In this study, we have proposed b-scale-based binary classification approach for automatic TIB pattern detection and quantification from chest CTs. The proposed system integrates 1) fast localization of candidate TIB patterns through b-scale filtering and scale selection, and 2) combined shape and textural features to identify TIB patterns. Note that texture-based recognition methods offer a complementary view to shape-based methods; therefore, the integration of spatial information and the proposed shape features achieves high detection rates. Moreover, our proposed local shape features illustrate the usefulness of the invariant properties, Willmore energy in particular, to analyze TIB patterns in chest CT. We have also compared computer scoring of the proposed CAD system with subjective visual grading. A high correlation between objective (CAD) and subjective (visual grading) scores is obtained, which implies highly satisfactory accuracy of the proposed CAD system. Mannose-binding lectin deficiency and acute exacerbations of chronic obstructive pulmonary disease BACKGROUND: Mannose-binding lectin is a collectin involved in host defense against infection. Whether mannose-binding lectin deficiency is associated with acute exacerbations of chronic obstructive pulmonary disease is debated. METHODS: Participants in a study designed to determine if azithromycin taken daily for one year decreased acute exacerbations had serum mannose-binding lectin concentrations measured at the time of enrollment. RESULTS: Samples were obtained from 1037 subjects (91%) in the trial. The prevalence of mannose-binding lectin deficiency ranged from 0.5% to 52.2%, depending on how deficiency was defined. No differences in the prevalence of deficiency were observed with respect to any demographic variable assessed, and no differences were observed in time to first exacerbation, rate of exacerbations, or percentage of subjects requiring hospitalization for exacerbations in those with deficiency versus those without, regardless of how deficiency was defined. CONCLUSION: In a large sample of subjects with chronic obstructive pulmonary disease selected for having an increased risk of experiencing an acute exacerbation of chronic obstructive pulmonary disease, only 1.9% had mannose-binding lectin concentrations below the normal range and we found no association between mannose-binding lectin concentrations and time to first acute exacerbation or frequency of acute exacerbations during one year of prospective follow-up. Mannose-binding lectin (MBL) is a pattern-recognition collectin that is related to surfactant proteins A and D and has two roles in host defense. MBL activates complement via serine proteases, particularly MBL-associated serine protease-2, with which it circulates. 1,2 MBL is also involved in opsonophagocytosis, binding several types of pathogens to phagocytes via its carbohydrate recognition domain, triggering release of a number of proinflammatory cytokines [3] [4] [5] and facilitating clearance of apoptotic cells. 6 MBL is secreted primarily by the liver and circulates in the serum. Low MBL concentrations occur as a result of one of three single nucleotide polymorphisms on exon 1, but the most common cause of deficiency in Caucasians is the LXP haplotype resulting from polymorphisms of the promoter region of the gene, presenting either as a homozygous mutation or in combination with other haplotypes. [7] [8] [9] Several observations suggest that MBL deficiency may compromise host defense in the lungs. MBL binds to carbohydrates on the surface of a number of respiratory pathogens that are associated with acute exacerbations of chronic obstructive pulmonary disease (COPD), including Haemophilus influenzae, 10, 11 Mycoplasma pneumoniae, 12 and influenza. 13 Patients with cystic fibrosis and low MBL concentrations have decreased lung function, an increased prevalence of Burkholderia cepacia infection, and reduced survival relative to patients with cystic fibrosis and normal MBL concentrations. The difference in survival is particularly notable in those with chronic Pseudomonas aeruginosa infection and those with homozygous mutations in the MBL-2 gene. [14] [15] [16] [17] Low MBL concentrations have been associated with an increased risk of respiratory infections in immunocompetent subjects, [18] [19] [20] [21] with an increased frequency of respiratory syncytial virus infections, 22 and with worse outcomes in patients with community-acquired pneumonia and Streptococcus pneumoniae infections. [23] [24] [25] [26] MBL concentrations in bronchoalveolar lavage fluid obtained from a small number of current and former smokers with COPD are lower than those in fluid from healthy controls and tend to be higher in former smokers than in current smokers, 27, 28 but no association has been found between genotypes producing low MBL concentrations and the prevalence of COPD. 29 However, studies assessing the association of low MBL concentrations with acute exacerbations of COPD (AECOPDs) report conflicting results. [30] [31] [32] Accordingly, we prospectively measured MBL concentrations in a large cohort of subjects with COPD who were at increased risk of experiencing acute exacerbations and followed them for one year while tracking the number of acute exacerbations that occurred. Our hypothesis was that subjects with COPD who had an increased risk of experiencing an AECOPD would have more frequent acute exacerbations during one year of follow-up if they were deficient in MBL than if they were not.