Asymptotic consistency under large entropy sampling designs with unequal probabilities

A large part of survey sampling literature is devoted to unequal probabilities sampling designs without replacement. Brewer and Hanif (1983) provided a summary of these sampling designs. The maximum entropy designs is one of them. Consistency results have been proven for the maximum entropy sampling (Hájek, 1964). The aim is to give sufficient conditions under which Hájek (1964) consistency results still hold for large entropy sampling designs which are different from the maximum entropy design. These conditions involve modes of convergence of sampling designs towards the maximum entropy design. We show that these conditions are satisfied for the popular Rao-Sampford (Rao, 1965, Sampford, 1967) design. Our consistency results are applied to the Hájek (1964) simple variance estimator. This estimator does not require joint-inclusion probabilities and can be easily estimated using weighted least squares regression (Berger, 2004, 2005b). Deville (1999) conjectured that this estimator is suitable for any sampling designs (see also Brewer and Donadio, 2003). Our consistency result gives regularity conditions under which this estimator is consistent which justifies Deville’s (1999) conjecture

Variance estimation for measures of change in probability sampling

We propose to estimate the design variance of absolute changes between two cross-sectional estimators under rotating sampling schemes. We show that the variance estimator proposed is generally positive. We also propose possible extensions for stratified samples, with dynamic stratification; that is, when units move between strata and new strata are created at the second waves

A simple variance estimator for unequal probability sampling without replacement

Survey sampling textbooks often refer to the Sen-Yates-Grundy variance estimator for use with without replacement unequal probability designs. This estimator is rarely implemented, because of the complexity of determining joint inclusion probabilities. In practice, the variance is usually estimated by simpler variance estimators such as the Hansen-Hurwitz with replacement variance estimator; which often leads to overestimation of the variance for large sampling fraction that are common in business surveys. We will consider an alternative estimator: the Hájek (1964) variance estimator that depends on the first-order inclusion probabilities only and is usually more accurate than the Hansen-Hurwitz estimator. We review this estimator and show its practical value. We propose a simple alternative expression; which is as simple as the Hansen-Hurwitz estimator. We also show how the Hájek estimator can be easily implemented with standard statistical packages

Empirical likelihood confidence intervals and significance test for regression parameters under complex sampling designs

Confidence intervals based on ordinary least squares may have poor coverages for regression parameters when the effect of sampling design is ignored. Standard confidence intervals based on design variances may not have the right coverages when the sampling distribution is skewed. Berger and De La Riva Torres (2012) proposed an empirical likelihood approach which can be used for point estimation and to construct confidence intervals under complex sampling designs for a single parameter. We show that this approach can be extended to test the significance of a subset of model parameters and to derive confidence intervals. The proposed approach is not a straightforward extension of Berger and De La Riva Torres (2012) approach, because we consider the situation when the parameter is multidimensional and the parameter of interest is a subset of the parameter. This requires profiling which is not covered by Berger and De La Riva Torres (2012). The proposed approach intrinsically incorporates sampling weights, design variables, and auxiliary information. It may yield to more accurate confidence intervals when the sampling distribution of the regression parameters is not normal, the point estimator is biased, or the regression model is not linear. The proposed approach is simple to implement and less computer intensive than bootstrap. The proposed approach does not rely on re-sampling, linearisation, variance estimation, or design-effect

Open versus laparoscopically-assisted oesophagectomy for cancer: a multicentre randomised controlled phase III trial - the MIRO trial

<p>Abstract</p> <p>Background</p> <p>Open transthoracic oesophagectomy is the standard treatment for infracarinal resectable oesophageal carcinomas, although it is associated with high mortality and morbidity rates of 2 to 10% and 30 to 50%, respectively, for both the abdominal and thoracic approaches. The worldwide popularity of laparoscopic techniques is based on promising results, including lower postoperative morbidity rates, which are related to the reduced postoperative trauma. We hypothesise that the laparoscopic abdominal approach (laparoscopic gastric mobilisation) in oesophageal cancer surgery will decrease the major postoperative complication rate due to the reduced surgical trauma.</p> <p>Methods/Design</p> <p>The MIRO trial is an open, controlled, prospective, randomised multicentre phase III trial. Patients in study arm A will receive laparoscopic-assisted oesophagectomy, i.e., a transthoracic oesophagectomy with two-field lymphadenectomy and laparoscopic gastric mobilisation. Patients in study arm B will receive the same procedure, but with the conventional open abdominal approach. The primary objective of the study is to evaluate the major postoperative 30-day morbidity. Secondary objectives are to assess the overall 30-day morbidity, 30-day mortality, 30-day pulmonary morbidity, disease-free survival, overall survival as well as quality of life and to perform medico-economic analysis. A total of 200 patients will be enrolled, and two safety analyses will be performed using 25 and 50 patients included in arm A.</p> <p>Discussion</p> <p>Postoperative morbidity remains high after oesophageal cancer surgery, especially due to major pulmonary complications, which are responsible for 50% of the postoperative deaths. This study represents the first randomised controlled phase III trial to evaluate the benefits of the minimally invasive approach with respect to the postoperative course and oncological outcomes in oesophageal cancer surgery.</p> <p>Trial Registration</p> <p><a href="http://www.clinicaltrials.gov/ct2/show/NCT00937456">NCT00937456</a> (ClinicalTrials.gov)</p

Incidence of Sarcoma Histotypes and Molecular Subtypes in a Prospective Epidemiological Study with Central Pathology Review and Molecular Testing

International audienceBACKGROUND: The exact overall incidence of sarcoma and sarcoma subtypes is not known. The objective of the present population-based study was to determine this incidence in a European region (Rhone-Alpes) of six million inhabitants, based on a central pathological review of the cases. METHODOLOGY/PRINCIPAL FINDINGS: From March 2005 to February 2007, pathology reports and tumor blocks were prospectively collected from the 158 pathologists of the Rhone-Alpes region. All diagnosed or suspected cases of sarcoma were collected, reviewed centrally, examined for molecular alterations and classified according to the 2002 World Health Organization classification. Of the 1287 patients screened during the study period, 748 met the criteria for inclusion in the study. The overall crude and world age-standardized incidence rates were respectively 6.2 and 4.8 per 100,000/year. Incidence rates for soft tissue, visceral and bone sarcomas were respectively 3.6, 2.0 and 0.6 per 100,000. The most frequent histological subtypes were gastrointestinal stromal tumor (18%; 1.1/100,000), unclassified sarcoma (16%; 1/100,000), liposarcoma (15%; 0.9/100,000) and leiomyosarcoma (11%; 0.7/100,000). CONCLUSIONS/SIGNIFICANCE: The observed incidence of sarcomas was higher than expected. This study is the first detailed investigation of the crude incidence of histological and molecular subtypes of sarcomas

IL1B and DEFB1 Polymorphisms Increase Susceptibility to Invasive Mold Infection After Solid-Organ Transplantation

Background. Single-nucleotide polymorphisms (SNPs) in immune genes have been associated with susceptibility to invasive mold infection (IMI) among hematopoietic stem cell but not solid-organ transplant (SOT) recipients. Methods. Twenty-four SNPs from systematically selected genes were genotyped among 1101 SOT recipients (715 kidney transplant recipients, 190 liver transplant recipients, 102 lung transplant recipients, 79 heart transplant recipients, and 15 recipients of other transplants) from the Swiss Transplant Cohort Study. Association between SNPs and the end point were assessed by log-rank test and Cox regression models. Cytokine production upon Aspergillus stimulation was measured by enzyme-linked immunosorbent assay in peripheral blood mononuclear cells (PBMCs) from healthy volunteers and correlated with relevant genotypes. Results. Mold colonization (n = 45) and proven/probable IMI (n = 26) were associated with polymorphisms in the genes encoding interleukin 1β (IL1B; rs16944; recessive mode, P = .001 for colonization and P = .00005 for IMI, by the log-rank test), interleukin 1 receptor antagonist (IL1RN; rs419598; P = .01 and P = .02, respectively), and β-defensin 1 (DEFB1; rs1800972; P = .001 and P = .0002, respectively). The associations with IL1B and DEFB1 remained significant in a multivariate regression model (P = .002 for IL1B rs16944; P = .01 for DEFB1 rs1800972). The presence of 2 copies of the rare allele of rs16944 or rs419598 was associated with reduced Aspergillus-induced interleukin 1β and tumor necrosis factor α secretion by PBMCs. Conclusions. Functional polymorphisms in IL1B and DEFB1 influence susceptibility to mold infection in SOT recipients. This observation may contribute to individual risk stratificatio

N-Cadherin in Neuroblastoma Disease: Expression and Clinical Significance

One of the first and most important steps in the metastatic cascade is the loss of cell-cell and cell-matrix interactions. N-cadherin, a crucial mediator of homotypic and heterotypic cell-cell interactions, might play a central role in the metastasis of neuroblastoma (NB), a solid tumor of neuroectodermal origin. Using Reverse Transcription Quantitative PCR (RT-qPCR), Western blot, immunocytochemistry and Tissue MicroArrays (TMA) we demonstrate the expression of N-cadherin in neuroblastoma tumors and cell lines. All neuroblastic tumors (n = 356) and cell lines (n = 10) expressed various levels of the adhesion protein. The N-cadherin mRNA expression was significantly lower in tumor samples from patients suffering metastatic disease. Treatment of NB cell lines with the N-cadherin blocking peptide ADH-1 (Exherin, Adherex Technologies Inc.), strongly inhibited tumor cell proliferation in vitro by inducing apoptosis. Our results suggest that N-cadherin signaling may play a role in neuroblastoma disease, marking involvement of metastasis and determining neuroblastoma cell viability

Assessing associations between the AURKAHMMR-TPX2-TUBG1 functional module and breast cancer risk in BRCA1/2 mutation carriers

While interplay between BRCA1 and AURKA-RHAMM-TPX2-TUBG1 regulates mammary epithelial polarization, common genetic variation in HMMR (gene product RHAMM) may be associated with risk of breast cancer in BRCA1 mutation carriers. Following on these observations, we further assessed the link between the AURKA-HMMR-TPX2-TUBG1 functional module and risk of breast cancer in BRCA1 or BRCA2 mutation carriers. Forty-one single nucleotide polymorphisms (SNPs) were genotyped in 15,252 BRCA1 and 8,211 BRCA2 mutation carriers and subsequently analyzed using a retrospective likelihood appr