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Cough at 1000 km/h?

Cough at 1000 km/h?


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How fast does air move in the airways during a cough?

The following passage is from Talley and O'Connor's Clinical examination: a systematic guide to physical diagnosis (emphasis mine):

Cough is a common presenting respiratory symptom. It occurs when deep inspiration is followed by explosive expiration. Flow rates of air in the trachea approach the speed of sound during a forceful cough. Coughing enables the airways to be cleared of secretions and foreign bodies.

The speed of sound claim is unreferenced. I have found mention of coughs approaching the speed of sound in numerous popular sources (e.g. here, here, here (where it says 1000 km/h), and here), and innumerous books (e.g. here, here, here, here, here, and here); none of these references the claim. The same claim is also here. This book has a more exact (unreferenced!) claim:

Velocities as great as 28 000 cm/s (85% of the speed of sound) have been reported, but it is impossible to determine the gas velocity at points of airway constriction, where the greatest shearing forces will be developed. During this phase there is dynamic collapse in the bronchial tree, with large pressure gradients across the collapsed segment.

That speed is just over 1000 km/h. When I have searched for research literature behind this, I've only found much lower velocities at the mouth (rather than at a narrower location like the glottis), e.g. a peak cough velocity of 22m/s, also 11.2m/s, and 28.8m/s. The closest to a reference I found was this book with the following:

A cough comprises:… sudden opening of the glottis, causing air to explode outwards at up to 500 mph or 85% of the speed of sound (Irwin et al, 1998), shearing secretions off the airway walls.

Irwin et al isn't primary literature either, and references Comroe JH, Jr. Special acts involving breathing. In: Physiology of respiration: an introductory text. 2nd ed. Chicago: Year Book Medical Publishers, 1974; 230-31. I don't have access to this book (does anyone here?), but I expect the references only continue from there.


My question is this: how fast is a cough in the airways (I am interested because such an explosive rush of air could explain the substantial damage seen in chronic cough), and does anyone know where the 1000 km/h claim comes from, or can point me to a legitimate reference?


This reference from CHEST lists 21 clinically measured peak flow rates during various modes of coughing. Of these patients, and for unassisted cough, the highest peak flow is about 4 liters/sec. The human trachea ranges from 13 to 27 mm diameter. The relationship between velocity, $V$ and flow $Q$ is

$$ V=frac{Q}{A}$$

Assume the 4 liters/sec = 4000 cm^3/sec and minimum diameter, 13 mm = 1.3 cm, the cross section area being

$$A = pi (D/2)^2 = 1.3 cm^2$$

Plugging in

$$ V=frac{4000}{1.3} = 3077 cm/sec$$

which is a far cry from 28,000 cm/sec, so at this point I'm skeptical.

Things to consider is that the data taken in the paper was from sick humans so perhaps a healthy (and athletic) person may be able to exert much higher flow rates. But then healthy people generally are not stimulated to cough as much as a sick person with an airway compromised by sputum.

Although lower airways do have smaller diameters, the flow measured at the trachea is divided among them, so you wouldn't expect to see peak velocities in the lower airways, but rather the accumulation in the trachea.


Cough in exercise and athletes

In the general population, particularly in individuals with asthma, cough is a common symptom, often reported after exertion, although regular exercise may be associated with a reduction in the prevalence of cough. In athletes, exercise-induced cough is also a particularly frequent symptom. The main etiologies of cough in athletes are somewhat similar to non-athletes, including asthma/airway hyperresponsiveness, upper airways disorders such as allergic or non-allergic rhinitis , and exercise-induced laryngeal obstruction , although these conditions are more frequently observed in athletes. In these last, this symptom can also be related to the high ventilation and heat exchange experienced during exercise, particularly during exposure to cold/dry air or pollutants. However, gastroesophageal reflux, a common cause of cough in the general population, despite being highly prevalent in athletes, has not been reported as a main cause of cough in athletes. Cough may impair quality of life, sleep and exercise performance in the general population and probably also in athletes, although there are few data on this. The causes of cough should be documented through a systematic evaluation, the treatment adapted according to identified or most probable cough etiology and pattern of presentation, while respecting sports anti-doping regulations. More research is needed on exercise-induced persistent cough in the athlete to determine its pathophysiology, optimal management and consequences.


A mechanistic model and therapeutic interventions for COVID-19 involving a RAS-mediated bradykinin storm

Neither the disease mechanism nor treatments for COVID-19 are currently known. Here, we present a novel molecular mechanism for COVID-19 that provides therapeutic intervention points that can be addressed with existing FDA-approved pharmaceuticals. The entry point for the virus is ACE2, which is a component of the counteracting hypotensive axis of RAS. Bradykinin is a potent part of the vasopressor system that induces hypotension and vasodilation and is degraded by ACE and enhanced by the angiotensin1-9 produced by ACE2. Here, we perform a new analysis on gene expression data from cells in bronchoalveolar lavage fluid (BALF) from COVID-19 patients that were used to sequence the virus. Comparison with BALF from controls identifies a critical imbalance in RAS represented by decreased expression of ACE in combination with increases in ACE2, renin, angiotensin, key RAS receptors, kinogen and many kallikrein enzymes that activate it, and both bradykinin receptors. This very atypical pattern of the RAS is predicted to elevate bradykinin levels in multiple tissues and systems that will likely cause increases in vascular dilation, vascular permeability and hypotension. These bradykinin-driven outcomes explain many of the symptoms being observed in COVID-19.

Keywords: COVID-19 bradykinin computational biology human human biology hyaluronic acid medicine pathogenesis renin-angiotensin system systems biology.

Plain Language Summary

In late 2019, a new virus named SARS-CoV-2, which causes a disease in humans called COVID-19, emerged in China and quickly spread around the world. Many individuals infected with the virus develop only mild, symptoms including a cough, high temperature and loss of sense of smell while others may develop no symptoms at all. However, some individuals develop much more severe, life-threatening symptoms affecting the lungs and other parts of the body including the heart and brain. SARS-CoV-2 uses a human enzyme called ACE2 like a ‘Trojan Horse’ to sneak into the cells of its host. ACE2 lowers blood pressure in the human body and works against another enzyme known as ACE (which has the opposite effect). Therefore, the body has to balance the levels of ACE and ACE2 to maintain a normal blood pressure. It remains unclear whether SARS-CoV-2 affects how ACE2 and ACE work. When COVID-19 first emerged, a team of researchers in China studied fluid and cells collected from the lungs of patients to help them identify the SARS-CoV-2 virus. Here, Garvin et al. analyzed the data collected in the previous work to investigate whether changes in how the body regulates blood pressure may contribute to the life-threatening symptoms of COVID-19. The analyses found that SARS-CoV-2 caused the levels of ACE in the lung cells to decrease, while the levels of ACE2 increased. This in turn increased the levels of a molecule known as bradykinin in the cells (referred to as a ‘Bradykinin Storm’). . Previous studies have shown that bradykinin induces pain and causes blood vessels to expand and become leaky which will lead to swelling and inflammation of the surrounding tissue. In addition, the analyses found that production of a substance called hyaluronic acid was increased and the enzymes that could degrade it greatly decreased. Hyaluronic acid can absorb more than 1,000 times its own weight in water to form a hydrogel. The Bradykinin-Storm-induced leakage of fluid into the lungs combined with the excess hyaluronic acid would likely result in a Jello-like substance that is preventing oxygen uptake and carbon dioxide release in the lungs of severely affected COVID-19 patients. Therefore, the findings of Garvin et al. suggest that the Bradykinin Storm may be responsible for the more severe symptoms of COVID-19. Further experiments identified several existing medicinal drugs that have the potential to be re-purposed to treat the Bradykinin Storm. A possible next step would be to carry out clinical trials to assess how effective these drugs are in treating patients with COVID-19. In addition, understanding how SARS-Cov-2 affects the body will help researchers and clinicians identify individuals who are most at risk of developing life-threatening symptoms.


1,000-foot multi-rotor floating Windcatchers to power 80,000 homes each

Norway's Wind Catching Systems (WCS) has made a spectacular debut with a colossal floating wind turbine array it says can generate five times the annual energy of the world's biggest single turbines – while reducing costs enough to be immediately competitive with grid prices.

Standing more than 1,000 ft (324 m) high, these mammoth Windcatcher grids would deploy multiple smaller turbines (no less than 117 in the render images) in a staggered formation atop a floating platform moored to the ocean floor using established practices from the oil and gas industry.

Just one of these arrays, says WCS, could offer double the swept area of the world's biggest conventional wind turbines – the 15 MW Vestas V236 – and its smaller rotors could perform much better in wind speeds over 40 to 43 km/h (25 to 27 mph), when larger turbines tend to start pitching their blades to limit production and protect themselves from damage. The overall effect, says WCS, is a 500 percent boost in annual energy output, with each array making enough power to run 80,000 European homes.

Rather than using massive single components, these Windcatchers are built with smaller pieces that are much easier to work with. Once the floating base is installed, most of the rest can be done on deck, without cranes or specialized vessels, and the grid design allows easy access for ongoing maintenance. WCS says these arrays are ready for a 50-year service life, as opposed to the 30 years of a single large turbine.

The company says it's ready to start delivering offshore wind power on debut at grid parity – meaning at a levelized cost of energy (LCOE, taking capital costs into account) matching or beating the price of grid power. In Norway and the USA, that currently averages out at about US$105 per megawatt-hour. The US Energy Information Administration currently projects the capacity-weighted LCOE of new offshore wind assets coming online in 2026 to average $115.04 per megawatt-hour, with some regions capable of getting that under US$100.

To give you a sense of scale, WCS has pictured the Windcatcher grid alongside the 1,063-ft-high Eiffel Tower, among other things

So this will still be a relatively expensive way to generate electricity, especially compared to land-based wind and solar, but it could still be a cost saver for offshore wind. And WCS says its projections are based on an initial installation size that it believes will become significantly more economical as it scales up.

The company has the backing of investment companies North Energy and Ferd, and has developed the technology in conjunction with offshore wind supplier Aibel and the IFE Institute for Energy Technology.

WCS has not yet released further details about prototypes or first installations, so while it does have the appearance of a legit technology, it seems we'll have to wait some time before it proves its claims.


Minimum information required for a DMET experiment reporting

Aim: To provide pharmacogenomics reporting guidelines, the information and tools required for reporting to public omic databases.

Material & methods: For effective DMET data interpretation, sharing, interoperability, reproducibility and reporting, we propose the Minimum Information required for a DMET Experiment (MIDE) reporting.

Results: MIDE provides reporting guidelines and describes the information required for reporting, data storage and data sharing in the form of XML.

Conclusion: The MIDE guidelines will benefit the scientific community with pharmacogenomics experiments, including reporting pharmacogenomics data from other technology platforms, with the tools that will ease and automate the generation of such reports using the standardized MIDE XML schema, facilitating the sharing, dissemination, reanalysis of datasets through accessible and transparent pharmacogenomics data reporting.

Keywords: DMET bioinformatics minimum information requirement guidelines personalized genomics personalized medicine pharmacogenomics standardization.

Conflict of interest statement

Financial & competing interests disclosure

The CPGR is supported through institutional funding from TIA (Technology Innovation Agency) and the DST (Department of Science and Technology). This work is partially funded by NIH Common Fund Award/NHGRI Grant Number U41HG006941 through H3AbioNet project. M Macek was supported by NF-CZ11-PDP-3-003-2014, 00064203 and COST LD14073. The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript apart from those disclosed.


What is a supervolcano? What is a supereruption?

The term "supervolcano" implies a volcanic center that has had an eruption of magnitude 8 on the Volcano Explosivity Index (VEI), meaning that at one point in time it erupted more than 1,000 cubic kilometers (240 cubic miles) of material. In the early 2000s, the term “supereruption” began being used as a catchy way to describe VEI 8 eruptions. Explosive events of this size erupt so much magma that a circular-shaped collapse feature, called a caldera, forms above the evacuated magma storage region.

The largest (super) eruption at Yellowstone (2.1 million years ago) had a volume of 2,450 cubic kilometers. Like many other caldera-forming volcanoes, most of Yellowstone’s many eruptions have been smaller than VEI 8 supereruptions, so it is confusing to categorize Yellowstone as a “supervolcano.”

Other caldera-forming volcanoes that have produced exceedingly large pyroclastic eruptions in the past 2 million years include Long Valley in eastern California, Valles Caldera in New Mexico, Toba in Indonesia, and Taupo in New Zealand. Taupo erupted 22,600 years ago and is the most recent supereruption on Earth (with a volume of about 1,130 cubic kilometers).

Additional volcanoes capable of producing supereruptions include the large caldera volcanoes of Japan, Indonesia, and South America.

Comparison of volumes of magma erupted from selected volcanoes within the last 2 million years. (Public domain.)


What is a supervolcano? What is a supereruption?

The term "supervolcano" implies a volcanic center that has had an eruption of magnitude 8 on the Volcano Explosivity Index (VEI), meaning that at one point in time it erupted more than 1,000 cubic kilometers (240 cubic miles) of material. In the early 2000s, the term “supereruption” began being used as a catchy way to describe VEI 8 eruptions. Explosive events of this size erupt so much magma that a circular-shaped collapse feature, called a caldera, forms above the evacuated magma storage region.

The largest (super) eruption at Yellowstone (2.1 million years ago) had a volume of 2,450 cubic kilometers. Like many other caldera-forming volcanoes, most of Yellowstone’s many eruptions have been smaller than VEI 8 supereruptions, so it is confusing to categorize Yellowstone as a “supervolcano.”

Other caldera-forming volcanoes that have produced exceedingly large pyroclastic eruptions in the past 2 million years include Long Valley in eastern California, Valles Caldera in New Mexico, Toba in Indonesia, and Taupo in New Zealand. Taupo erupted 22,600 years ago and is the most recent supereruption on Earth (with a volume of about 1,130 cubic kilometers).

Additional volcanoes capable of producing supereruptions include the large caldera volcanoes of Japan, Indonesia, and South America.

Comparison of volumes of magma erupted from selected volcanoes within the last 2 million years. (Public domain.)


Exposure to virus and time of exposure determines infection

Erin gave an insight into how fast a person can get infected from the virus. In his analysis, Erin talks about a formula: Successful Infection = Exposure to Virus x Time. This formula shows that a successful infection depends upon the exposure to a number of virus particles for a particular period of time. Though he admits that this still needs to be determined experimentally, he states that the number can demonstrate how infection can occur.

According to many studies, as few as 1000 SARS-CoV2 infectious viral particles are needed to get someone infected. The professor states that infection may occur through 1000 infectious viral particles that one may receive in one breath or from one eye-rub, or 100 viral particles inhaled with each breath over 10 breaths, or 10 viral particles with 100 breaths. Each of these situations can lead to an infection.


Effects of Trophy Hunting on Lion and Leopard Populations in Tanzania

Department of Ecology, Evolution & Behavior, University of Minnesota, Saint Paul, MN 55108, U.S.A.

Durrell Institute of Conservation and Ecology, University of Kent, Canterbury, Kent CT2 7NR, U.K.

African Wildlife Foundation, Arusha, Tanzania

Tanzania Wildlife Research Institute, Arusha, Tanzania

Department of Ecology, Evolution & Behavior, University of Minnesota, Saint Paul, MN 55108, U.S.A.

Department of Wildlife, Fish & Conservation Biology, University of California, Davis, CA 95616, U.S.A.

Department of Ecology, Evolution & Behavior, University of Minnesota, Saint Paul, MN 55108, U.S.A.

Durrell Institute of Conservation and Ecology, University of Kent, Canterbury, Kent CT2 7NR, U.K.

African Wildlife Foundation, Arusha, Tanzania

Tanzania Wildlife Research Institute, Arusha, Tanzania

Department of Ecology, Evolution & Behavior, University of Minnesota, Saint Paul, MN 55108, U.S.A.

Department of Wildlife, Fish & Conservation Biology, University of California, Davis, CA 95616, U.S.A.

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Abstract

Abstract: Tanzania holds most of the remaining large populations of African lions (Panthera leo) and has extensive areas of leopard habitat (Panthera pardus), and both species are subjected to sizable harvests by sport hunters. As a first step toward establishing sustainable management strategies, we analyzed harvest trends for lions and leopards across Tanzania's 300,000 km 2 of hunting blocks. We summarize lion population trends in protected areas where lion abundance has been directly measured and data on the frequency of lion attacks on humans in high-conflict agricultural areas. We place these findings in context of the rapidly growing human population in rural Tanzania and the concomitant effects of habitat loss, human-wildlife conflict, and cultural practices. Lion harvests declined by 50% across Tanzania between 1996 and 2008, and hunting areas with the highest initial harvests suffered the steepest declines. Although each part of the country is subject to some form of anthropogenic impact from local people, the intensity of trophy hunting was the only significant factor in a statistical analysis of lion harvest trends. Although leopard harvests were more stable, regions outside the Selous Game Reserve with the highest initial leopard harvests again showed the steepest declines. Our quantitative analyses suggest that annual hunting quotas be limited to 0.5 lions and 1.0 leopard/1000 km 2 of hunting area, except hunting blocks in the Selous Game Reserve, where harvests should be limited to 1.0 lion and 3.0 leopards/1000 km 2 .

Abstract

Resumen: Tanzania mantiene la mayoría de las poblaciones remanentes de leones Africanos (Panthera leo) y tiene extensas áreas de hábitat de leopardo (Panthera pardus), y ambas especies son sujetas a cosechas considerables por cazadores deportivos. Como un primer paso hacia el establecimiento de estrategias de manejo sustentable, analizamos las tendencias de cosecha de leones y leopardos en los 300,000 km 2 de bloques de cacería de Tanzania. Sintetizamos las tendencias poblacionales de leones en áreas protegidas donde la abundancia de leones ha sido medida directamente, así como datos sobre la frecuencia de ataques de leones sobre humanos en áreas agrícolas altamente conflictivas. Ubicamos estos resultados en el contexto de la población humana en rápido crecimiento en Tanzania rural y los efectos concomitantes de la pérdida de hábitat, el conflicto humanos-vida silvestre y las prácticas culturales. Las cosechas de leones han declinado 50% en Tanzania entre 1996 y 2008, y las áreas de cacería con las cosechas iniciales más altas sufrieron las declinaciones más pronunciadas. Aunque cada parte del país está sujeto a alguna forma de impacto antropogénico por habitantes locales, la intensidad de la cacería deportiva fue el único factor significativo en el análisis estadístico de las tendencias poblacionales de leones. Aunque las cosechas de leopardos fueron más estables, regiones fuera de la Reserva de Caza Selous con las cosechas iniciales de leopardos más altas también mostraron las declinaciones más pronunciadas. Nuestros análisis cuantitativos sugieren que las cuotas anuales de cacería se limiten a 0.5 leones y 1.0 leopardo/1000 km 2 de área de cacería, excepto los bloques de cacería en la Reserva de Caza Selous, donde las cosechas deben limitarse a 1.0 león y 3.0 leopardos/1000 km 2 .


Acknowledgments

We acknowledge contributions from the following: O. Usmani, (Royal Brompton and Harefield NHS Trust and National Heart and Lung Institute, Imperial College, London, UK), J. Hull (Proctor and Gamble Ltd, Egham, UK), A. Rigby (Centre for Cardiovascular and Metabolic Research, Hull York Medical School, Cottingham, UK), C. Brightling (Respiratory Medicine, Glenfield Hospital, Leicester, UK) and A. Woodcock (Centre for Respiratory and Allergy, University of Manchester, University Hospital of South Manchester, Manchester, UK).


Watch the video: GPS A350-900 pushback, taxi, takeoff, climb, and goes over 1000 kmh (July 2022).


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