Ninety-Day Mortality: Redefining the Perioperative Period After Lung Resection.

Operative mortality is an important outcome for patients, surgeons, healthcare institutions, and policy makers. Although measures of perioperative mortality have conventionally been limited to in-hospital and 30-day mortality (or a composite endpoint combining both), there is a large body of evidence emerging to support the extension of the perioperative period after lung resection to a minimum of 90 days after surgery. Several large-volume studies from centers across the world have reported that 90-day mortality after lung resection is double 30-day mortality.

Evaluation of a Powered Vascular Stapler in Video-Assisted Thoracic Surgery Lobectomy.

Background: A narrow-profile powered vascular stapler (PVS) was developed to provide superior access and precise staple placement in thoracic procedures. The objective of this study was to determine if the PVS would yield an equivalent rate of hemostatic interventions compared with standard of care (SOC) staplers in video-assisted thoracoscopic surgery lobectomy.

Materials And Methods: A randomized, controlled, multicenter study was conducted comparing PVS with SOC staplers in lobectomies performed for non-small cell lung cancer.

Does induction chemoradiotherapy increase survival in patients with Pancoast tumour?

A best evidence topic in cardiothoracic surgery was written according to a structured protocol. The question addressed was whether induction (neoadjuvant) chemoradiotherapy (iCRT) compared with other therapeutic strategies improves survival in patients with Pancoast tumours. Altogether 248 papers were identified using the below-mentioned search.

Metastatic index of non-small-cell lung cancer and long-term survival.

Aim: We aimed to determine whether metastatic index is a factor determining long-term survival in patients undergoing curative resection for non-small-cell lung cancer.

Methods: There were 2695 consecutive pulmonary resections performed between October 2001 and September 2011 in our institution; 1795 were potentially curative resections for non-small-cell lung cancer with bronchial margin length data available. Benchmarking against the International Association for the Study of Lung Cancer data set was performed.

Prediction of in-hospital mortality following pulmonary resections: improving on current risk models.

Objectives: Using a large, prospectively collected and independently validated thoracic database, we created a risk-prediction tool for in-hospital mortality with the aim of improving on the accuracy of Thoracoscore.

Methods: A prospectively collected and independently validated database containing lung resections was utilized, N = 2574. Logistic regression analysis with bootstrapping, and by the use of a random training and test set was utilized.

Lung cancer staging: a physiological update.

The tumour-node metastasis (TNM) classification system is anatomically based. We investigated whether the addition of simple physiological variables, age and body mass index (BMI), would affect survival curves, i.e.

The Norwood procedure using a right ventricle-pulmonary artery conduit: comparison of the right-sided versus left-sided conduit position.

Objective: We proposed that a right-sided right ventricle-pulmonary artery conduit during the stage I Norwood procedure would facilitate pulmonary artery reconstruction during the stage II procedure.

Methods: Between 2002 and 2006, 153 patients underwent Norwood stage I reconstruction with a right ventricle-pulmonary artery conduit (125 in the right-sided group and 28 in the left-sided group). The previous 150 consecutive classic Norwood procedures (1997-2002) were used as a control group.

Alveolar macrophage secretory products effect type 2 pneumocytes undergoing hypoxia-reoxygenation.

Background: Activation of the alveolar macrophage is centrally important to the development of lung ischemia reperfusion injury. Alveolar macrophages and type 2 pneumocytes secrete a variety of proinflammatory mediators in response to oxidative stress. The manner in which they interact and how the macrophage may influence pneumocyte responses in lung ischemia reperfusion injury is unknown.

A comparison of phylogenetic network methods using computer simulation.

Background: We present a series of simulation studies that explore the relative performance of several phylogenetic network approaches (statistical parsimony, split decomposition, union of maximum parsimony trees, neighbor-net, simulated history recombination upper bound, median-joining, reduced median joining and minimum spanning network) compared to standard tree approaches, (neighbor-joining and maximum parsimony) in the presence and absence of recombination.

Principal Findings: In the absence of recombination, all methods recovered the correct topology and branch lengths nearly all of the time when the substitution rate was low, except for minimum spanning networks, which did considerably worse. At a higher substitution rate, maximum parsimony and union of maximum parsimony trees were the most accurate.

Poly (ADP) ribose synthetase inhibition in alveolar macrophages undergoing hypoxia and reoxygenation.

Background: Inhibition of the nuclear enzyme poly ribose synthetase (PARS) protects against in vivo lung ischemia reperfusion injury (LIRI). The effectiveness of intratracheal treatment suggests that PARS inhibition may primarily modulate alveolar macrophage (AM) activation. These studies attempted to characterize the effects of PARS on AM activation in response to oxidative stress.

Poly (ADP) ribose polymerase inhibition improves rat cardiac allograft survival.

Background: Heart transplantation is an accepted treatment modality for end-stage heart failure. However, acute cellular rejection (ACR) continues to be a morbid complication. Recently a novel mechanism of inflammatory allograft injury has been characterized which involves overactivation of the nuclear enzyme poly (ADP-ribose) polymerase (PARP).

Role of poly (ADP) ribose synthetase in lung ischemia-reperfusion injury.

Background: The activation of poly (adenosine diphosphate) ribose synthetase (PARS) is known to be important in the cellular response to oxidative stress. Previous studies have reported that PARS inhibition confers protection in models of endotoxic shock and ischemia-reperfusion. The purpose of this study was to determine the role of PARS inhibition in lung ischemia-reperfusion injury (LIRI).

Poly (ADP) ribose synthetase inhibition reduces obliterative airway disease in rat tracheal allografts.

Background: Obliterative bronchiolitis (OB) is the major long-term complication affecting lung transplant recipients, and is characterized pathologically by chronic inflammatory and fibroproliferative airway disease. Based on studies revealing anti-inflammatory and anti-apoptotic properties of poly (ADP)-ribose synthetase (PARS) inhibitors, we hypothesized that their administration would be protective in a heterotopic model of experimental OB.

Methods: We transplanted rat tracheas from Brown-Norway donors into Lewis recipients, and treated 2 groups with a novel PARS inhibitor, INO-1001.

FR167653 reduces obliterative airway disease in rats.

Background: Obliterative bronchiolitis (OB) is the main cause of late mortality among long-term survivors of lung transplantation. Although p38 kinase is functional in multiple acute inflammatory injury models, its role in chronic lung rejection is undefined. p38 regulates the expression of the cytokines tumor necrosis (TNF)-alpha and interleukin (IL)-1beta, 2 mediators involved in the development of OB in a tracheal transplant model.

Intratracheal poly (ADP) ribose synthetase inhibition ameliorates lung ischemia reperfusion injury.

Background: We previously demonstrated that intravenous poly (ADP) ribose synthetase (PARS) inhibition protects against experimental lung ischemia reperfusion injury (LIRI) in an in situ, hilar occlusion model. This study determined its efficacy when administered intratracheally (IT).

Methods: Left lungs of rats were rendered ischemic for 90 minutes, and reperfused for up to 4 hours.

Alpha chemokines regulate direct lung ischemia-reperfusion injury.

Background: Alpha chemokines function predominantly to recruit and activate neutrophils, which are important effectors of acute lung injury. This study evaluated whether blockade of 2 potent alpha chemokines, macrophage inflammatory protein-2 (MIP-2) and cytokine-induced neutrophil chemoattractant (CINC), is protective against lung ischemia-reperfusion injury in a warm in situ hilar clamp model.

Methods: Left lungs of Long-Evans rats underwent normothermic ischemia for 90 minutes and reperfusion for up to 4 hours.

Early tumor necrosis factor-alpha release from the pulmonary macrophage in lung ischemia-reperfusion injury.

Objective: Tumor necrosis factor-alpha is a proinflammatory mediator required for the development of experimental lung ischemia-reperfusion injury. The alveolar macrophage is a rich source of tumor necrosis factor-alpha in multiple models of acute lung injury. The present study was undertaken to determine whether the alveolar macrophage is an important source of tumor necrosis factor-alpha in lung ischemia-reperfusion injury and whether suppression of its function protects against injury.

Beta-chemokine function in experimental lung ischemia-reperfusion injury.

Background: Although chemokines are functionally important in models of ischemia-reperfusion injury, little is known about their role in lung ischemia-reperfusion injury (LIRI). This study examined the role of the beta-chemokines, macrophage inflammatory protein (MIP)-1alpha, monocyte chemoattractant protein (MCP)-1, and regulated upon activation normal T cells expressed and secreted (RANTES) in LIRI.

Methods: Left lungs of Long-Evans rats underwent normothermic ischemia for 90 minutes and reperfusion for up to 4 hours.

Proinflammatory response of alveolar type II pneumocytes to in vitro hypoxia and reoxygenation.

Type II pneumocytes (T2P) are integral in preserving the integrity of the alveolar space by modulating the fluid composition surrounding the alveolar epithelium. There is also mounting evidence supporting their contribution to the development of acute inflammatory lung injury subsequent to oxidative stress. This study characterized the response of T2P to in vitro hypoxia and reoxygenation (H&R).

Endotracheal calcineurin inhibition ameliorates injury in an experimental model of lung ischemia-reperfusion.

Objectives: We previously demonstrated that calcineurin inhibitors given intravenously ameliorate experimental lung ischemia-reperfusion injury. This study evaluates whether these effects can be achieved when these agents are delivered endotracheally.

Methods: Left lungs of Long Evans rats were rendered ischemic for 90 minutes and reperfused for up to 4 hours.

Novel broad-spectrum chemokine inhibitor protects against lung ischemia-reperfusion injury.

Background: Functional roles for chemokines have been demonstrated in several models of ischemia-reperfusion injury. The redundancy inherent to chemokine pathways makes administration of neutralizing antibodies to any single chemokine ineffective in ameliorating injury. This study was undertaken to define the pattern of chemokine expression in lung ischemia-reperfusion injury (LIRI), and to determine whether a broad-spectrum chemokine inhibitor, NR58-3.

The role of the beta chemokines in experimental obliterative bronchiolitis.

Beta chemokines have been implicated in cardiac and renal allograft rejection. This study determined if antibody antagonization of beta chemokines conferred protection against the development of experimental obliterative bronchiolitis (OB) in a heterotopic rat tracheal allograft model. Rat tracheas were transplanted from Brown-Norway or Lewis donors into Lewis recipients.

Chemokine response of pulmonary artery endothelial cells to hypoxia and reoxygenation.

Background: Chemokines are inflammatory mediators that activate and recruit specific leukocyte subpopulations. We have recently shown a role for certain chemokines in a warm in situ rat model of lung ischemia reperfusion injury. After hypoxic stress, rat pulmonary artery endothelial cells (RPAECS) potentiate and direct neutrophil sequestration, and, therefore, contribute to the development of tissue injury.

Simvastatin ameliorates injury in an experimental model of lung ischemia-reperfusion.

Objectives: Statins are lipid-lowering drugs with anti-inflammatory and antioxidant properties. This study explores the potential of these commonly prescribed agents to ameliorate lung ischemia-reperfusion injury.

Methods: Left lungs of Long-Evans rats were rendered ischemic for 90 minutes and reperfused for up to 4 hours.