35例艾滋病患者高效联合抗反转录病毒治疗后血脂代谢及颈动脉中层厚度的研究

目的 研究获得性免疫缺陷综合征[艾滋病(AIDS)]患者经高效联合抗反转录病毒治疗(Highly active antiretroviral therapy,HAART)后所导致的血脂及心血管方面的副作用.方法 回顾性调查在我院治疗并门诊随访的35例男性人类免疫缺陷病毒1型(HIV-1)感染者,均接受相同HAART方案(d4T+3TC+EFV),平均年龄为38.5±15.3岁,平均抗病毒时间为24.6±17.5月,抗病毒治疗前平均CD4计数为69.5±34.6个/μl,比较抗病毒治疗前、后患者空腹血脂变化(包括三酰甘油、总胆固醇、高密度脂蛋白、低密度脂蛋白)并进行统计学分析.其中22例在本系列研究最后1次血脂测定时接受高分辨B超测定颈动脉内膜中层厚度(IMT)测定.结果 35例AIDS患者HAART前、后血三酰甘油分别为1.44±0.35mmol/L和2.07±0.54mmol/L(P ＜0.001);总胆固醇分别为4.96±0.46mmol/L和6.15±0.83mmol/L(P＜0.001);血高密度脂蛋白分别为1.06±0.01mmol/L和 1.04±0.01mmol/L(P＞0.05);血低密度脂蛋白分别为2.29±0.33 mmol/L和3.11±0.29mmol/L(P＜0.001).22例患者经Philips5000彩色B超仪测定IMT平均为0.86±0.14 mm,明显高于文献报道的正常值0.7±0.2mm.结论 HAART治疗艾滋病患者与血脂代谢异常及部分心血管并发症相关.     

apoE_4近交系转基因鼠的高脂血症表现和自发变换行为损害

建立相关疾病的动物模型 ,研究apoE4在脂质代谢和早老性痴呆等疾病中的作用 .通过显微注射法建立人apoE4近交系转基因鼠 .经Southern和Northern印迹杂交 ,鉴定apoE4基因的整合与表达 .98只新生鼠中鉴定出 2只首建鼠 ,定名为TgN(apoE4) 1QiL和TgN(apoE4) 2QiL .外源基因整合的拷贝数分别为 1和 2 .F1代杂合鼠的脑 ,肾脏 ,心脏和肝脏中均有人apoE4基因的表达 .血清脂质水平通过酶法检测 ,自发变换行为经Y迷宫试验检测 .转基因鼠的血清胆固醇和甘油三酯明显升高 ,自发变换行为受到损害 .结果表明 ,近交系转基因鼠过量表达人apoE4基因可导致血清脂质升高 ,并对其空间记忆能力造成损害 .     

中老年男性患者血脂代谢特点及与年龄等因素的相关分析

目的:探讨中老年男性患者血脂代谢特点及与年龄等因素的相关性。方法:资料来自2006年6月于我院干部门诊进行健康查体的1603例中老年男性患者(排除正在服用降脂药物的患者),采用全自动生化分析仪对血清总胆固醇(TC)、血清甘油三酯(TG)、血清低密度脂蛋白胆固醇(LDL-c)、血清高密度脂蛋白胆固醇(HDL-c)、空腹血糖(FBG)、血肌酐(Cr)及血尿酸(UA)等指标进行测定,同时记录身高、体重及血压等基本资料。结果:入选患者血脂异常总检出率为56.27%,其中TC、TG、HDL-c及LDL-c异常检出率分别为36.74%、28.20%、10.79%及6.92%,以TC、TG异常为主。与50~59岁组相比,80岁以上高龄老年组TG异常及HDL-c异常检出率显著降低,TC及TG水平显著降低,HDL-c水平显著升高(P<0.05)。在校正BMI、SBP、DBP、UA、FBG及CCr等危险因素影响后的多元线性回归分析发现,年龄每升高10岁,TC、TG分别降低约0.097 mmol/L及0.087 mmol/L,HDL-c升高约0.113 mmol/L。结论:中老年男性患者血脂异常以高TC和高TG为主,TC、TG与年龄呈负相关,HDL-c与年龄呈正相关,需针对高龄老年患者血脂代谢特点进行合理调脂治疗。     

超滤得到的海蜇酶解产物的降血脂功能评价

目的:探讨超滤对于海蜇酶解产物降血脂功能的提高作用。方法:海蜇通过中性蛋白酶酶解后,将超滤过的酶解产物和未超滤的酶解产物分别按照高、中、低三个剂量组喂食高血脂症大鼠模型42d,测定各组血脂水平并进行对照分析。结论:未超滤组的高、中剂量组和超滤组高中低剂量组喂食42d后均观察到大鼠血清总胆固醇(TC)、甘油三酯(TG)的降低,其中未超滤中剂量组(灌胃剂量5 mg/kg.BW)血清总胆固醇(TC)值为2.45±0.28mmol/L,超滤低剂量组(灌胃剂量0.3mg/kg.BW)血清总胆固醇(TC)值为2.61±0.33mmol/L,均明显低于高脂模型对照组(3.38±0.22 mmol/L),未超滤低剂量组(灌胃剂量3mg/kg.BW)血清总胆固醇(TC)值为2.82±0.38mmol/L,相对于高脂模型对照组(3.38±0.22 mmol/L)无显著差异;未超滤中剂量组(灌胃剂量5 mg/kg.BW)甘油三酯(TG)值为0.90±0.21mmol/L,超滤低剂量组(灌胃剂量0.3mg/kg.BW)甘油三酯(TG)值为0.93±0.14 mmol/L,均明显低于高脂模型对照组(1.21±0.20 mmol/L),未超滤低剂量组(灌胃剂量3mg/kg.BW)甘油三酯(TG)值为1.18±0.12mmol/L,相对于高脂模型对照组(1.21±0.20 mmol/L)无显著差异。结论:海蜇多肽的酶解产物具有降血脂功能,超滤能够有效提高海蜇酶解产物的降血脂活性。     

野生猕猴应激与抗应激的研究

本文以野生猕猴为实验对象 ,以血清皮质醇含量为指标 ,研究了野生猕猴被捕获与给予氯丙嗪、Vc 等药物后上述指标的变化。结果表明 :(1)野生猕猴在被捕获后的 1～ 2周内 ,血清皮质醇一直维持在一个高水平状态 (2 4 78± 0 2 0 μg/dl,2 4 88± 0 5 8μg/dl) ;(2 )氯丙嗪可使动物行为处于一种安静状态 ,但并不降低血清皮质醇水平 (2 8 73± 6 16 μg/dl) ,(3)Vc 可改善动物的精神状态 ,使血清皮质醇略低 (2 1 0 0± 2 90 μg/dl) (P >0 0 5 ) ,(4)氯丙嗪和Vc 合用后 ,血清皮质醇与单独使用氯丙嗪无明显差异 (2 8 0 7± 4 45 μg/dl)。     

化痰脉通片对高脂血症大鼠血脂、肝功能、脂肪肝的影响

目的:探讨国医大师沈宝藩临床运用三十余年的化痰脉通片对高脂血症大鼠脂肪肝、肝功能的干预效果,了解其改善肝功能,治疗脂肪肝作用疗效。方法:选取SD大鼠75只,随机分为正常组、模型组、氟伐他汀组、化痰脉通中剂量组、化痰脉通高剂量组,每组15只,观察对比各组治疗后血脂水平、肝功能的变化,并通过病理切片,对比各组脂肪肝疗效。结果:正常组、氟伐他汀组、化痰脉通中剂量组、化痰脉通高剂量组总胆固醇(TC)、甘油三酯(TG)、低密度脂蛋白胆固醇(LDL-C)均显著低于模型组(P0.05),而高密度脂蛋白胆固醇(HDL-C)显著高于模型组(P0.05);正常组及化痰脉通高剂量组TC、TG、LDL-C均显著低于化痰脉通中剂量组及氟伐他汀组(P0.05),而HDL-C显著高于化痰脉通中剂量组及氟伐他汀组(P0.05),且化痰脉通中剂量组及氟伐他汀组血脂水平无显著性差异(P0.05);正常组TC、TG、LDL-C[(1.28±0.38)mmol/L,(0.40±0.16)mmol/L,(0.39±0.07)mmol/L]显著低于化痰脉通高剂量组[(5.18±1.42)mmol/L,(0.51±0.24)mmol/L,(2.07±0.46)mmol/L](P 0.05),而HDL-C[(3.78±0.34)mmol/L]显著高于化痰脉通高剂量组[(2.89±0.78)mmol/L](P0.05)。正常组、氟伐他汀组、化痰脉通中剂量组、化痰脉通高剂量组丙氨酸转氨酶(ALT)、谷草转氨酶(AST)均显著低于模型组(P0.05);正常组[(10.38±1.46)mmol/L,(10.85±1.24)mmol/L]、化痰脉通中剂量组[(15.97±3.64)mmol/L,(16.52±1.18)mmol/L]、化痰脉通高剂量组[(10.54±1.01)mmol/L,(10.62±1.67)mmol/L]AST、ALT均显著低于较氟伐他汀组[(25.47±2.38)mmol/L,(21.34±2.39)mmol/L](P0.05),而组间AST、ALT比较无显著性差异,不具有统计学意义(P0.05)。在肝脏病理切片的对比中,随着化痰脉通片剂量的增加,脂肪肝的程度减轻。结论:化痰脉通片具有良好的降脂效果,且与剂量有关,其对肝功能具有良好的保护作用并对脂肪肝具良好的治疗作用,其治疗机制可能与调脂作用有关。     

兰州地区健康体检者血脂水平分析

目的:通过检测兰州地区健康体检者空腹血脂水平了解本地区人群血脂水平现状及血脂异常情况,建立本地区血脂参考值。方法:采用全自动生化分析仪检测兰州市2328名健康体检者,血清胆固醇(TC)、甘油三酯(TG)、高密度脂蛋白胆固醇(HDL-C)、低密度脂蛋白胆固醇(LDL-C)。比较不同年龄、性别血脂水平差异。结果:本地区2328名被检者,女性TC平均(4.54±0.94)mmol/L,TG中位数1.24mmol/L、HDL-C平均(1.34±0.26)mmol/L、LDL-C平均(2.61±0.76)mmol/L;男性TC平均(4.52±0.84)mmol/L、TG中位数1.56mmol/L mmol/L、HDL-C平均(1.20±0.23)mmol/L LDL-C平均(2.76±0.72)mmol/L,血脂水平随年龄增加逐渐升高(P<0.05)。血脂参考范围为女性TC:2.70~6.38 mmol/L、TG:0.52~3.66 mmol/L、HDL-C:0.83~1.85 mmol/L、LDL-C:1.12~4.10 mmol/L男性:TG:2.87~6.17 mmol/L、0.65~4.00 mmol/L、0.75~1.65 mmol/L、1.35~4.17 mmol/L。男性高TC、高TG、低HDL-C和高LDL-C患病率为18.2%、42.8%、19.6%和28%,女性高TC、高TG、低HDL和高LDL的患病率分别为22.1%、25.5%、2.7%和23.5%。结论:兰州地区血脂水平随年龄、性别、地区不同存在较大差异,临床上不能采用统一标准衡量,而应根据本地区建立的参考值诊断高脂血症。积极控制血脂水平、降低高脂血症患病率预防心脑血管疾病发生。     

降浊颗粒预防性给药对实验性高脂血症大鼠血脂含量的影响

目的:研究降浊颗粒对实验性高脂血症大鼠血脂含量的影响。方法:采用高脂高胆固醇饲喂大鼠4周,建立大鼠高脂血症模型,造模同时给药,分别于给药第2、4周后剪尾取血,检测血清中总胆固醇(TC)、甘油三酯(TG)、高密度脂蛋白胆固醇(HDL-C)和低密度脂蛋白胆固醇(LDL-C)含量。结果:降浊颗粒分别以800mg/kg、400mg/kg和200mg/kg给大鼠预防性灌胃2周及4周时,均具有明显降低高脂模型动物血清TC、TG和LDL-cho含量,同时使TC/HDL-cho比值也明显降低的作用(与模型组比较分别为(P<0.001;P<0.01或P<0.05),并具有良好的量-效关系。结论:降浊颗粒可明显抑制实验性大鼠高脂血症的形成,主要能明显降低血清总胆固醇、甘油三酯和低密度脂蛋白胆固醇含量。     

马麝生理生化正常值的测定

对甘肃兴隆山国家级自然保护区人工养麝场的马麝 3项临床指标、6项血液生理指标和 1 3项血清生化指标进行了测定。结果表明 ,成麝体温为 ( 39 94± 0 87)℃ ,呼吸 ( 1 2 4 67± 1 7 2 9)次 min ,心率( 1 2 4 67± 1 7 2 9)次 min;红细胞 ( 2 0 1 9± 4 95 )× 1 0 12 L ,白细胞计数 ( 1 2 4 76± 5 4 96)× 1 0 9 L ,PCV 0 5 78±0 0 3;血糖 ( 8 2 64± 2 0 5 6)mmol L ,K( 4 4 85± 0 2 4 3)mmol L ,Na ( 1 38 2± 1 6 64)mmol L ,Ca ( 2 75 8± 0 31 )mmol L ,总蛋白 ( 74 70 5± 8 1 5 9)g L ,白蛋白 ( 5 2 77± 2 2 32 )g L ,球蛋白 ( 2 1 4 8± 7 2 76)g L等。     

高复制HBV转基因小鼠模型对抗病毒药物拉米夫定评价的研究

[目的]探讨乙型肝炎病毒(HBV)转基因小鼠模型筛选抗HBV药物的可行性。[方法]用公认抗HBV复制药物拉米夫定对我们建立高复制HBV转基因鼠进行实验,选我们建立的1.3copy高复制HBV转基因小鼠20只,随机分成两组,每组10只。采用灌胃针灌胃法给药。对照组灌喂生理盐水,实验组灌喂拉米夫定,剂量为100mg/kg,每天2次,连续灌21d,每7d采血1次。荧光定量PCR检测血清中HBVDNA。[结果]实验组用拉米夫定前小鼠血清HBVDNA5.50±0.42(拷贝数log10数值),3周后HBVDNA已显著降低(4.63±0.57),4周后,小鼠血清HBVNDA为4.08±0.51,停药1周后,再次检测血清HBVDNA,小鼠血清HBVDNA又恢复正常水平(5.70±0.39)。[结论]我们建立的高复制HBV转基因小鼠模型验证了拉米夫定对HBV复制的抑制程度和持续时间,表明该模型可应用于抗HBV药物的筛选、评价研究。     

甲型H1N1流感病毒在季流病毒、禽流感病毒共感染时变异可能性的验证

目的 甲型H1N1流感病毒A/California/7/2009分别与A/Brisbane/10/07和A/ShenZhen/406H/06共感染小型香猪,预测甲流病毒在与季流H3N2病毒/甲流病毒与禽流感病毒共感染时是否会发生变异.方法 分别将A/California/7/2009(CA7)与A/Brisbane/10/07(H3N2),A/California/7/2009与A/Shenzhen/406H/06(H5N1)对5～6月龄小型猪共感染,小型猪经复方氯胺酮0.1 mL/kg麻醉后进行滴鼻感染,感染后第5天安乐死动物,取动物肺组织作病毒测序分析.结果 A/California/7/2009(CA7)与A/Brisbane/10/07(H3N2)共感染后,A/California/7/2009病毒PB1基因993位G→A突变,PA基因1659位G→A突变,没有氨基酸的变异.A/California/7/2009与A/Shenzhen/406H/06(H5N1)共感染后A/California/7/2009病毒PB2基因1711位T→C突变.碱基的突变未引起氨基酸的变异.结论 A/California/7/2009(CA7)与A/Brisbane/10/07(H3N2),A/California/7/2009与A/Shenzhen/406H/06(H5N1)共感染后在猪的体内没有发生病毒重组、变异.     

Pathogenesis of primary defects in mitochondrial ATP synthesis

Maternally inherited mutations in the mtDNA-encoded ATPase 6 subunit of complex V (ATP synthase) of the respiratory chain/oxidative phosphorylation system are responsible for a subgroup of severe and often-fatal disorders characterized predominantly by lesions in the brain, particularly in the striatum. These include NARP (neuropathy, ataxia, and retinitis pigmentosa), MILS (maternally inherited Leigh syndrome), and FBSN (familial bilateral striatal necrosis). Of the five known pathogenic mutations causing these disorders, four are located at two codons (156 and 217), each of which can suffer mutations converting a conserved leucine to either an arginine or a proline. Based on the accumulating data on both the structure of ATP synthase and the mechanism by which rotary catalysis couples proton flow to ATP synthesis, we propose a model that may help explain why mutations at codons 156 and 217 are pathogenic.     

Glycoprofiling with micro-arrays of glycoconjugates and lectins

To facilitate deciphering the information content in the glycome, thin film-coated photoactivatable surfaces were applied for covalent immobilization of glycans, glycoconjugates, or lectins in microarray formats. Light-induced immobilization of a series of bacterial exopolysaccharides on photoactivatable dextran-coated analytical platforms allowed covalent binding of the exopolysaccharides. Their specific galactose decoration was detected with fluorescence-labeled lectins. Similarly, glycoconjugates were covalently immobilized and displayed glycans were profiled for fucose, sialic acid, galactose, and lactosamine epitopes. The applicability of such platforms for glycan profiling was further tested with extracts of Caco2 epithelial cells. Following spontaneous differentiation or on pretreatment with sialyllactose, Caco2 cells showed a reduction of specific glycan epitopes. The changed glycosylation phenotypes coincided with altered enteropathogenic E. coli adhesion to the cells. This microarray strategy was also suitable for the immobilization of lectins through biotin-neutravidin-biotin bridging on platforms functionalized with a biotin derivatized photoactivatable dextran. All immobilized glycans were specifically and differentially detected either on glycoconjugate or lectin arrays. The results demonstrate the feasibility and versatility of the novel platforms for glycan profiling.     

Analysis of the two active sites of the hyaluronan synthase and the chondroitin synthase of Pasteurella multocida

Type A Pasteurella multocida produces a hyaluronan (HA) capsule to enhance infection. The 972-residue HA synthase, pmHAS, polymerizes the linear HA polysaccharide composed of alternating beta3N-acetylglucosamine (GlcNAc)-beta4glucuronic acid (GlcUA). We demonstrated previously that pmHAS possesses two independent glycosyltransferase sites. Here we further define the sites and putative motifs. Deletion of residues 1-117 does not affect HA polymerizing activity. The carboxyl-terminal boundary of the GlcUA-transferase resides within residues 686-703. Both transferase sites contain a DXD motif essential for HA synthase activity. D247N or D249N mutants possessed only GlcUA-transferase activity, whereas D527N or D529N mutants possessed only GlcNAc-transferase activity, further confirming our assignment of the two active sites within the synthase polypeptide. A potential role of the DXD motif in substrate binding was supported by experiments utilizing high UDP-sugar concentrations that partially rescued the activity of certain mutants. The WGGED sequence motif is involved in GlcNAc-transferase activity because mutants with substitutions at E369 or D370 possessed only GlcUA-transferase activity. Type F P. multocida synthesizes an unsulfated chondroitin (beta3GalNAc-beta4GlcUA) capsule. A chimeric enzyme consisting of residues 1-427 of pmHAS and residues 421-704 of pmCS, the homologous chondroitin synthase, was an active HA synthase. The converse chimeric enzyme consisting of residues 1-420 of pmCS and residues 428-703 of pmHAS was a functional chondroitin synthase. Analyses of a panel of pmHAS/pmCS chimeric enzymes identified a 44-residue region, corresponding to pmHAS residues 225-265, involved in UDP-hexosamine selectivity. Overall, these findings further support the model of two independent transferase sites within a single polypeptide.     

Heparin sequencing

Heparin is a highly sulfated glycosaminoglycan widely used as an anticoagulant. Modifications in its relatively uniform structure appear to be key to its recognition and modulation of serine proteases, growth factors, chemokines, and extracellular proteins, as has been most clearly demonstrated in the antithrombin binding site. We sequenced the major oligosaccharides released from mastocytoma heparin by partial nitrous acid using a highly sensitive technique tailored for sequencing of metabolically radiolabeled heparin. It utilizes partial nitrous acid cleavage to allow simultaneous sequencing of the internal components of the oligosaccharide under investigation by specific lysosomal exoenzymes. Sequencing revealed that although the majority of the heparin disaccharides are N-, 2-O-, and 6-O-sulfated, the less sulfated disaccharides (lacking 2-O- or 6-O-sulfates) seem to be spaced out along the chain. The technique may be particularly useful for characterizing heparin from novel sources, such as the glial progenitor cells and Ascidia, as well as for sequencing protein binding sites.     

A new kind of carbohydrate array,its use for profiling antiglycan antibodies,and the discovery of a novel human cellulose-binding antibody

In this study, we use a novel glycan array to analyze the glycan-binding antibody repertoire in a pool of affinity-purified IgG collected from a healthy human population. The glycan array used is based on mono- and oligosaccharides covalently linked to the surface via a long linker at their reducing ends. They are thus presented to the medium with a well-defined orientation and are accessible for specific binding by glycan-binding proteins, such as antibodies and lectins. A novel anticellulose antibody was detected that binds specifically to beta4-linked saccharides with a preference for glucopyranose over galactopyranose residues. We also found previously known antiglycan antibodies against mono- and oligosaccharides that are constituents of commonly occurring bacterial polysaccharides. We propose that this array can facilitate high-throughput screening of glycan-binding proteins and the search for biomarkers for personalized medicine.     

N-glycan branching requirement in neuronal and postnatal viability

The structural variations among extracellular N-glycans reflect the activity of glycosyltransferases and glycosidases that operate in the Golgi apparatus. More than other types of vertebrate glycans, N-glycans are highly branched oligosaccharides with multiple antennae linked to an underlying mannose core structure. The branching patterns of N-glycans consist of three types, termed high-mannose, hybrid, and complex. Though most extracellular mammalian N-glycans are of the complex type, some cells variably express hybrid and high-mannose forms. Nevertheless, a requirement for hybrid and complex N-glycan branching exists in embryonic development and postnatal function among mice and humans inheriting defective Mgat1 or Mgat2 alleles. The resulting defects in formation N-glycan branching patterns cause multiple abnormalities, including neurologic defects, and have inferred the presence of distinct functions for hybrid and complex N-glycan branches among different cell lineages. We have further explored N-glycan structure-function relationships in vivo by using Cre-loxP conditional mutagenesis to abolish hybrid and complex N-glycan branching specifically among neuronal cells. Our findings show that hybrid N-glycan branching is an essential posttranslational modification among neurons. Loss of Mgat1 resulted in a unique pattern of neuronal glycoprotein deficiency concurrent with caspase 3 activation and apoptosis. Such animals exhibited severe locomotor deficits, tremors, paralysis, and early postnatal death. Unexpectedly, neuronal Mgat2 deletion resulting in the loss of complex but not hybrid N-glycan branching was well tolerated without phenotypic markers of neuronal or locomotor dysfunction. Structural features associated with hybrid N-glycan branching comprise a requisite posttranslational modification to neuronal glycoproteins that permits normal cellular function and viability.     

Detailed glycan analysis of serum glycoproteins of patients with congenital disorders of glycosylation indicates the specific defective glycan processing step and provides an insight into pathogenesis

The fundamental importance of correct protein glycosylation is abundantly clear in a group of diseases known as congenital disorders of glycosylation (CDGs). In these diseases, many biological functions are compromised, giving rise to a wide range of severe clinical conditions. By performing detailed analyses of the total serum glycoproteins as well as isolated transferrin and IgG, we have directly correlated aberrant glycosylation with a faulty glycosylation processing step. In one patient the complete absence of complex type sugars was consistent with ablation of GlcNAcTase II activity. In another CDG type II patient, the identification of specific hybrid sugars suggested that the defective processing step was cell type-specific and involved the mannosidase III pathway. In each case, complementary serum proteome analyses revealed significant changes in some 31 glycoproteins, including components of the complement system. This biochemical approach to charting diseases that involve alterations in glycan processing provides a rapid indicator of the nature, severity, and cell type specificity of the suboptimal glycan processing steps; allows links to genetic mutations; indicates the expression levels of proteins; and gives insight into the pathways affected in the disease process.     

Carbohydrate-recognition domains of galectin-9 are involved in intermolecular interaction with galectin-9 itself and other members of the galectin family

Galectin-9 (Gal-9) is a tandem-repeat-type member of the galectin family associated with diverse biological processes, such as apoptosis, cell aggregation, and eosinophil chemoattraction. Although the detailed sugar-binding specificity of Gal-9 has been elucidated, molecular mechanisms that underlie these functions remain to be investigated. During the course of our binding study by affinity chromatography and surface plasmon resonance (SPR) analysis, we found that human Gal-9 interacts with immobilized Gal-9 in the protein-protein interaction mode. Interestingly, this intermolecular interaction strongly depended on the activity of the carbohydrate recognition domain (CRD), because the addition of potent saccharide inhibitors abolished the binding. The presence of multimers was also confirmed by Ferguson plot analysis of result of polyacrylamide gel electrophoresis and matrix-assisted laser-desorption/ionization time-of-flight (MALDI-TOF) mass spectrometry (MS). Moreover, this intermolecular interaction was observed between Gal-9 and other galectin members, such as Gal-3 and Gal-8, but not Gal-1. Because such properties have not been reported yet, they may explain an unidentified mechanism underlying the diverse functions of Gal-9.