The purinergic signaling system is an evolutionarily conserved and critical regulatory circuit that maintains homeostatic balance across various organ systems and cell types by providing compensatory responses to diverse pathologies. Despite cardiovascular diseases taking a leading position in human morbidity and mortality worldwide, pulmonary diseases represent significant health concerns as well. The endothelium of both pulmonary and systemic circulation (bronchial vessels) plays a pivotal role in maintaining lung tissue homeostasis by providing an active barrier and modulating adhesion and infiltration of inflammatory cells. However, investigations into purinergic regulation of lung endothelium have remained limited, despite widespread recognition of the role of extracellular nucleotides and adenosine in hypoxic, inflammatory, and immune responses within the pulmonary microenvironment. In this review, we provide an overview of the basic aspects of purinergic signaling in vascular endothelium and highlight recent studies focusing on pulmonary microvascular endothelial cells and endothelial cells from the pulmonary artery vasa vasorum. Through this compilation of research findings, we aim to shed light on the emerging insights into the purinergic modulation of pulmonary endothelial function and its implications for lung health and disease.

Mitochondria, pivotal organelles governing cellular biosynthesis, energy metabolism, and signal transduction, maintain dynamic equilibrium through processes such as biogenesis, fusion, fission, and mitophagy. Growing evidence implicates mitochondrial dysfunction in a spectrum of respiratory diseases including acute lung injury/acute respiratory distress syndrome, bronchial asthma, pulmonary fibrosis, chronic obstructive pulmonary disease, and lung cancer. Consequently, identifying methods capable of ameliorating damaged mitochondrial function is crucial for the treatment of pulmonary diseases. Extracellular vesicles (EVs), nanosized membrane vesicles released by cells into the extracellular space, facilitate intercellular communication by transferring bioactive substances or signals between cells or organs. Recent studies have identified abundant mitochondrial components within specific subsets of EVs, termed mitochondrial extracellular vesicles (mitoEVs), whose contents and compositions vary with disease progression. Moreover, mitoEVs have demonstrated reparative mitochondrial functions in injured recipient cells. However, a comprehensive understanding of mitoEVs is currently lacking, limiting their clinical translation prospects. This Review explores the biogenesis, classification, functional mitochondrial cargo, and biological effects of mitoEVs, with a focus on their role in pulmonary diseases. Emphasis is placed on their potential as biological markers and innovative therapeutic strategies in pulmonary diseases, offering fresh insights for mechanistic studies and drug development in various pulmonary disorders.

Introduction Heart failure (HF) poses a substantial and escalating medical and economic challenge, marked by significant morbidity and mortality. It stands as the primary cause of hospital admissions among the elderly, contributing significantly to healthcare expenditures in developed nations. Evaluating cardiac and pulmonary function remains challenging, necessitating careful interpretation to mitigate misdiagnosis and inappropriate treatment. Remote monitoring has emerged as a preventive strategy to curb HF-related hospitalizations, emphasizing the importance of early detection of impending acute HF decompensation. Implantable cardiac defibrillators (ICDs) capture various parameters, including heart rhythm, pacing percentages, thoracic impedance, and physical activity. Objective In this study, we aim to investigate the effectiveness of HeartLogic (Boston Scientific, Marlborough, Massachusetts) parameters in accurately distinguishing HF patients from individuals with alternative diagnoses. Methods This cross-sectional study was conducted at Cabell Huntington Hospital, St. Mary\'s Medical Center in Huntington, West Virginia, between 2021 and 2022. The study involved a retrospective chart review of electronic medical records, approved by the institutional review board, encompassing patients aged >18 admitted with Heartlogic-capable devices. The analysis included demographic variables, admission and discharge diagnoses, length of hospital stays, health literacy index, and thoracic impedance. Results Of the initially included 26 patients, 19 met all inclusion criteria. The demographic profile highlighted a predominantly older population with a male preponderance and a notable incidence of congestive heart failure (CHF). Physiological changes, particularly in thoracic impedance and the HeartLogic Index, demonstrated significant alterations. Logistic regression analysis revealed that changes in health literacy index and thoracic impedance significantly contributed to predicting the change in CHF diagnosis. Conclusion This study, conducted in a rural setting, demonstrates the capability of the HeartLogic algorithm in predicting HF events, providing valuable insights into its utility in diverse clinical environments. The findings emphasize the potential of this technology to enhance diagnostic accuracy and improve patient outcomes. Despite inherent limitations, this analysis contributes unique perspectives, particularly in the context of a specific and underexplored rural population in West Virginia.

This work proposes a novel technique called Enhanced JAYA (EJAYA) assisted Q-Learning for the classification of pulmonary diseases, such as pneumonia and tuberculosis (TB) sub-classes using chest x-ray images. The work introduces Fuzzy lattices formation to handle real time (non-linear and non-stationary) data based feature extraction using Schrödinger equation. Features based adaptive classification is made possible through the Q-learning algorithm wherein optimal Q-values selection is done via EJAYA optimization algorithm. Fuzzy lattice is formed using x-ray image pixels and lattice Kinetic Energy (K.E.) is calculated using the Schrödinger equation. Feature vector lattices having highest K.E. have been used as an input features for the classifier. The classifier has been employed for pneumonia classification (normal, mild and severe) and Tuberculosis detection (presence or absence). A total of 3000 images have been used for pneumonia classification yielding an accuracy, sensitivity, specificity, precision and F-scores of 97.90%, 98.43%, 97.25%, 97.78% and 98.10%, respectively. For Tuberculosis 600 samples have been used. The achived accuracy, sensitivity, specificity, precision and F-score are 95.50%, 96.39%, 94.40% 95.52% and 95.95%, respectively. Computational time are 40.96 and 39.98 s for pneumonia and TB classification. Classifier learning rate (training accuracy) for pneumonia classes (normal, mild and severe) are 97.907%, 95.375% and 96.391%, respectively and for tuberculosis (present and absent) are 96.928% and 95.905%, respectively. The results have been compared with contemporary classification techniques which shows superiority of the proposed approach in terms of accuracy and speed of classification. The technique could serve as a fast and accurate tool for automated pneumonia and tuberculosis classification.

Poor oral health negatively impacts overall health, quality of life and well-being. Increasing evidence suggests that provision of basic dental care for elderly Americans would improve outcomes for a variety of systemic diseases and reduce the overall cost of health care. As a result, recent changes have been implemented to include some dental benefits in the Medicare program. This article outlines evidence, rationale and approaches required for inclusion of dental benefits for more Americans through the Medicare program. Improving access to dental services through Medicare to help prevent and manage common chronic diseases is an important step towards integration of dental care with general healthcare to improve the overall health, quality of life, and well-being for many older Americans.

Introduction: Primary ciliary dyskinesia (PCD) is caused by the dysfunction of motile cilia resulting in insufficient mucociliary clearance of the lungs. This study aimed to map novel PCD variants and determine their pathogenicity in PCD patients in Kuwait. Methods: Herein, we present five PCD individuals belonging to a cohort of 105 PCD individuals recruited from different hospitals in Kuwait. Genomic DNAs from the family members were analysed to screen for pathogenic PCD variants. Transmission electron microscopy (TEM) and immunofluorescence (IF) analyses were performed on the nasal biopsies to detect specific structural abnormalities within the ciliated cells. Results: Genetic screening and functional analyses confirmed that the five PCD individuals carried novel pathogenic variants of DNAH5 causing PCD in three Arabic families. Of these, one multiplex family with two affected individuals showed two novel homozygous missense variants in DNAH5 causing PCD with situs inversus; another multiplex family with two affected individuals showed two newly identified compound heterozygous variants in DNAH5 causing PCD with situs solitus. In addition, novel heterozygous variants were identified in a child with PCD and situs solitus from a singleton family with unrelated parents. TEM analysis demonstrated the lack of outer dynein arms (ODAs) in all analysed samples, and IF analysis confirmed the absence of the dynein arm component of DNAH5 from the ciliary axoneme. Conclusion: The newly identified pathogenic variants of DNAH5 are associated with PCD as well as variable pulmonary clinical manifestations in Arabic families.

UNASSIGNED: Previous observational studies have reported a close association between socioeconomic status and pulmonary disease-related morbidity. However, the inherent causal effects remain unclear. Therefore, this bidirectional Mendelian randomization (MR) study aimed to identify the causal relationship between household income and genetic susceptibility to pulmonary diseases.
UNASSIGNED: An MR study was conducted on a large cohort of European individuals, using publicly available genome-wide association study datasets using a random-effects inverse-variance weighting model as the main standard. Simultaneously, MR-Egger regression, weighted median, and maximum likelihood estimation were applied as supplements. Sensitivity analysis, comprising a heterogeneity test and horizontal pleiotropy test, was performed using the Cochran\'s Q, MR-Egger intercept, and MR-PRESSO tests to ensure the reliability of the conclusion.
UNASSIGNED: A higher household income tended to lower the risk of genetic susceptibility to chronic obstructive pulmonary disease (COPD, OR: 0.497, 95% CI = 0.337-0.733, p < 0.001), asthma (OR: 0.687, 95% CI = 0.540-0.876, p = 0.002), and lung cancer (OR: 0.569, 95% CI = 0.433-0.748, p < 0.001), and further indicated potential causality with pneumonia (OR: 0.817; 95% CI = 0.686-0.972, p = 0.022). No association was evident with COVID-19 (OR: 0.934, 95% CI = 0.764-1.142, p = 0.507), tuberculosis (OR: 0.597, 95% CI = 0.512-1.189, p = 0.120), or bronchiectasis (OR: 0.680, 95% CI = 0.311-1.489, p = 0.400). Reverse MR analysis suggested no reverse causal relationship between pulmonary disease and household income status, while sensitivity analysis verified the reliability of the results.
UNASSIGNED: The results revealed that the population with a higher household income tended to have a lower risk of genetic susceptibility to COPD, asthma, and lung cancer.

Dyslipidemia is one of the most common diseases worldwide. As a component of metabolic syndrome, the prevalence and mechanism by which dyslipidemia promotes cardiovascular diseases has been well studied, although the relationship between pulmonary diseases is not well understood. Because the lung is a respiratory organ with a large surface area and is exposed to the environment outside the body, it continuously inhales various substances. As a result, pulmonary diseases have a vast diversity, including chronic inflammatory diseases, allergic diseases, cancers, and infectious diseases. Recently, growing evidence has suggested that dyslipidemia plays a role in the pathogenesis and prognosis of various pulmonary diseases. We herein review the current understanding of the relationship between dyslipidemia and pulmonary diseases, including chronic obstructive pulmonary diseases, asthma, and lung cancer, and infectious pulmonary diseases, including community-acquired pneumonia, tuberculosis, nontuberculous mycobacterial pulmonary disease, and COVID-19. In addition, we focus on recent evidence of the utility of statins, specifically 3-hydroxy-3-methylglutaryl-coA reductase inhibitors, in the prevention and treatment of the various pulmonary diseases described above.

Advanced glycation end products (AGEs) are compounds formed via non-enzymatic reactions between reducing sugars and amino acids or proteins. AGEs can accumulate in various tissues and organs and have been implicated in the development and progression of various diseases, including lung diseases. The receptor of advanced glycation end products (RAGE) is a receptor that can bind to advanced AGEs and induce several cellular processes such as inflammation and oxidative stress. Several studies have shown that both AGEs and RAGE play a role in the pathogenesis of lung diseases, such as chronic obstructive pulmonary disease, asthma, idiopathic pulmonary fibrosis, cystic fibrosis, and acute lung injury. Moreover, the soluble form of the receptor for advanced glycation end products (sRAGE) has demonstrated its ability to function as a decoy receptor, possessing beneficial characteristics such as anti-inflammatory, antioxidant, and anti-fibrotic properties. These qualities make it an encouraging focus for therapeutic intervention in managing pulmonary disorders. This review highlights the current understanding of the roles of AGEs and (s)RAGE in pulmonary diseases and their potential as biomarkers and therapeutic targets for preventing and treating these pathologies.

The brain and lungs, vital organs in the body, play essential roles in maintaining overall well-being and survival. These organs interact through complex and sophisticated bi-directional pathways known as the \'lung-brain axis\', facilitated by their close proximity and neural connections. Numerous studies have underscored the mediation of the lung-brain axis by inflammatory responses and hypoxia-induced damage, which are pivotal to the progression of both pulmonary and neurological diseases. This review aims to delve into how pulmonary diseases, including acute/chronic airway diseases and pulmonary conditions, can instigate neurological disorders such as stroke, Alzheimer\'s disease, and Parkinson\'s disease. Additionally, we highlight the emerging research on the lung microbiome which, drawing parallels between the gut and lungs in terms of microbiome contents, may play a significant role in modulating brain health. Ultimately, this review paves the way for exciting avenues of future research and therapeutics in addressing respiratory and neurological diseases.