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Biomedical subjects

Y Takada

Publications and source records attributed to Y Takada.

At least 271 records · Page 15Linked to original sources
PubMed1996

Purification of membrane-bound ATPase of a psychrophilic marine bacterium, Vibrio sp. strain ABE-1 and characterization as a F0F1-type enzyme.

The ATPase bound to the inner membrane of a psychrophilic marine bacterium, Vibrio sp. strain ABE-1 (Vibrio ABE-1) was extracted with Triton X-100 and purified by fractionation with polyethylene glycol, sucrose density gradient centrifugation, and DEAE-Toyopearl 650M column chromatography. The molecular masses of subunits constituting the purified ATPase were estimated as 54, 49, 33.5, 27, 23.5, 18.5, and 15 kDa by SDS-PAGE. The composition and molecular masses of the subunits of the purified ATPase were similar to those of Escherichia coli F0F1-ATPase (EF0F1). The 54-, 49-, and 18.5-kDa polypeptides of the Vibrio ABE-1 ATPase strongly cross-reacted with the antibodies against the EF0F1 alpha, beta, and b subunits, respectively. However, the Vibrio ABE-1 ATPase contained no cross-reactive polypeptide with the antibodies against A and B subunits of V-type H(+)-ATPase from mung bean tonoplasts. The ATPase activity showed two pH optimum peaks at pH 5.3 and 8.0 and was strongly inhibited by N,N'-dicyclohexyl carbodiimide (DCCD) and NaN3. It hydrolyzed ATP, GTP, and ITP at similar rates. These properties confirm that the purified ATPase is a F0F1-type. The optimum temperature for the ATP-hydrolyzing activity of the enzyme was observed at 50 degrees C, but the DCCD-sensitivity of the enzyme was markedly decreased above 30 degrees C, suggesting that the F1-moiety is released from the enzyme complex at high temperatures. This characteristic is compatible with the psychrophilic nature of Vibrio ABE-1.

Cross Reactions↗
PubMed1996

Expression of basic fibroblast growth factor mRNA in developing choroidal neovascularization.

PURPOSE: Basic fibroblast growth factor (bFGF) is an angiogenic peptide that may be important in the pathogenesis of choroidal neovascularization. We attempted to determine the transcription of the bFGF gene during the development of experimentally induced choroidal neovascularization. METHODS: Rat bFGF cDNA was inserted in the pBluescript to prepare antisense and sense riboprobes. Multiple krypton laser burns were applied to the posterior poles of the eyes of pigmented rats according to a protocol described for producing subretinal neovascularization in these animals. At intervals of up to 4 weeks after photocoagulation, the eyes were removed and cut into thin sections. The sections were subjected to histopathological analysis, cell proliferation study, or in situ hybridization with digoxigenin (DIG)-labeled single-strand riboprobes synthesized from rat bFGF cDNA. RESULTS: In normal adult rat retinas, bFGF mRNA expression was mainly observed in the ganglion cell layer and the inner nuclear layer. After laser photocoagulation, proliferation of RPE cells, fibroblast-like cells and cells in the choroid in the lesions were observed. Expression of bFGF mRNA was observed in the lesions 3 days to 2 weeks after laser treatment. Signals of bFGF mRNA were detected in the proliferating RPE-like cells, choroidal vascular endothelial cells and fibroblast-like cells, all of which are essential for neovascularization. However, bFGF mRNA expression was no longer detectable in these cells 4 weeks after photocoagulation. CONCLUSIONS: Our findings indicate that bFGF is normally transcribed in ganglion cells and the inner nuclear cell layer. During the neovascularization that followed laser photocoagulation, bFGF mRNA expression was detected within the laser lesions. It is thus probable that bFGF acts as a mediator in the neovascularization process.

Animals↗
PubMed1996

Induction of experimental bone metastasis in mice by transfection of integrin alpha 4 beta 1 into tumor cells.

Cell adhesion receptors (eg, integrins and CD44) play an important role in invasion and metastasis during tumor progression. The increase in integrin alpha 4 beta 1 expression on primary melanomas has been reported to significantly correlate with the development of metastases. alpha 4 beta 1 is a cell surface heterodimer that mediates cell-cell and cell-extracellular matrix interactions through adhesion to vascular cell adhesion molecule (VCAM)-1 and to the IIICS region of fibronectin. To test the effects of alpha 4 beta 1 expression on tumor cell metastasis, Chinese hamster ovary cells were transfected with human alpha 4 cDNA. Whereas alpha 4-negative Chinese hamster ovary cells developed only pulmonary metastasis, alpha 4-positive Chinese hamster ovary cells developed bone and pulmonary metastasis in 3 to 4 weeks when injected intravenously into nude mice. Bone metastasis was inhibited by antibody against alpha 4 or VCAM-1. Expression of alpha 3 beta 1, alpha 6 beta 1, or alpha V beta 1 did not induce bone metastasis. Expression of alpha 4 beta 1 also induced bone metastasis in K562 human erythroleukemia cells injected into SCID mice. These results demonstrate that alpha 4 beta 1 can induce tumor cell trafficking to bone, probably via interaction with VCAM-1 that is constitutively expressed on bone marrow stromal cells.

Animals↗
PubMed1996

[Morphological and clinical study of acoustic tumor with respect to enlargement of internal auditory canal: mechanism of bone destruction].

The mechanism of widening of the internal auditory canal (IAC) by an acoustic tumor is still unknown. Degree of IAC enlargement was expressed as "IAC ratio' calculated from the measurement of bilateral horizontal diameters from bone-imaging CT. Comparing IAC ratio to radiological findings of tumors, such as size, solidity, mode of attachment to pyramidal bone and the presence of ventricular dilatation, we found a positive correlation between the ratio and the volume of solid tumors (especially of smaller ones) and more marked destruction of IAC in association with ventricular dilatation. Preoperative degrees of hearing ability or facial nerve function didn't correlate with that of IAC enlargement. It is our hypothesis that the mechanism involved in the destruction of IAC is as follows: (1) The repeated strokes of the tumor caused by brain pulsation gradually erode the bony wall of IAC (especially, that of the posterior wall). The apparently less destruction of IAC in cases with mostly cystic large tumors might be due to the restriction of this pulsatile movement. (2) Increased CSF pressure on the site has some influence on the mechanism of bone erosion as also does solidity of the tumor.

Bone and Bones↗
PubMed1996

[Effect of timing of granulocyte-colony stimulating factor administration on leukopenia induced by systemic chemotherapy in patients with non-small-cell lung cancer--multi-center randomized crossover study].

Sixty-six chemotherapy-naive patients with non-small-cell carcinoma of the lung were given two courses of systemic chemotherapy consisting of mitomycin C, vindesine, and cisplatin. The effect of the timing of administration of grannulocyte colony-stimulating factor (G-CSF) on the incidence of neutropenic fever, the nadir leukocyte count, the duration of neutropenia ( < or = 1000/mm3), and the time needed for recovery from neutropenia was studied. Patients were assigned at random to begin receiving G-CSF (50 microns/m2, subcutaneously) either when the leukocyte count was less than or equal to 1000/mm3 (group I) or when it was between 1000/mm3 and 2000/mm3 (group II), in a crossover fashion. The nadir leukocyte count was lower in group I than in group II (859/mm3 and 1215/mm3, respectively). The duration of leukopenia (defined as a leukocyte count less than or equal to 1000/mm3) was greater in group I than in group II (1.5 days and 0.8 day, respectively), as was the time needed for recovery to a leukocyte count of 2000/mm3 (1.9 days and 1.6 days, respectively) (p < 0.05). No differences were found in the incidence of neutropenic fever (group I: 44%, group Ii: 45%), in the duration of fever (group I: 2.3 days, group II: 2.8 days), or in the duration of G-CSF use (group I: 6.3 days, group II: 6.8 days). There were no treatment-related deaths in either group. We conclude that when this type of combination chemotherapy is given for non-small-cell carcinoma of the lung, administration of G-CSF can be postponed without clinical problems until the leukocyte count is less than of equal to 1000/mm3.

Antineoplastic Combined Chemotherapy Protocols↗
PubMed1996

Effect of alacepril on 24-hour blood pressure in elderly hypertensive patients.

The effect of administration of an angiotensin-converting enzyme inhibitor, alacepril, on 24-hour blood pressure in the elderly hypertensive patients was investigated. Thirteen elderly hypertensive patients (mean age 71 +/- 5; 6 male and 7 female) participated in the present study. After 2 weeks of control period alacepril was administered 25-50 mg/day for 8 weeks. Ambulatory blood pressure monitoring with cuff-oscillometric method was performed at the end of both control and treatment periods. Alacepril administration for 8 weeks significantly decreased 24-hour blood pressure while it had little effect on heart rate. Daytime blood pressure was significantly decreased from 154 +/- 10/91 +/- 5 mmHg to 145 +/- 8/85 +/- 5 mmHg, while the change in nocturnal blood pressure was not significant: from 137 +/- 17/79 +/- 7 mmHg to 130 +/- 15/75 +/- 9 mmHg. Hyperbaric area of systolic blood pressure was also significantly decreased (from 295 +/- 185 mmHg x hour/day to 172 +/- 111 mmHg x hour/day), indicating that pressure load to the heart was effectively reduced. Administration of alacepril did not cause tachycardia in response to the decrease in blood pressure. Acrophase of both blood pressure and heart rate was changed to 11:00 a.m. These findings indicate that blockade of the renin-angiotensin system in the elderly hypertensive patients decreased blood pressure effectively without causing tachycardia or deterioration of diurnal variations of blood pressure. These hemodynamic changes produced by alacepril administration are favorable for the treatment of the elderly patients with cardiovascular disease.

Aged↗
PubMed1996

[Late phase II study of LY188011 (gemcitabine hydrochloride) in patient with non-small-cell lung cancer. Gemcitabine Late Phase II Cooperative Study Group A)].

A late phase II study of LY188011 (gemcitabine hydrochloride), a new synthetic anticancer agent, was conducted at 20 Japanese institutions to evaluate the efficacy and safety of the agent administered alone in patients previously untreated with chemotherapy for primary non-small-cell lung cancer (NSCLC). All of the total 73 patients enrolled were eligible and 69 completed at least one course of LY188011 therapy. All patients were evaluated for safety. The response rate was 26.0% (19/73) of eligible patients. The most common adverse reactions included decreased hemoglobin, leukopenia, neutropenia, anorexia, nausea/vomiting, and malaise. Most adverse reactions were of grade 1 or 2 and only a few grade 3 or 4 reactions were reported. However, since a death occurred due to interstitial pneumonia, careful observation for this event is needed. Based on these results, it may be concluded that LY188011, a new anticancer agent, has adequate efficacy for the treatment of NSCLC and causes few clinically relevant adverse reactions.

Adenocarcinoma↗
PubMed1996

FGF receptor 1 expression in experimental choroidal neovascularization.

Fibroblast growth factor (FGF) is an important factor in neovascularization. To clarify the role of FGF, we demonstrated the expression of FGF receptor 1 mRNA in experimentally induced choroidal neovascularization using in situ hybridization. Krypton laser photocoagulation was applied to the posterior retina of colored rats to induce choroidal neovascularization; the eyes were removed at various intervals after photocoagulation. Chorioretinal sections were made, and FGF receptor 1 cDNA fragments were used to make antisense and sense probes for in situ hybridization. In normal chorioretinal tissue, stain indicating FGF receptor 1 mRNA was observed in the ganglion cells and the inner nuclear layer. After photocoagulation, FGF receptor 1 mRNA appeared in the retinal pigment epithelial cells, in melanocytes of the choroid and in the choroidal blood vessel wall of the photocoagulation lesions. This suggests that FGF is involved in the process of neovascularization. Previous studies have reported that the capillary endothelial cells and retinal pigment epithelial cells produce basic FGF in vitro; FGF may affect the cells in an autocrine or paracrine manner.

Animals↗
PubMed1995

Critical amino acid residues for ligand binding are clustered in a predicted beta-turn of the third N-terminal repeat in the integrin alpha 4 and alpha 5 subunits.

Integrin alpha 4 beta 1 is a receptor for vascular cell adhesion molecule (VCAM)-1 and fibronectin (CS-1). The alpha 4 beta 1-ligand interaction is involved in the pathogenesis of diseases and is, therefore, a therapeutic target. Here, we identified critical residues of alpha 4 for ligand binding using alanine-scanning mutagenesis of the previously localized putative ligand binding sites (residues 108-268). Among 43 mutations tested, mutations of Tyr187, Trp188 and Gly190 significantly inhibited cell adhesion to both VCAM-1 and CS-1. This inhibition was not due to any gross structural changes of alpha 4 beta 1. These critical residues are clustered in a predicted beta-turn structure (residues 181-190) of the third N-terminal repeat in alpha 4. The repeat does not contain divalent cation binding motifs. Notably, the mutations within the corresponding region of alpha 5 significantly reduced fibronectin-alpha 5 beta 1 interaction. These findings suggest that the predicted beta-turn structure could be ubiquitously involved in ligand binding of non-I domain integrins.

Amino Acid Sequence↗
PubMed1995

Changes in blood and plasma serotonergic measurements in rats--effect of nicotine and/or exposure to different stresses.

Effects of two kinds of stress on plasma and whole blood serotonergic measurements were studied in nicotine administered rats. Plasma tryptophan levels increased after footshock stress. Stress given to nicotine administered rats resulted in decrease in plasma tryptophan levels. Although there was no change in 5-HT levels in whole blood, footshock increased plasma levels of 5-HT, and restraint stress decreased its levels. Plasma and whole blood 5-HIAA levels increased in rats given stress and nicotine. 5-HIAA/5-HT ratio (the turnover rate of 5-HT) in plasma and blood increased only in rats given stress and nicotine. These results indicate that nicotine administration may decrease stress induced increase in plasma 5-HT levels by increasing its degradation.

Analysis of Variance↗
PubMed1995

Inhibition of cell cycle progression by the alternatively spliced integrin beta 1C.

Integrins regulate cell growth, differentiation, and behavior in many systems. Integrin beta 1C (beta 1S) is an alternatively spliced variant of integrin beta 1 with a specific cytoplasmic domain and is expressed in several human tissues. Human beta 1c transiently expressed in mouse 10T1/2 fibroblasts showed a diffuse pattern of cell surface staining, whereas beta1 localized to focal adhesions. Moderate concentrations of beta 1C had no effect on actin stress fibers or focal adhesions, but markedly inhibited DNA synthesis. Inhibition by beta 1C mapped to the late G1 phase of the cell cycle, near the G1-S boundary. Thus, alternative splicing of beta1 results in transmission of distinct signals that may regulate growth in vivo.

Alternative Splicing↗