Marshall University

This paper aims to present a non-destructive, optimized variational mode decomposition (VMD)-based ground-penetrating radar (GPR) method developed for identifying void defects in reinforced concrete (RC) structures. This study also presents an enhanced framework for defect detection in RC by integrating advanced spectrum analysis with deep learning techniques. A GPR investigation was conducted on an RC bridge deck with known structural defects to generate a representative dataset reflecting both intact and void-defective conditions. In addition to conventional spectral techniques such as fast Fourier transform (FFT), spectrogram, and scalogram, an optimized variational mode decomposition (VMD) method was implemented. The VMD approach decomposes GPR signals into intrinsic mode functions, enabling refined feature extraction beyond traditional spectral methods and allowing clear differentiation between intact and defective signals. The limited availability and quality of GPR small datasets have restricted the application of a functional 1D-CNN which generally requires at least several hundred datasets. To address this challenge, a data augmentation strategy is adopted. FFT-based features were successfully utilized to train a one-dimensional convolutional neural network (1D-CNN) for automated defect identification. The results demonstrate that both the advanced spectrum-based approach and the hybrid framework combining spectral analysis with deep learning significantly improve defect detection performance. Overall, the proposed methodology provides an effective and intelligent solution to support timely, data-driven decision-making for maintenance and safety assurance of bridge infrastructure.

Nicotine damages the cardiovascular system in a variety of ways, from promoting inflammation to causing oxidative stress to prompting unnecessary autophagy. The alteration to the nervous system that yields nicotine dependence further exacerbates the negative impact that nicotine use has on public health. Nicotine use has also been found to cause alterations in exosome content, especially miRNA. Conversely, exosomes have also had promising results as treatments for nicotine-mediated alterations in protein and miRNA levels. However, although nicotine has been shown to both alter exosome content and exacerbate stroke outcomes, the relationship between these two functions is poorly understood. This review examines multiple sources to compare available data. Several factors in nicotine's effect on exosome content were thus found that imply a correlation. Also, exosome contents are not only a viable biomarker for multiple conditions, including ischemic brain damage and tobacco use, but they are also able to influence the cells of test subjects, both as a treatment for ischemic stroke and as a regulator of healthy brain function in stroke-free test subjects. Taken together, previous evidence suggests that nicotine-mediated alterations in neuronal exosome content have an effect on the progression of stroke in nicotine users.

Telomeres safeguard the genome, acting as sentinels of oxidative stress and preventing chromosome ends from eliciting a DNA damage response. PROTECTION OF TELOMERES 1 (POT1) is a highly conserved telomere protein, essential for chromosome integrity and telomeric DNA replication. Arabidopsis thaliana encodes two divergent POT1 paralogs: AtPOT1a stimulates telomerase activity, but AtPOT1b function is unknown. Here we show that AtPOT1b modulates reactive oxygen species (ROS) homeostasis. Oxidative stress induces AtPOT1b expression and telomeric accumulation, while AtPOT1b inactivation elevates ROS, increases telomeric and genome-wide oxidation, and causes stochastic telomere length changes. To address how AtPOT1b controls ROS, we report its localization in nuclei and peroxisomes, and association with catalases and peroxidases that enhance ROS scavenging. Impairing AtPOT1b-CAT2 interaction increases ROS accumulation and telomeric oxidation. Moss or human POT1 rescues ROS overaccumulation in Arabidopsis pot1b mutants, but not telomere deficiency in pot1a pot1b mutants, supporting a conserved role for POT1 in modulating ROS homeostasis and genome stability, distinct from canonical telomeric functions.

Heart failure continues to portend significant morbidity and mortality within the United States. Data regarding the efficacy of mineralocorticoid receptor antagonists (MRAs) in heart failure with preserved ejection fraction (HFpEF) remains unclear. Finerenone, a non-steroidal MRA, has demonstrated reduction in hospitalizations in this population. However, the comparative efficacy of different MRA classes in these patients remains elusive. We conducted a retrospective observational cohort study using the TriNetX research network. We applied 1:1 propensity score matching to compare patients with HFpEF initiated on finerenone versus spironolactone. We examined 1-year risks of heart failure exacerbation, acute kidney injury, electrolyte derangements, and cardiovascular outcomes. We identified 254,417 patients with HFpEF and MRA use. After propensity score matching, each cohort contained 491 patients. Analysis revealed that finerenone use was associated with a significantly lower risk of heart failure exacerbation (HR = 0.63 [95% CI: 0.54, 0.74], p < 0.001), all-cause mortality (HR = 0.38 [95% CI: 0.23, 0.64], p < 0.001), and hypokalemia (HR = 0.58 [95% CI: 0.40, 0.85], p = 0.001). The aforementioned results, along with a reduction in AKI risk, were statistically significant after stratified subgroup analysis by DM and CKD. In this large real-world HFpEF cohort, finerenone use was associated with lower risks of heart failure exacerbation and all-cause mortality compared with spironolactone. These observational findings are hypothesis-generating and warrant confirmation in randomized trials.