千屈菜对富营养化水体中磷的去除作用

试验于 2 0 0 1年 8月 11日～ 9月 10日进行。千屈菜选用整齐健壮的 6月份扦插苗 (株高约 2 0cm) ,用清水洗净后置于总P浓度不同的营养液中 (以NaH2 PO4·2H2 O配制 )。选用能净化富营养化水体的凤眼莲为对照植物 ,置于总P浓度为 0 0 5和 0 4mg·L-1 的水体中。植株用打孔的泡沫板固定在培养箱中 ,每框用水均为 10L ,定期以蒸馏水补足蒸发失去的水分。 3次重复 ,完全随机排列。塑料温室内空气流通 ,光照为自然散射光。试验共 30d ,每 5d采集水样 1次 ,用钼酸铵分光光度法测定总P浓度。从试验结果 (表 1)可以看出 ,在总P 0～0 4mg·…     

控制条件下CO2与养分交互作用对番茄幼苗生长动态的影响

在营养液栽培条件下,以番茄(合作906)为供试作物,设计不同的CO2及养分浓度处理,研究了CO2与养分的交互作用对番茄生长的影响.结果表明:CO2施肥能增加番茄幼苗各个取样阶段的鲜干生物量、株高、茎粗、壮苗指数,而这些指标对CO2响应的强弱依赖于营养液浓度的高低,高浓度营养液能够强化番茄幼苗对CO2的响应.CO2施肥降低了番茄幼苗根的长度,但增加了根干物质含量,在同一CO2条件下,营养液浓度低有利于根增长,不利于根干物质的积累.根冠比、干鲜比对CO2的响应随营养液浓度改变并不发生有规律的变化.总的趋势是CO2施肥在高浓度营养液条件下增加根冠比,干鲜比.     

营养液中不同氮素水平对基质栽培番茄产量和品质的影响

以荷兰温室园艺研究所的番茄无土栽培营养液配方为对照,改变营养液中的氮素(N)浓度及营养液的电导率(EC)值,第1阶段设置3个N浓度处理,分别是184.8(HN)、123.2(LN),154.0(CK)mg/L,确立N浓度后,第2阶段分别设EC 1.5(T1)、2.5(CK)、3.5(T2)、4.5(T3)mS/cm 4个处理,研究了其对基质盆栽番茄的生长发育、果实产量与品质的影响。结果表明:营养液中不同N浓度对番茄的株高、茎粗等与生长有关的要素没有显著影响,而单株番茄产量和平均单果重以LN处理的最高。LN营养液的不同EC值对番茄株高、茎粗没有显著影响;EC值1.5mS/cm时番茄具有最高的单株产量,而营养生长期叶绿素值以EC值4.5mS/cm时为最高。番茄果实的可溶性糖含量、维生素C含量及总酸度均以EC值4.5mS/cm时为最高。     

营养液浓度对花叶芋水插的影响

花叶芋 (Ｃａｌａｄｉｕｍｈｏｒｔｕｉａｎｕｍ)可水养 ,经常换水 ,水中营养可使花叶芋保持绿色并且生长。但花叶芋生长在自来水中 ,品质是否受到影响 ,营养液在何浓度时花叶芋品质好 ,尚有待进一步探索。1　材料与方法　　试验于 1999年 7月～ 9月在玻璃温室中进行。营养液配方为 :Ｃａ(ＮＯ3) 2 ·4Ｈ2 Ｏ 590ｍｇ/Ｌ、ＫＮＯ340 4ｍｇ/Ｌ、ＫＨ2 ＰＯ4 136ｍｇ/Ｌ、ＭｇＳＯ4 ·7Ｈ2 Ｏ 2 4 6ｍｇ/Ｌ ,微量元素采用通用配方。用ＥＣ值为 0 .2 7ｍｓ/ｃｍ的自来水配制营养液。试验处理营养液浓度剂量为 :0 (自来水 )、0 .1、0 .5、1.0、1…     

贮藏环境对甜樱桃拮抗酵母菌生长和链格孢菌生物防治的影响(英文)

拮抗酵母菌(Rhodotorulaglutinis)在20～25℃的室温下生长较快,即使20%CO2亦不能抑制其生长,但菌落直径扩展速度与CO2浓度(0～20%)呈显著负相关(r=-0.8999～-0.9383)。R.glutinis在低温(1℃)条件下,对CO2较敏感,15%CO2浓度可以抑制该拮抗菌在低温下生长,但将其移到常温下培养2d后即可生长。另外,5%或15%CO2单独使用不能抑制Alternariaalternata(1×104个孢子/mL,15μL)在红灯樱桃果实上萌发,但可极显著地抑制其病斑在樱桃果实上的扩展速度。R.glutinis悬浮液(108cfu/mL)与5%或15%CO2结合使用则可完全抑制A.alternata在樱桃果实上生长。     

几种制剂及配方对巨峰葡萄硬枝扦插生长的影响

1　材料与方法　　试验以巨峰硬枝插条为试材 ,设ＮＡＡ10 0ｍｇ·ｌ- 1(Ａ)、ＩＢＡ5 0ｍｇ·ｌ- 1(Ｂ)、ＡＢＤ5 0ｍｇ·ｌ- 1(Ｃ)、ＮＡＡ10 0ｍｇ·ｌ- 1+ＩＢＡ5 0ｍｇ·ｌ- 1(Ｄ)、ＮＡＡ10 0ｍｇ·ｌ- 1+ＡＢＤ5 0ｍｇ·ｌ- 1(Ｅ)、ＩＢＡ5 0ｍｇ·ｌ- 1+ＡＢＤ5 0ｍｇ·ｌ- 1(Ｆ)、ＮＡＡ10 0ｍｇ·ｌ- 1+ＩＢＡ5 0ｍｇ·ｌ- 1+ＡＢＤ5 0ｍｇ·ｌ- 1(Ｇ)及清水对照共8个处理 ,3次重复。每重复 4 0根插条 ,每根插条留两个芽 ,插条下面紧靠芽部斜剪 ,上面在芽上 2ｃｍ处平剪。2 0 0 0年 2月 2 3日 ,将剪好的插条分别用 8种处理处理 2 …     

不同生长阶段营养液浓度对水培生菜产量和品质的影响

以生菜为材料,采用水培法研究了不同生长阶段营养液浓度对生菜产量和品质的影响。试验结果表明,与C1处理(营养液每20 d更换一次,营养液浓度在整个生长期均为1/2霍格兰配方)相比,C2处理(营养液每10 d更换一次,1~10 d为1/4霍格兰配方,11~20 d为1/2霍格兰配方,21~30 d为1/2霍格兰配方)、C3处理(营养液每10 d更换一次,1~10 d为1/8霍格兰配方,11~20 d为1/4霍格兰配方,21~30 d为1/2霍格兰配方)的生菜叶片数、全株鲜质量、地上部鲜质量和地上部干质量,VC、可溶性蛋白、硝酸盐和叶绿素含量均无显著差异;C2与C1处理的生菜可溶性糖含量也无显著差异,但C3与C1处理相比,生菜可溶性糖含量则显著降低。     

不同色膜处理对番茄叶片光合作用特性的影响

以不同色膜(红、蓝、绿、黄、紫、白色(CK))为试材,以番茄为试验对象,研究了温室环境因子条件下不同光质对番茄幼苗叶片光合作用特性的影响。结果表明:红、蓝、绿、紫、黄膜的处理番茄的光补偿点为45μmol·m-2·s-1,紫光的光饱和点为400μmol.m-2·s-1,白膜、红膜、蓝膜、绿膜处理的光饱和点为1 000μmol.m-2·s-1,黄膜处理的光饱和点为1 500μmol.m-2·s-1。6种色膜处理的CO2补偿点均约为100μL/L,另外红膜、黄膜、白膜、紫膜的CO2饱和点为800μL/L左右,其它2种蓝膜和绿膜均大于1 000μL/L,其中以蓝膜的CO2饱和点最高。白膜处理的叶片叶绿素含量最高,绿膜最低。对影响叶片光合速率主要因子的通径系数分析表明,影响白色膜处理的为胞间CO2浓度、蒸腾速率,影响红色膜处理为胞间CO2浓度、空气相对湿度,影响蓝膜处理为大气CO2浓度、光合有效辐射,影响黄膜处理为胞间CO2浓度、空气湿度,影响紫膜处理为大气CO2浓度、胞间CO2浓度,影响绿膜处理为胞间CO2浓度、空气相对温度。     

营养液浓度对番茄营养生长期生长发育的影响

以珍珠岩栽培番茄为试验材料,分别浇施1/3、2/3、1、4/3倍标准浓度的营养液,结合常规测定方法,分析营养液浓度对番茄生长指标、干物质累积和根系特征参数的影响,为基质栽培中养分的管理提供参考依据。结果表明:随着营养液浓度的升高,番茄株高、茎粗、叶面积均呈抛物线增长趋势,1倍营养液浓度处理株高最高,4/3倍浓度处理茎粗和叶面积最大;番茄植株的干物质量随营养液浓度提高而增大,根冠比随营养液浓度的提高而减小,且二者均与营养液浓度有很好的二次曲线关系,相关性均达到极显著水平;根系特征参数均随营养液浓度升高呈先增大后减小的趋势,且拟合关系较好,其中以1/3倍浓度处理最小,其它处理间均未达到差异显著性水平;试验表明,1倍和4/3倍营养液浓度处理番茄植株的生长状况相比其它2个低浓度处理更好,更有利于番茄植株营养生长期的生长发育。     

日光温室厚皮甜瓜光合特性研究

试验以蜜世界、伊丽莎白和新状元3个厚皮甜瓜品种为试材,测定了其在日光温室(冬暖大棚)中的光合特性。结果表明:3个品种在各个时期功能叶的光合速率日变化均呈双峰曲线,有明显的“午休”现象。3个品种均具有较高的光合速率(8～20μmolCO2·m-2·s-1);植株伸蔓期各叶片光合速率为中位叶>下位叶>上位叶;坐果期则出现了2个光合速率高峰,1个在上位叶的中部,另1个在坐果节叶位。新状元单个叶片的光合速率在叶龄18天时达到最高值;其光饱和点为1690.7μmol·m-2·s-1,光补偿点为116.5μmol·m-2·s-1;CO2饱和点为1233.2μl·L-1,CO2补偿点为152.5μl·L-1。     

Effect of new Qing Yi Tang decoction on expression of inhibitor kappa B-alpha in pancreas and liver tissues of rats with acute pancreatitis

AIM:To investigate the expression of inhibitor kappa B alpha (IκBα) in pancreas and liver tissues of rats with experimental acute pancreatitis (AP) and to explore the therapeutic mechanism of Chinese medicine new Qing Yi Tang (QYT) on AP. METHODS:70 SD rats were randomly divided into three groups:normal control group (n=10), AP+QYT group (n=30), and AP+normal saline (NS) group (n=30). AP model was induced by retrograded injection of 4% sodium deoxycholate into the pancreatic duct. QYT or NS was infused to the rats respectively by a gastric catheter repeatedly every five hours after AP induction. At 1 h, 4 h, 10 h after operation, rats were sacrificed, and the pancreas and liver were moved out individually. Real-time RT-PCR was performed to detect IκBα mRNA expression in the liver. Western blotting was applied to detect IκBα protein expression in the liver and pancreas. IκBα proteins including phosphorylated form (IκBα-p) and non-phosphorylated form (IκBα-n) were tested. Serum level of leukotriene C4 (LTC4) was detected by ELISA. The pathological changes of pancreas and lung tissues stained with HE were observed under light microscope. RESULTS:Compared with the normal control group, expression of IκBα mRNA in liver was higher in AP rats in the observation period (P<0.01, or P<0.05). QYT treated group had lower expression of IκBα mRNA as compared with AP+NS group (P<0.05). Expression of IκBα protein (including IκBα-p and IκBα-n) in liver and pancreas were also higher in AP group as compared with that in control group (P<0.05). IκBα-p displayed an increased tendency during the observation period in AP+ NS group. However, QYT treatment induced a decrease in IκBα-p protein expression and an increase in IκBα-n expression. The serum LTC4 level in AP group was increased in a time-dependent manner, and QYT attenuated the increased LTC4 level in certain degree (P<0.05). The pathological changes in pancreas and lung tissues of AP rats, such as edema, hemorrhage, and inflammatory cell infiltration were lightly attenuated by QYT. CONCLUSION:QYT alleviated the inflammatory reaction of AP by inhibiting IκBα-p expression and then reducing the inflammatory mediators.     

Geniposide attenuates cognitive dysfunction in sleep-deprived rats by inhibiting TLR4/NF-κB signaling pathway

AIM To investigate the effects of geniposide （Gen） on Toll like receptor 4/nuclear factor-κB （TLR4/NF-κB） signaling pathway and cognitive dysfunction in sleep deprived rats. METHODS Wistar rats （n=120） were randomly divided into normal control （NC） group， model （M） group， low-dose （5 g·kg^-1·d^-1） Gen （Gen-L） group， medium-dose （10 g·kg^-1·d^-1） Gen （Gen-M） group， high-dose （20 g·kg^-1·d^-1） Gen （Gen-H） group and Gen-H+LPS （0.4 mg·kg^-1·d^-1， tail vein injection） group. After 7 days of intervention， the sleep deprivation model of rats in M group， Gen-L， Gen-M， Gen-H and Gen-H+LPS group was established by improved small platform water environment. The escape latency of Morris water maze experiment and the behavior correct rate of Y maze experiment were measured. The serum levels of S100B and neuron-specific enolase （NSE）， and the levels of interleukin-1β （IL-1β）， IL-6 and tumor necrosis factor-α （TNF-α） in hippocampus were detected by ELISA. The mRNA levels of TLR4 and NF-κB p65 were detected by RT-qPCR， and the protein levels of TLR4 and NF-κB p65 were determined by Western blot. RESULTS Compared with NC group， the escape latency， the serum levels of S100B and NSE， the hippocampal levels of IL-1β， IL-6 and TNF-α， and the mRNA and protein expression of TLR4 and NF-κB p65 were increased significantly in M group （P<0.01）， and the behavior correct rate was decreased significantly （P<0.01）. Compared with M group， the escape latency， the hippocampal levels of IL-1β， IL-6 and TNF-α， and the expression of TLR4 and NF-κB p65 at mRNA and protein levels were decreased significantly in Gen-L， Gen-M and Gen-H groups （P<0.01）， and the behavior correct rate was increased in turn （P<0.01）. Compared with Gen-H group， the escape latency， the serum levels of S100B and NSE， the hippocampal levels of IL-1β， IL-6 and TNF-α， and the expression of TLR4 and NF-κB p65 at mRNA and protein levels were increased significantly in Gen-H+LPS group （P<0.01）， and the behavior correct rate was decreased significantly （P<0.01）. CONCLUSION Geniposide may inhibit the TLR4/NF-κB p65 signaling pathway to effectively improve cognitive function in sleep-deprived rats and reduce hippocampus inflammation.     

Effects of thalidomide on the expression of NF-κB and TNF-α in experimental hepatic fibrotic rats

AIM: To study the effects of thalidomide on the expressions of nuclear factor κB (NF-κB) and tumor necrosis factor-α (TNF-α) in rat liver fibrosis.METHODS: The fibrosis of rat liver was induced by intraperitoneal injection of carbon tetrachloride thrice weekly.Meanwhile thalidomide (10 mg·kg^-1·d^-1 or 100 mg·kg^-1·d^-1) was given daily by the intragastric route for 8 weeks.Serum alanine aminotransferase (ALT),aspartate aminotransferase (AST),prealbumin (PA),hyaluronic acid (HA) and laminin (LN),and hydroxyproline (HYP) contents in the liver,NF-κB p65 and α-smooth muscle actin (α-SMA) protein in the liver,IκBα and TNF-α protein in cytoplasm and NF-κB p65 protein in nucleus and TNF-α mRNA levels in the liver were studied.RESULTS: Compared with the model group,the Knodell score,serum ALT,AST,HA,LN levels and HYP contents in liver,NF-κB p65 protein in nucleus and α-SMA protein in the liver,and TNF-α mRNA and protein in the liver of rats given high dose of thalidomide were decreased significantly (P<0.01).Meanwhile PA level and IκBα protein in cytoplasm were elevated significantly (P<0.01).CONCLUSION: Thalidomide exerts its effect on the down-regulation of NF-κB-induced TNF-α via inhibiting dissociation and degradation of IκB and prevents liver fibrosis in rats.     

Effects of PDS on rat brain cortical nuclear factor kappa B in LPS shock

AIM:To explore the molecular mechanism of brain tissue injury induced by lipopolysaccharide (LPS),the effects of panaxadiol (PDS) on the expression of nuclear factor kappa B (NF-κB) in cerebral cortex of rat with LPS shock were studied. METHODS:Rats were randomly divided into LPS roup,LPS+dexamethasone group,LPS+PDS group and control group. The DNA binding activity and protein expression of NF-κB were observed. These indices were assayed at 1 h and 4 h after intravenous injection of LPS (4 mg·kg^-1). RESULTS:EMSA showed that PDS inhibited NF-κB DNA-binding activity in nuclear extracts at both 1 h and 4 h after LPS injection,compared with the LPS group (P<0.01). Western blotting showed that PDS down-regulated the expression of p65 and p50 protein in the nuclear extracts compared with the LPS group. However,the expression of p65 and p50 protein from cytosolic extracts did not show any significant change. CONCLUSION:PDS may alleviate brain injury by inhibiting NF-κB activation.     

Inhibitory effects of CCK-8 on NF-κB activities stimulated by LPS in rat PIMs

AIM: To investigate the inhibitory effects of cholecystokinin octapeptide (CCK-8) on nuclear factor-κB (NF-κB) activities stimulated by lipopolysaccharide (LPS) by using forskolin, the activator of adenylate cyclase, and PKA inhibitor H-89 in rat pulmonary interstitial macrophages (PIMs).METHODS: PIMs were isolated and purified.EMDA was applied to detect NF-κB activities and Western blotting was used to analyze the IκB-α protein level in rat PIMs.RESULTS: The NF-κB activity was not detected in normal control rat PIMs.The NF-κB activity in LPS-treated rat PIMs was obviously higher than that in control group (P<0.01).The IκB-α protein level in endochylema decreased obviously compared to control group (P<0.01).No obvious change of NF-κB activity and IκB-α protein level in CCK or Fsk treated rat PIMs was observed (P>0.05).The NF-κB activity in CCK＋LPS group and LPS＋Fsk group were obviously lower than that in LPS group (P<0.05).The IκB-α protein level was obviously higher (P<0.01).In LPS＋CCK＋H-89 group, the NF-κB activity in rat PIMs was obviously higher than that in CCK＋LPS group (P<0.01), while the IκB-α protein level decreased (P<0.01).CONCLUSIONS: The activation of cAMP-PKA signaling pathway inhibits the increase in NF-κB activity and the decrease in IκB-α protein level stimulated by LPS in rat PIMs.The anti-inflammatory effects of CCK-8 were taken effect by activating cAMP-PKA signaling pathway and further inhibiting the NF-κB activity.     

Role of IRAK-4 activity in inhibitory effects of lipopolysaccharide pretreatment on hepatic ischemia/reperfusion injury

AIM:To observe the changes of interleukin-1 receptor associated kinase-4 (IRAK-4) in ischemia/reperfusion (I/R) liver pretreated with lipopolysaccharide (LPS) and to explore the protective mechanisms of LPS pretreatment against hepatic I/R injury. METHODS:Male Sprague-Dawley rats, weighing 240-280 g, were divided into three groups:control, ischemia/reperfusion group (I/R group) and LPS-pretreated group (LPS group). On the first day, LPS group received 0.1 mg/kg LPS via the tail vein, followed by 0.5 mg/kg on the 2nd, 3rd, 4th and 5th day. I/R group received the equivalent volumes (0.5 mL) of sterile PBS. Experiments of I/R injury was induced by temporary ischemia of the left lateral liver lobe for 90 min followed by 3 h reperfusion on 2 days after the last LPS treatment. At 0 min, 60 min and 180 min after reperfusion, the expression of IRAK-4 gene and protein level were determined by RT-PCR and Western blotting. The activity of NF-κB and the serum TNF-α level were also detected by ELISA. RESULTS:Although the level of IRAK-4 gene and protein were higher in the LPS group than that in I/R group and control group (P<0.01), no difference of the activities of NF-κB and the TNF-α level was observed between the LPS group and I/R group (P>0.05) at 0 min after reperfusion. However, all those indexes were evidently lower in the LPS group than those in I/R group (P<0.01) at 60 min and 180 min after reperfusion. CONCLUSION:This data suggests that the protective effects induced by LPS pretreatment against hepatic I/R injury may be via down-regulation of IRAK-4 expression.     

Effect of advanced glycation end products on inflammation in cultured cardiomyocytes

AIM: To investigate the effect of advanced glycation end products on inflammation in cultured cardiomyocytes.METHODS: Primary cardiomyocytes were isolated from Sprague-Dawley neonatal (1 to 2 days old) rats ventricles.The insulin resistant cardiomyocyte model was established.Neonatal rat ventricular myocytes were exposed to AGEs for 24 hours.TNF-α mRNA and PPAR-γ mRNA expressions were determined by RT-PCR.Activation of NF-κB in the cells was examined by using immunocytochemistry.The ultrastructure of the cells was detected by transmission electron microscope.RESULTS: The exprssion of TNF-α mRNA and the activation of NF-κB increased,the expression of PPAR-γ mRNA decreased compared with control group (P<0.05).The differences among different AGE-BSA groups were significant (P<0.05).The numbers of chondriosome and smooth endoplasmic reticulum increased.CONCLUSION: AGEs significantly increase TNF-α mRNA expression and NF-κB activation,and restrain the expression of PPAR-γ mRNA.These data suggest that AGEs play an important role in the onset of diabetic cardiomyopathy.