Neonatal microglia transplantation at early stage but not late stage after traumatic brain injury shows protective effects in mice.

The transplantation of neonatal microglia suppresses neuroinflammation caused by traumatic brain injury (TBI). This research aimed to explore the optimal time point of neonatal microglia transplantation for the best effect on the improvement of long-term cognitive function and inflammatory response in mouse models. qPCR and immunoblotting showed that the level of Iba1 gradually increased to the highest on day 7 and then gradually declined in TBI mice. Furthermore, it was observed that the level of CD86 and TNF-α increased to the highest after 7 days and subsequently was maintained until day 21, whereas the level of CD206 and IL-10 increased to the highest after 24 h and subsequently decreased until day 21 by qPCR and enzyme-linked immunosorbent assay. Afterward, it was shown that the neonatal microglia transplantation within 1 h significantly attenuated anxiety-like behavior and improved cognitive impairments in TBI mice. Mechanism exploration showed that the neonatal microglia could significantly decrease the level of cleaved caspase-3, M1/M2 polarization, and inflammatory cytokine (TNF-α) while increasing the level of anti-inflammatory factor IL-10 in TBI mice after transplantation within 1 h. Here, our findings demonstrated that neonatal microglia transplantation within 1 h significantly attenuated anxiety-like behavior and cognitive impairments caused by TBI.NEW & NOTEWORTHY The study demonstrated that neonatal microglia transplantation within 1 h significantly inhibited the pathogenesis of traumatic brain injury (TBI) in mouse models through inhibition of M1 polarization and promotion of M2 polarization.

Relation of serum uric acid levels to readmission and mortality in patients with heart failure.

Data on the association between uric acid (UA) levels and clinical outcomes, such as readmission and mortality, in patients with heart failure are scarce. This study explores whether UA exhibits an independent association with the composite endpoint (clinical outcome during 6 months after discharge, including mortality and 6-month readmission) in patients with chronic heart failure while controlling for other covariates. This study was an observational retrospective study. A cohort of 1943 consecutive patients diagnosed with chronic heart failure, who were admitted between December 2016 and June 2019, was included in the study. Data were sourced from PhysioNet. The independent variable analyzed was the UA level, and the dependent variable was a composite endpoint comprising mortality and 6-month readmission. The study had 1943 participants, of which 91.04% were aged more than 60 years and 58.05% were female. The fully-adjusted model yielded a positive correlation between UA levels (per 10 µmol/L) and the composite endpoint as well as readmission, following adjustment for confounding variables (HR = 1.01, 95% CI 1.00-1.01). Notably, a non-linear relationship was observed between UA levels and the composite endpoint, particularly readmission, with a J-shaped correlation observed between UA levels and both the composite endpoint and readmission. Overall, we found that the serum UA levels at admission were independently and positively associated with the risk of the composite endpoint (clinical outcomes during 6 months after discharge), especially readmission after adjusting other covariates. A J-shaped relationship was observed between UA levels and the composite endpoint and readmission.