Search PubMed⌕ Search

Biomedical subjects

K Muraki

Publications and source records attributed to K Muraki.

107 records · Page 6Linked to original sources
PubMed1983

A case of hypophosphataemic vitamin D-resistant rickets treated with initial massive doses of 1 alpha-hydroxy-vitamin D3 alone.

A 1 5/12-year-old girl with hypophosphataemic vitamin D-resistant rickets was treated with initial massive doses of 1 alpha-hydroxy-vitamin D3 (1 alpha-OH-D3) alone. A dramatic improvement of bone lesions and growth rate and normalization of the characteristic biochemical defects were noted within four months after the start of massive 1 alpha-OH-D3 therapy. The results of this study suggest that early therapy with massive doses of 1 alpha-OH-D3 alone improves the radiological findings and restores to normal the biochemical defects and the growth rate as early as possible. This regimen may improve motor strength and endurance and obviate the need for corrective orthopaedic procedures.

Bone and Bones↗
PubMedDate not supplied

Neurotensin elevates hematocrit and plasma levels of the leukotrienes, LTB4, LTC4, LTD4 and LTE4, in anesthetized rats.

The IV injection of neurotensin (NT) into anesthetized rats produced a marked increase in hematocrit, labored breathing and peripheral blood stasis with cyanosis. This effect could also be produced by the NT-related peptides, neuromedin-N and xenopsin; however, it was not observed when nine other biologically active peptides, including bradykinin and substance P, were tested. Associated with these responses were increases in the plasma levels of histamine (measured radioenzymatically) and the leukotrienes, LTB4, LTC4, LTD4, and LTE4 (measured by RIA and HPLC). The increment in hematocrit after varying doses of NT correlated to the increase in plasma levels of LTC4. Histamine and LTC4 were both capable of elevating hematocrit when given IV; however, LTC4 was approximately 1000 times more potent than histamine and active doses of histamine elevated LTC4 levels. Furthermore, the effects of NT on plasma LTC4 and hematocrit were reduced by pretreating animals with antagonists to histamine and serotonin. Pretreatment with the specific mast cell degranulating agent, compound 48/80, also blocked NT's ability to elevate plasma levels of histamine, LTB4 and LTC4 and prevented the increased hematocrit and cyanosis. These results indicate that NT-related peptides are very potent and specific stimulators of leukotriene release and that this action is mediated by mast cells and associated with loss of plasma volume and blood stasis. A working hypothesis is that histamine, released from mast cells in response to NT, stimulates LTC4 production by other cells.

Anesthesia, General↗
PubMedDate not supplied

Xenopsin-related peptide(s) are formed from xenopsin precursor by leukocyte protease(s) and cathepsin D.

Lysates of isolated rat polymorphonuclear leukocytes and macrophages were found to generate xenopsin-related peptides when incubated with a liver extract used as a source of precursor. The lysosomal enzyme, cathepsin D, was also shown to display this property and to share with the lysate a similar pH dependence (optimum, approximately pH 3.5) and sensitivity to the acid protease inhibitor, pepstatin A (ID50: lysate, 10 nM; cathepsin D, 30 nM). When subjected to HPLC on mu-Bondapak C-18, the xenopsin-related peptides generated by the lysate eluted near to those formed by cathepsin D and when tested in a radioreceptor assay for neurotensin, they displayed similar cross-reactivities (peak 2, approximately 50%; peak 1, approximately 100%). These results indicate that cathepsin D from lysed granulocytes can process precursor protein(s) to form radioreceptor-active xenopsin-related peptides.

Amino Acid Sequence↗
PubMedDate not supplied

Enhanced expression of neurotensin/neuromedin N mRNA and products of NT/NMN precursor processing in neonatal rats.

Intestinal levels of immunoreactive neurotensin (iNT) and neuromedin N (iNMN), as well as mRNA for the NT/NMN precursor, were elevated during the suckling period in rats. While transient expression of NT/NMN was observed at 1-5 days of age in the proximal small intestine and colon, NT/NMN levels in the ileum increased to peak at 10-20 days of age and then decreased to adult levels. The levels of these peptides were not elevated in the central nervous system and pituitary over this time period. Chromatographic analyses of jejunoileal extracts indicated that large molecular forms of iNT and iNMN were present, constituting approximately 1.3% of total iNT and approximately 56% of total iNMN, respectively. Treatment of the large forms with pepsin, which is known to generate the fully immunoreactive peptides, NT(3-13), NT(4-13), and NMN, increased immunoreactivity tenfold (iNT) and 1.2-fold (iNMN). Thus, large forms actually constituted approximately 13% (iNT) and approximately 60% (iNMN). Based upon its physicochemical properties, large molecular iNMN was tentatively identified as a 125 residue peptide with NMN at its C-terminus [i.e., rat prepro-NT/NMN(23-147)]. The properties of large molecular iNT were most similar to those predicted for the entire precursor [i.e., rat prepro-NT/NMN(23-169)]. These results indicate a) that enhanced expression of NT/NMN occurs in a tissue-specific manner in rats during the suckling period; b) that the pattern of precursor processing in intestine yields primarily NT and a large molecular form of NMN.

Animals↗
PubMedDate not supplied

Ontogenic development of neurotensin-like immunoreactivity in the gastrointestinal tract and the influence of dietary changes in rats.

The ontogenic development of neurotensin-like immunoreactivity (NTLI) in the gastrointestinal tract was studied in three groups of male rats on different diets. Group I rats were weaned physiologically. Group II rats received only mother's milk until 25 days of age. Group III rats were fed mother's milk alone for 20 days and then switched abruptly to laboratory chow. The NTLI concentration in the gastrointestinal tract from the esophagus to the small intestine was almost the same as that in adult rats before weaning. It increased after weaning to a peak on day 20 or 25, and then decreased to the adult level. The NTLI concentration in the cecum and large intestine, however, decreased from high neonatal level, reaching the adult level on day 20 or 25, and it remained constant thereafter. Prolonged mother's milk feeding alone enhanced neurotensin production in the esophagus and postponed the physiological decrement of NTLI concentrations in the duodenum and small intestine. The sudden change from mother's milk to laboratory chow accelerated the decrement of intestinal NTLI concentrations.

Animals↗