ABSTRACT
Carbon nanotubes (MWCNTs) and nano-silica (nano-SiO2) are widely used in the field of life science because of their special physical and chemical properties. In this study, the effects of different concentrations of MWCNTs (0 mg·L-1, 200 mg·L-1, 400 mg·L-1, 800 mg·L-1 and 1200 mg·L-1) and nano-SiO2 (0 mg·L-1, 150 mg·L-1, 800 mg·L-1, 1500 mg·L-1 and 2500 mg·L-1) on maize seedling growth and relative mechanisms were explored. The main results are as follows: MWCNTs and nano-SiO2 can promote the growth of maize seedlings, and promote plant height, root length, the dry and fresh weight of seedlings, root-shoot ratio and so on. The ability to accumulate dry matter increased, the relative water content of leaves increased, the electrical conductivity of leaves decreased, the stability of cell membranes improved and the water metabolism ability of maize seedlings increased. The treatment of MWCNTs with 800 mg·L-1 and nano-SiO2 with 1500 mg·L-1 had the best effect on seedling growth. MWCNTs and nano-SiO2 can promote the development of root morphology, increase root length, root surface area, average diameter, root volume and total root tip number and improve root activity, so as to improve the absorption capacity of roots to water and nutrition. After MWCNT and nano-SiO2 treatment, compared with the control, the contents of O2·- and H2O2 decreased, and the damage of reactive oxygen free radicals to cells decreased. MWCNTs and nano-SiO2 can promote the clearance of reactive oxygen species and maintain the complete structure of cells, so as to slow down plant aging. The promoting effect of MWCNTs treated with 800 mg·L-1 and nano-SiO2 treated with 1500 mg·L-1 had the best effect. After treatment with MWCNTs and nano-SiO2, the activities of key photosynthesis enzymes PEPC, Rubisco, NADP-ME, NADP-MDH and PPDK of maize seedlings increased, which promoted the opening of stomata, improved the fixation efficiency of CO2, improved the photosynthetic process of maize plants and promoted plant growth. The promoting effect was the best when the concentration of MWCNTs was 800 mg·L-1 and the concentration of nano-SiO2 was 1500 mg·L-1. MWCNTs and nano-SiO2 can increase the activities of the enzymes GS, GOGAT, GAD and GDH related to nitrogen metabolism in maize leaves and roots, and can increase the content of pyruvate, so as to promote the synthesis of carbohydrates and the utilization of nitrogen and promote plant growth.
ABSTRACT
Rice breeders are now developing new varieties with semi-high or even high plant height to further increase the grain yield, and the problem of lodging has re-appeared. We identified a major quantitative trait locus (QTL), qSCM4, for resistance to lodging by using an F2 segregant population and a recombinant self-incompatible line population from the cross between Shennong265 (SN265) and Lijiangxintuanheigu (LTH) after multiple years and multiple environments. Then, the residual heterozygous derived segregant population which consisted of 1781 individual plants, and the BC3F2 segregant population which consisted of 3216 individual plants, were used to shorten the physical interval of qSCM4 to 58.5 kb including 11 genes. DNA sequencing revealed the most likely candidate gene for qSCM4 was Os04g0615000, which encoded a functional protein with structural domains of serine and cysteine. There were 13 DNA sequence changes in LTH compared to SN265 in this gene, including a fragment deletion, two base changes in the 3' UTR region, six base changes in the exons, and four base changes in the introns. A near-isogenic line carrying qSCM4 showed that it improved the lodging resistance through increasing stem thickness by 25.3% and increasing stem folding resistance by 20.3%. Furthermore, it was also discovered that qSCM4 enhanced the primary branch per panicle by 16.7%, secondary branch by per panicle 9.9%, and grain number per panicle by 14.7%. All the above results will give us a valuable genetic resource for concurrently boosting culm strength and lodging resistance, and they will also provide a basis for further research on the lodging resistance mechanism of rice.
Subject(s)
Oryza , Quantitative Trait Loci , Oryza/genetics , Oryza/metabolism , Edible Grain/genetics , Edible Grain/metabolism , Plant Proteins/genetics , Plant Proteins/metabolism , IntronsABSTRACT
Corn straw is an abundant lignocellulose resource and by-product of agricultural production. With the continuous increase in agricultural development, the output of corn straw is also increasing significantly. However, the inappropriate disposal of straw results in wasting of resources, and also causes a serious ecological crisis. Screening microorganisms with the capacity to degrade straw and understanding their mechanism of action is an efficient approach to solve such problems. For this purpose, our research group isolated three actinomycete strains with efficient lignocellulose degradation ability from soil in the cold region of China: Streptomyces sp. G1T, Streptomyces sp. G2T and Streptomyces sp. G3T. Their microbial properties and taxonomic status were assessed to improve our understanding of these strains. The three strains showed typical characteristics of the genus Streptomyces, and likely represent three different species. Genome functional annotation indicated that most of their genes were related to functions like carbohydrate transport and metabolism. In addition, a similar phenomenon also appeared in the COG and CAZyme analyses, with a large number of genes encoding carbohydrate-related hydrolases, such as cellulase, glycosidase and endoglucanase, which could effectively destroy the structure of lignocellulose in corn straw. This unambiguously demonstrated the potential of the three microorganisms to hydrolyze macromolecular polysaccharides at the molecular level. In addition, in the straw-returning test, the decomposing consortium composed of the three Streptomyces isolates (G123) effectively destroyed the recalcitrant bonds between the various components of straw, and significantly reduced the content of active components in corn straw. Furthermore, microbial diversity analysis indicated that the relative abundance of Proteobacteria, reportedly associated with soil antibiotic resistance and antibiotic degradation, was significantly improved with straw returning at both tested time points. The microbial diversity of each treatment was also dramatically changed by supplementing with G123. Taken together, G123 has important biological potential and should be further studied, which will provide new insights and strategies for appropriate treatment of corn straw.
ABSTRACT
Sepsis-associated encephalopathy (SAE) is the cognitive impairment resulting from sepsis and is associated with increased morbidity and mortality. Hydrogen has emerged as a promising therapeutic agent to alleviate SAE. The mechanism, however, remains unclear. This research aimed to determine whether hydrogen alleviates SAE by regulating microglia polarization and whether it is mediated by the mammalian target of rapamycin (mTOR)-autophagy pathway. Septic models were established by cecal ligation and puncture (CLP) performed on mice. The Morris Water Maze was used to evaluate cognitive function. M1/M2 microglia polarization was assessed by immunofluorescence. Inflammatory cytokines were determined by ELISA. Septic cell models were established using BV-2 cells incubated with 1 µg/ml lipopolysaccharide (LPS). M1/M2 microglia polarization was assessed by flow cytometry. Inflammatory cytokines from culture medium supernatant were determined by ELISA, and associated protein expression levels of mTOR-autophagy pathway were assessed by Western blot. Hydrogen inhalation attenuated sepsis-induced cognitive impairment with improved escape latency, time spent in the target platform quadrant and number of times crossing the target platform. In both animal and cell research, hydrogen reduced TNF-α, IL-6 and HMGB1 levels and M1 polarization, but increased IL-10 and TGF-ß levels and M2 polarization. Hydrogen treatment decreased the ratio of p-mTOR/mTOR and the expression of p62 and increased the ratio of p-AMPK/AMPK, LC3II/LC3I and the expression of TREM-2 and Beclin-1 in LPS-treated BV-2 cells. MHY1485, an mTOR activator, abolished the protective effects of hydrogen in vitro. Taken together, these results demonstrated that hydrogen attenuated sepsis-induced neuroinflammation by modulating microglia polarization, which was mediated by the mTOR-autophagy signaling pathway.
Subject(s)
Anti-Inflammatory Agents/therapeutic use , Hydrogen/therapeutic use , Microglia/immunology , Neurogenic Inflammation/therapy , Sepsis/therapy , TOR Serine-Threonine Kinases , Animals , Autophagy , Cell Differentiation , Cell Line , Humans , Male , Mice , Mice, Inbred C57BL , Microglia/drug effects , Signal Transduction , TOR Serine-Threonine Kinases/metabolismABSTRACT
The interaction of remifentanil with glutamate systems has an important role in remifentanil-induced thermal and mechanical hyperalgesia. A previous study by our group suggested that the trafficking and function of glutamate receptor 1 (GluR1) subunits contributes to remifentanil-induced hyperalgesia by regulating the phosphorylation of GluR1 in dorsal horn neurons. The present study demonstrated that δ opioid receptor (DOR) inhibition prevented thermal and mechanical hyperalgesia, which was induced by remifentanil infusion via attenuating GluR1 subunit trafficking and α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor (AMPAR) function in dorsal horn neurons. Sprague Dawley rats received a plantar incision and remifentanil infusion to induce a model of postoperative hyperalgesia. Thermal and mechanical pain was tested at 8 different time-points. Expression of AMPAR subunits GluR1 and DOR, as well as the phosphorylation status of GluR1 were evaluated by western blot analysis. Furthermore, the function of AMPAR in the spinal dorsal horn was measured by whole-cell patch-clamp recording. Remifentanil-induced thermal and mechanical hyperalgesia appeared after the 60-min infusions, reaching a peak level on day 2 and persisting for 5 days. Remifentanil infusion led to upregulation of membrane expression of the AMPAR subunit GluR1 and DOR (P=0.003 and 0.001, respectively) no change in total GluR1 and DOR expression levels (P=0.244 and 0.531, respectively). Selective DOR inhibitor naltrindole caused a reduction of remifentanil-induced hyperalgesia, which was accompanied by downregulation of membrane levels of GluR1 in the spinal cord (P=0.0013). In addition, DOR inhibition led to downregulation of GluR1 phosphorylated at Ser845. Furthermore, the AMPAR-mediated miniature excitatory post-synaptic current was increased in frequency and in amplitude in dorsal horn neurons (P=0.002 and 0.0011, respectively), which was decreased by incubation with naltrindole. Combined behavioral, western blot and electrophysiological evidence indicated that remifentanil-induced hyperalgesia was mediated by DOR activation, followed by phosphorylation-dependent GluR1 trafficking and AMPAR function enhancement in the spinal cord. DOR appears to be required for remifentanil and incision-induced hyperalgesia development and to be a potential biochemical target for treating opioid-induced postoperative hyperalgesia.
ABSTRACT
UNLABELLED: Research suggests that the addition of dexmedetomidine to local anesthetics can prolong peripheral nerve blocks; however, it is not known whether dexmedetomidine can reduce the quantity of local anesthetic needed. We hypothesized that adding dexmedetomidine as an adjuvant to an obturator nerve block could reduce the median effective concentration of lidocaine. In this double-blinded randomized trial, 60 patients scheduled for elective transurethral resection of bladder tumors on the lateral wall were randomly divided into two groups: the control group (C group, n = 30) and the dexmedetomidine group (D group, n = 30). Two main branches of the obturator nerve (i.e., anterior and posterior) were identified using neural stimulation at the inguinal level, with only lidocaine used for the C group and 1 µg/kg dexmedetomidine combined with lidocaine used for the D group. The median effective concentration was determined by an up-and-down sequential trial. The ratio of two consecutive concentrations was 1.2. The median effective concentration (95% confidence interval) of lidocaine was 0.57% (0.54%-0.62%) in the C group and 0.29% (0.28%-0.38%) in the D group. The median effective concentration of lidocaine was significantly lower in the D group than in the C group (p < 0.05). These results indicate that dexmedetomidine (1 µg/kg) in combination with lidocaine for obturator nerve block decreases the median effective concentration of lidocaine. TRIAL REGISTRATION: ClinicalTrials.gov NCT02066727.
Subject(s)
Adjuvants, Pharmaceutic , Analgesics, Non-Narcotic/administration & dosage , Anesthetics, Local/therapeutic use , Dexmedetomidine/administration & dosage , Lidocaine/therapeutic use , Nerve Block , Obturator Nerve/drug effects , Adolescent , Adult , Aged , Aged, 80 and over , Analgesics, Non-Narcotic/adverse effects , Anesthetics, Local/administration & dosage , Anesthetics, Local/adverse effects , Dexmedetomidine/adverse effects , Dose-Response Relationship, Drug , Female , Humans , Lidocaine/administration & dosage , Lidocaine/adverse effects , Male , Middle Aged , Muscle Strength/drug effects , Muscle, Skeletal/drug effects , Muscle, Skeletal/innervation , Nerve Block/methods , Young AdultABSTRACT
AIM: To establish and validate a simple quantitative assessment method for nonalcoholic fatty liver disease (NAFLD) based on a combination of the ultrasound hepatic/renal ratio and hepatic attenuation rate. METHODS: A total of 170 subjects were enrolled in this study. All subjects were examined by ultrasound and (1)H-magnetic resonance spectroscopy ((1)H-MRS) on the same day. The ultrasound hepatic/renal echo-intensity ratio and ultrasound hepatic echo-intensity attenuation rate were obtained from ordinary ultrasound images using the MATLAB program. RESULTS: Correlation analysis revealed that the ultrasound hepatic/renal ratio and hepatic echo-intensity attenuation rate were significantly correlated with (1)H-MRS liver fat content (ultrasound hepatic/renal ratio: r = 0.952, P = 0.000; hepatic echo-intensity attenuation r = 0.850, P = 0.000). The equation for predicting liver fat content by ultrasound (quantitative ultrasound model) is: liver fat content (%) = 61.519 × ultrasound hepatic/renal ratio + 167.701 × hepatic echo-intensity attenuation rate -26.736. Spearman correlation analysis revealed that the liver fat content ratio of the quantitative ultrasound model was positively correlated with serum alanine aminotransferase, aspartate aminotransferase, and triglyceride, but negatively correlated with high density lipoprotein cholesterol. Receiver operating characteristic curve analysis revealed that the optimal point for diagnosing fatty liver was 9.15% in the quantitative ultrasound model. Furthermore, in the quantitative ultrasound model, fatty liver diagnostic sensitivity and specificity were 94.7% and 100.0%, respectively, showing that the quantitative ultrasound model was better than conventional ultrasound methods or the combined ultrasound hepatic/renal ratio and hepatic echo-intensity attenuation rate. If the (1)H-MRS liver fat content had a value < 15%, the sensitivity and specificity of the ultrasound quantitative model would be 81.4% and 100%, which still shows that using the model is better than the other methods. CONCLUSION: The quantitative ultrasound model is a simple, low-cost, and sensitive tool that can accurately assess hepatic fat content in clinical practice. It provides an easy and effective parameter for the early diagnosis of mild hepatic steatosis and evaluation of the efficacy of NAFLD treatment.
Subject(s)
Adiposity , Kidney/diagnostic imaging , Liver/diagnostic imaging , Non-alcoholic Fatty Liver Disease/diagnostic imaging , Adult , Area Under Curve , Case-Control Studies , Female , Humans , Kidney/physiopathology , Liver/physiopathology , Male , Middle Aged , Non-alcoholic Fatty Liver Disease/physiopathology , Predictive Value of Tests , Prognosis , Proton Magnetic Resonance Spectroscopy , ROC Curve , Reproducibility of Results , Severity of Illness Index , UltrasonographyABSTRACT
OBJECTIVE: To explore the effect of ulinastatin (UTI) continuous infusion combined Rivaroxaban on the deep vein thrombosis in patients undergoing major orthopedic surgery. METHODS: Forty-five patients undergoing major orthopedic surgery were randomly divided into three groups:ulinastatin continuous infusion (Uc) group, ulinastatin single injection (Us) group and control (C) group. All patients received patient-controlled intravenous analgesia (PCIA) after operation, and took Rivaroxaban 10 mg orally 12 hours after operation. Ulinastatin (5 000 U/kg) was given intravenously to both Uc and Us groups preoperatively. Group C was given isometric normal saline, group Uc was pumped UTI continuous intravenously at the end of surgery (10 000 U/kg) to 48 hours through PCIA pump. The values of hematocrit (HCT), thrombomodulin (TM), Interleukin (IL-6), thrombin-antithrombin complex (TAT), D-Dimer (D-D) were normally tested before surgery (T1), at the end of the surgery (T2), 12 hours (T3), 24 hours (T4) and 48 hours (T5) after surgery. RESULTS: Compared with T1, there was an upward tendency in TM, IL-6, TAT, and D-D after operation in group C group (P<0.05). The values of them were significantly increased from nearly 24-hour after surgery in Us group (P<0.05). In group Uc, there were no significant changes in these indices after operation (P>0.05). CONCLUSIONS: During the perioperative period, ulinastatin continuous infusion combined Rivaroxaban can correct blood hypercoagulability through different approaches in patients undergoing major orthopedic surgery.
ABSTRACT
Oxidative damage plays a critical role in many diseases of the central nervous system. This study was conducted to determine the molecular mechanisms involved in the putative anti-oxidative effects of sevoflurane against experimental stroke. Focal cerebral ischemia was performed via 1h of middle cerebral artery occlusion followed by reperfusion. At the onset of reperfusion, rats were subjected to postconditioning with sevoflurane or without sevoflurane for 1h. Neurological deficit score was assessed at different time points after reperfusion. Cerebral infarct volume, oxidative stress level and the binding activity of Nrf2 to antioxidant response element were assessed, meanwhile the expression of nuclear factor-erythroid 2-related factor 2 (Nrf2), quinine oxidoreductase 1 (NQO1), protein kinase B (Akt) and phosphor-Akt was examined by Western blot at 72h after reperfusion. Sevoflurane postconditioning administration significantly reduced neurological deficit score, infarct volume and oxidative stress levels, while increased the expression of phosphorylation Akt, NQO1, Nrf2 and the binding activity of Nrf2 to ARE in middle cerebral artery occlusion rats. These neuroprotective effects were all suppressed by LY294002, a selective PI3K blocker. Taken together, these findings provided evidence that sevoflurane postconditioning protects brain against ischemic/reperfusion injury, and this neuroprotective effect involves the Akt/Nrf2 pathway.