Background: Finger cuff technologies allow continuous noninvasive arterial blood pressure (AP) and cardiac output/index (CO/CI) monitoring. Methods: We performed a meta-analysis of studies comparing finger cuff-derived AP and CO/CI measurements with invasive measurements in surgical or critically ill patients. We calculated overall random effects model-derived pooled estimates of the mean of the differences and of the percentage error (PE; CO/CI studies) with 95%-confidence intervals (95%-CI), pooled 95%-limits of agreement (95%-LOA), Cochran's Q and I 2 (for heterogeneity). Results: The pooled mean of the differences (95%-CI) was 4.2 (2.8 to 5.62) mm Hg with pooled 95%-LOA of e14.0 to 22.5 mm Hg for mean AP (Q¼230.4 [P<0.001], I 2 ¼91%). For mean AP, the mean of the differences between finger cuff technologies and the reference method was 5±8 mm Hg in 9/27 data sets (33%). The pooled mean of the differences (95%-CI) was e0.13 (e0.43 to 0.18) L min À1 with pooled 95%-LOA of e2.56 to 2.23 L min À1 for CO (Q¼66.7 [P<0.001], I 2 ¼90%) and 0.07 (0.01 to 0.13) L min À1 m À2 with pooled 95%-LOA of e1.20 to 1.15 L min À1 m À2 for CI (Q¼5.8 [P¼0.326], I 2 ¼0%). The overall random effects model-derived pooled estimate of the PE (95%-CI) was 43 (37 to 49)% (Q¼48.6 [P<0.001], I 2 ¼63%). In 4/19 data sets (21%) the PE was 30%, and in 10/19 data sets (53%) it was 45%. Conclusions: Study heterogeneity was high. Several studies showed interchangeability between AP and CO/CI measurements using finger cuff technologies and reference methods. However, the pooled results of this meta-analysis indicate that AP and CO/CI measurements using finger cuff technologies and reference methods are not interchangeable in surgical or critically ill patients. Clinical trial number: PROSPERO registration number: CRD42019119266.

Intestinal ischemia/reperfusion (I/R) injury causes inflammation and tissue damage and is associated with high morbidity and mortality. Uncontrolled activation of the innate immune system through toll-like receptors (Tlr) plays a key role in I/R-mediated tissue damage but the underlying mechanisms have not been fully resolved. Here, we identify post-transcriptional upregulation of the essential Tlr signalling molecule interleukin 1 receptor-associated kinase (Irak) 1 as the causative mechanism for post-ischemic immune hyper-responsiveness of intestinal epithelial cells. Increased Irak1 protein levels enhanced epithelial ligand responsiveness, chemokine secretion, apoptosis and mucosal barrier disruption in an experimental intestinal I/R model using wild-type, Irak1−/− and Tlr4−/− mice and ischemic human intestinal tissue. Irak1 accumulation under hypoxic conditions was associated with reduced K48 ubiquitination and enhanced Senp1-mediated deSUMOylation of Irak1. Importantly, administration of microRNA (miR)-146a or induction of miR-146a by the phytochemical diindolylmethane controlled Irak1 upregulation and prevented immune hyper-responsiveness in mouse and human tissue. These findings indicate that Irak1 accumulation triggers I/R-induced epithelial immune hyper-responsiveness and suggest that the induction of miR-146a offers a promising strategy to prevent I/R tissue injury.

Objective. Patients with autoimmune diseases such as systemic lupus erythematosus (SLE) and granulomatosis with polyangiitis (Wegener's) (GPA) have a 3-20-fold increased risk of herpes zoster compared to the general population. The aim of this study was to evaluate if susceptibility is due to decreased levels of cellular and/or humoral immunity to the varicellazoster virus (VZV).Methods. A cross-sectional study of VZV-specific immunity was performed in 38 SLE patients, 33 GPA patients, and 51 healthy controls. Levels of IgG and IgM antibodies to VZV were measured using an in-house glycoprotein enzyme-linked immunosorbent assay (ELISA). Cellular responses to VZV were determined by interferon-␥ (IFN␥) enzyme-linked immunospot (ELISpot) assay and carboxyfluorescein succinimidyl ester (CFSE) dye dilution proliferation assay.Results. Levels of IgG antibodies to VZV were increased in SLE patients as compared to healthy controls, but levels of IgM antibodies to VZV were not. Antibody levels in GPA patients did not differ significantly from levels in healthy controls. In response to stimulation with VZV, decreased numbers of IFN␥ spot-forming cells were found among SLE patients (although not GPA patients) as compared to healthy controls. Proliferation of CD4؉ T cells in response to stimulation with VZV was decreased in SLE patients but not GPA patients.Conclusion. SLE patients have increased levels of IgG antibodies against VZV, while cellular immunity is decreased. In GPA patients, antibody levels as well as cellular responses to VZV were comparable to those in healthy controls. These data suggest that increased prevalence of herpes zoster in SLE patients is due to a poor cellular response. Vaccination strategies should aim to boost cellular immunity against VZV.Herpes zoster (shingles) is caused by reactivation of the varicella-zoster virus (VZV) (1,2). It presents as an acute neurocutaneous disease characterized by severe pain and rash in a dermatomal distribution (3). Postherpetic neuralgia, defined as pain lasting Ͼ90 days after onset of rash, is the most common complication of herpes zoster and is estimated to occur in 8-27% of patients (4-7). Herpes zoster and postherpetic neuralgia can have a major impact on quality of life and productivity of a patient (4,5). In particular, elderly individuals and individuals with compromised immune systems are at increased risk of developing herpes zoster and, accordingly, postherpetic neuralgia (3,6).Systemic lupus erythematosus (SLE) and granulomatosis with polyangiitis (Wegener's) (GPA) both are autoimmune inflammatory rheumatic diseases. Patients with an autoimmune inflammatory rheumatic disease are at increased risk of infections including herpes zoster, as a result of the immunosuppressive effect of the disease and/or the use of immunomodulatory medication (8-10). Herpes zoster is found in 15-91 cases per 1,000 patient-years among SLE patients and 45 cases per 1,000 patient-years among GPA patients (3,11,12). Since the incidence of herpes zoster in developed countries is...