Dexmedetomidine Versus Propofol Sedation Improves Sublingual Microcirculation After Cardiac Surgery: A Randomized Controlled Trial

ObjectivesTo compare the effects of dexmedetomidine and propofol on sublingual microcirculation in patients after cardiac surgery.DesignA prospective, randomized, single-blind study.SettingUniversity hospital.ParticipantsAdult patients undergoing elective valve surgery with cardiopulmonary bypass.InterventionsOn arrival in the intensive care unit (ICU), patients were assigned randomly to receive either dexmedetomidine (0.2-1.5 μg/kg/h) or propofol (5-50 μg/kg/min) with open-label titration to a target Richmond Agitation-Sedation Scale of 0 to –3.Measurements and Main ResultsSublingual microcirculation was recorded using sidestream dark-field imaging at ICU admission (baseline [T1]) and 4 hours (T2) and 24 hours after ICU admission (T3). At T2, median changes in perfused small-vessel density and the De Backer score from baseline were significantly greater in the dexmedetomidine group (n = 29) than in the propofol group (n = 32) (1.3 v 0 mm/mm2, p = 0.025; 0.9 v –0.1/mm, p = 0.005, respectively); median changes in small-vessel density and the proportion of perfused small vessels from baseline also tended to be higher in the dexmedetomidine group compared with the propofol group (1.0 v –0.1 mm/mm2, p = 0.050; 2.1% v 0.5%, p = 0.062, respectively). At T3, there still was a trend toward greater improvements in the small vessel density, proportion of perfused small-vessels, perfused small-vessel density, and De Backer score from baseline in the dexmedetomidine group than in the propofol group.ConclusionsThis trial demonstrated that dexmedetomidine sedation may be better able to improve microcirculation in cardiac surgery patients during the early postoperative period compared with propofol

Vessel co-option: a unique vascular-immune niche in liver cancer

Tumor vasculature is pivotal in regulating tumor perfusion, immune cell infiltration, metastasis, and invasion. The vascular status of the tumor is intricately linked to its immune landscape and response to immunotherapy. Vessel co-option means that tumor tissue adeptly exploits pre-existing blood vessels in the para-carcinoma region to foster its growth rather than inducing angiogenesis. It emerges as a significant mechanism contributing to anti-angiogenic therapy resistance. Different from angiogenic tumors, vessel co-option presents a distinctive vascular-immune niche characterized by varying states and distribution of immune cells, including T-cells, tumor-associated macrophages, neutrophils, and hepatic stellate cells. This unique composition contributes to an immunosuppressive tumor microenvironment that is crucial in modulating the response to cancer immunotherapy. In this review, we systematically reviewed the evidence and molecular mechanisms of vessel co-option in liver cancer, while also exploring its implications for anti-angiogenic drug resistance and the immune microenvironment, to provide new ideas and clues for screening patients with liver cancer who are effective in immunotherapy

Phenotypic Plasticity of Staphylococcus aureus in Liquid Medium Containing Vancomycin

Phenotypic plasticity enables individuals to develop different phenotypes in a changing environment and promotes adaptive evolution. Genome-wide association study (GWAS) facilitates the study of the genetic basis of bacterial phenotypes, and provides a new opportunity for bacterial phenotypic plasticity research. To investigate the relationship between growth plasticity and genotype in bacteria, 41 Staphylococcus aureus strains, including 29 vancomycin-intermediate S. aureus (VISA) strains, were inoculated in the absence or presence of vancomycin for 48 h. Growth curves and maximum growth rates revealed that strains with the same minimum inhibitory concentration (MIC) showed different levels of plasticity in response to vancomycin. A bivariate GWAS was performed to map single-nucleotide polymorphisms (SNPs) associated with growth plasticity. In total, 227 SNPs were identified from 14 time points, while 15 high-frequency SNPs were mapped to different annotated genes. The P-values and growth variations between the two cultures suggest that non-coding region (SNP 738836), ebh (SNP 1394043), drug transporter (SNP 264897), and pepV (SNP 1775112) play important roles in the growth plasticity of S. aureus. Our study provides an alternative strategy for dissecting the adaptive growth of S. aureus in vancomycin and highlights the feasibility of bivariate GWAS in bacterial phenotypic plasticity research