Table_1_Categorizing numeric nutrients criteria and implications for water quality assessment in the Pearl River Estuary, China.docx

Coastal eutrophication, the over-enrichment of water with nutrients, has become a global ecological problem. As coastal waters are subjected to great pressure due to anthropogenic influences and climate change, establishing numeric nutrient criteria for coastal waters has been exceedingly complex at present. To control and improve the water quality of the Pearl River Estuary (PRE), based on the data from 2015 to 2020, the nutrient criteria of the PRE and adjacent waters were established using frequency statistical analysis. Based on the spatiotemporal salinity patterns, the coastal waters of the PRE were divided in three subareas namely freshwater (Zone I), mixed (Zone II), and seawater (Zone III) using cluster analysis. The recommended criteria values of dissolved inorganic nitrogen (DIN) were 0.573, 0.312, and 0.134 mg·L-1 in Zones I, II, and III, respectively. The total nitrogen (TN) criterion for Zone III (0.222 mg·L-1) was much lower than those for Zone I (0.902 mg·L-1) and Zone II (0.885 mg·L-1).The dissolved inorganic phosphorus (DIP) criteria were different for the three Zones, ranging from 0.004 to 0.009 mg·L-1, and the total phosphorus (TP) recommended criteria in Zones I, II, and III were 0.039, 0.028, and 0.020 mg·L-1, respectively. In the water quality assessment, the categorizing numeric nutrients criteria can be referred and applied into fresh, mixed, and seawater zones of PRE. The results of this study provide a new nutrient reference condition in the PRE, which could be helpful in establishing integrated land-ocean unified nutrient criteria and water quality assessment, and implementing effective coastal eutrophication control in the future.</p

Forest plot of ORs for CAD in the dominant model (CC + AC vs.AA) of the <i>SELE</i> gene A561C polymorphism stratified by ethnicity.

<p>White diamonds denote the pooled ORs in the fixed effect. Black squares indicate the OR in each study, with square sizes inversely proportional to the standard error of the OR. Horizontal lines represent 95% CIs. ^aOne study with different types of populations.</p

Pooled measures on the relationship of the <i>SELE</i> gene A561C polymorphism with CAD.

<p>Dominant model: CC + AC versus AA; Codominant model: C versus A.</p><p>FEM: fixed effect model, REM: random effect model, DHWE: deviated from Hardy–Weinberg equilibrium.</p>**<p><i>P</i><0.01.</p><p><i>P</i>_h: <i>P</i> value of <i>Q</i>-test for heterogeneity test.</p

Forest plot of ORs for CAD in the dominant model (TT + GT vs.GG) of the <i>SELE</i> gene G98T polymorphism stratified by ethnicity.

<p>White diamonds denote the pooled ORs in the fixed effect. Black squares indicate the OR in each study, with square sizes inversely proportional to the standard error of the OR. Horizontal lines represent 95% CIs. ^aOne study with different types of populations.</p

Characteristics of the <i>SELE</i> gene A561C polymorphism genotype distributions in studies included in this meta-analysis.

<p>CHD: coronary heart disease, CAD: coronary artery disease, MI: myocardial infarction, AP: angina pectoris, AMI: acute myocardial infarction.</p><p>ACS: acute coronary syndrome, N: total number of subjects in each study, F: the C allele frequency in control, Na: not available. * <i>P</i><0.05.</p>a<p><i>P</i> for Hardy–Weinberg equilibrium in the control group.</p>b<p>Only the median age of cases and controls was available from the original article.</p>c/d<p>One study with different populations.</p>e<p>ACS mainly included unstable angina pectoris, myocardial infarction, coronary death in the original article.</p

Analysis of the influence of individual studies on the pooled estimate in the dominant model (TT + GT vs. GG) of the <i>SELE</i> gene G98T polymorphism.

<p>Open circles indicate the pooled OR, given the named study is omitted. Horizontal lines represent the 95% CIs. ^aOne study with different types of populations.</p

Characteristics of the <i>SELE</i> gene G98T polymorphism genotype distributions in studies included in this meta-analysis.

<p>CHD: coronary heart disease, CAD: coronary artery disease, N: total number of subjects in each study, F: the T allele frequency in control.</p><p>Na: not available.</p>a<p><i>P</i> for Hardy –Weinberg equilibrium in control group.</p>b<p>One study with different populations.</p

Analysis of the influence of individual studies on the pooled estimate in the dominant model (CC + AC vs. AA) of the <i>SELE</i> gene A561C polymorphism.

<p>Open circles indicate the pooled OR, given the named study is omitted. Horizontal lines represent the 95% CIs. ^aOne study with different types of populations.</p

Pooled measures on the relationship of the <i>SELE</i> gene G98T polymorphism with CAD.

<p>Dominant model: TT + GT versus GG; Codominant model: T versus G.</p><p>FEM: fixed effect model, REM: random effect model.</p><p><i>P</i>_h: <i>P</i> value of <i>Q</i>-test for heterogeneity test.</p

PTEN knockdown increased Akt activation both in the presence and absence of IFN-γ.

<p>The protein expression level of PTEN, Akt and phospho-Akt^Ser473 were determined by Western blotting. β-actin was used to verify equal loading. Representative images are selected from performed experiments repeated in triplicates.</p