Correlations Between Polymorphisms of Extracellular Superoxide Dismutase, Aldehyde Dehydrogenase-2 Genes, as Well as Drinking Behavior and Pancreatic Cancer

Objective To investigate the correlation between drinking behavior combined with polymorphisms of extracellular superoxide dismutase （EC-SOD） and aldehyde dehydrogenase-2 （ALDH2） genes and pancreatic cancer. Methods The genetic polymorphisms of EC-SOD and ALDH2 were analyzed by polymerase chain reaction restriction fragment length polymorphism in the peripheral blood leukocytes obtained from 680 pancreatic cancer cases and 680 non-cancer controls. Subsequently the frequency of genotype was compared between the pancreatic cancer patients and the healthy controls.The relationship of drinking with pancreatic cancer was analyzed. Results The frequencies of EC-SOD （C/G） and ALDH2 variant genotypes were 37.35% and 68.82% respectively in the pancreatic cancer cases, and were significantly higher than those in the healthy controls （21.03% and 44.56%, all P〈0.01）. People who carried EC-SOD （C/G） （0R=2.24, 95% C1= 1.81-4.03, P〈0.01） or ALDH2 variant genotypes （OR=2.75, 95% CI=1.92-4.47, P〈0.01） had a high risk to develop pancreatic cancer. Those who carried EC-SOD （C/G） genotype combined with ALDH2 variant genotype had a high risk for pancreatic cancer （29.56% vs. 6.76%, 0R=7.69, 95% CI=3.58-10.51, P〈0.01）. The drinking rate of the pancreatic cancer group （64.12%） was significantly higher than that of the control group （40.15%; OR=2.66, 95% CI=1.30-4.42, P〈0.01）. An interaction between drinking and EC-SOD （C/G）/ALDH2 variant genotypes increased the risk of occurrence of pancreatic cancer （OR=25.00, 95% CI= 11.87-35.64, P〈0.01）. Conclusion EC-SOD （C/G）, ALDH2 variant genotypes and drinking might be the risk factors of pancreatic cancer.

Phytosphinganine Affects Plasmodesmata Permeability via Facilitating PDLP5-Stimulated Callose Accumulation in Arabidopsis

Plant plasmodesmata (PDs) are specialized channels that enable communication between neighboring cells. The intercellular permeability of PDs, which affects plant development, defense, and responses to stimuli, must be tightly regulated. However, the lipid compositions of PD membrane and their impact on PD permeability remain elusive. Here, we report that the Arabidopsis sld1 sld2 double mutant, lacking sphingolipid long-chain base 8 desaturases 1 and 2, displayed decreased PD permeability due to a significant increase in callose accumulation. PD-located protein 5 (PDLP5) was significantly enriched in the leaf epidermal cells of sld1 sld2 and showed specific binding affinity to phytosphinganine (t18:0), suggesting that the enrichment of t18:0-based sphingolipids in sld1 sld2 PDs might facilitate the recruitment of PDLP5 proteins to PDs. The sld1 sld2 double mutant seedlings showed enhanced resistance to the fungal-wilt pathogen Verticillium dahlia and the bacterium Pseudomonas syringae pv. tomato DC3000, which could be fully rescued in sld1 sld2 pdlp5 triple mutant . Taken together, these results indicate that phytosphinganine might regulate PD functions and cell-to-cell communication by modifying the level of PDLP5 in PD membranes.

Targeted Lipidomics Studies Reveal that Linolenic Acid Promotes Cotton Fiber Elongation by Activating Phosphatidylinositol and Phosphatidylinositol Monophosphate Biosvnthesis

The membrane lipids from fast-elongating wild-type cotton （Gossypium hirsutum） fibers at 10 days post- anthesis, wild-type ovules with fiber cells removed, and ovules from the fuzzless-lintless mutant harvested at the same age, were extracted, separated, and quantified. Fiber cells contained significantly higher amounts of phosphatidylinositol （PI） than both ovule samples with PI 34：3 being the most predominant spe- cies. The genes encoding fatty acid desaturases （415GhFAD）, PI synthase （PIS） and PI kinase （PIK） were expressed in a fiber-preferential manner. Further analysis of phosphatidylinositol monophosphate （PIP） indicated that elongating fibers contained four- to five-fold higher amounts of PIP 34：3 than the ovules. Exog- enously applied linolenic acid （C18：3）, soybean L-α-PI, and PIPs containing PIP 34：3 promoted significant fiber growth, whereas a liver PI lacking the C18：3 moiety, linoleic acid, and PIP 36：2 were completely ineffec- tive. The growth inhibitory effects of carbenoxolone, 5-hydroxytryptamine, and wortmannin were reverted by C18：3, PI, or PIP, respectively, suggesting that PIP signaling is essential for fiber cell growth. Furthermore, cotton plants expressing virus-induced gene-silencing constructs that specifically suppressed Gh15FAD, GhPIS, or GhPIK expression, resulted in significantly short-fibered phenotypes. Our data provide the basis for in-depth studies on the roles of PI and PIP in mediating cotton fiber growth.

Interaction of Polymorphisms of Resistin Gene Promoter -420C/G, Glutathione Peroxidase -1 Gene Pro198Leu and Cigarette Smoking in Nonalcoholic Fatty Liver Disease

Background： Many studies have suggested that cigarette smoking and polymorphisms of resi stin and glutathione peroxidase-1 （GPx-1） genes are closely correlated with tile pathogenesis of nonalcoholic lhtty liver disease （NAFLD）. However, few reports have investigated these associations with respect to NAFLD susceptibility. We, therefore, exalnined the distribution of polymorphisms in GPx-l and resistin genes in NAFLD patients and healthy controls and analyzed the relationship between these polymorphisms and smoking status. Methods： Nine hundred NAFLD patients and 900 healthy controls were selected, and the genetic polymorphisms of resistin gene promoter- 420C/G and GPx- 1 gene Pro 198Leu were analyzed by polymorphism-polymerase chain reaction （PCR） in DNA extracted from peripheral blood leukocytes. Interactions between tile two mutants and the gene-environment interaction with cigarette smoking were also analyzed. Results： Genotype frequencies of 420C/G （GG） and Pro198Leu （LL） were significantly higher in NAFLD cases （49.56% and 50.11%, respectively） compared with healthy controls （23.67% and 24.22%, respectively） （P = 0.0069： P= 0.0072）. Moreover, the risk of NAFLD with 420C/G （GGJ was significantly higher than in controls （odds ratio [OR] =3.1685, 95% confidence interval （（7） 1.9366-5.2073）. Individuals carrying Pro198Leu （LL） had a high risk of NAFLD （OR - 3.1424, 95% C/= 1.7951 5.2367）. Combined analysis of the polymorphisms showed that the -420C/G （GG）/Pro198Leu （LL） genotype was significantly more common in the NAFLD group than in the control group （39.44% vs. 12.78%, respectively, P 0.0054）, while individuals with -420C/G （GG）/Pro198Leu （LL） had a high risk of NAFLD （OR = 5.（1357, 95% CI= 3.1852 7.8106）. Moreover, the cigarette smoking rate in the NAFLD group was significantly higher than in tile control group （OR = 1.8990, P = 0.0083 in the smoking index （SI） _〈400 subgroup： OR = 5.0937, P = 0.0051 in the SI 〉400 subgroup）, and statistical analysis suggested a positive interaction between cigarette smoking and 420C/G （GG） （y = 5.6018 in tile SI≤400 subgroup; γ - 4.4770 in the SI 〉400 subgroup） and Pro198Leu （LL） （y = 5.7715 in the SI ≤400 subgroup： γ 4.5985 in the SI 〉400 subgroup） in increasing the risk of NAFLD. Conclusion： NAFLD risk factors include -420C/G （GG）, Pro198Leu （LL） and cigarette smoking, and these three factors have a significant additive effect on NAFLD risk.