庭藤种综内分类群间变异式样的相关性

在种子植物中,种内的分化类型之呈连续的数量性状变异式样者屡见不鲜。毛叶石楠Photinia villosa(Thunb.)DC^[1]、短葶山麦冬Liri-ope muscari (Decne.)Bailey^[2]和胡枝子Lespedeza bicolor Turcz.^[3]就是很好的例证。     

科达穗和羽杉化石在新疆准噶尔盆地南缘的发现

近年来,笔者在系统研究了新疆准噶尔盆地南缘的古生代植物化石后,发现了两种早已绝灭了的科达(Cordaites)的生殖器官化石,一种是长苞科达穗(Cordaianthus volkmannii(Ett.)Zeiller),另一种是短苞科达穗(比较种)(Cordaianthus of.curtus Sze);同时还发现了一种最古老的松柏类化石——双羽杉(比较种)(Walchia of.bipinata Gu et Zhi)这些化石产生在准噶尔盆地南缘的乌鲁木齐市东南的下芨芨槽子群中,其地质时代隶属於早二叠晚期(P₁²)。     

栝楼上星盾炱属一新种

星盾炱属新种栝楼星盾炱Asterinatrichosanthis寄生在葫芦科植物毛果栝楼Trichosanthesmushaensis的叶上。新种有拉丁文和英文描述,附了显微结构图。模式标本保存在广东省微生物研究所标本室(HMIGD)。     

栝楼上星盾炱属一新种

星盾炱属新种栝楼星盾炱Asterina trichosanthis寄生在葫芦科植物毛果栝楼Trichosanthes mushaensis的叶上。新种有拉丁文和英文描述,附了显微结构图。模式标本保存在广东省微生物研究所标本室(HMIGD)。     

鱼鳞云杉种子油中顺-5,9,12-十八碳三烯酸的分离和鉴定

在东北松科鱼鳞云杉(Picea jezoensis Carr.)种子油脂肪酸的分析中,发现有三种不常见脂肪酸未予鉴定,其中一种含量高达25.9％。对此我们进行了分离鉴定,确证为顺-5,9,12-十八碳三烯酸。此酸芬兰Eero Elomaa已有报导。 本实验分析了东北松科其余11种种子油脂肪酸的组成,发现它们都含有顺-5,9,12-十八碳三烯酸,但在我们分析过的东北其他科属180种种子油的脂肪酸中,未发现上述不     

中国唇柱苣苔属校订(Ⅰ)

英国学者D.Don于1822年代F.Buchanan发表了Chirita Buch.-Ham.ex D.Don,^[30],于1825年描述了这属的三个种^[13]:C.urticifolia Buch.Ham.ex Don,C.bifolia D.Don及C.pumila D.Don.Chirita属于苦苣苔亚科Cyrtandroideae的长蒴苣苔族Didy-mocarpeae,与这族的另一大属长茹苞苔属Didymccarpus Wall.近缘,二者的主要区别在于柱头的特征上^{[1] [13] [17] [28]},本属的柱头为位于花柱下方的一个薄片,而上方的柱头财完全消失,在长茹筐苔属,柱头呈扁球形或盘状,可能是由二枚柱头合生而成。     

含α-桐酸的两种油料植物

自然界的植物种子油中,桐酸的存在是比较少见的。以前一度认为它是大戟科(Euphorbiaceae)油桐(Vernicia Lour.)中特有的脂肪酸。后来不仅在大戟科的其它属中,而且在蔷薇科(Rosaceae),葫芦科     

木本植物花药培养的进展

近十年来,已从木本植物的8个科、9个属、约23 个种中获得了单倍体植株,它们是：茄科的滨黎叶拘祀 (Lycium halimifolzum Mill.)^[33],宁夏拘祀(L. barbarum L.)t'3拘祀(L. chinense Mill.)^[2]。杨柳科的 黑杨（Populus nigra L. )[33,小叶杨X黑杨（P. simonit Carr. X P. nigra L.),大青杨（P. ussuriensis Komar. )^[32],加拿大白杨X香杨（P. canadensis Moench X P. koreana Rehd.),哈青杨X钻天杨(P. harbinensis Wang et Skv. X P. pyramidalis Roz.)^[4],银白杨X小 叶杨（P. albs L. X P. simonii Carr.)^[5],中东杨（P. berolinensis Dipp. ),中东杨X钻夭杨(P. berolinensis Dipp. X P. pyramidalis Roz. ),小青杨（P. pseudo-simonii Kitagawa.)^[6],小青杨X钻天杨（P. pseudo-stmonzi Kitagawa. X P. pyramidalis Roz.)^[5],小叶杨（P. simonii Carr.) M,胡杨（P. euphratica Oliv. )^[7][8]。芸香科的权 壳（Poncirus trifolata (L.) Raf.)^[25], 柑桔（Citrus microcarpa Bge.)^[9] 葡萄科的葡萄(Vitis vinifera L.)^[10]蔷薇科苹果属的揪子（Malus pruni f olia (Wi- 11d.) Borkh.)^[11]以及苹果（Malus pumilea Mill.)^[12]。七叶树科的欧洲七叶树（Aesculus hippocastanum L.)^[30] 无患子科的荔枝（Litchi chinensis Sonn.)^[13]。此外,在 我国已从杉木花药培养获得小植株^[14],油茶也已从花 药愈伤组织分化出绿芽点^[15]。     

中国荨麻科冷水花属的研究

冷水花属Pilea Lindl.是荨麻科藤麻族Trib.Prccrideae^[22]中的一个较原始的属,也是荨麻科最大的一个属,约600^[14]种,约占该科全部种数的三分之一^*,主要分布于美洲、亚洲、非洲和大洋洲的新几内亚的热带和亚热带地区,温带地区较少。在我国,原记录有70余种,经研究整理后,本文记载了85种(其中存疑种2种),8亚种,7变种,其中新种31种,我国新记录9种,还有部分标本暂时难以作出鉴定,它们代表了大约六、七种,这样,估计我国冷水花属植物约有90余种,为我国尊麻科的一个大属(另一大属楼梯草属Elatostema, 108种) (王文采,中国植物志手稿,未发表),主要分布于长江流域以南地区,少数种类可分布到东北省区。这属植物喜好生长于山坡阴湿处,是为这些地区山坡阴湿环境草本植被的重要建群植物。     

黄渤海甲壳类的分类多样性

为了解黄渤海甲壳类的分类多样性特征, 我们统计了2010-2015年中国水产科学研究院黄海水产研究所调查捕获的黄渤海甲壳类(软甲纲: 十足目与口足目)物种名录。结合历史文献, 进一步系统整理得到黄渤海甲壳类物种总名录。基于这2个名录, 应用分类阶元包含指数(the inclusion index at taxonomic level, TINCL_i)、平均分类差异指数(average taxonomic distinctness index, Δ⁺)和分类差异变异指数(variation in taxonomic distinctness index, Λ⁺)研究了其分类多样性特征。结果显示: 2010-2015年调查名录中, 甲壳类共93种, 隶属于2目39科66属, 其中10种为新分布种; 对虾科、藻虾科、长臂虾科、梭子蟹科和弓蟹科的物种数最多, 合计占总物种数的38.71%; TINCL_i分别为1.41种/属和2.38种/科; Δ⁺和Λ⁺分别为50.25和35.20。总名录中, 甲壳类共228种, 隶属于2目53科123属, 其中藻虾科、豆蟹科、对虾科、弓蟹科和鼓虾科的物种数最多, 合计占总物种数的30.70%; TINCL_i分别为1.85种/属和4.30种/科, Δ⁺和Λ⁺分别为50.18和30.87。对虾科的相对丰富度指数(the relative richness index, R_r)最高(100), 其次是梭子蟹科(71.43)和长臂虾科(62.50), 豆蟹科最低(6.25)。黄渤海甲壳类的平均分类差异指数(Δ⁺)明显小于鱼类(P < 0.05)。2010-2015年调查的Δ⁺计算值高于理论值, 且在理论值的95%置信区间内, 说明黄渤海甲壳类群落正处在中等程度的干扰中。     

Combined transgenic expression of Punica granatum conjugase (FADX) and FAD2 desaturase in high linoleic acid Arabidopsis thaliana mutant leads to increased accumulation of punicic acid

Main conclusion

Arabidopsis was engineered to produce 21.2 % punicic acid in the seed oil. Possible molecular factors limiting further accumulation of the conjugated fatty acid were investigated. Punicic acid (18:3Δ^{9cis,11trans,13cis} ) is a conjugated linolenic acid isomer and is a main component of Punica granatum (pomegranate) seed oil. Medical studies have shown that punicic acid is a nutraceutical with anti-cancer and anti-obesity properties. It has been previously demonstrated that the conjugated double bonds in punicic acid are produced via the catalytic action of fatty acid conjugase (FADX), which is a homolog of the oleate desaturase. This enzyme catalyzes the conversion of the Δ¹²-double bond of linoleic acid (18:2Δ^9cis,12cis ) into conjugated Δ^11trans and Δ^13cis -double bonds. Previous attempts to produce punicic acid in transgenic Arabidopsis thaliana seeds overexpressing P. granatum FADX resulted in a limited accumulation of punicic acid of up to 4.4 %, accompanied by increased accumulation of oleic acid (18:1?^9cis ), suggesting that production of punicic acid in some way inhibits the activity of oleate desaturase (Iwabuchi et al. 2003). In the current study, we applied a new strategy to enhance the production of punicic acid in a high linoleic acid A. thaliana fad3/fae1 mutant background using the combined expression of P. granatum FADX and FAD2. This approach led to the accumulation of punicic acid at the level of 21 % of total fatty acids and restored the natural proportion of oleic acid observed in the A. thaliana fad3/fae1 mutant. In addition, we provide new insights into the high oleate phenotype and describe factors limiting the production of punicic acid in genetically engineered plants.     

Punicic Acid a Conjugated Linolenic Acid Inhibits TNFα-Induced Neutrophil Hyperactivation and Protects from Experimental Colon Inflammation in Rats

Background

Neutrophils play a major role in inflammation by releasing large amounts of ROS produced by NADPH-oxidase and myeloperoxidase (MPO). The proinflammatory cytokine TNFα primes ROS production through phosphorylation of the NADPH-oxidase subunit p47phox on Ser345. Conventional anti-inflammatory therapies remain partially successful and may have side effects. Therefore, regulation of neutrophil activation by natural dietary components represents an alternative therapeutic strategy in inflammatory diseases such as inflammatory bowel diseases. The aim of this study was to assess the effect of punicic acid, a conjugated linolenic fatty acid from pomegranate seed oil on TNFα-induced neutrophil hyperactivation in vitro and on colon inflammation in vivo.

Methodology and Principal Findings

We analyzed the effect of punicic acid on TNFα-induced neutrophil upregulation of ROS production in vitro and on TNBS-induced rat colon inflammation. Results show that punicic acid inhibited TNFα-induced priming of ROS production in vitro while preserving formyl-methionyl-leucyl-phenylalanine (fMLP)-induced response. This effect was mediated by the inhibition of Ser345-p47phox phosphorylation and upstream kinase p38MAPK. Punicic acid also inhibited fMLP- and TNFα+fMLP-induced MPO extracellular release from neutrophils. In vivo experiments showed that punicic acid and pomegranate seed oil intake decreased neutrophil-activation and ROS/MPO-mediated tissue damage as measured by F2-isoprostane release and protected rats from TNBS-induced colon inflammation.

Conclusions/Significance

These data show that punicic acid exerts a potent anti-inflammatory effect through inhibition of TNFα-induced priming of NADPH oxidase by targeting the p38MAPKinase/Ser345-p47phox-axis and MPO release. This natural dietary compound may provide a novel alternative therapeutic strategy in inflammatory diseases such as inflammatory bowel diseases.     

Formation of conjugated Delta11Delta13-double bonds by Delta12-linoleic acid (1,4)-acyl-lipid-desaturase in pomegranate seeds.

For the biosynthesis of punicic acid (18:3Delta9Z,11E,13Z) a (11,14)-linoleoyl desaturase activity has been proposed. To isolate this acyl-lipid-desaturase, PCR-based cloning was used. This approach resulted in the isolation of two complete cDNAs. The first isolated full-length cDNA harbors a sequence of 1350 bp encoding a protein of 395 amino acids. The second cDNA was 1415 bp long encoding a protein of 387 amino acids. For functional identification proteins encoded by the cDNAs were expressed in Saccharomyces cerevisiae, and formation of newly formed fatty acids was analyzed by gas chromatography-free induction decay (GC-FID) and GC/MS. The expression of the heterologous enzymes resulted in the first case in a significant amount of linoleic acid and in the second case, after linoleic acid supplementation, in formation of punicic acid. The results presented here identify one cDNA coding for a classical Delta12-acyl-lipid-desaturase. The other one codes for a new type of (1,4)-acyl-lipid-desaturase that converts a cis double bond located in the Delta12-position of linoleic acid or gamma-linolenic acid, but not in alpha-linolenic acid, into a conjugated cis-trans double bond system.     

Fatty acid changes during maturation of Momordica charantia and Trichosanthes Anguina Seeds

Changes in fatty acids were studied during maturation of Momordica charantia and Trichosanthes anguina seeds, which contain cis-9, trans-11, trans-13-octadecatrienoic acid (α-eleostearic) and cis-9, trans-11, cis-13-octadecatrienoic acid (punicic), respectively. The two seeds matured 30 and 35 days after flowering, respectively. Total lipids as well as α-eleostearic acid accumulated rapidly from 10 to 20 days in M. charantia. In T. anguina the active period of lipid synthesis was from 15 to 30 days but punicic acid continued to be synthesized until maturity. In both species, the disappearance of linolenic acid and the reduction in concentration of linoleic acid were concomitant with the formation of conjugated fatty acids. The conjugated fatty acids were absent from monoacylglycerols and phospholipids of both species, and also from the diacylglycerols of M. charantia, throughout maturation     

Synergistic effect of conjugated linolenic acid isomers against induced oxidative stress,inflammation and erythrocyte membrane disintegrity in rat model

Background

α-Eleostearic acid and punicic acid, two typical conjugated linolenic acid (CLnA) isomers present in bitter gourd and snake gourd oil respectively, exhibit contrasting cis-trans configuration which made them biologically important.

Methods

Rats were divided into six groups. Group 1 was control and group 2 was treated control. Rats in the groups 3 and 4 were treated with mixture of α-eleostearic acid and punicic acid (1:1) (0.5% and 1.0% respectively) while rats in the groups 5 and 6 were treated with 0.5% of α-eleostearic acid and 0.5% of punicic acid respectively along with sodium arsenite by oral gavage once per day.

Results

Results showed that increase in nitric oxide synthase (NOS) activity, inflammatory markers expression, platelet aggregation, lipid peroxidation, protein oxidation, DNA damage and altered expression of liver X receptor-α (LXR-α) after arsenite treatment were restored with the supplementation of oils containing CLnA isomers. Altered activities of different antioxidant enzymes such as superoxide dismutase, catalase, glutathione peroxidase, glutathione reductase and ferric reducing ability of plasma (FRAP) also restored after oil supplementation. Altered morphology and fluidity of erythrocyte membrane studied by atomic force and scanning electron microscopy, after stress induction were significantly improved due to amelioration in cholesterol/phospholipid ratio and fatty acid profile of membrane. Oils treatment also improved morphology of liver and fatty acid composition of hepatic lipid.

Conclusions

Overall two isomers showed synergistic antioxidant and anti-inflammatory effect against induced perturbations and membrane disintegrity.

General significance

Synergistic antioxidant and anti-inflammatory role of these CLnA isomers were established by this study.     

Conjugated fatty acid synthesis: residues 111 and 115 influence product partitioning of Momordica charantia conjugase

Conjugated linolenic acids (CLNs), 18:3 Δ(9,11,13), lack the methylene groups found between the double bonds of linolenic acid (18:3 Δ(9,12,15)). CLNs are produced by conjugase enzymes that are homologs of the oleate desaturases FAD2. The goal of this study was to map the domain(s) within the Momordica charantia conjugase (FADX) responsible for CLN formation. To achieve this, a series of Momordica FADX-Arabidopsis FAD2 chimeras were expressed in the Arabidopsis fad3fae1 mutant, and the transformed seeds were analyzed for the accumulation of CLN. These experiments identified helix 2 and the first histidine box as a determinant of conjugase product partitioning into punicic acid (18:3 Δ(9cis,11trans,13cis)) or α-eleostearic acid (18:3 Δ(9cis,11trans,13trans)). This was confirmed by analysis of a FADX mutant containing six substitutions in which the sequence of helix 2 and first histidine box was converted to that of FAD2. Each of the six FAD2 substitutions was individually converted back to the FADX equivalent identifying residues 111 and 115, adjacent to the first histidine box, as key determinants of conjugase product partitioning. Additionally, expression of FADX G111V and FADX G111V/D115E resulted in an approximate doubling of eleostearic acid accumulation to 20.4% and 21.2%, respectively, compared with 9.9% upon expression of the native Momordica FADX. Like the Momordica conjugase, FADX G111V and FADX D115E produced predominantly α-eleostearic acid and little punicic acid, but the FADX G111V/D115E double mutant produced approximately equal amounts of α-eleostearic acid and its isomer, punicic acid, implicating an interactive effect of residues 111 and 115 in punicic acid formation.     

Use of reversed phase HP liquid chromatography to assay conversion of N-acylglycines to primary fatty acid amides by peptidylglycine-alpha-amidating monooxygenase

Primary fatty acid amides (R-CO-NH2) and N-acylglycines (R-CO-NH-CH2-COOH) are classes of compounds that have only recently been isolated and characterized from biological sources. Key questions remain regarding how these lipid amides are produced and degraded in biological systems. Relative to the fatty acids, little has been done to develop methods to separate and quantify the fatty acid amides and N-acylglycines. We describe reversed phase HPLC methods for the separation of C2-C12 primary fatty acid amides and N-acylglycines and also C12-C22 fatty acid amides. Separation within each class occurs primarily on the basis of simple interactions between the acyl chain and the chromatographic stationary phase, but the polar headgroups on these and related fatty acids and N-acylethanolamides modulate the absolute retention in reversed phase mode. We use these methods to measure the enzyme-mediated, two-step conversion of N-octanoylglycine to octanoamide.     

Substrate inhibition of pigeon liver fatty acid synthetase and optimum assay conditions for over-all synthetase activity

The effects of the substrates acetyl-CoA, malonyl-CoA, and NADPH on the activity of pigeon liver fatty acid synthetase have been studied over a wide range of concentrations. Double-reciprocal coordinate plots for each of the substrates have been found to be linear at low concentrations. At higher concentrations two of the substrates, acetyl-CoA and malonyl-CoA, inhibit the rate of fatty acid synthesis. This double substrate inhibition is apparently of a competitive type. Inhibition by acetyl-CoA is very strong as compared to that by malonyl-CoA. At a 4:1 ratio of acetyl- to malonyl-CoA, inhibition is about 75%, whereas at a 4:1 ratio of malonyl- to acetyl-CoA fatty acid synthesis proceeds at the maximum rate.These results are consistent with the hypothesis that a competition between acetyl-CoA and malonyl-CoA occurs for the occupany of the 4′- phosphopantetheine site, a prosthetic group of the synthetase complex, and possibly also for the hydroxyl binding site (or sites). The relative concentrations of these substrates and the binding constants for each then determine whether these sites are occupied by acetyl or malonyl groups, and whether inhibition of fatty acid synthesis occurs. Based on our results, assays for pigeon liver fatty acid synthetase activity should be conducted at substrate concentrations of 15 μm, 60 μm, and 100 μm for acetyl-CoA, malonyl-CoA, and NADPH, respectively.     

Inhibition of c-Jun-N-terminal kinase increases cardiac peroxisome proliferator-activated receptor alpha expression and fatty acid oxidation and prevents lipopolysaccharide-induced heart dysfunction

Septic shock results from bacterial infection and is associated with multi-organ failure, high mortality, and cardiac dysfunction. Sepsis causes both myocardial inflammation and energy depletion. We hypothesized that reduced cardiac energy production is a primary cause of ventricular dysfunction in sepsis. The JNK pathway is activated in sepsis and has also been implicated in impaired fatty acid oxidation in several tissues. Therefore, we tested whether JNK activation inhibits cardiac fatty acid oxidation and whether blocking JNK would restore fatty acid oxidation during LPS treatment. LPS treatment of C57BL/6 mice and adenovirus-mediated activation of the JNK pathway in cardiomyocytes inhibited peroxisome proliferator-activated receptor α expression and fatty acid oxidation. Surprisingly, none of the adaptive responses that have been described in other types of heart failure, such as increased glucose utilization, reduced αMHC:βMHC ratio or induction of certain microRNAs, occurred in LPS-treated mice. Treatment of C57BL/6 mice with a general JNK inhibitor (SP600125) increased fatty acid oxidation in mice and a cardiomyocyte-derived cell line. JNK inhibition also prevented LPS-mediated reduction in fatty acid oxidation and cardiac dysfunction. Inflammation was not alleviated in LPS-treated mice that received the JNK inhibitor. We conclude that activation of JNK signaling reduces fatty acid oxidation and prevents the peroxisome proliferator-activated receptor α down-regulation that occurs with LPS.