with an even greater increase in the incidence of hemorrhagic stroke (RR 6.118 95% CI 5.265-7.108, P < 0.001). CONCLUSION: Our meta-analysis showed that TBI was associated with a more than two-fold increase in the risk of stroke. However, owing to the high degree of heterogeneity, decisions should be made on a patient-by-patient basis. The occurrence of TBI is associated with the development of both hemorrhagic and ischemic stroke, and the risk of hemorrhagic stroke is much higher than that of ischemic stroke in TBI patients.

Ursolic acid protects against cisplatin­induced ototoxicity by inhibiting oxidative stress and TRPV1­mediated Ca2+­signaling.

Cisplatin (CDDP) is widely used in clinical settings for the treatment of various cancers. However, ototoxicity is a major side effect of CDDP, and there is an associated risk of irreversible hearing loss. We previously demonstrated that CDDP could induce ototoxicity via activation of the transient receptor potential vanilloid receptor 1 (TRPV1) pathway and subsequent induction of oxidative stress. The present study investigated whether ursolic acid (UA) treatment could protect against CDDP­induced ototoxicity. UA is a triterpenoid with strong antioxidant activity widely used in China for the treatment of liver diseases. This traditional Chinese medicine is mainly isolated from bearberry, a Chinese herb. The present results showed that CDDP increased auditory brainstem response threshold shifts in frequencies associated with observed damage to the outer hair cells. Moreover, CDDP increased the expression of TRPV1, calpain 2 and caspase­3 in the cochlea, and the levels of Ca2+ and 4­hydroxynonenal. UA co­treatment significantly attenuated CDDP­induced hearing loss and inhibited TRPV1 pathway activation. In addition, UA enhanced CDDP­induced growth inhibition in the human ovarian cancer cell line SKOV3, suggesting that UA synergizes with CDDP in vitro. Collectively, the present data suggested that UA could effectively attenuate CDDP­induced hearing loss by inhibiting the TRPV1/Ca²+/calpain­oxidative stress pathway without impairing the antitumor effects of CDDP.