ADARRI: a novel method to detect spurious R-peaks in the electrocardiogram for heart rate variability analysis in the intensive care unit

We developed a simple and fully automated method for detecting artifacts in the R-R interval (RRI) time series of the ECG that is tailored to the intensive care unit (ICU) setting. From ECG recordings of 50 adult ICU-subjects we selected 60 epochs with valid R-peak detections and 60 epochs containing artifacts leading to missed or false positive R-peak detections. Next, we calculated the absolute value of the difference between two adjacent RRIs (adRRI), and obtained the empirical probability distributions of adRRI values for valid R-peaks and artifacts. From these, we calculated an optimal threshold for separating adRRI values arising from artifact versus non-artefactual data. We compared the performance of our method with the methods of Berntson and Clifford on the same data. We identified 257,458 R-peak detections, of which 235,644 (91.5%) were true detections and 21,814 (8.5%) arose from artifacts. Our method showed superior performance for detecting artifacts with sensitivity 100%, specificity 99%, precision 99%, positive likelihood ratio of 100 and negative likelihood ratio <0.001 compared to Berntson’s and Clifford’s method with a sensitivity, specificity, precision and positive and negative likelihood ratio of 99%, 78%, 82%, 4.5, 0.013 for Berntson’s method and 55%, 98%, 96%, 27.5, 0.460 for Clifford’s method, respectively. A novel algorithm using a patient-independent threshold derived from the distribution of adRRI values in ICU ECG data identifies artifacts accurately, and outperforms two other methods in common use. Furthermore, the threshold was calculated based on real data from critically ill patients and the algorithm is easy to implement.     

Post-operative Weaning of Opioids After Ambulatory Surgery: the Importance of Physician Stewardship

Purpose of Review

We performed a systematic review to elucidate the current guidelines on weaning patients from opioids in the post-operative ambulatory surgery setting, and how pain management intraoperatively can impact this process.

Design

The review highlights the most up-to-date research from clinical trials, patient reports, and retrospective studies regarding both the current guidelines and weaning of opioid analgesia in ambulatory surgery setting.

Recent Findings

A striking paucity of convincing evidence exists on ambulatory postoperative pain management discontinuation or weaning of pain medications. However, retrospective and patient-reported studies suggest our approach should be similar to acute pain management strategies. The first steps include identifying high-risk patients and devising an appropriate pain plan. This may be accomplished by implementing multimodal analgesia, anticipating opioid needs, and the proper use of regional anesthesia. The increasing roles for Transitional Pain Service (TPS), Perioperative Surgical Home (PSH), and Enhanced Recovery After Surgery (ERAS) may also guide us in this process.

Summary

Patients discharged from same-day surgery may lack the additional infrastructure of a hospital or medical establishment to monitor postoperative recovery. As such, weaning of pain medications in ambulatory surgery settings requires teams that are adept at treating varied patient populations through a tailored, novel means that invoke multimodal analgesia. Given the growth of surgeries moving toward the ambulatory sector, more data and practice guidelines are needed to direct postoperative pain regimen titration for the patients.

     

Gene-Specific Differential DNA Methylation and Chronic Arsenic Exposure in an Epigenome-Wide Association Study of Adults in Bangladesh

Background: Inorganic arsenic is one of the most common naturally occurring contaminants found in the environment. Arsenic is associated with a number of health outcomes, with epigenetic modification suggested as a potential mechanism of toxicity.Objective: Among a sample of 400 adult participants, we evaluated the association between arsenic exposure, as measured by blood and urinary total arsenic concentrations, and epigenome-wide white blood cell DNA methylation.Methods: We used linear regression models to examine the associations between arsenic exposure and methylation at each CpG site, adjusted for sex, age, and batch. Differentially methylated loci were subsequently examined in relation to corresponding gene expression for functional evidence of gene regulation.Results: In adjusted analyses, we observed four differentially methylated CpG sites with urinary total arsenic concentration and three differentially methylated CpG sites with blood arsenic concentration, based on the Bonferroni-corrected significance threshold of p < 1 × 10^–7. Methylation of PLA2G2C (probe cg04605617) was the most significantly associated locus in relation to both urinary (p = 3.40 × 10^–11) and blood arsenic concentrations (p = 1.48 × 10^–11). Three additional novel methylation loci—SQSTM1 (cg01225779), SLC4A4 (cg06121226), and IGH (cg13651690)—were also significantly associated with arsenic exposure. Further, there was evidence of methylation-related gene regulation based on gene expression for a subset of differentially methylated loci.Conclusions: We observed significant associations between arsenic exposure and gene-specific differential white blood cell DNA methylation, suggesting that epigenetic modifications may be an important pathway underlying arsenic toxicity. The specific differentially methylated loci identified may inform potential pathways for future interventions.Citation: Argos M, Chen L, Jasmine F, Tong L, Pierce BL, Roy S, Paul-Brutus R, Gamble MV, Harper KN, Parvez F, Rahman M, Rakibuz-Zaman M, Slavkovich V, Baron JA, Graziano JH, Kibriya MG, Ahsan H. 2015. Gene-specific differential DNA methylation and chronic arsenic exposure in an epigenome-wide association study of adults in Bangladesh. Environ Health Perspect 123:64–71; http://dx.doi.org/10.1289/ehp.1307884     

Differences in COVID-19 Preventive Behavior and Food Insecurity by HIV Status in Nigeria

AIDS and Behavior - The aim of the study was to assess if there were significant differences in the adoption of COVID-19 risk preventive behaviors and experience of food insecurity by people living...     

Impaired survival of peripheral T cells, disrupted NK/NKT cell development, and liver failure in mice lacking Gimap5

The loss of Gimap5 (GTPase of the immune-associated protein 5) gene function is the underlying cause of lymphopenia and autoimmune diabetes in the BioBreeding (BB) rat. The in vivo function of murine gimap5 is largely unknown. We show that selective gene ablation of the mouse gimap5 gene impairs the final intrathymic maturation of CD8 and CD4 T cells and compromises the survival of postthymic CD4 and CD8 cells, replicating findings in the BB rat model. In addition, gimap5 deficiency imposes a block of natural killer (NK)- and NKT-cell differentiation. Development of NK/NKT cells is restored on transfer of gimap5(-/-) bone marrow into a wild-type environment. Mice lacking gimap5 have a median survival of 15 weeks, exhibit chronic hepatic hematopoiesis, and in later stages show pronounced hepatocyte apoptosis, leading to liver failure. This pathology persists in a Rag2-deficient background in the absence of mature B, T, or NK cells and cannot be adoptively transferred by transplanting gimap5(-/-) bone marrow into wild-type recipients. We conclude that mouse gimap5 is necessary for the survival of peripheral T cells, NK/NKT-cell development, and the maintenance of normal liver function. These functions involve cell-intrinsic as well as cell-extrinsic mechanisms.     

Plasma cortisol transport and primate evolution

Primates have diverged into three major evolutionary groups: prosimians, Old World primates, and New World primates; the last group is distinguished by high circulating cortisol concentrations and resistance to the action of glucocorticoids. We have studied a large spectrum of primate species within these groups to characterize the phylogenetic relationships of cortisol-binding globulin (CBG) among them. The CBG in each species was found to be glycosylated, as judged from lectin interactions, and to exhibit an electrophoretic mobility similar to that of human CBG. Although the CBG affinity for cortisol differed among species, the effects of changes in temperature on the CBG affinity were similar. Strikingly, the CBG-binding capacity of plasma in the New World primates was 1/10th to 1/100th those in the Old World primates and prosimians, while the CBG-binding affinity for cortisol was lower. The reduced capacity and affinity of CBG result in a markedly higher fraction of unbound plasma cortisol in the New World primates than in the Old World primates or the prosimian species examined. This evolutionary pattern of CBG may be a compensatory mechanism for the target organ resistance to glucocorticoids that characterizes the New World monkeys.