Prediction of topsoil organic matter and clay content from measurements of spectral reflectance and electrical conductivity

Soil organic matter (SOM) and clay content of a soil characterized as a coarse sandy loam were modelled using hyperspectral reflectance data acquired with a spectrometer and soil electrical conductivity (SEC) data acquired with an EM38 instrument manufactured by Geonics Ltd. The partial least squares (PLS) regression method was applied and the results validated using cross validation. First, the models were calibrated using only spectral reflectance data; then EM38 data were included in the X-matrix of predictors. Although SEC is significantly correlated with clay content, the results showed that EM38 data did not improve model performance for the estimation of soil organic matter content and clay content, despite the fact that EM38 showed significant correlation with clay content.     

Effect of bim silencing by siRNA on hypoxia-induced apoptosis of rat cardiomyocytes

AIM：To investigate the effect of BH3-only protein Bim (Bcl-2 interacting mediator of cell death) on apoptosis of rat cardiomyocytes induced by hypoxia. METHODS：Rat cardiomyocytes were isolated from infant rats aged 1~3 days and then primarily cultured. The antibody targeting α-actin of striated muscle was used to identify the cardiomyocytes. The siRNAs of bim were transfected into the cardiomyocytes with liposome, and the expression of Bim was determined by Western blotting. The cardiomyocytes were divided into blank control group, hypoxia group, hypoxia+liposome group, hypoxia+negative control siRNA group and hypoxia+bim-siRNA group.The frequency and rhythm of cardiomyocyte beating were observed and recorded under inverted microscope. The activity of lactate dehydrogenase (LDH) in the culture medium was assessed by automatic biochemical analyzer. The viability of the cells was analyzed by MTT assay. The cell apoptotic rate was measured by flow cytometry. The protein expression of Bim, Bax, Bcl-2, p-p38 MAPK and p38 MAPK was detected by Western blotting. RESULTS：Immunohistochemical identification confirmed that the rat cardiomyocytes were successfully cultured. The expression of Bim was obviously inhibited after transfected with bim-siRNAs and the silencing efficiency of bim-siRNA-2 was the highest (86.73%). The frequency of cardiomyocyte beating was slowed down after hypoxia and the rhythm was disordered, while the frequency of beating was obviously increased after silencting the expression of bim. Compared with control group, the LDH in the culture medium was increased (P<0.01), and the viability of the cardiomyocytes was reduced in hypoxia group (P<0.05). The apoptotic rate was increased (P<0.01). After transfection with bim-siRNA, the release of LDH was decreased, and the viability of the cardiomyocytes was increased. The apoptotic rate was decreased. The results of Western blotting showed that hypoxia increased the expression of Bax and p-p38 MAPK (P<0.05), and decreased the expression of Bcl-2 (P<0.01), while transfection with bim-siRNA reduced the effects caused by hypoxia (P<005). These were greatly related to the decrease of apoptosis. However, the expression of p38 MAPK was not changed. CONCLUSION：The apoptosis of cardiomyocytes induced by hypoxia can be inhibited by silencing the expression of bim gene by down-regulation of p-p38 MAPK and Bax expression and up-regulation of Bcl-2 expression.     

p38 MAPK/ATF-2 pathway is involved in C-relative protein-induced endothelial cell activation

AIM: To investigate the role of p38 MAPK/ATF-2 pathway in C-relative protein (CRP)-induced endothelial cell activation. METHODS: Human coronary artery endothelial cells (HCAEC) were cultured and were used between passages 3 and 7. CRP served as a stimulus for endothelial cell activation. Western blotting was performed to determine the expression and phosphorylation of eNOS, p38 and ATF2. ELISA was carried out to detect the levels of ICAM-1, VCAM-1 and MCP-1 released from HCAEC. Pharmacological p38 inhibitors SB203580 and SB202190 were used to determine the effect of p38/ATF-2 pathway. RESULTS: CRP reduced the p-eNOS level in a concentration-dependent manner and induced the release of ICAM-1, VCAM-1 and MCP-1. The p38/ATF-2 pathway was activated by CRP treatment. SB203580 and SB202190 partially rescued p-eNOS level and suppressed the secretion of ICAM-1, VCAM-1 and MCP-1. CONCLUSION: p38MAPK/ATF-2 pathway participates in CRP-induced endothelial activation.     

GnIH通过p38MAPK信号通路对猪卵巢颗粒细胞自噬与凋亡的影响

【目的】细胞自噬和凋亡存在着相互制约,p38MAPK信号通路作为细胞凋亡的主要调控通路之一,也对细胞自噬存在促进和抑制的双重作用。已有研究表明,促性腺激素抑制激素(gonadotropin-inhibitory hormone , GnIH)对细胞自噬与凋亡均有影响,但作用机制尚不明确。故探究GnIH通过p38MAPK信号通路对猪卵巢颗粒细胞（pGCs）自噬与凋亡的影响及其机理,为解决母猪的产子率以及同期发情等问题提供参考。【方法】min、10 min、30 min、60 min、90 min)分组,用Western blot检测猪卵巢颗粒细胞p38与p-p38的蛋白表达量变化;2、验证GnIH对p38MAPK信号通路的影响：按（空白对照、GnIH、p38激活剂（U-46619）、U-46619+GnIH）分组,用Western blot检测p38与p-p38的蛋白表达量变化;3、探究不同浓度GnIH对自噬和凋亡的影响：按（空白对照、10 ^-6mol·L ^-1 GnIH、10 ^-8mol·L ^-1 GnIH、10 ^-10mol·L ^-1 GnIH、10 ^-12mol·L ^-1 GnIH）分组,用Western blot检测自噬与凋亡标志性蛋白的表达量变化;4、验证不同浓度GnIH通过p38信号通路对自噬和凋亡的影响：将细胞分成6组（空白对照、U-46619、U-46619+10 ^-6 mol·L ^-1 GnIH、U-46619+10 ^-8mol·L ^-1 GnIH、U-46619+10 ^-10mol·L ^-1 GnIH、U-46619+10 ^-12mol·L ^-1 GnIH）,用Western blot检测自噬与凋亡标志性蛋白的表达量变化。【结果】1. GnIH孵育10 min后,显著降低p38与p-p38的蛋白表达量（P<0.05）,提示,GnIH对p38MAPK信号通路的最佳作用时间为10 min;2. U-46619显著促进pGCs的p38磷酸化水平（P<0.05）,GnIH显著抑制pGCs的p38磷酸化水平（P<0.05）,提示,U-46619使p38MAPK信号通路活化,GnIH对p38MAPK信号通路的活化有抑制作用;3. 当 GnIH的浓度为10 ^-6 mol·L ^-1时,pGCs的自噬和凋亡水平显著升高（P<0.05）,随着GnIH浓度的降低,pGCs的自噬水平逐渐升高（P<0.05）,pGCs的凋亡水平逐渐降低（P<0.05）,提示,高浓度GnIH可以促进自噬和凋亡,随着GnIH浓度的降低,自噬水平逐渐升高,而凋亡水平逐渐下降;4. 加入U-46619后,GnIH使pGCs的自噬显著上调（P<0.05）,并且使pGCs的凋亡显著下调（P<0.05）,提示,不同浓度GnIH通过p38MAPK信号通路影响pGCs的自噬和凋亡。【结论】GnIH可能通过抑制p38MAPK信号通路的活化,上调pGCs的自噬,减少pGCs的凋亡。     

基于EMI的小泊湖退化湿地土壤盐分的空间分布

采用电磁感应(EMI)、地统计学半变异函数和Kriging空间插值方法研究小泊湖退化湿地土壤盐分的空间分布。结果表明:土壤表观电导率(ECa)和0—40cm土壤盐分含量呈线性显著正相关,说明在小泊湖湿地土壤表观电导率的变化可以用以反映土壤盐分含量的变化;半变异函数分析表明,土壤盐分具有强空间相关性[C/(C0+C)0.5],其空间分布主要是由结构性因素引起的;高斯模型(R2=0.98)插值土壤盐分表明,土壤盐分空间分布与退化湿地的空间分布表现出明显的一致性,放牧活动强烈的退化区域土壤盐分相对较高,说明小泊湖湿地退化后土壤盐分含量高于未退化湿地,土壤盐分含量在一定程度上能反映湿地退化的程度,可为湿地退化防治监测提供依据。     

基于VRML的土壤电导率三维空间变异性虚拟实现建模研究

如何表达土壤属性的三维空间变异性对传统的土壤剖面采样、空间变异分析和三维可视化表达提出了挑战。本研究以浙江省围垦海涂水稻田土壤盐分为例,采用EM38电磁感应线性模型结合二阶Tikhonov正则化方法反演剖面0~110 cm范围内10个土层深度的土壤电导率作为三维空间变异性研究的数据源;然后利用三维反距离权重方法进行土壤盐分的三维空间插值;最后分别采用虚拟现实建模语言（VRML）的球体、切片、地柱模型对土壤电导率剖面离散点、二维空间变异切片、三维变异土体模型进行三维虚拟现实可视化建模,并实现模型的网络发布。结果表明,在田间尺度上,三维反距离权重方法可较好的对土壤电导率在三维空间的分布进行预测插值;通过VRML方法进行可视化建模可较好的展示及解析土壤电导率的三维空间分布规律;水平方向上,土壤盐分从西北面向东南面逐渐增大,垂直方向上,土壤盐分随土层深度的增加而增大,且东南角土壤盐分最大;另外,用户可利用IE浏览器实现虚拟现实模型的可视化及对模型进行平移、放大、缩小、旋转等基本操作。基于VRML的虚拟建模方法可为土壤属性的三维变异性可视化及网络共享提供新途径。     

基于电磁感应仪的土壤盐渍化剖面特征解译研究

为了快速、精准解译区域尺度土壤盐分特征,有必要建立土壤剖面盐分信息精确解译模型。以新疆农灌区不同土壤质地的盐渍化土壤为研究对象,利用电磁感应式大地电导率仪EM38获取土壤表观电导率,构建了基于EM38的两种土壤质地剖面分层盐分解译模型,并对盐分解译回归模型进行了精度检验。结果表明:两种质地的土壤剖面盐分含量变异均较大,中壤土各层电导率变异系数在58%~98%,呈现中等变异强度,而砂土表层(0~40 cm)变异系数达到100%以上,属于强变异强度,深层土壤变异系数介于76%~88%属于中度变异强度。两种质地土壤电导率与磁感表观电导率EMh、EMv间呈显著的相关关系,水平和垂直测量模式都能够对不同深度土盐层分进行预测,且以EMh+EMv为自变量的二元回归解译模型具有较高的精度,相关系数R达到0.94以上。中壤土EM38的盐分预测在不同深度土层的验证结果决定系数达到0.59以上,砂土质地土壤盐分预测验证R2达到0.36以上,预测精度与土壤剖面盐分变异性呈现显著负相关,其相关系数为-0.86,中壤土质地的解译效果优于砂土质地。分析EM38在预测不同土壤质地盐分精度上的差异性,构建了电磁感应式土壤剖面盐分含量的预测模型。研究结果引入土壤质地变量,可为大面积土壤盐渍化的快速精确测定提供理论依据。     

Analysis of Potassium Uptake by Rice Roots Treated with Aluminum Using a Positron Emitting Nuclide, 38K

We investigate the effect of Al on K⁺ uptake by rice roots. Potassium-38 (³⁸K), a positron emitting nuclide (the half-life: 7.61 min), was used to trace K⁺ behavior. When a rice root was treated with 10μM Al for 24 h, the uptake of ³⁸K in the root was increased in the range of 1 to 2 cm from the root tip compared with that of the control sample. Because the root continued to grow without showing any damage of plasma membrane during the Al treatment, it was suggested that the ³⁸K uptake was not occurred through diffusion into the cells. The uptake of ³⁸K in both treatments, with/without Al, was decreased by VO₄^3- (inhibitor of H⁺-ATPase on plasma membrane) and DNP (H⁺ ionophore) treatment, which suggested that the K⁺ uptake was performed through an active transport, such as H⁺:K⁺ transport or H⁺ gradient promoted by an Al treatment.     

Asiaticoside attenuates hypoxic pulmonary hypertension in mice by inhibiting NF-κB/p38 signaling pathway

AIM: To investigate whether asiaticoside attenuates hypoxic pulmonary hypertension by inhibiting p38/NF-κB signaling pathway. METHODS: BALB/c mice (n=30) were randomly divided into normoxia (N) group, hypoxia (H) group, and hypoxia+asiaticoside group. Right ventricular systolic pressure (RVSP), mean carotid artery pressure (mCAP), the weight ratio of right ventricle/(left ventricle+ventricular septum)[RV/(LV+S)], the ratio of right ventricle/body weight (RV/BW), vessel wall area/vessel total area (WA/TA) and vessel wall diameter/vessel wall total diameter (WT/TT) were determined after the model was established. The protein levels of p38, p-p38, NF-κB and p-NF-κB in the lung tissues were detected by Western blot. The fluorescence intensity of p-p38 and p-NF-κB were measured by immunofluorescence method. The serum levels of interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α) were measured by ELISA. RESULTS: Compared with N group, the levels of RVSP, RV/(LV+S), RV/BW, WA/TA and WT/TT were significantly increased in H group, while administration of asiaticoside decreased the levels of RVSP, RV/(LV+S), RV/BW, WA/TA and WT/TT (P<0.05). Compared with N group, the relative protein levels of p-p38 and p-NF-κB in H group were significantly increased (P<0.05), and the concentrations of IL-6 and TNF-α were significantly increased, which were apparently attenuated by asiaticoside injection. CONCLUSION: Inhibition of p38/NF-κB signaling pathway and reduction of inflammatory responses may be the important mechanisms of asiaticoside in the prevention and treatment of hypoxic pulmonary hypertension.     

TPX2 induces apoptosis of rectal cancer HR-8348 cells through p38 MAPK signaling pathway

AIM: To study the effect of targeting protein for Xenopus kinesin-like protein 2 (TPX2) expression knockdown on the apoptosis of rectal cancer HR-8348 cells.METHODS: The HR-8348 cells transfected with TPX2 small interfering RNA (siRNA) served as TPX2 siRNA group. The non-transfected cells were used as control group. The cells transfected with siRNA negative control (siRNA-NC) were used as siRNA-NC group. The TPX2 siRNA-transfected cells exposed to p38 MAPK inhibitor SB203580 served as TPX2 siRNA+SB203580 group. The expression of TPX2 at mRNA and protein levels was determined by RT-qPCR and Western blot. The cell viability was measured by MTT assay, the apoptosis was analyzed by flow cytometry. The protein levels of p38 MAPK, p-p38 MAPK, cleaved caspase-3 and Bcl-2 in the HR-8348 cells were determined by Western blot.RESULTS: After transfection, the expression of TPX2 at mRNA and protein levels was decreased in TPX2 siRNA-transfected cells (P<0.05). Transfection with siRNA-NC had no effect on TPX2 mRNA and protein levels in the cells. After knockdown of TPX2 expression, the viability of rectal cancer HR-8348 cells and the expression of Bcl-2 were decreased, while the apoptotic rate and the protein levels of cleaved caspase-3 and p-p38 MAPK/p38 MAPK were increased significantly reduced (P<0.05). Compared with TPX2 siRNA group, the apopto-tic rate and the protein levels of cleaved caspase-3 and p-p38 MAPK/p38 MAPK in TPX2 siRNA+SB203580 group were significantly decreased, while the viability was significantly increased (P<0.05).CONCLUSION: Knockdown of TPX2 expression promotes apoptosis of rectal cancer HR-8348 cells by activating p38 MAPK signaling pathway.