The enzyme activity of <i>P. haitanensis</i> in responding to heat shock.

<p>A, NADPH oxidase activities and B, SOD activities of thallus and conchocelis after heat shock at 35°C for 30 min. ^*<i>P</i><0.05, ^**<i>P</i><0.01 (n = 3) compared with those of control without heat shock. ^##<i>P</i><0.01 (n = 3) compared with those of the groups of thallus.</p

H₂O₂ concentrations in the medium of <i>P. haitanensis</i> during 30 min exposure to 35°C heat shock.

<p>H₂O₂ concentrations in the medium of <i>P. haitanensis</i> during 30 min exposure to 35°C heat shock.</p

The gene expression of <i>P. haitanensis</i> in responding to heat shock.

<p>A, The gene expression response of thallus to different periods of heat shock. ^*<i>P</i><0.05, ^**<i>P</i><0.01 (n = 3) compared with that in control without heat shock. B, The different responses of thallus and conchocelis to heat shock for 30 min. The thallus or conchocelis of <i>P. haitanensis</i> was treated under 35°C. At different periods, the samples were collected, the mRNA was extracted and the expression levels of <i>PhMn-sod</i>, <i>Phhsp70</i> and <i>Phrboh</i> were analyzed by QRT-PCR. C, The gene copies of <i>PhMn-sod</i>, <i>Phhsp70</i> and <i>Phrboh</i> of thallus and conchocelis without heat shock. Data represented mean ± SD from three individual experiments. ^*<i>P</i><0.05, ^**<i>P</i><0.01 (n = 3) compared with those of the groups of thallus.</p

The changes of fatty acids of thallus and conchocelis of <i>P. haitanensis</i> after heat shock (%).

a<p>“-” indicated undetected.</p><p>*<i>p</i><0.05, **<i>p</i><0.01 compared with control.</p

The changes of floridoside of <i>P. haitanensis</i> in responding to heat shock.

<p>A, The changes of floridoside of thallus treated at 35°C for different periods. ^**<i>P</i><0.01 (n = 3) compared with those of control without heat shock. B, The different floridoside responses of thallus and conchocelis to heat shock after recovery for 3 h. The thallus or conchocelis of <i>P. haitanensis</i> was treated at 35°C for 30 min. The samples were then returned to 20°C and examined after the periods of 1 h and 3 h. The control samples were cultured under the same conditions without heat shock treatment. R-1 h and R-3 h indicated the samples returned to 20°C for 1 h and 3 h, respectively. ^*<i>P</i><0.05, ^**<i>P</i><0.01 (n = 3) compared with that of control without heat shock. ^#<i>P</i><0.05, ^##<i>P</i><0.01 (n = 3) compared with that of the groups of thallus.</p

The changes of volatiles of thallus and conchocelis of <i>P. haitanensis</i> after heat shock (μg/100 mg).

a<p>“-” indicated undetected.</p><p>*<i>p</i><0.05, **<i>p</i><0.01 compared with control.</p

Flow diagram of included and excluded studies.

<p>Flow diagram of included and excluded studies.</p

Forest plots showing the association of the TLR4 +896A/G polymorphism with H. Pylori infection in gastric cancer patients.

<p>A. AG vs. AA, B. G vs. A.</p

Association between TLR4 (+896A/G and +1196C/T) Polymorphisms and Gastric Cancer Risk: An Updated Meta-Analysis

<div><p>Background</p><p>Toll-like receptor 4 (TLR4) is a receptor of lipopolysaccharide in the signaling transduction of gastric epithelial cell. It plays a pivotal role in activation of innate immunity and pathogen recognition and thus acts as a modulator in the development and progression of gastric cancer. Growing studies explored the association of polymorphisms in TLR4 with susceptibility to gastric cancer, but the results have remained controversial and conflicting. To investigate the effect of two selected TLR4 (+896A/G and +1196C/T) polymorphisms on gastric cancer, we performed a meta-analysis.</p><p>Methods</p><p>A comprehensive search was conducted to identify all eligible case-control publications investigating the association between TLR4 polymorphisms and gastric cancer risk. Odds ratios (OR) and corresponding 95% confidence intervals (CI) were used to assess such association.</p><p>Results</p><p>Up to March 26 2014, 10 published case-control studies from PubMed and EMBase were available, involving a total of 1888 gastric cancer patients and 3433 control subjects. In the overall meta-analyses, a significantly increased gastric cancer risk was detected in TLR4 +896A/G polymorphism (heterozygous model, AG vs. AA: OR = 1.67, 95% CI, 1.39–2.01; additive model, G vs. A: OR = 1.64, 95% CI, 1.37–1.95) and TLR4 +1196C/T polymorphism (heterozygous model, CT vs. CC: OR = 1.42, 95% CI, 1.11–1.81; additive model, T vs. C: OR = 1.36, 95% CI, 1.08–1.72), similar results were obtained in the subgroup analyses of Caucasian, whereas no associations were detected in any genetic models of non-Caucasian.</p><p>Conclusions</p><p>The overall results suggest that TLR4 polymorphisms (+896A/G and +1196C/T) may be associated with a significantly increased gastric cancer risk in Caucasian.</p></div

Sensitivity analysis for heterogeneity.

<p>A. AG vs. AA; B. G vs. A; C. CT vs. CC; D. T vs. C.</p