不同处理对姜花属杂种种子发芽率的影响

[目的]研究不同处理对姜花属杂交种子发芽率的影响。[方法]分别用0（CK）、50、100、150、200 mg/L GA3浸泡种子,在24和28℃下进行发芽试验。[结果]经100 mg/L GA3浸泡后的杂交种子在28℃下发芽率最高,达97.6%。[结论]GA3处理可显著提高种子发芽率。     

Marker‐assisted introgression of rare allele of β‐carotene hydroxylase (crtRB1) gene into elite quality protein maize inbred for combining high lysine,tryptophan and provitamin A in maize

Vitamin A deficiency in humans is a widespread health problem. Quality protein maize (QPM) is a popular food rich in lysine and tryptophan, but poor in provitamin A (proA). Here, we report the improvement of an elite QPM inbred, HKI1128Q for proA using marker‐assisted introgression of crtRB1‐favourable allele. HKI1128 was one of the parental lines of three popular hybrids in India and was converted to QPM in our earlier programme. Severe segregation distortion for crtRB1 was observed in BC₁F₁, BC₂F₁ and BC₂F₂. Background selection by 100 SSRs revealed mean recovery of 91.07% recurrent parent genome varying from 88.78% to 93.88%. Across years, introgressed progenies possessed higher mean β‐carotene (BC: 9.22 µg/g), β‐cryptoxanthin (BCX: 3.05 µg/g) and provitamin A (proA: 10.75 µg/g) compared to HKI1128Q (BC: 2.26 µg/g, BCX: 2.26 µg/g and proA: 3.38 µg/g). High concentration of essential amino acids, viz. lysine (mean: 0.303%) and tryptophan (0.080%) in endosperm, was also retained. Multi‐year evaluation showed that introgressed progenies possessed similar grain yield (1,759–1,879 kg/ha) with HKI1128Q (1,778 kg/ha). Introgressed progenies with higher lysine, tryptophan and proA hold immense potential as donors and parents in developing biofortified hybrids.     

基于VLF/LF三维闪电探测系统的贵州省全闪分布特征分析

为进一步加强云闪分布特征分析,增强对雷暴云内物理过程的认识,利用2015—2017 年VLF/LF三维闪电探测系统的数据资料对贵州省闪电特征进行空间和时间分布特征分析。结果表明：无论云闪还是地闪,均以负闪为主;闪电发生主要集中在夏季,冬季闪电最少,闪电月际分布主要为单峰型,仅冬季Z比率大于1;闪电主要发生时段为16 时至次日凌晨2 时,Z比率与全闪频数随时间的变化呈正相关,相关系数0.618;全省闪电密度整体呈西高东低趋势,年均闪电密度为5.07 次/(a ·km2);云闪主要发生在高度2k~7 km,全年云闪高度呈下降趋势;雷电强度主要分布在5k~45 kA,平均陡度为7.34 kA/μs。本研究有利于对闪电特征开展更全面的探究和分析,同时对强对流天气监测和预警也有重要意义和价值。     

两种盐胁迫对苦楝幼苗光合特性的影响

以一年生苦楝实生苗为试材,采用温室盆栽方式,用浓度为0%(CK)、0.2%、0.4%与0.6%的Na2SO4和Na2CO3溶液分别对幼苗进行胁迫处理21 d,比较了2种盐胁迫下幼苗光合作用和叶绿素荧光参数的变化和差异。结果表明:0.2%盐浓度对Pn、Tr、Ci、Fv/Fm、Fv/Fo、qP和NPQ没有显著影响,0.6%盐浓度则影响显著。同时,各浓度盐处理对Chl a、Chl b、Chl(a+b)、Chl a/b、Fo和Fm没有显著影响。2种盐处理对苦楝幼苗叶绿素含量没有显著影响;Na2CO3胁迫通过非气孔限制引起Pn下降,而Na2SO4引起Pn下降分别为0.2%处理时是气孔限制,0.4%和0.6%处理时是非气孔限制;幼苗光合作用和光合机构对0.2%浓度胁迫有较强耐性,对0.6%浓度胁迫耐性较弱;同时,碱性盐Na2CO3胁迫对苦楝光合作用的影响整体大于中性盐Na2SO4。     

miR-140-3p inhibits viability,invasion and migration of non-small-cell lung cancer A549 cells by targeting PD-L1

AIM: To explore the target relationship between microRNA-140-3p (miR-140-3p) and programmed cell death ligand 1 (PD-L1) and their effect on the viability, migration and invasion of non-small-cell lung cancer A549 cells.METHODS: RT-qPCR was used to detect the miR-140-3p expression in HLF-1, A549 and H1299 cells, and then the A549 cells with the most significant difference were selected as the subsequent research object. TargetScan software and dual-luciferase reporter assay were performed to predict and confirm the target relationship between miR-140-3p and PD-L1. RT-qPCR and Western blot were used to determine the effects of miR-140-3p mimic and inhibitor on PD-L1 expression level. MTT assay was used to detect the viability of A549 cells. Transwell assay was performed to detect the migration and invasion abilities of the A549 cells.RESULTS: miR-140-3p was significantly down-regulated in the A549 cells and H1299 cells (P<0.05). Transfection with miR-140-3p mimic decreased the expression of PD-L1 and inhibited the viability, migration and invasion of the A549 cells. Transfection with pcDNA3.0-PD-L1 reversed the inhibitory effect of miR-140-3p on the viability, migration and invasion of the A549 cells.CONCLUSION: miR-140-3p inhibits the viability, migration and invasion of A549 cells by targeting PD-L1.     

Shikonin inhibits neuronal apoptosis induced by OGD through targeting PI3K/Akt signaling pathway

AIM: To explore the effect of shikonin on rat primary cortical neurons in oxygen-glucose deprivation (OGD)-induced injury model.METHODS: The neurons were pretreated with shikonin at different concentrations (0.02, 0.2, 2 and 20 μmol/L) followed by treatment with OGD. Lactate dehydrogenase (LDH) release assay and fluorescein diacetate/propidium iodide (FDA/PI) double staining were used to detect neuronal viability and apoptosis, and then the optimal concentration of shikonin was determined. LY294002 (PI3K/Akt signaling pathway inhibitor, 1 μmol/L) was added before the addition of shikonin, and the protein level of p-Akt (Ser473) in the neurons was determined by Wes-tern blot. LDH release assay and FDA/PI double staining were also used to detect neuronal viability and apoptosis.RESULTS: A certain concentration (0.2~20 μmol/L) of shikonin increased the viability of impaired neurons (P<0.05) and the protein level of p-Akt (Ser473) in the neurons (P<0.05). The effect of shikonin on neuronal p-Akt (Ser473) levels and the cell death were blocked by LY294002 (P<0.05).CONCLUSION: A certain concentration of shikonin reduces OGD-induced apoptosis of rat primary cortical neurons by activating PI3K/Akt signaling pathway.     

Astrocyte activity and autophagy after radiation-induced brain injury in rats

AIM: To investigate the activity of astrocytes and autophagy-related changes after radiation-induced brain injury (RBI) in rats.METHODS: A total of 36 Sprague-Dawley rats, weighing 180~200 g, were trained for 4 d in the Morris water maze. They were randomly divided into sham group, model group and 3-methyladenine (3-MA) group. The rats in model group and 3-MA group were given single whole-brain X-ray irradiation at a dose of 20 Gy after intraperitoneal anesthesia. After the irradiation was completed, the rats in model group was given 5 μL of NaCl into the lateral ventricle, and the rats in 3-MA group was injected with 3-MA at 600 nmol into the lateral ventricle. After 8 weeks of feeding, Morris water maze was used for measuring the learning and memory abilities. The brain tissues were taken and HE staining was used to observe the pathological changes of the hippocampus. The protein level of GFAP was determined by immunohistochemistry and Western blot for evaluating astrocyte activity. Dual fluorescence staining of GFAP and LC3 was performed for evaluating the changes of autophagy in the astrocytes. The protein level of cleaved caspase-3 detected by Western blot and TUNEL staining in the ipsilateral hippocampus were used to evaluate the apoptosis. The contents of tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) were examined by ELISA to assess the inflammatory response in the hippocampus.RESULTS: Radiation inhibited astrocyte activity, activated autophagy in astrocytes, and aggravated brain damage. 3-MA promoted the activation of astrocytes and promoted the repair of brain tissue damage.CONCLUSION: The injury of rat hippocampus after radiation is obvious, and the number of astrocytes is significantly reduced. 3-MA significantly attenuates the damage. This finding may provide a new approach for the treatment of radiation-induced brain injury.     

CUDC-907 induces DNA damage and autophagy in glioma cells

AIM:To investigate the effect of CUDC-907, a dual histone deacetylase (HDAC) and phosphatidylinositol 3-kinase (PI3K) inhibitor, on the DNA damage, cell cycle distribution and autophagy in human glioma U251 cells. METHODS:U251 cells were treated with CUDC-907 of different concentrations, and the cell viability was detected by MTT assay. The quantitative γ-H2AX foci were determined by laser scanning confocal microscopy. The cell cycle distribution of U251 cells was examined by flow cytometry. The protein expression was determined by Western blot analysis. RESULTS:CUDC-907 inhibited the cell viability and the phosphorylation of Akt and p70 ribosomal protein S6 kinase (p70s6K) in the U251 cells (P<0.05). In CUDC-907-treated cells, the number of γ-H2AX foci and protein expression of γ-H2AX were increased significantly (P<0.05). CUDC-907 also induced cell arrest in the G₂/M phase by up-regulating the expression of p21, and inhibiting the protein level of cyclin B1 and the phosphorylation of cell division cycle protein 2 (Cdc2). In addition, CUDC-907 triggered cell autophagy, and inhibition of autophagy increased CUDC-907-induced DNA damage of U251 cells. CONCLUSION:CUDC-907 significantly inhibits PI3K/Akt signaling pathway, induces DNA damage and arrests cell cycle in G₂/M phase. Blockage of autophagy promotes CUDC-907-induced DNA damage of U251 cells.