Biomedical subjects

M Takano

Publications and source records attributed to M Takano.

At least 235 records · Page 13Linked to original sources

PubMed1994

Diabetes-induced reduction of neuronal survival in hypotonic environments in culture.

Dorsal root ganglion (DRG) neurons from streptozotocin (STZ)-induced diabetic and normal C57BL mice were exposed to three different hypotonic environments (1/2, 1/4, and 1/8 osmolar solutions). After rapid applications of these hypotonic solutions to the neurons, the cell volume autoregulatory mechanism operated in 1/2 osmolar solution but was disrupted in superhypotonic solutions below 1/4 osmolar in both kinds of mice. None of the neurons could survive 12 h after treatment with superhypotonic solutions. On the other hand, a gradual reduction of osmolarity of the culture medium enabled neurons in the normal mice to survive in 1/2 and 1/4 osmolar solutions as well as in an isotonic solution. However, this reduction of osmolarity increased neuronal cell death in the diabetic mice. These results suggest that the ability of DRG neurons to survive in hypotonic environments in culture may be lost in diabetes.

Animals↗

PubMed1994

Regional differences in neurite regeneration of postnatal mouse retinal explants.

Retinal explants from mice at postnatal days 2-15 were three-dimensionally cultured in collagen gel. The regeneration of neurites from the explants was investigated at each stage after birth. The explants from the central region in the retina could not regenerate neurites after postnatal day 9, but those from peripheral regions expressed such ability until postnatal day 12. This regional difference in the disappearance stages of retinal regenerative capability coincides with that of retinal maturation.

Aging↗

PubMed1994

Cellular toxicity of aminoglycoside antibiotics in G418-sensitive and -resistant LLC-PK1 cells.

The effects of gentamicin and G418 on the cellular function of LLC-PK1 epithelial pig kidney cells were investigated. Exposing the cells for 2 days to these aminoglycoside antibiotics inhibited the increase in cell-associated apical membrane enzyme activity (alkaline phosphatase, aminopeptidase, and gamma-glutamyltransferase). Kinetic analysis revealed that the maximal activity of alkaline phosphatase was reduced by these aminoglycosides. Both aminoglycosides inhibited [3H]leucine incorporation into microsomes prepared from LLC-PK1 cells. The LLC-PK1 cells transfected with DNA encoding aminoglycoside 3'-phosphotransferase II, designated T2000B, were resistant to G418 as assessed by colony formation assay and the number of floating dead cells and by assay of apical enzyme activity. After a 4-hr exposure to G418, [3H]leucine incorporation in the host LLC-PK1 cells was inhibited, whereas that in T2000B cells was relatively unaffected. Gentamicin inhibited [3H]leucine incorporation similarly in both cells. The inhibition of protein synthesis by aminoglycosides occurred earlier than that of apical enzyme activity. These findings suggest that the inhibition of protein synthesis by aminoglycoside antibiotics is a possible cause of the reduction in cell viability as well as the apical enzymes in LLC-PK1 cells.

Alkaline Phosphatase↗

PubMed1994

A cis-acting element and a trans-acting factor involved in the wound-induced expression of a horseradish peroxidase gene.

The mechanisms that control the wound-induced expression of the prxC2 gene for horseradish peroxidase (HRP) have been investigated. Analysis of the regulatory properties of 5'-deleted promoters showed that a positive element involved in the response to wounding was located between -307 and -99 bp from the site of initiation of translation. In in vitro binding assays of tobacco nuclear proteins and DNA fragments of prxC2 promoter, the binding site was the Box 1 from -296 to -283 containing the CACGTG motif. To identify the functional role of Box 1, the prxC2 promoter that has been digested from the 5' end to -289 with a disrupted Box 1 was fused to a reporter gene for beta-glucuronidase (GUS). No induction of GUS activity was observed in transgenic tobacco plants with the prxC2 (-289)/GUS construct. These data indicated that the expression of prxC2 in response to wounding required the Box 1 sequence from -296 to -283. Furthermore, a tobacco cDNA expression library was screened and a cDNA clone for a protein, designated TFHP-1, that bound specifically to the Box 1 sequence was identified. The putative TFHP-1 protein contains a basic region and leucine zipper (bZip) motif and a helix-loop-helix (HLH) motif. The mRNA for TFHP-1 was abundant in roots and stems, and it was not induced by wounding in leaves. In tobacco protoplasts, antisense TFHP-1 suppressed the expression of prxC2(-529)/GUS.

Amino Acid Sequence↗

PubMed1994

The KATP and Kv channels are distinct entities: a reply to Edwards and Weston.

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Action Potentials↗

PubMed1994

Nucleotide sequence of a new cDNA for peroxidase from Arabidopsis thaliana.

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Arabidopsis↗

PubMed1994

Cloning, sequencing and expression in Escherichia coli of the gene for alpha antigen from Mycobacterium scrofulaceum.

The gene for the extracellular alpha antigen of Mycobacterium scrofulaceum (S-alpha) was cloned by using the alpha antigen gene fragments of Mycobacterium bovis BCG as probes. The complete nucleotide sequence was determined. The gene was expressed in Escherichia coli. The gene encodes 330 amino acids, including 40 amino acids for the signal peptide, followed by 290 amino acids for the mature protein. The deduced amino acid sequences were highly homologous to the alpha antigen of the species of other mycobacteria. Interestingly, the alpha antigens of MAIS complex (Mycobacterium avium-Mycobacterium intracellulare-M. scrofulaceum) were closely homologous even at the C-terminal regions which were variable among those of M. bovis BCG, Mycobacterium leprae and Mycobacterium kansasii.

Amino Acid Sequence↗

PubMed1994

Sexual dimorphism of urine angiotensinogen excretion in the rat.

To determine the source of angiotensinogen excreted in urine, urine angiotensinogen was measured in male and female rats during growth. Angiotensinogen in 24-hr urine, measured by direct radioimmunoassay with antibody against rat angiotensinogen, increased fourfold in males between the ages of 5 and 7 weeks, whereas no significant changes were observed in females or castrated males. Plasma levels of angiotensinogen, in contrast, showed no significant differences between these groups at any age. Castration of adult males caused a significant reduction of urinary angiotensinogen after 4 weeks. Consecutive s.c. administration of 17 alpha-methyltestosterone for 3 weeks in castrated males resulted in a threefold increase in the urinary excretion of angiotensinogen, as well as a twofold increase in the renal expression of angiotensinogen messenger RNA (mRNA). Renal levels of angiotensinogen mRNA in intact adult males were about threefold higher than those in females and castrated males, whereas there were no significant differences in hepatic angiotensinogen mRNA between these animals. These results suggest that the sexual differences in the urinary excretion of angiotensinogen are primarily due to the androgen-dependent dimorphic expression of angiotensinogen mRNA in the kidney; thus, levels of angiotensinogen in urine might reflect intrarenal production.

Age Factors↗

PubMed1994