Biomedical subjects

Junko Yoshida

Publications and source records attributed to Junko Yoshida.

3 recordsLinked to original sources

PubMed2003

Antiproliferative effect of Ca2+ channel blockers on human epidermoid carcinoma A431 cells.

The effects of Ca(2+) channel blockers on the proliferation of human epidermoid carcinoma A431 cells were investigated by microtiter tetrazolium (MTT) proliferation assay and bromodeoxyuridine (BrdU) incorporation assay. Dihydropyridine derivatives, such as amlodipine, nicardipine, and nimodipine inhibited A431 cell growth and the incorporation of BrdU into cells with IC(50) values of 20-30 microM, while verapamil, diltiazem and dihydropyridine nifedipine inhibited neither the cell growth nor BrdU incorporation at the same concentration. Though extracellular Ca(2+) is indispensable to the cell growth, an L-type Ca(2+) channel agonist, 1,4-dihydro-2,6-dimethyl-5-nitro-4-[2-(trifluoromethyl) phenyl]pyridine-3-carboxylic acid methyl ester (200 nM), did not affect the antiproliferative action of amlodipine. Thapsigargin, an inhibitor of Ca(2+)-ATPase of the endoplasmic reticulum, inhibited itself the growth of A431 cells and also showed a synergistic effect with the antiproliferative action of amlodipine. In the fluorimetric measurement of intracellular free Ca(2+) concentration in fura-2 or fluo-3 loaded A431 cells, amlodipine blunted the thapsigargin- or cyclopiazonic acid-induced Ca(2+) release from endoplasmic reticulum and the ensuing Ca(2+) influx through Ca(2+)-permeable channels. The effect on the thapsigargin-induced Ca(2+) responses could be reproduced by nicardipine and nimodipine but not by nifedipine or verapamil, lacking antiproliferative potency. These findings suggest that the intracellular Ca(2+) control system responsible for thapsigargin- and cyclopiazonic acid-sensitive endoplasmic reticulum, but not L-type Ca(2+) channels, may be modulated by amlodipine, which results in the inhibition of A431 cell growth.

Calcium↗

PubMed2003

Mass screening for early detection of congenital kidney and urinary tract abnormalities in infancy.

BACKGROUND: Recent widespread use of ultrasound has led to new efforts at screening for congenital kidney and urinary tract abnormalities. However, a standard screening methodology, criteria defining abnormalities, and follow-up procedures remain to be established. In order to establish screening criteria for these abnormalities, we performed a preliminary study in 800 1-month-old infants using provisional methods and criteria. METHODS: Based on the results of preliminary study, we screened 2700 1-month-old infants in a prospective study using the criteria of renal size (longitudinal diameter or=60 mm, or a difference between sides of >or=10 mm), and of pelvic dilatation (Society for Fetal Urology [SFU] grade 2 or higher) as positive at the first ultrasound screening. We used the SFU grading system instead of anteroposterior pelvic diameter measurements for pelvic dilatation. RESULTS: One hundred and twelve (4.1%) of the 2700 infants had abnormalities at the first ultrasound screening, while 18 (0.67%) had congenital kidney and urinary tract abnormalities on further examination. Use of the SFU grading system enabled us to reduce the false-positive rate at first screening, while maintaining a high diagnostic rate. The abnormalities consisted of ureteropelvic junction obstruction in seven infants, megaureter in two, hypoplastic kidney in four, vesicoureteral reflux in six (three were accompanied by hypoplastic kidneys or multicystic dysplastic kidney), multicystic dysplastic kidney in one, and horseshoe kidney in one. CONCLUSION: These results indicate that our screening methods and criteria are useful variables for detecting congenital kidney and urinary tract abnormalities.

Female↗

PubMed2003

Decrease in plasma NOx concentration by isosorbide dinitrate, an organic nitrate ester.

It has been suggested that isosorbide dinitrate (ISDN)-induced venodilation could be ascribed to preferential accumulation of the agent in venous tissues, resulting in higher concentrations of nitric oxide (NO). Here, the authors investigated whether the venodilating effect of ISDN is associated with a preferential increase in plasma concentrations of NOx (NO2- and NO3-, stable end-products of NO) in venous blood than arterial blood. Plasma NOx was measured by high-performance liquid chromatography-Griess system with a sensitivity of 0.01 microM for NO2- and 0.1 microM for NO3-. Arterial and venous blood samples were obtained after coronary angiography from the aorta and right atrium of patients with or without ischemic heart disease. Nicardipine, a calcium channel blocker, was used as a non-NO-related arteriovasodilator. At 1 mg i.v., it did not cause any changes in NOx concentration in arterial and venous blood irrespective of hemodynamic changes. However, ISDN (3 mg i.v.) increased NO2- and decreased NO3- in both arterial and venous blood, with concomitant venodilation. Further analysis revealed that plasma NO increased in the pulmonary circulation and this increase was preserved after nicardipine and ISDN, and that ISDN, but not nicardipine, increased plasma NO3- in the pulmonary circulation. The authors did not detect higher concentrations of NOx in venous blood relative to their level in arterial blood. Further studies are necessary to clarify the kinetics of NO and NO-related compounds in the whole body.

Aged↗