Root development across a chronosequence in a Japanese cedar (<Emphasis Type="Italic">Cryptomeria japonica</Emphasis> D. Don) plantation     

Reiji Fujimaki  Ryunosuke Tateno  Naoko Tokuchi 《Journal of Forest Research》2007,12(2):96-102

We investigated the biomass, vertical distribution, and specific root length (SRL) of fine and small roots in a chronosequence of Japanese cedar (Cryptomeria japonica D. Don) plantations in Nara Prefecture, central Japan. Roots were collected from soil blocks up to 50 cm in depth in five plantations of differing age: 4, 15, 30, 41, and 88 years old. Fine-root biomass reached a maximum (639 g m₋₂) in the 15-year-old stand before canopy closure, decreased in the 30-year-old stand (422 g m₋₂), and thereafter was stable. Except in the 30-year-old stand, fine-root biomass increased in deeper soil layers as stand age increased, and the depth at which the cumulative biomass of fine roots reached 90% exhibited a good allometric relationship with mean stem diameter. Both root-length density (root length per unit soil volume) and SRL decreased with soil depth in all stands, indicating that plants mainly acquire water and nutrients from shallow soils. The highest SRL was observed in the 4-year-old stand, but the relationship between SRL and stand age was unclear in older stands. The SRL in surface soils seemed to decrease with increases in root-length density, suggesting that branching of the fine-root system during development is related to density-dependent processes rather than age.  相似文献   

The Fc and not CD4 receptor mediates antibody enhancement of HIV infection in human cells   总被引：36，自引：0，他引：36  

J Homsy  M Meyer  M Tateno  S Clarkson  J A Levy 《Science (New York, N.Y.)》1989,244(4910):1357-1360

Antibodies that enhance human immunodeficiency virus (HIV) infectivity have been found in the blood of infected individuals and in infected or immunized animals. These findings raise serious concern for the development of a safe vaccine against acquired immunodeficiency syndrome. To address the in vivo relevance and mechanism of this phenomenon, antibody-dependent enhancement of HIV infectivity in peripheral blood macrophages, lymphocytes, and human fibroblastoid cells was studied. Neither Leu3a, a monoclonal antibody directed against the CD4 receptor, nor soluble recombinant CD4 even at high concentrations prevented this enhancement. The addition of monoclonal antibody to the Fc receptor III (anti-FcRIII), but not of antibodies that react with FcRI or FcRII, inhibited HIV type 1 and HIV type 2 enhancement in peripheral blood macrophages. Although enhancement of HIV infection in CD4+ lymphocytes could not be blocked by anti-FcRIII, it was inhibited by the addition of human immunoglobulin G aggregates. The results indicate that the FcRIII receptor on human macrophages and possibly another Fc receptor on human CD4+ lymphocytes mediate antibody-dependent enhancement of HIV infectivity and that this phenomenon proceeds through a mechanism independent of the CD4 protein.  相似文献