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Electrical impedance tomography (EIT) is a non-ionizing real-time bedside imaging modality for pulmonary imaging. Regional images of ventilation and perfusion and EIT-derived clinical measures have the potential to guide clinicians in ventilator settings and treatment decisions for patients with severe lung disease. An important question is how to present such data to clinicians in a concise and useful format. EIT-derived measures of lung function and inhomogeneity have been presented and studied on 2-D data, but not for data collected in a 3-D electrode and current pattern configuration. Here we consider regional ventilation images, EIT-derived time constants, the EIT-derived regional ventilation delay, and EIT-derived ventilation/perfusion ratio indices for a set of patients with acute respiratory distress syndrome receiving mechanical ventilation. The results demonstrate marked differences in these measures between the upper and lower lung lobes in these patients, suggesting there is added clinical value in the 3-D images and EIT-derived measures. [ABSTRACT FROM AUTHOR]

The first confirmed detection of COVID-19 was in December, 2019 with symptomatic fever, cough, chest pain, bilateral pneumonia, and acute respiratory distress syndrome [1]. It was observed among the RT-PCR tested patients in Wuhan, Hubei Province, China. Later due to community transmission worldwide, COVID-19 was designated as a global pandemic by the WHO in February, 2020. This virus builds mutation as it transmits forming variants of concern. The first appeared Alpha variant popped up in the United Kingdom in September 2020. While in India, Delta variant is spreading rapidly for which the developed vaccines could offer protection against serious hospitalization. [2] There has been numerous researches to build a measurable (statistical/ machine learning) model which can possibly predict the course of this pandemic to some extent. Time-Series forecasting is a widely deployed method adopted in studying breeding of pathogens, their resultant infections and possible epidemics. The Schalekamp et al[3], 2020 developed a risk model to forecast deaths using clinical reports. The Malki et al.,2020 [4] research formed a machine learning model using weather elements to evaluate transmission. In other parts of the scientific community, Hao, Xu, Hu, Wang generated a model [5] using Long Short-Term Memory (LSTM), Support Vector Machines (SVM) and Elman Neural Network. Ji et al., 2020[6] presented papers which generated powerful estimation techniques by means of Multivariate COX Regression. Nonetheless, the modified model built using susceptible-exposed-infectious-recovered (SIER) and Runge-Kutta methods is appraised to be remarkable.[7] All of these evaluate the effectiveness of policies and guidelines of a country. The objective is to detect such trends in COVID-19 cases, deaths and vaccinations and further analyze them using publicly available dataset distributed by Our World in Data [8] where each regional data is collected, merged and uploaded in comma-separated value (CSV) file. This dataset covers figures reported by governments and ministries of health from countries around the world from December 13, 2020 to the present day. [ABSTRACT FROM AUTHOR]

Coronavirus disease 2019 is an infection caused by severe acute respiratory syndrome coronavirus-2. The clinical spectrum of this illness ranges from asymptomatic infection to acute respiratory distress syndrome (ARDS), circulatory shock, multiorgan failure, and ultimately death. The aims of this study are to assess of lymphocyte count, to study of acute phase proteins inflammatory biomarker which include ferritin, lactate dehydrogenase, and D-dimer, and to study of renal function markers which include blood urea nitrogen and serum creatinine. The data accumulated throughout this selective case control study which were extended from September 1st, 2020, to December 1st, 2020. A total of 176 human serum samples were collected, and subdivided into four groups moderate, sever, critical and control, each group comprised of 44 individuals. Results: The data was analyzed using the SPSS-20 statistical package that was available (Statistical Packages for Social Sciences-version 20). The results showed a highly significant decrease in the mean of Lymphocyte in Covid-19 patients when compared to the control group, p.value = 0.000. But Lymphocyte showed no significant differences among moderate, severe, and critical groups p.value = 0.580, p.value = 192, p.value = 456 respectively, where all of them had low lymphocyte count. The means of lactate dehydrogenase, ferritin, and D-dimer a showed a highly significant increase in Covid-19 patients when compared to the control group, p.value = 0.000, p.value = 0.000, p.value = 0.000 respectively. The results showed a highly significant increase in BUN in COVID-19 patient when compared with control group, p.value = 0.001, but the creatinine doesn't show any significant differences in COVID-19 patient when compared with control group, p.value = 0.405. Lactate dehydrogenase showed highly significant increase in critical group when compared with moderate group, p.value = 0.004, and showed significant differences in severe group when compared with moderate group, p.value = 0.031, but did not show significant differences between severe and critical groups, p.value = 0.690. Ferritin and D-dimer showed highly significant increase in critical group when compared with moderate group, p.value = 0.009, p.value = 0.000 respectively, and severe group, p.value = 0.002, p.value = 0.000 respectively. While, showed no nay significant differences between severe and moderate groups, p.value = 0.579, p.value = 0.075 respectively. Urea showed highly significant increase in critical group when compared with sever group and moderate group, p.value = 0.000. Creatinine showed significant increase in critical group when compared with sever group and moderate group, p.value = 0.031, p.value = 0.034 respectively. Both urea and creatinine showed no significant differences between severe and moderate groups p.value = 0.747, p.value = 0.958 respectively. Conclusions: In COVID- 19 patients, lymphopenia is a prognostic factor, increase levels of acute phase protein lactate dehydrogenase, D-dimer, and ferritin associated with disease severity, and the blood urea nitrogen and serum creatinine among critical group were associated with disease severity. [ABSTRACT FROM AUTHOR]

The COVID-19 pandemic has been going on for more than a year. COVID-19 causes asymptomatic infection, severe infection, until death. Diagnosis of COVID-19 infection is made by blood tests, antigen swabs, PCR, as well as radiology and CT-scan examinations. Severe COVID-19 infection shows similar symptoms to acute radiation injury. The paper aims to describe the similarity of severe infection COVID-19 and syndrome of acute radiation injury. This paper is a literature review. Literature was searched in the Science Direct and PubMed databases. The keywords were severe COVID-19 infection, acute radiation syndrome, similarity. The similarities between the pathophysiology of severe COVID-19 infection and acute radiation injury are cytokine storms. Symptoms of severe COVID-19 infection are acute respiratory distress syndrome (ARDS), hypoxia, and damage to the cardiovascular system. Researchers are trying to look for symptoms similar to this severe COVID-19 infection so they can find better prevention and therapeutic measures. Study of biological radiation has shown complex organ failure after exposure to high doses of radiation. This condition is called the acute radiation syndrome (ARS). Severe inflammation accompanied by cytokine storms causes severe symptoms of COVID-19 or ARS infection. ARS is diagnosed with a variety of biomarkers of radiation exposure. The similarity of symptoms and pathophysiology may be used to plan better treatment for patients with severe COVID-19 infection in the future. The treatment would be the same. [ABSTRACT FROM AUTHOR]

A new "coronavirus disease-2019 (COVID-19)" has spread quickly as an acute respiratory distress syndrome (ARDS) among individuals worldwide. Moreover, the number of COVID-19 test kits available in hospitals is limited compared to the growing number of cases every day. Therefore, It is necessary to introduce an automatic detection system as a fast alternative diagnostic method to prevent the spread of COVID-19 among humans. The purpose of this study is to propose an automated method using a machine learning method (Convolutional Neural Network (SimpNet model)) for the identification of COVID-19 pneumonia-infected patients using chest computed tomography (CT) images. Threshold and mathematical morphology were used to segment lung tissue as a region of interest (ROI). The Convolutional Neural Network (CNN) based on multi - Image augmentation technique was applied as a deep feature extraction technique and to identify CT samples with Covid 19 and Non-Covid 19. Specificity, Sensitivity, Accuracy, F1- score, Area Under Curve (AUC) were used as criteria to estimate the classification's efficiency. The highest classification accuracy was achieved as 98.67%. [ABSTRACT FROM AUTHOR]

The angiotensin-converting enzyme docks onto the spike glycoprotein on the virion outward. The dimer of the enzyme{ACE}2 is an vital step in the mechanism of life-threatening acute respiratory failure. Human cells are infected with the syndrome coronavirus 2 (SARS-CoV-2).The systemic renin-angiotensin system stifles the expression of ACE2 (RAS) imbalance and advancement of multi-organ harm. In common, the RAS triggers vasoconstriction, hypertension, inflammation, fibrosis, and proliferation through the ACE/Ang II/Ang II type 1 receptor (AT1R) axis and triggers the switch impacts through the ACE2/ Ang (1-7)/Mas axis. The RAS may be triggered by chronic inflammation in hypertension, diabetes, heavy weight, and cancer. The ACE 2 /Ang {1-7} / Mas axis is deactivated by means of SARS-CoV-2-induced ACE2 internalization and shedding. As a result, we believe that two RAS hits are responsible for COVID-19 progression. In summary, the The ACE / Ang II/ AT1R axis is triggered by chronic inflammation, which is the first hit. The second stems from the disruption of the ACE2/Ang (1-7)/Mas axis by COVID-19 infection. Furthermore, the two RAS hits might be the primary cause of elevated numbers of death in COVID-19 patients and comorbidities, and they might be used as a clinical target for COVID-19 therapy. [ABSTRACT FROM AUTHOR]

SARS-Cov-2, a new strain of coronavirus that has never been found in humans before, has become one of the biggest public health issues in the 21st century. By March 2021, more than 100 million people around the world had been diagnosed with the disease. Confirmed cases of COVID-19 have ranged from mild symptoms to severe or even fatal. In the early stage of the disease, fever, fatigue, dry cough is the main clinical manifestations. About half of the patients developed dyspnea more than one week later, and the severe cases rapidly progressed to acute respiratory distress syndrome. Thus, the development of the COVID-19 vaccine is important because of the impact and damage caused by the virus worldwide. This paper will first introduce some information related to the vaccine, such as the safety and efficacy of the vaccine. Then, It will illustrate data on some COVID-19 vaccines that are on the market or still in development with comparison and analysis. [ABSTRACT FROM AUTHOR]

A finite deformation constitutive model for lung parenchyma—including stiffness contributions from dense soft tissue, surface tension, and internal air pressure—is constructed for dynamic loading protocols and eventual injury assessments. The material is approximated as a homogeneous isotropic, nonlinear viscoelastic solid. Internal energy depends on finite strain measures, entropy, and internal state variables. The equilibrium response in the hyperelastic limit follows from a strain energy function depending on strain attributes stemming from a Gram-Schmidt decomposition of deformation. For rapid loading, a composite closed-cell model is invoked to estimate an isentropic bulk modulus of the effective continuum that depends strongly on initial airway pressure and stress-free mass density. Viscoelasticity is addressed by internal state variables in a thermodynamically consistent manner. Stiffness degradation and injury mechanisms can be tracked by additional internal variables. Solutions for planar shock compression are reported, verifying wave speed predictions in the low amplitude limit, exhibiting moderate nonlinearity in shock velocity versus particle velocity profiles, and demonstrating strong influence of initial air pressure on Hugoniot responses. [ABSTRACT FROM AUTHOR]

In 2019, an outbreak of influenza A virus infection was detected in Romania with subsequent cases observed in many counties. According to the Ministry of Health At the national level, the total number of cases of acute respiratory infections (clinical flu, upper airway respiratory infections and pneumonia) was 52,991, 9.1% higher than in the same week of the previous season (48,546). The latest information from the National Center for Communicable Disease Control within the National Institute of Public Health shows that the number of people who died from influenza in the 2018-2019 season reached 192. Many of them have not been vaccinated for influenza. BACKGROUND Due to the immunosuppressive therapy, the transplant patients have an increased risk of serious infections [1]. Respiratory viral infections are common among kidney transplanted patients, and so, adequate diagnosis and management are extremely important. Since the pandemic caused by the new influenza A (H1N1/09) virus resurged in Romania in 2019, report cases showed severe complications that occurred in transplanted patients, including viral pneumonia, secondary bacterial infections and graft dysfunction, with high mortality [2]. Immunogenicity of the influenza vaccine in kidney transplant recipients varies with the vaccine strain, the time after transplantation, the immunosuppressive therapy and the net state of immunosuppression of the recipient [3,4]. Although some vaccines are contraindicated in kidney transplant recipients, the flu shot needs to be given once per year, usually in the fall before flu season begins [5,6]. This is a case report of a renal transplant patient with PCR-confirmed H1N1 respiratory tract infection. The patient showed a mild clinical course despite the graft condition and the stable immunosuppressive therapy during the respiratory infection without more deterioration of the graft function. CASE A 50-year old male with renal transplantation in 2008 from live donor with chronic kidney rejection presented to Emergency room with high fever (38 °C), chills, dry cough,myalgia and severe physical asthenia with exertional dyspnea for two days. At the time of admission, he was undertriple immunosuppression therapy with tacrolimus, mycophenolic acid and prednisone, and was diagnosed with chronic allograft renal dysfunction from 2012. Serum creatinine on admission was 4,15 mg/dL (previous creatinine, one month before, was 2,93 mg/dL) (MDRD eGFR i.e. estimated GFR by utilizing the Modification of Diet in Renal Disease (MDRD) Study equation= 15,6 mL/min/1.73 m²). Additional chest radiography revealed no pulmonary lesions, only increased interstitial and perihilar lung markings, and simultaneous testing of H1N1 in nasopharyngeal swabs was positive. Oseltamivir (30 mg b.i.d.), with temporary stop of mycophenolate led to a complete resolution of symptoms within 5 days. After discontinuation of oseltamivir, PCR testing revealed negative H1N1. Serum creatinine on discharge day was 3,14 mg/dL. CONCLUSION Prompt diagnosis and adequate management of Influenza Virus infection in kidney transplant recipients is life-saving. This case shows that early diagnosis and antiviral therapy associates fast and complete resolution without more damage to an organ with previous graft dysfunction. [ABSTRACT FROM AUTHOR]

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Introduction. High frequency oscillatory ventilation (HFOV) is an alternative mode of mechanical ventilation. HFOV has been shown to provide adequate ventilation and oxygenation in acute respiratory distress syndrome (ARDS) patients and may represent an effective lung-protective ventilation in patients where conventional ventilation is failing. The aim of this study is to evaluate effects of continuous distending pressure (CDP) on variables that contribute to the oxygenation in healthy and ARDS lung model pigs. Methods. In order to simulate a lung disease, lung injury was induced by lavage with normal saline with detergent in three pigs. HFOV ventilation was applied before and after the lung lavage. CDP was stepwise increased by 2 cmH2O, until the maximum CDP (before the lung lavage 32 cmH2O and after the lung lavage 42 cmH2O) and then it was stepwise decreased by 2 cmH2O to the initial value. In this paper we analyzed the following parameters acquired during our experiments: partial pressure of oxygen in arterial blood (PaO2), cardiac output (CO) and mixed venous blood oxygen saturation (SvO2). In order to find how both PaO2 and CO affected SvO2 during the increase of CDP before and after lavage, a nonlinear regression fitting of the response in SvO2 on the predictors (PaO2 and CO) was implemented. Results. Before the lavage, with increasing of CDP, PaO2 remained constant, CO strongly decreased and SvO2 slightly decreased. After the lavage, with increasing of CDP, PaO2 strongly increased, CO decreased and SvO2 increased. So, development of SvO2 followed the PaO2 and CO trends. Changes in PaO2 and CO occur at decisive CDP step and it was much higher after the lung lavage compared to the healthy lungs. The implemented nonlinear model gives a good goodness of fitting in all three pigs. The values of PaO2 and CO estimated coefficients changed at the same decisive step of CDP identified by the trends. Also the algorithm identified a CDP step much higher after the lung lavage. Conclusions. The novelty of this study consists of the implementing of a model that allows to predict how PaO2 and CO affect SvO2. It is possible to identify a certain level of CDP (higher in ARDS model pigs) at which the contribution of PaO2 and CO to SvO2 course changes their weights. Above this value, PaO2 plays a major role in SvO2 developments. This is in concordance with the clinical experience that HFOV is suitable for patient with more severe lung diseases when much higher CDP levels are required to assure an adequate oxygenation. [ABSTRACT FROM AUTHOR]

In healthy humans arterial PO2 is almost constant, showing virtually no oscillations within the respiratory cycle [1]. In Acute Respiratory Distress Syndrome (ARDS) [2], arterial PO2 is thought to oscillate widely due to breath-by-breath variations in pulmonary shunt as a consequence of atelectasis, when alveoli open and collapse during each respiratory cycle. Commercially-available fibre optic oxygen sensors [3] are not suitable for clinical intravascular use, and may not be sufficiently fast to detect these arterial PO2 oscillations at elevated respiratory rate (RR). We have developed an in house, fast (response time ~ 50 ms) fibre optic intravascular sensor [4] (which can be placed into standard arterial cannulae) to detect oxygen oscillations at different simulated RR, and compared the performance of our sensor with a commercially-available sensor (response time ~ 470 ms; Foxy-AL300, Ocean Optics, USA). The sensors were tested in an extracorporeal circuit comprising two standard paediatric oxygenators (Medos-HILITE1000) through which minimally heparinised lambs' blood was circulated at 39° C via two coupled peristaltic pumps [5]. This provided two independent parallel circuits, in which PO2 was 5 or 50 kPa, and PCO2 was 5 kPa; these values were constantly controlled by a precision gas mixing pump, and monitored through samples for gas analysis before each experiment. A computer-controlled electronic switch opened and closed solenoid valves that diverted the circuits exposing the sensor to PO2 values oscillating between 5 and 50 kPa, simulating arterial PO2 oscillations in ARDS, where severe cyclical shunt exists. The simulated RRs studied were 10, 30 and 50 breaths per minute (bpm). Figure 1 shows results from the PO2 oscillations' tests in blood. The in house and the AL300 sensors performed comparatively well at a simulated RR of 10 bpm, where they recorded the whole PO2 oscillation amplitude from 5 to 50 kPa. In contrast, only the in house sensor was able to detect the full dynamic range of the oxygen oscillation at simulated RRs of 30 and 50 bpm, where the AL300 sensor detected only about 70% of the actual PO2 oscillation amplitude. Improvements in fibre optic sensing technology and materials may afford the development of an intravascular sensor for real-time detection of rapid oxygen oscillations, and hence cyclical atelectasis, in ARDS. Further studies are needed to validate the use of this fast intravascular technology in vivo and in clinical trials of whether this information can better inform individualised ventilation management in adult and paediatric intensive care units. [ABSTRACT FROM AUTHOR]

The vascular endothelium interfacing between the blood and vessel wall has the vital functions of regulating tissue fluid balance and supplying the essential nutrients needed for the survival of the organism. It is known that loss of this function results in tissue inflammation, the hallmark of inflammatory diseases such as the Acute Respiratory Distress Syndrome. Dynamic interaction between adherens junctions and cell-matrix attachments plays a primary role in regulating endothelial permeability. However, counter-adhesive forces generated by actinomysin molecular motors activated upon inflammatory mediators such as thrombin, bradykinin, histamine, VEGF, and others upon binding to their receptors, disrupt the organization of adherens junctions and cell-matrix complexes, thereby opening the junctional barrier. An increase in cytosolic Ca2+ has been established as the initial pivotal signal that precedes endothelial cell shape change and opening of adherens junctions resulting in barrier dysfunction. Following cell stimulation with inflammatory mediators, an increase in cytosolic Ca2+ concentration is apparent. There is an initial transient peak as the result of Ca2+ release from endoplasmic reticulum (ER) stores, which is followed by more sustained response secondary to Ca2+ entry via plasmalemma channels. Ca2+ entry refills ER stores and sustains Ca2+ signaling. Proteins of the transient receptor channel (TRPC) family are non-selective cation channels present in endothelial cells that increase intracellular Ca2+, and play an important role in regulating actin-myosin motor activity and endothelial barrier-function. Human pulmonary endothelial cells highly expressed TRPC1 and TRPC6, whereas TRPC3, TRPC4, and TRPC7 are expressed only weakly. TRPC1, TRPC4, and TRPC5 are activated by depletion of ER stores, and are therefore called store-operated channels (SOCs), whereas TRPC3 andTRPC6 are activated independently of store depletion, and are referred to as receptor-operated channels (ROC). SOCs and ROCs provide the primary structures by which Ca2+ enters endothelial cells. Both SOC and ROC have been shown to induced actin-myosin induced endothelial cell contraction and thereby endothelial permeability. In contrast to Ca2+, an increase in the concentration of cAMP is known to stengthen endothelial barrier-function such that it prevents increased permeability in response to known permeability-increasing mediators in endothelial cells and intact microvessels. Evidence indicates that increased levels of cAMP can be endothelial barrier protective through the cAMP-dependent kinase, PKA as well as modulation of adherens junctions and cell-matrix attachments. Cyclic AMP response element binding (CREB) protein is a nuclear-transcriptional factor that regulates several cellular-functions such as inflammation, cell proliferation, differentiation, adaptation and survival. We have shown that CREB plays a pivotal role in regulating endothelial barrier-function by restricting endothelial contraction through regulating the expression of p190RhoGAP. These findings indicate that TRPC and cAMP-mediated signaling mechanisms must intersect with each other to regulate endothelial permeability. My objectives in this presentation will be to discuss the data from genetic, physiological, cellular, and morphological studies whether TRPC- and cAMP-mediated signaling intersects and how this intersection plays a role in regulating endothelial barrier-function. [ABSTRACT FROM AUTHOR]