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Surface sediment diatoms from the east coast of Lake Tanganyika were analysed using ordination and classification techniques, and compared with assemblages previously described from the northern part of the lake. Grain-size analyses were performed on subsamples. Four groups of diatom assemblages were recognised. The first group clusters samples taken in the north, far from the Rusizi river mouth. The second group comprises samples taken on silty sediment along the Tanzanian coast, including one sample taken near the mouth of the Malagarazi river and those from the northernmost part of the lake. The third group comprises surface sediments along the Burundian coast (near Ramba and Magara), and the fourth is characterised by epipsammic taxa. A sample taken near the central arm of the Malagarazi river is included in the latter group. The impact of small rivers on the diatom assemblages in the surface sediments is restricted to the mouth area. 相似文献
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S. H. Habib S.-E. Ooi Ond?ej Novák Danu?e Tarkowská Jakub Rol?ík Karel Dole?al S. S. R. Syed-Alwee C.-L. Ho P. Namasivayam 《Plant Growth Regulation》2012,68(2):313-317
Comparative mineral and hormonal analyses were made on tissue culture derived truncated leaf syndrome and wild type oil palm seedlings. Mineral analysis confirmed that Boron, Zinc and chlorophyll levels were significantly lower in truncated leaf syndrome leaves than those of wild type. Hormonal analysis also revealed various cytokinin derivatives such as trans-zeatin, trans-zeatin riboside, trans-zeatin O-glucoside and trans-zeatin riboside 5??mono phosphate were significantly higher in truncated leaf syndrome leaves compared to wild type leaves. Brassinolide level was also significantly higher in truncated leaf syndrome leaves than those of the wild type. These observations suggest that the truncated leaf syndrome abnormality could be associated to high cytokinin and brassinosteroid production which affects the uptake of Boron and Zinc. 相似文献
4.
Immunization of cancer patients with tumor-specific antigenic peptides is currently being tested in several clinical studies. We have examined the induction of CTL responses in mice after various modalities of peptide vaccination, to explore protocols that could be applied to humans. Our first model antigen was P198, which results from a point mutation in a normal gene. While two immunizations with peptide P198 in SBAS-1c adjuvant induced measurable CTL responses in less than 10% of DBA/2 mice, the addition of IL-12 to the peptide adjuvant mixture resulted in high CTL responses in nearly all mice. This strong enhancing effect of IL-12 was observed with 1,000 and 300 units and decreased gradually as the doses were reduced to 30 units. When IL-12 was replaced by other cytokines acting on T cells or antigen-presenting cells, such as IFN-gamma, IL-2, IL-6, IL-7, GM-CSF or MCP-3, no significant enhancing effect was observed. The same effect of IL-12 was obtained with peptide P1A, which is a major tumor-specific antigen of mastocytoma P815 and is encoded by a gene that is specifically activated in tumors. 相似文献
5.
Yi Ting Zhou Li Li Chew Sheng-cai Lin Boon Chuan Low 《Molecular biology of the cell》2010,21(18):3232-3246
The BNIP-2 and Cdc42GAP homology (BCH) domain is a novel regulator for Rho GTPases, but its impact on p50-Rho GTPase-activating protein (p50RhoGAP or Cdc42GAP) in cells remains elusive. Here we show that deletion of the BCH domain from p50RhoGAP enhanced its GAP activity and caused drastic cell rounding. Introducing constitutively active RhoA or inactivating GAP domain blocked such effect, whereas replacing the BCH domain with endosome-targeting SNX3 excluded requirement of endosomal localization in regulating the GAP activity. Substitution with homologous BCH domain from Schizosaccharomyces pombe, which does not bind mammalian RhoA, also led to complete loss of suppression. Interestingly, the p50RhoGAP BCH domain only targeted RhoA, but not Cdc42 or Rac1, and it was unable to distinguish between GDP and the GTP-bound form of RhoA. Further mutagenesis revealed a RhoA-binding motif (residues 85-120), which when deleted, significantly reduced BCH inhibition on GAP-mediated cell rounding, whereas its full suppression also required an intramolecular interaction motif (residues 169-197). Therefore, BCH domain serves as a local modulator in cis to sequester RhoA from inactivation by the adjacent GAP domain, adding to a new paradigm for regulating p50RhoGAP signaling. 相似文献
6.
Pyrolysis mass spectrometry of polysaccharides. 总被引:1,自引:0,他引:1
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Structure of the gene of tum- transplantation antigen P91A: the mutated exon encodes a peptide recognized with Ld by cytolytic T cells 总被引:19,自引:0,他引:19
C Lurquin A Van Pel B Mariamé E De Plaen J P Szikora C Janssens M J Reddehase J Lejeune T Boon 《Cell》1989,58(2):293-303
Mutagen treatment of mouse P815 tumor cells produces immunogenic mutants that express new transplantation antigens (tum- antigens) recognized by cytolytic T cells. We found that the gene conferring expression of tum- antigen P91A contains 12 exons, encoding a 60 kd protein lacking a typical N-terminal signal sequence. The sequence shows no significant similarity with sequences in current data bases. A mutation that causes expression of the antigen is located in exon 4; it is the only apparent difference between the normal and the antigenic alleles. A short synthetic peptide corresponding to a region of exon 4 located around this mutation makes P815 cells sensitive to lysis by anti-P91A cytolytic T cells. The mutation creates a strong aggretope enabling the peptide to bind the H-2 Ld molecule. Several secondary tumor cell variants that no longer express tum- antigen P91A were found to carry deletions in the gene. 相似文献
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A Lucas R Morley T J Cole M F Bamford A Boon P Crowle J F B Dossetor R Pearse 《BMJ (Clinical research ed.)》1988,296(6635):1495-1497
To investigate the effect of maternal fatness on the mortality of infants born preterm up to the corrected age of 18 months 795 mother-infant pairs were studied. Maternal fatness was defined by Quetelet''s index (weight/(height2)) and all infants weighed less than 1850 g at birth. In 771 mother-infant pairs maternal age, complications of pregnancy, mode of delivery, parity, social class, and the baby''s sex and gestation were analysed by a logistic regression model for associations with infant mortality (but deaths from severe congenital abnormalities and those occurring during the first 48 hours after birth were excluded). In a subgroup of 284 mother-infant pairs all infant deaths except those from severe congenital abnormalities were analysed in association with the infant''s birth weight and gestation and the mother''s height and weight; this second analysis included another 24 infants who had died within 48 hours after birth. In the first analysis mortality overall was 7% (55/771), rising from 4% (71/173) in thin mothers (Quetelet''s index <20) to 15% (6/40) in mothers with grades II and III obesity (Quetelet''s index >30). After adjusting for major demographic and antenatal factors, including serious complications of pregnancy, maternal fatness was second in importance only to length of gestation in predicting death of infants born preterm. In the second analysis mortality overall was 15% (44/284), rising from 9% (5/53) in thin mothers to 47% (8/17) in mothers with grades II and III obesity. In both analyses the relative risk of death by 18 months post-term was nearly four times greater in infants born to obese mothers than in those born to thin mothers. In addition, maternal fatness was associated with reduced birth weight, whereas it is associated with macrosomia in term infants.These data differ fundamentally from those reported in full term babies of obese mothers. It is speculated that the altered metabolic milieu in obesity may reduce the ability of the fetus to adapt to extrauterine life if it is born preterm. 相似文献