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Background: There are "blind spots" on chest computed tomography (CT) where pulmonary nodules can easily be overlooked. The number of missed pulmonary nodules can be minimized by instituting a training program with particular focus on the depiction of nodules at blind spots., Purpose: The purpose of this study was to assess the variation in lung nodule detection in chest CT based on location, attenuation characteristics, and reader experience., Materials and Methods: We selected 18 noncalcified lung nodules (6-8 mm) suspicious of primary and metastatic lung cancer with solid (n = 7), pure ground-glass (6), and part-solid ground-glass (5) attenuation from 12 chest CT scans. These nodules were randomly inserted in chest CT of 34 patients in lung hila, 1 st costochondral junction, branching vessels, paramediastinal lungs, lung apices, juxta-diaphragm, and middle and outer thirds of the lungs. Two residents and two chest imaging clinical fellows evaluated the CT images twice, over a 4-month interval. Before the second reading session, the readers were trained and made aware of the potential blind spots. Chi-square test was used to assess statistical significance., Results: Pretraining session: Fellows detected significantly more part-solid ground-glass nodules compared to residents (P = 0.008). A substantial number of nodules adjacent to branching vessels and posterior mediastinum were missed. Posttraining session: There was a significant increase in detectability independent of attenuation and location of nodules for all readers (P < 0.0008)., Conclusion: Dedicated chest CT training improves detection of lung nodules, especially the part-solid ground-glass nodules. Detection of nodules adjacent to branching vessels and the posterior mediastinal lungs is difficult even for fellowship-trained radiologists.

Background: Aortic valve calcification severity has been associated with higher rates of aortic regurgitation (AR) following TAVR, but scarce data exist on its impact with the use of newer generation transcatheter heart valves., Methods: This was a multicenter study including 626 patients with severe aortic stenosis who underwent TAVR with the SAPIEN 3 valve. Patients were divided in 2 groups according to the median index calcium score (iCS) for each sex: high CS (HCS, iCS ≥ median), and low iCS (LCS, iCS < median). Another analysis was performed in those patients with extreme iCS (ECS, iCS >75th percentile for each sex). Clinical and echocardiographic data were collected prospectively in a dedicated database., Results: The mean CS was 3758 ± 1417 AU and 1616 ± 691 AU in the HCS and LCS groups, respectively (p < 0.001). There were no differences between groups in 30-day mortality (HCS:2.6%, LCS:1.0%, p = 0.13) and stroke (HCS:2.6%,LCS:2.6%, p = 1.0) rates, but all cases (n = 5) of annulus rupture occurred in the HCS group (1.6% vs. 0%, p = 0.061). The incidence of moderate-severe AR post-TAVR was low in both groups (HCS:1.6%,LCS:1.6%, p = 1.0), and valve gradient and area were similar between groups. The results remained similar in the ECS group (mean CS:4607 ± 1424 AU), but a mildly increased mean transvalvular gradient post-TAVR was observed in ECS patients (12.1 ± 5.6 vs 11.0 ± 4.3 mmHg; p = 0.015)., Conclusion: Aortic valve calcification severity failed to impact mortality/stroke rates following TAVR with the SAPIEN 3 valve. Low rates of significant AR were observed irrespective of CS, and a mild increase in transvalvular gradient was observed in ECS patients., Competing Interests: Declaration of competing interest Dr. Rodés-Cabau has received institutional research grants from Edwards Lifesciences. The other authors have not reported any potential conflict of interest with respect to the content of this paper., (Copyright © 2020 Elsevier B.V. All rights reserved.)

Background: Inherited mutations in SERPINA1 coding for the alpha-1 antitrypsin (A1AT) protein is the only well established cause of hereditary emphysema. We aimed to identify the genetic ecause of early-onset emphysema in a five-generation French-Canadian family free of A1AT deficiency., Methods: Between Dec 1, 2014, and April 1, 2017, we investigated 63 individuals from a single pedigree, including 55 with DNA available. Whole-exome sequencing was done in a convenience sample of 14 individuals (nine with unambiguous expression of the typical form of emphysema observed in this family). We filtered rare non-synonymous variants that were predicted to be damaging to identify a single mutation in a biologically relevant gene shared among all affected individuals. We assessed segregation with the disease in additional family members who were not evaluated by whole-exome sequencing. The effect of the candidate variant on protein function was evaluated in vitro. mRNA and protein expression of the candidate gene was assessed in lung samples from unrelated individuals (n=80) with and without emphysema who underwent surgery for lung cancer at our institution., Findings: A rare in-silico-predicted damaging variant (Ala455Thr) was identified in the protein tyrosine phosphatase non-receptor type 6 (PTPN6) gene, also known as SHP-1, an important negative regulator of immune processes. 20 (95%) of 21 family members with computed tomography-confirmed emphysema were heterozygotes for the Ala455Thr mutation. No Thr455 homozygotes were identified. Emphysema or reduced diffusion capacity was observed in all heterozygotes with a history of smoking. Incomplete penetrance of the mutation and variable degrees of emphysema were observed in never smokers. The Ala455Thr mutation in SHP-1 caused a reduction in phosphatase activity in vitro, confirming the loss-of-function effect of the mutation. mRNA and protein expression of PTPN6 were upregulated in smokers, but were not associated with emphysema or severity of airflow limitation., Interpretation: An inherited variant in the gene PTPN6 is responsible for early-onset emphysema in this family. To our knowledge, this is the second form of hereditary emphysema since the discovery of A1AT deficiency in the 1960s, representing a breakthrough in understanding the genetics and pathogenesis of emphysema., Funding: Fonds sur les maladies respiratoires J.-D. Bégin-P.-H. Lavoie de l'Université Laval, Fondation de l'Institut universitaire de cardiologie et de pneumologie de Québec, CIHR/GSK research Chair on COPD at Université Laval, and the Canadian Institutes of Health Research., (Copyright © 2019 Elsevier Ltd. All rights reserved.)

We report the case of a 47-year-old woman whose primary mediastinal leiomyoma was incidentally found during evaluation of her persistent cough. The preoperative diagnosis of mediastinal leiomyoma is challenging because of its rarity and indeterminate features on chest radiography, computed tomography (CT), and positron emission tomography-CT. We highlight how magnetic resonance imaging can substantially contribute to mediastinal mass characterization and diagnostic specificity., (Copyright © 2016 The Society of Thoracic Surgeons. Published by Elsevier Inc. All rights reserved.)

Acute dyspnea is a common presenting complaint in the Emergency Room. Evaluation with chest radiography is vital for initial assessment and may reveal diffuse parenchymal abnormalities that require further assessment with computed tomography (CT). The aim of this review is to outline a pattern-based approach for the analysis of diffuse pulmonary abnormalities in an acutely dyspneic patient with emphasis on CT appearances. Specific disease entities may be differentiated by their distribution in the lungs and by their radiologic findings. Recognition of the predominant finding and its distribution can generate an appropriate differential diagnosis that is further refined by the presence or absence of ancillary findings. Incorporation of the clinical history, laboratory data, and prior studies narrows the differential diagnosis, indicates the optimum modality for further evaluation, and, in some situations, provides important prognostic data.

Objectives: Benign prostatic hyperplasia and prostate cancer are important public health issues. However, histologic markers for these diseases are limited., Methods: Immunocytochemistry was used to analyze the cellular localization of AIbZIP, Cdc47, androgen receptor and estrogen receptor-beta markers. AIbZIP is a protein recently found to be more abundant in prostate cancer than in benign prostatic tissue, and Cdc47 is a cell proliferation-associated protein. The localization and modulation of androgen receptor and estrogen receptor-beta through the carcinogenesis process have been examined in several studies but controversial results were obtained. These four proteins were evaluated as potential markers of prostatic diseases in 210 needle core biopsies, including normal prostate, benign prostatic hyperplasia, low-grade and high-grade prostatic intraepithelial neoplasia, and different Gleason grades of prostatic adenocarcinoma., Results: Androgen receptor and estrogen receptor-beta do not discriminate between benign and malignant specimens, while AIbZIP was able to distinguish between them. Cdc47, in contrast, discriminated not only between malignant and benign prostatic tissue, but also between benign prostatic hyperplasia and normal prostatic tissue., Conclusions: Cdc47 appears to be a sensitive marker of prostatic diseases since its expression gradually increased in parallel with the severity of the lesion. AIbZIP discriminated between benign tissue and cancer. AIbZIP and Cdc47 thus appear to be useful markers with diagnostic and prognostic values.