强化型EM菌剂对金针菇菌糠堆肥的影响

为提高EM菌剂在菌糠堆肥中的应用效果,加速腐熟进程,改善堆肥质量,采用纤维素酶与木聚糖酶高产菌株黑曲霉SNH-7、蛋白酶高产菌株枯草芽孢杆菌SNK-103与EM菌剂进行复配,研制强化型EM菌剂,并研究其对菌糠堆肥的影响。结果表明：与普通EM菌剂相比,接种强化型EM菌剂的处理堆肥过程中微生物代谢更加旺盛,温度、pH、EC值、总有机碳、可溶性有机碳、总氮、铵态氮、硝态氮、C/N、腐植酸和黄腐酸含量等理化指标的升高或降低幅度更大,腐熟进程加快;成品堆肥的GI提高,C/N降低,总氮、硝态氮、总腐植酸和游离腐植酸的含量升高,生物安全性更好、肥效更高。说明在EM菌剂中补充纤维素酶、木聚糖酶和蛋白酶高产菌株,可强化其对纤维素、木质素和蛋白质的降解能力,在无辅料、高C/N、低pH的不利条件下,添加该菌剂能加速堆肥进程,提高堆肥质量。     

栅藻B38营养成分分析及蛋白质营养价值评价

对栅藻B38的营养成分进行了全面分析,结果表明,栅藻藻粉中油脂含量14%,总糖含量13.86%,粗纤维3.52%,灰分4.28%,蛋白质49.0%,为高蛋白质类微藻。栅藻B38中含有23种脂肪酸。栅藻B38中氨基酸总量为852.58 mg/g,必需氨基酸占总氨基酸的47.45%,必需氨基酸指数为85.42%。两种模式的氨基酸比值系数分较接近,均在65以上;待评价物质的氨基酸品质与模式蛋白的贴近度接近1(0.93和0.88)。栅藻B38中共检测出23种矿物质元素,其中钠、钾、钙、镁、铁、铝含量较为丰富。重金属的含量均低于国家食品卫生标准。栅藻B38中维生素B3(106.02 mg/100 g)和维生素E(540.77 mg/100 g)的量较高。综上,栅藻B38的营养较丰富,可以进一步开发利用。     

Prevalence,geographic distribution and phenotypic differences of Piscirickettsia salmonis EM‐90‐like isolates

Early reports accounted for two main genotypes of Piscirickettsia salmonis, a fish pathogen and causative agent of piscirickettsiosis, placing the single isolate EM‐90 apart from the prototypic LF‐89 and related isolates. In this study, we provide evidence that, contrary to what has been supposed, the EM‐90‐like isolates are highly prevalent and disseminated across Chilean marine farms. Molecular analysis of 507 P. salmonis field isolates derived from main rearing areas, diverse hosts and collected over 6 years, revealed that nearly 50% of the entire collection were indeed typed as EM‐90‐like. Interestingly, these isolates showed a marked host preference, being recovered exclusively from Atlantic salmon (Salmo salar) samples. Although both strains produce undistinguishable pathological outcomes, differences regarding growth kinetics and susceptibility to the antibiotics and bactericidal action of serum could be identified. In sum, our results allow to conclude that the EM‐90‐like isolates represent an epidemiologically relevant group in the current situation of piscirickettsiosis. Based on the consistency between genotype and phenotype exhibited by this strain, we point out the need for genotypic studies that may be as important for the Chilean salmon industry as the continuous surveillance of antimicrobial susceptibility patterns.     

All-trans retinoic acid attenuates blood-brain barrier injury induced by cerebral ischemia-reperfusion in rats through JNK/P38 MAPK signaling pathway

AIM: To investigate the effect of all-trans retinoic acid (ATRA) on blood-brain barrier after cerebral ischemia-reperfusion (CIR) injury in rats and its possible role mechanism.METHODS: Male SD rats were randomly divided into sham group, model (CIR) group and CIR+ATRA (10, 30 and 90 mg/kg) groups. The rat model of CIR injury was established by MCAO thread occlusion method. After ischemia for 1.5 h and reperfusion for 24 h, the neurological functional behavioral score, cerebral infarction volume, brain water content and Evans blue content were determined. The activity of matrix metalloprotein-9 (MMP-9) was measured by gelatin zymography. The protein levels of claudin-5, occludin, ZO-1, JNK, p-JNK, P38, p-P38 and MMP-9 in the brain tissues were determined by Western blot.RESULTS: Compared with CIR model group, ATRA at 30 mg/kg significantly improved neurological function, and decreased cerebral infarction volume, brain water content, Evans blue content and the degradation of tight junction proteins in ischemic area (P<0.01). The activity and protein expression of MMP-9 in ischemic brain tissue were decreased (P<0.01). The phosphorylation of JNK and P38 was inhibited and the protein levels of p-JNK and p-P38 were decreased (P<0.01).CONCLUSION: ATRA reduces the damage of brain tissue and the destruction of blood-brain barrier induced by CIR in rats. The protective effect may be related to inhibiting the activation of JNK/P38 MAPK signaling pathway and MMP-9.     

β-carotene attenuates weaning-induced apoptosis via inhibition of PERK-CHOP and IRE1-JNK/p38 MAPK signalling pathways in piglet jejunum

Weaning may cause oxidative injury, immune response impairment, apoptosis and other injuries in piglets. Oxidative and endoplasmic reticulum stress (ERS) can elicit inflammatory responses, and persistent oxidative and ERS also may lead to apoptotic cascades, which is associated with the pathogenesis of multiple diseases. β-carotene, a natural carotenoid, has potential anti-inflammatory and antioxidant functions. However, the effect of β-carotene on apoptosis in weaned piglets and the detailed molecular mechanism remain unclear. In this study, we found that β-carotene decreased malondialdehyde (MDA) levels and increased the activities of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) in piglet serum. β-carotene could inhibit the mRNA levels of caspase-3 significantly, but had no significant inhibitory effect of the mRNA levels of caspase-9 and caspase-12 in the piglet jejunum. In addition, β-carotene decreased the activation of GRP78, CHOP, and JNK/p38 MAPK and the ratio of Bax/Bcl-2. Furthermore, β-carotene had a significant influence on the activation of ERS and apoptosis-related signals in TG-induced IPEC-J2. In the present study, β-carotene pre-treatment attenuated the ratio of Bax/Bcl-2 and prevented TG-induced increases in the level of PERK-CHOP and IRE1-JNK/p38 MAPK pathway activation in a dose-dependent manner. Overall, these findings indicate that β-carotene may protect weaning-induced apoptosis through inhibiting ERS.     

Minimally modified low-density lipoprotein up-regulates endothelin receptors in mouse mesenteric artery through p38 MAPK pathway

AIMTo investigate whether minimally modified low-density lipoprotein (mmLDL) affects the quantity and activity of endothelin （ET） type A (ET_A) and type B (ET_B) receptors in mouse mesenteric artery by activating p38 mitogen-activated protein kinase (MAPK) inflammatory pathway. METHODSThe KM mice were divided into normal saline (NS) group (injection of NS via caudal vein), mmLDL group (injection of mmLDL via caudal vein), LDL group (injection of LDL via caudal vein), mmLDL+SB 203580 group (injection of mmLDL via caudal vein and intraperitoneal injection of p38 MAPK pathway specific inhibitor SB 203580) and mmLDL+DMSO group (injection of mmLDL via caudal vein and intraperitoneal injection of DMSO). Mesenteric artery ring segment vasoconstriction dose-response curves affected by sarafotoxin 6c (S6c) and ET-1 were recorded by the myography system. The mRNA levels of ET_B receptor, ET_A receptor and interleukin-6 (IL-6) were detected by RT-qPCR. The protein levels of ET_B receptor, ET_A receptor, IL-6, p38 MAPK, p-p38 MAPK, NF-κB and p-NF-κB were determined by Western blot. The serum concentration of IL-6 was measured by ELISA. RESULTSThe contractile responses of the blood vessel segments to S6c and ET-1 were significantly increased by mmLDL (P<0.01). The mRNA and protein expression levels of ET_A receptor, ET_B receptor, and IL-6 significantly increased (P<0.01). The protein levels of p-p38 MAPK and p-NF-κB were significantly increased (P<0.01). The serum level of IL-6 was significantly increased (P<0.01). These effects of mmLDL were inhibited by p38 MAPK inhibitor SB 203580. CONCLUSION mmLDL increses the serum concentration of IL-6, up-regulates the expression of IL-6, ET_A receptor and ET_B receptor in mouse mesenteric artery, and enhances the vasoconstriction function medi?ated by ET_A and ET_B receptors, which is related to the activation of p38 MAPK inflammatory pathway and downstream NF-κB pathway.     

有效微生物群对生活污水中有机物的降解能力研究

采用正交试验方法．研究了有效微生物群（简称EM）对生活污水中有机物的降解能力．结果表明：EM能去除生活污水中的有机物，且在水温为25℃,水力停留时间（HRT）为48h，台液加入量（VEM／V污水）为1／104，曝气时间为HRT／3，进水PH值为8．0时处理效果最佳．在此最佳处理条件下，测定了污水中BOD5，CODcr随时问的变化情况，并与不加EM的测定结果进行了比较，加EM的污水中有机物去除率大大增加，2d后接近最高值并趋于稳定．EM在处理生活污水方面的优势是：较少或不产生污泥，曝气时间短，但如果要较好地应用于生活污水治理，必须提高污水中的EM浓度．     

基于PLC的直埋夹套管试验控制系统设计

在分析国家压力管道元件质量监督检验中心原有直埋夹套管试验设备局限性的基础上，采用PLC可编程控制对原有砂箱试验装置进行了改造，克服了原有砂箱设备笨重、工作效率低等缺点。为实现试验系统的自动化，采用PLC的EM253位置控制拓展模块输出高速脉冲来精确控制伺服电机的速度和位置，试验拉力通过EM231模拟量模块输出，确保总体抗压强度及工作管轴向移动性能试验结果可靠，并实现了自锁、互锁功能。     

EIAV Rev蛋白拮抗eqTRIM5α介导的AP-1信号通路的机制研究

为探究马传染性贫血病毒(EIAV)附属蛋白Rev负调控Tripartite motif-containing protein 5α(TRIM5α)介导的AP-1信号通路的机制,本研究将pEIAV-Rev-HA和pcDNA3.1质粒分别与含TRIM5α基因的质粒及pGL3-AP-1-Luc(AP-1报告质粒)共转染HEK 293T细胞,采用荧光素酶试验检测Rev对TRIM5α激活的AP-1信号通路的影响;将pEIAV-Rev-HA和pcDNA3.1质粒分别与含TAK1、TAB2、P38和c-Jun基因的质粒及pGL3-AP-1-Luc共转染HEK 293T细胞,采用荧光素酶试验检测Rev对TRIM5α下游转导分子(TAK1、TAB2、P38、c-Jun)激活的AP-1信号通路的影响;将pEIAV-Rev-HA和pcDNA3.1质粒分别与含TAK1、TAB2、P38基因的质粒共转染HEK293T细胞,利用western blot试验分别检测TAK1、TAB2、P38的表达水平;将pEIAV-Rev-HA和pcDNA3.1质粒分别与含P38基因的质粒共转染HEK 293T细胞后加入蛋白酶体抑制剂MG132,利用western blot检测P38蛋白的表达情况。结果显示,共转染EIAV-Rev-HA实验组中TRIM5α对AP-1的激活倍数为0.4,而共转染pcDNA3.1对照组中相应的激活倍数为26.0;共转染pEIAV-Rev-HA实验组中,TAK1、TAB2、P38和c-Jun对AP-1信号通路的激活倍数分别为7.7、0.1、0.6、9.8,而共转染pcDNA3.1对照组中对AP-1信号通路的激活倍数分别为60.0、1.5、6.3、12.0;转染pEIAV-Rev-HA+pP38-Flag组与转染pcDNA3.1+pP38-Flag组相比,前者P38蛋白的表达量显著降低;加入蛋白酶体抑制剂组则恢复了P38蛋白的表达。上述结果表明,EIAV Rev显著下调eqTRIM5α及其下游转导分子TAK1、TAB2、P38激活的AP-1信号通路,但不显著下调c-Jun激活的AP-1信号通路;EIAV Rev通过蛋白酶体途径降解P38蛋白的表达而抑制eqTRIM5α激活的AP-1信号通路。本研究结果为理解EIAV与宿主蛋白相互作用提供参考依据。