意大利蜜蜂工蜂幼虫肠道中ame-miR-bantam对靶基因USP和P300的表达调控

【目的】本研究旨在通过饲喂法对意大利蜜蜂Apis mellifera ligustica工蜂幼虫肠道中ame-miR-bantam进行过表达与敲减,明确ame-miR-bantam对靶基因USP和P300表达的调控作用。【方法】通过饲喂ame-miR-bantam模拟物(mimic-ame-miR-bantam)和抑制物(inhibitor-ame-miR-bantam)及相应的阴性对照mimic-NC-ame-miR-bantam和inhibitor-NC-ame-miR-bantam,对意大利蜜蜂工蜂4-6日龄幼虫肠道组织中的ame-miR-bantam分别进行过表达和敲减。利用生物信息学软件进行ame-miR-bantam的靶向预测及分析。通过RT-qPCR检测4-6日龄意大利蜜蜂工蜂幼虫肠道中ame-miR-bantam的过表达和敲减效果及靶基因USP和P300的相对表达量。【结果】相较于饲喂mimic-NC-ame-miR-bantam,饲喂mimic-ame-miR-bantam后,ame-miR-bantam在意大利蜜蜂4-6日龄工蜂幼虫肠道中均显著上调;相较于饲喂inh...     

碧桃朝鲜球坚蚧的出蛰若虫空间格局及应用

采用多种聚集度指标、Iwao法和Taylor幂函数法分析朝鲜球坚蚧出蛰若虫在碧桃上的空间格局。结果表明,出蛰若虫在碧桃上呈聚集分布,分布以个体群形式存在。碧桃不同段位上的聚集度指标和Iwao法均表明其为聚集分布,而Taylor幂函数法测定为上、中段均匀分布,下段聚集分布,综合分析其成因是各样地受害程度及垂直方向虫口密度差异显著所致。聚集均数λ值的测定结果表明,该虫的聚集原因主要由出蛰若虫自身的生物学习性和环境因素所引起。此外,利用空间格局参数确定了理论抽样数和序贯抽样模型。     

阿里山潜蝇茧蜂对橘小实蝇卵的寄生效能

在温度25℃、相对湿度75%、光周期L∶D=12∶12的条件下,研究了阿里山潜蝇茧蜂对橘小实蝇卵的寄生效能。结果表明:橘小实蝇卵的密度变化对阿里山潜蝇茧蜂的寄生作用有很大影响,可用功能反应模型HollingⅡ型模拟,其模拟方程为Na=0.9082N0/(1 0.0046N0);阿里山潜蝇茧蜂成虫的自身密度对寄生作用也有较大影响,可用Hassell-Varley模型模拟,其模拟方程为α=0.2858P-0.3448。     

藏北申扎地区下石炭统永珠组下部孢子组合的特征及意义

报道藏北申扎永珠区德日昂玛—下拉剖面的永珠组孢子组合,发现孢子43属,70余种(包括未定种)。组合特征如下:1)缺乏欧美植物地理区早石炭世典型的石松类植物的小孢子Lycospora属及早石炭世晚期(维宪期)重要孢子属;2)出现较多早石炭世早期(杜内期),甚至泥盆纪晚期分子。呈现出新老化石的混合现象;3)北半球和南半球孢子的混合组合,同时也是冷、暖微古植物群混合,既有相当于中国早石炭世晚期大塘期以及西欧维宪期典型属种,又有南半球澳大利亚(包括巴西和非洲大陆)的维宪期的典型种。从孢子化石混合现象看,永珠组应为近岸浅水或滨海条件下的沉积,下伏地层的孢子化石再沉积现象说明当时有一次很大的海平面下降,在邻近地区出现了大面积的剥蚀区。说明杜内期末期—维宪期初期,申扎地区出现一次由冈瓦纳大陆冰川发育造成海平面相对下降。形成区域上不整合界面———洛工组或“巴日阿朗寨段”底部的不整合界面。混合孢子组合中的寒冷气候条件下的孢子化石的发现,印证了杨式溥、范影年和林宝玉推断的冈瓦纳冰川自早石炭世维宪期(大塘期)开始就影响到西藏申扎的推论。     

青海省下三叠统巴颜喀拉山群下亚群的孢粉组合

首次对青海中部下三叠统巴颜喀拉山群下亚群孢粉组合进行综合研究。共发现孢粉:下岩组59属89种(包括1新种),按在组合中百分含量的平均值,蕨类植物孢子占55.71%,裸子植物花粉占36.3%,疑源类9属2种占7.36%,称之为Lundbladispora-Cycadopites-Veryhachium组合;上岩组86属119种(包括3新种),蕨类植物孢子占46.03%,裸子植物花粉占31.91%,疑源类13属16种占21.64%,称之为Limatulasporites?Cycadop-tes?Tubermonocolpites-Micrhystridium组合。上述孢粉组合特征,大体可与国内外早三叠世孢粉组合对比,因此,巴颜喀拉山群下亚群的时代应属早三叠世。     

Evidence that hepatic lipase and endothelial lipase have different substrate specificities for high-density lipoprotein phospholipids

Hepatic lipase (HL) and endothelial lipase (EL) are both members of the triglyceride lipase gene family. HL hydrolyzes phospholipids and triglycerides in triglyceride-rich lipoproteins and high-density lipoproteins (HDL). EL hydrolyzes HDL phospholipids and has low triglyceride lipase activity. The aim of this study was to determine if HL and EL hydrolyze different HDL phospholipids and whether HDL phospholipid composition regulates the interaction of EL and HL with the particle surface. Spherical, reconstituted HDL (rHDL) containing either 1-palmitoyl-2-oleoylphosphatidylcholine (POPC), 1-palmitoyl-2-linoleoylphosphatidylcholine (PLPC), 1-palmitoyl-2-arachidonylphosphatidylcholine (PAPC), or 1-palmitoyl-2-docosahexanoylphosphatidylcholine (PDPC) as the only phospholipid, apolipoprotein A-I as the only apolipoprotein, and either cholesteryl esters (CE) only or mixtures of CE and triolein (TO) in their core were prepared. The rHDL were similar in size and had comparable core lipid/apoA-I molar ratios. The CE-containing rHDL were used to determine the kinetics of HL- and EL-mediated phospholipid hydrolysis. For HL the V(max) of phospholipid hydrolysis for (POPC)rHDL > (PLPC)rHDL approximately (PDPC)rHDL > (PAPC)rHDL, while the K(m)(app) for (POPC)rHDL > (PDPC)rHDL > (PLPC)rHDL > (PAPC)rHDL. For EL the V(max) for (PDPC)rHDL > (PAPC)rHDL > (PLPC)rHDL approximately (POPC)rHDL, while the K(m)(app) for (PAPC)rHDL approximately (PLPC)rHDL > (POPC)rHDL > (PDPC)rHDL. The kinetics of EL- and HL-mediated TO hydrolysis was determined using rHDL that contained TO in their core. For HL the V(max) of TO hydrolysis for (PLPC)rHDL > (POPC)rHDL > (PAPC)rHDL > (PDPC)rHDL, while the K(m)(app) for (PLPC)rHDL > (POPC)rHDL approximately (PAPC)rHDL > (PDPC)rHDL. For EL the V(max) and K(m)(app) for (PAPC)rHDL > (PDPC)rHDL > (PLPC)rHDL > (POPC)rHDL. These results establish that EL and HL have different substrate specificities for rHDL phospholipids and that their interactions with the rHDL surface are regulated by phospholipids.     

Selective interleukin-12 synthesis defect in 12/15-lipoxygenase-deficient macrophages associated with reduced atherosclerosis in a mouse model of familial hypercholesterolemia

Targeted gene disruption or overexpression of 12/15-lipoxygenase in mice on the genetic background of apolipoprotein E or low density lipoprotein-receptor (LDL-R) deficiency has implicated 12/15-lipoxygenase in atherogenesis. The data support indirectly a role for 12/15-lipoxygenase in the oxidative modification of low density lipoprotein. In this study we set out to explore other potential mechanisms for 12/15-lipoxygenase in atherosclerosis using apolipoprotein B mRNA editing catalytic polypeptide-1/LDL-R double-deficient mice, a model highly related to the human condition of familial hypercholesterolemia. 12/15-Lipoxygenase deficiency in this strain led to approximately 50% decrease in aortic lesions in male and female mice at 8 months on a chow diet in the absence of cholesterol differences. While studying 12/15-lipoxygenase-deficient macrophages in culture, we discovered a remarkable selective defect (75-90% decrease) in interleukin-12 production but not in tumor necrosis factor-alpha or nitric oxide release, in response to lipopolysaccharide in the presence or absence of interferon-gamma priming. The lipopolysaccharide/interferon-gamma response was associated with a 33-50% decrease in nuclear interferon consensus sequence-binding protein, which is consistent with interferon consensus sequence-binding protein containing protein complex-dependent regulation of the interleukin-12 p40 gene. The decrease in interleukin-12 production was recapitulated in vivo in mouse aortas of the triple knockout group and was reflected in a marked decrease in interferon-gamma expression. The data provide support for a novel mechanism linking the 12/15-lipoxygenase pathway to a known immunomodulatory Th1 cytokine in atherogenesis.     

Acute inflammation increases selective uptake of HDL cholesteryl esters into adrenals of mice overexpressing human sPLA2

The acute-phase protein secretory phospholipase A2 (sPLA2) influences the metabolism of high-density lipoproteins (HDL). The adrenals are known to utilize HDL cholesterol as a source of sterols. The aim of the present study was to test the hypothesis that sPLA2 enhances the selective uptake of HDL into the adrenals in response to acute inflammation as a possible physiological role for the sPLA2-HDL interaction. Human sPLA2-transgenic mice, in which sPLA2 expression is upregulated by inflammatory stimuli, were used. Ten hours after induction of the acute-phase response (APR) by injection of bacterial lipopolysaccharide (LPS), plasma levels of HDL cholesterol decreased significantly in sPLA2-transgenic mice (-18%, P < 0.05) but remained unchanged in wild-type mice. The fractional catabolic rates of both 125I-labeled tyraminecellobiose (TC)-HDL and [3H]cholesteryl ether increased significantly in the sPLA2-transgenic mice after induction of the APR (0.18 +/- 0.01 vs. 0.21 +/- 0.01 pool/h, P < 0.05, and 0.31 +/- 0.02 vs. 0.42 +/- 0.05 pool/h, P < 0.05, respectively) but remained unchanged in the wild-type mice (0.10 +/- 0.01 vs. 0.22 +/- 0.02 pool/h, respectively). After induction of the APR, in both groups HDL holoparticle uptake by the liver was increased (P < 0.001). sPLA2-transgenic mice had 2.4-fold higher selective uptake into the adrenals after induction of the APR than wild-type mice (156 +/- 6 vs. 65 +/- 5%/ micro g tissue protein, P < 0.001). In summary, upregulation of sPLA2 expression during the APR specifically increases the selective uptake of HDL cholesteryl ester into the adrenals. These data suggest a novel metabolic role for sPLA2: modification of HDL during the APR to promote increased adrenal uptake of HDL cholesteryl ester to serve as source for steroid hormone synthesis.     

Overexpression of secretory phospholipase A(2) causes rapid catabolism and altered tissue uptake of high density lipoprotein cholesteryl ester and apolipoprotein A-I

Plasma levels of high density lipoprotein (HDL) cholesterol and its major protein component apolipoprotein (apo) A-I are significantly reduced in both acute and chronic inflammatory conditions, but the basis for this phenomenon is not well understood. We hypothesized that secretory phospholipase A(2) (sPLA(2)), an acute phase protein that has been found in association with HDL, promotes HDL catabolism. A series of HDL metabolic studies were performed in transgenic mice that specifically overexpress human sPLA(2) but have no evidence of local or systemic inflammation. We found that HDL isolated from these mice have a significantly lower phospholipid and cholesteryl ester and significantly greater triglyceride content. The fractional catabolic rate (FCR) of (125)I-HDL was significantly faster in sPLA(2) transgenic mice (4.08 +/- 0.01 pools/day) compared with control wild-type littermates (2.16 +/- 0.48 pools/day). (125)I-HDL isolated from sPLA(2) transgenic mice was catabolized significantly faster than (131)I-HDL isolated from wild-type mice after injection in wild-type mice (p < 0.001). Injection of (125)I-tyramine-cellobiose-HDL demonstrated significantly greater degradation of HDL apolipoproteins in the kidneys of sPLA(2) transgenic mice compared with control mice (p < 0.05). The fractional catabolic rate of [(3)H]cholesteryl ether HDL was significantly faster in sPLA(2)-overexpressing mice (6.48 +/- 0.24 pools/day) compared with controls (4.80 +/- 0.72 pools/day). Uptake of [(3)H] cholesteryl ether into the livers and adrenals of sPLA(2) transgenic mice was significantly enhanced compared with control mice. In summary, these data demonstrate that overexpression of sPLA(2) alone in the absence of inflammation causes profound alterations of HDL metabolism in vivo and are consistent with the hypothesis that sPLA(2) may promote HDL catabolism in acute and chronic inflammatory conditions.     

糖类在植物组织培养中的效应

糖类是影响植物组织培养成功与否的关键之一。迄今为止,已用于植物组织培养的糖类有５０多种。在植物体细胞组织培养中,蔗糖一直作为标准碳源,然而其他糖类物质如：葡萄糖、麦芽糖和山梨醇对植物体细胞培养也产生了一定的影响。在植物花药培养中,蔗糖较好,但应注意麦芽糖对花药培养的促进作用。