RESUMEN
WS2-C is produced from a hydrothermal reaction, in which WS2 nano-sheets are coated with carbon, using glucose as the carbon source. In order to investigate the tribological properties of WS2-C as a lubricant additive, WS2-C was modified by surfactant Span80, and friction tests were carried out on an MRS-10A four-ball friction and wear tester. The results show that Span80 can promote the dispersibility of WS2-C effectively in base oil. Adding an appropriate concentration of WS2-C can improve the anti-wear and anti-friction performance of the base oil. The friction coefficient reached its lowest point upon adding 0.1 wt % WS2-C, reduced by 16.7% compared to the base oil. Meanwhile, the wear scar diameter reached its minimum with 0.15 wt % WS2, decreasing by 26.45%. Moreover, at this concentration, the depth and width of the groove and the surface roughness on the wear scar achieved their minimum. It is concluded that WS2-C dispersed in oil could enter friction pairs to avoid their direct contact, thereby effectively reducing friction and wear. At the same time, WS2-C reacts with the friction matrix material to form a protective film, composed of C, Fe2O3, FeSO4, WO3, and WS2, repairing the worn surface.
RESUMEN
Phytophthora root and stem rot, a destructive disease of soybean [Glycine max (L.) Merr.], is caused by the oomycete Phytophthora sojae. However, how the disease resistance mechanisms of soybean respond to P. sojae infection remains unclear. Previously, we showed that GmWRKY31, which interacts with a sucrose non-fermenting-1(SNF1)-related protein kinase (SnRK), enhances resistance to P. sojae in soybean. Here, we report that the membrane-localized SnRK GmSnRK1.1 is involved in the soybean host response to P. sojae. The overexpression of GmSnRK1.1 (GmSnRK1.1-OE) increased soybean resistance to P. sojae, and the RNA interference (RNAi)-mediated silencing of GmSnRK1.1 (GmSnRK1.1-R) reduced resistance to P. sojae. Moreover, the activities and transcript levels of the antioxidant enzymes superoxide dismutase and peroxidase were markedly higher in the GmSnRK1.1-OE transgenic soybean plants than in the wild type (WT), but were reduced in the GmSnRK1.1-R plants. Several isoflavonoid phytoalexins related genes GmPAL, GmIFR, Gm4CL and GmCHS were significantly higher in "Suinong 10" and GmSnRK1.1-OE lines than these in "Dongnong 50," and were significantly lower in GmSnRK1.1-R lines. In addition, the accumulation of salicylic acid (SA) and the expression level of the SA biosynthesis-related gene were significantly higher in the GmSnRK1.1-OE plants than in the WT and GmSnRK1.1-R plants, moreover, SA biosynthesis inhibitor treated GmSnRK1.1-R lines plants displayed clearly increased pathogen biomass compared with H2O-treated plants after 24 h post-inoculation. These results showed that GmSnRK1.1 positively regulates soybean resistance to P. sojae, potentially functioning via effects on the expression of SA-related genes and increased accumulation of SA.
RESUMEN
Phytophthora root and stem rot of soybean [Glycine max (L.) Merr.] caused by the oomycete Phytophthora sojae, is a destructive disease worldwide. The molecular mechanism of the soybean response to P. sojae is largely unclear. We report a novel WRKY transcription factor (TF) in soybean, GmWRKY31, in the host response to P. sojae. Overexpression and RNA interference analysis demonstrated that GmWRKY31 enhanced resistance to P. sojae in transgenic soybean plants. GmWRKY31 was targeted to the nucleus, where it bound to the W-box and acted as an activator of gene transcription. Moreover, we determined that GmWRKY31 physically interacted with GmHDL56, which improved resistance to P. sojae in transgenic soybean roots. GmWRKY31 and GmHDL56 shared a common target GmNPR1 which was induced by P. sojae. Overexpression and RNA interference analysis demonstrated that GmNPR1 enhanced resistance to P. sojae in transgenic soybean plants. Several pathogenesis-related (PR) genes were constitutively activated, including GmPR1a, GmPR2, GmPR3, GmPR4, GmPR5a, and GmPR10, in soybean plants overexpressing GmNPR1 transcripts. By contrast, the induction of PR genes was compromised in transgenic GmNPR1-RNAi lines. Taken together, these findings suggested that the interaction between GmWRKY31 and GmHDL56 enhances resistance to P. sojae by regulating defense-related gene expression in soybean.
RESUMEN
OBJECTIVE: To evaluate the influence of anisodamine (Ani) on restoration of spontaneous circulation (ROSC) and cardiopulmonary resuscitation (CPR) rate in a randomized, blinded experimental study so as to explore a new treatment for CPR. METHODS: Forty-five Sprague-Dawley (SD) rats were randomized to three groups: control group (0.9% normal saline), epinephrine (Epi) group and Epi plus Ani group (combined group), 15 rats in each group. Ventricular fibrillation (VF) or asystole was induced by transoesophageal alternating current stimulation. A blinded drug administration and mechanical chest compression were used in this study (Epi 200 microg/kg, Ani 10 mg/kg). ROSC rate and resuscitation rate were compared among these groups. RESULTS: Combined group had higher ROSC rate(93.3% vs. 46.7%), resuscitation rate (80.0% vs.33.3%) and survival rate within 3 hours (83.3% vs.20.0%) compared with Epi group (all P<0.05). ROSC occurred only in one rat of control group. Mean arterial pressure (MAP) at the beginning of ROSC in Epi group was higher compared with combined group (P<0.05). After ROSC, MAP decreased in both drug groups, especially after 5 minutes of ROSC, and MAP in Epi group was lower than that of combined group. There was difference between the two groups till 30 minutes after ROSC (all P<0.05) . CONCLUSION: Administration of Epi plus Ani at the beginning of treatment for cardiac arrest could improve ROSC rate and resuscitation rate.