Biomedical subjects

Xiaoping Liu

Publications and source records attributed to Xiaoping Liu.

36 records · Page 2Linked to original sources

PubMed2004

Involvement of protein radical, protein aggregation, and effects on NO metabolism in the hypochlorite-mediated oxidation of mitochondrial cytochrome c.

Cytochrome c (cyt c)-derived protein radicals, radical adduct aggregates, and protein tyrosine nitration have been implicated in the pro-apoptotic event connecting inflammation to the development of diseases. During inflammation, one of the reactive oxygen species metabolized via neutrophil activation is hypochlorite (HOCl); destruction of the mitochondrial electron transport chain by hypochlorite is considered to be a damaging factor. Previous study has shown that HOCl induces the site-specific oxidation of cyt c at met-80. In this work, we have assessed the hypothesis that exposure of cyt c to physiologically relevant concentrations of HOCl leads to protein-derived radical and consequent protein aggregation, which subsequently affects cyt c's regulation of nitric oxide metabolism. Reaction intermediates, chemical pathways available for protein aggregation, and protein nitration were examined. A weak ESR signal for immobilized nitroxide derived from the protein was detected when a high concentration of cyt c was reacted with hypochlorite in the presence of the nitroso spin trap 2-methyl-2-nitrosopropane. When a low concentration of cyt c was exposed to the physiologically relevant levels of HOCl in the presence of 5,5-dimethyl-pyrroline N-oxide (DMPO), we detected DMPO nitrone adducts derived from both protein and protein aggregate radicals as assessed by Western blot using an antibody raised against the DMPO nitrone adduct. The cyt c-derived protein radicals formed by HOCl were located on lysine and tyrosine residues, with lysine predominating. Cyt c-derived protein aggregates induced by HOCl involved primarily lysine residues and hydrophobic interaction. In addition, HOCl-oxidized cyt c (HOCl-cyt c) exhibited a higher affinity for NO and enhancement of nonenzymatic NO synthesis from nitrite reduction. Furthermore, HOCl-mediated cyt c oxidation also resulted in a significant elevation of cyt c nitration derived from either NO trapping of the cyt c-derived tyrosyl radical or cyt c-catalyzed one-electron oxidation of nitrite.

Animals↗

PubMed2004

Biphasic modulation of vascular nitric oxide catabolism by oxygen.

Endothelium-derived nitric oxide (NO) plays an important role in the regulation of vascular tone. Lack of NO bioavailability can result in cardiovascular disease. NO bioavailability is determined by its rates of generation and catabolism; however, it is not known how the NO catabolism rate is regulated in the vascular wall under normoxic, hypoxic, and anaerobic conditions. To investigate NO catabolism under different oxygen concentrations, studies of NO and O2 consumption by the isolated rat aorta were performed using electrochemical sensors. Under normoxic conditions, the rate of NO consumption in solution was enhanced in the presence of the rat aorta. Under hypoxic conditions, NO consumption decreased in parallel with the O2 concentration. Like the inhibition of mitochondrial respiration by NO, the inhibitory effects of NO on aortic O2 consumption increased as O2 concentration decreased. Under anaerobic conditions, however, a paradoxical reacceleration of NO consumption occurred. This increased anaerobic NO consumption was inhibited by the cytochrome c oxidase inhibitor NaCN but not by the free iron chelator deferoxamine, the flavoprotein inhibitor diphenylene iodonium (10 microM), or superoxide dismutase (200 U/ml). The effect of O2 on the NO consumption could be reproduced by purified cytochrome c oxidase (CcO), implying that CcO is involved in aortic NO catabolism. This reduced NO catabolism at low O2 tensions supports the maintenance of effective NO levels in the vascular wall, reducing the resistance of blood vessels. The increased anaerobic NO catabolism may be important for removing excess NO accumulation in ischemic tissues.

Animals↗

PubMed2004

A novel PRPF31 splice-site mutation in a Chinese family with autosomal dominant retinitis pigmentosa.

PURPOSE: The autosomal dominant form of retinitis pigmentosa (ADRP) can be caused by mutations in 13 genes and a further locus for which the gene remains to be identified. This study was intended to identify mutations in a large Chinese pedigree with ADRP. METHODS: A genome scan was conducted in the family. The whole coding sequences and the intron-exon boundaries of candidate genes were amplified and sequenced. The reverse transcriptase polymerase chain reaction (RT-PCR) was performed to amplify the mutated mRNA. RESULTS: The strongest evidence of linkage was detected with three adjacent microsatellite markers genotyped between D19S902 and D19S210 on chromosome 19q13.33-13.43. Within the region, a single nucleotide change (G>A) at position -1 of Intron 5 of PRPF31 was found. The consensus AG doublet of the Intron 5 splice acceptor was changed to AA. The mutation co-segregated with the disease phenotype, suggesting that it was the disease-causing mutation in this family. This splicing site mutation is predicted to cause an erroneous splicing of Exon 6. By RT-PCR, we found the mutated nucleotide of Intron 5 (A) and the first nucleotide of Exon 6 (G) was regarded as a new splice acceptor, resulting in 1 bp deletion of the first codon of Exon 6 (GAG-to-AG) at the mRNA level. This change led to a frameshift and truncated protein of 196 amino acids with 56 novel amino acids prior to a premature stop. CONCLUSIONS: A novel splicing mutation (IVS5-1G>A) in the pre-mRNA splicing-factor gene PRPF31 causes retinitis pigmentosa in a large Chinese family. The mutation results in a truncated protein of PRPF31.

Asian People↗

PubMed2004

Characterization of the effects of oxygen on xanthine oxidase-mediated nitric oxide formation.

Under anaerobic conditions, xanthine oxidase (XO)-catalyzed nitrite reduction can be an important source of nitric oxide (NO). However, questions remain regarding whether significant XO-mediated NO generation also occurs under aerobic conditions. Therefore, electron paramagnetic resonance, chemiluminescence NO-analyzer, and NO-electrode studies were performed to characterize the kinetics and magnitude of XO-mediated nitrite reduction as a function of oxygen tension. With substrates xanthine or 2,3-dihydroxybenz-aldehyde that provide electrons to XO at the molybdenum site, the rate of NO production followed Michaelis-Menten kinetics, and oxygen functioned as a competitive inhibitor of nitrite reduction. However, with flavin-adenine dinucleotide site-binding substrate NADH as electron donor, aerobic NO production was maintained at more than 70% of anaerobic levels, and binding of NADH to the flavin-adenine dinucleotide site seemed to prevent oxygen binding. Therefore, under aerobic conditions, NADH would be the main electron donor for XO-catalyzed NO production in tissues. Studies of the pH dependence of NO formation indicated that lower pH values decrease oxygen reduction but greatly increase nitrite reduction, facilitating NO generation. Isotope tracer studies demonstrated that XO-mediated NO formation occurs in normoxic and hypoxic heart tissue. Thus, XO-mediated NO generation occurs under aerobic conditions and is regulated by oxygen tension, pH, nitrite, and reducing substrate concentrations.

Animals↗

PubMed2004

Effect of pH and concentration on the diffusion of radiostrontium in compacted bentonite--a capillary experimental study.

The effects of pH and Sr2+ solution concentration on diffusion and sorption of Sr2+ in compacted bentonite (rhob = 1000+/-30 kg/m3) were studied using an "in-diffusion" method at an ionic strength of 0.1M NaClO4. The results (distribution coefficients, Kd, apparent and effective diffusion coefficients, Da and De) derived from the capillary method are in good agreement with the literature data obtained for similar bentonite dry densities and fit Fick's second law very well. The results suggest that the diffusion of Sr2+ in compacted bentonite decreases slightly with increasing pH values and also increases slightly with increasing Sr2+ solution concentration. The distribution coefficients are weakly dependent on the solution concentrations and show a slight increase with increasing pH values. The average effective diffusion coefficient of Sr2+ in compacted bentonite is (1.2+/-0.2) x 10(-9) m2/s, surface diffusion effects are found for the diffusion of Sr2+ in compacted bentonite.

Journal Article↗

PubMed2004

An integrative radiation protection control system based on a CAN bus for the HT-7U tokamak fusion device.

A radiation protection control system has been designed, based on distributed computers and consideration of the features of the radiation source of the HT-7U fusion experimental device, for protecting the workers and the public against neutron and photon radiation, and especially for ensuring that workers cannot unexpectedly enter an area of high radiation level in any case. A multisubsystem (irradiation monitoring subsystem, access control subsystem, safety interlock subsystem and other related facilities) integration concept is proposed for the design. This system has been implemented on the basis of the up-to-date industrial field bus CAN, featuring simplicity and flexibility of installation and maintenance, capability for real-time long distance communication and multi-master protocol.

Humans↗

PubMed2004

Molecular regulation of gene expression of catecholamine biosynthetic enzymes by stress: sympathetic ganglia versus adrenal medulla.

Stress induces tyrosine hydroxylase (TH) and dopamine beta-hydroxylase (DBH) gene expression in sympathetic ganglia and adrenal medulla (AM). However, distinct molecular mechanisms appear to regulate these genes in these locations. The elevation of TH mRNA in response to single immobilization stress (IMO) in AM is robust, but transient, while the induction of TH and DBH mRNAs in sympathetic ganglia is slower and more long lasting. Injections of adrenocorticotropic hormone (ACTH) elicited induction of TH and DBH gene expression in rat sympathetic ganglia, but not in AM. The superior cervical (SCG) and stellate (StG) ganglia, but not AM, were found to express mRNA for the MC-2 receptor, the major ACTH responsive receptor in adrenal cortex. IMO led to increase in MC-2 receptor mRNA levels in SCG. Thus, ACTH, via the MC-2 receptor, may be directly involved in the stress-elicited regulation of norepinephrine biosynthesis in sympathetic ganglia. The signaling pathways triggered by IMO differed in these locations. In AM, IMO triggered activation of the MAP kinase, JNK, and induction of AP1 factors, Egr1 and phosphorylation of CREB. In contrast in the SCG, with IMO we did not observe changes in JNK and little binding to the AP1 motif of the TH promoter. However, there was an increase in CREB binding to the CRE site of the TH promoter. The results reveal differential mechanisms of regulation of catecholamine biosynthetic enzymes by stress in two components of the sympathoadrenal system and should provide basis for possible selective pharmacologic interventions.

Adrenal Medulla↗

PubMed2004

Differential effects of stress on gene transcription factors in catecholaminergic systems.

Long-term changes in catecholamine levels and expression of their biosynthetic enzymes are associated with several stress-related disorders such as elevated plasma norepinephrine in posttraumatic stress disorder and increased postmortem tyrosine hydroxylase in the locus coeruleus with major depression. Stress elevates tyrosine hydroxylase gene expression in the CNS and periphery. Increased transcriptional initiation was involved in this induction in the rat adrenal medulla and locus coeruleus in response to single as well as repeated immobilization stress (IMO). We examined the stress-triggered induction or phosphorylation of several transcription factors, which were previously shown to be able to modulate tyrosine hydroxylase transcription. A single episode of IMO triggered elevations of c-fos in both the adrenal medulla and locus coeruleus. With repeated daily IMO, Fra-2 was a major AP-1 factor induced in the adrenal medulla, but not in the locus coeruleus. Egr1 levels were markedly elevated in the adrenal medulla with both single and repeated IMO stress, but not in the locus coeruleus. In the locus coeruleus, increased phosphorylation of CREB was observed after both single and repeated IMO. Results implicate differential transcription pathways in mediating elevation of gene expression of tyrosine hydroxylase, and other target genes, in these locations.

Adrenal Medulla↗

PubMed2004

[Determination of fluorine in the environmental samples by combustion-hydrolysis-ion selective electrode method].

OBJECTIVE: To establish a fast and accurately method of determination of fluorine in coal, hair and food by combustion-hydrolysis-ion selective electrode method. METHODS: The influence factors on combustion-hydrolysis, such as silica weight, temperature and time of hydrolysis, sample weight and volume of distilled water were studied so that to determine the best of all testing conditions. RESULTS: The time for hydrolysis in this method was reduced by one third of that of GB/T4633-1997 standard of PRC method. The fluorine in standard reference material such as tea, poplar leaves, coal and capsicum, and corn was determined on precision and accuracy by this method. The relative standard deviation was less than 5%. The recovery varied from 90.3% to 107.6%. CONCLUSION: The method is suitable for determining fluorine in the various environmental samples.

Carbon↗

PubMed2003

Characterization of the magnitude and kinetics of xanthine oxidase-catalyzed nitrate reduction: evaluation of its role in nitrite and nitric oxide generation in anoxic tissues.

In addition to nitric oxide (NO) generation from specific NO synthases, NO is also formed during anoxia from nitrite reduction, and xanthine oxidase (XO) catalyzes this process. While in tissues and blood high nitrate levels are present, questions remain regarding whether nitrate is also a source of NO and if XO-mediated nitrate reduction can be an important source of NO in biological systems. To characterize the kinetics, magnitude, and mechanism of XO-mediated nitrate reduction under anaerobic conditions, EPR, chemiluminescence NO-analyzer, and NO-electrode studies were performed. Typical XO reducing substrates, xanthine, NADH, and 2,3-dihydroxybenz-aldehyde, triggered nitrate reduction to nitrite and NO. The rate of nitrite production followed Michaelis-Menten kinetics, while NO generation rates increased linearly following the accumulation of nitrite, suggesting stepwise-reduction of nitrate to nitrite then to NO. The molybdenum-binding XO inhibitor, oxypurinol, inhibited both nitrite and NO production, indicating that nitrate reduction occurs at the molybdenum site. At higher xanthine concentrations, partial inhibition was seen, suggesting formation of a substrate-bound reduced enzyme complex with xanthine blocking the molybdenum site. The pH dependence of nitrite and NO formation indicate that XO-mediated nitrate reduction occurs via an acid-catalyzed mechanism. With conditions occurring during ischemia, myocardial xanthine oxidoreductase and nitrate levels were determined to generate up to 20 microM nitrite within 10-20 min that can be further reduced to NO with rates comparable to those of maximally activated NOS. Thus, XOR catalyzed nitrate reduction to nitrite and NO occurs and can be an important source of NO production in ischemic tissues.

Animals↗

PubMed2003

The effect of costimulatory factors in the pathogenesis of chronic idiopathic thrombocytopenic purpura.

To investigate the effect of costimulatory factors in the pathogenesis of chronic idiopathic thrombocytopenic purpura (CITP), we examined the expression of CD80 on platelets and megakaryocytes in patients with CITP and the controls by FACS. By using CD80 monoclonal antibody (McAb) to inhibit interaction among cells which is mediated by costimulatory factors, we observed the effect of CD80 McAb on the growth and maturation of megakaryocytic progenitors of patients with CITP in vitro. The results showed the expression of CD80 on platelets and megakaryocytes in CITP group was significantly higher than that in controls (P<0.01). There was a significantly positive correlation between the expression of CD80 on platelets and serum PAIgG in CITP (r=0.86, P<0.05). The mean of various clone numbers (CFU-MK, BFU-MK and mCFU-MK) in CITP were all lower than those in controls (P<0.05). In megakaryocytes co-cultured with CD80 McAb, there was an increasing tendency of the number of CFU-MK and big CFU-MK (the number of megakaryocyte with GP IIIa positive was more than 20) and mediate CFU-MK (the number of megakaryocyte with GP IIIa positive was 11-20). When the concentration of CD80 McAb was 10 microg/L, there was a significant difference in the number of megakaryocytic colony formation (CFU-MK, BFU-MK and mCFU-MK) between the group with CD80 McAb and that without it (P<0.05). These showed the abnormality of costimulatory factors had important effect in the pathogenesis of CITP.

Adult↗

PubMed2003

[Identification on Herba Hedyotidis by X-ray diffraction Fourier fingerprint pattern method].

OBJECTIVE: To establish a new identification and analysis method of Herba Hedyotidis. METHOD: Powder X-Ray diffraction fourier fingerprint pattern method. RESULT: Experiment and analysis were carried out on eight samples. The standard X-Ray diffraction fourier fingerprint pattern method and characteristic diffraction peaks of Herba Hedyotidis were obtained. CONCLUSION: This method can be used for the identification of Herba Hedyotidis.

Drug Contamination↗

PubMed2002

Nitric oxide uptake by erythrocytes is primarily limited by extracellular diffusion not membrane resistance.

The process of NO transfer into erythrocytes (RBCs) is of critical biological importance because it regulates the bioavailability and diffusional distance of endothelial-derived NO. It has been reported that the rate of NO reaction with oxyhemoglobin (Hb) within RBCs is nearly three orders of magnitude slower than that by equal amounts of free oxyhemoglobin. Consistent with early studies on oxygen uptake by RBCs, the process of extracellular diffusion was reported to explain this much lower NO uptake by RBC encapsulated Hb (Liu, X., Miller, M. J., Joshi, M. S., Sadowska-Krowicka, H., Clark, D. A., and Lancaster, J. R., Jr. (1998) J. Biol. Chem. 273, 18709-18713). However, it was subsequently proposed that the RBC membrane provides the main resistance to NO uptake rather than the process of extracellular diffusion (Vaughn, M. W., Huang, K. T., Kuo, L., and Liao, J. C. (2000) J. Biol. Chem. 275, 2342-2348). This conclusion was based on competition experiments that were assumed to be able to determine the rate constant of NO uptake by RBCs without extracellular diffusion limitation. To test the validity of this hypothesis, we theoretically analyzed competition experiments. Here, we show that competition experiments do not eliminate the extracellular diffusion limitation. Simulation of the competition data indicates that the main resistance to NO uptake by RBCs is caused by extracellular diffusion in the unstirred layer surrounding each RBC but not by the RBC membrane. This extracellular diffusion resistance is responsible for preventing interference of NO signaling in the endothelium without the need for special NO uptake by intracellular hemoglobin or a unique membrane resistance mechanism.

Binding, Competitive↗

PubMed2002

Overestimation of NADH-driven vascular oxidase activity due to lucigenin artifacts.

Several limitations have recently been described for lucigenin, a probe frequently used to assess the activity of vascular NAD(P)H oxidase, a major superoxide source. The preferential reducing substrate of such oxidase remains unclear. We assessed whether lucigenin artifacts could affect detection of NAD(P)H oxidase activity. Initial chemiluminescence assays were performed with vascular rings or homogenates at 5, 50, or 250 microM concentrations. Results showed preferential signals with NADPH (vs. NADH) with 5 and 50 microM lucigenin, which were blocked by diphenylene iodonium (DPI), superoxide dismutase (SOD), or its cell-permeable mimetic MnTBAP. With 250 microM lucigenin, the relative signal with NADH became larger than with NADPH, and was poorly inhibited by all three antagonists above. All SOD/DPI-resistant signals were effectively blocked by the electron acceptor nitrobluetetrazolium. Spin trapping with DMPO showed an approximate doubling of DMPO-OH radical adduct signal upon addition of 5 microM lucigenin to homogenates incubated with either NADPH or NADH. With 50 or 250 microM lucigenin, much larger increases were observed with NADH, as opposed to NADPH. Furthermore, oxygen consumption measurements showed analogous results. In summary, our data suggest that: (i) Lucigenin redox-cycling is detectable in vascular tissue even at 5 microM concentrations, while at 250 microM redox-cycling becomes predominant and is markedly increased when NADH is the assayed substrate; and (ii) With 250 microM lucigenin, preferentially with NADH, signals are further overestimated by direct, oxidase-dependent, superoxide-independent two-electron transfer. Therefore, previous reports of preferential NADH affinity of the vascular oxidase may have been due to these artifacts.

Acridines↗

PubMed2002

[Expression of growth hormone receptor and its mRNA in cirrhotic livers].

OBJECTIVE: To investigate the expression of growth hormone receptor in human cirrhotic livers. METHODS: Radio-ligand binding assay and reverse transcription-polymerase chain reaction (RT-PCR) were used to examine the expression of growth hormone receptor and its mRNA in cirrhotic liver tissues near cancer in 32 cases and cirrhotic liver cells near cancer of 6 patients undergoing radical resection of liver cancers. The results were compared with those in 5 specimens of normal liver tissue and 3 specimens of normal liver cells. RESULTS: The binding capacity of growth hormone receptors in human cirrhotic liver tissues was significant lower than that in normal control [RT, (22.4 +/- 5.0) fmol/mg protein, n = 32 versus (41.3 +/- 5.3) fmol/mg protein, n = 5; P < 0.05] and decreased further along with the aggravation of cirrhosis (P < 0.05). The number of binding sites of growth hormone receptors in human cirrhotic liver cells were significantly lower than that in normal control [Site, (2.40 +/- 0.93) x 10(4)/cell, n = 6 versus (4.68 +/- 1.14) x 10(4)/cell, n = 3; P < 0.05]. The expression of growth hormone receptor mRNA in human cirrhotic liver tissues was significant lower than that in normal control [riOD, 30.8% +/- 8.2%, n = 32 versus 44.93% +/- 6.25%, n = 5; P < 0.05] and decreased further along with the aggregation of cirrhosis (P < 0.05). CONCLUSION: The expression of growth hormone receptor in human cirrhotic liver cells is downregulated. The more severe liver cirrhosis the more the downregulation. The decreased expression of growth hormone receptor mRNA may account for the downregulated expression of growth hormone receptor in cirrhotic liver tissues.

Adult↗

PubMed2002

Quantitation of superoxide generation and substrate utilization by vascular NAD(P)H oxidase.

In vascular tissues, an NAD(P)H oxidase is the main source of superoxide; however, there has been much uncertainty regarding its activity and the levels of superoxide it generates. This problem has limited overall progress in this field. Therefore, studies were performed and techniques developed to quantitatively assess the function of the vascular NAD(P)H oxidase, measuring its rate of superoxide production and substrate consumption in rat aortic homogenates and intact segments. NADPH/NADH oxidation was measured spectrophotometrically, and oxygen consumption was measured by electrochemical probe. Superoxide was detected and quantitated by electron paramagnetic resonance spin trapping. Under basal conditions, superoxide generation and oxygen consumption were negligible. After addition of NADPH or NADH (0.1 mM), superoxide was generated at rates of 0.41 +/- 0.03 or 0.36 +/- 0.04 nmol x mg protein(-1) x min(-1), respectively. Oxygen was consumed with a similar time course at rates of 1.5 +/- 0.2 or 1.3 +/- 0.3 nmol. mg protein(-1) x min(-1), and NADPH or NADH were oxidized at rates of 1.8 +/- 0.4 and 1.5 +/- 0.3 nmol x mg protein(-1) x min(-1), respectively. In intact aortic rings, superoxide was generated with rates of 4.0 +/- 0.7 or 3.7 +/- 0.7 pmol x mg tissue(-1) x min(-1), whereas oxygen was consumed at rates of 22.1 +/- 5.0 or 14.5 +/- 3.3 pmol x mg tissue(-1) x min(-1), for NADPH or NADH, respectively. These values are lower than those previously measured using lucigenin, which uncouples flavoenzymes, triggering additional superoxide generation. This quantitative approach for characterization of the vascular NAD(P)H oxidase activity should facilitate the further identification and cellular characterization of this enzyme(s) and its functional and signaling roles.

Acridines↗

PubMed2002

[Endovascular treatment for abdominal aortic aneurysm, a primary study].

OBJECTIVE: To summarize the initial experience of endoluminal stent-grafting in the treatment of abdominal aortic aneurysm (AAA). METHODS: Stent-graft of proper shape and size was selected according to the morphology of AAA and was inserted into the lumen of abdominal aortic aneurysm through femoral artery to reconstruct the blood flow under X-ray flouroscopy among 34 cases. Data on complications and morphological changes were obtained according to a strict follow-up plan. RESULTS: The stent-grafting procedure was technically successful in all 34 patients. None of them required open repair. Five patients (14.7%) suffered from primary endoleaks after stent-graft deployment and 1 patient suffered from paraplegia and acute graft thrombosis. No other complications (kidney infarction, limbs and colon ischemia, etc) were found. The average follow-up time was 21 +/- 4.7 months. Perioperative death rate was 0% and total death rate was 3%. Two cases with primary endoleak developed into lasting endoleak during the follow-up period with a rate of late endoleak (> 30 days) of 11.7%. Secondary endoleak was found in 2 cases. One case with limb stent disconnection accepted secondary intervention. The mean max aneurysm diameter in cases without endoleak decreased significantly 6 months to 2 years after operation (P < 0.01). The aneurysm in two cases with secondary type I endoleak increased and one of them underwent secondary intraluminal treatment. CONCLUSION: Endovascular technique is a reliable method of treating AAA with micro-trauma. Endoleak is the main complication of this technique. Follow-up is an important component of the treatment plan. The aim of endoluminal repair is to completely neglect the aneurysmal lumen and prevent the aneurysm from increasing during follow-up.

Aged↗

PubMed2002

[Dynamic study of platelets surface glycoprotein in Kawasaki disease].

OBJECTIVE: To study the activation of platelets in children with Kawasaki disease (KD) at molecular level. METHODS: The expression of platelet surface glycoproteins CD(41), CD(42a), CD(61), CD(62p) and CD(63) in 20 KD patients was measured by flow cytometry before and at 1, 2, 3 week after treatment with aspirin and high-dose (1 approximately 2 g/kg) intravenous gamma-globulin (IVIG). RESULTS: The expression of glycoprotein CD(41), CD(42a), CD(61), CD(62p) and CD(63) were higher in KD group than in control group. Aspirin and IVIG could not inhibit these high expression of glycoproteins. Higher expression of CD(62p) was observed in patients with coronary artery injury. CONCLUSION: Platelets were highly activated in KD patients which may be one of the most important pathophysiological step in KD. It provided a theoretical basis for treatment of KD with antagonist of glycoprotein of platelets. Obviously increase of CD(62p) can be taken as a criterion for predicting coronary artery injury in KD patients.

Aspirin↗