Association between Muscle Mass Index and Neurological Outcomes of Patients with Out-of-Hospital Cardiac Arrest.

Muscle mass depletion is associated with unfavorable outcomes in many diseases. However, its relationship with cardiac arrest outcomes has not been explored. This retrospective single-center study determined the relationship between muscle mass depletion and the neurological outcomes of patients with out-of-hospital cardiac arrest (OHCA) by measuring muscle mass at various locations. Adult patients with OHCA, who were treated with target temperature management, and who underwent abdominal or chest computed tomography (CT) within 3 months of the cardiac arrest were included. Skeletal muscle index (SMI) was measured at the third lumbar vertebra (L3) level, psoas muscle, fourth thoracic vertebra (T4) level, and pectoralis muscle. The Youden index was used to determine a low SMI based on sex-specific cutoff values. The outcome variables were "good neurological outcome" and "survival" at hospital discharge. Multivariable analyses revealed that patients with low T4 SMI level were significantly associated with good neurological outcomes at hospital discharge (odds ratio = 0.26, 95% confidence interval: 0.07-0.88, p = 0.036). However, no significant differences were observed between good neurological outcomes and low SMI at the L3 level and psoas and pectoralis muscles; SMIs were not associated with survival at hospital discharge. T4 level SMI depletion was inversely associated with good neurological outcomes in patients with OHCA. Thoracic muscle depletion may be crucial for predicting the neurological outcomes in patients with OHCA and further investigation in larger prospective study is warranted.

Ischemic stroke outcome after promoting CD4+CD25+ Treg cell migration through CCR4 overexpression in a tMCAO animal model.

The importance of neuroinflammation during the ischemic stroke has been extensively studied. The role of CD4+CD25+ regulatory T (Treg) cells during the recovery phase have shown infarct size reduction and functional improvement, possibly through the mitigation of inflammatory immune responses. We aimed to investigate the molecular factors involved in microglia-Treg cell communication that result in Treg trafficking. First, we observed the migration patterns of CD8+ (cytotoxic) T cells and Treg cells and then searched for chemokines released by activated microglia in an oxygen-glucose deprivation (OGD) model. The transwell migration assay showed increased migration into OGD media for both cell types, in agreement with the increase in chemokines involved in immune cell trafficking from the mouse chemokine profiling array. MSCV retrovirus was transduced to overexpress CCR4 in Treg cells. CCR4-overexpressed Treg cells were injected into the mouse transient middle cerebral artery occlusion (tMCAO) model to evaluate the therapeutic potential via the tetrazolium chloride (TTC) assay and behavioral tests. A general improvement in the prognosis of animals after tMCAO was observed. Our results suggest the increased mobility of CCR4-overexpressed Treg cells in response to microglia-derived chemokines in vitro and the therapeutic potential of Treg cells with increased mobility in cellular therapy.