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F Arai

Publications and source records attributed to F Arai.

At least 37 records · Page 2Linked to original sources
PubMed1998

Macrophage-stimulating protein (MSP) and its receptor, RON, stimulate human osteoclast activity but not proliferation: effect of MSP distinct from that of hepatocyte growth factor.

Stem cell-derived tyrosine kinase (STK) is a member of the hepatocyte growth factor (HGF) receptor family. The ligand for STK, macrophage-stimulating protein (MSP), is a serum protein activated by members of the coagulation cascade. The RON gene is a human homolog of the murine STK. In this study we examined the role of MSP-RON in the signal pathway of human osteoclasts. Using anti-RON antibody, we detected RON expressed in multinucleated osteoclast-like cells (OCLs) formed in cultures of human bone marrow cells. To determine bone resorption, we placed OCLs on thin films of ceramic calcium phosphate formed on quartz plate-coated slides (Millenium Biologix) and measured pit formation. MSP stimulated pit formation by OCLs in a dose-dependent manner. MSP (50 ng/mL) caused a fourfold increase in pit area compared with the control. Furthermore, we examined the effects of MSP and HGF on OCL formation by purified populations of hematopoietic progenitors. OCLs were phenotypically identified by their cross-reactivity with 23c6, a monoclonal antibody that preferentially binds to osteoclasts. HGF (50 ng/mL) stimulated the differentiation of progenitors to 23c6-positive OCLs but did not enhance bone absorption. In contrast, MSP did not affect proliferation of osteoclast precursors but stimulated bone resorption by OCLs. We conclude that the MSP signal transduction pathway plays a role in bone resorption that is distinct from that of HGF.

Bone Marrow Cells↗
PubMed1997

Expression, localization and alternative splicing pattern of fibronectin messenger RNA in fibrotic human liver and hepatocellular carcinoma.

BACKGROUND/AIMS: Fibronectin is a multifunctional glycoprotein and plays important roles in cell-to-cell or cell-to-matrix interaction. The molecular and functional diversity of fibronectin arises from alternative splicing of pre-mRNA at three variable regions, termed ED-A, ED-B and IIICS. Cellular fibronectin with ED-A and ED-B regions has different biological activities from plasma fibronectin lacking these regions. This study was aimed at investigating the type-specific expression of fibronectin in human liver diseases. METHODS: Immunohistochemistry with anti-total and anti-cellular fibronectin monoclonal antibodies, in situ hybridization with cDNA probes detecting common and ED-A regions and RT-PCR to amplify each variable region were performed in 35 specimens, including 4 control, 16 chronic hepatitis, 7 liver cirrhosis and 8 hepatocelular carcinoma. RESULTS: In control liver, there were slight deposits of cellular fibronectin [ED-A(+)fibronectin] in portal areas. In chronic hepatitis, it was strongly deposited at the margin of the fibrously enlarged portal areas where new collagen fibers were formed. Cellular fibronectin was evenly and abundantly accumulated in fibrotic septa in liver cirrhosis, and in fibrotic septa and capsules of tumor nodules in hepatocellular carcinoma. In control liver, cellular fibronectin mRNA was localized in a few hepatocytes and non-parenchymal cells around central veins, and was increased in the same cell populations near fibrously enlarged portal areas as hepatic fibrosis progressed. In hepatocellular carcinoma, it was expressed in most hepatoma cells. Fibronectin mRNA with three variable regions was detectable by RT-PCR in control liver as well as in each disease group. CONCLUSIONS: The expression of cellular fibronectin was increased in fibrotic human liver and hepatocellular carcinoma. In human liver, both non-parenchymal cells and hepatocytes participated together in cellular fibronectin production. In hepatocellular carcinoma, hepatoma cells were the main producer. Our results indicate that, in human liver, cellular fibronectin may participate in the hepatic fibrogenesis and in the malignant phenotypes of hepatocellular carcinoma.

Alternative Splicing↗
PubMed1994

Background levels of total mercury concentrations in blood and urine.

We investigated the background levels of total mercury in blood and urine samples from Japanese subjects without occupational exposure to mercury vapor. Blood and urine specimens were decomposed in sealed Teflon containers, and total mercury concentration was measured by reductive vaporization-gold amalgam capture-atomic absorption spectrophotometry. The mean total mercury concentration in the blood of 56 women aged 34-65 was 18.2 +/- 9.9 ng/ml (range 3.9-56.8 ng/ml). The mean total mercury concentration in the urine of 130 men aged 22-39 was 2.33 +/- 1.50 micrograms/l (range 0.27-10.26 micrograms/l). The mean total mercury concentration in urine adjusted by specific gravity was 2.19 +/- 1.15 micrograms/l (range 0.68-7.68 micrograms/l), and that adjusted by creatinine was 1.51 +/- 0.68 micrograms/g creatinine (range 0.39-4.21 micrograms/g creatinine). These concentrations did not differ greatly from those reported from Europe and Japan. In expressing the total mercury concentration in urine, the creatinine-adjusted range between the minimum and maximum values was smaller than the range adjusted by specific gravity.

Adult↗
PubMed1994

Blood and urinary levels of metals (Pb, Cr, Cd, Mn, Sb, Co and Cu) in cloisonne workers.

Blood and urine samples from cloisonne ware workers were assayed for Pb, Cr, Cd, Mn, Sb, Co and Cu for biological monitoring. Mean blood Pb levels were 47.8 +/- 27.3 micrograms/dl (111-13.3 micrograms/dl) for 49 cloisonne glaze workers, and 0.97 +/- 0.47 microgram/dl (2.4-0.6 microgram/dl) for 62 normal subjects. There was a distinct difference between the 2 groups, and slight differences (p < 0.01) in mean Cr, Cd and Mn levels. There was a distinct difference in mean urinary Pb level between the 2 groups, and slight differences (p < 0.01) in mean Cr, Cd and Mn levels. The correlation coefficient, r, between blood Pb and Cd levels was 0.631 (p < 0.01) for 132 subjects consisting of cloisonne ware workers and normal subjects. r between blood Pb and blood Cr levels was 0.501 (p < 0.01), and that between blood and urinary Pb levels, 0.794 (p < 0.01). The above assays showed that glaze workers at cloisonne plants suffer severe exposure to lead and slight exposure to Cd and Cr.

Antimony↗
PubMed1990

Excretion of tetramethyllead, trimethyllead, dimethyllead and inorganic lead after injection of tetramethyllead to rabbits.

Rabbits were divided to groups of 3, and injected either 9.9 mg of tetramethyllead (Me4Pb)/kg of body weight (7.7 mg Pb/kg) or 39.7 mg/kg (30.8 mg Pb/kg) into the ear vein once only, respectively, and urinary and fecal excretions of lead were studied for chemical species and total lead during the following 7 days. In the group injected 9.9 mg/kg, the urinary total lead excretion was composed of about 73% dimethyllead (Me2Pb2+), about 19% trimethyllead (Me3Pb+), about 6% inorganic lead (Pb2+), and about 2% Me4Pb on the day following the injection, and 100% Me3Pb+ 7 days after the injection. In the group injected 39.7 mg/kg, the urinary total lead excretion was composed of about 67% Me2Pb2+, about 14% Me3Pb+, about 17% Pb2+, and about 2% Me4Pb on the day following the injection, and about 8% Me2Pb2+, about 74% Me3Pb+, about 17% Pb2+, and about 1% Me4Pb 7 days after the injection. In both groups, the fecal total lead excretion during 7 days after the injection was entirely composed of Pb2+. During the 7 days, 1-3% of either administered dose was excreted in the urine, and 7-19% in the feces. The urinary total lead excretion in the rabbits injected Me4Pb was similar to that in the rabbits injected tetraethyllead, but the fecal total lead excretion in the former was extremely smaller. This extremely small fecal excretion of total lead appeared to have resulted from the less elimination of lead into the bile of Me4Pb-injected rabbits.

Animals↗
PubMed1986

[Excretion of triethyl lead, diethyl lead and inorganic lead in the urine and feces of rabbits treated with diethyl lead dichloride].

One group of rabbits were injected intraperitoneally with diethyllead dichloride (7.7 mg Pb/kg) and another group of rabbits were likewise injected with an equivalent lead dose of lead acetate. These rabbits were followed up for changes in the lead amounts excreted daily in the urine and feces from 24 h through 7 d after the injection, respectively. In the group of rabbits injected with diethyllead dichloride (one of 3 rabbits died during the observation), an amount of lead equivalent to about 25% of the injected dose was excreted in the urine during the first 24 h after the injection. Also, an amount of lead equivalent to about 28% of the injected lead was excreted in the feces during the first 3 d, and the total lead excretion during the 7 d after the injection corresponded to about 60% of the injected dose of diethyllead. One day after dosing, the total lead in the urine was made up of about 92% diethyllead, about 7% inorganic lead and about 1% triethyllead. One day after dosing, the total lead in the feces consisted of about 63% inorganic lead, about 28% diethyllead and about 9% triethyllead. Three days after dosing, the total lead in feces comprised about 98% inorganic lead, about 1% diethyllead and about 1% triethyllead. In the group of 3 rabbits injected with lead acetate, the total lead amount excreted in both the urine and feces during the 7 d after the injection corresponded to only about 9% of the injected dose of lead acetate.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗