Biomedical subjects

N Houki

Publications and source records attributed to N Houki.

8 recordsLinked to original sources

PubMed1999

A novel in-frame deletion mutation in a case of lactate dehydrogenase (LD) H subunit deficiency showing an atypical LD isoenzyme pattern in serum and erythrocytes.

OBJECTIVE: We report a case showing an atypical lactate dehydrogenase (LD) isoenzyme pattern involving deficiency only of LD-1 and LD-2 in serum and erythrocytes. LD activity in serum from this patient was extremely low, similar to complete LD-H deficiency, and also that in erythrocytes was low. DESIGN: The DNA fragment containing exon 1 through 7 of the LD-H gene were amplified by PCR and directly sequenced. Total RNA was prepared from venous blood and the proportion of LD-H cDNA to total LD cDNA was semiquantified. RESULTS: Genetic analysis by DNA sequencing detected a three base deletion (AAT) at codon 220 of exon 5, which caused a deletion of one asparagine. The present case did not show reduced LD-H expression at the mRNA level in whole blood. Residue 220 is involved in turning beta-J to alpha1-G and is not buried in the interior of the protein. The novel homozygous in-frame deletion mutation at codon 220 may cause a three-dimensional change of the subunit-binding domain.

Adult↗

PubMed1998

Induction of drug resistance to gold sodium thiomalate in a monocyte cell line, THP-1.

The expression of metallothionein, an intracellular heavy-metal-binding protein, and p-glycoprotein, an energy-dependent drug efflux pump, was examined to study the mechanism of cell resistance to gold sodium thiomalate (GST). THP-1, one of the monocyte-derived cell lines, was cultured for 6 months and resistance to 25 microg/ml of GST (GST-resistant cells) was thus induced. The GST-resistant cells were then cultured with bucillamine to examine the presence of cross-resistance. The intracellular GST concentration was examined by flameless atomic absorption spectroscopy. The cell viability was determined by the uptake of 3-4,5 dimethylthiazole-2,5 diphenyl tetrazolium bromide (MTT). The expression of p-glycoprotein was detected by Western blotting using monoclonal anti-p-glycoprotein antibody. The expression of metallothionein was detected using the indirect immunofluorescence technique. GST-resistant cells did not show any cross-resistance to bucillamine. The rate of cytoplasmic GST accumulation decreased in the GST-resistant cells, while the rate of GST efflux also decreased. The expression of p-glycoprotein in the GST-resistant cells was not significantly different from that in the cells not treated with GST. On the other hand, the GST-resistant cells showed a higher expression of metallothionein than cells not treated with GST. These findings suggest that the induced resistance to GST might partly be due to an induction of metallothionein.

ATP Binding Cassette Transporter, Subfamily B, Mem↗

PubMed1993

[Pathophysiology of cytoskeleton and extracellular matrix in failing myocardium].

Cytoskeleton of myocytes and extracellular matrix play an essential role for maintaining cellular function. Alterations in humoral factors observed in heart failure, e.g., excess of plasma norepinephrine and angiotensin II, injure the microtubule structure probably through Ca overload and increase the collagen synthesis of the cardiac fibroblast. Recent studies demonstrated that network structures of microtubules and intermediate filaments are disrupted in the myocardium obtained from patients with heart failure. Changes in cytoskeletons and extracellular matrix may affect the contractile function, since they organize the intra- and inter-cellular architectures. Pathophysiological roles of cytoskeletons and extracellular matrix in failing hearts deserve further studies.

Angiotensin II↗

PubMed1986