Correction to: Determination of the Genetic and Synergistic Suppression of a Methoxyfenozide-Resistant Strain of the House Fly Musca domestica L. (Diptera: Muscidae).

Due to an unfortunate turn of events, the surname of the last author appeared incorrectly in the original publication as the name should have read Binyameen.

Determination of the Genetic and Synergistic Suppression of a Methoxyfenozide-Resistant Strain of the House Fly Musca domestica L. (Diptera: Muscidae).

Musca domestica Linnaeus (house fly, Diptera: Muscidae) is a major veterinary and medical important pest all over the world. These flies have ability to develop resistance to insecticides. The present trial was performed to discover the inheritance mode (autosomal, dominance, number of genes involved) and preliminary mechanism of methoxyfenozide resistance in order to provide basic information necessary to develop resistance management strategy for this pest. A strain of M. domestica (MXY-SEL) was exposed to methoxyfenozide for 44 generations which developed a 5253.90-fold level of resistance to methoxyfenozide. The overlapping fiducial limits of LC50 values of the reciprocal crosses, F1 (MXY-SEL ♂ × Susceptible ♀) and F1† (MXY-SEL ♀ × Susceptible ♂), suggest that inheritance of methoxyfenozide resistance was an autosomal and likely completely dominant trait (DLC = 0.93 and 0.94 for F1 and F1†, respectively). Backcrosses of the F1 with the parental MXY-SEL or Susceptible population predict a polygenic mode of inheritance. Piperonyl butoxide significantly altered the LC50 values, suggesting enhanced detoxification by cytochrome P450-dependent monooxygenases is a major mechanism of resistance to methoxyfenozide in the MXY-SEL strain. The estimated realized heritability was 0.07 for methoxyfenozide. These results would be helpful for the better management of M. domestica.

Protein Quantitative Trait Loci Analysis Identifies Genetic Variation in the Innate Immune Regulator TOLLIP in Post-Lung Transplant Primary Graft Dysfunction Risk.

The authors previously identified plasma plasminogen activator inhibitor-1 (PAI-1) level as a quantitative lung injury biomarker in primary graft dysfunction (PGD). They hypothesized that plasma levels of PAI-1 used as a quantitative trait could facilitate discovery of genetic loci important in PGD pathogenesis. A two-stage cohort study was performed. In stage 1, they tested associations of loci with PAI-1 plasma level using linear modeling. Genotyping was performed using the Illumina CVD Bead Chip v2. Loci meeting a p < 5 × 10(-4) cutoff were carried forward and tested in stage 2 for association with PGD. Two hundred ninety-seven enrollees were evaluated in stage 1. Six loci, associated with PAI-1, were carried forward to stage 2 and evaluated in 728 patients. rs3168046 (Toll interacting protein [TOLLIP]) was significantly associated with PGD (p = 0.006). The increased risk of PGD for carrying at least one copy of this variant was 11.7% (95% confidence interval 4.9-18.5%). The false-positive rate for individuals with this genotype who did not have PGD was 6.1%. Variants in the TOLLIP gene are associated with higher circulating PAI-1 plasma levels and validate for association with clinical PGD. A protein quantitative trait analysis for PGD risk prioritizes genetic variations in TOLLIP and supports a role for Toll-like receptors in PGD pathogenesis.

Objective Estimates Improve Risk Stratification for Primary Graft Dysfunction after Lung Transplantation.

Primary graft dysfunction (PGD) is a major cause of early mortality after lung transplant. We aimed to define objective estimates of PGD risk based on readily available clinical variables, using a prospective study of 11 centers in the Lung Transplant Outcomes Group (LTOG). Derivation included 1255 subjects from 2002 to 2010; with separate validation in 382 subjects accrued from 2011 to 2012. We used logistic regression to identify predictors of grade 3 PGD at 48/72 h, and decision curve methods to assess impact on clinical decisions. 211/1255 subjects in the derivation and 56/382 subjects in the validation developed PGD. We developed three prediction models, where low-risk recipients had a normal BMI (18.5-25 kg/m(2) ), chronic obstructive pulmonary disease/cystic fibrosis, and absent or mild pulmonary hypertension (mPAP<40 mmHg). All others were considered higher-risk. Low-risk recipients had a predicted PGD risk of 4-7%, and high-risk a predicted PGD risk of 15-18%. Adding a donor-smoking lung to a higher-risk recipient significantly increased PGD risk, although risk did not change in low-risk recipients. Validation demonstrated that probability estimates were generally accurate and that models worked best at baseline PGD incidences between 5% and 25%. We conclude that valid estimates of PGD risk can be produced using readily available clinical variables.

Preoperative plasma club (clara) cell secretory protein levels are associated with primary graft dysfunction after lung transplantation.

Inherent recipient factors, including pretransplant diagnosis, obesity and elevated pulmonary pressures, are established primary graft dysfunction (PGD) risks. We evaluated the relationship between preoperative lung injury biomarkers and PGD to gain further mechanistic insight in recipients. We performed a prospective cohort study of recipients in the Lung Transplant Outcomes Group enrolled between 2002 and 2010. Our primary outcome was Grade 3 PGD on Day 2 or 3. We measured preoperative plasma levels of five biomarkers (CC-16, sRAGE, ICAM-1, IL-8 and Protein C) that were previously associated with PGD when measured at the postoperative time point. We used multivariable logistic regression to adjust for potential confounders. Of 714 subjects, 130 (18%) developed PGD. Median CC-16 levels were elevated in subjects with PGD (10.1 vs. 6.0, p<0.001). CC-16 was associated with PGD in nonidiopathic pulmonary fibrosis (non-IPF) subjects (OR for highest quartile of CC-16: 2.87, 95% CI: 1.37, 6.00, p=0.005) but not in subjects with IPF (OR 1.38, 95% CI: 0.43, 4.45, p=0.59). After adjustment, preoperative CC-16 levels remained associated with PGD (OR: 3.03, 95% CI: 1.26, 7.30, p=0.013) in non-IPF subjects. Our study suggests the importance of preexisting airway epithelial injury in PGD. Markers of airway epithelial injury may be helpful in pretransplant risk stratification in specific recipients.

Localization of peripheral pulmonary nodules for thoracoscopic excision: value of CT-guided wire placement.

OBJECTIVE: One of the indications for the rapidly expanding use of thoracoscopic surgery as an alternative to thoracotomy is the excision of peripheral lung nodules. Nodules judged too small or too far from the pleural surface to be seen or palpated during thoracoscopy must be localized beforehand. The purpose of this study was to evaluate the feasibility and effectiveness of percutaneous placement of spring hookwires to localize such nodules before video-assisted thoracoscopy. SUBJECTS AND METHODS: Under CT guidance, 17 nodules in 14 patients were preoperatively localized with the Kopans breast lesion localization system. Three patients who had solitary nodules had thoracoscopic resections for diagnosis because a previous transthoracic needle or transbronchial biopsy had been unsuccessful. Four patients who had lesions less than 8 mm in diameter had thoracoscopic biopsies because transthoracic fine-needle aspiration biopsy was not likely to be diagnostic. Seven patients, who had a total of 10 nodules, had therapeutic wedge resections of either limited metastases or a second bronchogenic carcinoma. Mean nodule diameter was 10 mm (range, 3-20 mm). The mean distance from nodule to costal pleura was 9 mm (range, 0-25 mm). At the end of the procedure, wire placement was confirmed by CT scanning. After thoracoscopy, the surgeons were questioned about the stability and utility of each hookwire localization. RESULTS: In all 17 procedures, a hookwire was placed successfully. In one case, the wire dislodged before thoracoscopy (after a 6-hr preoperative delay and severe bending of the wire during induction of anesthesia). In 16 of the 17 resections, the surgeon thought that thoracoscopic identification of the lesion would not have been possible without hookwire localization. Only one localization, across a major fissure, required placement of a second wire to localize a nodule. Wire-related complications included two instances of serious pain, five cases of clinically insignificant pneumothorax, and one large pneumothorax requiring drainage before a second nodule in the same lung was localized. CT scanning showed presumed local pulmonary hemorrhage in six cases without hemoptysis or hemothorax. CONCLUSION: CT-guided hookwire localization is easily and safely performed and permits thoracoscopic resection of lung nodules, which might otherwise be impossible.

Pulmonary function tests in bronchopleural fistula.

A 53-year-old white man underwent a left pneumonectomy for alveolar cell carcinoma. His postoperative course was complicated by pneumonia. At a follow-up clinic visit, the patient complained of a "roaring sound" during respiration. A follow-up PFT did not show the expected loss of volume (nitrogen washout) from a preoperative PFT, suggesting a bronchopleural fistula. A chest x-ray film and xenon lung scan confirmed the diagnosis. The fistula was surgically repaired.