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Bronchial hyperresponsiveness (BHR), a hallmark of bronchial asthma, is typically diagnosed through a methacholine inhalation test followed by spirometry, known as the methacholine challenge test (MCT). While spirometry relies on proper patients' cooperation and precise execution of forced breathing maneuvers, we conducted a comparative analysis with the portable nanomaterial-based sensing device, SenseGuard™, to non-intrusively assess tidal breathing parameters. In this prospective study, 37 adult participants with suspected asthma underwent sequential spirometry and SenseGuard™ measurements after inhaling increasing methacholine doses. Among the 37 participants, 18 were MCT responders, 17 were non-responders and 2 were excluded due to uninterpretable data. The MCT responders exhibited a significant lung function difference when comparing the change from baseline to maximum response. This was evident through a notable decrease in forced expiratory volume in 1 ​s (FEV 1) levels in spirometry, as well as in prominent changes in tidal breathing parameters as assessed by SenseGuard™, including the expiratory pause time (T rest) to total breath time (T tot) ratio, and the expiratory time (T ex) to T tot ratio. Notably, the ratios T rest /T tot (∗p ​= ​0.02), T ex /T tot (∗p ​= ​0.002), and inspiratory time (T in) to T ex (∗p ​= ​0.04) identified MCT responders distinctly, corresponding to spirometry (∗p ​< ​0.0001). This study demonstrates that tidal breathing assessment using SenseGuard™ device reliably detects clinically relevant changes of respiratory parameter during the MCT. It effectively distinguishes between responders and non-responders, with strong agreement to conventional spirometry-measured FEV 1. This technology holds promise for monitoring clinical respiratory changes in bronchial asthma patients pending further studies. [ABSTRACT FROM AUTHOR]

Respiration is an essential and primary mechanism for speech production. We first inhale and then produce speech while exhaling. When we run out of breath, we stop speaking and inhale. Though this process is involuntary, speech production involves a systematic outflow of air during exhalation characterized by linguistic content and prosodic factors of the utterance. Thus speech and respiration are closely related, and modeling this relationship makes sensing respiratory dynamics directly from the speech plausible, however is not well explored. In this article, we conduct a comprehensive study to explore techniques for sensing breathing signal and breathing parameters from speech using deep learning architectures and address the challenges involved in establishing the practical purpose of this technology. Estimating the breathing pattern from the speech would give us information about the respiratory parameters, thus enabling us to understand the respiratory health using one's speech. • Speech and Respiration relationship. • Estimating breathing signal and breathing parameters from speech is plausible. • Speech could be used as a pathological indicator for respiratory conditions. [ABSTRACT FROM AUTHOR]

Background Chronic obstructive pulmonary disease (COPD) affects respiratory functioning and psychosocial factors. However, little is known about perceived ability of people with COPD to engage in a regular exercise program. This study assessed respiratory parameters, exercise capacity, psychosocial factors and their relations in people with COPD. Methods This cross-sectional study involved patients with COPD recruited from a Nigerian university teaching hospital. Respiratory parameters including forced expiratory volume in 1 sec (FEV 1 ) and forced vital capacity (FVC) were assessed by using a spirometer and FEV 1 /FVC ratio was calculated. Participants were sitting upright in a comfortable chair and wearing a nose clip for measurements. The procedure was performed in accordance with the American Thoracic Society criteria. Exercise capacity was assessed by the 6-min walk test (6MWT). Gait speed was assessed by the distance covered in 6 min. Perceived exercise self-efficacy (PESE) and rating of perceived exertion (RPE) were assessed by exercise self-efficacy and Borg scales, respectively. Data were analysed using descriptive and inferential statistics. Alpha level was set at P < 0.05. Results The mean age of the 125 participants was 62.0 ± 7.1 years (60% male). The mean values for FEV 1 , FVC and FEV 1 /FVC were 1.8 ± 0.6 L, 2.4 ± 0.5 L and 58.0 ± 8.8%, respectively, and the mean 6MWT and PESE values were 291.1 ± 41.6 m 63.1 ± 11.2%. Exercise capacity was correlated with mean values for the respiratory parameters FEV 1 ( r = 0.29; P = 0.035), FVC ( r = 0.32; P = 0.045) and FEV 1 /FVC ratio ( r = 0.37; P = 0.007), and both exercise capacity and PESE were correlated with gait speed ( r = 0.96, P = 0.001 and r = 0.57; P = 0.042) and RPE ( r = 0.42, P = 0.050 and r = −0.44; P = 0.032), but PESE was not correlated with respiratory parameter values ( P > 0.05). Conclusion Participants with COPD demonstrated reduced respiratory parameter values and low exercise capacity but moderate PESE. We found significant correlations between exercise capacity and respiratory parameter values, but PESE was correlated with only gait speed and RPE. The study has implications for respiratory health promotion and exercise adherence. [ABSTRACT FROM AUTHOR]

The development of graphical user interfaces (GUIs) has been an emergent demand in the area of healthcare technologies. Specifically for respiratory healthcare there is a lack of tools to produce a complete multimedia database, where respiratory sounds and other clinical data are available in a single repository. This is essential for a complete patient's assessment and management in research/clinical settings. Therefore, this study aimed to develop a usable interface to collect and organise respiratory-related data in a single multimedia database. A GUI, named LungSounds@UA, composed by a multilayer of windows, was developed. The usability of the user-centred interface was as-sessed in a pilot study and in an evaluation session. The users testified the utility of the application and its great potential for research/clinical settings. However, some drawbacks were identified, such as a certain difficulty to intuitively navigate in the great amount of the available information, which will inform future developments. [ABSTRACT FROM AUTHOR]

We recently demonstrated that peripheral and central administration of nesfatin-1 in fasting and satiety states generate hyperventilation activity by increasing tidal volume (TV), respiratory rate (RR), and respiratory minute ventilation (RVM). The present study aimed to investigate the mediation of central cholinergic receptors effective in respiratory control in the hyperventilation activity of nesfatin-1. Besides this, we intended to determine possible changes in blood gases due to hyperventilation activity caused by nesfatin-1 and investigate the mediation of central cholinergic receptors in these changes. Intracerebroventricular (ICV) administration of nesfatin-1 revealed a hyperventilation response with an increase in TV, RR, RMV, and pO 2 and a decrease in pCO 2 in saturated Sprague Dawley rats. ICV pretreatment with the muscarinic receptor antagonist atropine partially blocked the RR, RMV, pO 2 , and pCO 2 responses produced by nesfatin-1 while completely blocking the TV response. However, central pretreatment with nicotinic receptor antagonist mecamylamine blocked the respiratory and blood gas responses induced by nesfatin-1. The study's conclusion demonstrated that nesfatin-1 had active hyperventilation effects resulting in an increase in pO 2 and a decrease in pCO 2. The critical finding of the study was that activation of central cholinergic receptors was involved in nesfatin-1-evoked hyperventilation and blood gas responses. [ABSTRACT FROM AUTHOR]

• ICV injected AA produces pressor and bradycardic cardiovascular effects. • ICV administrated AA causes hyperventilation response. • Centrally injected AA increases p O 2 and decreases p CO 2. • Central lipoxygenase pathway mediate AA-evoked cardiorespiratory and blood gases responses. We previously reported that intracerebroventricularly (ICV) injected arachidonic acid (AA) could produce pressor and bradycardic responses on the cardiovascular system and hyperventilation effect on the respiratory system by activating cyclooxygenase (COX). We also demonstrated that centrally injected AA-induced cardiovascular and respiratory responses were mediated by COX-metabolites, such as thromboxane A 2 (TXA 2), prostaglandin (PG) D, PGE, and PGF 2α. Brain tissue is also able to express the lipoxygenase (LOX) enzyme and LOX-induced AA-metabolites. The current study was designed to investigate the possible mediation of the central LOX pathway in AA-induced cardiorespiratory effects in anesthetized rats. Central pretreatment with different doses of a non-selective LOX inhibitor, nordihydroguaiaretic acid (NDGA) (500 and 1000 μg; ICV) partially blocked the AA (0.5 μmol; ICV)-evoked pressor and bradycardic cardiovascular responses in male anesthetized Sprague Dawley rats. Pretreatment with different doses of NDGA (500 and 1000 μg; ICV) also reduced AA-induced hyperventilation responses, with an increase in tidal volume, respiratory rate and minute ventilation, in the rats. Moreover, AA-induced increasing p O 2 and decreasing p CO 2 responses were diminished by central NDGA pretreatment. In summary, our findings show that the central LOX pathway might mediate, at least in part, centrally administered AA-evoked cardiorespiratory and blood gases responses. [ABSTRACT FROM AUTHOR]