Search PubMed⌕ Search

Biomedical subjects

S Kato

Publications and source records attributed to S Kato.

At least 1,243 records · Page 69Linked to original sources
PubMed1990

[The effect of 1, 25-dihydroxyvitamin D3 on cultured human hair follicle cells from a patients with vitamin D-dependent rickets type II with alopecia].

We examined the effects of 1, 25-dihydroxyvitamin D3 on the growth and differentiation of cultured human hair follicle cells from a patient with vitamin D-dependent rickets type II [DDR-II] with alopecia. In the presence of 100 nM 1, 25-dihydroxyvitamin D3, the clonal growth of normal hair follicle cells was inhibited and terminal differentiation was markedly stimulated. However, the cells from a patient with DDR-II with alopecia did not respond to the hormone, suggesting a lack of the specific receptors in the cells. The difference in the cellular response to the hormone between the normal hair follicle cells and those from a patient were clear and easily distinguished, and these studies may provide a basis for the rapid diagnosis of DDR-II. Large number of hairs were difficult to obtain from patients with alopecia, and we developed a new culture method to accomplish these studies. Our system may be useful in the culture of HFC from only a few hair follicles.

Alopecia↗
PubMed1990

[Result of allogeneic bone marrow transplantation from unrelated donor].

Two patients treated by unrelated bone marrow transplantation were reported. Case 1 was an eight-year-old boy with Morquio's disease received bone marrow graft from an HLA one-locus mismatched, MLC non reactive unrelated donor. The patient was prepared with conventional dose of cyclophosphamide, and thoracoabdominal irradiation. For the prophylaxis of GVHD, three drug regimen consisted of methotrexate (MTX), cyclosporine A (CsA), and prednisolone (PSL) was administered. Engraftment was prompt, and grade I of acute GVHD developed, which resolved with increased dose of PSL. Case 2 was a ten-month-old boy with juvenile chronic myelogenous leukemia received bone marrow graft from an HLA fully matched, MLC non reactive unrelated donor. Preconditioning regimen consisted of total body irradiation, VP-16, and cytosine arabinoside. MTX, CsA, and methylprednisolone were administered to prevent GVHD, but grade II of acute GVHD developed, which resolved with prolonged course of PSL. Both cases are alive and well, without chronic GVHD. In conclusion, unrelated donor bone marrow transplantation may be a useful to treat hematologic malignancies, aplastic anemia, and some inherited diseases.

Bone Marrow Transplantation↗
PubMed1989

Role of peroxisomal fatty acid beta-oxidation in ethanol metabolism.

The contribution of peroxisomal fatty acid beta-oxidation to ethanol metabolism was examined in deermice hepatocytes. Addition of 1 mM oleate to hepatocytes isolated from fasted alcohol dehydrogenase (ADH)-positive deermice in the presence of 4-methylpyrazole or to hepatocytes from fasted or fed ADH-negative deermice produced only a slight and statistically not significant increase in ethanol oxidation. Lactate (10 mM), which is not a peroxisomal substrate, showed a greater effect on ethanol oxidation. There was also a lack of oleate effect on the oxidation of ethanol by hepatocytes of ADH-positive deermice. Furthermore, in ADH-negative deermice, the catalase inhibitor azide (0.1 mM) did not inhibit the increase in ethanol oxidation by oleate and lactate. The rate of oleate oxidation by hepatocytes from fasted ADH-negative deermice was much lower than that of ethanol. These results indicate that in deermice hepatocytes, peroxisomal fatty acid oxidation does not play major role in ethanol metabolism.

Alcohol Dehydrogenase↗
PubMed1989

Postnatal changes in dolichol-pathway enzyme activities in rat liver.

The activity of hepatic protein N-glycosylation was compared in rats of different ages by incubating UDP-[14C]glucose with liver microsomes. Dolichyl-phosphate [14C]glucose, [14C]glucosyl-oligosaccharide-lipid and [14C]glycoproteins formed were increased after birth to maximal levels at 2 weeks; thereafter dolichylphosphate [14C]glucose remained constant, while [14C]glucosyl-oligosaccharide-lipid and [14C]glycoproteins were decreased to constant levels at 4 weeks. The postnatal change in the formation of [14C]glycoproteins was similar to the change in the hexosamine content of N-glycans in liver microsomes and plasma, suggesting that the N-glycosylation of proteins in rat liver increases after birth to a maximum at 2 weeks, and thereafter decreases to a constant level at 4 weeks. The possibility of a regulatory role for dolichyl phosphate in glycoprotein synthesis in rat liver during postnatal development was eliminated by demonstrating the inefficiency of exogenous dolichyl phosphate on the postnatal changes in [14C]glycoprotein formation. The transfer of [14C]glucose from UDP-[14C]glucose to denatured alpha-lactalbumin in liver microsomes increased to a maximum at 2 weeks and then decreased to a constant level, as with transfer to endogenous proteins (i.e. the formation of [14C]glycoproteins). On the other hand, the transfer of oligosaccharide from exogenous [14C]glucosyl-oligosaccharide-lipid to denatured alpha-lactalbumin reached a maximum at 2 weeks and then remained constant. These results strongly suggest that oligosaccharide-lipid available for N-glycosylation is limiting in rat liver after 2 weeks post partum. The activities of dolichyl-phosphate glucose, dolichyl-phosphate mannose and dolichyl-pyrophosphate N-acetylglucosamine synthases increased until 2 weeks post partum. Thereafter, the activity of dolichyl-pyrophosphate N-acetylglucosamine synthase decreased to a constant level at 4 weeks, while the activities of dolichyl-phosphate glucose and dolichyl-phosphate mannose synthases remained constant. These results suggest that N-glycosylation of proteins in rat liver increases until 2 weeks post partum, and that this depends on the activities of dolichol-pathway enzymes as a whole rather than on the activity of specific enzymes. N-Glycosylation then decreases to a constant level at 4 weeks due to decreases in the activities of enzymes responsible for oligosaccharide assembly on lipids, including dolichyl-pyrophosphate N-acetylglucosamine synthase.

Animals↗
PubMed1989

The microsomal ethanol oxidizing system mediates metabolic tolerance to ethanol in deermice lacking alcohol dehydrogenase.

Metabolic tolerance to ethanol has been attributed to enhanced mitochondrial reoxidation of reducing equivalents produced in the alcohol dehydrogenase (ADH) pathway or to non-ADH mechanisms. To resolve this issue, deermice lacking low Km hepatic ADH were fed for 2 weeks a liquid diet containing ethanol or isocaloric carbohydrate and hepatocytes were isolated. Ethanol (50 mM) oxidation increased (9.8 vs 4.5 nmol/min/10(6) cells in controls). To differentiate which of two non-ADH pathways (the microsomal ethanol oxidizing system (MEOS) or catalase) was responsible for the induction, four approaches were used. First, MEOS was assayed in hepatic microsomes and found to be increased (24.4 vs 6.8 nmol/min/mg protein in controls). Second, hepatocyte ethanol metabolism was measured after addition of the catalase inhibitor azide (0.1 mM) and found to be unchanged. By contrast, the competitive MEOS inhibitor, 1-butanol, depressed metabolism in a concentration-dependent manner. A third approach relied on measurement of isotope effects known to be different for MEOS and catalase. From the isotope effect values, MEOS was calculated to contribute 85% or more of total ethanol oxidation by cells from both ethanol-fed and control animals. A fourth approach involved in vivo pretreatment with pyrazole (300 mg/kg/day for 2 days), which reduced peroxidation by catalase to 13% of control values in liver homogenates while inducing MEOS activity to 152% of controls. Hepatocytes from pyrazole-treated deermice showed a 47% increase in ethanol metabolism, paralleling the MEOS induction and contrasting with the catalase suppression. These results indicate that since metabolic tolerance occurs in the absence of ADH, it is not necessarily ADH mediated, and further, that MEOS rather than catalase accounts for basal ethanol metabolism and its increase after chronic ethanol treatment.

1-Butanol↗
PubMed1989

Effects of brefeldin A on the synthesis and secretion of egg white proteins in primary cultured oviduct cells of laying Japanese quail (Coturnix coturnix japonica).

We investigated the effect of brefeldin A (BFA) and monensin on the secretion of egg white proteins in primary cultured oviduct cells. Monensin inhibited the secretion of egg white proteins, but this drug also caused morphological changes of the cells and inhibited their protein synthesis. BFA inhibited protein secretion without any remarkable morphological changes of the cells and without significant inhibition of protein synthesis. In the presence of BFA at 1 microgram/ml, only 10% of synthesized ovalbumin was secreted into the medium even after 6 h. A similar effect of BFA was shown in the case of conalbumin. When the cells were cultured in the presence of BFA, precursors of mature ovalbumin accumulated which were not secreted. Their affinity for lectin binding affinity columns (Con-A Sepharose and WGA-agarose) suggested that they contained immature high-mannose-type chains. The above results suggest that the conversion of high-mannose-type oligosaccharides to hybrid-type ones, which is not usually observed in mammalian species but only in avian oviduct tissues, proceeds between the Golgi complex and the endoplasmic reticulum.

Animals↗
PubMed1989

Characteristics of butanol metabolism in alcohol dehydrogenase-deficient deermice.

Deermice lacking the low-Km alcohol dehydrogenase eliminated butan-1-ol, a substrate for microsomal oxidation but not for catalase, at 117 mumol/min per kg body wt. Microsomal fractions and hepatocytes metabolized butan-1-ol also (Vmax. = 6.7 nmol/min per nmol of cytochrome P-450, Km = 0.85 mM; Vmax. = 5.3 nmol/min per 10(6) cells, Km = 0.71 mM respectively). These results are consistent with alcohol oxidation by the microsomal system in these deermice.

Alcohol Dehydrogenase↗
PubMed1989

Lipid peroxidation and antioxidant defense systems in rat liver after chronic ethanol feeding.

The effects of chronic ethanol feeding on hepatic lipid peroxidation, ascorbic acid, glutathione and vitamin E levels were investigated in rats fed low or adequate amounts of dietary vitamin E. Hepatic lipid peroxidation was significantly increased after chronic ethanol feeding in rats receiving a low-vitamin E diet, indicating that dietary vitamin E is an important determinant of hepatic lipid peroxidation induced by chronic ethanol feeding. No significant change was observed in hepatic non-heme iron content, but hepatic content of ascorbic acid and glutathione was increased by ethanol feeding. Both low dietary vitamin E and ethanol feeding significantly reduced hepatic alpha-tocopherol content, and the lowest hepatic alpha-tocopherol was found in rats receiving a combination of low vitamin E and ethanol. Plasma alpha-tocopherol was elevated after ethanol feeding, probably because of the associated hyperlipemia. Both the ratio of plasma alpha-tocopherol/plasma lipid and the red blood cell alpha-tocopherol were reduced by ethanol feeding. Furthermore, ethanol feeding caused a marked increase of hepatic alpha-tocopheryl quinone, a metabolite of alpha-tocopherol by free radical reactions. Ethanol feeding caused little changes of alpha-tocopherol and alpha-tocopheryl quinone content in mitochondria, whereas a striking increase in alpha-tocopheryl quinone was observed in microsomes. These data suggest that ethanol feeding causes a marked alteration of vitamin E metabolism in the liver and that the combination of ethanol with a low-vitamin E intake results in a decrease of hepatic alpha-tocopherol content which renders the liver more susceptible to free radical attack.

Animals↗
PubMed1989

Induction of the acrosome reaction in ejaculated goat spermatozoa by preincubation in chemically defined medium.

The aim of the present study was to examine the effects of the elimination of energy substrate from the medium and the effects of the preincubation vessel, temperature, and time on the induction of the acrosome reaction in ejaculated goat spermatozoa in chemically defined medium. Washed spermatozoa were resuspended in Brackett-Oliphant (BO) medium or substrate-free BO medium to give a high concentration and preincubated in open test tubes or sealed glass tubes at 37.0 or 39.5 degrees C for 1, 2, or 3 h. Sperm acrosome reaction was evaluated using a simplified triple-stain technique and a hamster test. It was found that the goat sperm acrosome reaction occurred more readily in the sealed glass tubes than in open test tubes, in substrate-free BO medium than in BO medium, and at 39.5 than at 37.0 degrees C. During preincubation with substrate-free BO medium in sealed glass tubes at 39.5 degrees C, the optimum time necessary to induce the acrosome reaction in goat spermatozoa was 2-3 h.

Acrosome↗
PubMed1989

Induction of the acrosome reaction in goat spermatozoa in simple physiological salt solution.

The present study was carried out to determine whether K+, Mg2+, PO4(3-), and HCO3- in a medium are necessary for inducing the acrosome reaction in ejaculated goat spermatozoa. Washed goat spermatozoa were resuspended in K-1 medium, containing NaCl, KCl, CaCl2, MgCl2, NaH2PO4, and NaHCO3; in K-2 medium, containing NaCl, CaCl2, NaH2PO4, and NaHCO3; in K-3 medium, containing NaCl, CaCl2, and NaHCO3; and in K-4 medium, containing only NaCl and CaCl2, followed by preincubation in a sealed glass tube at 39.5 degrees C for 1, 2, or 3 h. The sperm acrosome reaction was evaluated by the trypan blue-Giemsa method and hamster test. The results were essentially the same in all cases. Following preincubation for 1 h, however, the percentage of acrosome-reacted spermatozoa, the proportion of zona-free hamster eggs penetrated by spermatozoa, and the average number of spermatozoa in the vitellus of these penetrated eggs were low; all values indicated a significant increase with preincubation for 2 and 3 h. The presence of K+, Mg2+, PO4(3-), and HCO3- in the medium thus does not appear necessary for inducing the acrosome reaction in goat spermatozoa, since they can undergo the reaction during preincubation in a simple physiological salt solution containing only NaCl and CaCl2 when preincubated in sealed glass tubes at 39.5 degrees C.

Acrosome↗
PubMed1989

Ultrastructural and ultracytochemical studies on the blood-brain barrier in chronic relapsing experimental allergic encephalomyelitis.

We induced chronic relapsing experimental allergic encephalomyelitis (EAE), and studied the ultrastructural and ultracytochemical changes of the blood-brain barrier (BBB) in the demyelinating lesions of various stages of EAE. In the chronic, inactive stage with gliosis and perivascular fibrosis, the basal lamina (BL) of the perivascular processes of astrocytes was formed only partially, and neural parenchyma was not fully separated from the perivascular mesenchymal tissues by the BL of astrocytic processes. Vascular permeability of the BBB was studied using exogenous horseradish peroxidase (HRP) as the tracer: HRP extravasation was marked during the stages of both active myelin breakdown and removal of debris, and was recognized even at the inactive stage, although the degree was reduced to a very low level. The functions of the endothelia, assessed by ouabain-sensitive, K+-dependent p-nitrophenylphosphatase activity, were impaired as EAE progressed. The decrease in HRP leakage at the inactive stage suggests the endothelial impairment of active transport of metabolites including HRP. Along with the development of inflammatory demyelination in EAE, the BBB in affected areas became more and more altered, and gradual morphological and functional impairment of the BBB developed.

Animals↗
PubMed1989

Mitochondria covered with a net of parallel and latticed filaments in nigral neurons of monkeys with experimental parkinsonism.

Nigral neurons of crab-eating monkeys treated with 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) showed a peculiar configuration occasionally in mitochondria. The outer membrane of mitochondria was covered with a net of fine parallel or latticed filaments, which turned spirally about the long axis of the mitochondria. The filaments were approximately 8 nm in diameter: parallel filaments were arranged at intervals of about 13 nm from center to center; and latticed filaments intersected each other at an angle of almost 135 degrees. When mitochondria were present in groups, the intermitochondrial gap was occasionally filled with the same parallel filaments. The netted mitochondria were frequently associated with intramitochondrial abnormalities such as small floculent inclusions and disintegrated cristae. Only one or two netted mitochondria were counted in the perikaryon of one section of an injured neuron. They appeared in about one-third of mildly or moderately injured neurons in three of six MPTP-treated monkeys, and not in normal surviving and recovering neurons of treated animals, or in neurons of control animals. We consider the netted mitochondria to be a pathological configuration related to a metabolite of oxidation of MPTP, and to be different from the stubby mitochondria reported in amyotrophic lateral sclerosis (ALS) and a non-ALS case.

1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine↗
PubMed1989

Reappraisal of neurofibrillary tangles. Immunohistochemical, ultrastructural, and immunoelectron microscopical studies.

We have studied the immunohistochemical reactivity and ultrastructure of both neurofibrillary tangles (NFTs) occurring with severe neurofibrillary diseases, and Pick bodies (PBs) associated with Pick's disease. The NFTs and PBs did not react immunohistochemically with the anti-nonphosphorylated neurofilament monoclonal antibody irrespective of whether they were pretreated with alkaline phosphatase. In granular neurons of the dentate fascia of Ammon's horn in cases of dementia of the Alzheimer type (DAT), NFTs either resembled PB-like inclusion bodies (Horoupian's inclusion bodies) in form, or had a perinuclear structure. Immunohistochemically and ultrastructurally, the NFTs in the dentate fascia in cases of DAT, including Horoupian's inclusion bodies, were similar to the NFTs in the pyramidal neurons of Ammon's horn, which are found most frequently in association with severe neurofibrillary diseases. Under a light microscope, Horoupian's inclusion bodies and PBs could not be differentiated and appeared to be argyrophilic round cytoplasmic inclusions in granular neurons of the dentate fascia. There were, however, ultrastructural differences. Horoupian's inclusion bodies consisted of bundles made up of straight tubules (STs), each about 15 nm in diameter. These bundles were intermixed with a few paired helical filaments which occurred at intervals of about 80 nm. On the other hand, PBs were composed of randomly distributed 15-nm-wide STs, intermixed with a very few fibrillary structures. These fibrils had a periodicity of about 160 nm, and ranged in width from about 15 nm to 30 nm. Horoupian's inclusion bodies associated with DAT and PBs associated with Pick's disease are different in this neuropathological aspect.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1989

Inhibition of HIV-1 replication and syncytium formation by synthetic CD4 peptides.

Only one peptide of CD4 (amino acid residues 70-132) among 16 synthetic peptide fragments selectively inhibited HIV-1 replication and HIV-1-induced syncytium formation. Several smaller peptides within this region did not show any activity, except for the peptide (86-132) which showed somewhat lower activity.

Antigens, Differentiation, T-Lymphocyte↗
PubMed1989

Quantitative assessment of aqueous flare intensity in diabetes.

Aqueous flare intensity was measured with the laser flare-cell meter in 231 eyes of diabetic patients and 31 eyes of normal age-matched controls. Diabetic patients were divided into four groups based on the degree of retinopathy: (1) non-retinopathy, 42 eyes; (2) background retinopathy, 72; (3) preproliferative retinopathy, 23; and (4) proliferative retinopathy, 94. There was no significant difference between the normal controls and the non-retinopathy group, whereas the rest of the diabetic groups showed significantly higher flare values than did normal controls (P less than 0.001). Flare intensity increased with the progression of retinopathy. Our results demonstrate that clinical use of the flare-cell meter enables the quantitative assessment of blood-aqueous barrier function in diabetics and suggest that diabetic iridopathy, as one of the manifestations of diabetes in the anterior part of the eye, exists even in the early stages of this disease and progresses in parallel with retinopathy.

Aqueous Humor↗
PubMed1989

Locations of peptic ulcers in children.

The locations of peptic ulcers in children were studied in a total of 55 cases; 19 with gastric ulcers, 31 with duodenal ulcers and 5 with a combination of both. The male children were predominantly affected with these three types. The mean age of the children with gastric ulcers was significantly lower than those with duodenal ulcers (P less than 0.005). Gastric ulcer was markedly predominant in the antrum, and commonly present in the anterior and posterior walls of the stomach, and infrequently on the greater curvature. Ten of 24 cases (42%) had ulcerations on the anterior wall of the antrum. In seven cases, ulcerations were located on the posterior wall. Duodenal ulcers mostly occurred in the bulb. The anterior and/or posterior walls of the bulb were commonly associated with ulcerations. The present observations concerning gastric and duodenal ulcer location are essentially in agreement with results from adult studies. Perforations were demonstrated in the anterior wall or lesser curvature in both gastric and duodenal ulcers. In five of seven relapse cases, ulcerations had recurred in the same area.

Adolescent↗
PubMed1989

Gastric acid secretion in a child with postbulbar duodenal ulcer.

A 14-year-old case was reported with a primary postbulbar duodenal ulcer, which was confirmed by barium meal study and duodenoscopy. In the preoperative study, the patient showed marked gastric hyperacidity: maximal and peak acid output were 0.980 and 1.434 mEq/kg/hr, respectively. As previously described, hyperacidity appears to be a main factor in the pathogenesis of postbulbar duodenal ulcer. Fasting and postprandial serum gastrin secretion was not thought to be responsible for gastric hyperacidity in the present case. Upon histological investigation, the operatively resected stomach did not suggest a possible relationship between hyperacidity and an enlarged parietal cell mass.

Adolescent↗