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Low temperature has become a major abiotic stress factor that can reduce maize yield and cause a number of economic loss. This study was designed to identify key genes and pathways associated with coldresistance of maize. The gene expression profile GSE46704, including 4 control temperature treated plants and 4 low temperature treated plants, was downloaded from the Gene Expression Omnibus database. Differentially-expressed genes (DEGs) were identified by limma package. Then, protein-protein interaction (PPI) network and module selection were constructed using Cytoscape. Moreover, the DEGs were re-matched based on the Zea mays L. gene ID and symbol data from PlantRegMap. Finally, the re-matched DEGs were performed functional and pathway enrichment analyses by the DAVID online tool. A total of 750 DEGs were screened (including 387 up-regulated and 363 down-regulated genes) In the PPI network, GRMZM2G070837_P01 and GRMZM2G114578_P01 had higher degrees. Besides, carbohydrate metabolic process, starch and sucrose metabolism and biosynthesis of secondary metabolites were significantly enriched in functional and pathway enrichment analysis. GRMZM2G070837_P01 and GRMZM2G114578_P01 might play a critical role in cold-resistance of maize. Meanwhile, carbohydrate metabolic process, starch and sucrose metabolism and biosynthesis of secondary metabolites might function in cold-resistance of maize.

Objective This study was designed to investigate the action and mechanism of cordyceps polysaccharide on rat acute liver failure (ALF). Methods Sixty rats were randomly divided into five groups: normal group, model group, and cordyceps polysaccharide groups with high, middle and low doses (20, 10 and 5 mg/ml). Apoptosis was detected through TUNEL method. Protein expressions of caspase 1, IL-18, IL-10, VEGF, and SDF-1α in liver tissue are detected by Western Blot. PCNA and sIRPα1 contents were measured by PCR method. Rat ALF is modeled with a D-galactosamine induced by lipopolysaccharide (LPS). Results The results after modelling showed tissue HE staining wiith typical manifestation of acute liver injury. Compared with the medicated group, serum ALT and AST, as well as hepatocyte apoptosis are significantly higher in the liver failure group, in a time-dependent way. This suggests that medication can effectively inhibit the expression of caspase 1, IL-18, and IL-10, while simultaneously increasing the expression of VEGF and SDF-1α, as well as of PCNA and sIRPα1. Cordyceps polysaccharide can alleviate the immune inflammatory response in acute liver failure, and may be specifically homing to the damaged liver, thus promoting the secretion of VEGF, proliferation of hepatocyte, regeneration of liver vessels, and repair of liver tissues. Conclusion Medication can reduce the IL-10 level, regulate the equilibrium of pro-inflammatory and anti-inflammatory factors, and decrease the level of caspase 1 and IL-18 (Tab. 2, Fig. 1, Ref. 18).

Based on the catalytic oxidation, the cross-linked silk fibroin membrane and the chitosan-modified silk fibroin membrane are prepared by means of tape-casting method. Compared with the silk fibroin membrane without cross-linking, the cross-linked membrane has lower water solubility and higher breaking strength. The structural differences between control and cross-linked membrane are confirmed by Atomic Force Microscope and X-ray Photoelectron Spectroscopy measurements. The analysis of Sodium Dodecyl Sulfate Polyacrylamide Gel Electrophoresis further proves that the silk fibroin is cross-linked by tyrosinase. The chitosan-modified silk fibroin membrane shows excellent antibacterial activity against Escherichia coli, and the inhibition rate is about 95%. Our results indicate the potential application of this blend membrane in biomedical material.

We investigated the mechanism of the effect of lentinan on 3T3-L1 fat cell formation by inhibiting the peroxisome proliferator-activated receptor gamma (PPARγ)/protein kinase B (AKT) signaling pathway. 3T3-L1 fat cells were treated with 80 mM lentinan with or without the PPARγ activator, 100 mM rosiglitazone for 24 h. Reverse transcription-polymerase chain reaction was applied to detect PPARγ and AKT mRNA expression levels. Western blotting was used to detect AKT protein expression level. Compared with the control group, 80 mM lentinan increased PPARγ mRNA expression and downregulated AKT mRNA expression. After treatment with rosiglitazone, PPARγ mRNA expression increased by 78% (P < 0.05), while AKT mRNA expression decreased by 71% (P < 0.05). Lentinan treatment decreased AKT protein expression by 33%, and AKT protein expression in the lentinan and rosiglitazone co-treatment group was reduced by 28% compared with the lentinan treatment group. We found that 80 mM lentinan increased PPARγ mRNA expression and reduced AKT mRNA. Combination treatment with rosiglitazone increased this effect. This suggests that lentinan can depress 3T3-L1 fat cell formation by inhibiting the PPARγ/AKT signaling pathway.

SummaryPineapple (Ananas comosus L. ‘Comte de Paris’) fruit at commercial maturity (180 fruit per treatment, three replicates) were immersed in 0, 1.0, 3.0, or 5.0 mM salicylic acid (SA) for 15 min, then stored at 10oC and 90% relative humidity (RH) for 20 d. After 20 d in cold storage, they were moved to 20oC for 2 d to simulate shelf-life. Physiological and biochemical responses were studied. The results showed that the 3.0 or 5.0 mM SA treatments lowered the internal browning (IB) index, while the 5.0 mM SA treatment decreased the soluble solids content (SSC), titratable acidity (TA), and soluble sugar content, but increased ascorbic acid (AsA) levels at the end of shelf-life. Furthermore, during cold storage, all SA treatments significantly decreased the rate of tissue respiration in pineapple fruit. SA at 5.0 mM significantly decreased the activities of peroxidase (POD), polyphenol oxidase (PPO), and phenylalanine ammonia-lyase (PAL), but increased the activities of superoxide dismutase (SOD) and asc...