Cuntz-Pimsner C*-algebras associated with subshifts

By using C*-correspondences and Cuntz-Pimsner algebras, we associate to every subshift (also called a shift space) $X$ a C*-algebra $O_X$, which is a generalization of the Cuntz-Krieger algebras. We show that $O_X$ is the universal C*-algebra generated by partial isometries satisfying relations given by $X$. We also show that $O_X$ is a one-sided conjugacy invariant of $X$.Comment: 28 pages. This is a slightly updated version of a preprint from 2004. Submitted for publication. In version 2 the Introduction has been changed, two remarks (Remark 7.6 and 7.7) have been added and the list of references has been update

Inhaled nebulized adrenaline improves lung function in infants with acute bronchiolitis

Abstractβ2-agonists have questionable symptomatic effect in infants with acute bronchiolitis, whereas inhaled, nebulized racemic adrenaline, commonly used in Norway, appears (clinically) to be effective. Limited lung function observations during acute bronchiolitis exists, and less for assessing possible effects inhaled adrenaline.In this preliminary study, tidal flow-volume loops were measured in 16 infants with acute bronchiolitis and seven healthy controls (mean age 7·9 and 4·4 months, respectively), with repeated measurements 15 min after inhaled nebulized racemic adrenaline (4 mg diluted in 2 ml saline) in nine bronchiolitis patients.The ratio of time to reach peak tidal expiratory flow to total expiratory time (tPTEF/tE) was significantly reduced in children with acute bronchiolitis (mean, 95% CI) (0·08, 0·05–0·10) compared to controls (0·31, 0·18–0·43), with significant improvement after inhaled racemic adrenaline 0·19 (0·13–0·25), parallel with significant clinical improvement.Lung function (tPTEF/tE) was reduced in infants with acute bronchiolitis and improved significantly after inhaled racemic adrenaline. Inhaled racemic adrenaline is potentially an important alternative for treating infants with acute bronchiolitis

Lung function in children with Duchenne's muscular dystrophy

AbstractDuchenne's muscular dystrophy (DMD), characterized by gradually developing muscular weakness, leads to respiratory symptoms and reduced lung function. We aimed to assess lung function in 25 patients with DMD in relationship to age and muscular function. The 25 boys, mean age 13 years, comprized patients in southern Norway with DMD, taking part in an epidemiological follow-up study. None had chronic respiratory disease. Lung function was measured by maximum expiratory flow–volume loops and whole body plethysmography, and repeated after 1 year (n=14). Lung function was reduced compared to predicted values for healthy children. Forced expiratory volume in 1 sec (FEV1)% predicted and forced vital capacity (FVC)% predicted correlated (significantly) inversely to age. FEV1and FVC decreased annually 5·61 and 4·2% of predicted, respectively. Absolute values of FVC (litres) and FEV1(l sec−1) increased until mean age 14 years, decreasing thereafter. Values in % predicted decreased steadily throughout the age range (6–19 years). Lung function correlated closely to upper limb muscle function

A new "breath" from the European Respiratory Society School

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Influence of renal transplantation and living kidney donation on large artery stiffness and peripheral vascular resistance

BACKGROUND: Vascular status following renal transplantation (RT) may improve while living kidney donation (LKD) is possibly associated with an increased cardiovascular risk. METHODS: We prospectively assessed glomerular filtration rate (mGFR, 51Chrome EDTA clearance) and intermediate vascular risk factors in terms of blood pressure (BP), pulse wave velocity (PWV), central augmentation index (AIx), excess pressure (Pexcess) and forearm vascular resistance in donors (n=58, 45±13 years) and recipients (n=51, 50±12 years) before and one year following LKD or RT. RESULTS: After kidney donation mGFR decreased by 33% to 65±11 ml/min/1.73m2 while recipients obtained a mGFR of 55±9 ml/min/1.73m2. Ambulatory 24-hour mean BP (MAP) remained unchanged in donors but decreased by 5 mmHg in recipients (P<0.05). Carotid-femoral PWV increased by 0.3 m/s in donors (P<0.05) but remained unchanged in recipients. AIx was unaltered after LKD but decreased following RT (P<0.01) while Pexcess did not change in either group. Resting forearm resistance (Rrest), measured by venous occlusion plethysmography, increased after LKD (P<0.05) but was unaffected by RT, while no changes were seen in minimum resistance (Rmin). ΔPWV showed a positive linear association to Δ24-hour MAP in both groups. Multiple linear regression analysis (adjusting for age, gender and the baseline value of the studied parameter) did not detect independent effects of graft function on 24-hour MAP, PWV, AIx, vascular resistance or Pexcess, whereas low post-donation GFR was related to higher AIx and Rrest. CONCLUSIONS: RT reduced BP and AIx without affecting PWV whereas LKD resulted in increased PVW and Rrest, despite unchanged BP

Hyperactivation of NF-κB via the MEK signaling is indispensable for the inhibitory effect of cAMP on DNA damage-induced cell death

With cAMP signaling having a profound inhibitory effect on DNA damage-induced apoptosis in B-cell precursor acute lymphoblastic leukemia (BCP-ALL) cells, understanding how this signaling pathway affects the survival capacity of the cell has important implications for cancer therapy. We have recently shown that p53 is critical for the inhibitory effect of cAMP on genotoxic agents-mediated apoptosis in BCP-ALLs. Here, we show that elevation of cAMP levels in cells exposed to DNA damage enhances the nuclear translocation and DNA binding of NF-κB by accelerating the phosphorylation of IKKβ and thereby phosphorylation and degradation of IκBα. Furthermore, we show that the ability of cAMP to potentiate the ionizing radiation-induced activation of NF-κB requires the activity of MEK. Importantly, pharmacological or genetic ablation of NF-κB reversed the inhibitory effect of cAMP on DNA damage-induced apoptosis, demonstrating that, in addition to p53, cAMP relies on the activity of NF-κB to provide cells with a survival advantage in the face of DNA damage. Collectively, our results uncover a novel and important interaction between the cAMP and NF-κB pathways that may have implications for the targeted treatment of lymphoid malignancies, such as BCP-ALL, in which aberrant NF-κB activity functions as a driving force for treatment resistance