Une faune de petits mammiferes d'age turolien moyen(Miocene superieur) a Cucuron (Vaucluse); donnees nouvelles sur le genre Stephanomys (Rodentia) et consequences stratigraphiques

A small mammal fauna, including rodents and a new species of Murid, Stephanomys stadii n. sp., has been found in a continental formation underlying the deposits with the famous big mammal fauna of Mont Luberon. This fauna of small mammals is a little younger than the fauna of Los Mansuetos (Spain), so, the Pikermian fauna of Mont Luberon, which is said to be of the same age as the fauna of Pikermi is younger than the fauna of big and small mammals of Los Mansuetos.     

Synthesis of glycosyl halides and glycosides via 1-O-sulfonyl derivatives

The reaction of an aldose derivative containing a free anomeric hydroxyl group with trifluoromethanesulfonic anhydride or methanesulfonic anhydride, in the presence of halide ion and s-collidine, furnishes a glycosyl halide; if an alcohol is then introduced, glycoside synthesis is effected in an overall, “one-pot” reaction. Several α-d-glucopyranosides, including disaccharides, have been prepared in high yield by using 2,3,4,6-tetra-O-benzyl-d-glucose as the aldose, and generating the corresponding glycosyl bromide(s) in situ. As a halide-exchange step is incorporated in the reaction sequence, orthoacetate formation was favored in reactions of 2,3,4,6-tetra-O-acetyl-d-glucose, such as occurs with per-O-acetylglycosyl halides. Methanesulfonic anhydride promotes glycosidation or orthoester formation in the absence of halide ion, as well as in its presence, whereas formation of an intermediate glycosyl halide appears to be necessary in order to moderate the more vigorous reactions of the trifluoro derivative. The analogous reaction of methanesulfonyl chloride with an aldose provides a ready route to glycosyl chlorides. Under the conditions employed for these various syntheses, acid-sensitive protecting groups may be used, including cyclic and acyclic acetals and O-trityl substituents.     

Reduction of oxidized inorganic nitrogen compounds by a new strain of Thiobacillus denitrificans

Denitrification by Thiobacillus denitrificans "RT" strain was investigated using manometry and gas chromatography. 1. From nitrate, resting cells produced only nitrogen anaerobically with thiosulfate as the electron donor. The data suggest that nitrate was assimilated and dissimilated by the same nitrate reductase, assayed with benzyl-viologen as the electron donor. 2. From nitrite, whole cells produced nitric oxide, nitrous oxide and nitrogen, using thiosulfate as the electron donor; nitrogen was the final product of the reduction. Crude extract reduced nitrite to nitrogen with p-phenylene-diamine and dimethyl-p-phenylene diamine as the electron donors, and produced nitric oxide, nitrous oxide and nitrogen with tetramethyl-p-phenylene-diamine as the electron donor. Nitrite was reduced to nitric oxide and nitrous oxide by crude extract using ascorbate-phenazine methosulfate as the electron donor. 3. From nitric oxide, whole cells produced nitrous oxide and nitrogen using thiosulfate as the electron donor, nitrogen was the final reduction product. Nitric oxide was reduced to nitrous oxide by crude extract with the ascorbate-phenazine methosulfate system. 4. Whole cells reduced nitrous oxide to nitrogen with thiosulfate as the electron donor. It was not possible to detect any nitrous oxide reductase activity in crude extract. 5. A scheme was of denitrification by Thiobacillus denitrificans "RT" strain.     

模拟打制实验及其在丁村角页岩石器研究中的应用

模拟打制是史前考古研究中的重要实验考古方法之一,对于正确认识考古标本的类型和技术、解读当时人类的认知水平和知识积累具有不可取代的作用。本文简要回溯了模拟打制实验的发展史,并评述其应用现状。模拟打制实验在欧美有较长的发展与应用历史,但最终趋向了不同的发展方向。传统的模拟打制实验研究在欧洲得到了更加深入的继承和发展,而美国在上世纪90年代后期逐渐发展起了以定量控制、数理统计为核心的实验方法。本文以近期在山西丁村开展的角页岩模拟打制实验为例,介绍传统的模拟打制实验的基本流程和内容,包括实验的内容设计、实施及记录和分析等。本次实验结果肯定了硬锤锤击技术在丁村角页岩石核剥片和修理中的广泛应用,并在一定程度上否定了以往对使用碰砧法的推测。文章最后对模拟打制实验存在的问题和应用前景作了讨论和展望。     

Dendritic cells and cytokines in human inflammatory and autoimmune diseases

Dendritic cells (DCs) produce cytokines and are susceptible to cytokine-mediated activation. Thus, interaction of resting immature DCs with TLR ligands, for example nucleic acids, or with microbes leads to a cascade of pro-inflammatory cytokines and skewing of T cell responses. Conversely, several cytokines are able to trigger DC activation (maturation) via autocrine, for example TNF and plasmacytoid DCs, and paracrine, for example type I IFN and myeloid DCs, pathways. By controlling DC activation, cytokines regulate immune homeostasis and the balance between tolerance and immunity. The increased production and/or bioavailability of cytokines and associated alterations in DC homeostasis have been implicated in various human inflammatory and autoimmune diseases. Targeting these cytokines with biological agents as already is the case with TNF and IL-1 represents a success of immunology and the coming years will expand the range of cytokines as therapeutic targets in autoinflammatory and autoimmune pathology.     

Distinct Biology of Kaposi’s Sarcoma-Associated Herpesvirus from Primary Lesions and Body Cavity Lymphomas

The DNA sequence for Kaposi’s sarcoma-associated herpesvirus was originally detected in Kaposi’s sarcoma biopsy specimens. Since its discovery, it has been possible to detect virus in cell lines established from AIDS-associated body cavity-based B-cell lymphoma and to propagate virus from primary Kaposi’s sarcoma lesions in a human renal embryonic cell line, 293. In this study, we analyzed the infectivity of Kaposi’s sarcoma-associated herpesvirus produced from these two sources. Viral isolates from cultured cutaneous primary KS cells was transmitted to an Epstein-Barr virus-negative Burkitt’s B-lymphoma cell line, Louckes, and compared to virus induced from a body cavity-based B-cell lymphoma cell line. While propagation of body cavity-based B-cell lymphoma-derived virus was not observed in 293 cell cultures, infection with viral isolates obtained from primary Kaposi’s sarcoma lesions induced injury in 293 cells typical of herpesvirus infection and was associated with apoptotic cell death. Interestingly, transient overexpression of the Kaposi’s sarcoma-associated herpesvirus v-Bcl-2 homolog delayed the process of apoptosis and prolonged the survival of infected 293 cells. In contrast, the broad-spectrum caspase inhibitors Z-VAD-fmk and Z-DEVD-fmk failed to protect infected cell cultures, suggesting that Kaposi’s sarcoma-associated herpesvirus-induced apoptosis occurs through a Bcl-2-dependent pathway. Kaposi’s sarcoma-associated herpesvirus isolates from primary Kaposi’s sarcoma lesions and body cavity-based lymphomas therefore may differ and are likely to have distinct contributions to the pathophysiology of Kaposi’s sarcoma.