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M Katsumata

Publications and source records attributed to M Katsumata.

At least 19 recordsLinked to original sources
PubMed2004

Effect of heat exposure on uncoupling protein-3 mRNA abundance in porcine skeletal muscle.

Exposure to cold increases abundance of mRNA for uncoupling protein-3 (UCP3) in skeletal muscle, whereas the influence of exposure to heat is unknown. Thus, we conducted a study to investigate the influence of heat exposure on UCP3 mRNA abundance in porcine skeletal muscle. Three pigs aged 110 to 120 d, with an average BW of 75 kg, from each of eight litters were used. Each littermate was assigned to one of three treatment groups; one group was reared at 32 degrees C and fed ad libitum (32AL) for 4 wk, whereas the other two groups were maintained at 23 degrees C for the same period, and either pair-fed the intake of their 32AL littermates (23PF), or fed ad libitum (23AL). The RNase protection assay revealed that UCP3 mRNA abundance in longissimus dorsi and rhomboideus muscles was higher (P < 0.05) in the 32AL group than the 23PF group. The 23AL group also had significantly higher UCP3 mRNA abundance than the 23PF group in these muscles. Plasma total 3,5,3'-triiodothyronine concentration of the 32AL group was lower (P < 0.05) than that of the 23PF group, whereas mRNA abundance of thyroid hormone receptor (TR) isoforms, TRalpha1 and TRalpha2, in these muscles was not affected, suggesting that the 32AL group was in a relatively hypo-thyroid state. Because thyroid hormone up-regulates UCP3 expression, these results indicate that factors other than thyroid hormone may play a role in regulating UCP3 mRNA abundance in skeletal muscle of heat-exposed pigs.

Animals↗
PubMed2002

Effects of human recombinant calcitonin on a rat osteopenia model induced by TPTX and arotinoid.

Recombinant human calcitonin (rh-CT) has been developed as an agent for patients with excessive bone resorption to replace calcitonins from animal species, which are associated with tolerance problems. In this study, inhibitory effects of rh-CT against bone resorption were examined in thyroparathyroidectomized (TPTX) rats, the animal model of accelerated bone resorption induced by administering a synthetic retinoid (arotinoid). The arotinoid-treated TPTX rats exhibited signs of stimulated bone resorption, such as hypercalcemia, reduced bone mineral density, and inferior bone strength. Significant improvements were seen in all of these changes after a daily treatment with rh-CT (30, 300 U/kg s.c.) for 1 week. A histomorphometrical analysis showed that the treatment with rh-CT markedly suppressed the reduction of trabecular bone volume and that of cortical thickness in the femur of arotinoid-treated TPTX rats. These results suggest that rh-CT may prevent osteopenia caused by accelerated bone resorption.

Animals↗
PubMed2001

Nutrition-hormone receptor-gene interactions: implications for development and disease.

Nutrition profoundly alters the phenotypic expression of a given genotype, particularly during fetal and postnatal development. Many hormones act as nutritional signals and their receptors play a key role in mediating the effects of nutrition on numerous genes involved in differentiation, growth and metabolism. Polypeptide hormones act on membrane-bound receptors to trigger gene transcription via complex intracellular signalling pathways. By contrast, nuclear receptors for lipid-soluble molecules such as glucocorticoids (GC) and thyroid hormones (TH) directly regulate transcription via DNA binding and chromatin remodelling. Nuclear hormone receptors are members of a large superfamily of transcriptional regulators with the ability to activate or repress many genes involved in development and disease. Nutrition influences not only hormone synthesis and metabolism but also hormone receptors, and regulation is mediated either by specific nutrients or by energy status. Recent studies on the role of early environment on development have implicated GC and their receptors in the programming of adult disease. Intrauterine growth restriction and postnatal undernutrition also induce striking differences in TH-receptor isoforms in functionally-distinct muscles, with critical implications for gene transcription of myosin isoforms. glucose transporters, uncoupling proteins and cation pumps. Such findings highlight a mechanism by which nutritional status can influence normal development, and modify nutrient utilization. thermogenesis. peripheral sensitivity to insulin and optimal cardiac function. Diet and stage of development will also influence the transcriptional activity of drugs acting as ligands for nuclear receptors. Potential interactions between nuclear receptors, including those for retinoic acid and vitamin D, should not be overlooked in intervention programmes using I or vitamin A supplementation of young and adult human populations

Diet↗
PubMed2000

T cell receptor-induced calcineurin activation regulates T helper type 2 cell development by modifying the interleukin 4 receptor signaling complex.

The activation of downstream signaling pathways of both T cell receptor (TCR) and interleukin 4 receptor (IL-4R) is essential for T helper type 2 (Th2) cell development, which is central to understanding immune responses against helminthic parasites and in allergic and autoimmune diseases. However, little is known about how these two distinct signaling pathways cooperate with each other to induce Th2 cells. Here, we show that successful Th2 cell development depends on the effectiveness of TCR-induced activation of calcineurin. An inhibitor of calcineurin activation, FK506, inhibited the in vitro anti-TCR-induced Th2 cell generation in a dose-dependent manner. Furthermore, the development of Th2 cells was significantly impaired in naive T cells from dominant-negative calcineurin Aalpha transgenic mice, whereas that of Th1 cells was less affected. Efficient calcineurin activation in naive T cells upregulated Janus kinase (Jak)3 transcription and the amount of protein. The generation of Th2 cells induced in vitro by anti-TCR stimulation was inhibited significantly by the presence of Jak3 antisense oligonucleotides, suggesting that the Jak3 upregulation is an important event for the Th2 cell development. Interestingly, signal transducer and activator of transcription (STAT)5 became physically and functionally associated with the IL-4R in the anti-TCR-activated developing Th2 cells that received efficient calcineurin activation, and also in established cloned Th2 cells. In either cell population, the inhibition of STAT5 activation resulted in a diminished IL-4-induced proliferation. Moreover, our results suggest that IL-4-induced STAT5 activation is required for the expansion process of developing Th2 cells. Thus, Th2 cell development is controlled by TCR-mediated activation of the Ca(2+)/calcineurin pathway, at least in part, by modifying the functional structure of the IL-4R signaling complex.

Amino Acid Sequence↗
PubMed2000

Impaired Ca/calcineurin pathway in in vivo anergized CD4 T cells.

Clonal anergy is one of the mechanisms that may account for self tolerance induced in T cells in the periphery. In this study we used the well-documented system of in vivo administration of a superantigen, staphylococcal enterotoxin B (SEB), to induce a state of hyporesponsiveness (anergy) in murine peripheral T cells to decipher the intracellular biochemical basis for this process. The TCR-induced Ca response of in vitro activated T cells was found to be impaired with significant defects in the phosphorylation of phospholipase C-gamma 1. Experiments with calcium ionophore and newly established transgenic mouse lines that express an active form of calcineurin suggested that in vivo SEB-induced anergy is established and/or maintained by a selective impairment in the TCR-induced activation of the Ca/calcineurin pathway.

Animals↗
PubMed2000

Growth hormone receptor gene expression in porcine skeletal and cardiac muscles is selectively regulated by postnatal undernutrition.

During mild postnatal undernutrition, growth hormone receptor (GHR) mRNA abundance decreases in liver but increases in longissimus dorsi muscle. We tested the following hypotheses: 1) GHR gene expression is related to the metabolic and contractile characteristics of different muscles, and 2) the GHR response to nutrition depends on muscle type. Eight pairs of littermate pigs were weaned at 3 wk and given an optimal [60 g/(kg.d)] or low [(20 g/(kg.d)] food intake for the next 3 wk. All pigs grew, but at a slower rate in the low food intake group (P: < 0.001). Functionally distinct muscles were assessed for GHR mRNA (RNase protection analysis), oxidative myofibers (succinate dehydrogenase histochemistry) and type I slow myofibers (myosin immunocytochemistry). There were striking muscle-specific differences in GHR gene expression (P: < 0.001) and in its regulation by nutritional status. Relative expression of GHR mRNA in the optimal food intake group occurred in ascending order as follows: longissimus < diaphragm approximately rhomboideus < cardiac < soleus. There was a positive correlation with the proportion of oxidative myofibers (P: < 0.001) but not with type I myofibers (P: > 0.10). Compared with the high intake pigs, hepatic GHR mRNA was downregulated in the low intake pigs by 59% (P: < 0.01), whereas in the four muscles examined it was upregulated as follows: longissimus, 124% (P: < 0.05); rhomboideus, 19% (P: > 0.4); soleus, 65% (P: < 0. 05); cardiac, 51% (P: < 0.05). Moreover, the proportion of skeletal muscle fibers with high oxidative capacity was also greater in the low intake group (P: < 0.05). We conclude that postnatal GHR gene expression and its regulation by mild undernutrition are related to the metabolic, contractile and specific functional properties of different muscles.

Animals↗
PubMed2000

[A study of metallic mercury polluting a room after being spilled from a sphygmomanometer].

Mercury spilled from a mercurial sphygmomanometer on a hot carpet can vaporize and pollute the environment. We observed the vaporization of mercury in model experiments. Mercury (0.15g) was heated on a hot carpet and the near-by air was sampled with a midget impinger. The evaporated mercury levels were 5.0, 6.3, 8.1 and 10.0mg/m(3) at 20, 40, 60 and 80 minutes, respectively at a height of 30cm from carpet. The result indicated that even if a small quantity of mercury remained on the hot carpet, it could evaporate and pollute the indoor air. Little is known about the influence on human health of low mercury exposure, especially on children. In order not to pollute the air, we need to pay attention to mercury.

Accidents, Home↗
PubMed1999

Suboptimal energy balance selectively up-regulates muscle GLUT gene expression but reduces insulin-dependent glucose uptake during postnatal development.

The major facilitative glucose transporters in muscle, GLUT1 (insulin-independent) and GLUT4 (insulin-dependent), are essential for normal growth and metabolism, but factors controlling their expression during postnatal development are poorly understood. We have therefore determined the role of energy status in regulating muscle GLUT gene expression and function in young, growing pigs on a high (H) or low (L) food intake (H =2L) at 35 degrees C or 26 degrees C. RNase protection assays revealed selective up-regulation of GLUT1 and GLUT4 by mild undernutrition 20-24 h after feeding: mRNA levels were elevated in longissimus dorsi (P<0.001) and rhomboideus (P<0.05), but not in diaphragm or cardiac muscles. Assessment of 2-deoxy-glucose uptake in a small isolated muscle, flexor carpi radialis, showed that the 26L group, which had suboptimal energy balance and the greatest GLUT4 expression, had the highest insulin-independent glucose uptake but the lowest insulin-dependent increment: 20% compared with 70% in the other groups. These novel findings are directly relevant to an understanding of mechanisms underlying the development of insulin resistance and demonstrate 1) muscle-specific up-regulation of GLUT gene expression by postnatal undernutrition that is not related simply to myofiber type, but to whole-body function; and 2) that the degree of GLUT up-regulation and the subcellular distribution and function of GLUT proteins are dependent on energy status.

Animals↗
PubMed1999

[Methemoglobin].

Explore the source record for details and available documents.

Humans↗
PubMed1998

Two novel oleanolic acid saponins having a sialyl Lewis X mimetic structure from Achyranthes fauriei root.

Two novel triterpene glycosides, achyranthosides E and F, were isolated as methyl esters from the root of Achyranthes fauriei, an antiinflammatory medicinal plant. Their structures were characterized as oleanolic acid glucuronides having unique substituents composed of C6H9O5 and C9H15O7, respectively, at the C-3 position of glucuronic acid. These compounds are active components which can inhibit the excess recruiting of neutrophiles to injured tissues 1,000 times more potently than sialyl Lewis X.

Magnetic Resonance Spectroscopy↗
PubMed1998

Biological monitoring of metabolites of sarin and its by-products in human urine samples.

More than 20,000 passengers of Tokyo underground trains were intoxicated with warfare toxic chemicals. Most of the patients examined had marked miosis and decreased serum cholinesterase activity. Transient increase of serum CPK activity after 3 days of the exposure was the another sign. We intensively analyzed the metabolites in the urine of 4 patients. The following analytic results indicated the exposure to sarin as well as contaminated compounds such as diisopropyl methylphosphonate (DIMP), ethyl methylphosphonate fluoridate (EMPF, or ethylsarin), diethyl methylphosphonate (DEMP), and ethyl isopropyl methylphosphonate (EIMP). (1) Isopropanol (IPA) and ethanol (EtOH) were detected of large quantities in the urine samples, and were thought to be derived from sarin and the sarin counterpart, EMPF, DIMP, DEMP and EIMP. (2) Monoalkyl methylphosphonic acids (isopropyl methylphosphonic acid (IMPA) and ethyl methylphosphonic acid (EMPA) also were excreted in large amounts with taking the similar excretion pattern of IPA and EtOH. (3) The metabolite only derived from sarin and ethylsarin is F anions whose integral output in the urine was less than the equimolar level of the excreted (IMPA + EMPA + IPA + EtOH). (4) Other corroborative findings were low lethality: of more than 5,510 patients treated, 11 were acutely dead. (5) Nine exposed males had higher sister chromatid exchange (SCE) rate (5.00 +/- 1.48/cell) than the control (3.81 +/- 0.697/cell), because dialkyl methylphosphonates seemed to have alkylating activity and producing DNA adducts. The SCE rate also increased after the in vitro exposure of lymphocytes to dialkyl methylphosphonates.

Chemical Warfare Agents↗
PubMed1997

Method for the analysis of the methylphosphonic acid metabolites of sarin and its ethanol-substituted analogue in urine as applied to the victims of the Tokyo sarin disaster.

An analysis method for the methylphosphonic acid metabolites of sarin in urine using trimethylsilyl derivatization and flame photometric detection is described in this report. Authentic reference standards of isopropyl methylphosphonic acid (IMPA) and ethyl methylphosphonic acid (EMPA) as well as methylphosphonic acid were employed to estimate the concentration in human urine. A sample pretreatment procedure was developed for urine using a column of cation-loaded ion-exchange resins (Ag+ -, Ba2+ - or H+ -Dowex) and adjusting the pH of the eluate from the column to 3.75-3.85 improved recovery of the target compounds. The eluate was evaporated to dryness under vacuum prior to trimethylsilylation, to remove water and any hydroxy- or amino-carrying volatile substances. The sarin metabolites, because of their low volatility, were concentrated and could be derivatized for analysis. The use of synthesized authentic sarin and ethylsarin metabolites, i.e., IMPA and EMPA, made it possible to establish the necessary sample pretreatment procedures for derivatization and gas chromatography-flame photometric detection (GC-FPD) analysis. The detection limits were 0.025 ppm both for EMPA and [MPA, and 0.625 microM for MPA, respectively. This method can be useful for estimating the exposure level to sarin by assaying the metabolites in urine and it is applicable to a large numbers of samples.

Chemical Warfare Agents↗
PubMed1997

Murine thioredoxin peroxidase delays neuronal apoptosis and is expressed in areas of the brain most susceptible to hypoxic and ischemic injury.

Thioredoxin peroxidase (TPx) is an antioxidant protein that limits the activity of reactive oxygen species (ROS). We cloned the cDNA encoding the mouse homolog of TPx from an E14.5 brain cDNA library and analyzed its distribution and function in murine tissues. Comparison of the amino acid sequence of mouse TPx with those of other species revealed that TPx was highly conserved across all species. Mouse TPx had broad tissue distribution, but its expression was especially marked in cells that metabolize oxygen molecules at high levels such as erythroid cells, renal tubular cells, cardiac and skeletal muscle cells, and certain types of neurons. Levels of increased expression of TPx in the brain were coincident with regions known to be especially sensitive to hypoxic and ischemic injury in humans. Models of erythroid differentiation and neuronal survival were employed to study the function of TPx. Murine erythroleukemia cells (MEL cells) increased TPx transcription when in a chemically differentiated state. Furthermore, expression of mouse TPx in PC12 pheochromocytoma cells prolonged their survival in the absence of nerve growth factor (NGF) and serum, indicating that TPx could promote neuronal cell survival. We propose that TPx contributes to antioxidant defense in erythrocytes and neuronal cells by limiting the destructive capacity of oxygen radicals. These findings identify a novel gene that appears to be relevant to hypoxic brain injury and may be of importance in development of new approaches to abrogate the effects of ischemic- and hypoxic-related injury in the central nervous system (CNS).

Amino Acid Sequence↗
PubMed1997

Comparative sequence analyses of the genes coding for 16S rRNA of Lactobacillus casei-related taxa.

The primary structures of the 16S rRNA genes of the type strains of Lactobacillus casei and related taxa were determined by PCR DNA-sequencing methods. The sequences of Lactobacillus casei, Lactobacillus zeae, Lactobacillus paracasei, and Lactobacillus rhamnosus were different. The Knuc values ranged from 0.0040 to 0.0126. On the basis of the Knuc values and the levels of DNA-DNA relatedness among the strains of these species, the L. casei-related taxa should be classified in the following three species: L. zeae, which includes the type strains of L. zeae and L. casei; a species that includes the strains of L. paracasei and L. casei ATCC 334; and L. rhamnosus.

DNA Primers↗
PubMed1997

Herbal medicine-associated lead intoxication.

A female patient visited our hospital with abdominal pain and anemia. Examination for a gastrointestinal disease gave no diagnostic information. Laboratory studies of the parameters of heme biosynthesis revealed an enzymatic inhibition by lead. The diagnosis of lead poisoning was confirmed by detection of an elevated blood lead level. Excessive lead ingestion was thought to be caused by herbal medicines and/or by an earthen teapot.

Abdominal Pain↗
PubMed1996

bcl-2 alters the antigen-driven selection of B cells in mukappa but not in mu-only Xid transgenic mice.

A point mutation in the pleckstrin homology domain of the mouse Bruton's tyrosine kinase (btk) gene results in an X-linked immune defect, Xid, characterized by immunologic unresponsiveness to polymeric carbohydrate Ags. In Xid mice, B cells specific for phosphocholine (PC) do not develop in peripheral lymphoid tissues because they either fail to be positively selected from the marrow or they are clonally deleted via an Ag-driven, receptor-mediated process. Overexpression of the bcl-2 gene allows PC-specific B cells to survive and mature in Xid mukappa anti-PC transgenic mice, but PC-specific B cells are not rescued by bcl-2 in Xid mu-only transgenic mice. The failure of bcl-2 to rescue PC-specific B cells, in mu-only transgenic mice suggests that either it does not correct the btk defect in the Ag-driven selection process that occurs in pre-B cells and/or in very immature B cells or that a btk-dependent proliferative phase is required for the selection and amplification of the PC-specific B cells in mu-only transgenic mice. The rescue of PC-specific B cells in mukappa transgenic mice indicates that bcl-2 can alter receptor-mediated B cell selection at late stages in B cell development. The rescued PC-specific B cells in Xid male mice do not exhibit an altered proliferation profile in response to B cell-stimulating agents compared with B cells from unmanipulated Xid mice; thus, they fail to respond to soluble anti-mu, or PC-dextran, but they proliferate in response to PC, anti-mu, or anti-id conjugated to Sepharose.

Animals↗
PubMed1996

Inhibition of apoptosis and augmentation of lymphoproliferation in bcl-2 transgenic Fas/Fas ligand-defective mice.

Mice defective in Fas (CD95 or APO-1) or its ligand (lpr or gld mice) develop age-dependent lymphadenopathy and systemic autoimmune disease. T cells accumulating in the lymph nodes of these mice express reduced levels of Bcl-2 protein and are susceptible to spontaneous and glucocorticoid-induced apoptosis. We backcrossed bcl-2 transgenic mice to lpr and gld mice to homozygosity to determine the effects of Bcl-2 overexpression. T cells in these mice were resistant to spontaneous and glucocorticoid-induced apoptosis in vitro. Moreover, the accumulation of CD4(-)CD8(-) T cells in the lymph nodes and the spleens was augmented, suggesting that a Bcl-2-dependent mechanism regulating the number of T cells residing in the peripheral lymphoid organs in addition to the Fas-mediated pathway exists.

Animals↗