An automatic model of the respiratory control system
Cybernetic feedback connections for automatic model of respiratory control
SEARCH · Engineering Papers
Search indexed NASA NTRS and DOE OSTI research on propulsion, heat transfer, battery materials and energy systems. Follow report and document links to the original sources.
Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.
Cybernetic feedback connections for automatic model of respiratory control
A system is described for monitoring the respiratory process in which the gas flow rate and the frequency of respiration and expiration cycles can be determined on a real time basis. A face mask is provided with one-way inlet and outlet valves where the gas flow is through independent flowmeters and through a mass spectrometer. The opening and closing of a valve operates an electrical switch, and the combination of the two switches produces a low frequency electrical signal of the respiratory inhalation and exhalation cycles. During the time a switch is operated, the corresponsing flowmeter produces electric pulses representative of the flow rate; the electrical pulses being at a higher frequency than that of the breathing cycle and combined with the low frequency signal. The high frequency pulses are supplied to conventional analyzer computer which also receives temperature and pressure inputs and computes mass flow rate and totalized mass flow of gas. From the mass spectrometer, components of the gas are separately computed as to flow rate. The electrical switches cause operation of up-down inputs of a reversible counter. The respective up and down cycles can be individually monitored and combined for various respiratory measurements.
Mathematical models for transient oxygen at input of human body respiratory control center
Personal portable oxygen respiratory support equipment
Hydrogen sulfide (H 2 S) has not historically been detected in spacecraft, but the possible evolution of volatile components from polar ice on the lunar surface is a potential concern for NASA’s planned Artemis missions. Numerous case reports and occupational epidemiological studies document that exposure to H 2 S at high concentrations has effects on the respiratory system, potentially leading to unconsciousness followed by debilitating neurological effects. Studies in rodents demonstrate sensitivity of the respiratory system to lower concentrations of H 2 S. Adverse respiratory effects have also been indicated in workers chronically exposed to H 2 S. The objective of the present publication is to develop Spacecraft Maximum Allowable Concentrations (SMACs) for H 2 S for all current standard durations of exposure for spaceflight (1-hour, 24-hours, 7-days, 30-days, 180-days, and 1000-days). Summary sources and literature review were used to identify relevant studies to inform SMAC development. Space flight mission specific activities and most probable exposure scenarios were used to determine the relevant toxicity endpoints and supporting studies. SMACs were established for hydrogen sulfide of 5 ppm for 1-hour, 1.3 ppm for 24-hours, 1.3 ppm for 7-days, 1.3 ppm for 30-days, and 0.3 ppm for 180-days. Data are not sufficient currently to establish a 1000-day SMAC value. SMACs for H 2 S will support development of handling protocols and proper containment for lunar sample collection.
On-line time sharing data processing and computer analysis techniques, and acceleration effects on cardiovascular and respiratory systems
Sampled-data regulator for investigating both steady-state and transient responses of respiratory system of humans to reduced oxygen at fixed levels of carbon dioxide
The popularity of electronic cigarettes and vaping products has launched the outbreak of a condition affecting the respiratory system of users, known as electronic-cigarette/vaping-associated lung injury (EVALI). The build-up of vitamin E acetate (VEA), a diluent of some illicit vaping oils, in the bronchoalveolar lavage of patients with EVALI provided circumstantial evidence as a target for investigation. In this work, we provide a fundamental characterization of the interaction of VEA with lung cells and pulmonary surfactant (PS) models to explore the mechanisms by which vaping-related lung injuries may be present. We first confirm the localization and uptake of VEA in pulmonary epithelial cells. Further, as PS is vitally responsible for the biophysical functions of the lungs, we explore the effect of added VEA on three increasingly complex models of PS: dipalmitoylphosphatidylcholine (DPPC), a lipid-only synthetic PS, and the biologically derived extract Curosurf. Using high-resolution techniques of small-angle X-ray scattering, small-angle neutron scattering, neutron spin–echo spectroscopy, and neutron reflectometry, we compare the molecular-scale behaviors of these membranes to the bulk viscoelastic properties of surfactant monolayer films as studied by Langmuir monolayer techniques. While VEA does not obviously alter the structure or organization of PS membranes, a consistent softening of membrane systems—regardless of compositional complexity—provides a biophysical explanation for the respiratory distress associated with EVALI and yields a new perspective on the behavior of the PS system.
Inhaled radioactive materials can pose a long-term health concern, as the material can be incorporated into the body’s metabolic pathways and remain in organs and tissues for extended durations. During the retention period, the radioactive material may localize in a source organ and irradiate adjacent target organs and tissues. Distribution of these materials changes over time, requiring biokinetic modeling to evaluate their movement through various tissues and organs. The evolving distribution depends on multiple inputs characterizing the inhaled material, such as particle size and size distribution, particle density, aspect ratio, specific radionuclide, the chemical form, and solubility. In addition, biological parameters such as breathing rate, breathing type (nasal or nasal/oral), respiratory system morphometry, tidal volume, functional residual capacity, and anatomical dead space all influence material transport. These aerosol properties and physiological characteristics of the respiratory tract jointly define a range of initial conditions that influence the time-dependent distribution of radioactive material. To evaluate both uncertainty in the initial conditions of inhalation exposure and the final output (committed effective dose) from biokinetic models, a Python-based software tool, Radiological Exposure Dose Calculator (REDCAL), was developed to propagate uncertainty within the human respiratory tract model. Focusing on deposition fraction uncertainty, the primary objective was to characterize the initial activity distribution across respiratory regions as a function of anticipated particle sizes and distributions. The impact of the deposition fraction uncertainty was propagated to committed effective dose coefficients for selected radionuclides in a companion publication. For each particle size, a lognormal distribution, characterized by its geometric mean as defined within ICRP Publication 66, serves as the basis for introducing uncertainty into the physical processes governing deposition in various lung regions. Finally, this study addresses the deposition process and examines how uncertainty in deposition mechanisms affects activity distribution in the airways, ultimately presenting the expected range and standard deviation of deposited activity as a function of particle size.
All hydrocarbon- (HC-) fueled heat engine exhaust (tailpipe) emissions (<10 to 140 nm) contribute as health hazards, including emissions from transportation vehicles (e.g., aircraft) and other HC-fueled power systems. CO2 emissions are tracked, and when mapped, show outlines of major transportation routes and cities. Particulate pollution affects living tissue and is found to be detrimental to cardiovascular and respiratory systems where ultrafine particulates directly translocate to promote vascular system diseases potentially detectable as organic vapors. This paper discusses aviation emissions, fueling, and certification issues, including heat engine emissions hazards, detection at low levels and tracking of emissions, and alternate energy sources for general aviation.
Determining the fate of inhaled aerosols in the respiratory system is essential in assessing the potential toxicity of inhaled airborne materials, responses to airborne pathogens, or in improving inhaled drug delivery. The availability of high-resolution clinical lung imaging and advances in the reconstruction of lung airways from CT images have led to the development of subject-specific in-silico 3D models of aerosol dosimetry, often referred to as computational fluid-particle-dynamics (CFPD) models. As CFPD models require extensive computing resources, they are typically confined to the upper and large airways. These models can be combined with lower-dimensional models to form multiscale models that predict the transport and deposition of inhaled aerosols in the entire respiratory tract. Understanding where aerosols deposit is only the first of potentially several key events necessary to predict an outcome, being a detrimental health effect or a therapeutic response. To that end, multiscale approaches that combine CFPD with physiologically-based pharmacokinetics (PBPK) models have been developed to evaluate the absorption, distribution, metabolism, and excretion (ADME) of toxic or medicinal chemicals in one or more compartments of the human body. CFPD models can also be combined with host cell dynamics (HCD) models to assess regional immune system responses. Here, this paper reviews the state of the art of these different multiscale approaches and discusses the potential role of personalized or subject-specific modeling in respiratory health.
Pentachlorophenol (PCP) was extensively utilized as an organochlorine pesticide and wood preservative in the United States from the 1930s until the Environmental Protection Agency (EPA) imposed restrictions due to concerns about its toxicity and potential carcinogenic properties. Although it is no longer widely used, PCP remains a concern due to its environmental persistence and potential for long-term health effects. Significant occupational and environmental exposures have likely occurred, with the health and economic costs of PCP exposure potentially being substantial given its known toxicity. Notably, PCP exhibits rapid absorption through both the skin and respiratory system and has been shown to cause hepatotoxicity, developmental toxicity, immunotoxicity, irritation, and carcinogenicity in laboratory animal studies. PCP exposure induces oxidative stress, a key mechanism underlying its inflammatory and toxic effects, which can activate cellular stress responses including upregulation of heat shock protein 70 (Hsp70). Previous studies in lung and liver epithelial cells have shown that Hsp70 and oxidative stress play pivotal roles in triggering autophagy. This study establishes the critical role of the Hsp70-reactive oxygen species (ROS)-autophagy axis in regulating cellular responses to PCP exposure in human alveolar (A549) and liver carcinoma (HepG2) epithelial cells. Our research elucidated the molecular mechanisms underlying PCP's cellular effects, demonstrating that its exposure resulted in increased expression of autophagy-related proteins (Beclin-1, LC3B, ATG12, and ATG16), subunits of NADPH oxidase (NCF-1, NCF-2, NOX2, and Rac), and antioxidant proteins (SOD and GPx) in both lung and liver cell types. Notably, PCP augmented the interaction between Hsp70 and the autophagy regulator Beclin-1. Pretreatment with the ROS inhibitor N-acetylcysteine or Hsp70 knockdown markedly reversed PCP-induced responses. Our in-silico protein–protein docking analysis and molecular dynamics simulation studies revealed enhanced interactions and/or stable confirmations maintained throughout the simulations for TLR4-Hsp70 and Hsp70-Beclin-1 complexes in the presence of PCP. These findings provide a strong foundation for future studies, employing in vivo experimental models and human populations to identify promising targets for PCP-induced toxicity and cellular injury. As a result, these findings may have far-reaching implications for public health and environmental policy, ultimately leading to the identification of biomarkers and the development of more effective interventions for environmentally induced toxicity and diseases.
Inhalation of uranium aerosols produced via human activities such as mining can pose a threat to human respiratory systems. Uranium oxide particulates emit short-range alpha particles that elicit DNA and direct damage, beyond associated physiochemical heavy-metal toxicity, to internal epithelial tissues. The availability of reliable in vitro models to study radiation exposure can greatly enhance our ability to understand and combat the biological impacts of exposure. However, the toxicological effects of alpha emissions and/or the oxidation states of uranium particulates vary across different human lung epithelial cell models and have not been systematically compared. We have endeavored to address this limitation by comparing impacts in three different human lung cell models: primary human bronchial and tracheal epithelial cells, primary human small airway epithelial cells, and human adenocarcinoma alveolar basal epithelial cells. Other studies have mainly investigated the toxicity of depleted uranium. Here, we compared the exposure of uranium oxide particulates (U 3 O 8 and UO 3 ) of different enrichment states on the chosen cell systems. Each cell model was exposed to 0.1, 1, 10, 50, 100, and 500 µg/mL of depleted U 3 O 8 , highly-enriched U 3 O 8 , and natural UO 3 particulates for 24 hours in submerged monolayer cultures. We compared viability and superoxide dismutase activity results across cell lines and uranium enrichment/ oxidative states. The results showed that 1) the oxide state of the particulates affected cell viability, implying that uranium’s different oxidation states contribute to different toxicological responses, and 2) each cell model reacts differently when exposed to uranium oxides, which may provide insights into the mechanistic processes associated with the exposure of radiological particulates on different biological systems. For instance, increased uranium enrichment corresponds to increased toxicity for the primary cells, but not for the immortalized cells. Our study shows that a holistic approach that incorporates similarities between model systems and types of radionuclides is required to truly develop empirical solutions for radiation exposure.
Chronic exposure of rats to gaseous environments of varied composition and pressure, noting exposure capsules, gas flow system, respiratory gas analyzer, etc
Respiratory system and oxygen metabolism regulation in man and animals
Pulmonary capillary gas exchange and venous admixture model and inclusion into respiratory system model, discussing pressure and concentration gradients, pathological effects, etc
In an attempt to develop guidelines for classification by degree of intensity of various kinds of physical work performed by women, the effects of different work loads on women as compared to men were studied under industrial and experimental conditions, including response of the cardiovascular and respiratory systems to specified physical exercises of increasing intensity. Physiological criteria for assessing female labor in terms of intensity are proposed.
In chamber thermodegradation procedures were used to access the lethality to rats of the pyrolysis/combustion products of three foams, an adhesive backed metallic tape and RTV silicone rubber adhesive sealant used in spacecraft construction. The role of carbon monoxide in the overall pyrolysate toxicity was also investigated. Post exposure observation of the rats, histological evaluation of selected organs, carbon monoxide concentration in the chamber atmosphere during exposure and the percent carboxyhemoglobin in the animals expiring in the chamber are discussed. Thermogravimetric analysis and dosage response results are given. The lethal effect of the RTV silicon appears to be due to physical obstruction of the respiratory system by particulate matter from pyrolysis.