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Objective: Many hospitals were unprepared for the surge of patients associated with the spread of coronavirus disease 2019 (COVID-19) pandemic. We describe the processes to develop and implement a surge plan framework for resource allocation, staffing, and standardized management in response to the COVID-19 pandemic across a large integrated regional healthcare system.Setting: A large academic medical center in the Cleveland metropolitan area, with a network of 10 regional hospitals throughout Northeastern Ohio with a daily capacity of more than 500 intensive care unit (ICU) beds.Results: At the beginning of the pandemic, an equitable delivery of healthcare services across the healthcare system was developed. This distribution of resources was implemented with the potential needs and resources of the individual ICUs in mind, and epidemiologic predictions of virus transmissibility. We describe the processes to develop and implement a surge plan framework for resource allocation, staffing, and standardized management in response to the COVID-19 pandemic across a large integrated regional healthcare system. We also describe an additional level of surge capacity, which is available to well-integrated institutions called “extension of capacity.” This refers to the ability to immediately have access to the beds and resources within a hospital system with minimal administrative burden.Conclusions: Large integrated hospital systems may have an advantage over individual hospitals because they can shift supplies among regional partners, which may lead to faster mobilization of resources, rather than depending on local and national governments. The pandemic response of our healthcare system highlights these benefits.

Background Relative enlargement of the pulmonary artery (PA) on chest CT imaging is associated with respiratory exacerbations in patients with COPD or cystic fibrosis. We sought to determine whether similar findings were present in patients with asthma and whether these findings were explained by differences in ventricular size. Methods We measured the PA and aorta diameters in 233 individuals from the Severe Asthma Research Program III cohort. We also estimated right, left, and total epicardial cardiac ventricular volume indices (eERVVI, eELVVI, and eETVVI, respectively). Associations between the cardiac and PA measures (PA-to-aorta [PA/A] ratio, eERVVI-to-eELVVI [eRV/eLV] ratio, eERVVI, eELVVI, eETVVI) and clinical measures of asthma severity were assessed by Pearson correlation, and associations with asthma severity and exacerbation rate were evaluated by multivariable linear and zero-inflated negative binomial regression. Results Asthma severity was associated with smaller ventricular volumes. For example, those with severe asthma had 36.1 mL/m2 smaller eETVVI than healthy control subjects (P = .003) and 14.1 mL/m2 smaller eETVVI than those with mild/moderate disease (P = .011). Smaller ventricular volumes were also associated with a higher rate of asthma exacerbations, both retrospectively and prospectively. For example, those with an eETVVI less than the median had a 57% higher rate of exacerbations during follow-up than those with eETVVI greater than the median (P = .020). Neither PA/A nor eRV/eLV was associated with asthma severity or exacerbations. Conclusions In patients with asthma, smaller cardiac ventricular size may be associated with more severe disease and a higher rate of asthma exacerbations. Trial Registry ClinicalTrials.gov; No.: NCT01761630; URL: www.clinicaltrials.gov

Introduction As the headspace of the blood, our exhaled breath contains a vast array of substances and molecules that hold great promise for monitoring our health and for the diagnosis and management of various lung and systemic diseases. This includes substances we produce endogenously as part of our normal (or disease-related) metabolism whether this is local in the lung or systemic in origin. Since we are constantly inhaling air from our environment as we breathe in the ambient air, exhaled breath can also reflect our environmental exposure(s). Furthermore, our breath contains volatile compounds produced by our “internal environment”: the bacteria in our gut and mouth. Add to all of those volatile byproducts generated from our diet, medications, drugs, or toxins that we are exposed to and you get a very rich matrix that has great potential to revolutionize and personalize medicine. Recent Advances in Breath Analysis With continued advances in technology, essentially anything in the blood that is potentially volatile or has a volatile metabolite can be measured in exhaled breath. Sensor array (electronic nose) devices can be trained to recognize patterns or “smell-prints” in exhaled breath that allow identification of certain diseases or disorders. However, this technology is not well-suited to identify the specific compounds that contribute to a recognized pattern. The mass spectrometry approach to breath analysis on the other hand, allows the identification of specific individual compounds in the breath, but it is not well-suited to recognize patterns commonly seen in disease. Methods In our group, we have used both approaches to analyze breath and have come to recognize the strengths a weaknesses of both approaches. More recently we started to use an approach that combines the strengths of both methods. By approaching each compound (or peak) on the mass spectrometry output as its own sensor, we are able to recognize patterns or “breath-prints” in mass spectrometry data in a way similar to how the sensor arrays recognize “smell-prints”. Unlike pattern recognition by the sensor array based systems, the major strength of our approach is that we are able to identify the single components that contribute to each pattern we recognize. Results and Conclusions With this best-of-both-worlds approach, we are able to identify unique “breath-prints” in patients with liver disease (fetor hepaticus) as well as heart and kidney disease. We are further able to analyze these patterns to identify single molecules in the breath of these patients and link them to the underlying pathobiology of the disease. References 1. Dweik RA (Guest Editor), Amann A. Exhaled breath analysis: the new frontier in medical testing. Journal of Breath Research (JBR). 2008; 2 (030301):1-3. 2. Hunter GW, Dweik RA. Applied Breath Analysis: An Overview of the Challenges and Opportunities in Developing and Testing Sensor Technology for Human Health Monitoring in Aerospace and Clinical Applications. Journal of Breath Research (JBR). 2008; 2 (037020):1-7. 3. Mashir A and Dweik RA. Exhaled Breath Analysis: the New Interface between Medicine and Engineering. Advanced Powder Technology. 2009; 20: 420–25. 4. Paschke KM, Mashir A, Dweik RA. Clinical applications of breath testing. F1000 medicine reports 2010;2:56. 5. Mondal SP, Dutta PK, Hunter GW, Ward BJ, Laskowski D, Dweik RA. Development of High Sensitivity Potentiometric NOx Sensor and its Application to Breath Analysis. Sensors & Actuators:. 2011;158: 292– 298. 6. Hunter GW, Xu JC, Biaggi-Labiosa A, Laskowski D, Dutta PK, Mondal S, Ward BJ, Makel DB, Liu CC , Chang CW, Dweik RA. Smart Sensors Systems for Human Health Breath Monitoring Applications. J Breath Res. 2011; 5(3). 7. Dweik RA. The great challenge for exhaled breath analysis: embracing complexity, delivering simplicity. J Breath Res. 2011; 5(3):030201. 8. Cikach Jr, FS and Dweik RA. Cardiovascular Biomarkers In Exhaled Breath. Progress in Cardiovascular Disease. 2012; 55:34-43. 9. Braun PX, Gmachl GF, Dweik RA. Bridging the Collaborative Gap: Realizing the Clinical Potential of Breath Analysis for Disease Diagnosis and Monitoring. IEEE sensors. 2012; 12: 3258-3270. 10. Samara MA, Tang WHW, Cikach F, Gul Z, Tranchito L, Paschke KM, Viterna J, Wu Y, Dweik RA. Single Exhaled Breath Metabolomic Analysis Identifies Unique Breathprint in Patients with Acute Decompensated Heart Failure. J Am Coll Cardiol. 2013; 61: 1463-4 11. Hanouneh IA, Zein NN, Cikach F, Dababneh L, Grove D, Alkhouri N, Lopez R, Dweik RA. The breathprints in patients with liver disease identify novel breath biomarkers in alcoholic hepatitis. Clin Gastroenterol Hepatol. 2014 Mar; 12(3):516-23.

Hydrogen sulfide (H2S) plays important roles in metabolism and health. Its enzymatic generation from sulfur-containing amino acids (SAAs) is well characterized. However, the existence of non-enzymatic H2S production from SAAs, the chemical mechanism, and its biological implications remain unclear. Here we present non-enzymatic H2S production in vitro and in blood via a reaction specific for the SAA cysteine serving as substrate and requires coordinated catalysis by Vitamin B6, pyridoxal(phosphate), and iron under physiological conditions. An initial cysteine-aldimine is formed by nucleophilic attack of the cysteine amino group to the pyridoxal(phosphate) aldehyde group. Free or heme-bound iron drives the formation of a cysteine-quinonoid, thiol group elimination, and hydrolysis of the desulfurated aldimine back to pyridoxal(phosphate). The reaction ultimately produces pyruvate, NH3, and H2S. This work highlights enzymatic production is inducible and robust in select tissues, whereas iron-catalyzed production contributes underappreciated basal H2S systemically with pathophysiological implications in hemolytic, iron overload, and hemorrhagic disorders., Jie Yang et al. show the non-enzymatic production of hydrogen sulfide from sulfur-containing amino acids (SAA) in vitro and in blood. They find that the reaction uses SAA cysteine as a substrate, and requires coordinated catalysis by Vitamin B6 and iron, all under physiological conditions.