浙江省洞头拟裸长角虫兆属一新种（长角虫兆科：弹尾纲）

记述浙江省洞头岛拟祼长角虫兆属1无眼新种,岛屿拟裸长角虫兆Coecobrya islandica Shi&Pan sp.nov.。此新种的鉴定特征为无眼,弹器基具"光滑"刚毛,胫胕节内侧无"光滑"刚毛,下唇MREL1L2为光滑刚毛,X和X4为光滑刺状小刚毛,上唇基刚毛,腹部第II–IV节的感觉毛以及背部毛序。该新种与短毛拟裸长角虫兆Coecobrya brevis Xu et al.,2012最相似。本文给出了该新种的特征图及与相似种的详细特征比较。模式标本保存于台州学院生命科学学院和南京农业大学植保学院昆虫系。     

刺齿虫兆属温州一新种及浙江分种检索表（弹尾纲：长角虫兆科）

记述刺齿虫兆属温州 1 新种:六毛刺齿虫兆Homidia hexaseta sp. nov.,该种的鉴别特征包括体色,下唇具光滑毛L1,头背部顶区具6根大刚毛,胸部第Ⅱ节具p4系列大刚毛,腹部第Ⅲ节中间具a2大刚毛,腹部第Ⅳ节具B6和Ae5-7大刚毛以及端节亚顶端齿远大于顶端齿。同时,本文还给出了浙江省刺齿虫兆属分种检索表。正模:♀,浙江省温州市泰顺县乌岩岭国家自然保护区,采集号C9271-4,2005-Ⅶ-29;副模:5♀♀。其中两头雌性副模标本保存于台州学院生命科学学院,其余标本保存于南京大学生命科学学院。     

刺齿(虫兆)属温州—新种及浙江分种检索表(弹尾纲:长角(虫兆)科)

记述刺齿(虫兆)属温州1新种:六毛刺齿(虫兆) Homidia hexaseta sp.nov.,该种的鉴别特征包括体色,下唇具光滑毛L1,头背部顶区具6根大刚毛,胸部第Ⅱ节具p4系列大刚毛,腹部第Ⅲ节中间具a2大刚毛,腹部第Ⅳ节具B6和Ae5-7大刚毛以及端节亚顶端齿远大于顶端齿.同时,本文还给出了浙江省刺齿(虫兆)...     

浙江省大雷山刺齿虫兆属一新种描述（弹尾纲：长角虫兆科）

记述浙江省大雷山刺齿虫兆属 1 新种,张氏刺齿虫兆Homidia zhangi sp. nov., 该种鉴别特征有体色,光滑下唇毛 L1,腹部第 4 节后侧中间 3+3 根大刚毛及长度相近的特化毛,腹部第 1 节和第 5 节特化毛的相对位置以及腹管侧瓣和弹器端区的大量纤毛状刚毛。模式标本保存于南京大学生命科学学院和台州学院生命科学学院。     

中国西部刺齿(虫兆)属Homidia一新种(弹尾纲:长角(虫兆)科)

本文记述中国西部剌齿(虫兆)属1新种:中带剌齿(虫兆)H.mediofascia,sp.nov..该种区别属内其他种的主要特征是本种胸部第2节到腹部第2节背部中间具色带,第1腹节具大刚毛a1,腹部第4节后缘大刚毛7+7,粘管后侧面具光滑刚毛4根.本文还对属内5个相近种进行了比较.正模:早,陕西省安康市,2006-Ⅵ-15;副模:8♀♀,1♂以及8头酒精标本,陕西省安康市,2006-Ⅵ-15.1♀和1头酒精标本保存于南京大学,其他标本保存于台州学院生命科学学院.     

浙江台州刺齿䖴属一新种及其一龄幼体描述（弹尾纲：长角䖴科）

记述了浙江省刺齿属一腹部第四节前缘"眉毛"仅具4根大刚毛的新种:四毛刺齿Homidia quadriseta Pan sp.nov.。此新种的鉴定特征是腹部第3节整节以及第4节的后半节为深色,腹部第3节中间具1根大刚毛,腹部第4节前缘"眉毛"具2+2大刚毛,后侧中间具3根大刚毛,上唇基具12根刚毛,齿节内侧刺少(7–8根)且多数呈细纤毛状;同时,本文还描述了该新种的一龄幼虫。模式标本保存于台州学院生命科学学院。     

中国颚毛(虫兆)属二新种(弹尾目,疣(虫兆)科)

记述了采白海南和浙江省的弹尾目疣[虫兆]科颚毛[虫兆]属Crossodonthina Yosii,2新种,海南颚毛yao C．hainana sp．nov．和天童颚毛yao C．tiantongshana sp．nov．。海南颚毛[虫兆]头部每侧有眼2个,弹器痕上有6根刚毛,非常容易与本属其它已知种类分开。天童颚毛[虫兆]与上海产的Crossodonthina tridentiens Yue＆Yin,1999相似,两者的主要区别是：新种的上颚有两条长的、羽毛状分支和具5齿的片状突起,且基部齿长而细;下颚的内颚叶端部及近基部各有1齿;新种腹部第5节有3＋3个疣状突起,而C．tridentiens有2＋2个疣状突起;新种的爪部内侧有2个小齿,1个大齿,C．tridentiens只有1大齿。模式标本保存于上海生命科学研究院,植物生理生态所昆虫标本馆。     

中国浙江省刺齿虫兆属一新种(弹尾目:长角虫兆科)

本文记述了中国刺齿虫兆属１新种——天台刺齿虫兆Ｈｏｍｉｄｉａｔｉａｎｔａｉｅｎｓｉｓ,ｓｐ．ｎｏｖ．。该种色斑明显不同于此属所有已知种。它的许多特征与朝鲜的Ｈ．ｆｌａｖｏｎｉｇｒａＳｚｅｐｔｙｃｋｉ,１９７３相似,但上唇、下唇和弹器齿节基部等处的刚毛及腹部第ＩＩ节的毛序可区分两者。正模♀,浙江天台山,采集号８５３７,１９９６－ＶＩＩ－１６;副模５♀♀,采集号８５３５、８５３６和８５３７,其它同正模。模式标本保存于南京大学生物系。     

广东丽虫兆属一新种（弹尾纲：爪虫兆科）

记述广东弹尾纲 1 新种广东丽虫兆Callyntrura (Javaphysa) guangdon gensis sp. nov.,该新种与C. (J.) javana Yosii,1992 在上唇和下唇上比较相似,但是它们在体色、齿节刚毛、头部 V0 大毛、胸部第2节毛序有较大的区别。     

福建省刺齿虫兆属（弹尾纲：长角虫兆科）一新种描述

记述福建省刺齿属1新种:拟中华刺齿Homidia pseudosinensis sp.nov.。该新种的鉴定特征有胸部第2节后侧具近似M型的横条带,下唇毛序及腹部第4节毛序。本文提供了该物种的特征图及福建省刺齿属分种检索表。     

Intra-H-2 recombination inH-2b/H-2t1 heterozygotes in the mouse

Four cases of intra-H-2 recombination were detected during serological screening of 1066 backcross animals produced fromH-2^b/H-2^t1 heterozygous mice. Three of the intra-H-2 recombinants received theK region fromH-2^t1 and theD region from theH-2^b parental chromosome. The remaining recombinant received theK region from theH-2^b parental chromosome and theD region fromH-2^t1. Three of the four recombinants have been developed into inbred lines TBR2, TBR3, and TBR4 and were assigned the haplotype designations at², at³, and at⁴. Ss typing revealed that TBR2 and TBR3 originated fromK- S interval crossover events, while the remaining two recombinants resulted from crossing over in theS- D interval.     

The relationship between theH-2 loss mutations ofH-2da andH-2db in the mouse

The mouse strain B10.D2-H-2^da carries the mutantH-2^da allele, derived after chemical induction, and this has been shown to be a gain and loss mutation involving theH-2D^d locus.BALB/c- H-2^db, derived spontaneously, is a loss mutation only, and appears not to involve theH-2D^d, but rather theH-2L^d locus. The two mutations effectboth graft rejection and serologically detected H-2 specificities (Type II mutation). In the experiments described in this study, theloss mutations in theH-2^da andH-2^db mutants have been compared by skin grafting, and by direct and absorption serological techniques: (1) By skin grafting, using the well established complementation method, it has been shown thatH-2^da andH-2^db do not complement each other, i.e., the mutation in both occurred at the same locus. However, by appropriate selection of donor and recipient, it has become clear thatH-2^da had a greater loss than didH-2^db, althoughH-2^da includes the loss found inH-2^db. (2) Serological studies have demonstrated that H-2D.4 was altered inH-2^da, but not inH-2^db; H-2.28 (detected by D-28b and D-29) was decreased or lost in both mutants;H-2^db anti-BALB/c failed to react withH-2^da; both mutants reacted similarly with D-28 sera. In addition, sera made usingH-2^da as donor did not contain an anti-H 2.28 antibody. The loss mutation involvingH-2^da therefore appears to have led also to the loss of H-2.28 as found inH-2^db. We conclude that theH-2^da strain arose after a complex mutation or recombination event which involvedboth theH-2D^d locus and the closely linkedH-2L^d locus, whereasH-2^db affects only theH-2L locus.     

Intra-H-2 recombination in the mouse

Serological characterization of threeK-S interval recombinant strains, TBR2 (H-2 ^at2 ), TBR3 (H-2 ^at3 ) and AIR1 (H-2 ^a2 ) was performed using anti-H-2, Ia, Ss and Slp antisera. The data presented here reveal that the crossover events in both TBR2 and TBR3 occurred between theI-A andI-E subregions. In both cases, theH-2K andI-A subregions were derived from theH-2 ^t1 chromosome, while theI-E, S andH-2D regions were derived from theH-2 ^b chromosome (K ^s A ^k E ^b S ^b D ^b ). TheH-2 ^a2 chromosome resulted from a crossover event between theH-2 ^a1 andH-2 ⁱ⁹ chromosomes. Ia and Ss typing of AIR1 suggested that theK toI-E regions originated fromH-2 ^a1 and theS andD regions originated fromH-2 ⁱ⁹ (K ^k A ^k E ^k S ^b D ^d ).     

Study ofH-2 mutations in mice

The serologically defined H-2.5 specificity was tested on spleen cells and red blood cells (RBC) of theH-2 ^b haplotype and a number of its mutants. Thebm8 (bh) mutant was barely distinguishable fromb in a variety of tests made. On spleen cells ofbm1 (ba) the H-2.5 specificity seemed to be unchanged, while it was virtually absent from RBC of this mutant. Mutantsbm4 (bf),bm5 (bg1), andbm6 (bg2) were similar tobm1, with slight differences between them. The mutantbm3 (bd) retained an unchanged quantity of H-2.5 on its spleen cells, while the specificity was substantially increased on its RBC. The H-2.5 ofbm3 is not identical to that ofH-2 ^a . Possible mechanisms causing differential serology of theH-2 ^b mutants are discussed.     

OsVIL2 functions with PRC2 to induce flowering by repressing OsLFL1 in rice

Flowering is exquisitely regulated by both promotive and inhibitory factors. Molecular genetic studies with Arabidopsis have verified several epigenetic repressors that regulate flowering time. However, the roles of chromatin remodeling factors in developmental processes have not been well explored in Oryza sativa (rice). We identified a chromatin remodeling factor OsVIL2 (O. sativa VIN3‐LIKE 2) that promotes flowering. OsVIL2 contains a plant homeodomain (PHD) finger, which is a conserved motif of histone binding proteins. Insertion mutations in OsVIL2 caused late flowering under both long and short days. In osvil2 mutants OsLFL1 expression was increased, but that of Ehd1, Hd3a and RFT1 was reduced. We demonstrated that OsVIL2 is bound to native histone H3 in vitro. Chromatin immunoprecipitation analyses showed that OsVIL2 was directly associated with OsLFL1 chromatin. We also observed that H3K27me3 was significantly enriched by OsLFL1 chromatin in the wild type, but that this enrichment was diminished in the osvil2 mutants. These results indicated that OsVIL2 epigenetically represses OsLFL1 expression. We showed that OsVIL2 physically interacts with OsEMF2b, a component of polycomb repression complex 2. As observed from osvil2, a null mutation of OsEMF2b caused late flowering by increasing OsLFL1 expression and decreasing Ehd1 expression. Thus, we conclude that OsVIL2 functions together with PRC2 to induce flowering by repressing OsLFL1.     

Linkage of lactate dehydrogenase-2, Ldh-2, in the mouse

An electrophoretically detectable variant of lactate dehydrogenase-2 in Mus musculus has been found and used to locate the structural gene, Ldh-2, on chromosome 6. Gene order and recombination frequencies are estimated as Sig—36.0±4.8—Lc 21.0±4.1—Mi ^wh—20.0±4.0—Ldh-2.     

Phospholipase A2 in astrocytes

Astrocytes comprise the major cell type in the central nervous system (CNS) and they are essential for support of neuronal functions by providing nutrients and regulating cell-to-cell communication. Astrocytes also are immune-like cells that become reactive in response to neuronal injury. Phospholipases A₂ (PLA ₂) are a family of ubiquitous enzymes that degrade membrane phospholipids and produce lipid mediators for regulating cellular functions. Three major classes of PLA ₂ are expressed in astrocytes: group IV calcium-dependent cytosolic PLA ₂ (cPLA₂), group VI calcium-independent PLA ₂ (iPLA₂), and group II secretory PLA ₂ (sPLA₂). Upregulation of PLA ₂ in reactive astrocytes has been shown to occur in a number of neurodegenerative diseases, including stroke and Alzheimer’s disease. This review focuses on describing the effects of oxidative stress, inflammation, and activation of G protein-coupled receptors on PLA ₂ activation, arachidonic acid (AA) release, and production of prostanoids in astrocytes.     

H-2 effects on cell-cell interactions in the response to single non-H-2 alloantigens

Immune response (Ir) genes mapping in theI region of the mouseH-2 complex appear to regulate specifically the presentation of a number of antigens by macrophages to proliferating T cells. We have investigated the possibility that similarIr genes mapping in theH-2K andH-2D regions specifically regulate the presentation of target antigens to cytotoxic effector T cells. We report that the susceptibility of targets expressing specific non-H-2 H alloantigens to lysis by H-2-compatible, H-antigen-specific cytotoxic effector T cells is controlled by polymorphicH-2K/D genes. This control of susceptibility to lysis is accomplished through what we have defined operationally as antigen-specific regulation of non-H-2 H antigen immunogenicity. High immunogenicity of the H-4.2 alloantigen is determined by a gene mapping in theH-2K region ofH-2 ^b . However, high immunogenicity of H-7.1 is determined by a gene mapping in theH-2D region ofH-2 ^b . High immunogenicity of the H-3.1 alloantigen is determined by genes mapping in both theH-2K andH-2D regions ofH-2 ^b . Therefore, genes mapping in theH-2K andH-2D regions serve a function in presenting antigen to cytotoxic effector T cells. This function is analogous to that played byI-regionIr genes expressed in macrophages which present antigen to proliferating T cells. We present arguments for classification of theseH-2K/D genes as a second system ofIr genes and discuss the implications of twoH-2-linkedIr-gene systems, their possible functions, and their evolution.