Petrosal bones of metatherian mammals from the Late Palaeocene of Itaboraí (Brazil), and a cladistic analysis of petrosal features in metatherians

Metatherian petrosal bones were recovered from the early Late Palaeocene Itaboraí, Brazil, and are formally described. A cladistic analysis of the distribution of 56 petrosal and basicranial characters among extant and fossil metatherians was conducted, resulting in seven parsimonious trees. Relationships among metatherian ingroup taxa are congruent with current understanding of metatherian phylogeny. Metatheria is diagnosed by eight petrosal synapomorphies: stapedial artery absent in adults; reduced, intramural prootic canal; extrabullar internal carotid artery; inferior petrosal sinus between petrosal, basisphenoid, and basioccipital; cava supracochleare and epiptericum completely separated; reduction of the lateral flange; reduction of the anterior lamina; separation of the jugular foramen from the opening for the inferior petrosal sinus. The Palaeocene taxa Mayulestes , Pucadelphy s, and Andinodelphys from Tiupampa, and Petrosal Type II from Itaboraí are the sister groups of all other South American and Australian metatherians. This analysis confirms previous results showing the South American 'monito del monte' Dromiciops nested within the Australasian radiation. Within this australidelphian clade, Dromiciops is closely related to the dasyurids. The South American Caenolestes appears more closely related to the Australidelphia than to the South American didelphids. The Petrosal Types I, III, IV and V from Itaboraí are the stem taxa of the clade Australidelphia plus Caenolestes . The significant synapomorphies supporting this relationship are: enlargement of the fossa subarcuata that produces a bulbous ventral aspect of the mastoid and loss of post-temporal canal.  Journal compilation © 2007 The Linnean Society of London, Zoological Journal of the Linnean Society , 2007, 150 , 85–115. No claim to original French government works.     

益生菌粉（副干酪乳酪杆菌207-27）的毒理学安全性评价

评估益生菌粉（副干酪乳酪杆菌207-27）的毒理学安全性,为其应用提供依据。

通过大鼠急性经口毒性试验、细菌回复突变试验、小鼠红细胞微核试验、小鼠精母细胞染色体畸变试验及大鼠28 d经口毒性试验研究益生菌粉（副干酪乳酪杆菌207-27）的安全性。

大鼠急性经口毒性试验结果显示,益生菌粉（副干酪乳酪杆菌 207-27）对大鼠的经口急性毒性LD₅₀均大于15.00 g/（kg•BW）,根据急性毒性分级标准属实际无毒。细菌回复突变试验、小鼠红细胞微核试验及小鼠精母细胞染色体畸变试验结果均显示阴性。大鼠28 d经口毒性试验结果表明,实验组大鼠体质量、摄食量、食物利用率、眼部状况、血液学指标、血液生化指标、脏器指数、大体及病理学检查结果与对照组相比差异均无统计学意义。

益生菌粉（副干酪乳酪杆菌207-27）具有良好的毒理学安全性。

     

The nonhomologous DNA end joining pathway is important for chromosome stability in primary fibroblasts

There are two types of chromosome instability, structural and numerical, and these are important in cancer. Many structural abnormalities are likely to involve double-strand DNA (dsDNA) breaks. Nonhomologous DNA end joining (NHEJ) and homologous recombination are the major pathways for repairing dsDNA breaks. NHEJ is the primary pathway for repairing dsDNA breaks throughout the G0, G1 and early S phases of the cell cycle [1]. Ku86 and DNA ligase IV are two major proteins in the NHEJ pathway. We examined primary dermal fibroblasts from mice (wild type, Ku86(+/-), Ku86(-/-), and DNA ligase IV(+/-)) for chromosome breaks. Fibroblasts from Ku86(+/-) or DNA ligase IV(+/-) mice have elevated frequencies of chromosome breaks compared with those from wild-type mice. Fibroblasts from Ku86(-/-) mice have even higher levels of chromosome breaks. Primary pre-B cells from the same animals did not show significant accumulation of chromosome breaks. Rather the pre-B cells showed increased cell death. These studies demonstrate that chromosome breaks arise frequently and that NHEJ is required to repair this constant spontaneous damage.     

Localization of multiple melanoma tumor-suppressor genes on chromosome 11 by use of homozygosity mapping-of-deletions analysis

Loss-of-heterozygosity (LOH) studies have implicated one or more chromosome 11 tumor-suppressor gene(s) in the development of cutaneous melanoma as well as a variety of other forms of human cancer. In the present study, we have identified multiple independent critical regions on this chromosome by use of homozygosity mapping of deletions (HOMOD) analysis. This method of analysis involved the use of highly polymorphic microsatellite markers and statistics to identify regions of hemizygous deletion in unmatched melanoma cell line DNAs. Regions of loss were defined by the presence of an extended region of homozygosity (ERH) at > or =5 adjacent markers and having a statistical probability of < or =.001. Significant ERHs were similar in nature to deletions identified by LOH analyses performed on uncultured melanomas, although a higher frequency of loss (24 [60%] of 40 vs. 16 [34%] of 47) was observed in the cell lines. Overall, six small regions of overlapping deletions (SROs) were identified on chromosome 11 flanked by the markers D11S1338/D11S907 (11p13-15.5 [SRO1]), D11S1344/D11S11385 (11p11.2 [SRO2]), D11S917/D11S1886 (11q21-22.3 [SRO3]), D11S927/D11S4094 (11q23 [SRO4]), AFM210ve3/D11S990 (11q24 [SRO5]), and D11S1351/D11S4123 (11q24-25 [SRO6]). We propose that HOMOD analysis can be used as an adjunct to LOH analysis in the localization of tumor-suppressor genes.     

The Finland-United States investigation of non-insulin-dependent diabetes mellitus genetics (FUSION) study. I. An autosomal genome scan for genes that predispose to type 2 diabetes

We performed a genome scan at an average resolution of 8 cM in 719 Finnish sib pairs with type 2 diabetes. Our strongest results are for chromosome 20, where we observe a weighted maximum LOD score (MLS) of 2.15 at map position 69.5 cM from pter and secondary weighted LOD-score peaks of 2.04 at 56.5 cM and 1.99 at 17.5 cM. Our next largest MLS is for chromosome 11 (MLS = 1.75 at 84.0 cM), followed by chromosomes 2 (MLS = 0.87 at 5.5 cM), 10 (MLS = 0.77 at 75.0 cM), and 6 (MLS = 0.61 at 112.5 cM), all under an additive model. When we condition on chromosome 2 at 8.5 cM, the MLS for chromosome 20 increases to 5.50 at 69.0 cM (P=.0014). An ordered-subsets analysis based on families with high or low diabetes-related quantitative traits yielded results that support the possible existence of disease-predisposing genes on chromosomes 6 and 10. Genomewide linkage-disequilibrium analysis using microsatellite marker data revealed strong evidence of association for D22S423 (P=.00007). Further analyses are being carried out to confirm and to refine the location of these putative diabetes-predisposing genes.     

三种绿叶挥发性物质对云南切梢小蠹寄主定位行为的干扰作用

为了研究环境中非寄主阔叶植物释放出的绿叶挥发性物质（GLVs）对针叶树蛀干害虫云南切梢小蠹Tomicus yunnanesis的影响, 选取了(E)-2-己烯醛、 (E)-2-己烯醇和(Z)-3-己烯醇3种释放量较大的绿叶挥发性物质, 通过室内松梢取食试验测试了单组分及两两混合后对云南切梢小蠹寄主定位行为的干扰作用。结果表明： 源于阔叶植物的3种绿叶挥发性物质及其混合物能够不同程度干扰云南切梢小蠹的寄主定位行为。当虫放入广口瓶12 h后, 3个单组分绿叶挥发性物质处理组［A： (E)-2-己烯醛, P＜0.01; B： (E)-2-己烯醇, P＜0.01; C： (Z)-3-己烯醇, P＜0.01］及2个混合组分［D： (E)-2-己烯醛+(E)-2-己烯醇, P＜0.01）; E： (E)-2-己烯醛+(Z)-3-己烯醇, P＜0.01］中滞留在松梢外部的虫数与对照组相比都有显著性差异, 绿叶挥发性物质的存在显著降低了云南切梢小蠹侵害云南松松梢的概率。但是, 24 h后只有D组（P＜0.01）和E组（P＜0.01）滞留在松梢外部的虫数与对照组相比具有显著性差异, 在48 h后只有D组（P＜0.01）与对照相比仍具有显著性差异。本研究为利用非寄主植物的次生代谢产物防治云南切梢小蠹进行了有益的探索。     

Overexpression of Cu/Zn superoxide dismutase is lethal for mice lacking double-strand break repair

The non-homologous DNA end joining (NHEJ) pathway is a major double-strand DNA break repair pathway in cells of multicellular eukaryotes. Ku is a heterodimeric protein consisting of Ku70 and Ku86, and it is thought to be the first component to bind to a broken double-strand DNA end. Mice lacking Ku86 show features of premature aging, live about 6-12 months, and show a characteristic loss of neurons in the central nervous system during development. Cells from mice lacking Ku have increased numbers of chromosome breaks, a significant fraction of which are caused by oxidative metabolism. Overexpression of the cytoplasmic Cu/Zn superoxide dismutase (SOD1) from a transgene is known to increase the number of chromosome breaks in primary cells (presumably by increasing reactive oxygen species). Here we show that SOD1 overexpression in a Ku86-/- mouse results in embryonic lethality. This striking effect is, however, subject to a strain-specific modifier. Genome-wide marker analysis is most consistent with the modifier being on mouse chromosome 13. Analysis of 10 markers on chromosome 13 suggests that the modifier is within the same region as a modifier of the murine amyotropic lateral sclerosis (ALS) phenotype when it is caused by overexpression of a mutant form of SOD1. Based on these results, we propose a model in which oxidative metabolism causes chromosome breaks, leading to neuronal death; and this neuronal death may account for that seen in NHEJ mutant animals and in mammals with SOD1-mediated ALS.     

云南切梢小蠹对初侵害云南松挥发物的电生理和行为反应

云南切梢小蠹Tomicus yunnanensis(Kirkendall and Faccoli)是一种蛀害云南松Pinus yunnanensis的本土害虫.为深入了解其寄主选择机制,用顶空动态法和浸提法分别提取了初侵染云南松针叶和松脂的挥发性化合物,并用气相色谱-质谱联用技术(GC-MS)、气相色谱-昆虫触角电位测量系统(GC-EAD)、生测法鉴定和筛选了对云南切梢小蠹具有活性功能的成分.结果表明:云南松针叶和松脂中共有18种化合物,均为萜烯类物质,但两者化学成分的构成有显著差异.针叶中单萜类占99.98％,主要是 α-蒎烯(80.82％)、β-蒎烯(8.78％)、D-柠檬烯(4.77％)、莰烯(2.86％)和β-月桂烯(1.42％),而松脂以单萜类和双萜类为主,前者以α-蒎烯(21.38％)、3-蒈烯(21.42％)和异松油烯(2.78％)为主要成分,后者仅有长叶松酸(51.13％)一种.云南切梢小蠹对α-蒎烯、β-蒎烯、3-蒈烯、γ-萜品烯和4-烯丙基苯甲醚有触角电位反应,其中α-蒎烯、3-蒈烯和γ-萜品烯具引诱作用,4-烯丙基苯甲醚和β-蒎烯则为驱避功能.研究可为开发植物源引诱剂或与性信息素结合进行种群监测和诱杀提供科学依据.