Association between serum nickel and oral cancer incidence using propensity score matching and inverse probability of treatment weighting

BackgroundThe association between serum nickel (Ni) and oral cancer incidence is unclear and most of the previous studies were observational studies that did not control for confounding factors between groups.ObjectiveTo assess the correlation of serum Ni with oral cancer incidence based on propensity score matching (PSM) and inverse probability of treatment weighting (IPTW).MethodsA cohort of 456 newly diagnosed oral cancer patients was recruited from the First Hospital of Fujian Medical University during November 2011 to May 2019, and residents ordered their health check-up in hospitals or local community health centers over the same period were selected as a control group, which included a total of 1410 participants. Serum Ni was evaluated by inductively coupled plasma mass spectrometry. Case-control pairs were selected using a 1:1 PSM (caliper value of 0.02), and the study subjects in the case group and control group were weighted for subsequent analysis by IPTW. The general characteristics of the study subjects were tested for equilibrium before and after matching by chi-square test and standardized mean difference (SMD). This was followed by exploring the potential nonlinear dose-response relationship between serum Ni and oral cancer using restricted cubic splines as well as analyzing the association between serum Ni and oral cancer incidence by conditional logistic regression and weighted logistic regression.ResultsAfter controlling for between-group covariates by PSM and IPTW, the dose-response curves demonstrated that the risk of developing oral cancer tended to decline and then increase with the increasing serum Ni level. The outcome of the analysis using PSM demonstrated that as compared to the control group, the risk of developing oral cancer in the 0.09-16.80 μg·L−1 serum Ni group was negatively correlated with serum Ni level (OR=0.36, 95%CI: 0.24-0.54), whereas the risk of developing oral cancer in the >16.80 μg·L−1 serum Ni group was positively correlated with serum Ni level (OR=5.43, 95%CI: 2.76-10.68). After applying IPTW, a negative association was found between the risk of oral cancer and serum Ni concentration within a serum Ni window ranging from 0.09 to 20.55 μg·L−1 (OR=0.39, 95%CI: 0.29-0.52), while a positive association with an OR and 95%CI of 5.54 (3.62-8.49) for the Ni concentration > 20.55 μg·L−1.ConclusionIn this study, a J-shaped relationship between serum Ni concentration and the risk of developing oral cancer is found, which shows that high serum Ni concentration (>20.55 μg·L−1) may be a risk factor for oral cancer

Improved Analytical Formula for the SAR Doppler Centroid Estimation Standard Deviation for a Dynamic Sea Surface

The existing formulas for the synthetic aperture radar (SAR) Doppler centroid estimation standard deviation (STD) suffer from various limitations, especially for a dynamic sea surface. In this study, we derive an improved version of these formulas through three steps. First, by considering the ocean wavenumber spectrum information, a new strategy for determining the number of independent samples of the sea wave velocity field is adopted in the new formula. This is contrary to the method used in the existing formulas, where the number of SAR geometric resolution cells is taken as the number of samples assuming that adjacent SAR resolution cells are statistically uncorrelated. Second, the pulse repetition frequency and Doppler bandwidth are decoupled in the new formula, unlike in the existing formulas where they are unchangeably related to each other. Third, the effects of thermal noise and Doppler aliasing are jointly quantified in a mathematically exact manner instead of being treated separately, as in the existing formulas. Comprehensive SAR raw data simulations for the ocean surface show that the new formula has a better performance in predicting the Doppler centroid estimation STD than the existing formulas

Improved Analytical Formula for the SAR Doppler Centroid Estimation Standard Deviation for a Dynamic Sea Surface

The existing formulas for the synthetic aperture radar (SAR) Doppler centroid estimation standard deviation (STD) suffer from various limitations, especially for a dynamic sea surface. In this study, we derive an improved version of these formulas through three steps. First, by considering the ocean wavenumber spectrum information, a new strategy for determining the number of independent samples of the sea wave velocity field is adopted in the new formula. This is contrary to the method used in the existing formulas, where the number of SAR geometric resolution cells is taken as the number of samples assuming that adjacent SAR resolution cells are statistically uncorrelated. Second, the pulse repetition frequency and Doppler bandwidth are decoupled in the new formula, unlike in the existing formulas where they are unchangeably related to each other. Third, the effects of thermal noise and Doppler aliasing are jointly quantified in a mathematically exact manner instead of being treated separately, as in the existing formulas. Comprehensive SAR raw data simulations for the ocean surface show that the new formula has a better performance in predicting the Doppler centroid estimation STD than the existing formulas

TUSC2P suppresses the tumor function of esophageal squamous cell carcinoma by regulating TUSC2 expression and correlates with disease prognosis

Abstract Background Pseudogenes are RNA transcripts with high homology with its parent protein-coding genes. Although pseudogenes lost the ability to produce protein, it still exert import biological function, and play important role in the pathogenesis of a wide varity of tumors; However, the role of pseudogenes in esophageal squamous cell carcinoma (ESCC) is poorly understood. Methods TUSC2P function in ESCC were explored using both in vitro and in vivo experiments cell proliferation, invasion and apoptosis assay was performed to evaluated the effect of TUSC2P on the tumor biology of ESCC. Expression of relative genes was assessed by quantitative real-time PCR (qRT-PCR) and western blotting in EC109 and TE-1 cell, as well as ESCC patients. 3’UTR luciferase assay was used to confirm the direct binding of miRNAs with TUSC2 and TUSC2P 3’UTR. Relation betweenTUSC2P, TUSC2 and ESCC prognosis was predicted by survival analysis (n = 56). Results Pseudogene TUSC2P was down regulated in ESCC tissues compared with paired normal adjacent tissues, and the expression of TUSC2P was significantly correlated with survivalof ESCC patients. Over expression of TUSC2P in EC109 and TE-1 cells resulted in altered expression of TUSC2, thus inhibited proliferation, invasion and promoted apoptosis. Dual luciferase assay demonstrated that TUSC2P 3’UTR decoyed miR-17-5p, miR-520a-3p, miR-608, miR-661 from binding to TUSC2. Conclusions TUSC2P can suppresses the tumor function of esophageal squamous cell carcinoma by regulating TUSC2 expression and may also serve as a prognostic factor for ESCC patients