Combinatorial classification of quantum lens spaces

We answer the question of how large the dimension of a quantum lens space must be, compared to the primary parameter $r$, for the isomorphism class to depend on the secondary parameters. Since classification results in C*-algebra theory reduces this question to one concerning a certain kind of $SL$-equivalence of integer matrices of a special form, our approach is entirely combinatorial and based on the counting of certain paths in the graphs shown by Hong and Szyma\'nski to describe the quantum lens spaces.Comment: 27 pages, 2 figure

COL4A3 is degraded in allergic asthma and degradation predicts response to anti-IgE therapy.

BACKGROUND: Asthma is a heterogeneous syndrome substantiating the urgent requirement for endotype-specific biomarkers. Dysbalance of fibrosis and fibrolysis in asthmatic lung tissue leads to reduced levels of the inflammation-protective collagen 4 (COL4A3). OBJECTIVE: To delineate the degradation of COL4A3 in allergic airway inflammation and evaluate the resultant product as a biomarker for anti-IgE therapy response. METHODS: The serological COL4A3 degradation marker C4Ma3 (Nordic Bioscience, Denmark) and serum cytokines were measured in the ALLIANCE cohort (paediatric cases/controls: n=134/n=35; adult cases/controls: n=149/n=31). Exacerbation of allergic airway disease in mice was induced by sensitising to ovalbumin (OVA), challenge with OVA aerosol and instillation of poly(cytidylic-inosinic). Fulacimstat (chymase inhibitor; Bayer) was used to determine the role of mast cell chymase in COL4A3 degradation. Patients with cystic fibrosis (n=14) and cystic fibrosis with allergic bronchopulmonary aspergillosis (ABPA; n=9) as well as patients with severe allergic uncontrolled asthma (n=19) were tested for COL4A3 degradation. Omalizumab (anti-IgE) treatment was assessed using the Asthma Control Test. RESULTS: Serum levels of C4Ma3 were increased in asthma in adults and children alike and linked to a more severe, exacerbating allergic asthma phenotype. In an experimental asthma mouse model, C4Ma3 was dependent on mast cell chymase. Serum C4Ma3 was significantly elevated in cystic fibrosis plus ABPA and at baseline predicted the success of the anti-IgE therapy in allergic, uncontrolled asthmatics (diagnostic OR 31.5). CONCLUSION: C4Ma3 levels depend on lung mast cell chymase and are increased in a severe, exacerbating allergic asthma phenotype. C4Ma3 may serve as a novel biomarker to predict anti-IgE therapy response

More than just a barrier: The immune functions of the airway epithelium in asthma pathogenesis.

Allergic bronchial asthma is a chronic disease of the airways that is characterized by symptoms like respiratory distress, chest tightness, wheezing, productive cough, and acute episodes of broncho-obstruction. This symptom-complex arises on the basis of chronic allergic inflammation of the airway wall. Consequently, the airway epithelium is central to the pathogenesis of this disease, because its multiple abilities directly have an impact on the inflammatory response and thus the formation of the disease. In turn, its structure and functions are markedly impaired by the inflammation. Hence, the airway epithelium represents a sealed, self-cleaning barrier, that prohibits penetration of inhaled allergens, pathogens, and other noxious agents into the body. This barrier is covered with mucus that further contains antimicrobial peptides and antibodies that are either produced or specifically transported by the airway epithelium in order to trap these particles and to remove them from the body by a process called mucociliary clearance. Once this first line of defense of the lung is overcome, airway epithelial cells are the first cells to get in contact with pathogens, to be damaged or infected. Therefore, these cells release a plethora of chemokines and cytokines that not only induce an acute inflammatory reaction but also have an impact on the alignment of the following immune reaction. In case of asthma, all these functions are impaired by the already existing allergic immune response that per se weakens the barrier integrity and self-cleaning abilities of the airway epithelium making it more vulnerable to penetration of allergens as well as of infection by bacteria and viruses. Recent studies indicate that the history of allergy- and pathogen-derived insults can leave some kind of memory in these cells that can be described as imprinting or trained immunity. Thus, the airway epithelium is in the center of processes that lead to formation, progression and acute exacerbation of asthma

Belastungskollektive von Schiffsantriebsanlagen und ihr Einfluss auf die Zuverlaessigkeit - INTACT

SIGLEAvailable from TIB Hannover: RR 9547(99-108),2 / FIZ - Fachinformationszzentrum Karlsruhe / TIB - Technische InformationsbibliothekBundesministerium fuer Bildung und Forschung, Berlin (Germany)DEGerman

Serological neo-epitope extracellular matrix related markers reflecting collagen or elastin degradation are elevated in a mouse model of allergic asthma exacerbation

Asthma is a chronic inflammatory disease, characterized by symptoms including increased mucus production, reversible airway obstruction and lung inflammation: all of which are exaggerated during asthma exacerbations. Extracellular matrix remodeling is associated with the release of ECM protein fragments (neo-epitopes) to the circulation. We sought to investigate the relationship between serological assessment of ECM remodeling markers (neo-epitopes) and the level of symptoms in a mouse model of exacerbated asthma. The hypothesis was, that an increase in ECM remodeling would be observed as a consequence of airway inflammation during exacerbations. Balb/C mice were sensitized to ovalbumin (OVA) (i.p.), acute exacerbations were provoked by i.n. instillation of poly-cytidylic-inosinic acid. Markers of matrix metalloproteinase (MMP) degraded collagen type I (C1M), type III (C3M), type IV (C4M), elastin (ELM7), and laminin (LAMa5) were assessed in serum. Analysis-software: JMP13 (SAS). Serum levels of C1M and LAMa5 individually correlated with bronchoalveolar lavage cells (BAL). Furthermore, the increase of airway resistance (C4M rs = -0.42, p <0.01; C1M, rs -0.55, p <0.001), the absolute airway resistance (C1M, rs = -0.51, p <0.001) and the dynamic compliance (C1M, rs = -0.47, p <0.01), were correlated with the ECM remodeling markers. Additionally, C1M showed a distinct correlation with the amount of mucus producing cells (Pearson coefficient 0.60, p = 0.0006). These data suggest, that serological neo-epitope markers may be valuable tools for objectively assessing the extent of airway remodeling especially during disease aggravation

Distal airways are protected from goblet cell metaplasia by diminished expression of IL-13 signaling components.

BACKGROUND: Increased mucus production is a critical factor impairing lung function in patients suffering from bronchial asthma, the most common chronic inflammatory lung disease worldwide. OBJECTIVE: This study aimed at investigating whether goblet cell (GC) metaplasia and mucus production are differentially regulated in proximal and distal airways. METHODS: Female Balb/c mice were sensitized to ovalbumin (OVA) and challenged with an OVA-aerosol on two consecutive days for one week (acute) or twelve weeks (chronic). Real-time RT-PCR analysis was applied on microdissected airways. RESULTS: In acutely and chronically OVA-challenged mice GC metaplasia and mucus production was observed in proximal but not in distal airways. In contrast, inflammation reflected by the infiltration of eosinophils and expression of the TH2-type cytokines IL-4 and IL-13 was increased in both, proximal and distal airways. Abundance of IL-13R&alpha;1 was lower in distal airways of healthy control mice. Under acute and chronic OVA-exposure, activation of IL-13R&alpha;1-dependent signaling cascade, reflected by Spdef and Foxo3A transcription factors, was attenuated in distal compared to proximal airways. CONCLUSION &amp; CLINICAL RELEVANCE: These data indicate that distal airways might be less sensitive to IL-13 induced GC metaplasia and mucus production through lower expression of IL-13R&alpha;1 and attenuated activation of downstream signaling. This might represent a protective strategy in order to prevent mucus plugging of distal airways and thus, impaired ventilation of attached alveoli

DIgestive COmplications in DIabetes - the DICODI population study

Background Diabetes type 1 and type 2 may develop gastrointestinal complications e.g., gastroparesis and gastroenteropathy. Concomitant celiac disease and pancreatic exocrine insufficiency occur with high prevalence in diabetes and with symptomatic overlap. Consequently, it is a challenge to disentangle symptoms of these conditions and separate them from functional dyspepsia. We aim to develop a clinical decision-support tool to differentiate the underlying disease in a plethora of gastrointestinal symptoms. Methods An internet-based computerized survey will collect basic characteristics (diabetes type, age, gender, duration, HbA1c, treatment) and patient reported outcomes by validated questionnaires focusing on (1) gastroparesis using Gastroparesis Cardinal Symptom Index; (2) gastroenteropathy using Gastrointestinal Symptom Rating Scale; (3) celiac disease using Celiac Symptom Index and (4) pancreatic exocrine insufficiency with Pancreatic Exocrine Insufficiency Questionnaire. Logistic regression and multiple regression analyses will identify risk factors and gastrointestinal complications. Cluster analyses and machine learning will classify different symptoms and co-existing presentations, into a likely diagnosis. We seek biomarkers for autonomic neuropathy by characterizing development of retinopathy using the Visual Function Questionnaire-25 and peripheral neuropathy by the Michigan neuropathy questionnaire. Participants are re-examined yearly for disease progression over time. Results From focus group studies gastrointestinal symptoms are of major concern in diabetes. Potentially, estimates of symptom prevalence, risk factor identification and classifications of gastrointestinal complications can be unraveled for feedback to health care providers. Conclusion The web-based DICODI project will open up possibilities to detect gastrointestinal complications of diabetes in a societal setting, benefitting people living with diabetes, health care professionals, and society