Table_1_Diabetic retinopathy risk in patients with unhealthy lifestyle: A Mendelian randomization study.pdf

PurposeThis study aimed to investigate the causal association between unhealthy lifestyle factors and diabetic retinopathy (DR) risk and to determine better interventions targeting these modifiable unhealthy factors.DesignTwo-sample Mendelian randomization (MR) analysis was performed in this study. The inverse variance-weighted method was used as the primary method.MethodOur study included 687 single-nucleotide polymorphisms associated with unhealthy lifestyle factors as instrumental variables. Aggregated data on individual-level genetic information were obtained from the corresponding studies and consortia. A total of 292,622,3 cases and 739,241,18 variants from four large consortia (MRC Integrative Epidemiology Unit [MRC-IEU], Genetic Investigation of Anthropometric Traits [GIANT], GWAS & Sequencing Consortium of Alcohol and Nicotine Use [GSCAN], and Neale Lab) were included.ResultIn the MR analysis, a higher body mass index (BMI) (odds ratio [OR], 95% confidence interval [CI] = 1.42, 1.30–1.54; P ConclusionOur findings suggest that higher BMI, WHR, and smoking are likely to be causal factors in the development of DR, whereas genetically higher HC is associated with a lower risk of DR, providing insights into a better understanding of the etiology and prevention of DR.</p

Means of microclimate factors of <i>Nitraria tangutorum</i> nebkhas.

<p>Means of microclimate factors of <i>Nitraria tangutorum</i> nebkhas.</p

Results of ANOVA for the effect of the aspect and size class on clonal reproduction and biomass allocation of <i>Nitraria tangutorum</i>.

<p>RatRs, DenAR, BaLeaf, BaStem and BaRoot represent rate of ramet sprouting (%), density of adventitious roots formation points (number/cm), biomass allocation of leaf (%), biomass allocation of stem (%) and biomass allocation of adventitious root (%), respectively.</p

Effects of aspect and size class of layering module on biomass allocation of 3 modules of <i>Nitraria tangutorum</i>.

<p>BaLeaf, BaStem, BaRoot and BioLm represent biomass allocation of leaf (%) (A and B), biomass allocation of stem (%) (C and D), biomass allocation of root (%) (E and F) and layering biomass (G), respectively; Open bars (A, C and E) are grand means of four aspect sections across two size classes of layering. Grayscale bars (B, D and F) are means of four aspect sections and two size classes of layering combinations; Error bars represent standard errors of the means; the letters above the error bar are groupings from Duncan's multiple range tests. Bars with a different letters are significantly different at <i>P</i> = 0.05.</p

Depth of axillary bud germination points of <i>Nitraria tangutorum</i> and their frequency distribution.

<p>Treatments with different letters are significantly different (p<0.05) according to a one-way ANOVA with aspect as the factor. Error bars represent standard errors of the means.</p

Effects of aspect and size class of layering module on clonal reproduction of <i>Nitraria tangutorum</i>.

<p>RatRs and DenAR represent the rate of ramet sprouting (%) (A and B)and density of adventitious root formation points (number/cm) (C and D), respectively. BioLm represents the layering biomass; Open bars (A and C) are grand means of four aspect sections across two size classes of layering. Grayscale bars (B and D) are means of the four aspect sections and two size classes of layering; the error bars represent standard errors of the means; the letters above the error bar are the groupings from Duncan's multiple range tests. Bars followed by different letters are significantly different at <i>P</i> = 0.05.</p

Knockdown of endogenous Smyd1b advances the timing of sarcomeric localization of Smyd1b_tv1^myc in zebrafish embryos.

<p><b>A.</b> Smyd1b E9I9-MO was injected into Smyd1b_tv1^myc or Smyd1b_tv1^myc transgenic zebrafish embryos at 1–2 cell stages. Western blot analysis shows the expression of myc-tagged Smyd1b_tv1^myc and Smyd1b_tv1^myc in un-injected control or E9I9-MO injected transgenic zebrafish embryos at 24 hpf. γ-Tubulin was used as loading control. <b>B and C.</b> Immunostaining using anti-myc antibody shows the cytoplasmic (B) or sarcomeric localization (C) of <i>smyd1b_tv1^myc</i> in control (B) or E9I9-MO injected (C) transgenic zebrafish embryos at 24 hpf. <b>D and E.</b> Immunostaining using anti-myc antibody shows the cytoplasmic localization of <i>smyd1b_tv2^myc</i> in control or E9I9-MO injected transgenic zebrafish embryos at 24 hpf. Scale bar: 30 µm.</p

The Serine 225 is required for the enhanced sarcomeric localization of Smyd1b_tv1.

<p><b>A.</b> Sequence comparison shows that the alternative splicing of smyd1b in various vertebrates and the conserved serine and threonine residues within the 13 aa insertion. <b>B and C.</b> Immunostaining using anti-myc antibody shows the sarcomeric localization of Smyd1b_tv1^myc in myofibers of zebrafish embryos at 38 hpf. C represents the highlighted box area in A. <b>D–G.</b> Immunostaining using anti-myc antibody shows the sarcomeric localization of Smyd1b_tv1^myc mutant proteins that carry substitutions at S217A and T221A (D), S225A (E), S225T (F), S225D (G). Scale bars: B = 40 µm; C = 20 µm.</p

Rescue of myofibril organization defect in smyd1b knockdown embryos by expression of Smyd1b_tv1-EGFP or Smyd1b_tv2-EGFP fusion protein.

<p><b>A.</b> DNA constructs encoding Smyd1b_tv1-EGFP, or Smyd1b_tv2-EGFP fusion proteins or EGFP control were generated and injected into zebrafish embryos. <b>B and C.</b> Myofibers expressing Smyd1_tv1-EGFP (B) or Smyd1_tv2-EGFP (C) was directly observed by GFP. <b>D and E.</b> Myosin thick filaments organization was determined by F59 antibody staining in Smyd1_tv1-EGFP (D) or Smyd1_tv2-EGFP (E) co-injected embryos. <b>F and G.</b> Double staining shows the colocalization of normal fibers with Smyd1_tv1-EGFP (F) or Smyd1_tv2-EGFP (G) expression. Scale bars: 20 µm.</p

The effect of <i>hsp90α1</i> mutation or knockdown on Smyd1b_tv1 sarcomeric localization.

<p><b>A and D.</b> Immunostaining using anti-myomesin antibody shows the organization of myomesin in <i>hsp90α1</i> mutant (A), or control (D) <i>smyd1b_tv1^myc</i> transgenic embryos at 72 hpf. <b>B and E.</b> Immunostaining using anti-myc antibody shows the localization of Smyd1b_tv1^myc in <i>hsp90α1</i> mutant (B), or control (E) <i>smyd1b_tv1^myc</i> transgenic embryos at 72 hpf. <b>C and F.</b> F59 staining shows the organization of slow muscle myosin in <i>hsp90α1</i> mutant (C), or control (F) <i>smyd1b_tv1^myc</i> transgenic embryos at 72 hpf. <b>G and H.</b> DNA construct <i>Smyd1_tv1-EGFP</i> was injected alone or together with <i>hsp90α1</i> ATG-MO into zebrafish embryos. Smyd1_tv1-EGFP localization was determined in myofibers of the control (G), or <i>hsp90α1</i> knockdown (H) at 48 hpf. Scale bars: D = 40 µm; G = 15 µm.</p