UNASSIGNED: Neurologic complications seriously affect the survival rate and quality of life in patients with extracorporeal cardiopulmonary resuscitation (ECPR) undergoing cardiac arrest. This study aimed to repurpose selective hypothermic cerebral perfusion (SHCP) as a novel approach to protect the brains of these patients.
UNASSIGNED: Rats were randomly allocated to Sham, ECPR, and SHCP combined ECPR (CP-ECPR) groups. In the ECPR group, circulatory resuscitation was performed at 6 minutes after asphyxial cardiac arrest by extracorporeal membrane oxygenation. The vital signs were monitored for 3 hours, and body and brain temperatures were maintained at the normal level. In the CP-ECPR group, the right carotid artery catheterization serving as cerebral perfusion was connected with the extracorporeal membrane oxygenation device to achieve selective brain cooling (26-28 °C). Serum markers of brain injury and pathomorphologic changes in the hippocampus were evaluated. Three biological replicates further received RNA sequencing in ECPR and CP-ECPR groups. Microglia activation and inflammatory cytokines in brain tissues and serum were detected.
UNASSIGNED: SHCP rapidly reduced the brain-targeted temperature and significantly alleviated nerve injury. This was evident from the reduced brain injury serum biomarker levels, lower pathologic scores, and more surviving neurons in the hippocampus in the CP-ECPR group. Furthermore, more differentially expressed genes for inflammatory responses were clustered functionally according to Kyoto Encyclopedia of Genes and Genomes pathway analysis. And SHCP reduced microglia activation and the release of proinflammatory mediators.
UNASSIGNED: Our preliminary data indicate that SHCP may serve as a potential therapy to attenuate brain injury via downregulation of neuroinflammation in patients with ECPR.

UNASSIGNED: Many studies have investigated a comparison of the potency and safety of PCV versus VCV modes in spinal surgery in prone position. However, controversy about the maximal benefits of which ventilation modes remains. The main purpose of this meta-analysis was to investigate which one is the optimal ventilation for surgery patients undergoing spine surgery in prone position between the two ventilation modes as PCV and VCV.
UNASSIGNED: We conducted a comprehensive search of PubMed, Embase, Web of Science, the Cochrane Library, and Google Scholar for potentially eligible articles. The continuous outcomes were analyzed using the mean difference and the associated 95% confidence interval. Meta-analysis was performed using Review Manager 5.4 software.
UNASSIGNED: Our meta-analysis included 8 RCTs involving a total of 454 patients between 2012 and 2020. The results demonstrated that IOB, Ppeak and CVP for VCV are significantly superior to PCV in spinal surgery in prone position. And PCV had higher Cdyn and PaO2/FiO2 than VCV. But there was no significant difference between PCV and VCV in terms of POB, Hb, HCT, HR and MAP.
UNASSIGNED: The PCV mode displayed a more satisfying effect than VCV mode. Compared to VCV mode in same preset of tidal volume, the patients with PCV mode in prone position demonstrated less IOB, lower Ppeak and CVP, and higher PaO2/FiO2 in spinal surgery. However, there is no obvious difference between PCV and VCV in terms of hemodynamics variables (HR and MAP).

Osteoarthritis (OA) is no longer regarded as a simple wear-and-tear problem of articular cartilage. Instead, OA is a whole joint disorder involving both cartilaginous and non-cartilaginous tissues such as subchondral bone and synovium. Among them, subchondral bone undergoes constant remodeling in response to the changes of mechanical environment. Current understanding of subchondral bone disturbance in OA is limited to its link with an altered local mechanical loading as a result of ligament or meniscus injury. Very recently, hypertension, the most common vascular morbidity, has been emerged as an independent risk factor of OA. It might suggest a plausible role of systemic hemodynamic mechanical stress in subchondral bone remodeling and the pathogenesis of OA. However, their relationship remains not fully understood. Based on our preliminary clinical observation on the association of hemodynamic parameters with subchondral bone mass and microstructure in late-stage knee OA patients, we formulate a vascular etiology hypothesis of OA from a mechanobiology perspective. Noteworthily, hemodynamic stress associated with subchondral bone mineral density; yet compressive mechanical loading does not. Furthermore, hemodynamic parameters positively correlated with subchondral plate-like trabecular bone volume but negatively associated with rod-like trabecular bone volume. In contrast, compressive mechanical loading tends to increase both plate-like and rod-like trabecular bone volume. Taken together, it warrants further investigations into the distinct role of hemodynamic or compressive stress in shaping subchondral bone in the pathophysiology of OA.
UNASSIGNED: This work provides a new insight, from the angle of biomechanics, into the emerging role of vascular pathologies, such as hypertension, in the pathogenesis of OA. It might open up a new avenue for the development of a mechanism-based discovery of novel diagnostics and therapeutics.