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Biomedical subjects

H Masukawa

Publications and source records attributed to H Masukawa.

16 recordsLinked to original sources
PubMed2002

Disruption of the uptake hydrogenase gene, but not of the bidirectional hydrogenase gene, leads to enhanced photobiological hydrogen production by the nitrogen-fixing cyanobacterium Anabaena sp. PCC 7120.

In order to determine the effects of the deletion of hydrogenase genes on nitrogenase-based photobiological H(2) productivity by heterocystous N(2)-fixing cyanobacteria, we have constructed three hydrogenase mutants from Anabaena sp. PCC 7120: hupL(-) (deficient in the uptake hydrogenase), hoxH(-) (deficient in the bidirectional hydrogenase), and hupL(-)/ hoxH(-) (deficient in both genes). The hupL(-) mutant produced H(2) at a rate four to seven times that of the wild-type under optimal conditions. The hoxH(-) mutant produced significantly lower amounts of H(2) and had slightly lower nitrogenase activity than wild-type. H(2) production by the hupL(-)/ hoxH(-) mutant was slightly lower than, but almost equal to, that of the hupL(-) mutant. The efficiency of light energy conversion to H(2) by the hupL(-) mutant at its highest H(2) production stage was 1.2% at an actinic visible light intensity of 10 W/m(2) (PAR) under argon atmosphere. These results indicate that deletion of the hupL gene could be employed as a source for further improvement of H(2) production in a nitrogenase-based photobiological H(2) production system.

Anabaena↗
PubMed1999

Klinefelter's syndrome accompanied by mixed connective tissue disease and diabetes mellitus.

We report a rare case of Klinefelter's syndrome (KS) with mixed connective tissue disease (MCTD), diabetes mellitus (DM) and several endocrine disorders. A 57-year-old man presented with polyarthritis and tapering fingers with Raynaud's phenomenon on admission. In addition to a karyotype of 47, XXY, a marked restrictive change in respiratory functional test, a myogenic pattern in electromyogram, the positive tests for anti-RNP antibody indicated that this was a case of KS complicated with MCTD. The patients also presented DM with insulin resistance, hyperprolactinemia, slight primary hypothyroidism and hypoadrenocorticism. The mechanism for these coincidences remains to be elucidated.

Arthritis↗
PubMed1998

Cat eye syndrome with hypogonadotropic hypogonadism.

A 17-year-old male diagnosed as having Cat Eye Syndrome (CES) with hypogonadotropic hypogonadism showed short stature and no development of secondary sex characteristics. Exogeneous gonadotropin replacement therapy combining human chorionic gonadotropin (hCG) and human menopausal gonadotropin (hMG) was started. As a result, the short stature and androgen deficiency were relieved. The critical region of CES was tetrasomy of 22 pter-->q11. Abnormalities of other chromosomes which cause hypogonadotropic hypogonadism may exist, thus further investigation is needed.

Abnormalities, Multiple↗
PubMed1987

Effect of lidamidine on transepithelial potential difference evoked by prostaglandin E2 in human jejunum.

The effect of the infusion of lidamidine, an antidiarrheal drug, on the change in transepithelial potential difference (TPD) induced by the infusion of prostaglandin E2 (PGE2) was examined in perfused human jejunum in vivo. The increase in luminal negativity of TPD produced by 3 X 10(-7) M PGE2 was significantly decreased from 2.8 +/- 0.5 mV to 1.2 +/- 0.5 mV by the superimposed infusion of 2 X 10(-3) M lidamidine. This result may suggest that lidamidine has an inhibitory effect on intestinal Cl secretion which is stimulated by PGE2.

Action Potentials↗
PubMed1986

Electrical measurement of chloride secretion in the perfused human jejunum: effects of theophylline and prostaglandin E1.

The effects of intraluminal theophylline or prostaglandin E1 (PGE1) on transepithelial potential difference (PD) were examined in the human jejunum in vivo with a quadruple lumen perfusion tube. To measure transepithelial PDs, we placed one of the Ag/AgCl electrodes in the jejunal lumen and the other in the subcutaneous region of the left forearm of the subjects. Infusion of theophylline or PGE1 into the jejunal lumen produced a change in the PD, the lumen being more negatively charged. The magnitude of the change in PD for 2.4 X 10(-3) M theophylline was 3.3 +/- 0.48 mV (mean +/- S.E., n = 6) and that for 10(-6) M PGE1 was 5.0 +/- 0.60 mV (n = 6). In addition, the change in the PD induced by simultaneous infusion of both 2.4 X 10(-3) M theophylline and 10(-7) M PGE1 was about twice as large as the sum of those induced by individual infusion of the same concentration of theophylline or PGE1. We concluded that these PD changes occurred primarily by stimulation of electrogenic Cl secretion in the jejunum. Further exploitation of this method to determine PD might be useful for clinical investigation of the intestinal secretion.

Adult↗
PubMedDate not supplied

Stimulatory effect of endothelin-1 on Na-dependent phosphate transport and its signaling mechanism in osteoblast-like cells.

Endothelin-1 (ET-1) has been reported to modulate bone metabolism both in vivo and in vitro. In the present study, we investigated the effect of ET-1 on inorganic phosphate (Pi) transport in osteoblast-like cells, which is now considered to be important for the initiation of bone matrix calcification. ET-1 time- and dose-dependently stimulated Na-dependent Pi transport in mouse calvaria-derived osteoblast-like MC3T3-E1 cells, and this effect was dependent on transcriptional and translational process. Kinetic analysis indicated that the change in Pi transport activity induced by ET-1 was due to alteration in the number of the Pi transporter. BQ123, a selective antagonist for ET(A) receptor, suppressed the ET-1-induced Pi transport, but BQ788, a selective antagonist for ET(B) receptor, had no effect. The inhibition of phosphoinositide hydrolysis by phospholipase C (PLC) partially attenuated the Pi transport by ET-1. Propranolol, which inhibits phosphatidic acid phosphohydrolase, also suppressed ET-1-induced Pi transport. On the contrary, indomethacin did not affect the stimulatory effect of Pi transport by ET-1. Calphostin C, a protein kinase C (PKC) inhibitor, significantly blunted the stimulatory effect of ET-1 on Pi transport. Combined effect of PMA and ET-1 on Pi transport was not additive. Pi transport induced by ET-1 was also suppressed in PKC down-regulated cells. In conclusion, the results of the present study indicate that in MC3T3-E1 osteoblast-like cells, ET-1 acting through ET receptor links to a stimulation of Pi transport via activation of PKC through both phosphoinositide and phosphatidylcholine hydrolyses.

Animals↗