Oviposition behaviour of Tamarixia radiata: effects of host density and exposure time

1. The number of hosts attacked as a function of host density is considered to be an important characteristic of parasitoid behaviour and is used to estimate key parameters such as handling time and ‘instantaneous rate of discovery’. However, little has been done to validate functional response models by direct observation of parasitoid oviposition behaviour. 2. Tamarixia radiata is the most promising parasitoid for biological control attacking Diaphorina citri. Mass rearing and augmentative release seen as a potential strategy for suppression of D. citri has been documented in abandoned citrus, residential areas, and organic groves. Nevertheless, parasitism rates in culture and in the field are only moderate, leading to questions about oviposition behaviour in response to host density. 3. Behaviours of gravid T. radiata females presented with susceptible host instars were categorised and documented by direct observation for 30 min and by camera recordings made over 12 h. Frequency of searching and antennating increased with host density during the 30 min. Probing rejection rates and search duration increased significantly with host density over 12 h. These factors resulted in significantly lower fecundity than expected, possibly due to host mark‐mediated deterrence within the small searching area. Females took approximately 3.6–4.2 min to probe and parasitise a host regardless of host density and exposure duration. These results were markedly different from the 52.2 min estimated from the functional response equation. 4. Further experiments are required to assess the range and persistence of the putative host‐marking pheromone, and to better understand the relationship between functional response parameters and actual behaviour.     

茶色金龟子和铜色白纹金龟子的初步研究

1.本文所述的两种金龟子,其一为茶色金龟子,属鞘翅目,金龟子科中的Rutelinae亚科,其二为铜色白纹金龟子,属Cetoniinae亚科。 2.茶色金龟子在莲塘一年发生二代。其第1次成虫盛期多在6月。第2次则在8月;铜色白纹金龟子,一年仅发生一代,其成虫出现期为6至9月,少数可延长到10月中旬。 3.茶色金龟子的成虫,为夜出性,傍晚7时半后,即开始出土,停息在多种寄主植物的叶片上,取食或交配,拂晓时飞返土中。铜色白纹金龟子的成虫,为日出性,取食成熟果子,玉米苞穗及多种树木的浆汁,亦喜取食。既钻入后,可连续数日不出。 4.两种金龟子的幼虫,都栖息在土中。茶色金龟子幼虫以在菜园土中、丘陵黄土地及属于粘壤性质的田塍内为多,对于土壤性质选择,较不严格。铜色白纹金龟子幼虫则多集中在腐熟的堆肥及腐殖质极丰富的土中,对于土壤,有比较严格的选择性。 5.关于防治方法:茶色金龟子在成虫期曾试用了0.5％γ体666粉及25％DDT乳剂(1份加水250份〕喷撒,第1种药适用于叶面较粗糙的植物,第2种则可用于叶面较光滑的植物,只要喷撒1次,便能在整个成虫发生期中,避免其飞来取食。铜色白纹金龟子的成虫,则可采用竹筒诱杀,筒高12—16寸,筒内盛腐熟果子及蜜,贴靠枝杆悬挂,能将圆内所有成虫,全部诱入筒中。此外,前一种成虫,并可利用外出     

各种昆虫耐饥力的观察

昆虫耐饥力的强弱,为昆虫的生物学特性之一。对於这个问题,以前还没有人作过系统性的观察。1950—1951两年,我们在这方面,曾经化了一些时间,并已初步得出一些结果,现在把它整理出来,以供大家讨论。     

AngⅡ和PKC对心肌细胞AngⅡ 1型受体的转录调节

利用体外培养的心肌细胞,观察血管紧张素Ⅱ（ＡｎｇⅡ）和蛋白激酶Ｃ（ＰＫＣ）在诱导ＡｎｇⅡ１型受体（ＡＴ１）基因表达及蛋白质代谢中的作用．研究结果表明：ＡｎｇⅡ可诱导ＡＴ１ｍＲＮＡ水平一过性下调,呈时间及剂量依赖性,１０ｎｍｏｌ／ＬＡｎｇⅡ刺激细胞６ｈ,引起ＡＴ１ｍＲＮＡ水平降低幅度最大,降至对照的５１．６％±９．５％,然后逐渐回升,２４ｈ恢复至对照水平．３０μｍｏｌ／ＬＨ－７（ＰＫＣ抑制剂）能阻断ＡｎｇⅡ诱导的ＡＴ１ｍＲＮＡ水平的下调．０．３μｍｏｌ／Ｌ的ＰＭＡ（ＰＫＣ激活剂）单独应用可诱导ＡＴ１ｍＲＮＡ水平下调达对照的４３％±８％,加入ＡＴ１拮抗剂ＤＭＰ８１１及Ｄｕｐ７５３均可阻断ＡｎｇⅡ诱导的ＡＴ１ｍＲＮＡ水平的下调．１０ｎｍｏｌ／Ｌ的ＡｎｇⅡ刺激心肌细胞９６ｈ可使蛋白含量降低至对照的７３．４％±５．６％,而加药持续刺激１４４ｈ可使蛋白含量较对照增加３３．８％±６．３％,Ｈ－７不能阻断ＡｎｇⅡ诱导的蛋白含量降低,但可有效地抑制蛋白含量的增加．以上结果提示：ＡｎｇⅡ对心肌细胞ＡＴ１基因的转录和细胞的蛋白代谢有调节作用,而ＰＫＣ则参与了ＡｎｇⅡ的这种调节作用     

Eucalyptus leachate inhibits reproduction in a freshwater fish

1. Dissolved organic carbon (DOC) can induce lethal and sub‐lethal effects in exposed biota via hypoxic blackwater events and the toxicity of leached compounds. Little is known of how DOC exposure affects fish reproduction despite the fact that its release can coincide with spawning‐associated flow pulses. 2. River red gum (Eucalyptus camaldulensis) leaf leachate is a major source of DOC in Australian freshwaters and includes the toxic plant secondary metabolites polyphenols and tannins. High concentrations of leachate are released when leaves on floodplains or dry stream channels are inundated by water. 3. Southern pygmy perch (Nannoperca australis) from naturally high and naturally low Eucalyptus leachate environments in south‐east Australia were exposed to elevated leachate levels to investigate the effects of DOC on reproduction and to explore whether response patterns were consistent with populations becoming locally adapted to historical leachate levels. 4. Fish exposed to leachate were half as likely to reach sexual maturity as control fish. Fish from a naturally high‐exposure population tended to reach sexual maturity earlier than those from a naturally low‐exposure population. Leachate exposure had no effect on either egg size or fecundity. 5. Our results suggest that leachate‐exposed mothers did not reproduce because they were physiologically stressed or perceive the environment to be unsuitable, which raises the potential of plastic or adaptive responses to this stressor. The negative sub‐lethal effects observed have important fitness implications for individuals, the viability of populations and the management of environmental flows and riparian zones.     

Isocitrate dehydrogenase 1 R132C mutation occurs exclusively in microsatellite stable colorectal cancers with the CpG island methylator phenotype

The CpG Island Methylator Phenotype (CIMP) is fundamental to an important subset of colorectal cancer; however, its cause is unknown. CIMP is associated with microsatellite instability but is also found in BRAF mutant microsatellite stable cancers that are associated with poor prognosis. The isocitrate dehydrogenase 1 (IDH1) gene causes CIMP in glioma due to an activating mutation that produces the 2-hydroxyglutarate oncometabolite. We therefore examined IDH1 alteration as a potential cause of CIMP in colorectal cancer. The IDH1 mutational hotspot was screened in 86 CIMP-positive and 80 CIMP-negative cancers. The entire coding sequence was examined in 81 CIMP-positive colorectal cancers. Forty-seven cancers varying by CIMP-status and IDH1 mutation status were examined using Illumina 450K DNA methylation microarrays. The R132C IDH1 mutation was detected in 4/166 cancers. All IDH1 mutations were in CIMP cancers that were BRAF mutant and microsatellite stable (4/45, 8.9%). Unsupervised hierarchical cluster analysis identified an IDH1 mutation-like methylation signature in approximately half of the CIMP-positive cancers. IDH1 mutation appears to cause CIMP in a small proportion of BRAF mutant, microsatellite stable colorectal cancers. This study provides a precedent that a single gene mutation may cause CIMP in colorectal cancer, and that this will be associated with a specific epigenetic signature and clinicopathological features.