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Respiratory Tract Diseases - Top 30 Publications

Acute Respiratory Distress Syndrome.

Acute Respiratory Distress Syndrome.

Fitness cost of reassortment in human influenza.

Reassortment, which is the exchange of genome sequence between viruses co-infecting a host cell, plays an important role in the evolution of segmented viruses. In the human influenza virus, reassortment happens most frequently between co-existing variants within the same lineage. This process breaks genetic linkage and fitness correlations between viral genome segments, but the resulting net effect on viral fitness has remained unclear. In this paper, we determine rate and average selective effect of reassortment processes in the human influenza lineage A/H3N2. For the surface proteins hemagglutinin and neuraminidase, reassortant variants with a mean distance of at least 3 nucleotides to their parent strains get established at a rate of about 10-2 in units of the neutral point mutation rate. Our inference is based on a new method to map reassortment events from joint genealogies of multiple genome segments, which is tested by extensive simulations. We show that intra-lineage reassortment processes are, on average, under substantial negative selection that increases in strength with increasing sequence distance between the parent strains. The deleterious effects of reassortment manifest themselves in two ways: there are fewer reassortment events than expected from a null model of neutral reassortment, and reassortant strains have fewer descendants than their non-reassortant counterparts. Our results suggest that influenza evolves under ubiquitous epistasis across proteins, which produces fitness barriers against reassortment even between co-circulating strains within one lineage.

Genetic variants of SULT1A1 and XRCC1 genes and risk of lung cancer in Bangladeshi population.

Lung cancer is one of the most frequently occurring cancers throughout the world as well as in Bangladesh. This study aimed to correlate the prognostic and/or predictive value of functional polymorphisms in SULT1A1 (rs9282861) and XRCC1 (rs25487) genes and lung cancer risk in Bangladeshi population. A case-control study was conducted which comprises 202 lung cancer patients and 242 healthy volunteers taking into account the age, sex, and smoking status. After isolation of genomic DNA, genotyping was done by polymerase chain reaction-restriction fragment length polymorphism method and the lung cancer risk was evaluated as odds ratio that was adjusted for age, sex, and smoking status. A significant association was found between SULT1A1 rs9282861 and XRCC1 rs25487 polymorphisms and lung cancer risk. In case of rs9282861 polymorphism, Arg/His (adjusted odds ratio = 5.06, 95% confidence interval = 3.05-8.41, p < 0.05) and His/His (adjusted odds ratio = 3.88, 95% confidence interval = 2.20-6.82, p < 0.05) genotypes were strongly associated with increased risk of lung cancer in comparison to the Arg/Arg genotype. In case of rs25487 polymorphism, Arg/Gln heterozygote (adjusted odds ratio = 4.57, 95% confidence interval = 2.79-7.46, p < 0.05) and Gln/Gln mutant homozygote (adjusted odds ratio = 4.99, 95% confidence interval = 2.66-9.36, p < 0.05) were also found to be significantly associated with increased risk of lung cancer. This study demonstrates that the presence of His allele and Gln allele in case of SULT1A1 rs9282861 and XRCC1 rs25487, respectively, involve in lung cancer prognosis in Bangladeshi population.

Sleep Apnea and Cardiovascular Disease: Lessons From Recent Trials and Need for Team Science.

Emerging research highlights the complex interrelationships between sleep-disordered breathing and cardiovascular disease, presenting clinical and research opportunities as well as challenges. Patients presenting to cardiology clinics have a high prevalence of obstructive and central sleep apnea associated with Cheyne-Stokes respiration. Multiple mechanisms have been identified by which sleep disturbances adversely affect cardiovascular structure and function. Epidemiological research indicates that obstructive sleep apnea is associated with increases in the incidence and progression of coronary heart disease, heart failure, stroke, and atrial fibrillation. Central sleep apnea associated with Cheyne-Stokes respiration predicts incident heart failure and atrial fibrillation; among patients with heart failure, it strongly predicts mortality. Thus, a strong literature provides the mechanistic and empirical bases for considering obstructive sleep apnea and central sleep apnea associated with Cheyne-Stokes respiration as potentially modifiable risk factors for cardiovascular disease. Data from small trials provide evidence that treatment of obstructive sleep apnea with continuous positive airway pressure improves not only patient-reported outcomes such as sleepiness, quality of life, and mood but also intermediate cardiovascular end points such as blood pressure, cardiac ejection fraction, vascular parameters, and arrhythmias. However, data from large-scale randomized controlled trials do not currently support a role for positive pressure therapies for reducing cardiovascular mortality. The results of 2 recent large randomized controlled trials, published in 2015 and 2016, raise questions about the effectiveness of pressure therapies in reducing clinical end points, although 1 trial supported the beneficial effect of continuous positive airway pressure on quality of life, mood, and work absenteeism. This review provides a contextual framework for interpreting the results of recent studies, key clinical messages, and suggestions for future sleep and cardiovascular research, which include further consideration of individual risk factors, use of existing and new multimodality therapies that also address adherence, and implementation of trials that are sufficiently powered to target end points and to support subgroup analyses. These goals may best be addressed through strengthening collaboration among the cardiology, sleep medicine, and clinical trial communities.

Epidemiology and molecular characterization of influenza viruses, human parechoviruses and enteroviruses in children up to 5 years with influenza-like illness in Northern Italy during seven consecutive winter seasons (2010-2017).

Besides the influenza virus (IV), several other viruses are responsible for influenza-like illness (ILI). Although human parechoviruses (HPeVs) and enteroviruses (EVs) may impact on ILI, limited data on their epidemiological characteristics are available. During seven consecutive winter seasons (from 2010-2011 to 2016-2017), within the framework of an influenza surveillance system (InfluNet), 593 respiratory swabs were collected from children ≤5 years of age with ILIs. Molecular detection showed that 58.3 % of swabs were positive for at least one of the viruses under study: 46 % for IV, 13 % for EV and 5.4 % for HPeV. A single virus was identified in 51.3 % of samples while more than one virus was detected in 7 % of the samples. The risk of contracting IV was higher than the risk associated with EV, which in turn was higher than the risk of contracting HPeV. The risk of developing an IV infection was twofold greater in children >3 years than in those ≤3 years, who had higher risk of EV/HPeV infection. The frequency of EV/HPeV-positive swabs increased significantly during the 2016-2017 winter season compared to the previous six seasons. Sixteen EV genotypes were identified belonging to species A and B. HPeV-1 was the most frequently detected genotype, followed by -6 and -3. In this study, IV was mainly responsible for ILI, however EV and HPeV were also involved and particularly affected children ≤3 years of age. Influenza surveillance samples could provide us with valuable insight into the epidemiological features of viruses involved in ILI.

Natural Selection on Genes Related to Cardiovascular Health in High-Altitude Adapted Andeans.

The increase in red blood cell mass (polycythemia) due to the reduced oxygen availability (hypoxia) of residence at high altitude or other conditions is generally thought to be beneficial in terms of increasing tissue oxygen supply. However, the extreme polycythemia and accompanying increased mortality due to heart failure in chronic mountain sickness most likely reduces fitness. Tibetan highlanders have adapted to high altitude, possibly in part via the selection of genetic variants associated with reduced polycythemic response to hypoxia. In contrast, high-altitude-adapted Quechua- and Aymara-speaking inhabitants of the Andean Altiplano are not protected from high-altitude polycythemia in the same way, yet they exhibit other adaptive features for which the genetic underpinnings remain obscure. Here, we used whole-genome sequencing to scan high-altitude Andeans for signals of selection. The genes showing the strongest evidence of selection-including BRINP3, NOS2, and TBX5-are associated with cardiovascular development and function but are not in the response-to-hypoxia pathway. Using association mapping, we demonstrated that the haplotypes under selection are associated with phenotypic variations related to cardiovascular health. We hypothesize that selection in response to hypoxia in Andeans could have vascular effects and could serve to mitigate the deleterious effects of polycythemia rather than reduce polycythemia itself.

Genome-wide association study for genetic variants related with maximal voluntary ventilation reveals two novel genomic signals associated with lung function.

Genome-wide association studies (GWAS) for spirometry parameters have been limited to forced vital capacity (FVC), forced expiratory volume in 1 second (FEV1), and their ratio. This study examined to identify genetic variants associated with maximal voluntary ventilation (MVV), an important spirometry parameter presenting inspiratory muscle strength.A total of 8842 Korean subjects participated in the Korean Association REsource Consortium were used to identify nucleotide variants associated with MVV and other spirometry parameters through a GWAS. Genetic associations were determined by employing a mixed model that can control background polygenic effects.The analysis revealed 3 nucleotide variants associated with MVV (P < 5 × 10). One (rs1496255) was also associated with FVC and FEV1. The other 2 variants were identified only for MVV and located in the genes of LOC102724340 (rs41434646) and FHIT (rs9833533). In particular, FHIT represses transcriptional activity of β-catenin, a critical protein for growth of skeletal muscle, and thus might have influenced the level of MVV.The current study revealed 2 novel nucleotide variants as genetic association signals for MVV. The association signals were suggested specific for neuromuscular diseases with a restrictive ventilatory impairment. Further studies are required to understand underlying mechanisms for their influence to restrictive lung diseases.

Sonography used in the infantile desmoid fibromatosis of postcricoid area: A case report.

Infantile desmoid fibromatosis of the postcricoid area is a rare disease and is characterized by a proliferation of fibrous tissue with non-metastasis, local infiltration, and a high rate of recurrence after surgical resection. Currently, ultrasound is scarcely used in the hypopharynx and larynx area.

Clinical features of secondary pulmonary alveolar proteinosis associated with myelodysplastic syndrome: Two case reports.

Pulmonary alveolar proteinosis (PAP) is a rare lung disorder characterized by the abnormal accumulation of alveolar surfactant protein in alveolar spaces. Secondary PAP can result from myelodysplastic syndrome (MDS).

Disease burden of hospitalized community-acquired pneumonia in South Korea: Analysis based on age and underlying medical conditions.

Pneumonia is a leading cause of hospitalization and mortality worldwide. Despite recognition of the importance of community-acquired pneumonia (CAP) in adults, limited epidemiologic information is available in South Korea. This study aimed to evaluate the disease burden of hospitalized CAP in adults aged ≥19 years and its epidemiologic trend using Health Insurance and Review Assessment (HIRA) data.This is a retrospective study using the HIRA database from year 2009 to 2013. We estimated the incidence rate and direct medical cost of hospitalized CAP in adults aged ≥19 years in South Korea. These were further analyzed with respect to age and underlying medical conditions.During 2009 to 2013, 1216,916 hospitalizations were recorded. On average, the annual age-adjusted incidence rate of hospitalized CAP was 626 per 100,000 persons, with the rate increasing with age. When stratified by age- and risk groups, elderly people ≥75 years showed the highest incidence rate of hospitalized CAP over 5-year study periods. With respect to the risk groups based on underlying medical conditions, incidence rate ratios were 2.04 to 5.86 for the high-risk group versus the low-risk group and 1.28 to 5.49 for the moderate-risk group versus the low-risk group. Overall, mean direct medical cost for hospitalized CAP was 1851 USD per capita during the 5-year period: 1263 USD in the low-risk group, 2353 USD in the moderate-risk group, and 2841 USD in the high-risk group.This study shows that the incidence and medical cost of hospitalized CAP were consistently high over the 5-year study period. In particular, elderly people and adults with underlying medical conditions were at increased risk for hospitalized CAP.

Immune-related adverse events associated with PD-1 and PD-L1 inhibitors for nonsmall cell lung cancer: Protocol for a systematic review and meta-analysis.

Nonsmall cell lung cancer accounts for approximately 80% of all lung cancers, and approximately 75% of cases are diagnosed in the middle and late stages of disease. Unfortunately, limited treatment does not improve the prognosis of advanced disease. Monoclonal antibodies targeting programmed cell death protein-1 (PD-1) and programmed death-ligand 1 (PD-L1) represent a new treatment paradigm for nonsmall cell lung cancer. Nevertheless, the immune-related adverse events (irAEs) associated with PD-1 and PD-L1 inhibitors are unique, and early recognition and treatment of these events are essential.

Determining the contribution of <em>Streptococcus pneumoniae</em> to community-acquired pneumonia in Australia.

To evaluate trends in the proportion and severity of community-acquired pneumonia (CAP) attributable to Streptococcus pneumoniae (pneumococcus) in Australians aged 18 years and over.

Reducing antibiotic prescribing in Australian general practice: time for a national strategy.

In Australia, the antibiotic resistance crisis may be partly alleviated by reducing antibiotic use in general practice, which has relatively high prescribing rates - antibiotics are mostly prescribed for acute respiratory infections, for which they provide only minor benefits. Current surveillance is inadequate for monitoring community antibiotic resistance rates, prescribing rates by indication, and serious complications of acute respiratory infections (which antibiotic use earlier in the infection may have averted), making target setting difficult. Categories of interventions that may support general practitioners to reduce prescribing antibiotics are: regulatory (eg, changing the default to "no repeats" in electronic prescribing, changing the packaging of antibiotics to facilitate tailored amounts of antibiotics for the right indication and restricting access to prescribing selected antibiotics to conserve them), externally administered (eg, academic detailing and audit and feedback on total antibiotic use for individual GPs), interventions that GPs can individually implement (eg, delayed prescribing, shared decision making, public declarations in the practice about conserving antibiotics, and self-administered audit), supporting GPs' access to near-patient diagnostic testing, and public awareness campaigns. Many unanswered clinical research questions remain, including research into optimal implementation methods. Reducing antibiotic use in Australian general practice will require a range of approaches (with various intervention categories), a sustained effort over many years and a commitment of appropriate resources and support.

Half of rifampicin-resistant Mycobacterium tuberculosis complex isolated from tuberculosis patients in Sub-Saharan Africa have concomitant resistance to pyrazinamide.

Besides inclusion in 1st line regimens against tuberculosis (TB), pyrazinamide (PZA) is used in 2nd line anti-TB regimens, including in the short regimen for multidrug-resistant TB (MDR-TB) patients. Guidelines and expert opinions are contradictory about inclusion of PZA in case of resistance. Moreover, drug susceptibility testing (DST) for PZA is not often applied in routine testing, and the prevalence of resistance is unknown in several regions, including in most African countries.

Non-small cell lung cancer (NSCLC), EGFR downstream pathway activation and TKI targeted therapies sensitivity: Effect of the plasma membrane-associated NEU3.

Adenocarcinoma of Non-Small Cell Lung Cancer (NSCLC) is a severe disease. Patients carrying EGFR mutations may benefit from EGFR targeted therapies (e.g.: gefitinib). Recently, it has been shown that sialidase NEU3 directly interacts and regulates EGFR. In this work, we investigate the effect of sialidase NEU3 overexpression on EGFR pathways activation and EGFR targeted therapies sensitivity, in a series of lung cancer cell lines. NEU3 overexpression, forced after transfection, does not affect NSCLC cell viability. We demonstrate that NEU3 overexpression stimulates the ERK pathway but this activation is completely abolished by gefitinib treatment. The Akt pathway is also hyper-activated upon NEU3 overexpression, but gefitinib is able only to decrease, and not to abolish, such activation. These findings indicate that NEU3 can act directly on the ERK pathway through EGFR and both directly and indirectly with respect to EGFR on the Akt pathway. Furthermore, we provide evidence that a healthy mucosa cell line (with EGFR wild-type gene sequence) is slightly sensitive to gefitinib, especially in the presence of NEU3 overexpression, thus hypothesizing that NEU3 overexpressing patients may benefit from EGFR targeted therapies also in absence of EGFR point mutations. Overall, the expression of NEU3 may be a novel diagnostic marker in NSCLC because, by its ability to stimulate EGFR downstream pathways with direct and indirect mechanisms, it may help in the identification of patients who can profit from EGFR targeted therapies in absence of EGFR activating mutations or from new combinations of EGFR and Akt inhibitors.

Effect of Rho-kinase inhibition on complexity of breathing pattern in a guinea pig model of asthma.

Asthma represents an episodic and fluctuating behavior characterized with decreased complexity of respiratory dynamics. Several evidence indicate that asthma severity or control is associated with alteration in variability of lung function. The pathophysiological basis of alteration in complexity of breathing pattern in asthma has remained poorly understood. Regarding the point that Rho-kinase is involved in pathophysiology of asthma, in present study we investigated the effect of Rho-kinase inhibition on complexity of respiratory dynamics in a guinea pig model of asthma. Male Dunkin Hartley guinea pigs were exposed to 12 series of inhalations with ovalbumin or saline. Animals were treated by the Rho-kinase inhibitor Y-27632 (1mM aerosols) prior to each allergen challenge. We recorded respiration of conscious animals using whole-body plethysmography. Exposure to ovalbumin induced lung inflammation, airway hyperresponsiveness and remodeling including goblet cell hyperplasia, increase in the thickness of airways smooth muscles and subepithelial collagen deposition. Complexity analysis of respiratory dynamics revealed a dramatic decrease in irregularity of respiratory rhythm representing less complexity in asthmatic guinea pigs. Inhibition of Rho-kinase reduced the airway remodeling and hyperreponsiveness, but had no significant effect on lung inflammation and complexity of respiratory dynamics in asthmatic animals. It seems that airway hyperresponsiveness and remodeling do not significantly affect the complexity of respiratory dynamics. Our results suggest that inflammation might be the probable cause of shift in the respiratory dynamics away from the normal fluctuation in asthma.

New targets bring hope in squamous cell lung cancer: neurotrophic tyrosine kinase gene fusions.

Neurotrophic tyrosine kinase genes encode for the Trk-family proteins TrkA, TrkB, and TrkC, which have an important role in the development of the nervous system; however, they have been identified as oncogenic fusions in solid tumors (NTK-1, NTRK-2, and NTRK-3) and are associated with poor survival in lung cancer. These three new fusions can be detected by fluorescent in situ hybridization or next-generation sequencing in less than 5% of the lung tumors. There are several ongoing clinical trials of NTRK oncogenes in lung cancer and other tumors. The agents entrectinib (RXDX-101), a multi-kinase small molecule inhibitor that selectively inhibits NTRK1, NTRK2, and NTRK3, ROS1 and ALK, and LOXO-101, an ATP-competitive pan-NTRK inhibitor, have shown responses in patients with lung cancer with an acceptable toxicity profile. Although these oncogenic fusions are not very prevalent, the high prevalence of lung cancer makes these findings very relevant and suggests the feasibility of these oncogenes as targets in lung cancer. New data from Ozono and collaborators presented in this issue suggest that BDNF/TrkB signal promotes proliferating migratory and invasive phenotypes and cellular plasticity in squamous cell carcinoma (SCC) of the lung but that it also represents a druggable target that may bring hope to squamous lung cancer patients.

Memory and Executive Screening for the Detection of Cognitive Impairment in Obstructive Sleep Apnea.

Obstructive sleep apnea (OSA) is commonly associated with cognitive dysfunction, which is more apparent in severe OSA and impairs quality of life. However, the clinical screening methods for these impairments in OSA are still limited. In this study, we evaluated the feasibility of using the Memory and Executive Screening (MES) for assessing cognitive performance in OSA.

Correlation Between Tumor Necrosis Factor-α and Interleukin-1β in Exhaled Breath Condensate and Pulmonary Function.

Exhaled breath condensate (EBC) has emerged as a noninvasive method for assessing inflammation in lung diseases. Our aim is to investigate the correlation between tumor necrosis factor α (TNF-α) and interleukin 1β (IL-1β) in EBC and in lung tissue, and between these values in EBC with pulmonary function tests in patients with chronic obstructive pulmonary disease (COPD).

Eosinophilic Lung Disease.

Eosinophils are involved in the pathogenesis of a number of lung diseases. Recent advances in eosinophil biology have now produced clinically applicable therapies that seek to counter eosinophilia in blood and lungs. This article reviews the basic biology of eosinophils and their role in mediating T-helper 2 cell responses. The current status of anticytokine therapy for eosinophilic lung disease is discussed. A clinical approach to eosinophilic lung disease based on symptoms and radiography is generated. The clinical significance of persistent eosinophilia in lung transplant patients and patients with asthma will receive special emphasis.

Treatment Outcomes of In-Office KTP Ablation of Vocal Fold Granulomas.

To determine the effectiveness of in-office potassium-titanyl-phosphate (KTP) treatment of vocal fold granulomas and identify any predictors of complete lesion resolution.

Gender Differences in the Reporting of Vocal Fatigue in Teachers as Quantified by the Vocal Fatigue Index.

Occupational voice users report higher instances of vocal health problems. Women, who are more likely than men to report voice problems, are the largest members of some occupational voice users, such as teachers. While a common complaint among this population is vocal fatigue, it has been difficult to quantify. Therefore, the goal of this study is to quantify vocal fatigue generally in school teachers and investigate any related gender differences.

Personalized therapy of lung cancer - current standard and future challenges.

So called "personalized therapy" has revolutionized the care of non-small cell lung cancer (NSCLC). The discovery of more and more driver mutations in NSCLC has led to a molecular defined sub classification of lung cancer patients. For four driver mutations (EGFR(mut), ALK(transl), ROS1(transl), BRAF-V600(mut)) firstline approved drugs are available and became the treatment of choice. Further drugs are in clinical development or can be used as off-label treatment. The emergence of resistance under targeted therapy, the development of new drugs for further driver mutations and the broad implementation of molecular diagnostics for all lung cancer patients are future challenges.

A lethal disease model for New World hantaviruses using immunosuppressed Syrian hamsters.

Hantavirus, the hemorrhagic causative agent of two clinical diseases, is found worldwide with variation in severity, incidence and mortality. The most lethal hantaviruses are found on the American continent where the most prevalent viruses like Andes virus and Sin Nombre virus are known to cause hantavirus pulmonary syndrome. New World hantavirus infection of immunocompetent hamsters results in an asymptomatic infection except for Andes virus and Maporal virus; the only hantaviruses causing a lethal disease in immunocompetent Syrian hamsters mimicking hantavirus pulmonary syndrome in humans.

Combining MAD and CPAP as an effective strategy for treating patients with severe sleep apnea intolerant to high-pressure PAP and unresponsive to MAD.

This study aimed to determine the effect of combining positive airway pressure (PAP) therapy and mandibular advancement device (MAD) in patients with severe obstructive sleep apnea (OSA) who were pressure intolerant for PAP and were unresponsive to MAD.

Toxoplasma gondii serine-protease inhibitor-1: A new adjuvant candidate for asthma therapy.

Serine-proteases are important players in the pathogenesis of asthma, promoting inflammation and tissue remodeling. It's also known that many serine protease inhibitors display immunomodulatory properties. TgPI-1 is a Toxoplasma gondii protein that exhibits broad spectrum inhibitory activity against serine proteases. In view of the increased prevalence of atopic disorders and the need to develop new treatment strategies we sought to investigate the potential of TgPI-1 for treating respiratory allergies. For this purpose, we developed a therapeutic experimental model. BALB/c mice were rendered allergic by intraperitoneal ovalbumin-alum sensitization and airway-challenged. Once the asthmatic phenotype was achieved, mice were intranasally treated with rTgPI-1 alone or with a mixture of rTgPI-1 and ovalbumin (OVA). A week later mice were given a secondary aerosol challenge. Treatment with rTgPI-1 alone or co-administered with OVA diminished bronchoalveolar eosinophilia, mucus production and peribronchial lung infiltration. This effect was accompanied by a lung resistance reduction of 26.3% and 50.3% respectively. Both treatments resulted in the production of lower levels of IL-4, IL-5, IFN-γ and regulatory IL-10 by thoracic lymph node cells stimulated with OVA. Interestingly, significant decreases in OVA specific IgE and T cell proliferation, and increases in FoxP3+ T cells at local and systemic levels were only detected when the inhibitor was administered along with OVA. These results show that both rTgPI-1 treatments reduced asthma hallmarks. However, co-administration of the inhibitor with the allergen was more effective. Hence, rTgPI-1 emerges as a novel adjuvant candidate for asthma treatment.

Cytokine-induced killer cells: A novel treatment for allergic airway inflammation.

The effectiveness of cytokine-induced killer (CIK) cells for treatment of cancers has long been appreciated. Here, we report for the first time that CIK cells can be applied to treat allergic airway inflammation. Adopting from an established protocol with some modifications, we generated CIK cells ex vivo from mouse T cells, and examined their effectiveness in treatment of allergic airway inflammation using the ovalbumin-induced model of allergic airway inflammation. Based upon evaluation of bronchoalveolar lavage cellularity, T helper type2 cytokine levels and lung histology, all of which are important parameters for determining the severity of allergic airway inflammation, diseased mice treated with CIK cells showed significant reductions in all the parameters without any obvious adverse effects. Interestingly, the observed effects were comparable to those treated with dexamethasone. Thus, our study provides a novel application of CIK cells in treatment of allergic airway inflammation.

Asthma is associated with atherosclerotic artery changes.

Asthma is a chronic airway inflammation with a potential systemic impact. Atherosclerosis is a chronic inflammatory artery disease. The aim of our study was to prove if there is a correlation between the occurrence of asthma and increased atherosclerotic vessel disorders. Vessel status was compared between mild-to-moderate, severe allergic asthma and matched controls. Measurements of artery stiffness were calculated by central pulse wave velocity, ultrasonographic strain imaging and ankle-brachial index. Atherosclerotic plaque burden was assessed by colour-coded duplex sonography. Additionally, analysis of cardiovascular and asthma blood markers was conducted. Arterial stiffness expressed as an increased central pulse wave velocity and decreased circumferential and radial strains as well as the prevalence of media sclerosis were significantly higher among asthma patients compared to controls. Atherosclerotic plaque burden was relevantly increased in asthma groups vs. controls (severe asthma: 43.1%, mild-to-moderate asthma: 25.0%, control: 14.3% of study participants). Except for the elevated IgE and fibrinogen concentrations as well as leukocyte number there were no relevant differences in the blood parameters between the groups. Allergic asthma is associated with distinct atherosclerotic artery changes compared to the respectively matched control collective. The severity of asthma correlates with more pronounced pathological vessel alternations.

Patterns, factors associated and morbidity burden of asthma in India.

Asthma is a non-curable but preventable disease, responsible for higher morbidity worldwide. According to recent WHO report, nearly 235 million people are suffering from asthma leading to 383000 deaths in 2015. The burden of asthma morbidity is higher in developed countries and is increasing in developing countries.