Balance and gait performance after maximal and submaximal endurance exercise in seniors: is there a higher fall-risk?

Impaired balance and gait performance increase fall-risk in seniors. Acute effects of different exercise bouts on gait and balance were not yet addressed. Therefore, 19 healthy seniors (10 women, 9 men, age: 64.6 ± 3.2 years) were examined on 3 days. After exhaustive treadmill testing, participants randomly completed a 2-km treadmill walking test (76 ± 8 % VO_2max) and a resting control condition. Standing balance performance (SBALP) was assessed by single limb-eyes opened (SLEO) and double limb-eyes closed (DLEC) stance. Gait parameters were collected at comfortable walking velocity. A condition × time interaction of center of pressure path length (COP_path) was observed for both balance tasks (p < 0.001). Small (Cohen’s d = 0.42, p = 0.05) and large (d = 1.04, p < 0.001) COP_path increases were found after 2-km and maximal exercise during DLEC. Regarding SLEO, slightly increased COP_path occurred after 2-km walking (d = 0.29, p = 0.65) and large increases after exhaustive exercise (d = 1.24, p < 0.001). No significant differences were found for gait parameters. Alterations of SBALP after exhaustive exercise might lead to higher fall-risk in seniors. Balance changes upon 2-km testing might be of minor relevance. Gait is not affected during single task walking at given velocities.     

IL-33 signaling contributes to the pathogenesis of myeloproliferative neoplasms

Myeloproliferative neoplasms (MPNs) are characterized by the clonal expansion of one or more myeloid cell lineage. In most cases, proliferation of the malignant clone is ascribed to defined genetic alterations. MPNs are also associated with aberrant expression and activity of multiple cytokines; however, the mechanisms by which these cytokines contribute to disease pathogenesis are poorly understood. Here, we reveal a non-redundant role for steady-state IL-33 in supporting dysregulated myelopoiesis in a murine model of MPN. Genetic ablation of the IL-33 signaling pathway was sufficient and necessary to restore normal hematopoiesis and abrogate MPN-like disease in animals lacking the inositol phosphatase SHIP. Stromal cell–derived IL-33 stimulated the secretion of cytokines and growth factors by myeloid and non-hematopoietic cells of the BM, resulting in myeloproliferation in SHIP-deficient animals. Additionally, in the transgenic JAK2^V617F model, the onset of MPN was delayed in animals lacking IL-33 in radio-resistant cells. In human BM, we detected increased numbers of IL-33–expressing cells, specifically in biopsies from MPN patients. Exogenous IL-33 promoted cytokine production and colony formation by primary CD34⁺ MPN stem/progenitor cells from patients. Moreover, IL-33 improved the survival of JAK2^V617F-positive cell lines. Together, these data indicate a central role for IL-33 signaling in the pathogenesis of MPNs.