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141 protocols using microsoft excel

1

Yield and Fiber Traits Evaluation

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In the summer of 2018 and 2019, 289 ILs were planted in Dangtu, Anhui province (E1) and Shangqiu, Henan province (E2), respectively, based on a randomized complete block design with two replications. Then a randomized complete block design with three replicates was applied, 289 ILs were planted in Sanya of Hainan province (2019 winter) (E3), Shangqiu of Henan province (2020 summer) (E4), and Shihezi of Xinjiang province (2020 summer) (E5). For field experiments under five environments, the recipient TM-1 and donor SXY 1 were used as control. Twenty-five bolls from each ILs in the middle of each row were hand-harvested from the internal middle parts of the plants. The yield-related traits, i.e., boll weight (BW), lint percent (LP), seed index (SI), number of bolls per plant (BN), number of fruit branches (FBN), and plant height (PH) were tested. All fiber samples from the five different environments were ginned by a roller. The fiber qualities were evaluated by high volume instrument for 2.5% fiber length (FL, mm), fiber strength (FS, cN/tex), micronaire (MIC), fiber elongation (FE, %), and fiber uniformity (FU, %). Basic statistical parameters, correlation coefficients, and phenotypic variation were performed using Microsoft Excel and SPSS 20.0 (SPSS, Chicago, IL, USA). The heritability of all the traits was calculated using QTL IciMapping 4.2 software.
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2

Genetic Association Analysis of Gastric Cancer

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All statistical analysis was conducted using Microsoft Excel and SPSS 16.0 (SPSS, Chicago IL USA). Allele frequency of each SNP in the control subjects was analyzed using the exact test to determine whether the four SNPs departed from Hardy-Weinberg equilibrium (HWE). We used Chi-square test/Fisher's exact test to compare the differences in SNP allele and genotype distribution between GC cases and controls [27 (link)]. Then the association between each SNP and GC was assessed under three genetic models: dominant, recessive and additive model using PLINK software, a web-based program available at http://pngu.mgh.harvard.edu/purcell/plink/. Finally, the SHEsis software platform (http://www.nhgg.org/analysis) and Haploview software package (version 4.2) were used to analyze and visualize patterns of linkage disequilibrium (LD) and haplotype construction [28 (link)]. The odd ratio (OR) and 95% confidence intervals (CI), calculated by using unconditional logistic regression analysis with adjustments for age and gender, were used to assess the association between each SNP and the risk of GC [29 ]. Two-sided P≤0.05 was considered statistically significant for all statistical tests.
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3

Genetic Analysis of Esophageal Cancer

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For cases and controls, we analyzed the gender distribution using Pearson's χ2 test and the age distribution by Welch's t test. We analyzed the genotype frequencies in the controls with Fisher's exact test to determine whether the five SNPs departed from Hardy-Weinberg equilibrium. The differences in the SNP allele and genotype distributions between patients and controls were evaluated with Chi-squared test/Fisher's exact tests. Genetic model analyses (Dominant, Recessive and Additive) were performed with PLINK software to assess the significance of the SNPs. The associations of the SNPs with the risk of esophageal cancer were estimated from the odds ratios (ORs) and 95% confidence intervals (CIs), which were determined by unconditional logistic regression and adjusted for age and gender [32 (link)]. The P-values reported are two-sided, and values of P < 0.05 were considered to be statistically significant. We used the Haploview software package (version 4.2) platform for analyses of pairwise linkage disequilibrium (LD) and haplotype structure [10 (link)]. All statistical analyses were performed with Microsoft Excel and SPSS 19.0 (SPSS, Chicago, IL, USA).
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4

Genetic Associations with Coronary Artery Disease

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Statistical analyses were done using Microsoft Excel and SPSS 18.0 (SPSS, Chicago, IL, USA). All p values were two-sided, and p ≤ 0.05 was considered significant. Control genotype frequencies for each SNP were tested for departure from the HWE using Fisher's exact test. The χ2 test was used to compare the distribution of marker alleles and genotypes in the patients and controls [29 (link)]. Unconditional logistic regression analysis, adjusted for age, was used to test odds ratios (ORs) and 95% confidence intervals (CIs) [30 (link)]. Associations between SNPs and risk of CAD were tested in genetic models using SNP Stats software (http://bioinfo.iconcologia.net). Values of OR and 95% CI were calculated as above. Finally, SHEsis software (http://analysis.bio-x.cn/myAnalysis.php) was used to estimate pairwise linkage disequilibrium (LD) and haplotype construction [31 (link)].
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5

Genetic Variants and COPD Risk

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Statistical analysis was performed with Microsoft Excel and SPSS 18.0 (SPSS, Chicago, IL, USA). Welch’s t-tests (for continuous variables) and the Chi square test (χ2 test, for categorical variables) were used to assess the differences in the distribution of demographic characteristics of case and control groups. SNP frequencies in the control subjects were evaluated for departure from Hardy–Weinberg Equilibrium (HWE) by the Fisher’s exact test. Allele and genotype frequencies of each SNP in patient and control groups were compared by a χ2 test. The associations between these SNPs and COPD risk were assessed by calculating odds ratios (ORs) and 95% confidence intervals (CIs) using logistic regression analysis with adjustments for age and gender. Multiple inheritance models (codominant, dominant, recessive, and log-additive) were generated by PLINK software (http://www.cog-genomics.org/plink2/) to estimate the relationship between each SNP and COPD risk.25 (link),26 (link) Finally, we used the Haploview software package (version 4.2) for pairwise linkage disequilibrium (LD) and haplotype construction, and used SHEsis software for haplotype association analyses. All P-values were two-sided, and P<0.05 was considered statistically significant.
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6

Genetic Associations in Large Artery Atherosclerotic Stroke

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Statistical analyses were carried out using Microsoft Excel and SPSS 17.0 (SPSS, Chicago, IL, USA) software. Deviation from Hardy-Weinberg equilibrium (HWE) was tested for control subjects to measure the distribution of the polymorphism using a Chi-square test [42 ]. The Haploview software package (version 4.2) and SHEsis software platform (http://analysis.bio-x.cn/myanalysis.php) were used for analyses of linkage disequilibrium, haplotype construction [43 (link), 44 (link)]. Associations between haplotypes and LAA stroke risk were analyzed by SNPStats (http://bioinfo.iconcologia.net/SNPstats) [45 (link)]. We used the unconditional logistic regression analysis adjusted by age and gender to determine the association between the haplotyes and LAA stroke. Two-sided P-value less than 0.05 was considered statistically significant. The risk associated with individual genotypes and allele was calculated as the odds ratios (OR) with their 95% confidence interval (95% CI) based on logistic regression models analysis.
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7

Quantitative Analysis of let-7g/i Expression

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Data are presented as the mean ± standard deviation of four independent experiments. Statistical analyses were performed using Microsoft Excel and SPSS software, version 16.0 (SPSS Inc., Chicago, IL, USA). Quantitative PCR data were analyzed as follows: U6 snRNA was used to normalize let-7g/i expression levels. Let-7g/i expression levels were measured using the threshold cycle (Ct), and the fold-change in expression was calculated as 2−ΔΔCt. The relative expression of let-7g/i in hematoma cell lines was calculated using the following formula: ΔΔCt = (Ctlet-7g/i − CtU6) cancer − (Ctlet-7g/i − CtU6) L-02. The relative expression of let-7g/i after transfection was calculated using the equation: ΔΔCt = (Ctlet-7i/g − CtU6) post-transfection − (Ctlet-7g/i − CtU6) pro-transfection. Factorial analysis of variance was used to analyze the interaction between let-7g and let-7i in the EdU retention assay and cell apoptosis assay. P<0.05 was considered to indicate a statistically significant difference.
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8

Serum Trace Elements Analysis

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The data collected were tabulated and analysed using Microsoft Excel and SPSS version 20 for Windows (Chicago, IL, USA). The data collected were analysed using Microsoft Excel and SPSS version 21.0 (IBM SPSS Statistics, USA) for Windows. The data are expressed as median and IQR. Categorical variables were calculated as frequency and percentage; continuous variables were represented as median (IQR). The normality of the parameters was checked using the Shapiro–Wilk test and found to be non-parametric. The difference in serum trace elements levels between subgroups was analysed using Kruskal–Wallis and Mann–Whitney U test along with pairwise post-hoc analysis. Moreover, Spearman correlation analysis was used to find the significance of association between the variables. Variable selection for ROC was performed via stepwise AIC selection. Differences between ROC curves were assessed by the DeLong test for two correlated ROC curves. A p value < 0.05 was considered statistically significant.
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9

Genetic Association Analysis

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We performed statistical analysis using Microsoft Excel and SPSS 16.0 statistical package (SPSS, Chicago, IL). All P values in this study were two-sided. We considered P ≤ 0.05 the threshold for statistical significance. We tested genotypic frequencies in control subjects for each SNP for departure from HWE using an exact test. We compared genotype frequencies of case and control subjects using the Chi2 test. We calculated OR and 95% CI by unconditional logistic regression analysis. There were two factors of age and gender adjusted for the analysis. We used the Haploview program to estimate the pairwise LD between markers and partition haplotype blocks. We inferred haplotypes using the Haploview software package (version 4.2).
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10

Genetic Association Analysis of KBD

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Statistical analyses were performed using Microsoft Excel, SPSS 16.0 (SPSS, Chicago, IL) and PLINK 1.07 software. Deviation from Hardy–Weinberg equilibrium (HWE) was tested for control subjects to measure the distribution of the polymorphism using a Chi‐square test (Ren et al., 2016). Two‐side p‐value less than 0.05 were considered statistically significant. The risk associated with individual genotypes and allele was calculated as the odds ratios (OR) with their 95% confidence interval (95% CI) based on logistic regression models analysis (Bland & Altman, 2000). The Haploview software package (version 4.2) was used for analyses of linkage disequilibrium, haplotype construction (Barrett, Fry, Maller, & Daly, 2005; Shi & He, 2005). Associations between haplotypes and KBD risk were analyzed with PLINK. We used the unconditional logistic regression analysis adjusted for age and gender to determine the association between the haplotypes and KBD.
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