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Biomedical subjects

K Fukuda

Publications and source records attributed to K Fukuda.

At least 829 records · Page 46Linked to original sources
PubMed1985

The induction of peroxisome proliferation in rat liver by perfluorinated fatty acids, metabolically inert derivatives of fatty acids.

The induction of peroxisome proliferation in rat liver was examined after administration of perfluoro-n-decanoic acid (PFDA, C10), perfluoro-n-octanoic acid (PFOA, C8), perfluoro-n-butyric acid (PFBA, C4), 1-H,1-H-pentadecafluoro-n-octanol (PFOL, C8) perfluorododecane (PFD, C12), and perfluorooctane (PFO, C8). The peroxisome proliferation in the liver was detected by the following methods; 1) measurement of liver weight, 2) assay of hepatic catalase activity, 3) analysis of 600 X g supernatant of liver homogenates by SDS-polyacrylamide gel electrophoresis to observe the induction of the bifunctional enoyl-CoA hydratase in peroxisomes (80K-protein) and 4) observation by electron microscopy. The oral administration of powdered chow containing 0.02%-PFOA and PFBA to male rats of the Sprague-Dawley strain for 2 weeks and the single intraperitoneal injection of corn oil mixed with PFDA, PFOA, and PFOL at the dose of 100 mg/kg induced peroxisome proliferation markedly. PFOL, which has two hydrogen atoms around the hydroxylated carbon, should be metabolized to PFOA, which is an active inducer. Perfluorinated paraffins, PFD and PFO, did not show any induction, indicating the importance of the carboxylic group in the molecule for the peroxisome proliferation. Although the participation of thyroid hormone cannot be excluded, PFOA appears to act directly on the liver.

Animals↗
PubMed1985

Acute tolerance to the analgesic action of nitrous oxide does not develop in rats.

The time course of nitrous oxide analgesia was studied in rats with a behavioral criterion, the tail-flick test to radiant heat. All rats were placed individually in a Plexiglas tube and exposed to either nitrous oxide, 75% in oxygen, or room air (control) for 2 hr. Analgesic potency was evaluated by prolongation of the time required to induce tail-flick. Although individual animals showed variability in the tail-flick time during exposure to nitrous oxide, no animal showed a tendency toward the development of tolerance, and a statistically significant sustained prolongation of tail-flick time was produced.

Analgesics↗
PubMed1985

Pathogenesis of portal sclerosis in the liver with idiopathic portal hypertension. Observations of 19 autopsy cases and animal experiments.

The pathomorphological changes of intrahepatic portal veins were studied in 19 autopsy cases of idiopathic portal hypertension (IPH), and the pathogenesis of portal sclerosis was discussed by the observations on the human and experimental materials. The degree and morphological appearance of intimal lesions vary from vessel to vessel. Fibro-cellular proliferation of subendothelial tissue and incorporation of organized mural thrombi were suggested as the cause of intimal thickening in the portal veins. Animal experiment showed that injury of portal vein wall was followed by intimal hyperplasia and/or incorporation of mural thrombi, and resulted in portal sclerosis similar to that of IPH liver. The cause of portal phlebosclerosis in IPH can not be explained by passive congestion alone. There might be a certain possibility of direct injurious effect in the vessel wall in the pathogenesis of portal lesions of IPH. The following pathogenesis of portal sclerosis in IPH is postulated: phlebo-sclerotic changes of the portal veins are initiated by injury to the vessel wall due to unknown cause(s) and accelerated by secondary thrombosis and/or mechanical injury due to increased portal pressure.

Animals↗
PubMed1985

A Fukuyama type of congenital muscular dystrophy associated with atypical gyrate atrophy of the choroid and retina. A case report.

A three-year-ten-month old boy with the Fukuyama type of congenital muscular dystrophy (FCMD), early onset of muscular hypotonia, severe mental retardation, a slow progressive course and a characteristic fundus appearance similar to that of gyrate atrophy is described. Hyperornithinaemia and iminoglycinuria were not noted. To our knowledge, this is the first reported case of FCMD associated with atypical gyrate atrophy of the choroid and retina.

Amino Acids↗
PubMed1985

Modified anti-C3 immune complex assay which avoids interference by anti-F(ab')2 antibodies.

The present authors and Olds et al. reported that the anti-F(ab')2 antibodies (Abs) in serum interfere with the solid phase (SP) anti-C3 immune complex assay. The anti-F(ab')2 Abs in human sera bind solid phase F(ab')2 anti-C3 of rabbit or goat, and were measured erroneously as C3 bearing circulating immune complexes (CIC). Gel filtration analysis of SP anti-C3 assay revealed that C3 bearing CIC is detected only in heavy fractions and 7S CIC-like activity is not CIC but anti-F(ab')2 activity. As the molecular weight of such CIC is heavy enough to be precipitated by 5% polyethylene glycol (PEG) and IgG anti-F(ab')2 Abs and free C3 are not included in 5% PEG precipitates, 5% PEG precipitates of the test sera were used for SP anti-C3 (Modified SP anti-C3). CIC measured by modified SP anti-C3 were positive in 14/16 at active stage of SLE and positive only in 2/16 at inactive stage. CIC by this test were also correlated well to serum complement activity, and were thought to be clinically reliable and useful.

Antibodies↗
PubMed1985

Circulating immune complex-like materials which bind to heat inactivated C1q interfere with the C1q solid phase assay for immune complexes.

C1q solid phase assay (C1q SP) was devised based on the fact that immune complexes (IC) and aggregated human globulin (AHG) bind to C1q. Neither IC nor AHG was found to bind to heat inactivated C1q. On the other hand, circulating immune complex (CIC)-like materials in patients' sera were able to bind to heat inactivated C1q, indicating that these CIC-like materials are not true CIC. Gel filtration analysis showed that molecular size of such CIC-like materials was almost the same as monomeric IgG, while true CIC were in heavy fractions. True CIC did not bind to heat inactivated C1q but bind only to native C1q. The CIC-like activity is not due to rheumatoid factors. About 2/3 of CIC positive sera by C1q-SP are not really CIC positive but are due to interference by the CIC-like materials.

Animals↗
PubMed1985

A new and specific enzyme-linked immunosorbent assay for the detection of C3 nephritic factor.

C3 nephritic factor (C3 NeF) was measured by assessing its capacity to form complex with C3 and B using an enzyme-linked immunosorbent assay (ELISA). Incubation of C3 NeF with normal human serum in the presence of MgEGTA resulted in a dose-dependent increase of C3-B-IgG complex. No complex was formed in EDTA. The C3 NeF titer estimated in this way was in good accordance with those reported previously by other indirect methods.

Complement C3↗
PubMed1985

Relationship of occupation with cancer of the maxillary sinuses in Hokkaido, Japan.

The age-standardized mortality rates for cancers of the nose, middle ear, and maxillary sinuses in Japan were calculated for 1970 and compared with those for 1975 and 1980. Japan shows a downward trend of these rates in both sexes in recent years. Demographic correlation analyses revealed that only the proportion of persons engaged in the lumber industry was positively correlated with the male maxillary sinus cancer mortality rate. A matched-pair case-control study was performed in Hokkaido in 1982; we collected data by questionnaires mailed to 41 male patients with maxillary sinus cancer and their age-, sex-, and residence-matched community controls and 82 males with laryngeal cancer and their community controls. Family, educational, and past histories of chronic sinusitis were not correlated with either maxillary sinus or laryngeal cancer. A cluster of occupations comprised of workers exposed to some chemical substances, coal miners, and tailors showed a significant elevated risk for maxillary sinus cancer but not for laryngeal cancer.

Demography↗