No abstract

Chronic sympathoexcitation is implicated in ventricular arrhythmogenesis (VAs) following myocardial infarction (MI), but the critical neural pathways involved are not well understood. Cardiac adrenergic function is partly regulated by sympathetic afferent reflexes, transduced by spinal afferent fibers expressing the TRPV1 channel. The role of chronic TRPV1 afferent signaling in VAs is not known. We hypothesized that persistent TRPV1 afferent neurotransmission promotes VAs after MI. Using epicardial Resiniferatoxin (RTX) to deplete cardiac TRPV1‐expressing fibers, we dissected the role of this neural circuit in VAs after chronic MI in a porcine model. We examined the underlying mechanisms using molecular approaches, immunohistochemistry, in vitro and in vivo cardiac electrophysiology, and simultaneous cardio‐neural mapping. Epicardial RTX depleted cardiac TRPV1 afferent fibers and abolished functional responses to TRPV1 agonists. Ventricular tachycardia/fibrillation (VT/VF) was readily inducible in MI subjects by programmed electrical stimulation or cesium chloride administration, however, TRPV1 afferent depletion prevented VT/VF induced by either method. Mechanistically, TRPV1 afferent depletion neither altered cardiomyocyte action potentials and calcium transients; nor the expression of ion channels and calcium handling proteins. However, it attenuated fibrosis and mitigated electrical instability in the scar‐border zone. In vivo recordings of cardiovascular‐related stellate ganglion neurons (SGNs) revealed that MI enhances SGN function and disrupts integrated neural processing. Depleting TRPV1 afferents normalized these processes. Taken together, these data indicate that after MI, TRPV1 afferent‐induced adrenergic dysfunction promotes fibrosis, adverse cardiac remodeling, and worsens border zone electrical heterogeneity, resulting in electrically unstable ventricular myocardium. We propose targeting TRPV1‐expressing afferent to reduce VT/VF following MI. Support or Funding Information NIH/NHLBI DP2 OD024323‐01

Combining diffuse correlation spectroscopy (DCS) and near-infrared spectroscopy (NIRS) permits simultaneous monitoring of multiple cerebral hemodynamic parameters related to cerebral autoregulation; however, interpreting these optical measurements can be confounded by signal contamination from extracerebral tissue.Aim: We aimed to evaluate extracerebral signal contamination in NIRS/DCS data acquired during transient hypotension and assess suitable means of separating scalp and brain signals.Approach: A hybrid time-resolved NIRS/multidistance DCS system was used to simultaneously acquire cerebral oxygenation and blood flow data during transient orthostatic hypotension induced by rapid-onset lower body negative pressure (LBNP) in nine young, healthy adults. Changes in microvascular flow were verified against changes in middle cerebral artery velocity (MCAv) measured by transcranial Doppler ultrasound.Results: LBNP significantly decreased arterial blood pressure (−18% AE 14%), scalp blood flow (>30%), and scalp tissue oxygenation (all p ≤ 0.04 versus baseline). However, implementing depth-sensitive techniques for both DCS and timeresolved NIRS indicated that LBNP did not significantly alter microvascular cerebral blood flow and oxygenation relative to their baseline values (all p ≥ 0.14). In agreement, there was no significant reduction in MCAv (8% AE 16%; p ¼ 0.09). Conclusion:Transient hypotension caused significantly larger blood flow and oxygenation changes in the extracerebral tissue compared to the brain. We demonstrate the importance of accounting for extracerebral signal contamination within optical measures of cerebral hemodynamics during physiological paradigms designed to test cerebral autoregulation.

<p>Purpose- The purpose of this paper is to understand how the Internet of Things can be used to reshape the BFSI sector; to understand the current scenario and find various new avenues that can be developed.</p> <p>Design/methodology/approach- This study has used secondary research and literature reviews to get an understanding of the topic. Apart from that, emphasis was given to getting the primary information from the market. </p> <p>Brief Understanding- The Internet of Things is a network or interconnection of computing devices. For the network to exist, internet infrastructure is required, which is used as the facilitator of information transfer. Data gathering followed by analysis is the basic tenet of the Internet Of Things. Information Technology and semiconductor industries are essentially the brain and heart of the IOT. It is through these semiconductor devices that the information is stored and then through the use of the internet passed to the appropriate destination. IT acts as the brain of the system and is used for the analysis of the huge data collected.</p> <p>IOT can act as a game changer in Banking, Financial Services, and Insurance sector and till now has made its presence in the sector. Customer satisfaction and unique user experience are two of the fundamental objectives of Industry 4.0 and IOT can help in achieving these objectives.</p>

Purpose: Acute care of patients with exacerbation of chronic obstructive pulmonary disease (AECOPD) in the emergency department (ED) is crucial, however not studied extensively in Nepal. The purpose of this study is to identify the opportunities for succinct measures to optimize the AECOPD care in ED with a multifaceted bundle care approach in a resource-limited setting. Methods: We conducted a prospective cross-sectional observational study as an initial baseline stage of the quality improvement project. Demographic data, clinical characteristics, the current diagnosis and treatment performances of AECOPD were recorded. The primary outcome measures were 30-day ED revisit and near-fatal events which were compared with other variables and performances with binary and logistic regression. The multidisciplinary team performed the root cause and Pareto analysis to identify the potential gaps in the AECOPD care. Results: The AECOPD performance measures were suboptimal. Written AECOPD emergency management clinical guidelines and advice regarding pulmonary rehabilitation were absent. Among the 249 AECOPD encounters, bilevel positive-airway pressure ventilation was started in 6.4%. At discharge, 11.8% and 39.7% were given oral steroids and antibiotics respectively; 2.2% were advised vaccination. Near-fatal events and 30-day revisit occurred in 19% and 38.2% of the encounters respectively. Those who required domiciliary oxygen had significantly higher 30-day revisits (OR=2.5; 95% CI=1.43-4.4; P value =0.001) as did those who were previously admitted (OR=1.98; 95% CI 1.11-3.59; P value =0.022). Those who had a 30-day revisit had increased near-fatal events (OR=2.86; 95% CI=1.362-6.18; P value =0.006). The opportunities for improving the ED care were identified and feasible interventions and their indicators are summarized for future implementation. Conclusion: The current COPD performance measures were suboptimal with high 30-day revisit and near-fatal outcomes. We suggest the urgent implementation of the enlisted feasible bundles-care involving multifaceted team and protocol-based management plans for AECOPD in a busy resource-limited ED.