AbstractDibrachys Förster are studied from China, of which four new species, Dibrachysgolmudica Jiao & Xiao, sp. n., Dibrachyskunmingica Jiao & Xiao, sp. n., Dibrachysliaoi Jiao & Xiao, sp. n. and Dibrachysqinghaiensis Jiao & Xiao, sp. n., and four newly recorded species, Dibrachysbraconidis (Ferrière & Faure), Dibrachysconfusus (Girault), Dibrachyshians Bouček and Dibrachysmaculipennis Szelényi, are reported. A key to Chinese Dibrachys and illustrations of external features of the species are provided.Twelve species of  Dibrachys was erected by Förster in 1856, but without any species included in the genus. Pteromalusboucheanus Ratzeburg, 1844 as the type species and listed Pteromaluscavus Walker, 1835 as a synonym. Although the type material of Pteromalusboucheanus is lost . Consequently, Dibrachysmicrogastri (Bouché) is the senior synonym of both Dibrachysboucheanus (Ratzeburg) and Dibrachyscavus . is lost , ThomsonDibrachys Förster s. str. and Dibrachys (Allodibrachys Bouček). Nineteen valid species of Dibrachys are recognized, of which 13 are known from the Palearctic region, 8 from the Nearctic region, 4 from the Oriental region, 1 from the Australasian region, 1 from the Afrotropical region and 2 from the Neotropical region . However, as Dibrachyscavus.Based on differences in mandibular formula and fore wing marginal fringe, l region . Most spibrachys , includiDibrachys have previously been recorded in China  and four newly recorded species (Dibrachysbraconidis (Ferrière & Faure), Dibrachysconfusus (Girault), Dibrachyshians Bouček, and Dibrachysmaculipennis Szelényi).Only four species of Institute of Zoology, the Chinese Academy of Sciences (IZCAS). All material from our own collection was swept and preserved in 75% ethanol. Specimens were subsequently air dried, point-mounted and examined with a Nikon SMZ1500 stereomicroscope. Photographs were taken using a Nikon Multizoom AZ100 system, and the plates were compiled using Adobe Photoshop CS3 software. In addition, the author had examined specimens of Dibrachys deposited in the National History Museum, London, the Naturalis, Leiden and the Bavarian State Collections of Zoology in April, 2002.A total of 943 specimens was examined from the museum of Morphological terminology mostly follows that of PageBreakAbbreviations of morphological terms used are: funicular segment number Fun posterior ocellar distance POL ocellocular distance OOL gastral tergum number GtnTaxon classificationAnimaliaHymenopteraPteromalidaeFörster, 1856DibrachysPteromalusboucheanus Ratzeburg, designated by Diplolepismicrogastri Bouché, 1834: 168). Förster, 1856: 65. Type-species: Dibrachys Förster: CoelopisthoideaCoelopisthoideacladiae Gahan, 1913: 178–183. Synonymized by  Gahan, 1913: 178–183. Type-species: Body dark green. Head in frontal view round; antennal insertion placed on lower ocular line and face not protuberant at antennal insertion; antennal formula 11263 (rarely 11353); lower margin of clypeus with two sinuate teeth; both mandibles with four teeth or right mandible with four teeth and left mandible with three teeth; head in dorsal view with occiput margined by blunt or sharp, transverse ridge. Mesosoma slightly convex; pronotal collar not margined or slightly carinate medially; notauli incomplete and inconspicuous; scutellum without frenal groove; propodeum with plica complete, median carina developed or not. Fore wing without marginal fringe or at least bare between postmarginal vein and wing apex; postmarginal vein short, only inconspicuously longer than stigmal vein. Hind tibia with one spur. Gaster ovate.PageBreakWidespread world-wide distribution, see Taxon classificationAnimaliaHymenopteraPteromalidaeBoučekDibrachysAllodibrachys Bouček, 1965: 30. Type-species : Dibrachyshians Bouček, by original designation. sgen. The subgenus have the left mandible with three teeth and right mandible with four teeth; occipital carina transverse, closer to foramen than vertex; fore wing with marginal fringe except between marginal vein and wing apex; gaster mostly ovate, slightly longer than broad.Taxon classificationAnimaliaHymenopteraPteromalidaeBouček, 1965, new record to ChinaDibrachys (Allodibrachys) hians Bouček, 1965: 28.POL 2× OOL. Mesosoma 1.37× as long as broad, mid lobe of mesoscutum with regular sculpture. Propodeum with complete median carina and incomplete plica. Fore wing with marginal vein 1.8× as long as postmarginal vein; postmarginal vein as long as stigmal vein. Gaster 1.25× as long as broad, slightly broader than thorax width.Body length 1.6-2.0 mm Figs  1.32 × aTachinidae sp. on Ptycholomoidesaeriferanus Herrich-Schaffer, leg. Ding-Xi Liao; 1♂, 1♀, Heilongjiang: Dailing, 29.VI.1962, ex. Tachinidae sp. on Ptycholomoidesaeriferanus Herrich-Schaffer; 1♀, Jilin: Dunhua, 25.VI.1990; 1♂, 2♀, Beijing: Yanqing, 19.VII.1982, ex. Curculionidae sp. on elm, leg. Ding-Xi Liao.China: 3♀, Heilongjiang: Yichun, 13.VII.1962, ex. Pyralisfarinalis L . as a host and here we record Curculionidae sp. on elm, Tachinidae sp. on Ptycholomoidesaeriferanus Herrich-Schaffer (Lepidoptera: Tortricidae), and Tachinidae sp. on Laspeyresiagrunertiana (Ratzeburg) (Lepidoptera: Noctuoidea).China ; Palearctic and Nearctic regions.Taxon classificationAnimaliaHymenopteraPteromalidaeEuteruskojimae Ishii, 1938: 100.Dibrachyskojimae (Ishii): 1-Fu3 slightly long than wide, Fu4-Fu6 subquadrate. Head in dorsal view , leg. Tao-Qian Hou; 4♀, Hunan, 25.X.1979, ex. pupae of Pierisbrassicae L., leg. Ding-Xi Liao; 1♂, 7♀, Hunan: Chengbu, 16. VIII.1986, ex. pupae of Dendrolimuskikuchii Matsumura, leg. Zheng-Mao Li; 10♂, 15♀, Hunan: Daoxian, 29.XII.1979, ex. eggs of Lebedanobilis Walker, leg. Ding-Xi Liao; 1♂, 5♀, Hunan: Daoxian, 12.XI.1973, ex. eggs of Lebedanobilis Walker, leg. Xin-Wang Tong; 2♀, Guangxi: Nanning, VI.1975, ex. Eggs of Dendrolimus, leg. Lin Wei; 2♀, Guizhou: Anshun, 25.X.1980, ex. pupae of Dendrolimushoui Lajonquiere, leg. Jin-Rong Zhou; 6♀, Yunnan: Baoshan, 21.v.1975, ex. Dendrolimus, leg. Ding-xi Liao; 1♀, Tibet: Mêdog, 1100m, 26.I.1983, leg. Yin-Heng Han.China: 2♂, 16♀, Beijing: Miyun Reservoir, 10-20.VII.1983, ex. pupae of PageBreakDendrolimusspectabilis Butler (Lepidoptera: Lasiocampidae) as a host and here we report Dendrolimustabulaeformis Tsai et Liu, pupae/eggs of Dendrolimus, Dendrolimuspunctatus , Dendrolimuskikuchii Matsumura, Dendrolimushoui Lajonquiere, Lebedanobilis Walker (Lepidoptera: Lasiocampidae) and Pierisbrassicae L. (Lepidoptera: Pieridae).China ; Japan.Taxon classificationAnimaliaHymenopteraPteromalidaeYang, 1996Dibrachyskoraiensis Yang, 1996: 197–199, 323.1 and Fu2 slightly longer than broad, Fu3 and Fu4 quadrate, Fu4 and Fu6 slightly transverse. Head in dorsal view 1.88× as wide as long; eye length 2× temple length; POL 1.5× OOL. Mesosoma 1.7× as long as broad, mid lobe of mesoscutum with relatively coarse sculpture. Propodeum with complete plica and indistinct median carina. Fore wing length 2.2× width; submarginal vein 2× as long as marginal vein; marginal vein 2.53× as long as postmarginal vein, 2.13× as long as stigma vein; stigmal vein slightly longer than postmarginal vein (1.15×). Gaster 1.5× as long as broad, distinctly broader than thorax width (1.21×).Body length 2.5–2.7 mm; gaster long ovate. Head in frontal view 1.25× as wide as high; antennal scrobe extending upwards and reaching anterior ocellus; lower face slightly convex; antennal insertion placed on lower ocular line; clypeus with longitudinal striation and lower margin slightly protruded, emarginate, and with two blunt teeth; lower angle of gena not exceeding clypeal margin. Antennal scape slightly shorter than eye height (0.87×); length of pedicel and flagellum shorter than head width (0.8×); anelli transverse; FuChina: 1♀, Heilongjiang: Yichun, 3.VII.1972, leg. Ding-xi Liao; 1♀, Heilongjiang: Hailin, VI.1975, leg. Gui-you Zhang.Piceakoraiensis Nakai  built by the wood pest Orthotomicusgolovjankoi Pjatnitzky (Coleoptera: Curculionidae), the possible host.China (Heilongjiang).Taxon classificationAnimaliaHymenopteraPteromalidaeJiao & Xiaosp. n.http://zoobank.org/DC6570D7-7010-4813-89D4-570403E3A730subgenusAllodibrachys, and similar to Dibrachysyunnanensis Yang has the lower angle of the gena not exceeding the clypeal margin, and the stigmal vein slightly shorter than the postmarginal vein. The main differences are: marginal vein 2× as long as stigmal vein; propodeum with plica indistinct, only conspicuous basally; median carina absent.The species belongs to Female. Body .PageBreakTaxon classificationAnimaliaHymenopteraPteromalidaeYang, 1996Dibrachysyunnanensis Yang, 1996: 199–201, 324.1 and Fu5 quadrate, Fu6 distinctly transverse. Head in dorsal view, 1.9× as wide as long, eye length 1.79× temple length; POL 1.78× OOL. Mesosoma 1.5× as long as broad, mid lobe of mesoscutum with regular sculpture. Propodeum with plicae complete, median carina distinct on base part. Fore wing with submarginal vein more than 2× as long as marginal vein, marginal vein 1.5× as long as postmarginal vein, stigmal vein as long as postmarginal vein. Gaster 1.3× as long as broad, as broad as thorax width.Body squat, length 2.0–2.4 mm. Head in front view 1.3× as wide as high; antennal scrobe shallow, extending upwards and reaching anterior ocellus; antennal insertion placed on the lower ocular line; clypeus with longitudinal sculpture; lower margin of clypeus slightly protruded, median emarginate and with 2 sinuate teeth; gena evenly curved, lower angle of gena not exceeding clypeal margin. Antennal scape slightly shorter than eye height, length of flagellum and pedicel combined less than head width (0.74×); pedicel in lateral view 2.2× as long as broad; both anelli transverse; FuChina: 1♀, Yunnan: Nanjian, 2.VI.1980, leg. Ding-Xi Liao.Tomicuspiniperda L. (Coleoptera: Curculionidae) which harmful to Pinusyunnanensis  (This species parasitized on larvae and pupae of inaceae) .China (Yunnan).Taxon classificationAnimaliaHymenopteraPteromalidaeFörsterBoth mandibles with four teeth; occipital carina curving, closer to vertex than foramen; fore wing without marginal fringe; gaster spindle-shaped, distinctly longer than broad.Taxon classificationAnimaliaHymenopteraPteromalidae, new record to ChinaHomoporuslunigerbraconidis Ferrière & Faure, 1925, 11: 226.Dibrachysbraconidis (Ferrière & Faure): 1 to Fu3 slightly longer than broad, Fu4 to Fu6PageBreakquadrate. Head in dorsal view, 1.9× as wide as long; eye length 2× temple length; POL 1.44× OOL. Mesosoma 1.37× as long as broad. Propodeum with complete median carina and plicae. Fore wing 2.33× as long as broad; submarginal vein 2.24× as long as marginal vein; marginal vein 1.9× as long as postmarginal vein; stigmal vein as long as postmarginal vein. Gaster 1.37× as long as broad, 1.27× as broad as thorax width.Body slender, length 2.0–2.9 mm Figs , 16. HeaNeodiprionxiangyunicus Xiao et Zhou, leg. Zhen Zhang; 1♀, Yunnan: Nanjian, 2.VI.1980; Yunnan: Kunming, 13.VII.1977, ex. pupae of Diprioninae, leg. Jing-liang Qi; 2♀, Yunnan: Kunming, XII.1988, leg. Hong-ming Yang; 1♀, Tibet: Chamdo, 3400m, 15.VIII.2001, leg. Chao-dong Zhu.China: 30♂, 29♀, Sichuan: Xichang, V.1992, ex. Luffiaferchaultella, and Luffialapidella (Lepidoptera: Psychidae) and Apantelesglomeratus (L.) (Hymenoptera: Braconidae) . Here we newly report Neodiprionxianyunicus Xiao et Zhou and Diprionidae sp. (Hymenoptera: Symphyta).The species mainly parasitizes China ; Palearctic and Nearctic regions. This is the first record from the Oriental region.Taxon classificationAnimaliaHymenopteraPteromalidae, new record to ChinaCoelopisthiaconfusus Girault, 1916a: 246.Dibrachysconfusus (Girault): POL 1.46× OOL. Mesosoma 1.43× as long as broad, mesoscutum with regular sculpture. Propodeum with median carina complete , leg. Ding-Xi Liao.China: 3♀, Beijing: Yuanmingyuan Imperial Garden, 2.VI.1984, ex. larvae of Megachilerotundata (Fabricius) (Hymenoptera: Megachilidae) as a host and here we record the larvae of Lymantriadispar (L.)(Lepidoptera: Lymantriidae).China (Beijing); Palearctic, Nearctic and Neotropical regions.Taxon classificationAnimaliaHymenopteraPteromalidaeJiao & Xiaosp. n.http://zoobank.org/F39A82B6-44C1-4E9A-9D23-B4462E870754Dibrachyss. str., and the noticeable differences with other species of the subgenus by the following characters: in female, antennae with three anelli; the postmarginal vein being distinctly shorter than the stigmal vein (0.5×), and gaster being 2.5× as long as broad.The new species belongs to Female. Body length 2.2 mm ; stigmal vein slightly curved.Head 1.24× as broad as thorax. Mesosoma 1.6× as long as broad. Pronotum 0.65× as broad as mesoscutum, collar rounded, posterior band smooth. Mesoscutum 1.57× as broad as long, with regular reticulation, in anterior half weakly reticulate and posterior half with deep reticulation; notauli distinct but not complete. Scutellum convex, 1.07× as broad as long, frenal line absent; reticulation smaller than on mesoscutum, but regular and shallow. Propodeum medially ½ as long as scutellum, with fine, deep, dense reticulation; plica weak Fig. , only vi1 covering 1/4 of gaster, with posterior margin cambered; tergites beyond Gt1 equal in length; ovipositor exserted.Gaster spindle-shaped with apex pointed Fig. , 2.5× asMale. Head black except frons with yellowish-green, and antennae yellow; mesosoma black except thorax purplish laterally, legs yellow except coxae brown. Antennae with two distinctly transverse anelli, pedicel in lateral view 1.8× as long as broad, each funicular segment longer than broad; gaster oval, apex not pointed.36.26°N, 94.53°E, 14.IX.2001, leg. Chao-Dong Zhu. Paratype. 1♀, same data to holotype; 3♂, 6♀, Inner Mongolia: Ejin B., 11.VI.1981, ex. Dinorhopala on Populusdiversifolia, leg. Hua-Qiang Shao.Holotype. ♀, China: Qinghai: Golmud, Guolemude, 2880m, Named after the location where the holotype was collection.Dinorhopala (Coleoptera: Curculionidae) on Populusdiversifolia.Specimens from Inner Mongolia were reared from China .Taxon classificationAnimaliaHymenopteraPteromalidaeJiao & Xiaosp. n.http://zoobank.org/2418A0BD-799F-44D4-8A3B-BCCAB3FCF7C2Dibrachyss. str., and the mainly differences with Dibrachysmicrogastri (Bouché) as follows: Dibrachysliaoi sp. n. slightly blue-greenish, clypeal margin with two sharp teeth, Fu1 to Fu4 length slight longer than its width respectively, Fu5 and Fu6 quadrate, gaster 1.8× as long as broad; but in Dibrachysmicrogastri (Bouché), body yellow-green, clypeal margin with two blunt teeth, Fu1 to Fu5 quadrate, Fu6 transverse, gaster 2× as long as broad.The new species belongs to Female. Body ; middle length of pronotum almost 1/9 as long as length of mesoscutum; collar not margined anteriorly, posterior margin of collar with a smooth band. Mesoscutum 1.86× as broad as long, with regular and dense reticulation; notauli incomplete and unconspicuous. Scutellum convex, 1.09× as broad as long, frenal line absent; reticulation same as on mesoscutum but slightly large on posterior part of scutellum. Propodeum Fig.  medially1 covering 1/3 length of gaster, posterior margin of Gt1 cambered, median with an obvious hollow; following tergites with posterior margin straight; gaster terminal acute.Petiole invisible dorsally. Gaster Fig.  long ovaMale. Body length 2.1 mm; head and thorax blue-green; antenna light brownish except clava slightly dark, other segments yellow; legs yellow to yellowish brown except coxae concolorous with body; fore wing yellowish brown; gaster brown, with a yellow transverse bright ribbon at 1/3 base of gaster.40.29°N, 116.50°E, 18.VII.1983, ex. pupae of Dendrolimustabulaeformis, leg. Ju-Wen Wu. Paratypes: China: 1♂, 2♀, same data as holotype; 2♀, Beijing: Miyun Reservoir, 20.VII.1983, ex. pupae of Dendrolimustabulaeformis, leg. Ju-Wen Wu; 5♀, Beijing: Huairou, 15.VI.1982, ex. Illiberispruni, leg. Mr. Jin; 1♀, Beijing: Songshan, 26.VIII.1984, ex. Illiberispruni; 4♀, Beijing: Changping, 15.VI.1981, ex. Locastramuscosalis, leg. Zhen-Hua Liu; 1♀, Beijing: Yuanmingyuan Imperial Garden, 18.VII.1984, ex. larvae of Lymantriadispar, leg. Mu-Zong Cheng; 6♀, Beijing: Yuanmingyuan Imperial Garden, 2.VI.1984, ex. larvae of Lymantriadispar, leg. Ding-Xi Liao; 4♂, 5♀, Beijing: Mentougou, late July of 1983, ex. Prothesiasimilesxanthocampa, leg. Sui-Hua Zhao; 1♀, Beijing: Qingbaichang, leg. Ding-Xi Liao.Holotype: China: ♀, Beijing: Miyun Reservoir, In memory of professor Ding-xi Liao in China.Illiberispruni Dyar, Illiberisnigra Leech (Lepidoptera: Zygaenidae), Lymantriadispar (L.) (Lepidoptera: Noctuoidea) and Porthesiasimilis (Fueszly) (Lepidoptera: Lymantridae), pupae of Dendrolimustabulaeformis Tsai et Liu, Dendrolimussuperans (Butler) (Lepidoptera: Lasiocampidae), Illiberisulmivora Graeser, Pseudopanolisflavimacula Inaba (Lepidoptera: Noctuidae), Rogasdendrolimi (Matsumura) (Hymenoptera: Braconidae) and Tenthredinidae sp..Larvae of China .PageBreakTaxon classificationAnimaliaHymenopteraPteromalidaeSzelényi, 1957, new record to ChinaDibrachysmaculipennis Szelényi, 1957: 301, 307.1 to Fu3 slightly long than broad respectively, Fu4 and Fu5 quadrate, Fu6 slightly transverse; clava slightly clavate, 2× as long as broad. Head in dorsal view, 2× as wide as long; occipital carina strong; POL 1.5× OOL. Mesosoma 1.6× as long as broad, with regular reticulation. Propodeum  (Hymenoptera: Megachilidae) (Hyphantriacunea (Drury) (Lepidoptera: Erebidae)  and Apantelesbaoris Wilkinson (Hymenopter: Braconidae).Recorded hosts of the species were hilidae)  and Hyphrebidae) . Here weChina ; Palearctic, Nearctic and Neotropic regions.Taxon classificationAnimaliaHymenopteraPteromalidaeDiplolepismicrogastriZMH by  Bouché, 1834: 168; neotype female in Dibrachysmicrogastri (Bouché) Peters & Baur, 2011: 18; DibrachysmicrogastriPteromaluscavus Walker, 1835: 477–478; Pteromalusdecedens Walker, 1835: 478; Pteromalusalbinervis Ratzeburg, 1844: 199; Pteromalusboucheanus Ratzeburg, 1844: 196; Pteromalustenuis Ratzeburg, 1844: 195; Pteromaluszelleri Ratzeburg, 1848: 190; Pteromalusvesparum Ratzeburg, 1852: 233; Cleonymusclisiocampae Fitch, 1856: 431–432; Pteromalusboarmiae Walker in Newman, 1863: 8609, 8610; Cheiropachusnigro-cyaneus Norton, 1869: 327; Eupelmuscereanus Rondani, 1876: 38. 40; Pteromalusgelechiae Webster, 1883: 151; Pteromaluschionobae Howard, 1889: 1872, 1889; Arthrolytusapatelae Ashmead, 1893: 162; Arthrolytuspimplae Ashmead, 1894: 339; Trichomalustruyilloi Blanchard, 1938: 178; Tritneptiselegans Szelényi, 1981: 400.  Synonymy: 6 transverse; setae on antenna become an angle with antennal surface. Mesosoma 1.43× as long as broad; mid lobe of mesoscutum with coarse sculpture. Propodeum with complete plicae and weak median carina. Fore wing , leg. De-Yun Deng; 1♂, 1♀, Heilongjiang: Dailing, 18.IX.1975, ex. Rhyacioniabuoliana, leg. Ding-Xi Liao; 2♀, Jilin: Siping, VII.1980, ex. Coleophoridae sp., leg. Yu-Ying Qiu; 5♀, Liaoning: Liaoyang, 19.VI.1980, ex. larvae of Lymantriadispar L., leg. Yu-Bao Zhang and Gui-Zhi Zhang; 3♂, 7♀, Liaoning: Liaoyang, 17.VII.1979, ex. Muscadomestica , leg. Ding-Xi Liao; 1♀, Liaoning: Liaoyang, 10.VI.1979, ex. pupae of Cnidocampaflavescens , leg. Yu-Bao Zhang; 5♀, Liaoning: Jinzhou, vi.1970, ex. Nephoteryxpirivorella Matsumura, leg. Bin Liu; 1♂, 1♀, Liaoning: Shenyang, 11.VII.1978, ex. sawfly, leg. Gong-Tian Xu; 1♂, 1♀, Liaoning: Xingcheng, 25.V.1981, leg. Yan-Li Zhao; 4♀, Liaoning: Suizhong, 13.IX.1973, ex. pupae of Tachinidae sp., leg. Shu-Hai Wang; 5♀, Liaoning: Liaoyang, Yuejiadadui, 1979, ex. pupae of PageBreakLymantriadispar (L.) from Populus sp., leg. Yu-bao Zhang & Gui-Zhi Zhang; 1♀, Liaoning: Liaoyang, Beiling, 5.IX.1978, ex. Lymantriadispar (L.), leg. Gong-Tian Xu; 1♀, Liaoning: Fuxian, 25.VI.1976, ex. Tortricidae sp., leg. Ding-Xi Liao; 3♀, LiaonPageBreaking: Siping, VI.1989, ex. Yponomeutidae sp., leg. Gui-You Zhang; 8♀, Liaoning: Fusong, IX.1953, ex. eggs of Dendrolimus sp.; 2♀, Inner Mongolia: Urad Middle Banner, 17.VII.1980, ex. AnacampsisPopulella Clerck, leg. Xu-Chang Huang; 3♂, Inner Mongolia: Horinger, 4.VIII.1981, ex. Malacosoma sp., leg. Qiang-Hua Shao; 1♂, 2♀, Inner Mongolia: Baotou, 19.IX.1989, ex. pupae of gelechiid moth, leg. Zhong-Ren Liu; 2♂, 3♀, Inner Mongolia: Baotou, 24.VI.1989, ex. pupae of ichneumon, leg. Zhong-Ren Liu; 1♀, Inner Mongolia: Baotou, 28.vii.1985, ex. Scolytidae sp., Zhong-Ren Liu; 3♂, 7♀, Beijing, vii.1986, ex. pupae of Tachinidae sp., leg. Da-Wei Huang; 1♂, 9♀, Beijing, 21.VIII.1962, ex. Tortricid, leg. Ding-Xi Liao; 5♀, Beijing: Xijiao, 20.IX.1957, ex. pupae of Stilprotiasalicis, leg. Tai-Lu Chen; 1♀, Beijing: Miyun, 17.VI.1984, ex. Dendrolimustabulaeformis, leg. Da-Wei Huang; 2♂, 6♀, Beijing: Daxing, 1963, ex. obsolete honeycomb, leg. Zong-You Xu; 2♀, Beijing: Yuanmingyuan Imperial Garden, 25.vii.1984, ex. larvae of Lymantriadispar, leg. Mu-Zong Cheng; 4♀, Hebei: Zhangbei, VII-XII.1983, ex. Stilpnotiacandida, leg. Ding-Xi Liao; 8♂, 24♀, Hebei: Zhangbei, 21.VII.1983, larvae of Stilpnotiacandida, leg. Xing-Jun Li; 9♀, Hebei: Zhangbei, vii.1983, ex. Lymantridae sp., leg. Xing-Jun Li; 1♂, 5♀, Hebei: Zhangbei, ex. pupae of Gypsonomaminutara, leg. Jun-Rong Dai; 1♀, Hebei: Fengning, 20.v.1992, ex. Rogasdendrolimi (Matsumura), leg. Da-Zhou Wang; 2♂, 3♀, Shanxi: Taiyuan, 6.V.1991, ex. Eulecaniumgigantean, leg. Hui-Di Zhang; 2♀, Shanxi: Taigu, 8.VII.1979, ex. pupae of Yponomeutidae sp., leg. Zhan-Gui Li; 1♂, 2♀, Shanxi: Taiyuan, 19.vi.1990, ex. pupae of Yponomeutapolystinellus Felder, leg. Da-Wei Huang; 1♂, 1♀, Shanxi: Taiyuan, iv.1980, ex. pupae of Ancylissativa Liu, leg. Ci Yu; 3♀, Shanxi: Pingshun, 10.VIII.1978, ex. Pinustabuliformis Carrière; 1♂, 1♀, Shanxi: Taigu, 8.VII.1979, ex. pupae of Galleriamellonella, leg. Zhan-Gui Li; 3♀, Shanxi: Taigu, 15.VI.1979, ex. larvae of Illiberisnigra Leech, leg. Zhan-Gui Li; 4♀, Shanxi: Taigu, VII.1979, ex. Illiberisnigra Leech, leg. Zhan-Gui Li; 1♀, Shanxi: Taigu, VII.1979, ex. Lithocolletisringoniella Mats., leg. Zhan-Gui Li; 2♀, Shanxi: Shuoxian, 24.V.1984, ex. Braconidae on Coccinellaseptempunctata, leg.Yu-Zhi Niu; 3♂, 6♀, Shanxi: Shuoxian, 3-16.VI.1984, ex. Braconidae sp. on AnacampsisPopulella Clerck, leg.Yu-Zhi Niu; 3♂, 6♀, Shanxi: Shuoxian, 14-18.VI.1984, ex. AnacampsisPopulella Clerck, leg. Yu-Zhi Niu; 1♂, 2♀, Shanxi: Shuoxian, 20.VI.1983, ex. AnacampsisPopulella Clerck, leg.Yu-Zhi Niu; 1♂, 7♀, Shanxi: Shuoxian, V-VII.1984, ex. Tachinidae sp. on AnacampsisPopulella Clerck, leg.Yu-Zhi Niu; 1♀, Shangdong: Weihai, 3.VI.1958, leg. Jin-Long Mao; 1♀, Shangdong: Fushan, 26.X.1958, leg. Jin-Long Mao; 1♂, 4♀, Henan: Anyang, 20.V.1956, ex. Pectinophoragossypiella (Saunders), leg. Ding-Xi Liao; 3♀, Henan: Zhengzhou, 10.IX.1972, ex. larvae of Olethreutidae sp., leg. Ding-Xi Liao; 1♀, Shaanxi: Xianyang, 6.III.1975, ex. pupae of Eariascupreoviridis Walker, leg. Ding-Xi Liao; 2♂, 6♀, Ningxia: Luhuatai, 29.V.1982, ex. Ypsolophavittellus (Linnaeus), leg. Ding-Xi Liao; 3♀, Ningxia: ZhongweisShapotou, 15.VI.1981, leg. Ding-Xi Liao; 3♀, Ningxia: Yinchuang, 12.VI.1974, ex. pupae of Syrphidae sp. on Ulmuspumila L.; 1♂, 9♀, Gansu: Pingliang, VII.1966, ex. Tachinidae sp. & Illiberispruni, leg. Shou-Min Liu; 3♀12♂, Gansu: PingliPageBreakang, VII. 1966, ex. Illiberispruni, leg. Shou-Min Liu; 4♂, 22♀, Xinjiang: Altay, VI.1979, ex. larvae of Gelechiapinguinella Trietschke, leg. Jun-Wen Xia; 5♀, Xinjiang: Korla, collecting time unknown, ex. eggs of Macroglossumcorythusluteata (Butler), leg. Tai-Lu Chen; 3♀, Xinjiang: Urumchi, 12.VII.1980, ex. pest on Salix sp., leg. Jiu-Xiong Bai; 1♂, 5♀, Jiangsu: Nanjing, 4.VII.1963, leg. Ding-Xi Liao; 2♂, 5♀, Shanghai: Pudong New District, III.1972, ex. cottonseed; 4♀, Shanghai: Minhang, XII.1979, ex. Apantelesglomeratus (L.), leg. Ji-Long He; 6♀, Anhui: Dangshan, 7.XI.1975, ex. Pyraustanubilalis (Hubern) & Chiloinfuscatellus (Snellen), leg. Ding-Xi Liao; 12♀, Anhui:Huangfu Mountain, 19.VI1965, ex. larvae of Lepidoptera, leg. Ding-Xi Liao; 1♂, 4♀, Zhejiang: Hangzhou, X.1954, ex. Pectinophoragossypiella (Saunders); 2♂, 6♀, Zhejiang: Hangzhou, i.1963, leg. Ding-Xi Liao; 5♂, 2♀, Zhejiang: Hangzhou, I.1963, ex. Pectinophoragossypiella (Saunders), leg. Cui Hu; 1♂, 2♀, Hubei: Hong’an, V.1978, ex. pupae of Dendrolimuspunctatus Walker, leg. Ding-Xi Liao; 6♀, Hunan: Changsha, 20.III.1984, ex. Chilosuppressalis , leg. Ding-Xi Liao; 1♂, 9♀, Hunan: Liuyang, 24.IX.1979, ex. eggs of Dendrolimus sp. , leg. Ding-Xi Liao; 1♀, Hunan, collecting time unknown, leg. Xin-Wang Tong; 1♀, Yunnan: Kunming, 17.V.1967, ex. larvae of Macrocentrus sp. leg. Jing-Liang Qi; 1♀, Yunnan: Zhaotong, 5.IV.1973, ex. Chilosuppressalis , leg. Ding-Xi Liao; 1♂, 1♀, Tibet: Lhasa, 3650m, 27.VIII.2001, leg. Chao-Dong Zhu. 2♀, Sk. Ahus, 15.IV.1979. leg. K. J. Hedqvist, Dibrachycavus , det. K. J. Hedqvist; N. Zealand: 1♀, Lincoln, nr Christchurch RT., 1988, B.J. Donovan. Cult. Vespula gemanica, Dibrachysboarmiae , det. Z. Boucěk, 1988.China: 3♂, 7♀, Heilongjiang: Hailin, VI.1975, ex. pupae of Dibrachysmicrogastri has been widely recorded, and the primary parasite has been recorded more than 240 species from 45 families of seven insects orders and also recorded two species of Arachnida (Noyes 2002). In our study, the species was parasitic on Coleoptera (Scolytidae sp.), Diptera , Hemiptera (aphids on cabbage), Hymenoptera (Apantelesglomeratus (L.), Braconidae sp. on Coccinellaseptempunctata, larvae of Macrocentrus sp., pupae of Gelis sp. and Lepidoptera (Chiloinfuscatellus (Snellen), Chilosuppressalis , Lymantriadispar (L.), Malacosoma sp., Nephopteryxpirivorella (Matsumura), Pectinophoragossypiella (Saunders), Ptycholomoidesaeriferanus (Herrich-Schäffer), Pyraustanubilalis (Hübner), Ypsolophavittellus (Linnaeus), eggs of Dendrolimus sp., larvae of Gelechiapinguinella Trietschkeb and Olethreutidae sp., pupae of Anacampsispopulella Clerck, pupae of Cnidocampaflavescens , pupae of Dendrolimuspunctatus , pupae of Eariascupreoviridis Walker, pupae of Stilprotiasalicis (L.), pupae of Yponomeutapadella Linnaeus and so on).Hosts of China ; widespread world-wide distribution .PageBreakTaxon classificationAnimaliaHymenopteraPteromalidaeJiao & Xiaosp. n.http://zoobank.org/2C61C736-41D3-4EB0-8C0B-F3218A96B622Dibrachys s. str., and the mainly differences with Dibrachysmicrogastri (Bouché) are as follows: antenna of Dibrachysqinghaiensis sp. n. slender, each funicular segment at least slightly longer than its broad; antennal scape as long as eye height, and nearly reaching lower margin of anterior ocellus; but Dibrachysmicrogastri (Bouché) at least with several transverse funicular segment in distal of antenna, antennal scape distinctly shorter than eye height, and not reaching lower margin of anterior ocellus.The new species belongs to Female. Body .


ST6Gal-I sialyltransferase adds α2,6-linked sialic acids to the terminal ends of glycan chains of glycoproteins and glycolipids. ST6Gal-I is reportedly upregulated in many cancers, including hepatocellular carcinoma, ovarian cancer and breast cancer. However, the expression and function of ST6Gal-I in prostate cancer (PCa) and the mechanism underlying this function remain largely unknown. In this study, we observed that ST6Gal-I expression was upregulated in human PCa tissues compared to non-malignant prostate tissues. High ST6Gal-I expression was positively correlated with Gleason scores, seminal vesicle involvement and poor survival in patients with PCa. ST6Gal-I knockdown in aggressive prostate cancer PC-3 and DU145 cells significantly inhibited the proliferation, growth, migration and invasion capabilities of these cells. ST6Gal-I knockdown decreased the levels of several PI3K/Akt/GSK-3β/ β-catenin pathway components, such as p-PI3K, (Ser473)p-Akt, (Ser9)p-GSK-3β and β-catenin. Furthermore, targeting this pathway with a PI3K inhibitor or Akt RNA interference decreased p-Akt, p-GSK-3β and β-catenin expression, resulting in decreased PC-3 and DU145 proliferation, migration and invasion. Taken together, these results indicate that ST6Gal-I plays a critical role in cell proliferation and invasion via the PI3K/Akt/GSK-3β/β-catenin signaling pathway during PCa progression and that it might be a promising target for PCa prognosis determination and therapy. PCa is a growing public health problem worldwide and is the most common malignant neoplasm diagnosed in men in the United States and Western Europe, as well as the leading cause of death among men . The incSialic acids are widely expressed as terminal glycans on glycoconjugates of eukaryotic cells. Sialylation is associated with a variety of cellular functions, such as cell adhesion, signal recognition and protein stability –6. More ST6Gal-I is the main sialyltransferase responsible for α2,6-linked sialic acid formation on N-glycans. ST6Gal-I is reportedly highly expressed in many cancers, including hepatocellular carcinoma, colon cancer, renal carcinoma and ovarian cancer –15. For In this study, we reported the clinical relevance of ST6Gal-I in PCa and showed that ST6Gal-I is required to maintain PCa cell aggressiveness and malignant properties. ST6Gal-I expression increased with PCa progression and was closely correlated with clinical survival and seminal vesicle invasion. ST6Gal-I knockdown effectively inhibited PCa cell proliferation, migration and invasion ability. Furthermore, the expression levels of p-Akt, p-GSK-3β and β-catenin in the PI3K/Akt/GSK-3β/β-catenin signaling pathway were decreased upon ST6Gal-I downregulation. Wortmannin, a PI3K/Akt/GSK-3β/β-catenin pathway inhibitor, and Akt RNA interference significantly inhibited the proliferation, migration and invasion ability of PCa cells. Thus, ST6Gal-I may be a promising target for early PCa diagnosis and treatment.P < 0.05). According to staining intensity, we subdivided 92 PCa patients into the following two groups: a “low-ST6Gal-I” group containing 43 samples characterized by low ST6Gal-I staining (negatively and weakly stained) and a “high-ST6Gal-I” group containing 49 samples characterized by high staining . Specific cases with high and low ST6Gal-I expression in different Gleason score groups were shown in Figure P = 0.007) for ST6Gal-I expression and Gleason scores. Moreover, seminal vesicle involvement was also found to be positively correlated with ST6Gal-I expression (P = 0.007), and the correlation coefficient for ST6Gal-I expression and seminal vesicle involvement was 0.280 (P = 0.007). These results suggest that ST6Gal-I overexpression is significantly associated with PCa progression.To investigate the clinical relevance of ST6Gal-I expression in PCa, ST6Gal-I and α2,6-linked sialic acid levels in patient tumour lesions were assessed by immunohistochemistry. As shown in Figure P < 0.001; Figure P = 0.003) and higher pathologic stage  were independent prognostic factors for overall survival  and multivariate analysis following adjustments for pretreatment PSA, Gleason score and pathologic stage   . These rSambucus nigra agglutinin (SNA) staining p-Akt, (Ser9)p-GSK-3β, β-catenin, c-Myc, Cyclin D1, TCF1, TCF4 and MMP-7 expression Figure  and 5E. In this study, we reported that ST6Gal-I expression was significantly upregulated in PCa tumour tissues and that elevated ST6Gal-I expression was correlated with Gleason scores and PCa prognosis. Based on these findings, we believe that ST6Gal-I plays a key role in promoting malignant tumour progression. Here, we proved that ST6Gal-I silencing significantly attenuates PCa cell proliferation, migration and invasion capability. As mentioned previously, ST6Gal-I overexpression has been observed in many cancers, indicating that ST6Gal-I upregulation might be a common tumour characteristic. Thus, treatments targeting ST6Gal-I may have promise as anti-tumour therapies.in vivo by facilitating the accumulation of C/EBPα protein, a suppressor of E2F1 transactivation [in vivo by facilitating rapid nuclear exportation of androgen receptor [Glycogen synthase kinase-3β (GSK-3β) is widely known for its essential role in triggering β-catenin destabilization in the Wnt/β-catenin signaling pathway, which is hyper-activated in PCa . In PI3Ktivation . Moreovereceptor . Furtherreceptor . All theEctopic cell surface receptor N-glycosylation resulting from oncogenic transformation has been extensively linked to tumourigenicity and tumour progression regulation. Studies have shown that EGFR N-glycosylation critically determines the structural conformation of its ligand-binding ectodomain, which enhances ligand-dependent EGFR activation . FurtherIt is known that Akt phosphorylation induces GSK-3β phosphorylation and inactivation, leading to enhanced Wnt/β-catenin signaling . In our Metastasis is the leading cause of death in PCa patients, especially bone metastasis. To date, the potential mechanisms underlying PCa bone metastasis remain poorly understood. PC-3 cells are derived from PCa cells that have metastasized to bone, while DU145 cells are derived from PCa cells that have metastasized to the brain. It has been suggested that integrin α2β1, a collagen I receptor and sialylation target, promotes selective PCa bone metastasis –48. ThesIn conclusion, our data indicate that ST6Gal-I expression in PCa tissues is associated with poor survival in patients with PCa. In addition, we found that ST6Gal-I knockdown inhibits the malignant phenotypes of different PCa cell lines through the PI3K/Akt/GSK-3β/β-catenin signaling pathway. Thus, ST6Gal-I overexpression may be a promising target for early PCa diagnosis and treatment.Formalin-fixed, paraffin-embedded benign prostate hyperplasia, prostatic intraepithelial neoplasia, and PCa tissues were obtained from 105 patients at the First Affiliated Hospital of Dalian Medical University, and the tumour grades and Gleason scores of these tissues were confirmed by two observers. This study was carried out with the informed consent of all patients and the approval of the ethics committee of Dalian Medical University.After deparaffination in dimethylbenzene overnight and hydration in gradient alcohol, tissue slides were subjected to antigen retrieval in retrieval buffer at 120°C for 5 minutes. Then, the slides were disposed by hydrogen peroxide  to remove endogenous peroxidase. For ST6Gal-I staining, primary antibodies against ST6Gal-I  was incubated with the tissue samples for 2 hours at 37°C. For α2,6-linked sialic acid staining, biotin-labelled SNA was diluted as indicated (1:100), and the incubation time was prolonged to 4 hours. After being washed (three washes for 5 minutes each) with PBS, the slides were incubated with biotinylated secondary antibodies for 30 minutes at 37°C. After being washed again, the cells were incubated with HRP-conjugated streptavidin for 30 minutes at 37°C. Then, the cells were treated with DAB , which was applied as a developer, before being redyed with haematoxylin and dehydrated with gradient alcohol. Two observers independently evaluated the immunohistochemical staining results according to staining intensities and positive-staining percentages. Positive-staining percentages were classified as lows: negative, 0% (–); weakly positive, 1%–25% (+); moderately positive, 26%–50% (++); and strongly positive, > 50% (+++). Cut-off values were defined as follows: moderately (++) and strongly positive (+++) stained tissue sections were considered to have high protein expression, while negatively (–) and weakly (+) stained sections were considered to have low protein expression in subsequent statistical analysis.2. For PI3K/Akt/GSK-3β/β-catenin signaling inhibition assay, PCa cells were treated with the PI3K inhibitor wortmannin (Selleck) at 3 μM for 24 h.The human prostate cancer cell lines PC-3 and DU145 were purchased from the Cell Bank of Shanghai Life Science Institution, Chinese Academy of Sciences. PC-3 and DU145 cells were cultured in 1640 medium (Gibco) containing 10% foetal bovine serum (Gibco) in a humidified incubator (Thermo Scientific) at 37°C with 5% COAn RNA interference vector with small hairpin RNA (shRNA) sequences targeting ST6Gal-I and a negative control vector (shNC) were constructed as described previously . Cells i--ΔΔCT method. GAPDH was used as an internal control.Total RNA was extracted from PC-3 and DU145 cells, shNC and shST6Gal-I voctors transfected PC-3 and DU145 cells by Trizol (Invitrogen) reagent and was reverse-transcribed using a PrimeScript RT Reagent Kit (TaKaRa). Specific primers for glyceraldehyde 3-phosphate dehydrogenase (GAPDH) and ST6Gal-I were purchased from GenePharma. ST6Gal-I mRNA levels were detected by an MX3000P detection system (Stratagene), and the results were analyzed via the 2Cells were lysed using cell lysis buffer (Beyotime) and then quantified using a BCA assay kit (Beyotime). Primary antibodies against p-PI3K (Bioworld), PI3K (Bioworld), ST6Gal-I (Abcam), Akt (Abcam), p-Akt (Abcam), GSK-3β (Affinity biosciences Inc), phosphorylated Ser9 GSK-3β (Affinity biosciences Inc), β-catenin , p-β-catenin (Bioworld), Cyclin D1 (Affinity biosciences Inc), c-Myc (Bioworld), TCF1 , TCF4 (Bioworld), MMP-2 , MMP-7 (Bioworld), MMP-9 , β-actin (Bioworld) and GAPDH  were applied to polyvinylidene fluoride (PVDF) membranes , and these membranes were subsequently incubated at 4°C for 12 hours at room temperature before being incubated with the appropriate secondary antibody for 2 hours. Protein levels were detected and quantified by an ECL kit (Advansta) and Image Lab software (Bio-Rad).Proteins were extracted using cell lysis buffer (Beyotime). After being quantified with a BCA assay kit (Beyotime), these proteins were boiled with SDS-PAGE protein sample buffer at a ratio of 4:1. Then, a protein mixture containing 35 μg of protein was loaded onto a 10% SDS-polyacrylamide gel, then it was transferred onto an NC membrane. The membrane was blocked in 5% skim milk at 4°C for 12 hours before being incubated with biotin-labelled SNA  at a dilution of 1:2000 at room temperature for 2 hours and peroxidase-labelled streptavidin for 1 hour. Image Lab software (Bio-Rad) was used for detection.Cells were seeded on coverslips at 30% confluence. After fixation with 4% paraformaldehyde, the cells were incubated with primary antibodies against ST6Gal-I  and β-catenin  for 12 hours at 4°C. After being washed, these cells were incubated with FITC-conjugated goat anti-rabbit second antibody (BD Biosciences). Golgi was localized by GM130 . After being washed again, the cells were treated with 4′,6-diamidino-2-phenylindole (DAPI) and imaged under a confocal laser scanning microscope (BD Biosciences).Cells were harvested and fixed with 75% alcohol. Then, the cells were blocked with 1% bovine serum albumin (BSA) and incubated with 2 μg/ml FITC-conjugated SNA lectin on ice for 30 minutes. After being washed three times with PBS, the cells were analyzed with a flow cytometer (BD Biosciences).2. A TECAN microplate reader  was used to measure the OD values at 450 nm. For cell colony formation assay, 5000 cells were seeded in six-well plates and incubated for 14 days at 37°C with 5% CO2 in 1640 medium with 10% FBS. After being stained with 0.1% crystal violet and washed, the plates were photographed. We randomly selected ten different fields in each six-well plate at 400 × magnification and counted the numbers of cell clusters comprising more than 50 cells.Approximately 2000 cells were seeded into a 96- well plate in triplicate, and 10 μl of CCK8 reagent in 100 μl of 1640 medium with 10% FBS was added into each well for 4 hours of incubation at 37°C with 5% CO6 cells were transferred to each well. After these cells reached confluence, a 200 μl sterile pipette tip was used to make a gap in the monolayer. Then, the cells were washed with 1640 medium without FBS and photographed immediately with a microscope at 100 × magnification. After the cells were cultured for 16 hours in 1640 medium without FBS, the same areas were photographed again.Four lines were evenly marked on the back of each well of each six-well plate to ensure that the same areas were photographed at every time point. Then, approximately 2.5 × 104 cells in 150 μl of 1640 medium without FBS were added to the upper compartment of a 24-well transwell chamber , and 350 μl of 1640 medium with 20% FBS was added to the lower compartment. After incubating for 9.5 hours with 5% CO2 at 37°C, the upper chamber was washed three times with PBS, and the cells were subsequently stained and fixed with 0.1% crystal violet diluted with methanol for 2 hours. After being washed three times with PBS and dried, the cells were photographed with a microscope at 200× magnification. Finally, Image-Pro Plus 6.0 software was used to count the numbers of cells in four randomly chosen areas. For invasion assay, all the procedures were the same as those described above; however, the 24-well transwell chambers were coated with 40 μl of Matrigel (at a dilution of 1 to 8) on the upward-facing side of the polycarbonate membrane, 1.5 × 105 cells were added to upper chamber, and the culture time was prolonged to 48 hours.About 5 × 10χ2 and Fisher's exact tests. The correlation between ST6Gal-I expression in PCa tissues and clinicopathological characteristics was determined by Spearman correlation analysis. Overall survival (OS) was defined as the time from surgery to death or the last follow-up. Progression-free survival (PFS) was defined as the time from treatment to recurrence or progression . Kaplan–Meier curves were plotted to calculate the effects of ST6Gal-I expression on PFS and OS, and survival curves were compared using a log-rank test. Cox regression  was performed for multivariate analysis of prognostic predictors. Differences between groups were compared using Student's t test, and differences among three or four groups were analyzed using one-way ANOVA. Two-sided P values < 0.05 were considered statistically significant.Statistical analysis was performed using SPSS 13.0 software. Continuous variables were expressed as the mean ± SD. The relationship between ST6Gal-I expression and clinicopathological characteristics was analyzed by Pearson's


Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disease affecting upper and lower motoneurons (MNs). The etiology of the disease is still unknown for most patients with sporadic ALS, while in 5–10% of the familial cases, several gene mutations have been linked to the disease. Mutations in the gene encoding Cu, Zn superoxide dismutase (SOD1), reproducing in animal models a pathological scenario similar to that found in ALS patients, have allowed for the identification of mechanisms relevant to the ALS pathogenesis. Among them, neuroinflammation mediated by glial cells and systemic immune activation play a key role in the progression of the disease, through mechanisms that can be either neuroprotective or neurodetrimental depending on the type of cells and the MN compartment involved. In this review, we will examine and discuss the involvement of major histocompatibility complex class I (MHCI) in ALS concerning its function in the adaptive immunity and its role in modulating the neural plasticity in the central and peripheral nervous system. The evidence indicates that the overexpression of MHCI into MNs protect them from astrocytes’ toxicity in the central nervous system (CNS) and promote the removal of degenerating motor axons accelerating collateral reinnervation of muscles.  Neurodegenerative diseases are devastating conditions that result in a significant loss of function and quality of life. Among them, amyotrophic lateral sclerosis (ALS) is the most prevalent motoneuron (MN) disease in adults, specifically targeting MNs in the cerebral cortex, brainstem, and spinal cord, causing progressive denervation and the atrophy of skeletal muscles, which finally results in complete paralysis and death .Symptoms and signs emerge when axonal connections fail, that is, when the axon retracts and denervation of the lower MNs or the muscle occurs. In fact, terminal axonal degeneration and neuromuscular junction (NMJ) denervation occur well before the loss of MNs in mutant superoxide dismutase (mSOD1) mice and ALS patients .ALS was first described by the French neurologist Jean-Martin Charcot in 1869, as a neurodegenerative disease that begins in late adulthood. Nowadays, it is considered the fourth most common neurodegenerative cause of death in adults after Alzheimer’s, Parkinson’s, and Huntington’s disease with a prevalence of 4–8 per 100,000 individuals . The aveC9orf72 gene were recognized as the most frequent cause of fALS. They were found in about 40% of fALS and 10% of sALS [ALS is a complex disease that can be divided into two forms, namely sporadic and familial. The most common form of ALS is sporadic (sALS), whereas the dominantly inherited familial ALS (fALS) associated with mutations in more than 40 genes accounts for only about 5–10% of all affected patients ,7. Of th of sALS , are togOver the years, TDP43, FUS, and C9ORF72 animal models have been generated ,13. HoweTARDBP are associated with an accumulation of ubiquitinated TDP43 aggregates in MNs for almost all ALS patients [The exact mechanisms whereby SOD1 mutants make the MNs highly vulnerable and contribute to disease progression is not yet completely defined. However, in the last years, in vivo and in vitro studies, using transgenic mice carrying SOD1 mutations, demonstrated that the degeneration of MNs was driven by acquired toxicities of mutant protein rather than from reduced dismutase activity . A promipatients . Proteinpatients ,16,17,18patients ,20. In fpatients  and postpatients . Increaspatients . Howeverpatients ,26,27,28Other potential pathogenic mechanisms have been associated with the vulnerability of MNs, and the important role of neuroinflammation mediated by glial and immune cells that are active player in the pathogenesis of ALS is emerging . In factAlthough these observations point to the active role of non-neuronal cells in the development and progression of the pathology, the source(s) and interaction of these pathogenic processes leading to MN death in ALS remain largely unknown . Underst+ T cells, which also has an important function in the activity-dependent refinement and plasticity of connections in developing and adult CNS [It is becoming evident that MNs express an unusual number of molecules that were originally thought to be specific to immune functions ,43,44. Sdult CNS ,47,48,49Major histocompatibility complex I (MHCI), originally described as a molecule of the immune system, playing an important role in the presentation of antigens, has also become known for the non-immune functions in the nervous system ,49. MHCI−/− mice subjected to axonal transection strongly influenced pre-synaptic density and axonal regeneration of spinal alpha MNs. In fact, in β2m−/− mice, pre-synaptic detachments of lumbar MNs somata one week after peripheral sciatic nerve transection was more extensive than those in wild-type animals. This removal selectively involved clusters of inhibitory synapses without affecting the loss of excitatory synapses that remained the same between normal and β2m−/− mice. These results demonstrate that, after peripheral axon lesion, MNs preferentially remove excitatory inputs, maintaining a subset of inhibitory inputs on their somata, and this last effect is dependent on the presence of MHCI. Additionally, in the same study, Oliveira et al. [−/− mice compared to wild-type mice, suggesting a positive effect of MHCI in axonal regeneration. This was subsequently confirmed by other studies showing that wild-type mouse strains with a greater ability to upregulate neuronal MHCI expression after injury had more efficient axonal regrowth [In the spinal cord, Oliveira et al.  showed ta et al.  demonstrregrowth . Thus, tregrowth .−/−; Db−/− mice), after sciatic nerve injury, showed an abnormal pattern of innervation of hind limb muscles, profound defects at NMJs and a delay in the motor recovery compared with wild-type counterpart [Studies in axotomized mice revealed that, while lesioned MNs overexpress MHCI mRNA subunits, the level of the protein was barely detectable in MN somata. On the contrary, a clear accumulation of MHCI was observed in motor axons and terminals at NMJs in gastrocnemius muscles. Consistently, mice defective for MHCI heavy chains , in both MN somata and peripheral axons. This indicates that motor axons may locally produce and expose MHCI “loaded” with antigenic peptides to be presented to cytotoxic T cells that infiltrate the PNS of C57SOD1G93A mice [G93A mice that do show an earlier axonal impairment and NMJ denervation [G93A mice, when crossed with β2m−/− mice, showed an anticipation of motor dysfunction, which correlates with an earlier axonal impairment and denervation of hind limb muscles [In recent years, the role of MHCI has been thoughtfully investigated in SOD1e models ,61. We rerminals A,B and e93A mice . Interes muscles . On the  muscles .+ T cells infiltrating the sciatic nerves may be essential not only to promote the phagocytosis of myelin debris by macrophages but also to limit the activity of effector T cells and macrophages once the remyelination is completed (recovery phase) [In the PNS, successful axonal regeneration depends on the coordinated effort of non-neuronal cells that, while motor axon debris is removed, release extracellular matrix molecules, cytokines, and growth factors that support axon regrowth . In thisy phase) .G93A mice? As discussed above, proteinopathy and the neuroinflammation are key players in ALS. In fact, the accumulation in the MNs of misfolded proteins genetically modified  or oxidized, is most likely the primum movens in the cascade leading to MN degeneration. Usually, misfolded aberrant proteins activate a complex protein quality control system in cells that include the constitutive ubiquitin-proteasome pathway, the ERAD, and autophagy. Why is the MHCI activated in the MNs of C57SOD1G93A mice and ALS patients [G93A mice, Song et al. [We and other groups found that, while the ubiquitin-proteasome machinery is impaired in the MNs of mSOD1 mice, the immunoproteasome subunits Lmp7, Lmp2, and Lmp10 (responsible for the production of antigenic peptides through the MHC I pathway) become strongly activated . This supatients  with theg et al.  suggesteAlthough different studies have suggested the involvement of ER stress signaling in ALS ,68,69, hMHC class I complexes are assembled in the endoplasmic reticulum through the concerted action of multiple ER-resident proteins. In response to ER stress, cells induce a highly conserved cellular stress response called the unfolded protein response (UPR) in an attempt to maintain their homeostasis . In ordeIn the previous section, we focused on the expression of MHCI by MNs in pathological conditions. However, other non-neuronal cell types surrounding MNs within CNS and PNS activate MHCI in different pathological conditions .G93A mice during the disease progression [Bombeiro et al.  showed tgression . On the gression   exacerbates cell death and damage by releasing toxic pro-inflammatory mediators over an extended period of time . Successervation . These f+ T cells and the exacerbation of inflammation in the CNS. Thus, while increasing MHCI within MNs may be a useful strategy to counteract the denervation atrophy of muscles and delay disease progression, its activation in microglia could have a deleterious effect. Increasing evidence indicates that mechanisms related to the adaptive immune response play an important role in ALS. MNs, when damaged by either an acute injury or chronic disease such as ALS, activate a series of molecules closely associated with the immune response. In this review, we focused on the potential role of MHCI in the progression of this devastating disease. The expression of MHCI in lesioned MNs has been reported to activate a series of compensatory mechanisms aimed to protect themselves from cell autonomous and non-cell-autonomous toxic mechanisms and to promote the regeneration of their axons that eventually leads to muscle reinnervation. Taking into account results hitherto obtained, we formulated a hypothesis for the role of MHCI during ALS progression, which is illustrated in Based on this information, the function of MHCI in the CNS may be cell-type-dependent. To date, we know that neuronal MHCI plays a crucial role during development and plasticity in CNS, whereas the role for glial MHCI deserves further analysis. Furthermore, it is likely that MHCI involves different interacting counterparts and signaling depending on the environmental stimulus. In the ALS context, further investigations, wherein models different from those characterized by mSOD1 mutations are used, will be necessary in the future. The failure of anti-inflammatory and anti-immune therapies in clinical trials  support


AnxA6 also affected the cross-talk between Wnt/ß-catenin signaling and NF-κB signaling by decreasing ß-catenin activity and increasing NF-κB activity in Wnt3a-, interleukin-1beta (IL-1ß)-, and combined Wnt3a/IL-1ß-treated cells. Wnt3a treatment increased the mRNA levels of catabolic markers  to a much lesser degree than IL-1ß treatment in human articular chondrocytes, and decreased the mRNA levels of matrix metalloproteinase-13 (MMP-13) and articular cartilage markers . Furthermore, Wnt3a decreased the mRNA levels of catabolic markers and MMP-13 in IL-1ß-treated human articular chondrocytes. High expression of AnxA6 resulted in decreased mRNA levels of catabolic markers, and increased MMP-13 and articular cartilage marker mRNA levels in Wnt3a-treated human articular chondrocytes, whereas leading to increased mRNA levels of catabolic markers and MMP-13 in human articular chondrocytes treated with IL-1ß, or combined Wnt3a and IL-1ß. Our findings define a novel role for AnxA6 in articular chondrocytes via its modulation of Wnt/ß-catenin and NF-κB signaling activities and the cross-talk between these two signaling pathways.Annexin A6 (AnxA6) is expressed in articular chondrocytes at levels higher than in other mesenchymal cell types. However, the role of AnxA6 in articular chondrocytes is not known. Here we show that complete lack of AnxA6 functions resulted in increased ß-catenin activation in Wnt3a-treated murine articular chondrocytes, whereas AnxA6 expressing articular chondrocytes showed decreased ß-catenin activation. High expression of AnxA6 in human articular chondrocytes showed the highest inhibition of Wnt/ß-catenin signaling. Inhibition of Wnt/ß-catenin signaling activity by AnxA6 together with cytosolic Ca Currently, very little is known about the role of annexins in articular cartilage despite the rapid progress in the understanding of the role of annexins in various other tissues and diseases, including Alzheimer’s disease, autoimmunity, cancer, diabetes, and cardiovascular diseases –4. StudiIn recent years, the NF-κB and the canonical Wnt signaling pathways have been implicated to play an important role in cartilage homeostasis, maintenance and the pathophysiology of OA –10. Pro-The different signaling pathways involved in cartilage homeostasis and OA pathogenesis, including NF-κB and Wnt/ß-catenin signaling do not act in isolation but these signaling pathways interact and affect each other. In addition, these signaling pathways may also interact with each other in tissue or cell type-specific manners. Finally, it is not just the activation of a signaling pathway that contributes to disease pathology but also the degree and duration of activation. For example, as discussed above, low degree of canonical Wnt/ß-catenin signaling activation was suggested to be required for long-term maintenance and function of articular cartilage, whereas prolonged or chronic activation of Wnt/ß-catenin signaling has been shown to cause cartilage degradation and joint disease , 15, 16.2+ can bind to the inner leaflet of the plasma membrane [We and others have shown that annexins act as intracellular modulators of various signaling pathways –19. For membrane , we hypomembrane , 23, 24.membrane , 24, 25.The AnxA6-/- mice were provided to us by Dr. S. E. Moss, University College of London, UK. These mice have a C57BL/6 genetic background, and mice heterozygous for the mutation in AnxA6 were used for breeding . All pro6 / well into 6-well tissue culture plates and grown in monolayer cultures in Dulbecco’s modified Eagle’s medium  containing 10% fetal calf serum , 2mM L-glutamine , and 50U/ml of penicillin and streptomycin (Invitrogen) (complete medium). Human articular chondrocytes were isolated from articular cartilage samples obtained from patients (donor age range 48–67) undergoing total knee replacement surgery at NYU Langone Orthopedic Hospital. Knee cartilage was harvested from regions with no macroscopically evident degeneration. The collection of tissue from patients undergoing knee replacement surgery was ethically approved by the Institutional Regulatory Board at NYU School of Medicine. Tissue samples were obtained after informed written consent was obtained. Human chondrocytes were isolated from these cartilage samples as described by us [6 cells/well into 6-well tissue culture plate and cultured in complete medium as described above. Semiconfluent human or mouse chondrocytes were transfected with empty pcDNA expression vector or pcDNA expression vector containing AnxA6 cDNA (pcDNA-AnxA6) using X-tremeGene HP DNA transfection reagent per the manufacturer’s protocol . Briefly, 200 μl Opti-MEM reduced serum medium containing 2 μg plasmid DNA together with 6 μl X-tremeGENE HP DNA transfection reagent were incubated for 30 min at room temperature. After incubation, the transfection complex was added to the cells in a drop-wise manner. Cells were incubated for 24 h at 37°C followed by serum starvation. Twenty four hours after serum starvation cells were pretreated for 2 h either with vehicle  or 1,2-bis(2-aminophenoxy)ethane-N,N,N’,N’-tetraacetic acid tetra(acetoxymethyl) ester (BAPTA)-2AM, a cell permeant Ca2+ chelator  followed by treatment with Wnt3a  and/or IL-1ß (10ng/ml) for various time points. The concentrations used for Wnt3a and IL-1ß are the same concentrations, which have been used in previous studies, including the study by Ma et al. (17). We used the pcDNA vector, which contains a c-myc tag. We obtained a transfection rate between 50% to 70% as determined by immunostaining of transfected cells with FITC-labeled antibodies specific for c-Myc  and counterstaining of cell nuclei with DAPI (data not shown).Murine articular chondrocytes were isolated from the articular cartilage cap of the femoral head, femoral condyles and tibial plateau of 21–day-old AnxA6-/- mice and WT littermates as described previously . Cells wed by us . Cells wphosphatase (SEAP). Secreted SEAP activity was monitored with the chemiluminescent substrate CSPD (Clontech). Luciferase activities were measured using the Tristar LB 941 luminometer  and was measured 48 h after transfection with the luciferase reporters. All experiments were performed in triplicate and repeated three to five times.For luciferase assays to determine ß-catenin activity, cells were co-transfected with a firefly TCF/LEF-specific luciferase reporter vector  or FOPFlash reporter, which contains a mutated TCF/LEF binding site and therefore serves as a negative control and a constitutively expressed Renilla luciferase reporter, which served as an internal control for normalizing transfection efficiencies and monitoring cell viability. Luciferase activities from both reporters were measured using a dual luciferase assay kit . For luciferase assays to determine NF-κB activity, cells were co-transfected with a firefly NF-κB-specific luciferase reporter vector . Luciferase activity in the medium from the secreted Metridia luciferase reporter gene was monitored using the Ready-To-Glow Secreted Luciferase Reporter Assay (Clontech). Transfection efficiency was monitored by co-transfection with pSEAP vector (Clontech), which provides constitutive expression of secreted form of human placental alkaline TM System; Applied Biosystems, Foster City, CA) with the appropriate primers and SYBR Green. PCRs were performed with a SYBR Green PCR Master Mix kit (Applied Biosystems), with 95°C for 10 min followed by 40 cycles at 95°C for 15 s and 60°C for 1 min, and 1 cycle at 95°C for 15 s and 60°C for 1 min. The 18S RNA was amplified at the same time and used as an internal control. The cycle threshold values for 18S RNA and the samples were measured and calculated by computer software. Relative transcript levels were calculated as x = 2–ΔΔCt, in which ΔΔCt = ΔE– ΔC, ΔE = Ctexp−Ct18S, and ΔC = Ctctl−Ct18S.Total RNA was isolated from chondrocyte cultures using the RNeasy minikit . mRNA levels of aggrecan, cyclooxygenase (Cox)-2, IL-6, inducible nitric oxide synthase (iNOS), MMP-13, and type II collagen were quantified by real-time PCR as described previously . BrieflyTM Tissue Protein Extraction Reagent from Pierce Biology Products. To extract the nuclear and plasma membrane proteins from the cell cultures we used the NE-PERTM Nuclear and Cytoplasmic Extraction Reagent or the Mem-PERTM Plus Membrane Protein Extraction Kit from Pierce Biology Products and followed the manufacturer’s instructions. Thirty μg of total cytoplasmic, nuclear or plasma membrane protein fractions were analyzed by SDS PAGE and immunoblotting with antibodies specific for AnxA6 , ß-catenin , Dishevelled 1  as described previously [Total lysates were obtained from human articular chondrocyte cultures 48 h after transfection with empty pcDNA expression vector of pcDNA expression vector containing full length AnxA6 cDNA or from late stage human OA articular cartilage using T-PEReviously . For norThe data are expressed as mean ± standard deviation (SD). SPSS software 19.0 and GraphPad Prism 6.0 were used to analyze the data. Analysis of the variance (ANOVA) was used to assess differences among 3 or more groups, while comparison of two groups was made using unpaired t tests. If there were significant differences in ANOVA, pairwise tests were conducted to assess specific differences using Tukey’s multiple comparison procedure. A p value below 0.05 was considered statistically significant.To determine how AnxA6 affects Wnt/ß-catenin signaling, we used articular chondrocytes isolated from AnxA6-/- mice. Wnt3a treatment increased Wnt/ß-catenin signaling as indicated by increased luciferase activity from the TOPFlash reporter in AnxA6-/- articular chondrocytes and WT cells. Complete absence of AnxA6 resulted in increased Wnt/ß-catenin signaling as indicated by the increased luciferase activity from the TOPFlash reporter in vehicle-treated and Wnt3a-treated articular chondrocytes isolated from AnxA6-/- mice compared to vehicle-treated and Wnt3a-treated chondrocytes isolated from WT littermates. Transfection with FOPFlash reporter that encodes mutated LEF/TCF binding sites elicited no response . These f2+ to associate with the plasma membrane [2+ together with AnxA6 on the inhibition of Wnt/ß-catenin signaling. We first transfected WT and AnxA6-/- articular chondrocytes with the TOPFlash luciferase reporter. Twenty-four hours after transfection these cells were treated with the cytoplasmic Ca2+ chelator BAPTA-2AM followed by treatment with Wnt3a. Treatment of WT chondrocytes with BAPTA-2AM showed similar luciferase activity from the TOPFlash reporter as vehicle-treated cells, while BAPTA-2AM-treated AnxA6-/- chondrocytes showed lower luciferase activity compared to vehicle-treated AnxA6-/- cells. In the presence of BAPTA-2AM the luciferase activity from the TOPFlash reporter was increased in Wnt3a-treated WT and AnxA6-/- cells compared to Wnt3a-treated cells in the absence of BAPTA-2AM. This increase in AnxA6-/- cells, however, was less pronounced than the increase in WT cells. BAPTA-2AM resulted in a similar luciferase activity in Wnt3a-treated WT cells as in Wnt3a-treated AnxA6-/- chondrocytes. Transfection with FOPFlash reporter elicited no response  and analyzed the amounts of AnxA6 and Dvl1 in the plasma membrane fraction by immunoblot analysis. Wnt3a treatment of BAPTA-2AM-treated WT chondrocytes resulted in decreased amounts of AnxA6 in the plasma membrane fraction compared to WT cells not treated with BAPTA-2AM. No immunostaining for AnxA6 was obtained in the plasma membrane fraction of AnxA6-/- chondrocytes treated with BAPTA-2AM and Wnt3a. Furthermore, BAPTA-2AM resulted in increased amounts of Dvl1 in the plasma membrane fraction of WT chondrocytes to levels similar to the amount of Dvl1 in the plasma membrane fraction of BAPTA-2AM / Wnt3a-treated AnxA6-/- chondrocytes  reduced in Wnt3a-treated human articular chondrocytes transfected with AnxA6 containing expression vector compared to Wnt3a-treated cells transfected with empty expression vector. IL-1ß stimulated Wnt/ß-catenin signaling activity in human articular chondrocytes transfected with empty expression vector by ~1.5-fold compared to vehicle-treated human articular chondrocytes transfected with empty expression vector, whereas IL-1ß did not stimulate Wnt/ß-catenin signaling in human articular chondrocytes transfected with AnxA6 containing expression vector. The combined Wnt3a/IL-1ß treatment resulted in the highest activation of Wnt/ß-catenin signaling activity in human articular chondrocytes transfected with empty expression vector (~3.5-fold increase compared to vehicle-treated cells), whereas the combined Wnt3a/IL-1ß treatment did not further increase ß-catenin signaling activity in human articular chondrocytes transfected with AnxA6 containing expression vector compared to cells transfected with AnxA6 containing expression vector and treated with Wnt3a only. Very little luciferase activity and little or no changes with the various treatments were measured in cells transfected with FOPFlash, a negative control reporter . Formation of this signaling complex and its association with the plasma membrane leads to the inactivation of GSK3ß, the inactivation of ß-catenin degradation and the subsequent accumulation of ß-catenin in the nucleus , 31, 32.2+ these annexins interact with phospholipids and associate with cellular membranes, including the plasma membrane [2+ concentrations to associate with various cellular membranes [2+ was chelated by BAPTA-2AM, while AnxA6 was decreased demonstrates that cytoplasmic Ca2+ is required for AnxA6 to associate with the plasma membrane of chondrocytes and ultimately to inhibit Wnt/ß-catenin signaling. These findings suggest that cytoplasmic Ca2+ plays a major regulatory role in AnxA6-mediated inhibition of Wnt/ß-catenin signaling in articular chondrocytes.Annexins, including AnxA6, are cytoplasmic proteins present in a variety of cell types, including chondrocytes , 33. In membrane . A previembranes . Our stu2+/calmodulin-dependent protein kinase II pathway, which results in an increase in intracellular Ca2+ concentration [2+ concentration in articular chondrocytes [2+ concentration enable increased amounts of AnxA6 to associate with the plasma membrane resulting in the inhibition of Wnt/ß-catenin signaling.Our study shows that the amount of plasma membrane-associated AnxA6 increased in Wnt3a-treated WT chondrocytes compared to vehicle-treated WT cells. Recently, it was shown that Wnt3a stimulates the canonical and non-canonical pathways in mesenchymal stem cells and chondrocytes , 36. Thentration . In addidrocytes . These sA recent study showed that several annexins, including AnxA6 are expressed at higher levels in articular chondrocytes than in other mesenchymal cell types . FindingOur findings show that IL-1ß treatment resulted in much higher expression levels of catabolic markers and MMP-13 in human artiular chondrocytes than Wnt3a treatment, whereas Wnt3a treatment was more effective than IL-1ß in inhibiting aggrecan and type II collagen expression. Combined IL-1ß and Wnt3a treatment of human articular chondrocytes resulted in lower expression levels of catabolic markers and MMP-13 than IL-1ß treatment, whereas the combined treatment resulted in the highest decrease of aggrecan and type II collagen expression. High expression of AnxA6 resulted in further increase in catabolic marker and MMP-13 expression in IL-1ß-treated or combined IL-1ß and Wnt3a-treated human articular chondrocytes, whereas high AnxA6 expression decreased catabolic marker expression and increased MMP-13, aggrecan and type II collagen expression in Wnt3a-treated human chondrocytes. These findings suggest that Wnt/ß-catenin and NF-κB signaling contribute to cartilage degradation during OA by affecting chondrocyte functions and phenotype in different ways. In addition, these two signaling pathways interact with each other and this interaction affects the activity of each pathway. Finally, our findings suggest that AnxA6 acts as an intracellular modulator of the activities of both signaling pathways and the cross-talk between these two signaling pathways.Previous findings showing that both loss- and gain-of function of ß-catenin in articular cartilage of mice resulted in accelerated OA development and progression or chemical inhibitors of Wnt/ß-catenin signaling inhibited OA development and progression , 39–42, In summary, AnxA6 expression in human articular chondrocytes affects Wnt/ß-catenin and NF-κB signaling activities and the cross-talk between these two signaling pathways. Specifically, our findings reveal that AnxA6 expression in chondrocytes stimulates NF-κB signaling via direct interaction with p65 of the active NF-κB complex as shown previously by us , and ind


But less attention has been paid to the thermal properties of an SF6/N2 mixture, especially with insulation materials overheating happening simultaneously. In this paper, thermal decomposition properties of epoxy resin in SF6/N2 mixture with different SF6 volume rates were studied, and the concentrations of characteristic decomposition components were detected based on concentrations change of some characteristic gas components such as CO2, SO2, H2S, SOF2, and CF4. The results showed that thermal properties of 20% SF6/N2 (volume fraction of SF6 is 20%) mixture has faster degradation than 40% SF6/N2 mixture. As ratio of SF6 content decreases, thermal stability of the system decreases, and the decomposition process of SF6 is exacerbated. Moreover, a mathematical model was established to determine happening of partial overheating faults on the epoxy resin surface in SF6/N2 mixture. Also thermal decomposition process of epoxy resin was simulated by the ReaxFF force field to reveal basic chemical reactions in terms of bond-breaking order, which further verified that CO2 and H2O produced during thermal decomposition of epoxy resin can intensify degradation of SF6 dielectric property.As a promising alternative for pure SF Hence, it was listed as one of the six greenhouse gases in Kyoto Protocol in 1997. To reduce the use of SF6, researchers worldwide have developed new alternatives such as C4F7N, C5F10O, SF6/CO2, and SF6/N2 mixture as insulation gases and put them into practice [6/N2 mixture with low SF6 volume fraction has been widely used in electric equipment such as gas insulated transmission lines (GIL) [6/N2 (volume fraction of SF6 is 20%) were developed by SIMENS and put into use in Geneva, Switzerland, which proved to be of high economic benefits. The transmission lines of 10% SF6/N2 gases in Electricite De France (EDF) have been safely used up to the present.SFoperties ,4,5,6,7.practice ,5,8,9,10es (GIL) ,12,13,146 in electrical equipment, such as supporting spacers in GIL. In order to detect partial overheating failure as early as possible, it has been proposed to detect the thermal decomposition components of SF6  in the presence of organic solid insulation materials [2 molecules in the SF6/N2 mixture will make SF6 molecules burden uneven stress distribution, causing increase in the bonding energy of S-F [6/N2 mixture in the presence of epoxy resin has not been reported yet. Hence, this issue has been investigated in this paper.When there happens to be an overloading problem in GIL, partial overheating failure is likely to occur at the insulation defects spots, especially in the poor contact surface, which would do harm to the dielectric properties of the insulation material, and the defects will aggravate partial overheating failure in return. The deterioration of insulation material will lead to serious consequences, such as the failure of some key part, or even a blackout at worst ,16,17,18aterials . When pay of S-F ,22,23,246/N2 mixture with SF6 ratio of 20%, 30%, and 40% respectively . By analyzing TG/DSC curves and comparing them with those from epoxy resin decomposition under pure SF6 or N2, the effect of ratio of SF6 on the decomposition of epoxy resin was obtained. The variation of SF6 characteristic decomposition component concentration with temperature in three different proportions of mixed gases was observed by Shimadzu QP2010 Ultra GC/MS. Types of gases that could be used as the characteristic components to detect the partial overheating failure in the presence of epoxy resin have been determined. Also the criterion of sharp weight loss of epoxy resin is established based on the change of characteristic components ratio.Thermogravimetric analysis instrument was used to investigate the decomposition of epoxy resin in SF6/N2 mixture gas was supplied by Wuhan Newradar Gas Co., Ltd. . The mixture gas was prepared according to the reference material number GBW(E)061516 in China, so the original percentage content of O2 and H2O in the mixture gas were too low to be took into consideration. Therefore, the main resource of H2O in the heating process may come from the thermal decomposition of epoxy resin.In the experiment, the bisphenol-A epoxy resin E51 was purchased from Wuxi Lan-Star Petrochemical Co., Ltd. . Epoxy resin was cured by an amine curing agent dubbed as type 593, supplied by Wuhan Shen Chemical Reagents and Equipments Co., Ltd. . High-precision SF6/N2 mixture, TGA/DSC 3+ thermogravimetric analyzer of Mettler Toledo company was used in the experiment. At first three parameters including thermal conductivity, density and specific heat capacity were calculated in order to keep the accuracy of experiments after filling them in the sheet of parameters of TG/DSC instrument.In order to obtain the TG/DSC curves of epoxy resin decomposition in SF6/N2 mixture is given by:6; 2, 6 and N2 respectively in per mole of mixture. The calculation results are shown in The instrument uses gas density at 0 °C under standard atmospheric pressure. The density of SF6/N2 gas mixture is calculated as follows:6 and N2 gas under constant pressure respectively; 6 and N2 in per mole of mixture respectively. The calculation results are shown in The instrument uses heat capacity at 25 °C under standard atmospheric pressure. The heat capacity of SF6/N2 gas mixture 6 and N2 under atmospheric pressure, 6 and N2 in the mixture respectively, 6 and N2 under atmospheric pressure (kg·s/m2), 6 and N2, 6 and N2 under atmospheric pressure (K), T is the constant of 273.15 (K), The instrument uses thermal conductivity at 0 °C under standard atmospheric pressure. The thermal conductivity of SFThe calculated values of thermal conductivities are shown in 6/N2 mixture gas with the SF6 volume ratio from 20% to 40% were used in experiment, and the results were compared with those from pure SF6 and N2. The sample mass of cured epoxy resin was 20 mg. The gas flow rate was set as 20 mL/min, the heating rate as 10 °C/min heating in the temperature range from 250 °C to 650 °C.In this paper, SF2 condition, the decomposition of epoxy resin is most violent, with remaining mass of 1.59 mg, accounting for 7.97% of the total weight of experimental sample, while under SF6 condition, the amount of remaining mass of decomposed epoxy resin was 4.53 mg, accounting for 22.73% of the total weight of experimental sample. The decomposition extent of epoxy resin in three mixed gases follows: 20% SF6/N2 > 30% SF6/N2 > 40% SF6/N2, that is to say, in the mixture of 20% SF6/N2, weight loss of epoxy resin was more severe than in the mixture of 40% SF6/N2.6 is lower than that of N2, therefore, the poor thermal conductivity of SF6 is not conducive to the decomposition of epoxy resin. However, N2 has higher thermal stability due to its large molecular bond energy of 946 kJ/mol. So N2 will not decompose or react with epoxy resin in the experimental temperature range. In pure SF6, SF6 begins to decompose at about 260 °C, and reaction between SF6 and epoxy resin would help add to the whole weight of the residue. The decrease of SF6 content in gas mixture will reduce the thermal stability of the system, making epoxy resin easier to react with SF6.As the reaction gas, thermal conductivity of SF6/N2 > 30% SF6/N2 > 40% SF6/N2 > SF6 > N2.In the DSC curve, the convex peak represents an increase in enthalpy(exothermic) and the concave peak represents a decrease in enthalpy(endotherm). 6. In pure SF6, the temperature at the exothermic peak is about 370 °C versus 350 °C in pure N2. Besides, in the pure N2, around 400 °C there are also existing some exothermic peaks representing the intrinsic thermal decomposition of epoxy resin. With the amount of SF6 increasing, some consecutive small peaks showed up at about 385 °C. Thermal decomposition of epoxy resin is actually the process of breaking and regenerating chemical bonds. In epoxy resin, C-O bond and C-H bond account for the major chemical bonds, and they are easy to break due to low bond energy. After breaking, free C, H and O atoms are formed, and further combined to form small molecules such as H2O and CO2. As a highly thermal stable gas, chemical bonds in N2 do not break to form N atoms under experimental temperature conditions, therefore, epoxy resin has intrinsic bond breakage in N2. SF6 decomposes at 260 °C in the presence of organic insulating solids [6 decomposes continuously throughout the weight-losing temperature range, a continuous exothermic peaks were shown on the DSC curve, causing the peak values to shift to the high temperature zone compared with the results in N2, indicating that the exothermic behavior is affected by SF6 decomposition.During the exothermic behavior stage, the peak temperature at this stage is greatly affected by SF6 is exacerbated with temperature increasing, and more free S and F atoms exist in the reaction gas to form a large amount of sulfides and fluorides resulting in increase of the exothermic peak area. It also confirms the conclusion that the smaller volume fraction of SF6 in the mixture would result in lower thermal stability, although it proved that 20% SF6/N2 has better dielectric property than 40% SF6/N2 [6/N2 cannot guarantee a better thermal property.Decomposition of SF% SF6/N2 . Better 6/N2, 30% SF6/N2, and 40% SF6/N2 gas mixtures were selected as experimental gases and the heating temperature was in the range of 200 °C–650 °C. In order to detect the formation temperature of characteristic components as accurately as possible, small heating increment of 2 °C/min was selected, and time interval for continuous gas collection was 15 min, meaning that temperature rose by 30 °C. The volume of collected gas was about 0.3 L and the gas component concentration was detected by GC/MS instrument quickly. The average component concentration in 15 min reflects the component formation rate.In this study, 20% SF6 decomposition characteristic gases including CO2, SO2, H2S, SOF2, SO2F2, CF4, and CS2 were detected in our study. If the measured characteristic gas concentration is less than 0.05 ppm, it is considered to be below the detection limit of the instrument, meaning the gas is not generated. Judging by the above principle, in the entire temperature range of the experiment, no CS2 or SO2F2 was detected. Therefore, five gases including CO2, SO2, H2S, SOF2, and CF4 were selected as the characteristic decomposition components of overheating failure on epoxy resin surface.Seven SF2 with temperature. It can be seen that the initial temperature of CO2 formation was always 275 °C under three gas mixtures with different proportions and the rate of CO2 formation increased before 450 °C and the generation rate of CO2 was fastest in the 20% SF6/N2. The formation rate of CO2 tended to become constant during a small temperature range after 450 °C. Finally, the CO2 formation rates of all three gases began to decrease from 515 °C.4 generation with temperature. The initial temperature of CF4 formation was 455 °C under three different ratios of gas mixtures, and the formation rate of CF4 increased exponentially with the increase of temperature. The relationship of the initial formation concentration shows in the order: 20% SF6/N2 > 30% SF6/N2 > 40% SF6/N2, that is to say, CF4 has fastest formation rate in the 20% SF6/N2 mixture.2 and CF4 in the presence of epoxy resin in mixed gas is the same as the results in pure SF6 [2 and CF4, it can be concluded that the formation rate of CO2 became constant when CF4 started to be generated, and the rate of CO2 formation started to decrease versus the increase of CF4 generation rate, which is likely to be caused by the fact that C atom preferentially binds with F atom above 450 °C, which affects the formation rate of CO2.The initial formation temperature of CO2 and SOF2 with temperature respectively. The initial formation temperature of SO2 and SOF2 was 275 °C under three gas mixtures with different ratios. The formation rates of SO2 and SOF2 increased exponentially with the increase of temperature, and the relationship of the initial formation concentration shows in the order: 20% SF6/N2 > 30% SF6/N2 > 40% SF6/N2. With temperature increasing, the formation rate of SO2 was bigger than that of SOF2.6 atmosphere, the formation temperature of SO2 and SOF2 in the presence of epoxy resin is lower [2 reacts with H2O to form SO2. Therefore, it can be seen that the formation of SO2 is greatly affected by H2O. During the decomposition of epoxy resin, more H2O is produced because of the dehydration condensation during elimination reaction within the molecule, which objectively enhances the hydrolysis of SOF2 and the formation of SO2.Compared with the decomposition of epoxy resin in SF2S with temperature. The initial formation temperature of H2S in three gas mixtures with different ratios was about 335 °C. The H2S formation rate tended to be constant between 335 °C and 395 °C, and started to decrease above 425 °C. The formation of H2S and CF4 indicates that epoxy resin has entered the stage of rapid decomposition and weight loss. Early detection of this stage can effectively help avoid the serious consequences of further aggravation of overheating fault.6/N2 gas mixture conditions, main criteria for determining weight loss of epoxy resins can be concluded based on the concentration change of the characteristic components, such as H2S mainly generated in the range of 320 °C–350 °C while CF4 generated in the range of 440 °C–470 °C, the initial concentrations of H2S and CF4 had an obvious difference.It can be seen from the TG curves that the main weight loss temperature range of epoxy resin was 330 °C–470 °C. In this range, under SF2, SO2, H2S, SOF2, and CF4 were measured in the interval of 15 °C. Statistically the proportion of H2S and CF4 was used to determine whether the epoxy resin began to lose weight rapidly. When CF4 was not detected, the variation of H2S ratio was used as the criterion. 2S at different temperature range during the decomposition of epoxy resin under three gas mixtures. By the way, the concentrations represent the measured value at every interval rather than a cumulative value, reflecting formation rate of H2S. The formation rate of H2S decreased with temperature.In order to obtain the standard for detecting the occurrence of an overheating fault, during heating samples of epoxy resin, concentrations of five characteristic components of CO2S in 2S) represents the concentration of H2S. Before the occurrence of the CF4, the following criteria for determining the weight loss of epoxy resin can be obtained:To obtain a mathematical principle for detecting the sharp weight-losing of epoxy resin, the concentrations of H4 began to form from 440 °C. 4 formed at different temperature range during the decomposition of epoxy resin under three gas mixtures. The formation rate of CF4 increases exponentially with the increase of temperature.On the other hand, CF4 indicates that the rapid weight loss of epoxy resin has come to the late stage, and serious overheating fault has occurred. Setting the total concentration of five characteristic components as C(T), and C(CF4) as the concentration of CF4, the following criteria can be obtained for determining the weight loss range of epoxy resin.The appearance of CF6-infused electrical equipment are designed to have high thermal and dielectric properties. To assess the operating condition of the sealed equipment based on the concentration of characteristic gases change would help find the overheating fault at an early stage. Equation (7) reflects the decomposition of epoxy resin at an early stage and Equation (8) represents the severe condition that epoxy resin enters sharp weight-losing stage. Once partial overheating faults happen on the surface of insulating material, usually it would be a lasting process to cumulate heat slowly so carbonization of epoxy resin in a small defect spot need to be analyzed both by Equations (7) and (8).Epoxy resin in SF6 atmosphere. 6, indicating that some of the fluoride and sulfide are present in the residue. It is highly probable that fluorine is adsorbed in the form of CF4 by strong hydrogen bonds formed by carbonization of epoxy resin and the specific molecular structure deserves further study. The content of sulfur element is lower than that of fluorine element, indicating that the sulfur element interacts with the epoxy resin as long as it is released as SO2 gas. The chemical reaction mechanism of epoxy resin and SF6 gas also deserves further study.In 2 and H2O. Firstly, the molecular model of the bisphenol A epoxy resin after curing was constructed as shown in As to the intrinsic decomposition mechanism of epoxy resin at high temperature, the simulation analysis was carried out by using ReacFF force field in Materials Studio software to study the formation of small molecular gases such as CO3 was applied. After 300 ps NPT ensemble simulation followed by 1000 ps structural optimization, the final unit cell model with the density of 1.14 g/cm3 was obtained, which is shown in The steps are summarized as follows: Single epoxy resin molecule shown in 57H70O14. The decomposition of epoxy resin starts with the cleavage of the C-O bond at locations ① and ② in 2 molecule is directly generated, as shown in 2O are formed, as shown in 2O when encountering highly active H ions, as shown in 2 appears around 70 ps, followed by CH2O, and finally H2O. The concentration of CO2 is higher than that of H2O. CO2 mainly comes from the cleavage of the ester bond connecting the epoxy group, and H2O mainly comes from the elimination reaction of macromolecular ions and the dehydration condensation reaction between molecules.2O in the main air chamber of the SF6 gas-insulated equipment to be put into operation should not exceed 500 ppm and the air content should not exceed 1%. Therefore, when there is an early latent insulation fault inside the equipment, the content of each component produced by the decomposition of SF6 will increase with the duration of discharge and overheating, and then the rate of increase will gradually slow down, and finally will reach a state of dynamic equilibrium until further increase happens due to aggravated fault. The presence of organic insulating material is one of the factors that accelerate the deterioration. At high temperature, SF6 is decomposed into low fluorides such as SF4 and SF5, which then react with H2O and O2 molecules. The decomposition process is shown in Equations 9–15.It is conventionally stipulated that the maximum concentration of H2O molecules generated by epoxy resin due to heating will react with SF6 to form SO2F2, SOF2, SO2 and other gases, which greatly affects the concentrations of decomposition components of SF6. By detecting the changes in concentration of each type of gas and comparing that with the thermal decomposition components of pure SF6, the rule of concentration change of the characteristic gases of the SF6 thermal decomposition components in the presence of epoxy resin can be summarized, and a basic method for judging whether there is a thermal decomposition fault of the epoxy resin in the electrical equipment can be proposed.The H6/N2 mixture were studied. The concentration of characteristic decomposition components was detected. The following conclusions are drawn:2 > 20% SF6/N2 > 30% SF6/N2 > 40% SF6/N2 > SF6. The DSC curves show that the decomposition of epoxy resin under SF6 condition is a series of complex chemical reactions. Epoxy resin decomposition in the 20% SF6/N2 is more severe than in 40% SF6/N2.The TG curve shows that the main weight loss range of epoxy resin is 330 °C–470 °C. The degree of weight loss follows: N2, SO2, H2S, SOF2, and CF4 are selected as the characteristic decomposition components of SF6. CO2, SO2 and SOF2 are all formed at 275 °C and the formation rate increases exponentially, but the formation rate of CO2 gradually decreases after CF4 has been generated. The formation rate of SO2 is higher than that of SOF2. The reason is that the decomposition of epoxy resin produces H2O, promoting hydrolysis of SOF2.During heating from 200 °C to 650 °C, the five gases of CO2S was lower than in the pure SF6, and CF4 generation rate also relatively increased. Concentration change of H2S and CF4 can be used as the criteria for judging the sudden weight loss caused by overheating fault happening on the surface of epoxy resin. 20% SF6/N2, 30% SF6/N2, and 40% SF6/N2 share the same judging standard: When there is no CF4 generation, H2S is used as the criterion depicted as follow: C(H2S)/C(T) > 0.01; when CF4 is generated, CF4 is used as the criterion depicted as follow: C(CF4)/C(T) > 0.001, among which C(T) represents the total decomposition gas concentration.When epoxy resin was heated in the gas mixture, the initial generation temperature of H2 and H2O produced during thermal decomposition of epoxy resin can intensify degradation of SF6 dielectric property. To judge the operation situation of SF6-infused electrical equipment, the problem of overheating faults involving epoxy resin decomposition should draw more attention.Thermal decomposition process of epoxy resin was simulated by the ReaxFF force field to reveal basic chemical reactions in terms of bond-breaking order, which further verified that COThe thermal decomposition characteristics of epoxy resin in SF