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Biomedical subjects

H Okada

Publications and source records attributed to H Okada.

At least 451 records · Page 25Linked to original sources
PubMed1996

Leukaemia inhibitory factor and oncostatin M modulate expression of urokinase plasminogen activator and fibrinogen.

BACKGROUND: Pathogenetic effects of active immune cell products on the coagulation and fibrinolytic system proteins in liver and endothelial cells--primary sites of synthesis of these proteins--have not been elucidated. METHODS: We incubated highly differentiated human hepatoma cells (Hep G2) and human umbilical vein endothelial cells (HUVECs) for 24 h with recombinant human leukaemia inhibitory factor (LIF) and oncostatin M (OSM)--cytokines that are implicated in acute phase reactions during inflammation and which bind to the same cell surface receptor unit (glycoprotein gp 130). LIF was also given to mice in vivo. Contents of coagulation and fibrinolytic system proteins in cell culture supernatants and in mouse liver were determined. RESULTS: LIF increased the accumulation of urokinase plasminogen activator (u-PA) in the Hep G2 cell culture supernatants determined by enzyme-linked immunosorbent assay (ELISA) (0.21 +/- 0.03 (SE) ng/ml at baseline; 0.40 +/- 0.05 ng/ml at 100 U/ml, P < 0.05; 0.57 +/- 0.06 ng/ml at 500 U/ml, P < 0.01; n = 9) without altering total protein content. OSM elicited a similar effect (0.25 +/- 0.04 ng/ml at baseline, 0.62 +/- 0.19 ng/ml at 1 ng/ml; P < 0.05, n = 6). A monoclonal antibody against gp 130 abrogated the response to both agents (n = 9). Plasminogen activator inhibitor type-1 (PAI-1) (assayed by ELISA, n = 9), the PAI-1 binding protein, vitronectin (immunoprecipitation, n = 3) and tissue factor (ELISA, n = 3) were not affected by LIF, but fibrinogen production increased up to twofold with LIF (500 U/ml; Western blot, n= 3). In HUVECs, synthesis of tissue type plasminogen activator or PAI-1 was not altered by LIF or OSM (ELISA, n = 9). In vivo, intraperitoneal recombinant murine LIF (2 mu g) increased liver concentrations of u-PA by 30% and fibrinogen by 220% in mice. CONCLUSIONS: LIF and OSM produced by immune cells may modify fibrinolysis and coagulation by altering expression of u-PA and fibrinogen, thereby contributing to coagulopathy.

Animals↗
PubMed1996

Quantification of the CD55 and CD59, membrane inhibitors of complement on HIV-1 particles as a function of complement-mediated virolysis.

Previous studies have demonstrated that the murine monoclonal antibody (MoAb) NM-01 activates the human complement classical pathway resulting in lysis of human immunodeficiency virus (HIV). The present study was performed to determine the availability of the V3-loop of gp120 relative to the complement regulatory proteins, CD55 (DAF) and CD59 (HRF20) molecules on HIV. The results demonstrate that CD55 and CD59 exist on HIV virions, along with gp120 molecules. These findings suggest that activation of human complement on free viral particles is induced by MoAb NM-01 and that this occurs regardless of the presence of CD55 and CD59 molecules. The destruction of viral particles was demonstrated by a decrease in infectivity. The involvement of human complement in this process was confirmed with an immunoelectron microscopy technique by the presence of a human C9 to prove membrane attack complex (MAC). The results indicate that NM-01 can induce complement activation because of the ratios of CD55 and CD59 to gp120 molecules on HIV virions. The availability of the gp120 V3 domain on the virion is sufficient for binding of NM-01 and thereby the formation of MAC that results in virolysis.

Antibodies, Monoclonal↗
PubMed1996

Epithelial cell proliferation during colonic chemical carcinogenesis in the rat.

To define the significance of alterations in epithelial cell proliferation as a marker of high risk mucosa for colorectal cancer, we examined cell proliferative events in the colonic mucosa during chemical carcinogenesis using in vitro bromodeoxyuridine labelling and by analysing serial colonoscopic biopsy specimens from dimethylhydrazine (DMH)-treated rats. In both the rectum and flexure of the colon, an increased labelling index of colonic epithelial cells, an upward extension of the proliferating zone and an upward shift of the major area of DNA synthesis of epithelial cells were observed during DMH-induced colonic carcinogenesis in rats. These changes preceded the development of the colonic tumour and were observed in endoscopically normal rectal mucosa where the tumour was absent. We confirmed the altered cell proliferative events preceding the development of the tumour by examining serial colonoscopic biopsies. The results suggest that these alterations are features that identify premalignant colonic mucosa in DMH-treated rats.

Animals↗
PubMed1996

Metenkephalin in seminal plasma of infertile men.

BACKGROUND: Enkephalin is one of the opioids, which is expressed widely in reproductive organs. However, the function of enkephalin in male reproduction is not completely understood. The effect of metenkephalin on sperm motility remains especially controversial. In this study we examined the level of metenkephalin in seminal plasma from men with normal sperm production and patients with asthenospermia, oligospermia, and azoospermia to investigate the role of metenkephalin in seminal plasma on sperm function. We also investigated the effect of metenkephalin on sperm motility in vitro. METHODS: Sixty nine infertile patients (31 oligospermic, 21 asthenospermic, and 17 azoospermic) were included in this study. The level of metenkephalin in seminal plasma of these men was measured and the effect of the peptide on the motility of human sperm was examined in vitro. Seventeen men with normal seminograms were a control group. RESULTS: The level of metenkephalin in the seminal plasma of semen from asthenospermic men was significantly lower than that from the controls (P < 0.05). No significant correlations between the level of metenkephalin and the mean pathing or progressive velocity of sperm, or serum hormone levels were observed. In the in vitro study, which used semen from the controls, treatment of sperm with metenkephalin (50-200 pg/mL) maintained sperm motility for 4 hours. On the other hand, motility of sperm incubated without metenkephalin began to decrease at 3 hours. Metenkephalin levels of 50 pg/ mL in seminal plasma is considered to be necessary for maintaining sperm motility. CONCLUSION: These results suggest that metenkephalin in seminal plasma is an important clue in the investigation of decreased sperm motility.

Enkephalin, Methionine↗
PubMed1996

Comparison of hormonal therapy and chemohormonal therapy in patients with newly diagnosed clinical stage D prostatic cancer.

BACKGROUND: In order to examine the usefulness of chemohormonal therapy, we conducted a multicentered randomized trial comparing hormonal therapy, using a luteinizing hormone-releasing hormone (LH-RH) agonist, with chemohormonal therapy, hormonal therapy plus cyclophosphamide (CPM), in patients with newly diagnosed clinical stage D prostatic cancer. METHODS: Between January 1991 and March 1995, 41 evaluable patients with stage D prostatic cancer were randomized into 2 groups: group A (hormonal therapy alone), goserelin acetate depot 3.6 mg subcutaneously every 4 weeks: group B (chemohormonal therapy), goserelin acetate depot 3.6 mg subcutaneously and CPM 1000 mg/m2 intravenously every 4 weeks. The responses to the therapies were evaluated based on the criteria of The Japanese Urological Association. RESULTS: There were no significant differences between the 2 groups with regard to objective and subjective response rates. No advantage in chemohormonal therapy was observed in the survival rate and progression-free survival rate. However, the survival rate and progression-free survival rate of responders were significantly higher than those of nonresponders in both groups. When the results were categorized by histologic grade patients with poorly-differentiated adenocarcinoma had significantly higher response rates, survival rates, and disease-progression-free survival rates in Group B compared to similar patients in Group A. CONCLUSIONS: We conclude that chemohormonal therapy does not definitely improve the clinical response and prognosis of patients with stage D prostatic cancer; however, for patients with poorly-differentiated adenocarcinoma, chemohormonal therapy is a useful treatment.

Aged↗
PubMed1996

Antigen-presenting-cell function of interferon gamma-treated human gingival fibroblasts.

The present study was carried out to examine the antigen-presenting cell (APC) functions of human gingival fibroblasts (HGF) elicited with IFN gamma. Stimulation of HGF with IFN gamma clearly induced HLA-DR expression and enhanced expression of intercellular adhesion molecule-1 (ICAM-1) on HGF. Despite the phenotypical resemblance of IFN gamma-treated HGF to so-called APC, HLA-DR positive HGF were unable to induce proliferation of allo-reactive peripheral blood T cells (PBT) isolated from different donors. The failure of IFN gamma-treated HGF to stimulate unprimed allo-reactive PBT was not due to the lack of production of IL-1 or the immunosuppressive effect of PGE2 from HGF. On the other hand, the fact that detectable expression of CD80, ligand for CD28, was not found on IFN gamma-treated HGF may at least in part explain the ineffective function of HGF as APC. Interestingly, IFN gamma-treated HGF induced proliferation of primed allo-reactive CD4+ T cells in a HLA-DR dependent manner, suggesting that IFN gamma-treated HGF may have the ability to stimulate pre-activated T cells. We then confirmed that high levels of IFN gamma mRNA were detectable in inflamed gingival tissue. Although it cannot be concluded from this study that HGF are incapable of effectively presenting antigenic peptides to autologous T cells bearing appropriate T cell receptors, present results suggest that HGF may be affected by locally-secreted IFN gamma and that the IFN gamma-stimulated HGF may play a role in regulating immune responsiveness in inflammatory periodontal lesions.

Antigen-Presenting Cells↗
PubMed1996

Human pregnancy serum suppresses the proliferative response of lymphocytes to autologous PHA-activated T lymphoblasts.

PROBLEM: We have previously demonstrated that human serum can suppress the proliferative response in autologous mixed lymphocyte reaction (AMLR) in which phytohemagglutinin (PHA)-activated T lymphoblasts act as stimulators (T-TPHA AMLR). The aim of the present work was to determine whether pregnancy serum (PS) possesses an inhibitory capacity similar or different in magnitude. METHODS: Sixteen PS were added to T-TPHA AMLR cultures and the proliferative response was compared with that in the presence of human serum. The effect of PS on the IL-2 dependent proliferation of PHA-activated T Lymphoblasts was examined as well. RESULTS: PS induced a significantly more pronounced suppression of T-TPHA AMLR than human serum (P < 0.05). One PS tested was not inhibitory but rather stimulatory. This PS was obtained from a woman who subsequently had IUGR. The inhibition is related to the existence of a serum inhibitory factor and not to the lack of a serum supporting factor. PS inhibited not only T-TPHA AMLR of the same woman but also T-TPHA AMLR of other individuals as well, implying that the inhibitor is a non-MHC restricted factor. IL-2 dependent cell proliferation was not inhibited by PS, implying that the inhibitor detected in T-TPHA AMLR is not a general cell proliferation inhibitor. CONCLUSIONS: These results suggest that a non-MHC restricted inhibitory factor present in PS may play an important biological role in regulating local immune responses in the fetal-placental unit mediated by autoreactive T cells restricted to autologous activated T lymphocytes.

Antilymphocyte Serum↗
PubMed1996

Diagnostic strategies of periodontitis based on the molecular mechanisms of periodontal tissue destruction.

OBJECTIVE: Periodontitis is a disease showing differences in disease progression between patients and between sites within a patient. Routine clinical examinations today are not useful enough to distinguish susceptible patients and active lesions from resistant patients and chronic lesions. Diagnostic markers should be pathogenic and inflammatory factors participating in periodontal tissue destruction. These are both local and systemic factors. MATERIALS AND METHODS: First of all, pathogenic factors and proinflammatory cytokines or mediators in gingival crevicular fluid (GCF) were examined and the difference was found between active and inactive periodontitis lesions distinguished by attachment loss. Active lesions were detected by discriminant-function analysis of these examinations, although the sensitivity of differential diagnosis was low. Then, we established a novel needle biopsy for understanding the pathophysiological conditions elicited in active and chronic inflammatory processes of periodontal tissue destruction. A variety of cytokines and mediators were detected in biopsied specimens by reversed transcription polymerase chain reactions (RT-PCR). Cytokine profiles were varied in inflammed periodontal biopsies. As IFN gamma mRNA expression was enhanced in inflamed gingiva, antigen-presenting-cell (APC) functions of human gingival fibroblasts (HGF) were examined. RESULTS: Despite the phenotypical resemblance of IFN gamma-treated HGF to so-called APC, HLA-DR positive HGF could not induce proliferation but suppressed proliferation of alloreactive peripheral blood T cells (PBT). However, HLA-DR positive HGF stimulated the proliferative responses of PBT which had been primed with allo-APC. Regulatory immune responses by IFN gamma were different in T cell conditions. CONCLUSIONS: Various kinds of cytokines participated in periodontal inflammation, and every cytokine is multi-functional. Complex and compound inflammatory processes can be clarified by examining cytokine networks and the precise effects of each cytokine on each of the cell types comprising periodontal tissue. It is, therefore, necessary for establishing diagnostic strategies to integrate pathogenic and inflammatory factors in periodontal tissue destruction.

Antibodies, Bacterial↗
PubMed1996

Two types of novel dipeptidyl aminopeptidases from Pseudomonas sp. strain WO24.

Two kinds of dipeptidyl aminopeptidase I (DAP I [cathepsin C])-like activities which hydrolyze Gly-Phe-p-nitroanilide (Gly-Phe-pNA) were detected in Pseudomonas sp. strain WO24. They were purified and characterized. The isolated enzymes, named DAP BII and DAP BIII, were revealed to be homogeneous by sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE) and isoelectric focusing. DAP BII was estimated to have a molecular mass of 150,000 Da by gel filtration and a subunit size of 73,000 Da by SDS-PAGE, indicating it to be a homodimer. The molecular mass of DAP BIII was evaluated to be approximately 60,000 Da by gel filtration and 69,000 Da by SDS-PAGE, indicating that it is monomeric. The isoelectric points of DAP BII and DAP BIII were 6.1 and 5.0, and their optimal pHs were 8.0 and 8.5 to 9.0, respectively. The result of peptide mapping for DAP BII and DAP BIII showed that these enzymes consist of different components. Both enzymes were completely inhibited by diisopropylphosphofluoride but not by general thiol inhibitors, indicating that they are serine proteases. DAP BII and DAP BIII hydrolyzed Gly-Phe-pNA but not Gly-Arg-pNA, both of which are model substrates for mammalian DAP I. Despite these shared activities toward DAP I, DAP BII released dipeptides from Ala-Ala-pNA and Lys-Ala-4-methylcoumarinamide (a substrate for DAP II), whereas DAP BIII did not hydrolyze either of these compounds and was presumed to prefer substrates composed of bulky, hydrophobic amino acids at P1 and P1' positions. In addition, DAP BII showed no endopeptidase activity, whereas DAP BIII possessed the activity on N-terminally blocked peptide derivatives besides exopeptidase activity. Assays performed with bioactive peptides such as angiotensin I and neuromedin N as substrates indicate that DAP BII has a considerably broader substrate specificity than DAP BIII and is able to hydrolyze an X-Pro bond, an imido bond that few peptidases and no known DAPs can cleave. These characteristics, namely, substrate specificities, molecular mass, pI, peptide mapping, pH optimum, and effect of inhibitors, suggested that the two DAPs purified in this work are distinct enzymes and do not belong to any of the previously reported DAP classes.

Bacterial Proteins↗
PubMed1996

A novel dipeptidyl aminopeptidase from Pseudomonas sp. strain WO24.

An activity similar to that of dipeptidyl aminopeptidase I (DAP I) which releases dipeptide from Gly-Arg-p-nitroanilide (Gly-Arg-pNA) was detected in a Pseudomonas sp. An enzyme was isolated and purified about 400-fold by a series of column chromatographies. The enzyme, named DAP BI (DAP from bacteria, type I), was revealed to be homogeneous by sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE) and isoelectric focusing. The molecular mass was estimated to be 82 kDa by SDS-PAGE and 65 kDa by gel filtration, suggesting that the enzyme may be a monomer. The enzyme had an isoelectric point of 4.7. It is optimally active at pH 9.0. The Km and Vmax of the enzyme for Gly-Arg-pNA were 0.25 mM and 195 micromol/min/mg, respectively. The purified enzyme did not hydrolyze Gly-Phe-pNA, which was also a substrate for DAP I, whereas it hydrolyzed Arg-Arg-4-methoxy-beta-naphthylamide (Arg-Arg-MNA), a model substrate for DAP III. The Km and Vmax for Arg-Arg-MNA were 0.019 mM and 145 micromol/min/mg, respectively. This purified enzyme can also catalyze the removal of Asp-Arg from the N termini of angiotensins I and II. The enzyme activity was completely inhibited by Zn(II) (0.5 mM), tosyl-L-Lys-chloromethyl ketone (0.1 mM), and leupeptin (0.1 mM) and partially inhibited by Co(II) (0.5 mM) and chymostatin (0.1 mM), whereas the enzyme was not affected by general serine protease inhibitors (phenylmethylsulfonyl fluoride and diisopropylfluorophosphate) and thiol protease inhibitors. The substrate specificity, classification of catalytic site, and other enzymatic properties demonstrate that this enzyme is distinct from the previously described mammalian DAPs I and III and Saccharomyces cerevisiae DAP III. These results indicate that DAP BI may be a new type of the DAP family.

Amino Acid Sequence↗
PubMed1996

Interleukin-4 modulates collagen synthesis by human mesangial cells in a type-specific manner.

Several studies have suggested an involvement of interleukin (IL)-4 in the pathophysiology of glomerulonephritis (GN). To elucidate its possible role in GN, we have investigated the effect of IL-4 on collagen accumulation by human mesangial cells (MC). After incubation with IL-1 alpha and/or IL-4 for 48 h, type I, III, and IV collagens in both soluble and cell-associated forms were identified by Western blotting. IL-1 alpha stimulated type I and IV collagen synthesis, lacking significant effect on type III collagen synthesis. In contrast, IL-4 stimulated type III collagen synthesis without affecting type I and type IV synthesis. Enzyme-linked immunosorbent assay confirmed the dose-dependent effect of IL-4 on collagen type III secretion (2.0-fold at 10 ng/ml). Importantly, IL-1 alpha-stimulated type I and IV collagen synthesis was suppressed by concomitant IL-4 treatment. Northern analysis of type I and III procollagen mRNAs displayed consistent results. These data indicate that IL-4 selectively stimulates type III collagen synthesis but also suppresses IL-1 alpha-stimulated type I and IV collagen synthesis. Therefore IL-4 could potentially contribute to the pathological changes in glomerular diseases in cooperate with other cytokines.

Blotting, Western↗
PubMed1996

Delayed and diminished pressor response to muscle sympathetic nerve activity in the elderly.

We studied the effects of aging on alpha-receptor-mediated vasoconstrictive responses to sympathetic nerve activity in 16 healthy aged [75.8 +/- 2.7 (SE) yr] and young men (33.8 +/- 2.0 yr). Muscle sympathetic nerve activity (MSNA), heart rate, and blood pressure were analyzed during slow respiration (0.1 Hz). Peak amplitude and phase were calculated from a cosine function fitted with 0.1 Hz by using the least squares method. The latency of the pressor response to MSNA, defined as lag time from the peak of MSNA to diastolic blood pressure, was significantly longer in the aged than the young group (7.1 +/- 0.3 vs. 5.4 +/- 0.4 s; P < 0.01). The extent of pressor response to MSNA, defined as diastolic blood pressure rise in response to increase in total MSNA, was significantly lower in the aged than the young group (0.038 +/- 0.006 vs. 0.099 +/- 0.024 mmHg/unit, P < 0.001). These results suggest that alpha-receptor-mediated vasoconstrictive responses to MSNA may be attenuated in the elderly.

Adult↗
PubMed1996

Inhibition of human complement-dependent cell lysis by bovine aortic endothelial cells transfected with membrane-bound complement-regulatory factor (DAF and HRF20) gene using a retroviral vector.

The endothelial cells (EC) of xenografts are the target of hyperacute rejection induced by complement activation via the classical and/or the alternative pathway. To protect these cells from the attack of human complement, decay-accelerating factor (DAF, CD55) and homologous restriction factor 20 (HRF20, CD59), which belong to human complement regulatory factors, were transfected into bovine aortic EC (BAEC) using retroviral vector. Cell surface expression of DAF and HRF20 on BAEC transfectants (BAEC/DAF, BAEC/HRF20) is comparable to that on human umbilical vein EC. Phosphatidyl inositol-phospholipase C treatment diminished or abolished cell surface expression of DAF and HRF20 on BAEC. The addition of human serum to BAEC led to complement-dependent cell lysis, whereas practically no lysis was observed after addition of human serum to BAEC/DAF and BAEC/HRF20. The addition of human serum plus rabbit complement to BAEC/DAF and BAEC/HRF20 caused complement-dependent cell lysis that was comparable to that observed for BAEC. These data demonstrate that xenograft EC transfected with DAF or HRF20 cDNA using retroviral vector are protected from complement-dependent cell lysis.

Animals↗
PubMed1996

Evidence for the involvement of vasopressin in the pathophysiology of adriamycin-induced nephropathy in rats.

The effect of orally available, nonpeptide vasopressin V1 and V2 receptor antagonists on chronic progressive glomerular disease was investigated in Wistar rats with Adriamycin-induced nephropathy. At weeks 0 and 3, Adriamycin was injected twice, and at week 3 drugs started to be given as follows: groups 2 and 3 were treated with V1 and V2 antagonists, respectively, while the untreated group 1 served as control. To block the effects of vasopressin totally, both V1 and V2 antagonists were simultaneously administered (group 4). At weeks 8 and 10, V1 and V2 antagonists given either alone or combined significantly reduced the urinary protein excretion to the same levels. Urinary volume increased in groups 3 and 4 from week 4. Systolic blood pressure did not significantly increase in all groups during the study. Histological alterations in the kidney of groups 2, 3 and 4 were significantly attenuated compared to the control. These results suggest that both vasopressin V1 and V2 agonism plays a role in the pathophysiology of Adriamycin-induced nephropathy despite plasma levels of vasopressin within the normal range. These findings also lead to the notion that in some types of nephrotic patients these orally available V1 and/or V2 receptor antagonists may be effective for reduction of proteinuria and for retardation of progression of renal failure.

Animals↗
PubMed1996

Anticataract action of vitamin E: its estimation using an in vitro steroid cataract model.

The aim of this study was to estimate the anticataract action of vitamin E using an in vitro methylprednisolone (MP)-induced cataract model. The same severity of early cortical cataract was induced in lenses isolated from male Wistar rats aged 6 weeks by incubation with MP (1.5 mg/ml) in TC-199 medium. The cataractous lenses showed slight increases in lipid peroxide (LPO) content and Na+/K+ ratio and slight decreases in reduced glutathione (GSH) content and glyceraldehyde-3-phosphate dehydrogenase (GAP-DH), a sensitive index of oxidative stress, and Na+,K(+)-ATPase activities. When the cataractous lenses were further incubated in TC-199 medium with and without vitamin E (250 micrograms/ml) for 48 h, the progression of cataract was prevented in the vitamin E-treated lenses, but not in the vitamin E-untreated lenses. The vitamin E-untreated lenses showed a decrease in vitamin E content and an increase in water content in addition to further increases in LPO content and Na+/K+ ratio and further decreases in GSH content and GAP-DH and Na+,K(+)-ATPase activities. In contrast, the changes of these components and enzymes except for GSH were attenuated in the vitamin E-treated lenses. From these results, it can be estimated that vitamin E prevents in vitro cataractogenesis in rat lenses treated with MP by protecting the lenses against oxidative damage and loss of membrane function.

Animals↗
PubMed1996

CD44-hyaluronate interaction participates in the adherence of T-lymphocytes to gingival fibroblasts.

It has already been clarified that peripheral blood T-lymphocytes which had been activated with phorbol 12-myristate 13-acetate (PMA) acquired the ability to bind to human gingival fibroblasts (HGF) and that the adherence was mediated by VLA integrins. However, these studies also raised the possibility that molecules other than VLA integrins should be involved in the adherence between T-lymphocytes and HGF. In this study, the possible involvement of CD44, a hyaluronate receptor, in heterotypic cell-cell interactions was investigated. It was confirmed that PMA-activated T-lymphocytes strongly adhered to plate-coated hyaluronate and that the hyaluronate binding was clearly inhibited by the addition of OS/37, a newly established mAb specific for the hyaluronate-binding epitope on CD44. Interestingly, OS/37 also blocked the HGF binding of the activated T-lymphocytes when the adherence to HGF was assessed at 4 degrees C, at which temperature the adhesion of integrin molecules diminished, while that of CD44 functioned normally. Immunofluorescence staining revealed that hyaluronate was anchored along the cell surface of HGF. Furthermore, the binding of activated T-lymphocytes to HGF was significantly inhibited by the treatment of HGF with hyaluronidase. These results clearly demonstrated that CD44-hyaluronate interactions participated at least in part in the adhesiveness of T-lymphocytes to HGF.

Antibodies, Monoclonal↗