An Animation Framework for Improving the Comprehension of TinyOS Programs

To meet the increasing demand for monitoring of the physical world, there has been an increase in the development of wireless sensor network applications. The TinyOS platform has emerged as a de facto standard for developing these applications. The platform offers a number of advantages, with its support for concurrency, power-efficient operation, and resource-constrained hardware chief among them. However, the benefits come at a price. Even without the TinyOS platform, the inherent parallel and distributed nature of these applications makes it difficult for developers to reason about program behavior. Further, the TinyOS programming model adopts asynchronous, split-phase execution semantics. Developers must explicitly manage program control state across event-handlers, components, and devices. This makes the design, debugging, and comprehension of these programs even more difficult. In this work, we describe an animation framework for TinyOS programs, designed to enhance the comprehension of their runtime behavior. The framework enables application developers to specify, in the form of an XML configuration file, the runtime elements to be captured within a given system and the manner in which those elements should be displayed. The resulting visualization presents an animated play-back sequence of the events that occurred during execution. The framework also provides a visual representation that connects causally-related events in a distributed network. We describe the design and implementation of the animation framework and present an analysis of the runtime overhead it introduces

Updates on His bundle pacing: The road more traveled lately

His bundle pacing (HBP) has continued to evolve over the past decade and has started to become a global phenomenon. Evidence is mounting of its clinical benefits as compared to both right ventricular and left ventricular pacing. In this paper, we review recent data in support of His bundle pacing and some of the challenges facing us as we advocate its increasing role in clinical practice

Comparative analysis defines a broader FMRFamide-gated sodium channel family and determinants of neuropeptide sensitivity

FMRFamide (Phe-Met-Arg-Phe-amide, FMRFa) and similar neuropeptides are important physiological modulators in most invertebrates, but the molecular basis of FMRFa activity at its receptors is unknown. We therefore sought to identify the molecular determinants of FMRFa potency against one of its native targets, the excitatory FMRFa-gated sodium channel (FaNaC) from gastropod mollusks. Using molecular phylogenetics and electrophysiological measurement of neuropeptide activity, we identified a broad FaNaC family that includes mollusk and annelid channels gated by FMRFa, FVRIamides, and/or Wamides (or myoinhibitory peptides). A comparative analysis of this broader FaNaC family and other channels from the overarching degenerin (DEG)/epithelial sodium channel (ENaC) superfamily, incorporating mutagenesis and experimental dissection of channel function, identified a pocket of amino acid residues that determines activation of FaNaCs by neuropeptides. Although this pocket has diverged in distantly related DEG/ENaC channels that are activated by other ligands but enhanced by FMRFa, such as mammalian acid-sensing ion channels, we show that it nonetheless contains residues that determine enhancement of those channels by similar peptides. This study thus identifies amino acid residues that determine FMRFa neuropeptide activity at FaNaC receptor channels and illuminates the evolution of ligand recognition in one branch of the DEG/ENaC superfamily of ion channels.publishedVersio

Permanent His-bundle Pacing in Pediatrics and Congenital Heart Disease

Permanent His-bundle pacing has been gaining popularity in the adult population requiring cardiac resynchronization therapy. Initial procedural challenges are being overcome, and this method of pacing has been shown to improve left ventricular function and heart failure symptoms secondary to ventricular dyssynchrony. Though the etiologies of ventricular dyssynchrony may differ in children and those with congenital heart disease than in adults with structurally normal hearts, His-bundle pacing may also be a preferred option in these groups to restore more physiologic electric conduction and improve ventricular function. We present a review of the current literature and suggested directions involving deploying permanent His-bundle pacing in the pediatric and congenital heart disease population

Thyroid Hormone Levels in Cirrhosis Patients and their Association with Liver Disease Severity

Cirrhosis of the liver, which has a number of etiologies and progresses in a devastating manner, causes significant liver dysfunction. The intricate connection between liver illness and thyroid function has come to light recently in study. The purpose of this study was to determine whether the severity of liver disease in cirrhosis patients was correlated with thyroid hormone levels (free triiodothyronine [FT3], free thyroxine [FT4], and thyroid-stimulating hormone [TSH]). Methods: Over the course of 18 months (from February 2021 to August 2022) 97 cirrhosis patients were prospectively enrolled. The severity of the liver disease (as measured by the Child-Pugh and MELD scores) and the etiology of cirrhosis were also recorded. Standard assays were used to assess the serum concentrations of FT3, FT4, and TSH. Correlations, multivariate regression, and stratification by Child-Pugh class were all included in the statistical study. Results: Significant negative relationships between FT3 and FT4 levels and Child-Pugh scores showed that levels decreased as liver disease severity increased (p 0.001). Child-Pugh scores and TSH levels showed a slight positive connection (p = 0.002). The Child-Pugh score's independent predictive significance for the FT3 and FT4 levels was validated by multivariate regression. Further stratification by Child-Pugh class indicated progressively altered thyroid hormones with deteriorating liver disease. Conclusion: This study clearly links thyroid hormone levels to the severity of liver disease in individuals with cirrhosis. In cirrhosis, particularly in advanced stages, monitoring thyroid function is essential for complete patient care and may help to achieve better clinical results. To clarify underlying causes and treatment implications, more study is required

Permanent His Bundle Pacing: Electrophysiological and Echocardiographic Observations From Long-Term Follow-Up

Background Permanent His bundle pacing (HBP) is a physiological alternative to right ventricular pacing. It is not known whether HBP can cause His-Purkinje conduction (HPC) disease. The aim of our study is to assess His bundle capture and its effect on left ventricular (LV) function in long-term follow-up and to determine HPC at the time of pulse generator change (GC) in patients with chronic HBP. Methods HB electrograms were recorded from the pacing lead at implant and GC. HBP QRS duration (QRSd), His-ventricular (HV) intervals, and HB pacing thresholds at GC were compared with implant measurements. HPC was assessed by pacing at cycle lengths of 700 ms, 600 ms, and 500 ms at GC. LV internal diameters, ejection fraction (EF), and valve dysfunction at baseline were compared with echocardiography during follow-up. Results GC was performed in 20 patients (men 13; age 74 ± 14 years) with HBP at 70 ± 24 months postimplant. HV intervals remained unchanged from initial implant (44 ± 4 ms vs 45 ± 4 ms). During HBP at 700 ms, 600 ms, and 500 ms (n = 17), consistent 1:1 HPC was present. HBP QRSd remained unchanged during follow-up (117 ± 20 ms vs 118 ± 23 ms). HBP threshold at implant and GC was 1.9 ± 1.1 V and 2.5 ± 1.2 V @ 0.5 ms. Despite high pacing burden (77 ± 13%), there was no significant change in LVEF (50 ± 14% at implant) during follow-up (55 ± 6%, P = 0.06). Conclusions HBP does not appear to cause new HPC abnormalities and is associated with stable HBP QRSd during long-term follow-up. Despite high pacing burden, HBP did not result in deterioration of left ventricular systolic function or cause new valve dysfunction