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1.
Annual production rates of reproductive organs inFagus crenata forests in the lower area of the species' range were studied using 10 litter traps in 1980–1986. The production rates of
dispersed pollen were estimated by multiplying the number of fallen male inflorescences per ha per year by the mean amount
of pollen per inflorescence before anthesis. Large annual fluctuations in the production rates of male and female inflorescences
were recognized, whereas their annual trends were synchronized with each other. Pollen production rates were within the range
1.0–6900 (mean: 1630)×109ha−1 yr−1, the maximum/minimum ratio attaining 7000.F. crenata was the lowest producer of pollen among seven tree species studied: the number of pollen grains equivalent to a single ovule
was in the range 6.0–14×104. Furthermore, the mean dry weight of a single pollen grain (3.77×10−5mg) was higher than for wind-pollinated species. Three factors seemed to cause the low seed fertility ofF. crenata. The dry-matter production rate in the best seed year reached 3252 kg ha−1 yr−1, of which pollen accounted for 259 kg ha−1 yr−1. Unproductive years with less than 10% of the maximum production occurred four times in a 7-yr period. In such years there
were fewer male and female inflorescences, and more fruit dropped as a result of insect damage. Lower nut dissemination would
play an important role in suppressing any increase in nut predators, and fewer flowers would be produced to avoid wastage
of photosynthates in a cool-temperate climate. 相似文献
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Teruhiko Yoshihara Fumihiro Ohmori Kaoru Nakamori Michiko Amanuma Takashi Tsutsumi Akitami Ichihara Hideyuki Matsuura 《Journal of Plant Growth Regulation》2000,19(4):457-461
apd: 9 May 2001 相似文献
5.
Hiroshi Kadokura Michiko Saito Akio Tsuru Akira Hosoda Takao Iwawaki Kenji Inaba Kenji Kohno 《Biochemical and biophysical research communications》2013
ERdj5 (also known as JPDI) is a member of PDI family conserved in higher eukaryotes. This protein possesses an N-terminal J domain and C-terminal four thioredoxin domains each having a redox active site motif. Despite the insights obtained at the cellular level on ERdj5, the role of this protein in vivo is still unclear. Here, we present a simple method to purify and identify the disulfide-linked complexes of this protein efficiently from a mouse tissue. By combining acid quenching and thiol-alkylation, we identified a number of potential redox partners of ERdj5 from the mouse epididymis. Further, we show that ERdj5 indeed interacted with two of the identified proteins via formation of intermolecular disulfide bond. Thus, this approach enabled us to detect and identify redox partners of a PDI family member from an animal tissue. 相似文献
6.
Factors associated with the basal level of serum thyrotropin (TSH) were analyzed over a wide range of pathophysiological conditions by means of a large laboratory database on thyroid function. When data were analyzed two-dimensionally, serum TSH showed significant inverse correlations with total triiodothyronine (T3), free T3 index (FT3I), total thyroxin (TT4) and free T4 index (FT4I) in the order of increasing intensity. The three-dimensional analysis, however, revealed that 1) total hormone levels were actually unrelated to serum TSH when the levels of free hormone indices were held constant, 2) the relation between FT3I and TSH became obscure when the influence of FT4I was similarly removed. On the other hand, 3) the relation of FT4I with TSH was unaffected by the level of FT3I. These results suggest that free T4 is the main determinant of the serum TSH level. This study also implies that it is possible to use large amounts of laboratory data to elucidate the overall profile of a given patho-physiological system, whose structure is only partially revealed by conventional clinical or animal studies. 相似文献
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Yamaji K Ikegami H Fujisawa T Noso S Nojima K Babaya N Itoi-Babaya M Makino S Sakamoto T Ogihara T 《Biochemical and biophysical research communications》2005,331(2):536-542
Among polygenes conferring susceptibility to type 1 diabetes in the NOD mouse, Idd10 on distal chromosome 3 has been shown to be important for disease susceptibility. In this study, we investigated the candidacy of Fcgr1 and Cd101 for Idd10, by congenic mapping and candidate gene sequencing. Among seven NOD-related strains studied, the IIS mouse was found to possess a recombinant Idd10 interval with the same sequence at Fcgr1 as the NOD mouse, but a different sequence at Cd101 from that in the NOD mouse with 10 amino acid substitutions. The frequency of type 1 diabetes in NOD mice congenic for IIS Idd10 (NOD.IISIdd10) was significantly reduced as compared to that in the NOD mouse, despite the presence of the identical Fcgr1 sequence. These data indicate that IIS mice possess a resistant allele at Idd10, and suggest that Cd101, but not Fcgr1, is responsible for the Idd10 effect. 相似文献
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The tumor suppressor gene Smad4 (DPC4) at chromosome 18q21.1 belongs to the Smad family, which mediates the TGFbeta signaling pathway suppressing epithelial cell growth. This review summarizes the mutational events of the Smad4 gene in human cancer. The Smad4 gene is genetically responsible for familial juvenile polyposis, an autosomal dominant disease characterized by predisposition to gastrointestinal polyps and cancer. In this syndrome, polyps are formed by inactivation of the Smad4 gene through germline mutation and loss of the unaffected wild-type allele. In pancreatic and colorectal cancer, inactivation of the Smad4 gene through homozygous deletion or intragenic mutation occurs frequently in association with malignant progression. However, mutation of this gene is seen only occasionally in the rest of human cancers. The majority of Smad4 gene mutations in human cancer are missense, nonsense, and frameshift mutations at the mad homology 2 region (MH2), which interfere with the homo-oligomer formation of Smad4 protein and the hetero-oligomer formation between Smad4 and Smad2 proteins, resulting in disruption of TGFbeta signaling. Supporting evidence for the above observation was provided by genetically manipulated mice carrying either a heterozygote of the Smad4 gene or a compound heterozygote of the Smad4 and APC genes, which develop either gastrointestinal polyps/cancer mimicking familial juvenile polyposis or progressed colorectal cancer, respectively. 相似文献