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61.
Normal 0 false false false EN-US X-NONE X-NONE MicrosoftInternetExplorer4 st1\:*{behavior:url(#ieooui) } /* Style Definitions */ table.MsoNormalTable {mso-style-name:"Table Normal"; mso-tstyle-rowband-size:0; mso-tstyle-colband-size:0; mso-style-noshow:yes; mso-style-priority:99; mso-style-qformat:yes; mso-style-parent:""; mso-padding-alt:0in 5.4pt 0in 5.4pt; mso-para-margin:0in; mso-para-margin-bottom:.0001pt; mso-pagination:widow-orphan; font-size:11.0pt; font-family:"Calibri","sans-serif"; mso-ascii-font-family:Calibri; mso-ascii-theme-font:minor-latin; mso-fareast-font-family:"Times New Roman"; mso-fareast-theme-font:minor-fareast; mso-hansi-font-family:Calibri; mso-hansi-theme-font:minor-latin; mso-bidi-font-family:"Times New Roman"; mso-bidi-theme-font:minor-bidi;} Life forms and floral characteristics of plants at Arches National Park (desert communities), the Mt. Nebo complex, and a subalpine meadow in the Uinta Mountains (montane and subalpine communities) were compared. Characteristics observed were (1) life form, (2) longevity, (3) pollination system, (4) flower structure, (5) flower symmetry, and (6) flower color. Common families in each flora were also compared. Results showed that there is a significant overrepresentation of shrub species at Arches, and an underrepresentation of perennial forbs. Relative number of perennial forb species was significantly higher at Mt. Nebo and the subalpine meadow than at Arches National Park. Native annuals and wind-pollinated species were significantly overrepresented at Arches. Flowers with open structure that permit free access of most insects to nectar and pollen were overrepresented at Mt. Nebo and in the subalpine meadow. The distribution of flower colors also differs significantly among these ecologically contrasting floras, with yellow being best represented in the desert and white in the mountains. 相似文献
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Dorner M Horwitz JA Robbins JB Barry WT Feng Q Mu K Jones CT Schoggins JW Catanese MT Burton DR Law M Rice CM Ploss A 《Nature》2011,474(7350):208-211
Hepatitis C virus (HCV) remains a major medical problem. Antiviral treatment is only partially effective and a vaccine does not exist. Development of more effective therapies has been hampered by the lack of a suitable small animal model. Although xenotransplantation of immunodeficient mice with human hepatocytes has shown promise, these models are subject to important challenges. Building on the previous observation that CD81 and occludin comprise the minimal human factors required to render mouse cells permissive to HCV entry in vitro, we attempted murine humanization via a genetic approach. Here we show that expression of two human genes is sufficient to allow HCV infection of fully immunocompetent inbred mice. We establish a precedent for applying mouse genetics to dissect viral entry and validate the role of scavenger receptor type B class I for HCV uptake. We demonstrate that HCV can be blocked by passive immunization, as well as showing that a recombinant vaccinia virus vector induces humoral immunity and confers partial protection against heterologous challenge. This system recapitulates a portion of the HCV life cycle in an immunocompetent rodent for the first time, opening opportunities for studying viral pathogenesis and immunity and comprising an effective platform for testing HCV entry inhibitors in vivo. 相似文献
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Campbell PJ Yachida S Mudie LJ Stephens PJ Pleasance ED Stebbings LA Morsberger LA Latimer C McLaren S Lin ML McBride DJ Varela I Nik-Zainal SA Leroy C Jia M Menzies A Butler AP Teague JW Griffin CA Burton J Swerdlow H Quail MA Stratton MR Iacobuzio-Donahue C Futreal PA 《Nature》2010,467(7319):1109-1113
Pancreatic cancer is an aggressive malignancy with a five-year mortality of 97-98%, usually due to widespread metastatic disease. Previous studies indicate that this disease has a complex genomic landscape, with frequent copy number changes and point mutations, but genomic rearrangements have not been characterized in detail. Despite the clinical importance of metastasis, there remain fundamental questions about the clonal structures of metastatic tumours, including phylogenetic relationships among metastases, the scale of ongoing parallel evolution in metastatic and primary sites, and how the tumour disseminates. Here we harness advances in DNA sequencing to annotate genomic rearrangements in 13 patients with pancreatic cancer and explore clonal relationships among metastases. We find that pancreatic cancer acquires rearrangements indicative of telomere dysfunction and abnormal cell-cycle control, namely dysregulated G1-to-S-phase transition with intact G2-M checkpoint. These initiate amplification of cancer genes and occur predominantly in early cancer development rather than the later stages of the disease. Genomic instability frequently persists after cancer dissemination, resulting in ongoing, parallel and even convergent evolution among different metastases. We find evidence that there is genetic heterogeneity among metastasis-initiating cells, that seeding metastasis may require driver mutations beyond those required for primary tumours, and that phylogenetic trees across metastases show organ-specific branches. These data attest to the richness of genetic variation in cancer, brought about by the tandem forces of genomic instability and evolutionary selection. 相似文献
65.
A major pathway in the clearance of pathogens involves the coating of the pathogen with specific antibodies, and the binding of the antibody Fc region to cell receptors. This can trigger engulfment of the pathogen by phagocytes or lysis by killer cells. By oligonucleotide site-directed mutagenesis we have engineered a single amino acid change in a mouse IgG2b antibody (Glu 235----Leu) which now enables the antibody to bind to the FcRI (high affinity) receptor on human monocytes with a 100-fold improvement in affinity. This indicates that Leu 235 is a major determinant in the binding of antibody to FcRI and that the receptor may interact directly with the region linking the CH2 domain to the hinge. Tailoring the affinity of antibodies for cell receptors could help dissect their role in clearing pathogen. 相似文献
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Salvi M Toninello A Schweizer M Friess SD Richter C 《Cellular and molecular life sciences : CMLS》2002,59(7):1190-1197
Mitochondria contain a specific Ca2+ release pathway which operates when oxidized mitochondrial pyridine nucleotides are hydrolyzed. NAD+ hydrolysis and therefore Ca2+ release is possible when some vicinal thiols are cross-linked. Here we report that the thiol oxidant peroxovanadate inhibits
the specific Ca2+ release pathway. In mitochondria, peroxovanadate causes a complete loss of reduced glutathione, which is not accompanied
by formation of glutathione disulfide, and a partial loss of protein thiols. In model reactions, peroxovanadate oxidizes reduced
glutathione predominantly to the sulfonate derivative, but does not react with glutathione disulfide. When the vicinal thiols
relevant for Ca2+ release are cross-linked, Ca2+ release is no longer inhibited by peroxovanadate. Conversely, pretreatment of mitochondria with peroxovanadate makes them
insensitive to compounds promoting the disulfide state. These results suggest that peroxovanadate inhibits the prooxidant-induced
Ca2+ release from mitochondria by (i) depleting mitochondria of reduced glutathione and (ii) oxidizing the vicinal thiols relevant
for Ca2+ release to a state higher than disulfide, presumably the sulfonate state. The findings provide further insight into the regulation
of Ca2+ release from intact mitochondria, and may be relevant for a better understanding of the action of peroxovanadate in cells,
where the compound can be insulin mimetic.
Received 28 March 2002; received after revision 8 May 2002; accepted 15 May 2002 相似文献
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Summary As judged from 2-h blood level curves, adult female rats absorbed more FeII per cm2 of gross duodenal mucosa than adult male rats. By contrast, the 2-h blood level curves per cm2 of mucosa of proximal jejunum did not differ significantly in male and female rats although in both sexes, iron was absorbed
more efficiently from the duodenum.
This research was supported by grant RO1 AM 12381 from the National Institute of arthritis, Diabetes and Digestive and Kidney
Diseases, National Institutes of Health. 相似文献