we suggest that no additional diagnostic evaluation need be performed (Grade 2C) .Remark : This recommendation applies only to solid nodules. For guidance about follow-up of subsolid nodules, see Recommendations 6.5.1 to 6.5.4 . 2.3.3.In the individual with an indeterminate nodule that is identifi ed by chest radiography, we recommend that CT of the chest should be performed (preferably with thin sections Objectives: The objective of this article is to update previous evidence-based recommendations for evaluation and management of individuals with solid pulmonary nodules and to generate new recommendations for those with nonsolid nodules. Methods: We updated prior literature reviews, synthesized evidence, and formulated recommendations by using the methods described in the "Methodology for Development of Guidelines for Lung Cancer" in the American College of Chest Physicians Lung Cancer Guidelines, 3rd ed. Results: We formulated recommendations for evaluating solid pulmonary nodules that measure . 8 mm in diameter, solid nodules that measure Յ 8 mm in diameter, and subsolid nodules. The recommendations stress the value of assessing the probability of malignancy, the utility of imaging tests, the need to weigh the benefi ts and harms of different management strategies (nonsurgical biopsy, surgical resection, and surveillance with chest CT imaging), and the importance of eliciting patient preferences. Conclusions: Individuals with pulmonary nodules should be evaluated and managed by estimating the probability of malignancy, performing imaging tests to better characterize the lesions, evaluating the risks associated with various management alternatives, and eliciting their preferences for management. CHEST 2013; 143(5)(Suppl):e93S-e120SAbbreviations: AAH 5 atypical adenomatous hyperplasia; ACCP 5 American College of Chest Physicians; AIS 5 adenocarcinoma in situ; EBUS 5 endobronchial ultrasound; ENB 5 electromagnetic navigation bronchoscopy; FDG 5 fl uorodeoxyglucose; HU 5 Hounsfi eld unit; LR 5 likelihood ratio; SPECT 5 single-photon emission CT; TBB 5 transbronchial biopsy; TTNB 5 transthoracic needle biopsy; VATS 5 video-assisted thoracic surgery; VBN 5 virtual bronchoscopy navigation; VDT 5 volume doubling time
The use of extracorporeal membrane oxygenation (ECMO) for severe acute respiratory failure (ARF) in adults is growing rapidly given recent advances in technology, even though there is controversy regarding the evidence justifying its use. Because ECMO is a complex, high-risk, and costly modality, at present it should be conducted in centers with sufficient experience, volume, and expertise to ensure it is used safely. This position paper represents the consensus opinion of an international group of physicians and associated health-care workers who have expertise in therapeutic modalities used in the treatment of patients with severe ARF, with a focus on ECMO. The aim of this paper is to provide physicians, ECMO center directors and coordinators, hospital directors, health-care organizations, and regional, national, and international policy makers a description of the optimal approach to organizing ECMO programs for ARF in adult patients. Importantly, this will help ensure that ECMO is delivered safely and proficiently, such that future observational and randomized clinical trials assessing this technique may be performed by experienced centers under homogeneous and optimal conditions. Given the need for further evidence, we encourage restraint in the widespread use of ECMO until we have a better appreciation for both the potential clinical applications and the optimal techniques for performing ECMO.
Early detection of metastasis can be aided by circulating tumor cells (CTCs), which also show potential to predict early relapse. Due to the limited CTC numbers in peripheral blood in early stages, we investigated CTCs in pulmonary vein blood accessed during surgical resection of tumors. Pulmonary vein (PV) and peripheral vein (Pe) blood specimens from patients with lung cancer were drawn during the perioperative period and assessed for CTC burden using a microfluidic device. From 108 blood samples analyzed from 36 patients, PV had significantly higher number of CTCs compared to pre-operative Pe (p<0.0001) and intra-operative Pe (p<0.001) blood. CTC clusters with large number of CTCs were observed in 50% of patients, with PV often revealing larger clusters. Long term surveillance indicated that presence of clusters in pre-operative Pe blood predicted a trend toward poor prognosis. Gene expression analysis by RT-qPCR revealed enrichment of p53 signaling and extracellular matrix involvement in PV and Pe samples. Ki67 expression was detected in 62.5% of PV samples and 59.2% of Pe samples, with the majority (72.7%) of patients positive for Ki67 expression in PV having single CTCs as opposed to clusters. Gene ontology analysis revealed enrichment of cell migration and immune-related pathways in CTC clusters, suggesting survival advantage of clusters in circulation. Clusters display characteristics of therapeutic resistance, indicating the aggressive nature of these cells. Thus, CTCs isolated from early stages of lung cancer are predictive of poor prognosis and can be interrogated to determine biomarkers predictive of recurrence.
Background-The use of extracorporeal life support (extracorporeal membrane oxygenation [ECMO]) as a direct bridge to heart transplant in adult patients is associated with poor survival. Similarly, the use of an implantable left ventricular assist device (LVAD) to salvage patients with cardiac arrest, severe hemodynamic instability, and multiorgan failure results in poor outcome. The use of LVAD implant in patients who present with cardiogenic shock who have not been evaluated for transplantation or who have sustained a recent myocardial infarction also raises concerns. ECMO may provide reasonable short-term support to patients with severe hemodynamic instability, permit recovery of multiorgan injury, and allow time to complete a transplant evaluation before long-term circulatory support with an implantable LVAD is instituted. After acquisition of the HeartMate LVAD (Thermo Cardiosystems, Inc), we began using ECMO as a bridge to an implantable LVAD and, subsequently, to transplantation in selected high-risk patients. adult patients who presented with refractory cardiogenic shock (cardiac index Ͻ2.0 L ⅐ min Ϫ1 ⅐ m Ϫ2 , with systolic blood pressure Ͻ100 mm Hg and pulmonary capillary wedge pressure Ն24 mm Hg and dependent on Ն2 inotropes with or without intra-aortic balloon pump) were evaluated and accepted as candidates for mechanical assistance as a bridge to transplant. Of the 32 patients, 14 (group I) had a cardiac arrest or severe hemodynamic instability (systolic blood pressure Յ75 mm Hg) with evidence of multiorgan failure (defined as serum creatinine level Ͼ3 mg/dL or oliguria; international normalized ratio Ͼ1.5 or transaminases Ͼ5 times normal or total bilirubin Ͼ3 mg/dL; and needing mechanical ventilation). Group I patients were placed on ECMO support; 7 underwent subsequent LVAD implant and 1 was bridged directly to transplant. Six patients in group I survived to transplant hospitalization discharge. The remaining 18 patients (group II) underwent LVAD implant without ECMO support; 12 survived to transplant hospitalization discharge and 2 remained alive with ongoing LVAD support and awaited transplant. One-year actuarial survival from the initiation of circulatory support was 43% in group I and 75% in group II. One-year actuarial survival from the time of LVAD implant in group I, conditional on surviving ECMO, was 71% (PϭNS compared with group II). Conclusions-In appropriately selected high-risk patients, the rate of LVAD survival after initial ECMO support was not significantly different from the survival rate after LVAD support alone. An initial period of resuscitation with ECMO is an effective strategy to salvage patients with extreme hemodynamic instability and multiorgan injury. Use of LVAD resources is improved by avoiding LVAD implant in a very-high-risk cohort of patients who do not survive ECMO. (Circulation. 1999;100[suppl II]:II-206 -II-210.)
We employed next generation RNA sequencing analysis to reveal dysregulated long non-coding RNAs (lncRNAs) in lung cancer utilizing 461 lung adenocarcinomas (LUAD) and 156 normal lung tissues from 3 separate institutions. We identified 281 lncRNAs with significant differential-expression between LUAD and normal lung tissue. LINC00857, a top deregulated lncRNAs, was overexpressed in tumors and significantly associated with poor survival in LUAD. knockdown of LINC00857 with siRNAs decreased tumor cell proliferation, colony formation, migration and invasion in vitro, as well as tumor growth in vivo. Overexpression of LINC00857 increased cancer cell proliferation, colony formation and invasion. Mechanistic analyses indicated that LINC00857 mediates tumor progression via cell cycle regulation. Our study highlights the diagnostic/prognostic potential of LINC00857 in LUAD besides delineating the functional and mechanistic aspects of its aberrant disease specific expression and potentially using as a new therapeutic target.
Whole transcriptome analyses of next generation RNA sequencing (RNA-Seq) data from human cancer samples reveled thousands of uncharacterized non-coding RNAs including long non-coding RNA (lncRNA). Recent studies indicated that lncRNAs are emerging as crucial regulators in cancer processes and potentially useful as biomarkers for cancer diagnosis and prognosis. To delineate dysregulated lncRNAs in lung cancer, we analyzed RNA-Seq data from 461 lung adenocarcinomas (LUAD) and 156 normal lung tissues. FAM83H-AS1, one of the top dysregulated lncRNAs, was found to be overexpressed in tumors relative to normal lung and significantly associated with worse patient survival in LUAD. We verified this diagnostic/prognostic potential in an independent cohort of LUAD by qRT-PCR. Cell proliferation, migration and invasion were decreased after FAM83H-AS1 knockdown using siRNAs in lung cancer cells. Flow cytometry analysis indicated the cell cycle was arrested at the G2 phase after FAM83H-AS1 knockdown. Mechanistically, we found that MET/EGFR signaling was regulated by FAM83H-AS1. Our study indicated that FAM83H-AS1 plays an important role in lung tumor progression and may be potentially used as diagnostic/prognostic marker. Further characterization of this lncRNA may provide a novel therapeutic target impacting MET/EGFR signaling.
Prolonged ECMO use for adult respiratory failure was associated with a lower (45.4%) hospital survival rate, compared with prior reported survival rates of short duration ECMO. Prolonged ECMO survival significantly increased in recent years, and increasing ECMO duration did not alter the survival fraction in the 1989 to 2013 study cohort. Although P-ECMO survival rates are less than short ECMO runs, P-ECMO support is justified.
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