Numerical Algorithms For Analysis Of Dynamics Of Ideal Fluid With Free/moving Boundaries

This thesis proposes and examines various algorithms for analysis of steady ideal fluid capillary flows with free/moving boundary.;For this class of problems, the leading parameter is the capillary number C which for an established flow and fixed geometry of the solution domain is proportional to the ratio of a velocity scale and surface tension. When C {dollar}\ll{dollar} 1 the problem can be simplified and is solved using Small Deformation Theory (SDT). Conditions for validity of SDT are identified.;When C = 0(1) one has to seek a simultaneous solution for two dependent variables, i.e. a flow field and a free surface shape. Depending on the order of linearization of the governing equations one arrives at the Picard Algorithm (linearization of the first order) and the 1-Step Algorithm (of the second order). The latter one provides significantly faster convergence.;All algorithms are based on a finite-difference approximation and the Alternate Direction Implicite (ADI) scheme has been chosen as a method of solution. A thorough study of an algebraic stability of equations of the flow field and the free surface, has been carried out. This is supplemented by an analytical and numerical analysis of existence and uniqueness of the solutions to the free surface equation. The Wachspress optimization of relaxation parameters has been used in order to accelerate convergence of the ADI.;Finite differences discretization implemented in the thesis is based on the Hermitian equations, which generated compact difference schemes of the second and higher order accuracy. In the thesis one can find a rigorous study of the interrelationship between the order of differencing scheme and the rate of convergence of the computed results with grid refining. This rate, called \u27grid-convergence order\u27 has been used as the criterion for identification of the minimum dimensionality of the computational grid. It was found that higher order methods require much finer grids than second order methods, to provide desired grid-convergence order.;For higher order method, the new fourth order compact difference estimate (independent of coordinate direction) of a mixed derivative was found. Its application significantly improved the grid-convergence order.;The discussion of the algorithms is supplemented by a physical interpretation of the results obtained for a number of particular cases

Antileukotriene drugs in the treatment of obstructive lung diseases and rhinitis

Ostatnio opublikowane międzynarodowe raporty: Światowej Inicjatywy Zwalczania Astmy, PRACTicing ALLergology i Allergic Rhinitis and its Impact on Asthma rekomendują leki przeciwleukotrienowe w terapii astmy u dorosłych i u dzieci oraz w alergicznym nieżycie nosa. W niniejszym artykule przedstawiono argumenty za i przeciw lekom antyleukotrienowym w leczeniu obturacji dróg oddechowych.Recently published international recommendations including Global INitiative for Asthma, PRACTicing ALLergology and Allergic Rhinitis and its Impact on Asthma offer antileukotriene drugs for adult and childhood asthma and allergic rhinitis. In this article we discuss the arguments for and against antileukotriene drugs therapy in the treatment of obstructive lung diseases and rhinitis

Adult form of Pompe disease

Pompe disease (glycogen-storage disease type II) is an autosomal recessive disorder caused by a deficiency of lysosomal acid a-glucosidase (GAA), leading to the accumulation of glycogen in the lysosomes primarily in muscle cells. In the adult form of the disease, proximal muscle weakness is noted and muscle volume is decreased. The infantile form is usually fatal. In the adult form of the disease the prognosis is relatively good. Muscle weakness may, however, interfere with normal daily activities, and respiratory insufficiency may be associated with obstructive sleep apnea. Death usually results from respiratory failure. Effective specific treatment is not available. Enzyme replacement therapy with recombinant human GAA (rh-GAA) still remains a research area. We report the case of a 24-year-old student admitted to the Department of Pulmonary Diseases because of severe respiratory insufficiency. Clinical symptoms such as dyspnea, muscular weakness and increased daytime sleepiness had been progressing for 2 years. Clinical examination and increased blood levels of CK suggested muscle pathology. Histopathological analysis of muscle biopsy, performed under electron microscope, confirmed the presence of vacuoles containing glycogen. Specific enzymatic activity of a-glucosidase was analyzed confirming Pompe disease. The only effective method to treat respiratory insufficiency was bi-level positive pressure ventilation. Respiratory rehabilitation was instituted and is still being continued by the patient at home. A high-protein, low-sugar diet was proposed for the patient. Because of poliglobulia, low molecular weight heparin was prescribed. The patient is eligible for experimental replacement therapy with rh-GAA

Can alveolar hypoventilation due to kyphoscoliosis be a contraindication to driving?

Road accidents are among the main fatalities worldwide and drowsy driving is a significant cause of road deaths where drivers are at fault. There are well known diseases which impair sensory and cognitive functions and can cause sleepiness during driving. Such diseases can be an important contraindication to driving because they may have an adverse effect on its safety. Thus, medical examinations for drivers should also be directed at identifying any possible conditions posing risks for driving safety. Occupational medicine specialists should look for symptoms of locomotor and sleep-related breathing disorders as these are medical conditions which could preclude a person from driving. In this case report, the authors describe a professional driver with chest deformity and present a pioneering attempt at assessing his medical fitness to drive. It is also explained why scoliosis can impair driving ability and how it should be diagnosed and treated. Finally, the authors describe how they used driving simulator tests as part of their diagnosis and suggest a relevant treatment regimen

Treatment of acute respiratory failure in the course of COVID-19. Practical hints from the expert panel of the Assembly of Intensive Care and Rehabilitation of the Polish Respiratory Society

In 2019, a pandemic began due to infection with a novel coronavirus, SARS-CoV-2. In many cases, this coronavirus leads to the development of the COVID-19 disease. Lung damage in the course of this disease often leads to acute hypoxic respiratory failure and may eventually lead to acute respiratory distress syndrome (ARDS). Respiratory failure as a result of COVID-19 can develop very quickly and a small percent of those infected will die because of it. There is currently no treatment for COVID-19, therefore the key therapeutic intervention centers around the symptomatic treatment of respiratory failure. The main therapeutic goal is to main-tain gas exchange, mainly oxygenation, at an appropriate level and prevent the intensification of changes in the lung parenchyma. Depending on the severity of hypoxemia different techniques can be used to improve oxygenation. Medical staff dealing with COVID-19 patients should be familiar with both, methods used to treat respiratory failure and the epidemiological risks arising from their use. In some patients, conventional (passive) oxygen therapy alone is sufficient. In patients with worsening respiratory failure high flow nasal oxygen therapy (HFNOT) may be effective. The continuous positive airway pressure (CPAP) and non-invasive ventilation (NIV) methods can be used to a limited extent. With further disease progression, invasive ventilation must be used and in special situations, extracorporeal membrane oxygenation (ECMO) can also be administered.The authors of this article set themselves the goal of presenting the most current knowledge about the epidemiology and patho-physiology of respiratory failure in COVID-19, as well as the methods of its treatment. Given the dynamics of the developing pandemic, this is not an easy task as new scientific data is presented almost every day. However, we believe the knowledge contained in this study will help doctors care for patients with COVID-19. The main target audience of this study is not so much pneumonologists or intensivists who have extensive experience in the application of the techniques discussed here, but rather doctors of other specializations who must master new skills in order to help patients during the time of a pandemic

Adult form of Pompe disease

Choroba Pompego (glikogenoza typu II) jest to zaburzenie genetyczne dziedziczone w sposób autosomalny recesywny, spowodowane niedoborem lizosomalnej kwaśnej α-glukozydazy (GAA). Niedobór enzymu prowadzi do gromadzenia się patologicznej ilości glikogenu w lizosomach komórek, głównie mięśni prążkowanych. U osób dorosłych jeden z objawów choroby Pompego - osłabienie siły mięśniowej - ma istotny wpływ na codzienną aktywność. Zmniejszone napięcie mięśniowe może prowadzić do wystąpienia niewydolności oddechowej oraz bezdechów obturacyjnych w czasie snu. Nie ma specyficznego, w pełni skutecznego leczenia. Stosuje się dietę bogatobiałkową z małą zawartością węglowodanów, rehabilitację oddechową, nieinwazyjną wentylację mechaniczną ciągłym dodatnim ciśnieniem w drogach oddechowych. W pracy przedstawiono przypadek 24-letniego chorego z osłabieniem siły mięśniowej i niewydolnością oddechową, u którego potwierdzono chorobę Pompego na podstawie oceny histopatologicznej mięśnia szkieletowego oraz badań enzymatycznych i aktywności GAA leukocytów krwi obwodowej. W wyniku leczenia nieinwazyjną wentylacją mechaniczną ciągłym dodatnim ciśnieniem w drogach oddechowych, prowadzoną w systemie bi-level, rehabilitacji oddechowej, stosowania heparyny drobnocząsteczkowej oraz diety ubogocukrowej i bogatobiałkowej, stan kliniczny pacjenta uległ poprawie. Ustąpiły objawy osłabienia mięśni i cechy niewydolności oddechowej. Chory został członkiem międzynarodowej grupy wsparcia osób z chorobą Pompego. Zakwalifikowano go do terapii eksperymentalnej z zastosowaniem rhGAA.Pompe disease (glycogen-storage disease type II) is an autosomal recessive disorder caused by a deficiency of lysosomal acid α-glucosidase (GAA), leading to the accumulation of glycogen in the lysosomes primarily in muscle cells. In the adult form of the disease, proximal muscle weakness is noted and muscle volume is decreased. The infantile form is usually fatal. In the adult form of the disease the prognosis is relatively good. Muscle weakness may, however, interfere with normal daily activities, and respiratory insufficiency may be associated with obstructive sleep apnea. Death usually results from respiratory failure. Effective specific treatment is not available. Enzyme replacement therapy with recombinant human GAA (rh-GAA) still remains a research area. We report the case of a 24-year-old student admitted to the Department of Pulmonary Diseases because of severe respiratory insufficiency. Clinical symptoms such as dyspnea, muscular weakness and increased daytime sleepiness had been progressing for 2 years. Clinical examination and increased blood levels of CK suggested muscle pathology. Histopathological analysis of muscle biopsy, performed under electron microscope, confirmed the presence of vacuoles containing glycogen. Specific enzymatic activity of α-glucosidase was analyzed confirming Pompe disease. The only effective method to treat respiratory insufficiency was bi-level positive pressure ventilation. Respiratory rehabilitation was instituted and is still being continued by the patient at home. A high-protein, low-sugar diet was proposed for the patient. Because of poliglobulia, low molecular weight heparin was prescribed. The patient is eligible for experimental replacement therapy with rh-GAA

Subphenotypes of nonsteroidal antiinflammatory diseaseexacerbated respiratory disease identified by latent class analysis

Background Induced sputum (IS) allows to measure mediators of asthmatic inflammation in bronchial secretions. NSAID‐exacerbated respiratory disease (NERD) is recognized as a distinct asthma phenotype, usually with a severe course, eosinophilic airway inflammation, and increased production of pro‐inflammatory eicosanoids. A more insightful analysis of NERD patients has shown this phenotype to be nonhomogeneous. Objective We aimed to identify possible subphenotypes in a cohort of NERD patients with the means of latent class analysis (LCA). Methods A total of 95 asthma patients with aspirin hypersensitivity underwent sputum induction. High‐performance liquid chromatography or gas chromatography coupled with mass spectrometry was used to profile eicosanoids in induced sputum supernatant (ISS). Sixteen variables covering clinical characteristics, IS inflammatory cells, and eicosanoids were considered in the LCA. Results Three classes (subphenotypes) were distinguished within the NERD cohort. Class 1 subjects had mild‐to‐moderate asthma, an almost equal distribution of inflammatory cell patterns, the lowest concentrations of eicosanoids, and logLTE4/logPGE2 ratio. Class 2 represented severe asthma with impaired lung function despite high doses of steroids. High sputum eosinophilia was in line with higher pro‐inflammatory LTE4 in ISS and the highest logLTE4/logPGE2 ratio. Class 3 subjects had mild‐to‐moderate asthma and were also characterized by eosinophilic airway inflammation, yet increased production of pro‐ (LTE4, PGD2 and 11‐dehydro‐TBX2) was balanced by anti‐inflammatory PGE2. The value of logLTE4/logPGE2 was between values calculated for classes 1 and 3, similarly to disease control and severity. Conclusions LCA revealed three distinct NERD subphenotypes. Our results support a more complex pathobiology of aspirin hypersensitivity. Considering NERD heterogeneity, the relationship between inflammatory pathways and clinical manifestations of asthma may lead to more individualized treatment in difficult to treat patients in the future

Validation of the Polish-language version of the COPD Assessment Test

INTRODUCTION The COPD Assessment Test (CAT) is a standardized patient–completed tool dedicated to assessment of symptom severity. While the Polish CAT version has been used for a few years, it has not been validated so far. OBJECTIVES The aim of the study was to validate the Polish‑language version of the CAT questionnaire by assessing its reproducibility and reliability. PATIENTS AND METHODS Validation of the Polish‑language version of the CAT questionnaire was a substudy of the international multicenter observational cross‑sectional POPE survey of patients with chronic obstructive pulmonary disease (COPD) in Central and Eastern European countries. The study was completed in 395 outpatients with stable disease at least 4 weeks before the survey. Validation was performed with the use of the Spearman correlation and Cronbach α coefficients, Cohen κ test, and the Bland–Altman procedure. RESULTS The internal consistency assessed by the Cronbach α coefficient was 0.87 for the questionnaire and 0.84 to 0.86 for its separate items. The repeatability of the questionnaire was good to very good (Cohen κ, 0.76–0.85; P <0.01). The Spearman coefficient for the sum of scores of test–retest responses was 0.95 (P <0.01). The Bland–Altman analysis revealed very good test–retest and interrater reliability, with the mean difference between test I and test II results of –0.556 (95% CI, –0.345 to 0.767). CONCLUSIONS The Polish version of the CAT questionnaire is a reproducible and reliable instrument for evaluation of patients with COPD and should be recommended for use in clinical practice