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Biomedical subjects

T Ogata

Publications and source records attributed to T Ogata.

At least 235 records · Page 13Linked to original sources
PubMed1995

Turner syndrome and female sex chromosome aberrations: deduction of the principal factors involved in the development of clinical features.

Although clinical features in Turner syndrome have been well defined, underlying genetic factors have not been clarified. To deduce the factors leading to the development of clinical features, we took the following four steps: (1) assessment of clinical features in classic 45,X Turner syndrome; (2) review of clinical features in various female sex chromosome aberrations (karyotype-phenotype correlations); (3) assessment of factors that could lead to Turner features; and (4) correlation of the clinical features with the effects of specific factors. The results indicate that the clinical features in 45,X and in other female sex chromosome aberrations may primarily be determined by: (1) degree of global non-specific developmental defects caused by quantitative alteration of a euchromatic or non-inactivated region; (2) dosage effect of a pseudoautosomal growth gene(s), a Y-specific growth gene(s), and an Xp-Yp homologous lymphogenic gene(s); and (3) degree of chromosome pairing failure in meiocytes that are destined to develop as oocytes in the absence of SRY. 1991; Grumbach and Conte 1992). However, the pertinent factors have not been determined to date. The method to clarify the factors responsible for the development of the Turner phenotype can be broken down into the following steps: (1) assessment of clinical features in classic 45,X Turner syndrome; (2) review of clinical features in various female sex chromosome aberrations (karyotype-phenotype correlations); (3) assessment of factors that could lead to Turner features; and (4) correlation of the clinical features with the effects of specific factors. If the clinical features in 45,X and in other female sex chromosome aberrations are explained by the effects of specific factors, it can be said that such factors contribute to the development of Turner features. In this paper, we take each of the above steps, and propose the principal factors involved in the development of clinical features in Turner syndrome.

Chromosome Aberrations↗
PubMed1995

Refinement of the locus for X-linked recessive chondrodysplasia punctata.

Although the locus for X-linked recessive chondrodysplasia punctata (CDPX1) has been mapped to the region between PABX and DXS31 (the critical region is about 3 Mb long), the precise location within the critical region has not been determined. In this paper, we describe a boy with a 46,Y,der(X)t(X;Y)(p22.3;q11)mat karyotype and review the genotype-phenotype correlations in three male patients with the combination of apparent lack of clinical features of CDPX1 and a partial deletion of the critical region. The results suggest that the region defined by the two BssHII sites at 3180 and 3570 kb from the Xp telomere may be the target region for the CDPX1 locus.

Adolescent↗
PubMed1995

A possible mechanism for the hypoxia-hypoglycemia-induced release of excitatory amino acids from cultured hippocampal astrocytes.

In order to elucidate the mechanism of release of excitatory amino acid (EAA) induced by hypoxia-hypoglycemia (in vitro ischemia) from cultured hippocampal astrocytes, we compared the EAA release by in vitro ischemia with those by other treatments. The EAA release induced by in vitro ischemia treatment was rapid and reversible. The amount of released aspartate was comparable to that of glutamate, although the endogenous content of aspartate was one sixth that of glutamate. High-K (100 mM) treatment and the addition of 5 mM NaCN induced a rapid EAA release and the glutamate release was much greater than aspartate. Addition of 5 mM iodoacetate, a glycolysis inhibitor, induced a slow EAA release, and the amount of released aspartate was much higher than that of glutamate. On the other hand, the in vitro ischemia treatment and the addition of 5 mM NaCN induced only 20% reduction in ATP content for initial 5 min, whereas the addition of 5 mM iodoacetate induced a marked reduction. Our data suggest that ischemia-induced EAA release from astrocytes is a complex process in which local energy failure, inhibition of glycolysis, and depolarization of the cell membrane are involved.

Adenosine Triphosphate↗
PubMed1995

A morphological study on the histogenesis of human colorectal hyperplastic polyps.

BACKGROUND & AIMS: Little is known about the histogenesis of human colorectal hyperplastic polyp, although this polyp is clinically very common. Therefore, the structural features of the polyp and their implications regarding histogenesis were studied. METHODS: A total of 261 foci were examined using scanning electronmicroscopic observation of the isolated crypt and surface structure, NaOH cell maceration and scanning electron microscopy, dissecting microscopy, and standard histological analysis. RESULTS: In surface view, each polyp crypt was discretely demarcated as in the normal crypt, suggesting that the crypt epithelium had not replaced the adjoining crypt. Notches at the base and various stages of branching, observed in 21.8% of the isolated crypts, were considered to reflect crypt fission. Several polyps with a single crypt mouth consisting of fissioned multiple crypts suggested polyp origin from a single crypt and growth by fission. Juxtaposition of small polyps and their fusion suggested polycentric origin. Almost all polyps showed increased stromal inflammatory cell infiltration and/or a lymphoid follicle at the base. CONCLUSIONS: Hyperplastic polyps originate by the apparent fusion of single abnormal crypts within a small region of mucosa. The polyps grow by fission of the crypt and fusion of the polycentrically originated polyps. Chronic inflammation has some relation to this process.

Adenoma↗
PubMed1995

Calbindin-D 28k immunoreactivity in the cerebellum of spinocerebellar degeneration.

We studied immunoreactivity for calbindin-D 28k (CaBP), an intracellular calcium-binding protein, in the cerebellum of control subjects and of patients with spinocerebellar degeneration (SCD) including sporadic olivopontocerebellar atrophy and familial cortical cerebellar atrophy. In the cerebellum, CaBP immunoreactivity was seen exclusively in the Purkinje cell in both SCD and control groups. However, the number of CaBP-immunoreactive Purkinje cells was significantly reduced in SCD. CaBP immunohistochemistry also disclosed abnormal morphological changes of Purkinje cells, which was not visualized on conventional strains or not clearly demonstrated on immunohistochemistry for neurofilaments. Moreover, reduced CaBP immunoreactivity was observed even in some remaining Purkinje cells of SCD suggesting that loss of CaBP precedes neuronal loss of Purkinje cell. We conclude that CaBP is a useful marker for Purkinje cell degeneration, and that reduced CaBP expression might have some association with the mechanism of the Purkinje cell degeneration in SCD.

Aged↗
PubMed1995

Guanidine neurotoxins are released with the digestive fluid of crabs (Crustacea, Brachyura).

During agonistic interactions intertidal crabs, when exposed to air, produce a foam made of digestive secretions, sea water and air bubbles. They also may release their digestive secretions in water when disturbed. Crabs belonging to the families Majidae, Xanthidae and Portunidae from Atlantic and Pacific areas, not related with human poisoning, possess substances in their digestive secretion which are neurotoxic to mice, block action potentials in nerve preparations, and are reversible on washing. After purification in Bio-gel P-2 chromatography and HPLC analysis, the spontaneously regurgitated secretion, the digestive secretion collected by stomach cannulation of crabs, and the water aquarium replete of intertidal crabs kept overnight show the presence of guanidine neurotoxins.

Animals↗
PubMed1995

Neurotoxicity of acromelic acid in cultured neurons from rat spinal cord.

Acromelic acid A, which contains the kainic acid structure in its molecule, is known to cause selective damage of interneurons in the rat lower spinal cord. In the present study, the potent neurotoxicity of acromelic acid A was demonstrated in cultured rat spinal neurons in terms of the activity of lactate dehydrogenase that was released from degenerated neurons into the culture medium. Acromelic acid A increased the lactate dehydrogenase activity in time- and concentration-dependent manners, and its EC50 was about 2.5 microM, which was much lower than that of kainic acid (70 microM) and (RS)-alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (EC50; 11 microM). The maximum level of lactate dehydrogenase released by acromelic acid A was quite similar to that by kainic acid, but was about twice the level produced by (RS)-alpha-3-hydroxy-5-methyl-4-isoxazolepropionic acid. Exposure to acromelic acid A caused release of L-glutamate from the cells into the medium; however, the concentration of L-glutamate released was far below the level for inducing the neurotoxic effects. The neurotoxicity of 10 microM acromelic acid A was almost completely inhibited by 30 microM 6-nitro-7-sulphamoylbenzo(F)quinoxaline-2,3-dione and 6-cyano-7-nitroquinoxaline-2,3-dione, potent antagonists for non-N-methyl-D-aspartate receptors, but was partly (35%) reduced by 30 microM dizocilpine maleate. In cultured hippocampal neurons, the toxicity of acromelic acid A was significantly less effective (EC50: 18 microM) than that in spinal neurons, whereas the toxicity of kainic acid was almost the same in both neurons. These results suggest that acromelic acid A directly activates non-N-methyl-D-aspartate receptors on the cultured spinal neurons to induce neuronal death. A new type of non-N-methyl-D-aspartate receptors which is specific to acromelic acid A is suggested to be present at least in spinal neurons.

Amino Acids↗
PubMed1995

Expression of the multidrug resistance-associated protein (MRP) gene in non-small-cell lung cancer.

We examined the levels of expression of the multidrug resistance-associated protein (MRP) gene quantified by Northern blot analysis in comparison with those of the MDR1 gene determined by reverse transcription-polymerase chain reaction (RT-PCR) in 104 non-small-cell lung cancer (NSCLC) specimens [59 adenocarcinoma (Ad), 40 squamous cell carcinoma (Sq), four large cell carcinoma (La) and one adeno-squamous carcinoma (AdSq)]. Thirty-three (31.7%) of the 104 NSCLC expressed the MRP gene at various levels. The NSCLC showing high (++) levels of MRP gene expression (19 out of 33, 57.6%) were predominantly squamous cell carcinomas (Ad, 5; Sq, 13; La, 1) (P < 0.05). Six of the eight NSCLCs expressing high levels of MRP mRNA and no MDR1 (MRP ++, MDR1-) were squamous cell carcinomas. Sixty-one of the 104 NSCLC patients received chemotherapy with MRP-related anti-cancer drugs [vindesine (VDS) and etoposide (VP-16)]. Twenty-three patients (37.7%) with tumour expressing high or moderate levels of MRP showed significantly worse prognoses than those with non- or low-MRP-expressing tumours (P < 0.05). These results suggest that the level of MRP gene expression is related to the histopathology and prognosis of NSCLC.

ATP Binding Cassette Transporter, Subfamily B, Mem↗
PubMed1995

Transient increase of cyclic AMP induced by glutamate in cultured neurons from rat spinal cord.

We demonstrated that glutamate increased the cyclic AMP level in cultured neurons from rat spinal cord. A bath application of glutamate (300 microM) elicited a rapid increase of the cyclic AMP concentration reaching a level three times as high as the basal level in approximately 3 min, and its content then decreased to the control level in 15 min. The increase was not observed in a Ca(2+)-free medium and was inhibited by an antagonist of NMDA receptors or a voltage-sensitive Ca2+ channel blocker. Preincubation with W7 also inhibited the glutamate-evoked cyclic AMP increase. NMDA, aspartate, and high-K+ conditions also induced a cyclic AMP increase; however, a decreasing phase did not follow. The decreasing phase was observed when (2S,1'S,2'S)-2-(carboxycyclopropyl)-glycine, a potent agonist for metabotropic glutamate receptors, was combined with NMDA. These results suggest that the cyclic AMP increase is mediated by a Ca2+ influx via both NMDA receptors and voltage-sensitive Ca2+ channels followed by an activation of the Ca2+/calmodulin system, and the decreasing phase observed in the case of glutamate exposure is due to the activation of the metabotropic glutamate receptors.

Animals↗
PubMed1995

Activation of the nuclear oncogenes N-myc and c-jun in carcinoid [correction of cartinoid] tumors of transgenic mice carrying the human adenovirus type 12 E1 region gene.

The adenovirus (Ad) E1 region genes, E1A and E1B, are well known cooperatively to transform primary rodent cells and activate a number of cellular promoters, including nuclear oncogenes such as N-myc and c-jun, in transfected cell lines. However, there is still less information available on the in vivo mechanism(s) by which the E1 region gene, when chromosomally integrated in the living animals, exerts its effect on nuclear oncogene activation coupled with transformation. To investigate such in vivo activity of E1A we have used a series of microinjection experiments into fertilized eggs to generate three transgenic mice carrying the Ad12-type E1A/E1B genes under the control of the human renin gene. This transgene caused an early onset of bowel cartinoid tumors that express neural cell adhesion molecules, but do not metastasize to any region. Northern blot analysis revealed that the transgenes were considerably expressed in the tumors, but not in other tissues at detectable levels. Interestingly, the levels of N-myc and c-jun mRNAs in the cartinoid tumors were elevated 19- and 8-fold, respectively, as compared with those found in the control intestine. In contrast, the major histocompatibility complex (MHC) class I mRNA level was not altered between the tumor and control intestines, suggesting that this unchanged expression may reflect the loss of tumor metastasis. These findings provide the first in vivo evidence that the expression of the Ad12 E1 region gene induces cartinoid tumors associated with the activation of the nuclear oncogenes N-myc and c-jun.

Adenovirus E1 Proteins↗
PubMed1995

Genetic complementation of the immortal phenotype in group D cell lines by introduction of chromosome 7.

Human immortal cell lines have been classified into at least four (A-D) genetic complementation groups by cell-cell hybrid analysis, i.e., a hybrid derived from different groups becomes mortal. Recently we have demonstrated that introduction of human chromosome 7 suppresses indefinite division potential in the non-tumorigenic human immortalized fibroblast lines KMST-6 and SUSM-1, both assigned to complementation group D. By extending our microcell-mediated chromosome transfer, we found that chromosome 7 also suppresses division potential in the human hepatoma line HepG2 (again, assigned to group D). Chromosome 7 was thus shown to suppress indefinite growth in the above group D cell lines irrespective of their cell types, or whether they are tumorigenic or not. Since chromosome 7 had no such effect on representative cell lines derived from complementation group A, B or C, these results indicate that the senescence gene(s) commonly mutated in the group D cell lines is located on chromosome 7.

Base Sequence↗
PubMed1995

Orally administered bovine lactoferrin inhibits bacterial translocation in mice fed bovine milk.

Feeding of bovine milk to mice induced a high incidence of bacterial translocation from the intestines to the mesenteric lymph nodes, and the bacteria involved were mainly members of the family Enterobacteriaceae. Supplementation of the milk diet with bovine lactoferrin or a pepsin-generated hydrolysate of bovine lactoferrin resulted in significant suppression of bacterial translocation. Our findings suggest that this ability of lactoferrin to inhibit bacterial translocation may be due to its suppression of bacterial overgrowth in the guts of milk-fed mice.

Administration, Oral↗
PubMed1995

Chromosomal localisation of a Y specific growth gene(s).

Although a Y specific growth gene(s) has been postulated in the Yq11 region, the precise location has not been determined. To localise the growth gene(s), we correlated genotype with stature in 13 Japanese and four European non-mosaic adult male patients with a partial Yq deletion. Fourteen patients preserving the region between DYS11 and DYS246 did not have short stature (11 Japanese, 165-180 cm; three Europeans, 165-173 cm) whereas the remaining three patients with the region deleted had short stature (two Japanese, both 159 cm; one European, 157 cm). The results suggest that the region defined by DYS11 at interval 5C and by DYS246 at interval 5D may be the critical region for the Y specific growth gene(s).

Adult↗
PubMed1995

A novel spin probe with long life in vivo for ESR imaging.

A dextran-bonded nitroxide radical (TEMPO-DX) was synthesized to obtain a radical with long life in vivo for ESR imaging. TEMPO-DX was injected intravenously into a rat tail vein and the decrease in ESR intensity in the collected, circulating blood was followed. The result showed that the half life of TEMPO-DX in vivo was 30 min, the longest value reported so far and more than 30 times longer than the corresponding radicals of the six-membered piperidine ring, which means that the bonding of a radical to the polymer greatly prolonged life. The stabilities of TEMPO-DX against the reduction with L-ascorbic acid and the rat liver homogenate were also examined and compared with those of the 3-carbamoyl-2,2,5,5-tetramethylpyrolidin-1-yloxy (CPROXYL) known as a radical stable in vivo. TEMPO-DX was shown not to be as stable as CPROXYL, thus in vivo stability of TEMPO-DX arises from the fact that it is slowly absorbed into the tissues where the radicals are quenched. An ESR image of the mouse head domain was obtained only by an intravenous injection of TEMPO-DX solution into the tail vein.

Animals↗
PubMed1995

Three-dimensional organization of lymphatics in the dog small intestine: a scanning electron microscopic study on corrosion casts.

Casts of the lymphatics of the canine small intestine were made by direct injection of a low viscosity methacrylate resin into a large lymphatic in the submucosal layer, and observed under a scanning electron microscope. The lymphatics started with rod-like central lacteals in the villi of the jejunum and leaf-like ones in those of the ileum. The bases of the lacteals were connected by slender lymphatics forming a three-dimensional network, tentatively called the "superficial lamina propria lymphatic plexus". From this plexus, a few straight branches descended through the lamina propria to drain into a well developed "deep lamina propria lymphatic plexus", which was extended two-dimensionally closely above the lamina muscularis mucosae. From this plexus, a few short lymphatics extended and penetrated the muscularis mucosae and drained into the "superficial submucosal lymphatic plexus", a coarse mesh work of thick lymphatics. From this plexus, a few slender lymphatics descended to drain into a second lymphatic plexus, called the "deep submucosal lymphatic plexus", which extended two-dimensionally on the circular muscle layer. This deep submucosal plexus was a coarse network of thick knotty lymphatics. A large collecting lymphatic was occasionally seen running through the mesh. The tunica muscularis contained tubular lymphatics extending horizontally parallel to the muscle fiber, both circular and longitudinal.

Animals↗
PubMed1995

Ultra-high-resolution scanning electron microscopic studies on the membrane system of the rat parietal cells after tetragastrin stimulation.

The membrane system of the rat parietal cells in the resting state and after stimulation with tetragastrin (gastrin) was examined by ultra-high-resolution scanning electron microscopy after removal of the cytoplasmic matrix by the aldehyde-osmium-DMSO-osmium procedure. The intracellular canaliculus was lined with numerous microvilli. Viewed from the cytoplasmic side, the intracellular canaliculi appeared as an arborized system of cactus-like structures with numerous holes about 100 nm in diameter corresponding to the basal openings of the microvilli. The intracellular canaliculi were more developed after gastrin stimulation than in the resting state. In resting cells, most of the tubulovesicles were isolated, 100-200 nm in diameter, spherical or tubular in shape. After gastrin stimulation, these structures were interconnected by slender tubules of about 30 nm in diameter forming together tubulovesicular network. Stereo SEM views clearly demonstrated that the tubulovesicular network was connected with the intracellular canaliculus by the slender connecting tubulus. The increase in the canalicular membrane area and the depletion of tubulovesicles is explained by the transfer of the tubulovesicular membrane to the intracellular canaliculus. In the resting parietal cell, the microvilli are slender and their interior is packed with microfilaments. After gastrin stimulation, the microvilli are swollen and their interior is edematous. These morphological changes seem to indicate the accumulation of fluid in the microvilli after gastrin stimulation.

Animals↗