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Biomedical subjects

Y Zhu

Publications and source records attributed to Y Zhu.

At least 307 records · Page 17Linked to original sources
PubMed2000

Production of hepatocyte growth factor during acute myocardial infarction.

OBJECTIVE: To investigate the clinical significance of circulating hepatocyte growth factor (HGF) and the role of peripheral blood mononuclear cells (monocytes), which are a possible source of HGF, in patients with acute myocardial infarction. DESIGN AND PATIENTS: 37 patients with acute myocardial infarction and 13 normal control subjects were recruited. Peripheral venous blood samples were drawn from the infarct patients 1, 7, 14, and 21 days after onset. Monocytes were isolated from peripheral blood at those times. HGF concentrations in serum and in a culture medium of monocytes after incubation for 24 hours (monocyte HGF levels) were measured by enzyme linked immunosorbent assay. RESULTS: Serum HGF and monocyte HGF values within seven days after onset of myocardial infarction were significantly higher than those of control subjects and decreased by day 14. There were significant positive correlations between serum HGF and monocyte HGF levels on day 7; between maximum plasma creatine phosphokinase levels and serum HGF levels on day 1; between maximum plasma C reactive protein and serum HGF levels; and between maximum C reactive protein and monocyte HGF levels. Monocyte HGF levels were raised in the patients with progression of ventricular enlargement in the course of acute myocardial infarction. CONCLUSIONS: Early serum HGF concentrations reflect the extent of myocardial damage in acute myocardial infarction patients. Inflammation after acute myocardial infarction is supposed to be involved in enhanced HGF production. Monocytes may play an important role in ventricular remodelling after acute myocardial infarction by releasing the cardiovascular protective mitogen HGF.

Adult↗
PubMed2000

Lipoprotein promotes caveolin-1 and Ras translocation to caveolae: role of cholesterol in endothelial signaling.

To explore the role of LDL in caveolin-Ras regulation in human endothelial cells (ECs), we incubated confluent human umbilical vein endothelial cells (HUVECs) with LDL. This resulted in a high steady-state caveolin-1 (Cav-1) expression at both the mRNA and protein levels. LDL exposure appeared not to regulate the abundance of Cav-1. Immunofluorescence staining showed that Cav-1 protein migrated from the cytoplasm to the cell membrane after LDL exposure. Cav-1 protein and cholesterol partitioned mainly into the caveola fractions, and LDL increased both Cav-1 and cholesterol in these fractions. Ras protein in caveola fractions was also increased by LDL. Increased Ras was detected in Cav-1 immunoprecipitated samples, and conversely, increased Cav-1 was found in Ras-immunoprecipitated samples. We also demonstrated LDL-increased Ras activity in HUVECs by measuring the GTP/GTP+GDP ratio of Ras with [(32)P]orthophosphate labeling in the cells. Finally, we determined the binding of [(3)H]-labeled free cholesterol and recombinant H-Ras to Cav-1 fusion proteins in vitro. Both cholesterol and Ras bound to full-length GST-Cav-1, scaffolding domain (61-101), and C-terminal (135-178) Cav-1 fusion peptides. Addition of cholesterol enhanced Ras binding to the full-length and scaffolding domain of Cav-1 but not to the C-terminal Cav-1. These findings strongly suggest a role for Cav-1 in cholesterol trafficking and cholesterol-mediated intracellular signaling, which may mediate EC activation by LDL.

Biological Transport↗
PubMed2000

Modification of type I collagenous gels by alveolar epithelial cells.

Contraction of type I collagen gels is an in vitro model of tissue remodeling. In addition to fibroblasts, some epithelial cells can mediate this process. We therefore hypothesized that alveolar epithelial cells might contract extracellular matrices and have the potential to directly participate in the remodeling of the lung after alveolar injury. A549 cells were plated on top of collagen gels, and the gels were floated in culture medium. A549 cells contracted the gels in a time- and cell density-dependent manner. A549 cells, as well as human bronchial epithelial cells (HBEC) and rat alveolar epithelial cells (RalvEC) contracted collagen gels more when they were plated on top of the gel than when they were embedded inside, in contrast to human fetal lung fibroblast (HFL1), which contracted more when cast inside. The amount of hydroxyproline in the collagen gels remained unchanged throughout the contraction. Anti-beta(1) integrin antibody inhibited A549 cell-mediated contraction. Transforming growth factor beta augmented the contraction by A549 cells as well as that by HBEC and HFL1. Prostaglandin E(2) inhibited the contraction by HFL1 but did not affect the contraction by A549 cells, HBEC, or RalvEC. Cytomix (a mixture of tumor necrosis factor-alpha, interleukin-1beta, and interferon-gamma) inhibited the contraction by HFL1 but strongly enhanced the contraction by A549 cells. Cytomix also caused a morphologic change of A549 cells from a polygonal to a spindle shape. Immunocytochemistry showed that cytomix induced alpha-tubulin expression in A549 cells, whereas cytokeratin, vimentin, smooth muscle actin, beta(1) integrin, and paxillin expressions were not changed. This study thus demonstrates that alveolar epithelial cells can cause contraction of extracellular matrices and that this process is modulated by exogenous mediators, which also modify the microtubular system. Such an activity might contribute to alveolar remodeling after injury.

Animals↗
PubMed2000

Peroxisome proliferator-activated receptors, coactivators, and downstream targets.

Peroxisomes in liver parenchymal cells proliferate in response to structurally diverse nonmutagenic compounds designated as peroxisome proliferators (PP). Sustained induction of peroxisome proliferation and peroxisomal fatty acid beta-oxidation system in rats and mice leads to the development of liver tumors. Two mechanistic issues are important for consideration: elucidation of the upstream events responsible for the tissue and species specific induction of the characteristic pleiotropic responses by PPs; and delineation of the downstream events associated with peroxisome proliferation, and their role in the development of liver tumors in species that are sensitive to the induction of peroxisome proliferation. The induction of peroxisome proliferation is mediated by PP-activated receptor alpha (PPAR alpha), a member of a group of transcription factors that regulate the expression of genes associated with lipid metabolism and adipocyte differentiation. Three isotypes of this family of nuclear receptors, namely PPAR alpha, PPAR gamma, and PPAR delta (also called beta), have been identified as products of separate genes. Although PPAR alpha is responsible for the PP-induced pleiotropic responses, PPAR gamma seems to be involved in adipogenesis and differentiation, but the events associated with PPAR gamma do not directly involve peroxisomes and peroxisome proliferation. PPARs heterodimerize with 9-cis retinoic acid receptor (RXR), and bind to PP response element(s) (PPREs) on the target gene promoter to initiate inducible transcriptional activity. Tissue and species responses to PPs depend on pharmacokinetics, relative abundance of PPAR isotypes, nature of PPRE in the upstream regions of target genes, the extent of competition or cross-talk among nuclear transcription factors for PPAR heterodimerization partner retinoid X receptor and the modulating role of coactivators and corepressors on ligand-dependent transcription of PPARs. Using PPAR as bait in the yeast two-hybrid system, the authors recently cloned mouse steroid receptor coactivator-1 (SRC-1) and PPAR-binding protein (PBP), and identified them as PPAR coactivators. Both SRC-1 and PBP contain LXXLL signature motifs, considered necessary and sufficient for the binding of coactivators to nuclear receptors. A multifaceted approach, which includes the identification of additional coactivators that may be responsible for cell specific transcriptional activation of PPAR-mediated target genes, and generation of genetically modified animals (transgenic and gene disrupted), will be necessary to gain more insight into the upstream and downstream targets responsible for the induction of early and delayed PP-induced pleiotropic responses. In this context, it is important to note that mice deficient in fatty acyl-CoA oxidase, the first and rate-limiting enzyme of the peroxisomal beta-oxidation system, revealed that this enzyme is indispensable for the physiological regulation of PPAR alpha, and the absence of this enzyme leads to sustained transcriptional activation of genes regulated by this receptor.

Animals↗
PubMed2000

Engineering, purification and applications of His-tagged recombinant antibody fragments with specificity for the major birch pollen allergen, bet v1.

Type I allergy, an immunodisorder affecting almost 20% of the population worldwide, is based on the production of IgE antibodies against per se harmless allergens. We report the expression of hexahistidine-tagged antibody fragments (Fabs) with specificity for Bet v1, the major birch pollen allergen, in Escherichia coli. The cDNA coding for the heavy chain fragment of a mouse monoclonal anti-Bet v1 antibody, Bip 1, was engineered by PCR to contain a hexahistidine-encoding 3' end. The modified Bip1 heavy chain cDNA was co-expressed in E. coli XL-1 Blue with the Bip 1 light chain cDNA using the combinatorial plasmid pComb3H. His-tagged recombinant (r) Bip 1 Fabs were isolated by nickel affinity chromatography and rBip 1 Fabs without His-tag were purified via affinity to rBet v1. rBip 1 Fabs with and without His-tag bound specifically to rBet v1 and, like Bet v1 -specific human serum IgE and rabbit-anti rBet v1 antibodies, cross-reacted with Bet v1-related allergens in other plant-species (alder, oak, hazelnut). We demonstrate the usefulness of His-tagged rBip 1 Fabs (1) for the identification of pollen samples containing Bet v 1 by particle blotting, (2) forthe detection of Bet v1-specific IgE antibodies in human serum samples by sandwich ELISA and (3) for the quantification of Bet v1 in solution. Based on these examples we suggest to use rBip 1 Fabs for the detection of Bet v1 and Bet v1-related allergens in natural allergen sources for allergy prevention, as well as for the standardization of natural allergen extracts produced for diagnosis and immunotherapy of birch pollen allergy.

Allergens↗
PubMed2000

Selective activation of endothelial cells by the antioxidant pyrrolidine dithiocarbamate: involvement of C-jun N-terminal kinase and AP-1 activation.

The antioxidant agent pyrrolidine dithiocarbamate (PDTC) has been shown to protect endothelial cells (EC) from pro-inflammatory-induced and pro-oxidant-induced NF-kappaB activation. It also perturbs EC by altering activator protein-1 (AP-1) status and inducing ICAM-1. Experiments were performed to investigate the upstream mechanism by which PDTC produces these effects. We have demonstrated that PDTC not only induced AP-1 binding and ICAM-1 expression by itself, but it also augmented AP-1 activation and ICAM-1 induction in low-dose IL-1alpha treated cells. To dissect the mechanism of these effects, we measured c-Jun and c-Fos expression, and the activity of c-Jun NH2-terminal kinase (JNK) and extracellular signal regulated kinase (ERK) in human umbilical vein endothelial cells (HUVEC). We detected an increase in JNK activity in PDTC-treated HUVEC. Following cotransfection with JNK[K-M], a kinase-deficient JNK1, the PDTC-increased AP-1-driven-luciferase activity was attenuated. Utilizing a specific trans-reporting system we confirmed c-Jun activation by upstream signaling mechanisms. The results show that c-Jun activity was increased 9-fold after PDTC treatment. In addition, PDTC promoted more transient activation in ERK-c-fos. In contrast, PDTC produced sustained JNK-c-Jun activation, which translated into long-lasting ICAM-1 production. These results suggest that an antioxidant may contribute to chronic vascular endothelial activation.

Antioxidants↗
PubMed2000

[A study of ventricular repolarization duration variability and dependence of RTm/RR].

As an important electrophysiological parameter that reflects cardiac depolarization and repolarization process, ventricular repolarization duration has been drawing growing attention. It is influenced by several physiological and pathological factors and associated with several cardiac diseases. We studied repolarization duration variability (RDV) and dependence of RTm/RR among normal subjects of different age-groups, as well as between normal subjects and subjects with cardiac diseases. It was found that RDV and dependence of RTm/RR are related to age. There are significant differences in the slope of RTm/RR, coherence, CV ratio and RDV between normal subjects and subjects with cardiac diseases. The RDV and dependence of RTm/RR can be employed in providing a more useful evaluation of cardiac disease and function in clinical care.

Adult↗
PubMed2000

Deletions at 11q23 in different lymphoma subtypes.

BACKGROUND AND OBJECTIVES: Chromosome band 11q23 is frequently deleted in various types of neoplasm. The region represented by yeast artificial chromosome (YAC) clone 755b11 at 11q23 has been shown to be the minimal common region of deletion in mantle cell lymphoma (MCL) and B-cell chronic lymphocytic leukemia (B-CLL). The aim of the study was to determine the frequencies of 11q23 deletion in different lymphoma subtypes. DESIGN AND METHODS: We performed fluorescence in situ hybridization (FISH) analysis with YAC755b11 on either peripheral blood or lymph node biopsy (LN) specimens of patients diagnosed as having MCL (47), CLL/small lymphocytic lymphoma (SLL) (62), diffuse large cell lymphoma (DLCL) (17), follicular lymphoma (FL) (9), and Hodgkin's disease (HD) (11). Fifteen cases of reactive or normal lymph node biopsies were studied as controls. RESULTS: Forty of the 161 (25%) samples exhibited deletions in the region represented by YAC755b11. The 11q23 deletion was found only in MCL (23, 49%), CLL / SLL (13, 21%) and DLCL (4, 24%). Three cases were classified as Richter's syndrome and they all exhibited the deletion at 11q23. The deletion frequencies in the blood specimens of typical CLL (30%) and lymph node specimens of CLL/SLL (13%) were remarkably different. INTERPRETATION AND CONCLUSIONS: Our study demonstrated that the 11q23 deletion is not common in lymphomas other than MCL, CLL and DLCL. It also showed the possible correlation of the 11q23 deletion with the transformation of localized lymphoma to CLL, and with the development of Richter's syndrome.

Adolescent↗
PubMed2000

HFE gene mutations in patients with rheumatoid arthritis.

OBJECTIVE: To investigate the role of C282Y and H63D mutations in HFE gene in susceptibility to rheumatoid arthritis (RA). METHODS: The distribution of C282Y and H63D mutations in patients with RA and in healthy subjects was examined by restriction endonuclease digestion of polymerase chain reaction amplified genomic DNA. RESULTS: The prevalence of C282Y mutation in patients with RA was the same as in healthy controls. In contrast, the distribution of H63D mutation was significantly higher in the total RA patient population and in DRB1 QKRAA/QRRAA epitope positive patients compared to respective groups of controls. Analysis of data showed that (1) both H63D mutation and QKRAA/QRRAA DRB1 epitope are individually associated with RA susceptibility; (2) there is interaction between these 2 factors in development of RA; and (3) both these factors combined have stronger association with RA susceptibility than with these factors individually. CONCLUSION: H63D mutation appears to play a role in pathogenesis of RA. This study is small and must be regarded as preliminary. These data therefore need confirmation from independent studies.

Adult↗
PubMed2000

Dopamine receptor gene polymorphisms in Guangzhou Hans.

OBJECTIVE: To determine the distribution of dopamine D2, D3, and D5 receptor(DRD2, DRD3, DRD5) gene polymorphisms in Guangzhou Hans. METHODS: A total of 141 healthy Guangzhou Hans were studied by the use of polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) and PCR-amplification of specific allele (PASA) techniques. Current results were compared with the data on other ethnic groups. RESULTS: Within the 141 individuals tested, the frequencies of the A1(Taq I-) and A2(Taq I+) alleles of the TaqI A mutation site in the 3'non-coding region of the DRD2 gene were found to be 48% and 52%, respectively. The observed frequencies of the A1A1, A1A2 and A2A2 genotypes were found to be 17%, 52% and 31%, respectively, which met Hardy-Weinberg equilibrium. The frequencies of the A1 and A2 alleles of the Bal I mutation site in the exon 1 of DRD3 gene were found to be 73% and 27%, respectively. The observed frequencies of the A1A1, A1A2 and A2A2 genotypes were found to be 53%, 39% and 8%, respectively, which met Hardy-Weinberg equilibrium. The frequencies of the 1 and 2 alleles of the Msp I mutation site in the intron 5 of DRD3 gene were found to be 62.5% and 37.5%, respectively. The observed frequencies of the 1-1, 1-2 and 2-2 genotypes were found to be 35%, 55% and 10%, respectively, which met Hardy-Weinberg equilibrium. No linkage disequilibrium was observed between the Bal I and Msp I polymorphism in Guangzhou Hans(chi(2)=0165, P>0.05). The frequencies of the T and C alleles of the T978C mutation site of DRD5 gene were found to be 51% and 49%, respectively. The observed frequencies of the T/T, T/C and C/C genotypes were found to be 23.6%, 54.6% and 21.8%, respectively, which met Hardy-Weinberg equilibrium. CONCLUSION: The polymorphisms of DRD2, DRD3, DRD5 gene in Guangzhou Hans were high and different from those in other populations.

Adult↗
PubMed2000

Clinical observation on treatment of non-parvicellular carcinoma of the lung with jin fu kang oral liquid.

Jin Fu Kang Oral Liquid ([symbol: see text]), made of traditional Chinese drugs for supplementing qi and nourishing yin, was developed according to the common symptoms in lung carcinoma with deficiency of both qi and yin. Of the 96 cases in the Jin Fu Kang group, 1 case got complete remission (CR) after treatment, 8 cases partial remission (PR), 52 cases no change (NC), PR + NC covering 63.5%. Of the 52 cases in the group of Jin Fu Kang plus chemotherapy, 11 cases got PR after treatment, 26 cases NC, PR + NC covering 71.2%. Of the 25 cases in the chemotherapy group, 4 cases got PR after treatment, 11 cases NC, PR + NC covering 60.0%. The results show that the therapeutic effectiveness in the Jin Fu Kang group and the group of Jin Fu Kang plus chemotherapy was better than that in the chemotherapy group. The one-year survival rate and the two-year survival rate after treatment in the Jin Fu Kang group were 67.3% and 67.3% respectively; 66.7% and 66.7% in the group of Jin Fu Kang plus chemotherapy; and 40.3% and 0.0% in the chemotherapy group. The improvement of clinical symptoms, increase of body weight and improvement of health situation (KPS marks) after treatment in both the Jin Fu Kang group and the group of Jin Fu Kang plus chemotherapy were better than that in the chemotherapy group. Some indicators of immunology and hemogram after treatment were greatly improved in the Jin Fu Kang group, worse in the chemotherapy group, but no obvious improvement in the group of Jin Fu Kang plus chemotherapy.

Adenocarcinoma↗
PubMed2000

[Construction and bioassay of secondary recombinant baculovirus with two foreign gene].

Plasmid pAcLEneo which bears neomycin gene derived by the baculovirus IE1 promotor was digested and the gene was harvested. A transfer vector pAc34DZ2 in which the polyhedrin envelope gene has been inactivated by insertion of expression cassette of PIE1/neo was constructed by inserting the neo cassette into the SacI site of plasmid pAc34DZ1. We have constructed the polyhedrin positive recombinant virus (I) vAcPhBtT which was able to express Bt truncated endotoxin gene. In order to improve the insecticide efficiency of recombinant virus (I), an anti-neomycin recombinant virus (II) vAcPhBtTPE- was obtained by second co-transfection into the Sf9 cells with pAc34DZ2 and recombinant virus (I) DNA. Southern blot and SDS-PAGE analysis indicated that the recombinant virus (II) was still able to express the 80 kD Bt truncated delta-endotoxin, but did not express the 34 kD polyhedrin envelope protein. The recombinant virus (II) without envelope released virion faster than recombinant virus (I) after alkaline lysis. Bioassay was carried out using Spodoera exigua. LC50 of the recombinant virus (II) was about half of wild type virus and LT50 reduced about two days.

Animals↗
PubMed2000

Effect of dietary fatty acids on colon tumorigenesis induced by methyl nitrosourea in rats.

To study the effect of dietary fatty acid on the colon tumorigenesis induced by methyl nitrosourea in rats, male SD rats were fed five semi-synthetic diets composed of different proportions of beef tallow, soybean oil, alkana oil, corn oil and fish oil for 180 days. The experimental groups were injected with a solution of methyl nitrosourea in phosphate buffer intraperitoneally once a week for six weeks. The control groups were injected with phosphate buffer solution only. The incidence of colon cancer, the average volume of the tumors, proliferation cell nuclear antigen, cell kinetics, membrane lipid fluidity, alkaline phosphatase activities and the content of prostaglandin E2 in colon mucosa and the fatty acid of testis pad fat were measured at the end of the experiment. The results showed that the incidence of colon cancer and the average volume of tumors in animals fed with diets composed mainly of beef tallow, soybean oil or alkana oil were significantly higher than those that were fed fish oil. The most effective anticancer diet in our study contained saturated fatty acid, monounsaturated fatty acid and polyunsaturated fatty acid of fish oil in the proportion of 13.9%, 16.4% and 68.8% respectively. Inhibition of colon tumorigenesis appeared to be related to the regulation of membrane lipid fluidity, and a decrease in the proliferation of cell nuclear antigen in colon cells. In addition, a decrease was noted in the number of cells in S phase and alkaline phosphatase activity, along with inhibition of arachidonic acid products and a corresponding decrease in the amount of prostaglandin E2.

Alkylating Agents↗
PubMed2000

Improving synthetic lethal screens by regulating the yeast centromere sequence.

The synthetic lethal screen is a useful method in identifying novel genes functioning in an alternative pathway to the gene of interest. The current synthetic lethal screen protocol in yeast is based on a colony-sectoring assay that allows direct visualization of mutant colonies among a large population by their inability to afford plasmid loss. This method demands an appropriate level of stability of the plasmid carrying the gene of interest. YRp-based plasmids are extremely unstable and complete plasmid loss occurs within a few generations. Consequently, YCp plasmids are the vector of choice for synthetic lethal screens. However, we found that the high-level stability of YCp plasmids resulted in a large number of false positives that must be further characterized. In this study, we attempt to improve the existing synthetic lethal screen protocol by regulating the plasmid stability and copy number. It was found that by placing a yeast centromere sequence under the control of either inducible or constitutive promoters, plasmid stability can be significantly decreased. Hence, altering the conditions under which yeast cells carrying the plasmid PGAL1-CEN4 were cultivated allowed us to develop a method that eliminated virtually 100% of false positives and drastically reduced the time required to carry out a synthetic lethal screen.

Aminohydrolases↗
PubMed2000

[Analysis of phenylethanoid glycosides in the extract of herba Cistanchis by LC/ESI-MS/MS].

AIM: To analyze the phenylethanoid glycosides in Cistanche deserticola Y. D. Ma and its alternatives. METHODS: An HPLC/MS/MS method has been developed for the analysis of seven kinds of phenylethanoid glycosides in Cistanche deserticola Y. D. Ma, C. salsa (C. A. Mey) G. Beck and C. tubulosa (Schenk) R. Wight. The [M - H]- ions were observed for five standards and Cistanche extracts. The glycosidic linkages, the core, and the attached sugar (s) of the phenylethanoid glycosides can be determined from the collision-induced dissociation spectra of the molecular. RESULTS: Seven kinds of phenylethanoid glycosides (echinacoside, acteoside, cisacteoside, isoacteoside, 2'-acetylacteoside, cistanoside A, osmanthuside B) in Cistanche deserticola Y. D. Ma, six kinds (echinacoside, acteoside, cisacteoside, isoacteoside, 2'-acetylacteoside and cistanoside A) in C. salsa (C. A. Mey) G. Beck and five kinds (echinacoside, acteoside, cisacteoside, isoacteoside and 2'-acetylacteoside) in C. tubulosa (Schenk) R. Wight were detected. CONCLUSION: The difference of the relative distribution of these phenylethanoid glycosides in each extract was found out. Phenylethanoid glycosides are the specific constituents in Cistanchis, which can be used to distinguish different species in Genus Cistanchis.

Drugs, Chinese Herbal↗
PubMed2000

[The correlation of cytokines TNF alpha, IFN-gamma, Epo with anemia in rheumatoid arthritis].

OBJECTIVE: To elucidate the characteristics of anemia of chronic disease(ACD) in rheumatoid arthritis(RA), and the role of TNF alpha, IFN-gamma and Epo in the pathogenesis of ACD. METHOD: Serum TNF alpha and IFN-gamma levels in RA patients and serum Epo levels in RA with ACD were measured by ELISA. Serum iron status profile in RA patients were also detected. The effects of TNF alpha and IFN-gamma on cobalt-induced erythropoietin production in human hepatic cancer cells(HepG2) were examined. The effect of TNF alpha and IFN-gamma erythroid colony formation (CFU-E and BFU-E) of normal bone marrow cells, and the effect of serum from RA patients and Epo on CFU-E yields of RA bone marrow cells. RESULT: Serum TNF alpha or IFN-gamma in RA and RA with ACD patients were higher than those in normal controls, and were inversely correlated with hemoglobin, and serum iron levels. Serum Epo levels in ACD patients were lower than those in iron-deficiency anemia patients with comparable hemoglobin level. TNF alpha and IFN-gamma could specifically inhibit cobalt-induced Epo production in HepG2 cells, and suppressed normal bone marrow BFU-E and CFU-E growth in a dose-dependent manner. Bone marrow CFU-E yields of RA patients were also suppressed by their own serum. The inhibitory effects of TNF alpha, IFN-gamma or serum from RA patients on erythroid colony formation could be corrected by the addition of rhEpo. CONCLUSION: It suggested that there were hematopoietic inhibiting factors in the serum of RA patients. TNF alpha or IFN-gamma was involved in the pathogenesis of anemia in RA patients. Administration of rhEpo might be beneficial for anemia of RA patients.

Adolescent↗