Biomedical subjects

B Chen

Publications and source records attributed to B Chen.

At least 325 records · Page 18Linked to original sources

PubMed1998

The molecular clock revisited: the rate of synonymous vs. replacement change in Drosophila.

Rates of synonymous and nonsynonymous substitution were investigated for 24 genes in three Drosophila species, D. pseudoobscura, D. subobscura, and D. melanogaster. D. pseudoobscura and D. subobscura, two distantly related members of the obscura clade, differ on average by 0.29 synonymous nucleotide substitutions per site. D. melanogaster differs from the two obscura species by an average of 0.81 synonymous substitutions per site. Using a method developed by Gillespie, we investigated the variance to mean ratio, or Index of Dispersion, R, of substitutions along the three species' branches to test the fundamental prediction of the neutral theory of molecular evolution, E(R) = 1. For nonsynonymous substitutions, the average R, Ra is 1.6, which is not significantly different from the neutral theory prediction. Only 5 of the 24 genes had significantly large Ra valves, and 12 of the genes had Ra estimates of less than one. In contrast, the Index of Dispersion for synonymous substitutions was significantly large for 12 of the 24 genes, with an average of R(s) = 4.4, also statistically significant. These findings contrast with results for mammals, which showed overdispersion of nonsynonymous substitutions, but not of synonymous substitutions. Weak selection acting to maintain codon bias in Drosophila, but not in mammals, may be important in explaining the high variance in the rate of synonymous substitutions in this group of organisms.

Animals↗

PubMed1997

In vivo homologous regulation of mu-opioid receptor gene expression in the mouse.

Regulation of the mu-opioid receptor gene by opioid analgesic drugs has not been observed in rats and mice following in vivo treatments that produce tolerance. Although in vivo heterologous regulation of mu-opioid receptor mRNA by non-opioid compounds has been reported, the failure to observe changes in mu-opioid receptor mRNA levels in vivo after treatment with opioid agonists raised the possibility that in vivo homologous regulation by agonists may not occur. Therefore, in the present study, the effect of a high intrinsic efficacy opioid receptor agonist on opioid receptor density, gene expression and tolerance was determined. Mice were infused with etorphine for 7 days using an osmotic minipump, then the pump was removed and studies conducted 16-168 h later. Etorphine (50-250 microg/kg/day) infusion produced significant dose-dependent tolerance to the analgesic (tailflick) effects of etorphine, as well as dose-dependent mu-opioid receptor downregulation in brain at 16 h following the end of the infusion. Mu-opioid receptor density returned to control levels over a 168 h period following the end of etorphine (250 microg/kg/day) infusion. Similarly, the magnitude of tolerance decreased over the same period. Evaluation of changes in brain mu-opioid receptor mRNA 16 h following etorphine infusion indicated that there was dose-dependent increase in steady-state levels, with no significant change in GAPDH mRNA. The increase in mu-opioid receptor mRNA was approximately 55-65% over control at the highest etorphine infusion dose. Mu-opioid receptor mRNA returned to control levels over a 168 h period following the end of etorphine (250 microg/kg/day) infusion. These data suggest that the increase in mu-opioid receptor mRNA following the termination of etorphine treatment may drive the recovery of mu-opioid receptors. These data are the first demonstration of in vivo homologous regulation of mu-opioid receptor gene expression in the mouse by an opioid receptor agonist that produces tolerance and receptor downregulation.

Analgesics, Opioid↗

PubMed1997

De novo and DNA primer-mediated initiation of cDNA synthesis by the mauriceville retroplasmid reverse transcriptase involve recognition of a 3' CCA sequence.

The Mauriceville mitochondrial retroplasmid of Neurospora encodes a novel reverse transcriptase that initiates cDNA synthesis at a 3' tRNA-like structure of the plasmid transcript, either de novo (i.e. without a primer) or by using the 3' OH group of a DNA primer. Both the de novo and primer-mediated initiations involve recognition of structural features at the 3' end of the retroplasmid transcript, which ends with a 3' CCACCA. Here, detailed biochemical characterization of the retroplasmid reverse transcriptase shows that the 3' CCA of the plasmid transcript is the major structural feature recognized by the reverse transcriptase for both the de novo and primer-mediated initiations. Complementarity between the DNA primer and RNA template is not required for the primer-mediated initiation, although short (1 to 3 nt) base-pairing interactions can influence both the efficiency and site of initiation near the 3' end of the transcript. Single nucleotide changes in the 3' CCA lead to less efficient initiation in the upstream CCA with an increased propensity to add extra "non-coded" nucleotides to the 5' end of the cDNA during de novo initiation or to the 3' end of the primer during primer-mediated initiation. Secondary structure features upstream of the 3' CCA also influence the efficiency of initiation, but are not stringently required in vitro. Finally, we find that the retroplasmid reverse transcriptase does not efficiently use DNA primers that are base-paired to internal positions in the RNA template, nor does it use analogs of natural substrates used by non-long terminal repeat retrotransposon or retroviral reverse transcriptases. Our results indicate that the retroplasmid reverse transcriptase is uniquely adapted to initiate cDNA synthesis by recognizing a 3' CCA sequence. The ability to recognize a specific template sequence is common for RNA polymerases, but unprecedented for a reverse transcriptase.

Base Composition↗

PubMed1997

Protein-tyrosine phosphatase SHP-1 is dispensable for FcgammaRIIB-mediated inhibition of B cell antigen receptor activation.

The inhibitory Fc receptor, FcgammaRIIB, provides a signal that aborts B cell antigen receptor activation, blocking extracellular calcium influx. Because the protein-tyrosine phosphatase SHP-1 binds tyrosyl phosphorylated FcgammaRIIB and FcgammaRIIB-mediated inhibition is defective in motheaten (me/me) mice, which do not express SHP-1, it was proposed that SHP-1 mediates FcgammaRIIB signaling in B cells (D'Ambrosio, D., Hippen, K. L., Minskoff, S. A., Mellman, I., Pani, G., Siminovitch, K. A., and Cambier, J. C. (1995) Science 268, 293-297). However, SHP-1 is dispensable for FcgammaRIIB-mediated inhibition of FcepsilonRI signaling in mast cells (Ono, M., Bolland, S., Tempst, P., and Ravetch, J. V. (1996) Nature 383, 263-266), prompting us to re-examine the role of SHP-1 in FcgammaRIIB signaling in B cells. We generated immortalized sIgM+, FcgammaRIIB+ cell lines from me/me mice and normal littermates. Co-ligation of FcgammaRIIB and the sIgM antigen receptor inhibits calcium influx in both cell lines. Inhibition is reversed by preincubation with anti-FcgammaRIIB antibodies, indicating that it is mediated by FcgammaRIIB. The inositol 5' phosphatase SHIP is recruited to tyrosyl-phosphorylated FcgammaRIIB in both cell lines. FcgammaRIIB-mediated CD19 dephosphorylation also occurs in the presence or the absence of SHP-1. Our results establish that SHP-1 is dispensable for FcgammaRIIB-mediated inhibition of sIgM antigen receptor signaling.

Animals↗

PubMed1997

Tissue-specific expression of the K-ras allele from the A/J parent in (A/J x TSG-p53) F1 mice.

Tissue-specific expression of parental K-ras allele(s) was investigated by single-strand conformation polymorphism analysis of the 3' untranslated region of the K-ras gene in normal lung, spleen, liver and kidney from (A/J x TSG-p53) F1 mice. The expression of A/J K-ras allele was equal to that of C57BL/6J allele in normal spleen, liver and kidney. However, transcripts from A/J K-ras allele were found to be 2-12-times greater than those from C57BL/6J allele in lung tissues harvested over a 20-week period. Similar to our previous observation with dimethylnitrosamine- and benzo[a] pyrene-induced lung tumors, K-ras mRNA transcribed from A/J allele was 10-40-times more abundant than those from C57BL/6J allele in all of 40 (A/J x TSG-p53) F1 mouse lung tumors induced by 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone. In addition, K-ras mutations (G to A transitions at the second base of codon 12) were detected in 38 of 40 (95%) lung tumors and all of the mutations were found on the allele inherited from the A/J parent. These data demonstrate tissue-specific allele-specific transcription of the K-ras gene and provide further support to the thesis that K-ras allele itself is a primary mouse lung tumor susceptibility gene.

Alleles↗

PubMed1997

Physical and functional interactions between the transcriptional inhibitors Id3 and ITF-2b. Evidence toward a novel mechanism regulating muscle-specific gene expression.

We have used an interaction cloning strategy to identify an inhibitory isoform of the ITF-2 transcription factor, ITF-2b, that interacts with the transcriptional inhibitor Id3/HLH462. The interaction was confirmed in vitro, and inside intact myogenic C2C12 cells. As expected, overexpression of either Id3/HLH462 or ITF-2b effectively inhibited the activation of the muscle-specific creatine kinase promoter by the myogenic transcription factor MyoD. However, when overexpressed simultaneously, ITF-2b and Id3/HLH462 counteracted each other's inhibitory effect to produce a reduced overall inhibition. Moreover, while ITF-2b inhibited the creatine kinase promoter, it acted as a weak transactivator on an artificial promoter consisting of three tandem copies of the consensus myogenic factor DNA binding site. Further investigation indicated that the ITF-2b/MyoD heterodimer bound to its specific DNA binding site in vitro, and the DNA binding was effectively blocked by Id3/HLH462. Additional analysis revealed the presence of transcripts for both the activating (ITF-2a) and inhibitory (ITF-2b) isoforms in differentiating C2C12 cultures, suggesting that both isoforms might participate in regulating the differentiation process. Taken together, this study reveals a more complex pattern of regulatory interactions involving the helix-loop-helix proteins than was previously anticipated.

Actins↗

PubMed1997

Inhibition of muscle-specific gene expression by Id3: requirement of the C-terminal region of the protein for stable expression and function.

We have examined the role of an Id-like protein, Id3 (also known as HLH462), in the regulation of muscle-specific gene expression. Id proteins are believed to block expression of muscle-specific genes by preventing the dimerization between ubiquitous bHLH proteins (E proteins) and myogenic bHLH proteins such as MyoD. Consistent with its putative role as an inhibitor of differentiation, Id3 mRNA was detected in proliferating skeletal muscle cells, was further induced by basic fibroblast growth factor (bFGF) and was down-regulated in differentiated muscle cultures. Overexpression of Id3 efficiently inhibited the MyoD-mediated activation of the muscle-specific creatine kinase (MCK) reporter gene. Deletion analysis indicated that the C-terminal 15 amino acids of Id3 are critical for the full inhibitory activity while deleting up to 42 residues from the C-terminus of the related protein, Id2, did not affect its ability to inhibit the MCK reporter gene. Chimeric protein containing the N-terminal region of Id3 and the C-terminus of Id2 was also non-functional in transfected cells. In contrast, wild-type Id3, the C-terminal mutants, and the Id3/Id2 chimera could all interact with the E-protein E47in vitro. Additional studies indicated that truncation of the Id3 C-terminus might have adversely affected the expression level of the mutant proteins but the Id3/Id2 chimera was stably expressed. Taken together, our results revealed a more complex requirement for the expression and proper function of the Id family proteins than was hitherto expected.

Amino Acid Sequence↗

PubMed1997

The unexpected G0/G1 cell cycle status of mobilized hematopoietic stem cells from peripheral blood.

Treatment with a combination of cytokines and chemotherapy can effectively stimulate the release of hematopoietic stem cells (HSC) into the peripheral blood (PB), which can then be harvested for transplantation. The cell cycle status of the harvested HSC from mobilized PB (MPB) is of interest because of the impact that cell cycling may have on optimizing the conditions for ex vivo expansion, retrovirus-mediated gene transfer, and the engraftment of transplanted tissues. Therefore, we characterized the cell cycling status of mobilized HSC from mice and humans. The murine HSC, which express the phenotype c-kit+ Thy-1.1lo Lin-/lo Sca-1+, were purified from PB, bone marrow (BM), and spleen after the mice were treated with the mobilizing regimen of granulocyte colony-stimulating factor (G-CSF) or a combination of cyclophosphamide (CTX) and G-CSF. Human HSC (CD34+ Thy-1+ Lin-) and progenitor cells (CD34+ Thy-1-Lin-) were isolated from the BM of untreated healthy volunteers and from MPB of healthy volunteers and patients treated with G-CSF or a combination of CTX and GM-CSF. Cell cycle status was determined by quantitating the amount of DNA in the purified cells after staining with the dye Hoechst 33342. Fluorescence-activated cell sorting analysis of the progenitor cells from the murine and human samples showed an unexpected finding, ie, virtually none of the cells from the MPB was cycling. The G0/G1 status of HSC from MPB was surprising, because a significant proportion of HSC from BM are actively proliferating and, after mobilization, the HSC in the spleen and BM were also actively cycling.

Animals↗

PubMed1997

Bryostatin 1 (bryo1)-induced monocytic differentiation in THP-1 human leukemia cells is associated with enhanced c-fyn tyrosine kinase and M-CSF receptors.

Bryostatin 1 (bryo1), a naturally occurring macrocyclic lactone derived from the marine bryozoan Bugula neritina is a potent protein kinase C (PKC) activator. In this report, we investigated the role of c-fyn protein, a src-related protein tyrosine kinase (PTK), during bryo1-induced monocytic differentiation in a human leukemia cell line, THP-1. Bryo1 treatment for 24 h inhibited the proliferation of THP-1 cells and caused a major fraction of them to become adherent cells with distinct monocyte/macrophage features and enhanced expression of M-CSF receptors (M-CSFR), a hallmark of mature macrophages. The THP-1 cells in control cultures expressed low but detectable levels of c-fyn proteins. Treatment of THP-1 cells with bryo1 resulted in an enhanced expression of c-fyn proteins, but not c-lyn proteins, another member of the src-family of kinases. The bryo1 treatment also enhanced the levels of both c-fyn tyrosine kinase and autophosphorylation activities in THP-1 cells. Using a combined immunoprecipitation and immunoblot analysis, bryo1 was shown to promote an enhanced association between c-fyn kinase and M-CSFR. The inducing activity of bryo1 was associated with PKC activation; treatment of THP-1 cells with bryo1 led to a rapid and transient elevation of total PKC activity in THP-1 cells. These results show that enhanced expression and activation of fyn kinases are critical events associated with monocytic differentiation induced by bryo1 in THP-1 cells. Our findings may be of clinical relevance, as bryo1 has been used in clinical trials of cancer patients.

Antineoplastic Agents↗

PubMed1997

Induction of macrophage colony-stimulating factor receptor up-regulation in THP-1 human leukemia cells is dependent on the activation of c-fyn protein tyrosine kinase.

We investigated the role of fyn kinase on the expression of macrophage colony-stimulating factor (M-CSF) receptors (M-CSFR) and macrophage differentiation using a human myelomonocytic leukemic cell line THP-1. Treatment of THP-1 cells with Bryostatin 1 (bryo 1), a potent protein kinase C (PKC) activator, caused a major fraction of them to become adherent (AD) with distinct monocyte/macrophage characteristics. The differentiation was associated with an enhanced expression of M-CSFR and fyn tyrosine kinase activity, occurring primarily on cells in the AD fraction. Scatchard plot analysis showed that the enhanced expression of M-CSFR binding activity was due to an increase in total receptor number per AD cell, rather than an increase in the binding affinity. Fyn antisense (AS) phosphorothioate oligonucleotides (s-oligos) inhibited the up-regulation of both M-CSFR and c-fms transcripts in bryo 1-treated THP-1 cells. In contrast, fyn sense s-oligos did not affect the up-regulation of either M-CSFR or c-fms mRNA in bryo 1-treated cells. In addition, fyn AS s-oligos blocked the expression of AD capacity in bryo 1-treated THP-1 cells. The efficacy of fyn AS s-oligos as macromolecular inhibitors was verified by their ability to lower fyn-associated tyrosine kinase and in vitro autophosphorylation activity in bryo 1-treated THP-1 cells. Taken together, our results show a strong correlation between M-CSFR expression and monocytic differentiation in THP-1 cells, and suggest a possible role of c-fyn tyrosine kinase in mediating these processes.

Bryostatins↗

PubMed1997

Binding of vanadate to human erythrocyte ghosts and subsequent events.

Spectroscopic techniques were used to investigate the interaction between vanadate and human erythrocyte ghosts. Direct evidence from 51 V nuclear magnetic resonance (NMR) studies suggested that the monomeric and polymeric vanadate species may bind to the anion binding sites of band 3 protein of the erythrocyte membrane. The results of 51V NMR studies and the quenching effect of vanadate on the intrinsic fluorescence of the membrane proteins indicated that in the low concentration range of vanadate (< 0.6 mM), monomeric vanadate binds mostly to the anion sites of band 3 protein with the dissociation constant close to 0.23 mM. The experiments of sulfhydryl content titration by the method of Ellman and residue sulfhydryl-labeled fluorescence spectroscopies clearly displayed that vanadate reacts directly with sulfhydryl groups. The appearance of the anisotropic election spin resonance (ESR) signal of vanadyl suggests that a small (c.3%) amount of vanadate was reduced by sulfhydryl groups of membrane proteins. The fluidity and order of intact ghost membrane were reduced by the reaction with vanadate, as shown by the ESR studies employing the protein- and lipid-specific spin labels. It was concluded that although vanadates mainly bind to band 3 protein, a minor part of vanadate may oxidize the residue sulfhydryl groups of membrane proteins, and thus decrease the fluidity of erythrocyte membrane.

Anion Exchange Protein 1, Erythrocyte↗

PubMed1997

Inhibition of inducible nitric oxide synthase prolongs rat lung allograft survival.

Nitric oxide (NO) has been demonstrated to be an important immunoregulation molecule in the process of cellular immunologic interactions. Our recent results demonstrated that NO is produced in association with acute allograft rejection and NO inhibition may suppress rejection histologically. This data provides direct evidence of NO in allograft rejection and the immunosuppressive potential of NO inhibitors. In this paper, the effect of NO inhibition on allograft survival was evaluated to investigate the capacity of NO inhibitors as immunosuppressive agents. Seventeen rat left lung transplants from BN donors to F344 recipients were accepted for this study. After surgery, recipients were randomized into two groups and received either aminoguanidine (AG), a highly selective NO synthase inhibitor, 200 mg/kg, intra-peritoneal every 6h (n = 13) or normal saline treatment (n = 4). No production was determined from the recipient's serum nitrite and nitrate levels. Graft survival was monitored via semi-quantitative radiographic aeration scores (AS: 0 = opaque lung to 6 = normal appearing lung). The nitrite and nitrate levels were clearly detectable before the radiographic finding associated with rejection became obvious. Production of NO was significantly inhibited by AG treatment. AG treatment prolonged allograft survival radiographically (12.0 days and 6.0 days for treated and untreated groups respectively, p = 0.0001). These data suggest that the inducible NO is produced in association with acute lung allograft rejection and may serve as a sensitive rejection marker. NO inhibition significantly prolonged rat lung allograft survival but failed to induce immunological tolerance.

Animals↗

PubMed1997

Antenatal steroids and intraventricular hemorrhage after premature rupture of membranes at 24-28 weeks' gestation.

To determine whether antenatal corticosteroid administration after midtrimester premature rupture of membranes (PROM) reduces the incidence or severity of neonatal intraventricular hemorrhage, we identified a cohort of infants delivered between 24 to 28 weeks gestation (n = 75) by mothers with PROM. Information was obtained from a computerized database (n = 3716) of all newborns admitted to the neonatal intensive care unit at a single medical center from 1991 to 1996. We reviewed records of each mother-infant pair to determine antenatal corticosteroid administration, presence, and severity of neonatal intraventricular hemorrhage, and frequency of infectious complications. Using a logistic regression model, antenatal corticosteroid administration was associated with a significantly reduced risk of severe (grade 3-4) intraventricular hemorrhage (0.1 odds ratio, 0.006-0.57, 95% confidence interval), but not a reduced incidence of intraventricular hemorrhage (grade 1-4, 0.4 odds ratio, 0.12-1.05, 95% confidence interval).

Adult↗

PubMed1997

A novel portable grab sampler for tritiated water vapor.

The purpose of this work was to evaluate the applicability of a recently developed portable high-throughput liquid-absorption air sampler for measuring tritiated water vapor concentrations in nuclear facilities. A procedure for sampling tritiated water with a portable high-throughput liquid-absorption air sampler and measuring its concentration in air was developed with the aid of a theoretical model. Tritium concentrations in the air of a heavy water reactor currently being decommissioned, derived from samples obtained with a portable high-throughput liquid-absorption air sampler, a bubbler, and a cold trap, yielded comparable results, suggesting the applicability of the portable high-throughput liquid-absorption air sampler to tritium grab sampling.

Air Pollutants, Radioactive↗

PubMed1997

The use of a PID controller to model vecuronium pharmacokinetics and pharmacodynamics during liver transplantation. Proportional-integral-derivative.

A four-phase proportional-integral-derivative (PID) controller was evaluated under the extremely unstable conditions of liver transplantation. Vecuronium was delivered to achieve 80%-90% neuromuscular blockade as measured by electromyogram (EMG). The first two controller phases delivered boluses and a constant infusion calculated to rapidly achieve setpoint, followed by a proportional-derivative (PD) phase at 35% from setpoint, and PID within 10% of the setpoint. During liver transplantation, the sources of system instability included large blood losses, temperature changes, and loss of hepatic drug metabolism during removal and replacement. During prolonged surgery, and when blood losses were not severe, the EMG remained within 10% of setpoint. Controller performance was more variable during system instability. Plasma sampling and two-compartment modelling of the infusion and response with a weighting factor for blood loss allowed estimation of the sources and degree of instability for improved design of future controllers.

Adolescent↗

PubMed1997

Ameliorating effect of erythromycin on bleomycin-induced pulmonary fibrosis: role of alveolar macrophage activation and cytokine release.

The objective of this study was to evaluate the effectiveness of erythromycin (EM) on bleomycin-induced pulmonary fibrosis in rats and its possible mechanisms. Seventy-five rats were divided into three groups. Alveolar macrophages (AM) were harvested through bronchalveolar lavage (BAL) and consecutive changes of tumour necrosis factor-alpha (TNF-alpha) and platelet-derived growth factor (PDGF) in AM supernatant and bronchoalveolar lavage fluid (BALF) were assayed with ELISA and bioassay, respectively. The AM-derived TNF-alpha was elevated on day 3, peaked day 7 and then decreased but remained at higher level until day 28. The AM-derived PDGF was increased on day 3, peaked on day 7 then decreased to non-statistically significant higher level. The TNF-alpha in BALF was increased significantly on day 3 then decreased to normal level; the peak preceded that of AM-derived TNF-alpha. The PDGF in BALF was increased on day 3, peaked on day 7, and then decreased to normal, which exhibited a consecutive change similar to that of AM-derived PDGF. The EM significantly suppressed TNF-alpha and PDGF release by AM, markedly decreased TNF-alpha and PDGF levels in BALF. The EM also lessened the collagen deposition, the lung hydroxyproline comprised 75.44%, 72.72% and 56.24% that of bleomycin-treated group on day 7, 14 and 28, respectively. In conclusion, EM can ameliorate bleomycin-induced pulmonary fibrosis possibly through suppression of TNF-alpha and PDGF as well as the inhibition on accumulation of inflammatory cells in the lung.

Animals↗

PubMed1997

Dextromethorphan metabolic phenotyping in a Chinese population.

AIM: To establish a phenotyping of dextromethorphan (DM) oxidation polymorphism in a native Chinese population. METHODS: The urine concentrations of DM and its metabolite dextrophan (DX) were assayed by HPLC and metabolic ratios (MR) were calculated in 120 unrelated native Chinese subjects after ingestion of DM 20 mg. RESULTS: The incidence of poor metabolizers was 0.8% (one in 120 subjects). There were distinct dimodal distributions which divided extensive metabolizers into 43 intermediate metabolizers and 76 very extensive metabolizers. The 0-8 h urinary recoveries of DM and DX were 0.4% +/- s 0.5% and 26% +/- s 13%, respectively. There was no difference in 0-8 h urinary recoveries between male and female subjects. CONCLUSION: DM metabolic phenotyping provides a new information for debrisoquine 4-hydroxylation (CYP2D6) polymorphism in native Chinese.

Adolescent↗

PubMed1997

[Changes of extracellular matrix components in bronchoalveolar lavage fluid in patients with idiopathic pulmonary fibrosis].

To clarify the roles of extracellular matrix in pulmonary fibrosis, we determined the levels of fibronectin (FN), hyaluronan (HA) and procollagen III (PC III) in peripheral blood and in bronchoalveolar lavage fluid (BALF) in 13 patients with idiopathic pulmonary fibrosis (IPF) and 11 normal subjects. The levels of FN, HA and PC III in BALF in patient group were not only significantly higher than those in own peripheral blood, but also significantly higher than those in BALF in control group. In patient group, the levels of FN and HA in BALF were respectively correlated with total cell numbers and neutrophils. PC III levels were related to alveolar macrophages. Also, there were positive correlation between FN, HA and PC III in BALF. These results suggested that the productions of FN, HA and PC III within the lung in IPF were increased and that the levels of FN, HA and PC III in BALF might reflect the activity of the disease from different aspects and play a role in estimating prognosis.

Adult↗