56,215 research outputs found
Pulmonary complications in patients with hematological disorders: Pathobiological bases and practical approach
No full textPulmonary complications occur in up to 40 to 60% of patients with hematological disorders during the disease course and considerably influence morbidity and mortality. The main factors making the lung a clinically significant targeted organ in these patients may be summarized as follows. In the lung parenchyma a variety of inflammatory cells whose precursors are in the bone marrow pass through, park in, proliferate, and release microbicidal and cytohistotoxic substances. Constitutive parenchymal lung cells (bronchiolar and alveolar epithelial cells, endothelial cells, "interstitial" cells) may be a distinctive target for toxic substances or may have an important part in the inflammatory/reactive and reparative processes after an injury event. Pathogenic agents are allowed to reach the lung very easily through either or both the airways and the vascular bed and accumulate there in large amounts. Inflammatory/immunologic reactions may be particularly weak or, on the contrary strong, in the lungs either spontaneously or due to toxic action of drugs and radiation or to the immunodeficiency induced by hematological disorders, and finally to the presence of immunomodulatory viruses. The distinctive anatomical structure and function of the lung parenchyma (interactions between air spaces and capillary bed-gas exchange units) may render localized parenchymal damage clinically relevant. Allogeneic reactions may be overexpressed in the lung or the kinetics of the developing of graft versus host disease (GVHD)-related lung injury may be markedly different from the kinetics of GVHD in other organs. Hematological disorders may harbor in lung parenchymal structures at the onset (i.e., lympho-/myeloproliferative disorders primary in the lung) or during the disease course. Genetic predisposition, although probably involved, is not yet well understood. This article reviews the pathobiological bases of lung injury occurring in subjects with hematological disorders and suggests a practical diagnostic approach to these pulmonary complications
Clinical guidelines and indications for bronchoalveolar lavage (BAL): extrinsic allergic alveolitis.
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Clinical presentation, outcome and risk factors of late-onset non-infectious pulmonary complication after allogeneic transplantation
No full textThe term late-onset non-infectious pulmonary complications (LONIPCs) has been used to refer to events occurring later than 3 months after allogeneic hematopoietic stem transplant (HSCT), such as bronchiolitis obliterans, bronchiolitis obliterans with organizing pneumonia, and lymphocytic or idiopathic interstitial pneumonia. The incidence of LONIPCs varies widely, ranging between 10% and 26%. Median time for LONIPC development is about 8-12 months after HSCT. Clinical symptoms may be insidious and non specific at the beginning and can be present in different types of infections. The diagnosis is made on the basis of thoracic high-resolution computed tomography and pulmonary function tests (PFT). It usually requires that standard cultures for infective agents on bronchoalveolar lavage are negative and is confirmed by transbronchial or lung biopsy, whenever possible. Total body irradiation and high doses of drugs used in the conditioning regimens , HLA disparity between donor and recipient, and chronic graft-versus-host disease (GVHD) are the main risk factors for LONIPCs. Since patients with LONIPCs have an increased risk of mortality because of infections or respiratory failure, pre- and post-transplant PFTs are strongly recommended in order to timely identify affected patients. The administration of antithymocyte globulin before unrelated donor transplants and slow taper of cyclosporine after transplant have been shown to prevent chronic GVHD and, therefore, the occurrence of LONIPC
Hot of the breath: mortality as a primary end-point in IPF treatment trials: the best is the enemy of the good
No full textComment in "Idiopathic pulmonary fibrosis: is all-cause mortality a practical and realistic end-point for clinical trials?" [Thorax. 2013
A Dynamic Subfilter-scale Stress Model for Large Eddy Simulations Based on Physical Flow Scales
No full textWe propose a new definition of the length scale in an eddy-viscosity model for large-eddy simulations (LES). This formulation extends and generalizes a previous proposal [Piomelli, Rouhi and Geurts, Proc. ETMM10, 2014], in which the LES length scale was expressed in terms of the integral length-scale of turbulence determined by the flow characteristics and explicitly decoupled from the simulation grid; this approach was named Integral Length-Scale Approximation (ILSA). As in the original ILSA, the model coefficient was determined by the user, and required to maintain a desired contribution of the unresolved, subfilter scales (SFS) to the global transport. We propose a local formulation (local ILSA) in which the model coefficient is local in space, allowing a precise control over SFS activity as a function of location. This new formulation preserves the properties of the global model; application to channel flow and backward-facing step verifies its features and accuracy
Large-eddy simulation of a separated flow with a sub-filter scale model based on the integral length-scale
No full textA new sub-filter scale model for large-eddy simulations, which uses a length-scale proportional to the integral scale of the turbulence instead of the grid resolution to parametrize the modelled stresses, will be assessed in the prediction of the flow of a boundary-layer over a rough surface, which includes separation and reattachment
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