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Biomedical subjects

A Ando

Publications and source records attributed to A Ando.

At least 163 records · Page 9Linked to original sources
PubMed1994

Involvement of phosphoinositide 3-kinase in insulin- or IGF-1-induced membrane ruffling.

Insulin, IGF-1 or EGF induce membrane ruffling through their respective tyrosine kinase receptors. To elucidate the molecular link between receptor activation and membrane ruffling, we microinjected phosphorylated peptides containing YMXM motifs or a mutant 85 kDa subunit of phosphoinositide (PI) 3-kinase (delta p85) which lacks a binding site for the catalytic 110 kDa subunit of PI 3-kinase into the cytoplasm of human epidermoid carcinoma KB cells. Both inhibited the association of insulin receptor substrate-1 (IRS-1) with PI 3-kinase in a cell-free system and also inhibited insulin- or IGF-1-induced, but not EGF-induced, membrane ruffling in KB cells. Microinjection of nonphosphorylated analogues, phosphorylated peptides containing the EYYE motif or wild-type 85 kDa subunit (Wp85), all of which did not inhibit the association of IRS-1 with PI 3-kinase in a cell-free system, did not inhibit membrane ruffling in KB cells. In addition, wortmannin, an inhibitor of PI 3-kinase activity, inhibited insulin- or IGF-1-induced membrane ruffling. These results suggest that the association of IRS-1 with PI 3-kinase followed by the activation of PI 3-kinase are required for insulin- or IGF-1-induced, but not for EGF-induced, membrane ruffling.

Amino Acid Sequence↗
PubMed1994

Signal transduction pathways from insulin receptors to Ras. Analysis by mutant insulin receptors.

We have examined the involvement of insulin receptor (IR) substrate-1 (IRS-1) and/or Shc in the upstream of Ras activation in insulin signaling using Chinese hamster ovary (CHO) cell lines overexpressing wild-type (CHO-IR) cells) or mutant insulin receptors. In CHO-IR cells, insulin rapidly phosphorylated IRS-1 and Shc at tyrosine residues and stimulated the formation of the active GTP-bound Ras (Ras.GTP). In contrast, a CHO cell line overexpressing the kinase-negative mutant insulin receptor substituting Arg1018 for Lys1018 was unable to tyrosine-phosphorylate IRS-1 and Shc and failed to activate Ras in response to insulin. A CHO cell line overexpressing the mutant insulin receptor, substituting Ala960 for Tyr960 and which was known to exhibit impaired tyrosine phosphorylation of IRS-1 and biological effects evoked by insulin, showed severely impaired insulin-dependent tyrosine phosphorylation of Shc and moderately impaired activation of Ras. Another cell line overexpressing the mutant insulin receptor, lacking 82 amino acids of the C terminus of beta-subunit and which was recently reported to retain normal insulin-dependent tyrosine phosphorylation of IRS-1, showed slightly impaired Ras activation at 10(-7) M insulin with severely reduced tyrosine phosphorylation of Shc protein. Furthermore, insulin did not induce the association of tyrosine-phosphorylated IRS-1 and Shc in CHO-IR cells. These results suggest that Shc and IRS-1 lie in the separate signaling pathways and that the tyrosine phosphorylation of IRS-1 with or without some low level of Shc phosphorylation may be enough to stimulate the submaximal accumulation of Ras.GTP complex and may need synergistically the higher level of tyrosine phosphorylation of Shc to induce the full activation of Ras in insulin signaling.

Animals↗
PubMed1994

Biodistributions of radioactive bipositive metal ions in tumor-bearing animals.

Distributions of the nuclides 65ZnCl2, 85SrCl2, 58CoCl2 and 103PdCl2 in tumor-bearing animals were determined, and, in addition, the distributions of these nuclides in tumor tissues were observed. Their subcellular distribution in tumor and liver was also examined. Generally speaking, retention values of these bipositive metal ions in tumor were smaller than those of tri-, quadri- and pentavalent metal ions. In the case of 85SrCl2, a large amount of this nuclide was taken up by the bone and remained there for a long time. In the case of 103PdCl2, 103Pd was avidly taken up by the kidney and liver. Very little of the 103Pd taken up into the kidney and liver was excreted. 65Zn and 103Pd were concentrated in the viable tumor tissue and were not seen in necrotic tumor tissue. In the case of 58Co, lysosome played an important role in liver accumulation and played a minor role in tumor accumulation. The distribution of 58Co in tumor and liver was fairly similar to that of 67Ga, 111In, 169Yb, 46Sc, 51Cr, 95Zr, 181Hf, 95Nb and 182Ta which were reported previously. Lysosome did not play an important role in the accumulation of 65Zn, 85Sr and 103Pd into tumor and liver.

Animals↗
PubMed1994

Cloning of a new kinesin-related gene located at the centromeric end of the human MHC region.

We previously reported the presence of a new gene (HSET) with an unknown function, in the centromeric side of the class II gene region of the human major histocompatibility complex (MHC). cDNA clones corresponding to the HSET gene were isolated from a human testis cDNA library. A 2.4 kilobase transcript from the HSET gene was abundantly expressed in testis, B-cell, T-cell, and ovary cell lines but was not detected in lung or stomach. Analysis of the nucleotide sequence of the HSET cDNA clones revealed significant similarity to kinesin-related proteins in yeast, Drosophila, and human. Its predicted amino acid sequence contains a domain with strong sequence similarity to the ATP-binding and motor domains of a plus end-directed microtubule motor protein, kinesin, which might be involved in mitotic chromosome segregation, suggesting that the HSET gene encodes a novel kinesin-related protein.

Amino Acid Sequence↗
PubMed1994

Tumour affinity of 203Pb-chloride: comparison with 67Ga-citrate and 201Tl-chloride.

The radionuclide 203Pb decays completely by electron capture to stable 203Tl with a half-life of 52 h. The primary radiation from the decay is gamma-ray radiation 280 keV (80%). 203Pb is produced easily from the natural metal thallium by the method described below. 203Pb-chloride is a promising imaging agent for tumour scanning because of the large retention value for tumour tissue and the small value for normal organs, but the large value for the kidney and bone is a shortcoming when considering it as an imaging agent. The retention value of 203Pb in tumour tissue is larger than that of 201Tl and smaller than that of 67Ga. The tumour/inflammatory lesion retention ratio for 203Pb is very large in comparison with those for 67Ga and 201Tl. 203Pb accumulates to a large extent in viable tumour tissue, and less in necrotic tumour tissue and in inflammatory lesion. Therefore, 203Pb-chloride is far better for visualization of viable tumour tissue than 67Ga and 201Tl if the large retention values for the kidney and bone were reduced.

Animals↗
PubMed1994

Coexistence of vasoactive intestinal polypeptide and neuropeptide Y immunoreactivity within axon terminals in the canine and human lower esophageal sphincter: electron microscopy by a double immunogold labeling procedure.

Subcellular localization of vasoactive intestinal polypeptide (VIP) and neuropeptide Y (NPY) immunoreactivity within nerves was investigated in the lower esophageal sphincter of dogs and humans by double immunogold staining of sections prepared for electron microscopy. Coexistence of VIP and NPY immunoreactivity was clearly demonstrated in the large granular vesicles (LGVs) in axon terminals that were closely associated with the smooth muscle cells, as well as in the LGVs within the perikarya of neurons located in the myenteric plexus. Some LGVs appeared immunopositive only for VIP or NPY. This phenomenon might have been partly due to the fact that the double-labeling procedure with immunogold particles of different sizes was performed on both faces of each section. The results obtained in this study suggest that VIP and NPY are synthesized in the same neuron, stored in the same axon terminal, and released together to act on sphincter muscle cells.

Animals↗
PubMed1994

Long-term efficacy of acute thrombolytic therapy for myocardial infarction.

We conducted a retrospective study (1981-1990) to determine whether the efficacy of intracoronary thrombolysis (ICT) could be evaluated from data obtained solely after recanalization. We investigated 55 successful ICT patients (38 with anterior and 17 with inferior myocardial infarction (MI)), and 31 control infarct patients without recanalization. The total serum creatine phosphokinase release (sigma CPK), the extent of infarction measured by T1-201 single photon emission computed tomography (total DS) and the disturbance of regional wall motion (asyn.%) were investigated as parameters for distinguishing the successful ICT and control groups. Discriminatory ability for the two groups was highest with the total DS in all patients. Only the total DS differed significantly between the two groups in patients with inferior infarction. Misidentification of control patients as successful patients was least frequent (25.5%) when using the total DS. These findings suggest that the effectiveness of ICT for acute MI may be assessed on the basis of data obtained solely after recanalization, with the total DS being particularly useful.

Adult↗
PubMed1994

The c-kit ligand, stem cell factor, promotes mast cell survival by suppressing apoptosis.

Stem cell factor (SCF) and its receptor (SCFR), a member of the receptor tyrosine kinase III family that is encoded by the c-kit gene, critically regulate several complex biological programs including hematopoiesis, mast cell development, cutaneous pigmentation, and gametogenesis. We show herein that mouse mast cells die rapidly after the withdrawal of SCF in vivo or in vitro, and provide morphological evidence that such mast cells undergo programmed cell death or apoptosis. We also show that when in vitro-derived mouse mast cells maintained in SCF are removed from SCF-containing medium for only 5 or 6 hours, the cells' genomic DNA exhibits the ladder-like pattern of oligonucleosome-sized fragments typical of apoptosis. These findings demonstrate that SCF can regulate the survival of a cellular lineage which expresses the SCFR by suppressing apoptosis. They also identify a mechanism that can result in striking and rapid reductions in the size of tissue mast cell populations without histological evidence of the concomitant induction of a significant inflammatory response.

Animals↗
PubMed1994

Hemodynamic effects of the calcium channel blocker pranidipine on exercise-induced angina.

Hemodynamic effects of a newly developed calcium channel blocker, pranidipine, on dynamic exercise-induced angina were investigated. Ten patients with stable effort angina pectoris underwent symptom-limited bicycle ergometer exercise testings before and after a single oral administration of pranidipine, and effects of pranidipine on systemic, cardiac and coronary hemo-dynamics induced by dynamic exercise were evaluated invasively. Pranidipine administration reduced systemic vascular resistance (from 1,764 +/- 109 to 1,115 +/- 60 dynes.sec/cm5; p < 0.01 at test, and from 1,120 +/- 102 to 795 +/- 62 dynes.sec/cm5; p < 0.05 at peak exercise) and mean arterial pressure (from 93 +/- 5 to 76 +/- 3 mmHg; p < 0.01 at test, and from 85 +/- 7 to 72 +/- 6 mmHg; p < 0.05 at peak exercise) with the increase in heart rate and cardiac index throughout exercise. Pranidipine also decreased coronary vascular resistance from 1.29 +/- 0.21 to 0.89 +/- 0.17 mmHg/ml/min (p < 0.05) at resting condition. At peak exercise, rate-pressure product and myocardial oxygen consumption decreased (from 237 +/- 21 to 215 +/- 18 x 10(2); p < 0.05, and from 31.3 +/- 7.5 to 21.7 +/- 3.9 ml/min; p < 0.05, respectively), while coronary vascular resistance did not change significantly. Furthermore, pranidipine mitigated ST-segment depression and elevation of pulmonary artery wedge pressure at peak exercise (from 0.20 +/- 0.03 to 0.13 +/- 0.02 mV; p < 0.01, and from 25 +/- 3 to 11 +/- 2 mmHg; p < 0.01, respectively). These results suggest that the major therapeutic effects of pranidipine for dynamic exercise-induced angina would be to reduce myocardial oxygen demand by improving peripheral circulation and reducing preload and afterload.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1994

[Surgical treatment of pulmonary aspergillosis].

There is controversy about the optimal treatment for pulmonary aspergillosis. Eight patients with pulmonary aspergilloma underwent surgical treatment. Three patients had tuberculosis, one Sjögren syndrome, one aortitis syndrome, one malignant lymphoma. Lobectomy was performed in five patients, segmentectomy in three patients. All patients are alive and have no recurrence. We have obtained excellent results from surgery and advocate early surgery for localized lesions to prevent life-threatening hemoptysis. This will allow patients to continue with further treatment for the underlying disease. We encountered a granulocytopenic patient with rapidly progressive aspergillus infection resulting in occlusion of main pulmonary artery leading to death. Surgical intervention could not prevent this fatal outcome. The selection of the patients with diffuse lesions should be made carefully.

Adult↗
PubMed1994

[Rabson-Mendenhall syndrome].

Rabson-Mendenhall syndrome was initially reported in 1956 by Rabson et al., who described three children with familial hyperplasia of pineal gland and diabetes mellitus. Characteristic features of this syndrome are low birthweight, thickened nails, hirsutism, acanthosis nigricans, dental precosity and dysplasia, polycystic ovary, abdominal proturbance, phallic enlargement and insulin resistant diabetes mellitus. Most patients die of ketoacidosis and intercurrent infection associating with extreme insulin resistance during mid-childhood. This syndrome appears to show autosomal recessive inheritance. Recent reports provide evidence that mutations in the insulin-receptor gene are, at least in pant, the cause of this syndrome, and that recombinant IGF-I (insulin-like growth factor-1) reduces hyperglycemia in patients of this syndrome.

Acanthosis Nigricans↗
PubMed1993

Mast cells contribute to the changes in heart rate, but not hypotension or death, associated with active anaphylaxis in mice.

The mast cell is widely thought to contribute importantly to the cardiopulmonary changes associated with anaphylaxis, but much of the evidence for this is indirect. We, therefore, performed a detailed assessment of heart rate and pulmonary function during active anaphylaxis in genetically mast cell-deficient W/Wv or S1/S1d mice, the congenic normal (+/+) mice, and W/Wv mice repaired of their mast cell deficiency by transplantation of bone marrow from the congenic +/+ mice (+/+ BM-->W/Wv mice). For all five groups of mice, Ag challenge resulted in the death of more than two-thirds of the sensitized animals, whereas none of the nonsensitized control mice died as a result of Ag infusion. Sensitized normal (WBB6F1(-)+/+ or WCB6F1(-)+/+) mice and +/+BM-->W/Wv mice developed increases in heart rate that were significantly greater than those of nonsensitized +/+ mice or those of sensitized mast cell-deficient mice, indicating that mast cells contribute to the tachycardia observed in this form of active anaphylaxis. By contrast, even though some of the pulmonary changes associated with active anaphylaxis were more severe in +/+ than in mast cell-deficient mice, it was not clear to what extent this difference was mast cell dependent. W/Wv mice undergoing active anaphylaxis developed decreases in systemic arterial blood pressure that occurred more rapidly and were more severe than those observed in the congenic +/+ mice, indicating that the hypotension associated with this model of anaphylaxis also can occur by mast cell-independent mechanisms. We conclude that in this model of anaphylaxis mast cells: 1) are required for the development of the tachycardia response; 2) may contribute to, but are not essential for, production of decreases in lung function; and 3) are not necessary for the development of hypotension or death.

Age Factors↗
PubMed1993

Prognosis of undetected intrapulmonary metastases in resected lung cancer.

BACKGROUND: Between 1975 and 1989, 839 patients with lung cancer underwent pulmonary resection at Okayama University Medical School; for this study data of the 42 (5.0%) who had intrapulmonary metastasis were analyzed. RESULTS: The 5-year survival rate for the 42 patients was 25.7%, which was significantly better than that of patients with Stage IV disease and extrapulmonary metastasis, none of whom survived for 3 years. The 2-year survival rate was found to be significantly better in patients with one-lobe metastasis (n = 37; 41.5%) than in those with two-lobe metastasis (n = 5; 20.0%). Adenocarcinoma was the most common tumor (66.8%), followed by squamous cell carcinoma (28.6%), but the prognosis differed little between these two histologic types. Intrapulmonary metastasis did not unfavorably affect the prognosis when the primary tumor was 3 cm or less in greatest dimension and there were no lymph node metastases (T1N0). CONCLUSION: In patients with lung cancer and one-lobe intrapulmonary metastasis, particularly in those with T1N0, a favorable prognosis can be expected after surgery.

Adenocarcinoma↗
PubMed1993

Myocardial SPECT and left ventricular performance study using a single Tc-99m teboroxime injection. Comparison with thallium-201 myocardial SPECT.

Myocardial SPECT using teboroxime was compared to thallium SPECT in 26 patients undergoing cardiac catheterization. Agreement between thallium SPECT and teboroxime SPECT for the identification of myocardial segments was 209/235 (89%). A significant correlation was found in 15 patients between the left ventricular ejection fraction by teboroxime first-pass study and the ejection fraction by contrast ventriculography. In nine patients with myocardial infarction and/or multivessel coronary artery disease, the ejection fraction revealed a mean decrease from 0.52 at rest to 0.46 at exercise. Teboroxime makes it possible to perform an exercise first-pass study of left ventricular ejection fraction followed by myocardial perfusion imaging.

Adult↗
PubMed1993

An autopsied case of Williams syndrome complicated by moyamoya disease.

An 18 year old girl with typical clinical features of Williams syndrome suddenly died of intracerebral hemorrhage due to moyamoya disease. Autopsy revealed vascular abnormalities, such as supravalvular aortic stenosis (SAS) and an abnormal complicated cerebrovascular network in the cerebral arteries. The arterial wall of the SAS lesion consisted of thickened medial tissue showing elastic disorganization with prominence of the smooth muscle cells. The narrowed vessels of the circle of Willis showed intimal thickening with an extremely wavy internal elastic lamina and marked thinning of the media. To our knowledge, this is the first report of moyamoya disease associated with Williams syndrome.

Abnormalities, Multiple↗
PubMed1993

Effects of chronic treatment with the c-kit ligand, stem cell factor, on immunoglobulin E-dependent anaphylaxis in mice. Genetically mast cell-deficient Sl/Sld mice acquire anaphylactic responsiveness, but the congenic normal mice do not exhibit augmented responses.

We treated genetically mast cell-deficient WCB6F1-Sl/Sld mice and the congenic normal (WCB6F1(-)+/+) mice with the c-kit ligand recombinant rat stem cell factor164 (rrSCF164; 100 micrograms/kg per d, subcutaneously) or with vehicle for 21 d, then passively sensitized the mice with anti-dinitrophenol30-40 immunoglobulin E (IgE) antibodies, and 1 d later measured the changes in heart rate, pulmonary dynamic compliance, and pulmonary conductance, and assessed the death rates associated with intravenous challenge of these animals with specific antigen. rrSCF164 treatment induced the development of mast cells in Sl/Sld mice, and these mice exhibited tachycardia, but not death, after challenge with IgE and antigen. rrSCF164 treatment induced mast cell hyperplasia in +/+ mice, but the cardiopulmonary changes associated with passive anaphylaxis in these mice were virtually indistinguishable from those observed in control +/+ mice treated with vehicle instead of rrSCF164. Moreover, the highest dose of antigen challenge produced significantly fewer fatalities in rrSCF164-treated than in vehicle-treated +/+ mice (1/11 vs. 8/11, respectively, P < 0.01). Thus, in normal mice, chronic treatment with rrSCF164 induces mast cell hyperplasia but does not increase, and in certain respects diminishes, the severity of IgE-dependent anaphylactic reactions.

Anaphylaxis↗