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BackgroundArtificial intelligence is experiencing rapid growth, with continual innovation and advancements in the health care field. ObjectiveThis study aims to evaluate the application of artificial intelligence technologies across various domains of respiratory care. MethodsWe conducted a narrative review to examine the latest advancements in the use of artificial intelligence in the field of respiratory care. The search was independently conducted by respiratory care experts, each focusing on their respective scope of practice and area of interest. ResultsThis review illuminates the diverse applications of artificial intelligence, highlighting its use in areas associated with respiratory care. Artificial intelligence is harnessed across various areas in this field, including pulmonary diagnostics, respiratory care research, critical care or mechanical ventilation, pulmonary rehabilitation, telehealth, public health or health promotion, sleep clinics, home care, smoking or vaping behavior, and neonates and pediatrics. With its multifaceted utility, artificial intelligence can enhance the field of respiratory care, potentially leading to superior health outcomes for individuals under this extensive umbrella. ConclusionsAs artificial intelligence advances, elevating academic standards in the respiratory care profession becomes imperative, allowing practitioners to contribute to research and understand artificial intelligence’s impact on respiratory care. The permanent integration of artificial intelligence into respiratory care creates the need for respiratory therapists to positively influence its progression. By participating in artificial intelligence development, respiratory therapists can augment their clinical capabilities, knowledge, and patient outcomes.

BackgroundLung cancer is currently the most fatal form of cancer worldwide, ranking as the fourth most prevalent type in Saudi Arabia, particularly among males. This trend is expected to increase with growing population, lifestyle changes, and aging population. Understanding the awareness of the Saudi population regarding the risk factors and symptoms of lung cancer is necessary to attenuate the predicted increase in cases.MethodA cross-sectional, population-based survey was performed using a previously validated questionnaire (Lung CAM). Multiple linear regression analysis was used to assess variables associated with deficiency in knowledge and awareness of risk factors and symptoms of lung cancer.ResultsMajority of the 15,099 respondents were male (65%), aged between 18 and 30 years (53%), 50% of which were educated up to a bachelor’s degree level. Overall awareness of lung cancer signs and symptoms was 53%, with painful cough and coughing up blood being the best-known symptoms. Conversely, persistent shoulder pain (44%) and clubbing fingers (47%) were the least known lung cancer symptoms. Also, 60% of the respondents showed low confidence in identifying the signs and symptoms of lung cancer. The overall awareness of the risk factors for lung cancer development was 74%, with first-hand (74%) and second-hand (68%) smoking being the most known risk factors. However, only ≤ 62% know the other non-smoking risk factors. Awareness of the risk factors and symptoms of lung cancer depended on age, gender, education, marital and employment status (p < 0.001).ConclusionPublic awareness of the risk factors and symptoms of lung cancer in Saudi Arabia is inadequate and heavily dependent on education and socio-economic status. Awareness can be improved through campaigns to raise awareness about other lesser-known lung cancer risk factors and symptoms.

Background Few studies have looked at how SARS-CoV-2 affects pulmonary function, exercise capacity, and health-related quality of life over time. The purpose of this study was to evaluate these characteristics in post COVID-19 subjects 1 year after recovery. Methods The study included two groups. The case group included post COVID-19 subjects who had recovered after a year, and the control group included healthy participants who had never tested positive for COVID-19. Results The study screened 90 participants, 42 of whom met the eligibility criteria. The findings revealed that the majority of post COVID-19 subjects had relatively normal lung function 1-year post-recovery. A significant reduction in DLCO (B/P%) was observed in the case group vs. control. The exercise capacity test revealed a clinically significant difference in distance walked and a significant difference in the dyspnea post-walk test in the case group compared to the control group. The case group’s health-related quality of life domain scores were significantly affected in terms of energy/fatigue, general health, and physical function. Conclusions The post COVID-19 subjects were shown to have well-preserved lung function after 1 year. However, some degree of impairment in diffusion capacity, exercise capacity, and health-related quality of life remained.

Abstract Background Pulmonary hypertension is a common and serious complication of chronic obstructive pulmonary disease (COPD). Studies suggest that cigarette smoke can initiate pulmonary vascular remodelling by stimulating cell proliferation; however, the underlying cause, particularly the role of vasoactive prostanoids, is unclear. We hypothesize that cigarette smoke extract (CSE) can induce imbalanced vasoactive prostanoid release by differentially modulating the expression of respective synthase genes in human pulmonary artery smooth muscle cells (PASMCs) and endothelial cells (PAECs), thereby contributing to cell proliferation. Methods Aqueous CSE was prepared from 3R4F research-grade cigarettes. Human PASMCs and PAECs were treated with or without CSE. Quantitative real-time RT-PCR and Western blotting were used to analyse the mRNA and protein expression of vasoactive prostanoid syhthases. Prostanoid concentration in the medium was measured using ELISA kits. Cell proliferation was assessed using the cell proliferation reagent WST-1. Results We demonstrated that CSE induced the expression of cyclooxygenase-2 (COX-2), the rate-limiting enzyme in prostanoid synthesis, in both cell types. In PASMCs, CSE reduced the downstream prostaglandin (PG) I synthase (PGIS) mRNA and protein expression and PGI2 production, whereas in PAECs, CSE downregulated PGIS mRNA expression, but PGIS protein was undetectable and CSE had no effect on PGI2 production. CSE increased thromboxane (TX) A synthase (TXAS) mRNA expression and TXA2 production, despite undetectable TXAS protein in both cell types. CSE also reduced microsomal PGE synthase-1 (mPGES-1) protein expression and PGE2 production in PASMCs, but increased PGE2 production despite unchanged mPGES-1 protein expression in PAECs. Furthermore, CSE stimulated proliferation of both cell types, which was significantly inhibited by the selective COX-2 inhibitor celecoxib, the PGI2 analogue beraprost and the TXA2 receptor antagonist daltroban. Conclusions These findings provide the first evidence that cigarette smoke can induce imbalanced prostanoid mediator release characterized by the reduced PGI2/TXA2 ratio and contribute to pulmonary vascular remodelling and suggest that TXA2 may represent a novel therapeutic target for pulmonary hypertension in COPD.