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Biomedical subjects

K Kataoka

Publications and source records attributed to K Kataoka.

At least 163 records · Page 9Linked to original sources
PubMed1998

Pathophysiologic studies of experimental chronic pancreatitis in rats induced by injection of zein-oleic acid-linoleic acid solution into the pancreatic duct.

An experimental model of chronic pancreatitis was induced by a retrograde injection of a viscous solution consisting of zein-oleic acid-linoleic acid (0.05 ml/100 g body weight) into the rat pancreatic duct. Histologic and biochemical changes were investigated over a period of 6 months after induction of this model. The treated rats gained weight, but pancreatic weight decreased with time. Histologically, the widening of acinar lumen and cellular vacuolization occurred within 24 h at the parenchyma neighboring the small ducts filled with the injected solution. Degenerative parenchyma, interstitial edema, and inflammatory cell infiltration were pronounced 1 week later. Thereafter, duct-like tubular complex formation progressed, and the exocrine tissue exhibited marked atrophy of the gland with irregular fibrosis and fat replacement over a period of 6 months. Pancreatic contents of protein, amylase, DNA, and RNA markedly decreased, as did pancreatic weight, whereas hydroxyproline content increased. Oral administration of camostat did not affect pancreatic weight and contents of enzyme in this model. Urinary para-aminobenzoic acid (PABA) excretion in the BT-PABA test decreased to 54% at 6 weeks and 22% at 6 months. Although three quarters of pancreatic immunoreactive insulin (IRI) content was lost after 6 months, overt diabetes did not occur. The results suggest that an obstructive mechanism in the small ducts plays an important role in the genesis and development of chronic pancreatitis.

Amylases↗
PubMed1998

Effect of chronic amylase inhibition on pancreatic growth and acinar cell secretory function in rats.

Wheat amylase inhibitor (WAI) was given to growing rats to determine whether chronic inhibition of intraluminal amylase activity alters pancreatic growth, pancreatic enzyme composition, and secretory responsiveness to cholecystokinin octapeptide (CCK-OP) and carbachol. For 21 days 13 rats were fed amylase inhibitor (AI) as 2.72% of the weight of their food; 13 were pair-fed controls (PFC), and 12 were controls with free access to food (FAC). Amylase and lipase secretion was measured from isolated pancreatic acini in response to CCK-OP (10(-12)-10(-8) M) and carbachol (10(-8)-10(-3) M). AI and PFC rats had similar food intakes and weight gains, pancreatic weights, and contents of enzymes (amylase, lipase, trypsin, chymotrypsin), protein, and RNA, but these measurements were significantly reduced compared to those of FAC rats. DNA contents per milligram of pancreas and per gram of body weight and amylase/DNA and trypsin/DNA were similar among all groups. Lipase/DNA and chymotrypsin/DNA in AI rats were the same as in PFC rats but significantly lower than in FAC rats. In response to CCK-OP, amylase secretion was similar in all three groups, but in response to carbachol amylase secretion was significantly less in AI compared to PFC and FAC rats. Lipase secretion increased in response to CCK-OP in AI compared to PFC and FAC rats but was similar in all three groups in response to carbachol. Long-term inhibition of intraluminal amylase activity suppresses pancreatic growth and content of enzymes and RNA by reducing food intake and weight gain and also decreases acinar cell secretion of amylase in response to carbachol and increases lipase secretion in response to CCK-OP.

Amylases↗
PubMed1998

Culture supernatants of Lactobacillus acidophilus and Bifidobacterium adolescentis repress ileal ulcer formation in rats treated with a nonsteroidal antiinflammatory drug by suppressing unbalanced growth of aerobic bacteria and lipid peroxidation.

A nonsteroidal antiinflammatory drug, 5-bromo-2-(4-fluorophenyl)-3-(4-methylsulfonylphenyl) thiophene (BFMeT), induced ileal ulcers in rats after oral administration, while no ulcers were observed after subcutaneous injection. The ileal ulcer formation in BFMeT-treated rats was examined to correlate the administration of cultures of Lactobacillus acidophilus or Bifidobacterium adolescentis with intestinal bacteria in the ileal contents and lipid peroxidation of the small intestinal mucosa. Ileal ulcers were observed in more than 85% of the rats treated with BFMeT at a dose of 1,000 mg/kg when they were given tap water as drinking water. The incidence of ulcer formation was repressed by giving culture supernatants of L. acidophilus or B. adolescentis as drinking water, but not by giving the cell suspension as drinking water. Gram staining of the ileal contents of normal rats revealed that 97% of the stained bacteria were gram-positive rods and only 1.5% were gram-negative rods. The percentage of gram-negative rods 72 hr after BFMeT administration was 49.8% and increased over 30-fold in BFMeT-treated rats. However, the percentage of gram-negative rods was 9.7 % or 16%, respectively, in rats taking culture supernatants of L acidophilus or B. adolescentis. In addition, thiobarbituric acid-reactive substances in the ileal mucosa increased significantly in the rats given tap water for 72 hr after BFMeT treatment, but not in rats given the culture supernatants of L. acidophilus or B. adolescentis. Since BFMeT induced an unbalanced intestinal microflora, the effect of antibiotic treatment on ulcer formation in rats was examined. The magnitude of the ulcer formation in the antibiotic-treated rats was, in decreasing order, metronidazole >none > kanamycin > a mixture (bacitracin, neomycin and streptomycin). These results suggest that the intestinal microflora plays an important role in ulcer formation and that a metabolite(s) of L. acidophilus and B. adolescentis inhibits ileal ulcer formation by repressing changes in the intestinal microflora and lipid peroxidation in BFMeT-treated rats.

Administration, Oral↗
PubMed1998

Protective effects of a culture supernatant of Lactobacillus acidophilus and antioxidants on ileal ulcer formation in rats treated with a nonsteroidal antiinflammatory drug.

Ileal ulcers and thiobarbituric acid (TBA)-reactive substances in the ileal mucosa were induced in rats treated with a nonsteroidal antiinflammatory drug, 5-bromo-2-(4-fluorophenyl)-3-(4-methylsulfonylphenyl)thiophene (BFMeT), at a dose of 1,000 mg/kg administered with tap water as drinking water. However, the formation of ileal ulcers and TBA-reactive substances in the ileal mucosa was repressed by giving the animals a culture supernatant of Lactobacillus acidophilus as drinking water. We measured the antioxidative activity of the culture supernatant and found that the supernatant inhibited the formation of t-butyl hydroperoxide-induced TBA-reactive substances in erythrocyte membrane ghosts. Therefore, the effects of various known antioxidative compounds on the ileal ulcer formation induced by BFMeT were investigated. While alpha-tocopherol, t-butyl-1,4-hydroxyanisole and allopurinol did not repress ulcer formation after BFMeT treatment, ascorbic acid, dimethyl sulfoxide, glutathione and beta-carotene significantly inhibited formation. Among these compounds, ascorbic acid was the most effective. Accumulation of TBA-reactive substances in the ileal mucosa after BFMeT treatment also decreased significantly in rats treated with ascorbic acid. In addition, the percentage of gram-negative rods in the ileal contents of rats treated with BFMeT and tap water was dramatically increased, but it was not increased in rats treated with BFMeT and these antioxidants. A positive correlation between the percentage of gram-negative rods and the number of ileal ulcers was also observed. These results suggest that lipid peroxidation mediated by oxygen radicals plays an important role in the induction of ileal ulcers by BFMeT in rats, and that lipopolysaccharide-activated neutrophils probably produce highly reactive hypochlorous acid and hydrogen peroxide, which are inactivated by ascorbic acid and glutathione, respectively.

Animals↗
PubMed1998

A disrupted cholecystokinin A receptor gene induces diabetes in obese rats synergistically with ODB1 gene.

Otsuka Long-Evans Tokushima fatty (OLETF) rats develop hyperglycemia, hyperinsulinemia, and mild obesity, which are characteristic of human non-insulin-dependent diabetes mellitus. We have shown that two recessive genes, ODB1 mapped on the X chromosome and ODB2 mapped on chromosome 14, are involved in the induction of the diabetes in OLETF rats. Recently we found that OLETF rats are the naturally occurring cholecystokinin type A receptor (CCKAR) gene knockout rats. In this study, we focused on the genotype of CCKAR gene and the ODB1 gene in regulation of glucose homeostasis in the F2 cross of the OLETF rats. Relatively high plasma glucose levels were observed in the F2 offspring with the homozygously disrupted CCKAR gene. A synergistic effect for increasing plasma glucose levels in F2 rats between disrupted CCKAR gene and the ODB1 gene was shown. The CCKAR gene was found to map very close to ODB2 by a linkage analysis using microsatellite markers. These results suggest that CCKAR gene maintains normoglycemia in rats.

Animals↗
PubMed1998

Minimized platelet interaction with poly(2-hydroxyethyl methacrylate-block-4-bis(trimethylsilyl)methylstyrene) hydrogel showing anomalously high free water content.

Novel hydrophilic-hydrophobic block copolymers - poly(2-hydroxyethyl methacrylate-block-4-bis(trimethylsilyl)methylstyrene) (poly(HEMA-block-BSMS) or BH polymer) - were prepared as materials potentially useful for blood-contacting devices. Among the BH(X) series including poly(HEMA) itself, platelet adhesion and activation are minimum on the surface of BH(10), the block copolymer composed of 10 mol% of the hydrophobic segment. The unique physicochemical characteristics of BH(10) such as the high free water content and the increased mobility of PHEMA segments seem to play an important role in the prevention of platelet adhesion and activation. The water content of BH(10) was twice that of poly(HEMA) itself, even in the presence of 10 mol% of the hydrophobic moiety [poly(BSMS)]. Further, an anomalous increase in free water content was observed for the BH(10) sample measured by DSC. The glass transition temperature of BH(10) in the dry state was determined to be c. 10 degrees C, which was much lower than that observed for each of the homopolymers (c.f.: Tg [poly(HEMA)] = 70 degrees C; Tg [poly(BSMS)] = 160 degrees C), suggesting an increased mobility of tethered PHEMA segments in the BH(10) film.

Acrylic Resins↗
PubMed1998

[Intracellular gene delivery by polymer micelle vectors].

This review paper deals with the development of novel vector system for gene and antisense oligonucleotides. The system is based on the self-association of poly(ethylene glycol)-poly(L-lysine) block copolymer with DNA to form polyion complex micelles with unimodel size distribution in the range of 50-100 nm. DNA molecules are compactly assembled into the core of the micelle, surrounding with the dense corona of poly(ethylene glycol). High resistance to nuclease attack was demonstrated for micellized DNA in the serum-containing medium, indicating the potential of micelle vector system to stabilize DNA in physiological condition. Significant gene expression was confirmed by luciferase assay using 293 cell-line for these micelle vector systems with slightly cationic character.

Animals↗
PubMed1998

Activation of 1-nitropyrene by nitroreductase increases the DNA adduct level and mutagenicity.

1-Nitropyrene (1-NP) is a mutagenic nitro compound in the environment. We studied correlations between the mutagenicity of 1-NP for three strains of Salmonella typhimurium, the activity of bacterial nitroreductases and the amount of 1-NP-derived DNA adducts. Bacterial strains used in this study were S. typhimurium strains TA98, nitroreductase-less mutant TA98NR and YG1021 carrying a nitroreductase-producing plasmid. The mutagenicity of 1-NP was measured using the Ames assay, and the nitroreductase activities of these strains were assayed by quantification of 1-aminopyrene produced from 1-NP. The DNA adducts were measured by the 32P-postlabeling method. Among the three bacterial strains, strain YG1021 was the highest in mutagenicity of 1-NP, the nitroreductase activity and the DNA adduct level. However, S. typhimurium strain TA98NR had the lowest values of these three parameters. Nitroreductase activity, DNA adduct level and mutagenicity were strongly correlated with each other. These results indicate that bacterial nitroreductase plays an important role in forming the DNA adducts, and that the higher the adduct level the higher the level of mutagenicity.

DNA Adducts↗
PubMed1997

Effect of intestinal bacteria on formation of azoxymethane-induced aberrant crypt foci in the rat colon.

The effect of intestinal bacteria on formation of azoxymethane (AOM)-induced aberrant crypt foci (ACF) and DNA adducts in the rat colon was investigated. Male Sprague-Dawley rats were administered cultures of Lactobacillus acidophilus, Bifidobacterium adolescentis, Bacteroides fragilis, Escherichia coli and Clostridium perfringens for five weeks and given injections of AOM at 15 mg/kg body weight at the first and second weeks. The number of ACF five weeks after the start of the experiment was decreased in the rats treated with the cultures or culture supernatants of L. acidophilus and C. perfringens. The half-life of O6-methylguanine (O6-meG) in the L. acidophilus group was shorter than that in the GAM broth group. The half-life of 7-methylguanine did not differ among the groups. These results suggest that the metabolite(s) of L. acidophilus and C. perfringens inhibit(s) the ACF formation in rats treated with AOM and that the inhibitory effect of L. acidophilus is due to the enhanced removal of O6-meG from the colon mucosal DNA.

Animals↗
PubMed1997

Disrupted cholecystokinin type-A receptor (CCKAR) gene in OLETF rats.

OLETF rats develop hyperglycemia, hyperinsulinemia and mild obesity, which is characteristic of human non-insulin-dependent diabetes mellitus (NIDDM). We cloned and sequenced the cholecystokinin type-A receptor (CCKAR) gene in the rats. Comparing the DNA sequences of the OLETF CCKAR gene and LETO CCKAR gene, normal gene, we found a deletion in the OLETF gene, 6847 bases in length, which was flanked by two 3-base-pair direct repeats (5'-TGT-3') at positions -2407/-2405 and 4441/4443, numbered according to the LETO gene sequence, one of which was lost. The promoter region, the first and second exons were missing in the mutant. The region upstream and downstream of the deletion, including exons 3, 4 and 5, was conserved between the two strains, and did not contain any base changes. We found that the gene mapped to chromosome 14 in rats. OLETF rats are the naturally occurring knockout animals with the homozygously disrupted CCKAR gene.

Animals↗
PubMed1997

Efflux of glutamate into the perilymph of the cochlea following transient ischemia in the gerbil.

Using a microdialysis technique followed by an enzyme cycling analysis, we measured changes in the glutamate levels in the perilymph of gerbil cochleae before, during and after transient ischemic insult. The basal glutamate level in perilymph was 0.35 +/- 0.22 pmol/microl. An almost immediate and continuous rise in the level of glutamate occurred after the ischemic insult, which advanced even further after recirculation; the average concentration was higher than 40 pmol/microl 55 min after recirculation. The compound action potentials (CAP) monitoring the auditory function totally disappeared after ischemic insult. However, CAP reappeared after recirculation; the threshold for acoustic stimulation was higher than that observed at the pre-ischemic state.

Acoustic Stimulation↗
PubMed1997

Crystallization and preliminary X-ray studies of azurin-I and azurin-II from denitrifying bacterium Alcaligenes xylosoxidans GIFU 1051.

Two distinct azurins named azurin-I and azurin-II were isolated from Alcaligenes xylosoxidans GIFU 1051 (AzG-I and AzG-II). They have been purified and crystallized. The crystals of AzG-I belong to the monoclinic crystal system, space group C2, unit-cell parameters a = 130.6, b = 54.4, c = 74.7 A, beta = 96.1 degrees. The crystals of AzG-II belong to the tetragonal crystal system, space group P4(1)22 or P4(3)22, unit-cell parameters a = b = 52.6, c = 100.7 A. Both crystals diffract up to 2.0 A resolution and are suitable for X-ray crystallographic studies.

Journal Article↗
PubMed1997

Mouse cholecystokinin type-A receptor gene and its structural analysis.

The mouse cholecystokinin type-A receptor (CCK(A)R) gene was cloned and sequenced, and the exon/intron boundaries were determined by cDNA cloning. The gene, approximately 10 kb in length, contains the entire coding region, and consists of five exons. The deduced amino acid sequence was homologous with that of other species, with the exception of an additional DNA sequence encoding 7 amino acids in exon 5. A region of the 5' end of exon 2 appeared to be alternatively spliced, and generated an isoform shorter by 52 bases. The shorter isoform may encode an 48 amino acid open reading frame due to frameshift of translation. These two mRNA isoforms were expressed equally in the mouse gallbladders.

Alternative Splicing↗
PubMed1997

Continuous monitoring and regulating of brain temperature in the conscious and freely moving ischemic gerbil: effect of MK-801 on delayed neuronal death in hippocampal CA1.

Many glutamate antagonists have been reported to have a neuroprotective effect against ischemic brain damage; however, some of them have been also reported to induce hypothermia that confers remarkable neuroprotection against the damage. In order to avoid the confounding effects of hypothermia, we assembled a telemeter-based brain temperature control system that allows continuous monitoring and regulating of brain temperature during an ischemic insult and in the post-ischemic period in conscious and freely moving animals. Experiments were performed in gerbils that were subjected to administration of MK-801 (3, 5, and 10 mg/kg) and/or to 5-min ischemia. The system monitored continuous changes in brain temperature and regulated brain temperature at normothermic levels, revealing that a neuroprotective effect of 3 mg/kg MK-801 against ischemia-induced delayed hippocampal CA1 neuronal death was mainly due to hypothermia, whereas a high dose of MK-801 (5 and 10 mg/kg) produced a neuroprotective effect even when the brain temperature was maintained at normothermic levels. These results indicate that this system is very useful to test potential antiischemic agents, especially when the agents have hypothermic side effects.

Animals↗
PubMed1997

Genomic structure and promoter analysis of the gene encoding MM3, a member of transmembrane 4 superfamily.

We have isolated genomic clones encoding hamster MM3, a member of transmembrane 4 superfamily (TM4SF). Nucleotide (nt) sequence analysis revealed that it is composed of 5 exons spanning about 8 kb. The exon-intron organization of the MM3 gene was quite different from those of other TM4SF members. We also identified its transcription start points (tsp) and the promoter region. Deletion analysis of the promoter revealed that about 160-bp region containing TATA-box, CAAT-box and GC-box was necessary for efficient transcription in cultured cells.

Amino Acid Sequence↗
PubMed1997

Albumin enhances superoxide production in cultured microglia.

Microglial activation and disruption of blood-brain barrier (BBB) are known to occur and contribute to neuronal damages in cerebral ischemic conditions and in some neurodegenerative diseases. To investigate whether a serum factor leaked out from circulation enhances microglial activation, we examined the effect of normal rat serum on superoxide (O2-) production by cultured microglia. Microglia cultured from neonatal rat brains were studied on their O2- production induced by the addition of phorbol myristate acetate by a method of acetyl-cytochrome c reduction. The O2- production was significantly increased by the addition of 0.01% rat serum, and the maximal enhancement was observed at about 0.1% rat serum. After the serum was fractionated using a molecular sieve membrane, we observed the enhancing effect only in a greater molecular weight fraction (>50 kDa). Furthermore, three kinds of bovine serum albumin (BSA) with different purity, and human serum and plasma albumins, also enhanced O2- production to a similar extent to that by rat serum. However, other proteins tested showed no significant effect. The enhancement of O2- production by BSA was observed dose-dependently, and the effect of 50 microg/ml of purified BSA was equivalent to that of 0.1% rat serum, suggesting that albumin itself enhances O2- production by microglia. These results imply that albumin leaked out through impaired BBB may activate microglia and that the potentiation of O2- production by albumin results in the pathogenesis of neuronal damage in cerebral ischemia and some neurodegenerative diseases.

Albumins↗