Biomedical subjects

M Takeda

Publications and source records attributed to M Takeda.

At least 19 recordsLinked to original sources

PubMed1992

Assembly regulatory domain of glial fibrillary acidic protein. A single phosphorylation diminishes its assembly-accelerating property.

Phosphorylation of glial fibrillary acidic protein (GFAP) induces disassembly of the filaments. An amino-terminal fragment of bovine GFAP (G-Hf) was produced by lysylendopeptidase digestion. G-Hf formed ribbon-like filaments in the presence of GFAP even in low ionic strength, whereas the fragment itself did not form any structures. Only one (PK3) of the five V8 protease fragments of G-Hf accelerated GFAP assembly to the same degree as G-Hf did, whereas the other fragments did not. When PK3 was cleaved into two fragments, it lost the assembly-accelerating property. The sequence of PK3 was determined as RRRVTSATRRSYVSSSE, which corresponded to residues 3-19 of porcine GFAP. It was concluded that PK3 contains a sequence indispensable for GFAP assembly and that neither PK1 (RRRVTS) nor PK2 (ATRRSYVSSSE) included all of the sequence. A single phosphorylation of PK3 by cyclic AMP-dependent protein kinase diminished its assembly-accelerating property. The phosphorylation site was determined as Ser-12 of porcine GFAP. It was shown that single phosphorylation of the amino-terminal head domain, which contains an indispensable sequence for GFAP assembly, might be sufficient for GFAP disassembly.

Amino Acid Sequence↗

PubMed1992

Cloning and characterization of an androgen-induced growth factor essential for the androgen-dependent growth of mouse mammary carcinoma cells.

An androgen-dependent mouse mammary carcinoma cell line (SC-3) requires androgen for growth stimulation. We have shown previously that androgen acts on SC-3 cells to induce secretion of a fibroblast growth factor (FGF)-like growth factor, which in turn stimulates growth of the cells in an autocrine manner. In this study, the androgen-induced growth factor (AIGF) was purified from a conditioned medium of SC-3 cells stimulated with testosterone. cDNA cloning of AIGF by use of its partial amino acid sequence data revealed that AIGF is a distinctive FGF-like growth factor. An AIGF cDNA (pSC17) encodes a 215-amino acid protein with a putative signal peptide, which shares 30-40% homology with known members of the FGF family. The AIGF mRNA was markedly induced by 10 nM testosterone in Northern blot analysis. Expression of AIGF cDNA in mammalian cells clearly showed remarkable stimulatory effects of AIGF on growth of SC-3 cells in the absence of androgen. Thus, it is clear that the androgen-induced growth of SC-3 cells is mediated in an autocrine manner by AIGF, which is secreted by the tumor cells themselves in response to hormonal stimuli.

Amino Acid Sequence↗

PubMed1992

Immunochemical characterization of rat testicular asparagine synthetase.

We studied immunochemical properties of rat testicular asparagine synthetase. Western blot analysis of testis extract with polyclonal antibody raised against purified asparagine synthetase revealed an immunoreactive band at 62 kDa. The pancreas, brain, thymus, and spleen also showed 62-kDa bands. The intensities of these bands were roughly proportional to the specific activities of the enzyme in these tissues. The antibody showed some degree of cross-reactivity to asparagine synthetases from human, beef, pig, mouse, guinea pig, chicken, and frog, but not carp. But the enzyme from human HL-60 cells and lower vertebrates reacted with the antibody less strongly than enzyme from rats. The N-terminal amino acid sequence of the enzyme, determined by the Edman degradation method, in 10 recovered residues was identical to that of human asparagine synthetase deduced from corresponding cDNA (I.L. Andrulis et al., 1987, Mol. Cell. Biol. 7, 2435-2443). Immunohistochemical staining of the testis showed the presence of asparagine synthetase mainly in Sertoli cells in the seminiferous tubules.

Amino Acid Sequence↗

PubMed1992

Amyloid beta-protein precursor deposition in rat hippocampus lesioned by ibotenic acid injection.

Ibotenic acid was injected into 3 parts of the lateral rat hippocampus. The animals were sacrificed 100 days after treatment, and studied immunohistochemically. The lesioned side of the hippocampus was highly atrophic with extensive neuronal loss and gliosis. Although silver staining revealed no particular structures such as neurofibrillary tangles or senile plaques, globular and granular depositions of amyloid beta-protein precursor (APP) immunoreactivity was observed by immunostaining in the lesion with the monoclonal antibody (clone 22C11). Increased immunoreactivities of glial fibrillary acidic protein (GFAP) and ubiquitin were found in the lesioned area, while the immunoreactivities of microtubule-associated protein 2 (MAP2) and 200 kDa neurofilament subunit protein (NF-H) were diminished. The results indicate that APP deposition is formed in the lesioned area where neuronal degeneration is produced by ibotenic acid in rat hippocampus.

Amyloid beta-Protein Precursor↗

PubMed1992

Teratocarcinoma F9 cells induced to differentiate with sodium butyrate produce both tissue-type and urokinase-type plasminogen activators.

Sodium butyrate (NaB) can induce teratocarcinoma cell differentiation as retinoic acid (RA). However, the function of these two agents seems to be a little different [Kosaka et al., Exp Cell Res, 192:46-51, 1991]. F9 cells treated with NaB synthesize both tissue-type (tPA) and urokinase-type (uPA) plasminogen activator, though RA induces only tPA production. Urokinase-type PA is demonstrated to exist in association with membrane and to localize its activity to the close environment of the cell surface. This may cause the specific cell morphology and characteristics of differentiated F9 cells induced with NaB.

Animals↗

PubMed1992

Disposition of beta-hexachlorocyclohexane, p,p'-DDT, and trans-chlordane administered subcutaneously to monkeys (Macaca fascicularis).

To evaluate skin lipid analysis for the accumulation level of environmental pollutants, the correlations between organochlorine pesticide residues in adipose tissue, blood, and skin lipids of monkeys were studied. The mixture of beta-hexachlorocyclohexane (beta-HCH), p,p'-DDT, and trans-chlordane was subcutaneously given to monkeys once weekly for 5 weeks at dose levels of 1 and 10 mg/kg. The chemicals distributed in adipose tissue, blood, and skin lipids were determined six times after the last dosing at intervals of 4 to 9 weeks. Oxychlordane and p,p'-DDE were detected in all tissues together with the administered chemicals. In blood and adipose tissue, trans-chlordane decreased rapidly and oxychlordane and p,p'-DDE increased gradually and then remained at constant levels. beta-HCH and p,p'-DDT in adipose tissue increased until the 12th week and then decreased in all animals. The correlation coefficients between blood and adipose tissue regardless of dose level and collection time for each chemical ranged from 0.83 to 0.94. Correlation coefficients between skin lipids and adipose tissue varied with the chemical, namely, 0.31, 0.72, 0.81, 0.81, and 0.83 for p,p'-DDE, trans-chlordane, p,p'-DDT, beta-HCH, and oxychlordane, respectively. The results indicated that skin lipid analysis may be useful for the evaluation of specific pollutants in the body burden.

Adipose Tissue↗

PubMed1992

Cumulative white matter changes in the gerbil brain under chronic cerebral hypoperfusion.

An animal model of chronic brain hypoperfusion has been developed by applying coiled clips to the bilateral carotid artery of Mongolian gerbils. The brain tissue damage was neuropathologically studied after 1, 4, 8, and 12 weeks of hypoperfusion. The hippocampus, basal ganglia, and cerebral cortex of the chronically hypoperfused gerbil showed lesions with various severity which are probably due to ischemic episodes. In the cerebral white matter, however, two types of lesions were observed; one similar to those in the gray matter, and the other observed only in the white matter after more than an 8-week duration of brain hypoperfusion. The lesion specific to the white matter showed rarefaction and gliosis without locally associated ischemic changes. This type of the white matter lesion was never found in the gerbil brain before 8 weeks and, significantly, increased in number and size by 12 weeks post operation. The accumulation of the white matter lesions is characteristic in the gerbil with chronic hypoperfusion. The observed white matter-specific lesion resembles the histological changes in aged brain with cerebrovascular diseases.

Animals↗

PubMed1992

SP-40,40 is a constituent of Alzheimer's amyloid.

Cerebrospinal fluid (CSF), serum and seminal plasma contain a small amount of SP-40,40, a modulatory protein of the human complement system. The SP-40,40 in each body fluid was different in molecular size on SDS-PAGE, and glioblastoma cells, hepatoma cells and testicular tumor cells produced SP-40,40, while neuroblastoma cells did not. Therefore, it was estimated that CSF SP-40,40 originated in glia cells, serum SP-40,40 in liver cells and seminal plasma SP-40,40 in testicular cells. SP-40,40 concentrations in CSF of the patients with Alzheimer's disease and the patients with cerebral tumor were higher than those of normal donors. beta-Amyloid deposits in the brains of the patients with Alzheimer's disease were stained with an anti-SP-40,40 monoclonal antibody (mAb) but not with an anti-S-protein mAb, while cellular processes around beta-amyloid were stained with an anti-S-protein mAb but not with an anti-SP-40,40 mAb. Therefore, beta-amyloid contained SP-40,40 in a form different from that in the soluble membrane attack complex (SMAC, SC5b-9) of the complement, which contains S-protein as well as SP-40,40.

Alzheimer Disease↗

PubMed1992

Differential diagnosis of adrenal tumour and upper pole renal tumour by I-131 cholesterol adrenocortical scintigraphy.

A 27-year-old housewife with right hypochondralgia was admitted for treatment of a huge right adrenal or upper pole renal tumour. The tumour measured 10 x 8 x 8 cm and was hypovascular. The main blood supply derived from the right adrenal artery which originated from the abdominal aorta just proximal to the right renal artery. Although several diagnostic imaging studies suggested that the tumour arose from the right adrenal gland, the bilateral adrenal glands were equally visualized on I-131 cholesterol adrenocortical scintigraphy. After surgery and pathological examination, the tumour proved to be a renal cell cancer, while the right adrenal gland was intact. This case demonstrates that adrenocortical scintigraphy is useful in the differentiation of adrenal and renal tumours when a large tumour occupies the upper pole of the kidney or adrenal gland.

Adrenal Gland Neoplasms↗

PubMed1992

Change in the cytoskeletal system in fibroblasts from patients with familial Alzheimer's disease.

1. Fibroblasts were cultured from four patients, two patients from two independent family lines, clinically diagnosed as familial Alzheimer's disease. 2. Adhesion efficiency to the dish was significantly suppressed with fibroblasts from patients with familial Alzheimer's disease compared with the cells from the age-matched control. 3. Cytoskeletal systems were visualized by immunofluorescent staining with antibodies against tubulin, actin, and vimentin, showing unique dearrangement of vimentin fibers in fibroblasts from familial Alzheimer's disease. 4. Regrowth of vimentin fibers after colchicine treatment was slower with fibroblasts from familial Alzheimer's disease than that of the control. 5. Western blotting analysis showed no change in tubulin, actin, and vimentin, but the size of fodrin in familial Alzheimer fibroblasts were different from that of the control cell.

Actins↗

PubMed1992

Endothelin-1 receptor antagonist: effects on endothelin- and cyclosporine-treated mesangial cells.

Endothelin-1 (Et) has profound effects on glomerular microcirculation and mesangial cell contraction. A parameter of mesangial cell contraction was examined by measuring myosin light chain phosphorylation (MLCP) in glomerular mesangial cells in the presence and absence of a newly developed endothelin-1 receptor antagonist (EtA). Addition of Et alone (10 nM) caused a marked increase in MLCP, which, on average, rose by 53 +/- 6% above the level in cells exposed to vehicle (P less than 0.0005). This effect was shown to continue for at least one hour; MLCP at 60 minutes was 64 +/- 12% higher than controls, (P less than 0.025), constituting a unique observation of an in vitro parameter which parallels the characteristic in vivo effect of Et. Treatment of cells with EtA virtually abolished this Et-induced increase in MLCP, which rose by only 2 +/- 3% and -1 +/- 4% for doses of EtA of 44 nM and 66 nM, respectively. Examination of the intracellular calcium concentration, [Ca2+]i, revealed that EtA almost completely abolished the transient increase in [Ca2+]i evoked by Et and also suppressed the early portions of the sustained increase in [Ca2+]i. EtA was ineffective in abolishing [Ca2+]i increase in response to arginine vasopressin. Finally, to evaluate EtA's efficacy in a pathophysiologic setting, we also studied mesangial cells exposed to cyclosporine (Cs). Exposure of mesangial cells to Cs (10(-5) M) for 60 minutes caused a significant increase in MLCP, on average, by 38 +/- 6% above control (P less than 0.0005), while cells exposed to Cs in the presence of EtA increased MLCP significantly less, by only 15 +/- 9%. These data provide further evidence for Et's long-lasting cellular actions, and demonstrate inhibitory effects of an Et receptor antagonist after direct cellular exposure to Et and also after Cs exposure, a pathophysiologic setting which likely involves Et.

Amino Acid Sequence↗

PubMed1992

Detection of three distinct phospholipases A2 in cultured mast cells.

Phospholipase A2 activity in lysates of mast cells such as rat mastocytoma RBL-2H3 cells and mouse bone marrow-derived IL-3-dependent mast cells (BMMC) was measured using phosphatidylcholine (PC), phosphatidylethanolamine (PE), or phosphatidylserine (PS) as a substrate. Both types of cells exhibited phospholipase A2 activity with a similar pH profile; the optimum pH observed with PS as a substrate was 5.5-7.4, whereas that with PE or PC was 8.0-9.0. PE and PC bearing an arachidonate at the sn-2 position were cleaved more efficiently by PE, PC-hydrolyzing phospholipase A2 than phospholipids with a linoleate. A monoclonal antibody raised against rabbit platelet 85-kDa cytosolic phospholipase A2 absorbed the PE, PC-hydrolyzing activity. PS-hydrolyzing activity was purified from RBL-2H3 cells and BMMC by sequential heparin-Sepharose, butyl-Toyo-pearl, and reverse-phase HPLC. On reverse-phase HPLC, the PS-hydrolyzing activity of RBL cells was separated into two peaks, A and B. The peak B activity was inhibited by the anti-rat 14-kDa group II phospholipase A2 antibody, while the peak A activity was not. The partially purified peak A activity hydrolyzed PS about 10-fold more efficiently than PE at optimum pH of 5.5-7.4. No appreciable hydrolysis was observed with PC or phosphatidylinositol (PI). Thus, mast cells may express at least three distinct phospholipases A2; 14-kDa group II phospholipase A2, 85-kDa cytosolic arachidonate preferential phospholipase A2, and a novel phospholipase A2 that shows high substrate specificity for PS.

Animals↗

PubMed1992

Purification and characterization of a possible protooncogene fyn product, p59fyn, from a rat brain particulate fraction.

Four tyrosine-protein kinases that reacted with antibodies specific to p62c-yes, p60c-src, p60c-src+, and p59fyn, respectively, were solubilized from a rat brain particulate fraction and separated by casein-Toyopearl column chromatography. Possible p59fyn, with a pI of 6.5, was purified 490-fold as a single 59-kDa protein band on SDS-PAGE. The purified enzyme contained almost no phosphotyrosine residues but was autophosphorylated with Mg2+. ATP exclusively at tyrosine residues, with a concomitant increase in the kinase activity toward tyrosine-glutamate (1:4) copolymers. The rate of the copolymer phosphorylation was proportional to the square of the enzyme concentration, suggesting activation through intermolecular catalysis. In the presence of Mn2+, however, the reaction showed a first-order dependence on the enzyme concentration.

Animals↗

PubMed1992

Slowly progressive limb-kinetic apraxia with a decrease in unilateral cerebral blood flow.

We report two patients with slowly progressive motor disorders, whose principal manifestations were asymmetric limb-kinetic apraxia and muscle rigidity. In both patients MRI revealed no responsible lesion, whereas single photon emission computed tomography (SPECT) showed a decrease in cerebral blood flow (CBF) in the unilateral hemisphere. One patient with mainly right-sided apraxia had a decreased CBF in the left central region between the frontal and parietal cortices, and the other patient with left-sided apraxia in the right parietal cortex. In agreement with asymmetric clinical symptoms, the regional CBF decrease in the unilateral cortical areas including the frontal and parietal cortices may suggest a degenerative disease, presumably diagnosed as having cortico-basal degeneration.

Aged↗

PubMed1992

Mechanism of PGE2-induced cell swelling in distal nephron segments.

The effects of prostaglandin (PG) E2 on cell swelling were studied in isolated perfused tubules of rabbit kidney. PGE2 (1 microM) added to the bath induced cell swelling by 13.4, 7.2, and 9.6% in the connecting tubule, distal convoluted tubule, and cortical collecting duct, respectively, but it had no effect on the proximal convoluted tubule and cortical thick ascending limb. The response was dose dependent in the range of 1 nM to 1 microM. PGI2 exerted a similar effect, but PGF2 alpha had no effect. The swelling was completely blocked by basolateral Na+ removal and was attenuated by bilateral Cl- removal, suggesting that the swelling was mediated by basolateral Na+ entry in association with Cl- entry. In all segments except proximal tubule, PGE2 caused an initial transient peak followed by a sustained increase in intracellular Ca2+. Intracellular Ca2+ chelation or inhibition of Ca2+ release from intracellular stores abolished the PGE2-induced cell swelling, but extracellular Ca2+ removal did not. An inhibitor of the Na(+)-Ca2+ exchanger (3',4'-dichlorobenzamil, 100 microM) in the bath completely inhibited PGE2-induced cell swelling. Neither furosemide (1 mM) nor amiloride (1 mM) added to bath abolished the response, indicating that neither Na(+)-K(+)-2Cl- cotransport nor Na(+)-H+ exchange is involved in the action of PGE2. The swelling response to PGE2 was observed even in the presence of ouabain, indicating that the effect of PGE2 is independent of Na(+)-K(+)-adenosinetriphosphatase inhibition. Nicardipine added to bath partially inhibited the swelling response.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1992

Primary localized amyloidosis of the bladder: a case of AL (lambda) amyloid protein and combination therapy using dimethyl sulfoxide and cepharanthin.

We report a case of primary localized amyloidosis of the bladder with amyloid deposits which was characterized as being of immunoglobulin light chain origin (AL) including lambda type (A lambda) and P component (AP) using the KMnO4 pretreatment method and immunohistochemical procedures. The patient was treated successfully with intravesical dimethyl sulfoxide instillation and oral administration of high-dose cepharanthin after transurethral resection. Combination therapy with dimethyl sulfoxide and cepharanthin was shown to be useful for primary localized amyloidosis of the bladder.

Aged↗

PubMed1992

Bilateral metastatic sclerochoroidal calcification in a patient with hyperparathyroidism.

We present the case of a 39-year-old man with bilateral sclerochoroidal calcification with primary hyperparathyroidism. Both the calcium and parathyroid hormone levels were elevated. Funduscopic examination revealed slightly elevated, multiple yellow lesions in both eyes. Fluorescein angiography showed filling defects of the choroid. Ultrasonography showed elevated, highly reflective lesions, and a computed tomography scan of the globe disclosed sclerochoroidal lesions with high density. We discuss the mechanism of sclerochoroidal calcification.

Adult↗

PubMed1992

Fisher's syndrome without total ophthalmoplegia.

A 16-year-old boy with acute ophthalmoplegic polyneuritis (Fisher's syndrome) exhibited bilateral internal ophthalmoplegia, but only lateral rectus and superior oblique eye movements were affected. Gaze-evoked nystagmus was also present on left lateral gaze. Pupillary reflex recovered 7 weeks after onset, but neither cholinergic supersensitivity nor light-near dissociation were present during the recovery process. This is the first such case to be reported in which the site of the lesion responsible for the pupillomotor impairment was the Edinger-Westphal nucleus.

Adolescent↗