Alterations of polymorphonuclear leukocyte surface charge by stimulated lymphocyte supernatants

The effects of human lymphokines on the surface charge density of human polymorphonuclear (PMN) leukocytes have been determined using the laser Doppler technique of electrophoretic light scattering. Unfractionated antigen (streptokinase-streptodornase or candida)-stimulated lymphocyte supernatants were found to decrease the mode electrophoretic mobility by 14%. In order to identify the responsible factor, we subjected supernatants from concanavalin A-stimulated lymphocytes to gel filtration on Sephadex G-100 columns and assayed the fractions for their ability to alter PMN electrophoretic mobilities. Two distinct species in the molecular weight ranges of 30–60K and 10–20K, respectively, were found to decrease the electrophoretic mobilities of PMN leukocytes. We have observed no effect of leukocyte inhibitory factor (LIF) on the electrophoretic mobility distribution of PMN leukocytes over a varying period of time (0–8 hr) and over a range of 2- to 10-fold supernatant concentration. Pretreatment of PMN leukocytes with neuraminidase substantially reduced their electrophoretic mobility; the addition of LIF to these pretreated cells did not alter their electrophoretic mobility distribution further. The latter finding is particularly significant in view of the fact that neuraminidase pretreatment of the target cells is known to potentiate LIF activity. We conclude that the mechanism of the inhibition of leukocyte migration by LIF does not involve an alteration of the leukocyte surface charge density.     

Inhibition of lymphocyte transformation responses to phytohemagglutinin by normal human plasma.

Marked variability in lymphocyte transformation responses to a suboptimal phytohemagglutinin concentration (0.1 μg/ml) was observed when peripheral blood mononuclear cells of normal subjects were cultured in media containing 15% autologous plasma. Low responses were related to the plasma and were caused by direct inhibition rather than an inability to support the response. This inhibitory activity varied greatly among different plasma specimens and was also found in human and animal serum. It appeared to be specific for suboptimal concentrations of phytohemagglutinin and could be overcome by increasing the mitogen concentration. The inhibitory activity was heat stable, was not dialyzable, and appeared to affect a very early stage of the response since a delay in addition of the inhibitory plasma reversed its effect. Our interpretation of these results is that human plasmas vary greatly with respect to their ability to bind phytohemagglutinin so that the addition of different plasmas to lymphocyte cultures stimulated by a limiting concentration of phytohemagglutinin results in marked variability of the results obtained.     

Responsiveness of RNA degradation to amino acids in cultured rat hepatocytes: comparison with isolated rat hepatocytes.

The role of amino acids in the regulation of RNA degradation was investigated in cultured hepatocytes from fed rats previously labeled in vivo with [6-14C]orotic acid. Rates of RNA degradation were determined between 42 and 48 h of culture from the release of radioactive cytidine in the presence of 0.5 mM unlabeled cytidine. The fractional rate was about 4.4 +/- 0.4%/h in the absence of amino acids (0x). The catabolism of RNA was decreased to basal level (1.5 +/- 0.3%/h) by the addition of amino acids at 10 times normal plasma concentration (10x). The inhibition of RNA degradation, expressed as percentage of maximal deprivation-induced response (0x minus 10x), averaged 60% at normal plasma levels of amino acids. The degree of responsiveness was greatly improved as compared to freshly isolated hepatocytes (20%) and was similar to the sensitivity previously observed with perfused livers. In cultured hepatocytes, the sensitivity of RNA degradation to amino acids was not affected by varying the volume of medium from 1 to 4 ml per dish. In freshly isolated hepatocytes, the inhibitory effect of amino acids was not modified by changing the cell density from 0.5 to 5 x 10(6) cells per ml. In the range of normal plasma concentration of amino acids, the low sensitivity of RNA degradation in isolated hepatocytes persisted with inhibition ranging from 10 to 20%. These findings suggest that the control of RNA degradation in both cultured and isolated hepatocytes is not affected by the total quantity of amino acids available in the medium, but their concentration is crucial. Electron microscopy observations and the inhibitory effect of 3-methyl-adenine in cultured rat hepatocytes partially confirmed the role of the lysosomal system in the increase of RNA degradation and its regulation by amino acids.     

Thrombotest mixing experiments in congenital coagulation disorders of the prothrombin complex and in coumarin treated patients. An additional evidence against the presence of an inhibitor in the latter.

Thrombotest clotting times of mixtures of coumarin plasmas and normal plasma yielded a patterm similar to that observed in mixtures of plasma with congenital coagulation disorders and normal plasma. The presence of 10 or 20% of test plasma in the mixture failed to affect the clotting times which resulted in normal limits. The only exception to this rule was the hemophilia BM plasma. In this case even the presence of 10-20% of patient plasma in the mixture caused a prolongation of the clotting time. This indicates that no inhibitor is present in coumarin plasmas and in the plasma of congenital coagulation disorders of the prothrombin complex save for hemophilia BM plasma which does contain an inhibitor.     

Optimization of ascorbic and uric acid separation in human plasma by free zone capillary electrophoresis ultraviolet detection

In this paper we propose a new fast free zone capillary electrophoresis method for the simultaneous determination of ascorbic acid (AA) and uric acid (UA) in human plasma. We investigated the effect of analytical parameters, such as concentration and pH of borate running buffer, cartridge temperature, and sample treatment, on resolution, migration times, corrected peak areas, and efficiency. A good separation was achieved using a 60.2-cmx75-microm uncoated silica capillary and 100 mmol/L sodium borate buffer, pH 8, when metaphosphoric acid was employed as protein precipitant, in less than 4 min. These conditions gave a good reproducibility of migration times (CV 0.35 and 0.34%) and peak areas (CV 3.2 and 3.1%) for ascorbate and urate, respectively. The limit of detection was 0.5mg/L for both analytes when the detection was performed at 254 nm for AA and at 292 nm for UA. We compared the present method with a validated capillary electrophoresis assay by measuring plasma urate and ascorbate in 32 normal subjects and the obtained data were analyzed by the Passing and Bablok regression.     

血浆是引起血沉增快的主要因素

目的：阐明血沉增快的原因是血浆还是红细胞。方法：收集72例血沉异常的抗凝血标本,同时收集血型相对应的72例血沉正常标本,组成血型相同的血沉异常和正常标本72对,每对互换血浆后重新测定血沉,与原始血沉结果比较,并通过多元线性回归分析血沉与血浆蛋白及血脂浓度的关系。结果：血沉异常标本的红细胞加入血沉正常标本的血浆后,72例（100%）血沉均减慢,其中30例血沉下降90%以上,35例下降70%-90%,7例小于70%。血沉正常标本的红细胞加入血沉异常标本的血浆后,67例（93%）血沉加快,其中58例（81%）变为异常（18例血沉加快10倍以上,40例加快5-10倍）。球蛋白、白蛋白和纤维蛋白原与血沉具有线性关系,球蛋白（r=0.420,P〈0.001）和纤维蛋白原（r=0.673,P〈0.001）与血沉呈正相关,而白蛋白（r=-0.558,P〈0.001）与血沉呈负相关。结论：血沉增快主要与血浆因素相关,红细胞对于血沉的影响作用很小。     

Suspension cultures of human malignant lymphoma in the leukocyte migration test

The effects of supernatants of primary and secondary malignant human lymphoma cell cultures were analyzed as parameters of spontaneous secretion of factors by these cells using the leukocyte migration test (LMT). Spontaneous cultivation for up to five weeks was successful in four cases. The postulated production of mediators, i.e. the inhibitory and stimulating effects on leukocyte migration were characterized by testing the influence of (a) concentration, (b) temperature and (c) absorption with normal blood leukocytes on the effect. Reproducible stimulatory and inhibitory effects on the migration of normal leukocytes were dependent on concentration and temperature and were apparently mediated by one or more factors. The supernatants of a lymphoblastic lymphosarcoma of the T-cell type and of a lymphoblastic lymphosarcoma clearly revealed congruous and reproducible inhibitory effects. A further case of lymphoblastic lymphosarcoma that could not exactly be defined with immunological methods either and a case of centroblastic/centrocytic lymphosarcoma exhibited stimulating effects which could be reduced in a time-dependent manner through preincubation with blood leukocytes. The results of these studies support the assumption that malignant lymphoma cells are capable not only of secreting immunoglobulin, but also of other biologically effective secretion. The effects of such secretion are differentiated into stimulating and inhibitory ones. They might be important for the spreading of a tumor or for resistance of the organism to the disease.     

Susceptibility of mice to Trypanosoma evansi treated with human plasma containing different concentrations of apolipoprotein L-1

The aim of this study was to test the susceptibility of mice to Trypanosoma evansi treated with human plasma containing different concentrations of apolipoprotein L-1 (APOL1). For this experiment, a strain of T. evansi and human plasma (plasmas 1, 2, and 3) from 3 adult males clinically healthy were used. In vivo test used 50 mice divided in 5 groups (A to E) with 10 animals in each group. Animals of groups B to E were infected, and then treated with 0.2 ml of human plasma in the following outline: negative control (A), positive control (B), treatment with plasma 1 (C), treatment with plasma 2 (D), and treatment with plasma 3 (E). Mice treated with human plasma showed an increase in longevity of 40.9 ± 0.3 (C), 20 ± 9.0 (D) and 35.6 ± 9.3 (E) days compared to the control group (B) which was 4.3 ± 0.5 days. The number of surviving mice and free of the parasite (blood smear and PCR negative) at the end of the experiment was 90%, 0%, and 60% for groups C, D, and E, respectively. The quantification of APOL1 was performed due to the large difference in the treatments that differed in the source plasma. In plasmas 1, 2, and 3 was detected the concentration of 194, 99, and 115 mg/dl of APOL1, respectively. However, we believe that this difference in the treatment efficiency is related to the level of APOL1 in plasmas.     

叶下珠有效部位对血栓形成的影响及其作用机制初探

采用Born方法和改良的Hamburger方法分别测定叶下珠 (Phyllanthusurinaria)含corilagin的有效部位 (代号PUW )在体内外对血小板聚集功能和对血小板与中性粒细胞之间粘附反应的影响 ;应用Myers方法评价PUW灌胃对小鼠尾静脉注射花生四烯酸 (AA)引起猝死的保护作用 ;运用改良的Charl ton方法及陈长勋等方法分别观察PUW灌胃对电刺激大鼠颈动脉血栓形成和下腔静脉血栓形成的影响 ;采用Tomihisa方法 ,观察PUW对大鼠尾尖出血时间的影响。结果显示 ,PUW在体内外对ADP、AA或血小板活化因子 (PAF)诱导的血小板聚集均无明显抑制作用 ;PUW呈浓度依赖性明显阻抑AA激活的血小板与中性粒细胞之间的粘附反应 ,其半数抑制浓度 (IC50 )为 39 7mg/kg。PUW (10、2 0和 4 0mg/kg)灌胃呈剂量依赖性显著减少AA致小鼠死亡的数量 ,明显延长电刺激大鼠颈动脉血栓形成时间 ,减轻大鼠下腔静脉血栓的干、湿重。 2 0mg/kg的PUW对出血时间无明显影响 ,4 0mg/kg的PUW虽延长出血时间 ,但与阿司匹林 (2 0mg/kg)比较 ,出血时间明显缩短 (P <0 0 5 )。本实验结果提示 ,PUW灌胃在多种体内血栓模型中均具有明显的抗血栓形成作用 ,其机制可能与阻抑血小板和中性粒细胞之间的的粘附作用密切相关。     

Elimination of clonogenic tumor cells from bone marrow using methylprednisolone (MP) and etoposide VP16: an in vitro pharmacologic study

The ability to eliminate malignant cells from bone marrow (BM) while retaining sufficient numbers of normal progenitors to ensure engraftment, may well establish the future of autologous BM transplantation (ABMT) for hematologic malignancies. In this study, we describe the effects of methylprednisolone (MP) and etoposide (VP16) alone or in combination on 5 tumor cell lines (HL-60, a promyelocytic cell line; Molt-4, a T cell leukemia; Daudi, a Burkitt's lymphoma and R10/8226 and R40/8226, doxorubicin-resistant myeloma cell lines). The tumor cell kill efficiency of the drugs was assayed using the limiting dilution assay. We determined the toxic effect on progenitor cells by assaying granulocyte-macrophage colony-forming units (CFU). With a combination of MP at 10(-3) M and VP16 at 75 microM, we observed the following log reduction in tumor cell clones: HL-60, 4.695 +/- 0.001; Molt-4, 3.626 +/- 0.036; Daudi, 5.633 +/- 0.001; R10/8226, 3.052 +/- 0.544; R40/8226, 3.126 +/- 0.080. CFU recovery was 24% +/- 5%. Mixing tumor cell lines with a 20-fold excess of normal irradiated BM cells did not eliminate the inhibitory effect of the drug combination. We propose that MP and VP16 used in concert produce effective purging of malignant hematopoietic cells from BM while sparing normal progenitors needed for engraftment.     

Syntheses of 2,4,6-trisubstituted pyrimidine derivatives as a new class of antifilarial topoisomerase II inhibitors

A series of 21 compounds of trisubstituted pyrimidine derivatives have been synthesized and evaluated for their in vitro topoisomerase II inhibitory activity against filarial parasite Setaria cervi. Out of these, seven compounds (8, 11-14, 25 and 28) have shown 60-80% inhibition at 40 and 20 microg/mL concentration. Five compounds (12, 13, 14, 25 and 28) exhibited 70-80% inhibition at 10 microg/mL concentration and three compounds (13, 14 and 28) have shown 40-60% inhibition at 5 microg/mL concentration. All the above mentioned compounds have shown better topo II inhibitory activity than standard antifilarial drug (DEC) and enzyme topo II inhibitors (Novobiocin, Nalidixic acid).     

溶氧水平对红豆杉细胞悬浮培养的影响研究

紫杉醇 (Ｔａｘｏｌ)是源自红豆杉提取物的一种高度衍生化的二萜类化合物 ,临床实验结果表明紫杉醇对于卵巢癌、乳腺癌、胃肠道癌等具有明显的抗肿瘤活性[1] ,因而受到世界各国的广泛关注 ,并已被美国食品与药品管理局 (ＦＤＡ)批准用于卵巢癌与乳腺癌的治疗[2 ] 。到目前为止紫杉醇仍然主要从树皮中提取 ,但由于红豆杉生长缓慢 ,天然资源非常有限 ,加快其替代来源的研究势在必行。利用植物细胞悬浮培养生产紫杉醇作为一种可行的选择 ,近年来取得了较大的进展[3 ,4 ] 。本文研究了摇瓶及 2 0 Ｌ反应器培养过程的溶氧水平对细胞生长及紫杉醇…     

Physiologic inhibition of human activated protein C by alpha 1-antitrypsin

The plasma antithrombotic enzyme activated protein C (APC) has two major plasma inhibitors. One is heparin-dependent, has been characterized, and is known as protein C inhibitor. The second inhibitor was isolated based on its heparin-independent ability to inhibit and complex with APC. The purified inhibitor had the amino acid composition and NH2 terminus of alpha 1-antitrypsin and reacted with monoclonal antibodies to alpha 1-antitrypsin. The inhibitor was greater than 95% pure alpha 1-antitrypsin as judged by electroimmunoassay, inactivation of trypsin, and electrophoresis in two gel systems. To identify the second major plasma inhibitor of APC, immunoblot studies of enzyme-inhibitor complexes were made to compare APC addition to normal plasma and to plasma deficient in protein C inhibitor or alpha 1-antitrypsin. The results showed that alpha 1-antitrypsin is the second major plasma APC inhibitor. Given the association rate constant of alpha 1-antitrypsin for APC of 10 M-1 s-1 and its plasma concentration of approximately 40 microM, it accounts for approximately half of the heparin-independent APC inhibitory activity of plasma. Based on immunoblot analysis plasmas of 15 patients with intravascular coagulation contained APC-alpha 1-antitrypsin complexes suggesting that this inhibition reaction occurs in vivo. Thus, alpha 1-antitrypsin is a major physiologic inhibitor of APC.     

Negative regulation of epithelium-neutrophil interactions via activation of CD44

Polymorphonuclear neutrophil (PMN) migration across epithelia is a common feature of active inflammation. Given the suggested role of carbohydrates in this process, we examined the receptor CD44. The standard CD44 isoform was expressed at the cell surface of PMN. PMN migration across model polarized intestinal epithelia was reduced (by 60%) if the CD44 receptor was activated by either a specific antibody (clone IM7) or the natural soluble ligand, hyaluronic acid. This inhibitory effect following receptor activation occurred with both basolateral-to-apical- and apical-to-basolateral-directed migration. The anti-CD44 antibody similarly reduced PMN migration through filters in the absence of epithelia, while preincubation of the antibody with the epithelium did not alter subsequent PMN transepithelial migration. These data suggest that PMN, rather than epithelial, CD44 is responsible for these effects. A similar inhibitory effect of anti-CD44 antibody was also observed on migration of intraepithelial lymphocytes. The molecular mechanism involved in such negative signaling following CD44 activation may include modulation of outside-in cell signaling. While neither the anti-CD44 antibody nor CD44 ligand affected PMN mobilization of intracellular Ca(2+), both led to increased adenylate cyclase activity, an inhibitory signal for PMN migration. Together, these results suggest that CD44 of PMN may potentially serve as a negative regulator of leukocyte migration across biological surfaces such as columnar epithelia.     

Effect of thalidomide affecting VEGF secretion, cell migration, adhesion and capillary tube formation of human endothelial EA.hy 926 cells

Angiogenesis, new blood vessel formation, is a multistep process, precisely regulated by pro-angiogenic cytokines, which stimulate endothelial cells to migrate, proliferate and differentiate to form new capillary microvessels. Excessive vascular development and blood vessel remodeling appears in psoriasis, rheumatoid arthritis, diabetic retinopathy and solid tumors formation. Thalidomide [alpha-(N-phthalimido)-glutarimide] is known to be a potent inhibitor of angiogenesis, but the mechanism of its inhibitory action remains unclear. The aim of the study was to investigate the potential influence of thalidomide on the several steps of angiogenesis, using in vitro models. We have evaluated the effect of thalidomide on VEGF secretion, cell migration, adhesion as well as in capillary formation of human endothelial cell line EA.hy 926. Thalidomide at the concentrations of 0.01 microM and 10 microM inhibited VEGF secretion into supernatants, decreased the number of formed capillary tubes and increased cell adhesion to collagen. Administration of thalidomide at the concentration of 0.01 microM increased cell migration, while at 10 microM, it decreased cell migration. Thalidomide in concentrations from 0.1 microM to 10 microM did not change cell proliferation of 72-h cell cultures. We conclude that anti-angiogenic action of thalidomide is due to direct inhibitory action on VEGF secretion and capillary microvessel formation as well as immunomodulatory influence on EA.hy 926 cells migration and adhesion.     

The membrane attack complex in complement-mediated glomerular epithelial cell injury: formation and stability of C5b-9 and C5b-7 in rat membranous nephropathy

Using a model of rat membranous nephropathy (MN), we examined the relationship between the development of glomerular epithelial cell injury and the formation and stability of the membrane attack complex (MAC) of complement. Isolated rat kidneys were perfused with buffered bovine albumin (BSA) or various plasmas (complement source). Kidneys containing nephritogenic amounts of complement-fixing sheep antibody to glomerular epithelial antigens (aFx1A) perfused with BSA (n = 5), and normal kidneys perfused with normal human plasma in BSA (50% v/v, n = 6) excreted 0.30 +/- 0.02 mg protein/min/g during 90 min perfusion (control groups). When normal plasma was added to the perfusate of aFx1A kidneys at concentrations of 12.5, 25, and 50% v/v, protein excretion rose in a time- and concentration-dependent manner. Perfusions with 25% plasma resulted in baseline proteinuria from 0 to 20 min that increased to 2.8 +/- 0.9 mg/min/g at 20 to 40 min and 8.6 +/- 2.1 at 40 to 60 min (n = 4, p less than 0.01 vs control groups). Removal of plasma at 20 min did not prevent this rise in protein excretion (3.9 +/- 2.4 and 5.8 +/- 2.6 mg/min/g at 30 to 40 and 55 to 65 min respectively, p less than 0.01, n = 4). Perfusion of aFx1A kidneys with C8-deficient (C8D) human plasma (25% v/v, n = 4) or C6D rabbit serum (25% v/v, n = 2) independently produced low levels of proteinuria comparable with BSA, but in combination, the two reagents restored enhanced protein excretion (n = 2). In aFx1A kidneys containing C5b-7, addition of C8 and C9 (C6D serum) after intervals of 20, 60, or 90 min immediately reconstituted heavy proteinuria. Thus, the magnitude of MAC-induced glomerular epithelial injury in rat MN is related to the complement dose. Altered glomerular permeability is delayed with respect to the onset of complement activation. Once sufficient C5b-9 is formed, proteinuria can develop despite cessation of new MAC assembly, implying that C5b-9 persists after formation. Moreover, the C5b-7 MAC intermediate is not eliminated rapidly in this model.     

Model of disseminated intravascular coagulation

Vascular-thrombocytic and plasma hemostasis was studied in dogs after blood loss (40--50 ml/kg weight) and subsequent hypervolemic (60--65 ml/kg weight) transfusion of homologous (from 3 donors) platelet and leukocyte rich in plasma. After a short phase of hypercoagulation all the tested dogs displayed hypocoagulation accompanied by a decrease in the count of platelets and a fall of their aggregation function, prolongation of bleeding time, diminution of capillary wall resistance, a decrease of plasma fibrinogen concentration and factor XIII activity, and by a rise of blood fibrinolytic activity. The data obtained show the development of the acute disseminated intravascular coagulation syndrome (DIC). DIC model is porposed on the basis of the results obtained.     

Gene cloning of a new plasma CC chemokine, activating and attracting myeloid cells in synergy with other chemoattractants

Chemokines are important mediators of cell migration during inflammation and normal leukocyte trafficking. Inflammatory chemokines are induced in multiple cell types at sites of infection. Here, we describe a novel bovine CC chemokine, designated regakine-1, that is constitutively present at high concentrations in plasma. Cloning of its gene revealed an expected two intron/three exon organization, with a rather long first intron. In addition to a 21-residue signal peptide, the coding sequence corresponded to a 71-residue secreted protein. However, the natural regakine-1 protein missed the COOH-terminal lysine residue. Regakine-1 has only weak sequence similarity (<50% identical residues) with other animal or human chemokines. Northern blot analysis demonstrated regakine-1 RNA expression in spleen and lung. At physiological concentrations (30-100 ng/mL), natural 7.5 kDa regakine-1 stimulated gelatinase B release from neutrophils and chemoattracted immature myeloid HL-60 cells, as well as mature granulocytes. Regakine-1 was more potent on human myeloid cells than the human plasma CC chemokine hemofiltrate CC chemokine-1 (HCC-1). Moreover, regakine-1 synergized with the bacterial peptide N-formylmethionylleucylphenylalanine (fMLP), yielding a 10-fold increase in neutrophil chemotactic response above their additive effect. Regakine-1 did not compete with interleukin-8 (IL-8) for binding to neutrophils, nor did it affect fMLP-induced calcium signaling, suggesting that regakine-1 recognizes a different receptor. In view of its high constitutive plasma concentration, regakine-1 is believed to recruit myeloid cells into the circulation, whereas its synergy with other neutrophil chemoattractants suggests that it also enhances the inflammatory response to infection.     

Resolution of rat renin substrates by isoelectric focusing.

Pooled plasmas from normal or binephrectomized rats and perfusates of isolated livers were used as sources of renin substrate for isoelectric focusing. After desalting, preliminary fractionation (plasma only), and concentration, the preparations were focused in a pH 3--10 gradient on 20-cm glass plates layered with Sephadex slurry. The pH 4--6 region, containing all the substrate, was scraped from this plate and refocused in a pH 4--6 gradient. Substrate content of 1-cm strips of slurry from half of the plate was determined by both radioimmunoassay and bioassay of angiotensin resulting from incubation with added renin. Corresponding strips from the other half of the plate were incubated without renin as a control for any preformed angiotensin. The asymmetry and broad distribution (pH 4--5) of substrate from different sources suggested the existence of more than one form. Higher resolution achieved by using the high substrate concentration of postnephrectomy plasma and 0.5-cm strips of slurry on 20-cm or 40-cm plates revealed peaks and shoulders of substrate activity. Our data suggest that multiple forms of substrate are synthesized by the liver and circulate in plasma. Postnephrectomy rat plasma appears to contain relatively more substrate(s) with higher isoelectric points than in normal plasma, possibly an accumulation of forms ordinarily degraded by endogenous renal renin.     

杂交粳稻超高产群体的冠层结构特点研究

研究了杂交粳稻超高产群体的苗穗粒结构及干物重在冠层不同层次、不同器官的分布,叶面积配置及光强分布等冠层结构特点．结果表明,杂交粳稻超高产群体冠层总干物重及40cm以下、40～60cm、60～80cm和80cm以上4个层次的干物重分别比常规粳稻高32．29％及29．12％、13．95％、16．45％和100．17％．杂交粳稻叶片(同化器官)与穗(库器官)干重分别占总干物重的248％与12．8％．高于常规稻;而叶鞘与茎(贮藏器官)的干重分别占总干物重的33．6％和28．9％,低于常规粳稻．杂交粳稻超高产群体冠层叶面积配置比较合理,齐穗期40cm以上冠层LAI达5．44．冠层光强上下分布比较均匀,60cm以下冠层光强比常规稻高13．1％～37．0％,而60cm以上冠层光强比常规稻低5．9％～12．2％;20cm、20～40cm、40～60cm和60～80cm各层消光系数分别比常规粳稻低35．1％、13．5％、29．1％和17．2％．