Mild traumatic brain injury (mTBI) strongly associates with chronic neurodegenerative impairments such as post-traumatic stress disorder (PTSD) and mild cognitive impairment. Early detection of concussive events would significantly enhance the understanding of head injuries and provide better guidance for urgent diagnoses and the best clinical practices for achieving full recovery.

A smart helmet was developed with a single embedded fiber Bragg grating (FBG) sensor for real-time sensing of blunt-force impact events to helmets. The transient signals provide both magnitude and directional information about the impact event, and the data can be used for training machine learning (ML) models.

The FBG-embedded smart helmet prototype successfully achieved real-time sensing of concussive events. Transient data “fingerprints” consisting of both magnitude and direction of impact, were found to correlate with types of blunt-force impactors. Trained ML models were able to accurately predict (R

∼ 0.90) the magnitudes and directions of blunt-force impact events from data not used for model training.

The combination of the smart helmet data with analyses using ML models provides accurate predictions of the types of impactors that caused the events, as well as the magnitudes and the directions of the impact forces, which are unavailable using existing devices.

This work resulted in an ML-assisted, FBG-embedded smart helmet for real-time identification of concussive events using a highly accurate multi-metric strategy. The use of ML-FBG smart helmet systems can serve as an early-stage intervention strategy during and immediately following a concussive event.

This work resulted in an ML-assisted, FBG-embedded smart helmet for real-time identification of concussive events using a highly accurate multi-metric strategy. The use of ML-FBG smart helmet systems can serve as an early-stage intervention strategy during and immediately following a concussive event.Acute heart failure (AHF) is a complex, heterogeneous, clinical syndrome with high morbidity and mortality, incurring significant health care costs. Patients transition from home to the emergency department, the hospital, and home again and require decisions surrounding diagnosis, treatment, and prognosis at each step of the way. The purpose of this review is to examine the epidemiology, etiology, and classifications of AHF and specifically focus on practical information relevant to the clinician. We examine the mechanisms of decompensation relevant to clinical presentations-including precipitating factors, neuroendocrine interactions, and inflammation-along with how consideration of these factors may help select therapies for an individual patient. The prevalence and significance of end-organ manifestations such as renal, gastrointestinal, respiratory, and neurologic manifestations are discussed. We also highlight how the development of renal dysfunction relates to the choice of a variety of diuretics that may be useful in specific circumstances and review guideline-directed medical therapy. We discuss the practical use (and pitfalls) of a variety of evidence-based clinical scoring criteria available to risk stratify patients with AHF. Finally, evidence-based management of AHF is discussed, including both pharmacologic and nonpharmacologic therapies, including the lack of evidence for using old and new vasodilators and the recent evidence regarding initiation of newer therapies in hospital. Overall, we suggest that clinicians consider implementing the newer data in AHF and subject existing practice patterns and treatments to the same rigour as new therapies.The use of sulfur mustard (SM) in global terrorism is still a relevant threat to both civilian population and military personnel. Casualties exposed to SM may present mild, moderate or severe acute ocular lesions followed by a complete ocular resolution, chronic lesions or re-emerged ocular pathologies after a latent period. Current treatment for SM-induced ocular injury is based mainly on the clinical manifestation at the different stages of the injury and includes pharmaceutical and surgical interventions. Histone Demethylase inhibitor These therapeutic measures are beneficial but not sufficient, and the ocular injury remains a continuous challenge for medical professionals. This review focuses on treatment experience carried out in humans and studied in animal models, for both SM-induced ocular acute injury and late pathology. In general, therapeutic measures are based on clinical features of the ocular injury or on the involvement of specific factors during the ocular injury that point out towards potential treatments. Anti-inflammatory treatments and limbal stem cell transplantation techniques were developed based on the clinical manifestation of the ocular injury. Optional therapies for impaired corneal innervation and endothelium are suggested for future research. Additionally, studies on potential treatments with anti-matrix metalloproteinase (MMP), anti-vascular endothelial growth factor (VEGF) and anti-IL-6 agents are discussed. Consequently, future studies may reveal the potential of additional pharmacological and biological treatments or advanced cellular and molecular biology methods to serve as novel therapeutic measures and techniques for this complicated ocular injury.In France, part of the population is overexposed to cadmium by the diet. In our work, we first revised the tolerable daily intake (TDI) of 0.36 μg Cd.kg bw.d.-1 proposed by the European Food Safety Authority (EFSA), derived from effects on kidneys and based on the critical urinary Cd concentration of 1.0 μg Cd.g-1 creatinine for humans. After reviewing the epidemiological data on Cd toxicity published after 2011, bone effects were selected as the critical effects. Body burden data of 0.5 μg.g-1 creatinine was chosen for the critical threshold for human urinary cadmium concentrations. To be used for the derivation of the new oral toxicological reference value, we used a modified physiologically based pharmacokinetic model (PBPK). The reverse calculation on the PBPK model gave a TDI of 0.35 μg Cd.kg bw-1.day-1. This TDI is compatible with a urinary Cd concentrations not exceeding 0.5 μg Cd.g-1 creatinine, in a 60 year-old adult, assuming that ingestion is the only source of exposure to Cd at 60 years. After implementing the PBPK model with French physiological data, Cd biological reference values as a function of age were modelled so as to remain below the revised health-based guidance values.