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J Tateishi

Publications and source records attributed to J Tateishi.

At least 73 records · Page 4Linked to original sources
PubMed1994

An exon 8-spliced out transcript of neurofibromatosis 2 gene is constitutively expressed in various human tissues.

We succeeded in cloning the exon 8-spliced out transcript of neurofibromatosis 2 (NF2) gene in human glioma cell lines. We then investigated the expression of the spliced out form in various human tissues by PCR analysis followed by Southern blot hybridization and sequencing to evaluate whether it was generated by normal alternative splicing or by a splicing mutation. The analysis revealed the splicing out of exon 8 in the various tissues, and the transcript missing exon 8 should thus be considered as a product of normal alternative splicing. Our results further support the possibility that the NF2 gene expresses multiple alternatively-spliced transcripts variantly in different tissue types.

Base Sequence↗
PubMed1994

Japanese family with Creutzfeldt-Jakob disease with codon 200 point mutation of the prion protein gene.

We report the first Japanese case of familial Creutzfeldt-Jakob disease (CJD) with the heterozygous point mutation at codon 200 of the prion protein gene. This suggests that the mutation is not race-specific. The clinical and pathologic features of this case are not different from those of sporadic CJD without point mutations. Some healthy members of the family also carry the same mutation in the autosomal dominant inheritance expression.

Adolescent↗
PubMed1994

Creutzfeldt-Jakob disease transmitted by a cadaveric dura mater graft.

We report a case of Creutzfeldt-Jakob disease developing in a 31-year-old woman 56 months after she received a cadaveric dura mater graft after the removal of a giant pituitary adenoma. Creutzfeldt-Jakob disease was confirmed by a brain autopsy and the existence of an abnormal isoform of prion protein, verified by both immunohistochemical and Western blot analysis. Moreover, prion protein gene analysis was shown in this case to possess a wild-type genotype. The characteristics of Creutzfeldt-Jakob disease after a cadaveric dura mater graft are reviewed and discussed.

Adenoma↗
PubMed1994

An immunohistochemical study of tissue transglutaminase in gliomas with reference to their cell dying processes.

Tissue transglutaminase is a Ca(2+)-dependent enzyme that catalyzes the formation of protein cross-links by an acyl transfer reaction. Recent reports have suggested that tissue transglutaminase is induced by tumor progression and apoptosis. In this study we immunohistochemically investigated a series of gliomas by using an antiserum against a dodecapeptide from the COOH-terminal of tissue transglutaminase. Among the gliomas the presence of positive immunoreactivity tended to increase in malignant counterparts. It is also noteworthy to mention that glioblastoma cells surrounding the zonal necrosis in a palisade fashion were strongly immunolabeled. The degenerating products in tumor cells, such as round granulated bodies, were primarily immunopositive, whereas Rosenthal fibers were negative. Dying cells through apoptosis in the metastatic brain tumors could be easily recognized by the presence of tissue transglutaminase. In conclusion, tissue transglutaminase may therefore be valuable in the prognostic characterization of gliomas with respect to the detection of dying cells. However, the appearance of tissue transglutaminase-positive neoplastic cells was not limited to apoptotic bodies but could also be detected in necrobiotic cell nests.

Amino Acid Sequence↗
PubMed1993

Immunohistochemical distribution of amyloid precursor protein during normal rat development.

This study focused on the immunohistochemical identification of the beta/A4 amyloid precursor protein (APP) in various developmental stages of both the rat central nervous system (CNS) and the peripheral nervous system (PNS). A comparative study with myelin basic protein (MBP) and synaptophysin (SYP) facilitated the understanding of neuronal maturation and synaptogenesis on both prenatal and postnatal development. Our immunohistochemical study revealed APP to be widely distributed through the nervous system while existing mainly in the cytoplasm, dendrites and axons of the neurons. However, immunoreactivity was also observed in either the ependymal cells or the choroid plexus epithelial cells. Our immunostaining was carried out by the hydrated autoclaving method and revealed the expression of APP at embryonic day 15 in the neuron of the mesencephalic nucleus of the trigeminal nerve and the anterior horn of the spinal cord, trigeminal and spinal ganglion, ependymal cells and the choroid plexus. We thus observed dramatic changes of APP expression in the cerebellum from the embryonic stage. The maturation of synaptogenesis in the cerebellar molecular layer was parallel to the extension of the dendrites of Purkinje cells, which revealed immunoreactivity for APP. These findings suggested that APP played an important role in neuronal maturation and synaptogenesis. Thus, APP is considered to be a useful marker for neuronal development.

Amyloid beta-Protein Precursor↗
PubMed1993

An amber mutation of prion protein in Gerstmann-Sträussler syndrome with mutant PrP plaques.

We found an amber mutation in the open reading frame of the prion protein (PrP) gene. The codon 145 mutation (tyrosine to stop) was recognized on a PrP allele of a patient with Alzheimer-type clinical course. Pathologic examination revealed many amyloid plaques and neurofibrillary changes. However, the amyloid plaques in this patient were not composed of beta/A4 protein, but of PrP. Both wild and mutant PrP alleles were detected in the cerebral mRNA; however, only C-terminal truncated PrP was detected in the kuru plaques. We herein present evidence that only mutant PrP aggregates to make kuru plaques in the central nervous system.

Adult↗
PubMed1993

Novel missense variants of prion protein in Creutzfeldt-Jakob disease or Gerstmann-Sträussler syndrome.

We found 3 novel missense variants in the open reading frame of the prion protein (PrP) gene. The codon 105 point mutation (proline to leucine) was found on a codon 129 (Valine) PrP allele in 4 patients from 3 different Japanese families with Gerstmann-Sträussler syndrome. The codon 180 variant PrP (valine to isoleucine) was found in Creutzfeldt-Jakob disease (CJD) patients with a similar clinical course to that of codon 178 mutation. The codon 232 variant PrP (methionine to arginine) was documented in the CJD patients with typical clinical and pathological findings. These variant PrP molecules were not detected in 200 normal Japanese PrP alleles. PrP has a large repertoire of variant forms, and each primary structure of PrP corresponds to the distinct phenotype of prion diseases.

Base Sequence↗
PubMed1993

A new inherited prion disease (PrP-P105L mutation) showing spastic paraparesis.

We report the clinicopathological findings of 5 patients with an inherited prion disease with a codon 105 (Pro to Leu) mutation. All of the patients had a spastic gait disturbance and progressive dementia without either cerebellar signs, myoclonus, or periodic synchronous discharges. Autopsy of 3 patients revealed numerous amyloid plaques in the cerebral cortex, especially in the motor cortex and the frontal lobe where neuronal loss and severe gliosis were observed in the absence of spongiform changes. The cerebellum was preserved histologically except for only a few amyloid plaques. The pyramidal tracts in the brainstem and spinal cord showed vacuolated changes and a loss of myelin, but no prion protein accumulations. Thus, the prion protein codon 105 mutation is considered to correspond to a new variant of the Gerstmann-Sträussler syndrome with spastic paraparesis.

Adult↗
PubMed1993

Small heat-shock protein is expressed in meningiomas and in granulofilamentous inclusion bodies.

FF cellular expression of estrogen receptor-related small heat-shock protein (HSP27) in meningiomas was investigated immunologically. A cytoplasmic distribution of HSP27 was demonstrated in surgical specimens of 22 of 26 cases with meningiomas and cultured meningioma cells derived from two individuals. By Western blotting, HSP27 was detected in every tissue homogenate of 17 cases studied. Thus, HSP27 appears to be constitutively expressed in most meningiomas. In anaplastic portions of one papillary meningioma, there were numerous granulofilamentous inclusion bodies [Goldman JE et al. (1980) Cancer 46:156-161]. The inclusion bodies were immunopositive for HSP27 despite the negativity of the tumor cytoplasms. Thus, HSP27 seems to participate in the formation of certain inclusion bodies in meningioma cells, like alpha B-crystallin which participates in the formation of Rosenthal fibers in astrocytes.

Adult↗
PubMed1993

Widespread distribution of tau in the astrocytic elements of glial tumors.

Recently tau immunoreactivity has been observed in astrocytes in Alzheimer's disease and other neurological diseases. We examined the immunohistochemical localization of tau in 110 human brain tumors. Tau was widely distributed in the glial neoplastic cells and the reactive astrocytes in tumor tissues. In human surgical specimens positive immunostaining for tau was frequently observed in astrocytic tumors, oligodendroglial tumors, and glioblastoma, as well as neuronal tumors. The astrocytic neoplastic cells in medulloblastoma and other poorly differentiated tumors were also stained. In contrast, no immunoreactivity was observed in meningiomas and schwannomas. The expression of tau in brain tumors was mainly restricted to those cells with astrocytic features rather than small immature cells. The expression of tau mRNA was also demonstrated in astrocytic tumors. In conjunction with the findings of tau-positive astrocytes in some degenerative disorders, astrocytes are considered to have a potential to express tau through neoplastic transformation and reactive processes.

Animals↗
PubMed1993

Alzheimer's amyloid precursor protein mRNA without exon 15 is ubiquitously expressed except in the rat central nervous system.

The expression of L-beta A4 amyloid precursor protein (L-APP) mRNA, which is a splicing product excluding exon 15 of the APP gene, was investigated in various tissues of adult rats by a polymerase chain reaction analysis of reverse-transcribed RNA (RT-PCR). L-APP mRNA was ubiquitously expressed in all the examined tissues including the liver, kidney, heart, skeletal muscle, spleen, thymus, adrenal, stomach, submandibular gland, testis and ovary, except for the central nervous system (CNS) tissues such as the brain and spinal cord. The DNA sequence analysis of the RT-PCR products from adult rat liver showed an L-APP cDNA form, in which exon 14 was spliced from exon 14 to exon 16, and exon 15 of the APP gene was excluded. In addition, regarding as the brain and liver, L-APP mRNA expression was examined during the development of the embryonic stage. In the brain, no L-APP mRNA expression was detected even in the embryonic stage, whereas L-APP mRNA expression of the liver was still found in the embryonic stage. These results suggest that the splicing event excluding exon 15, which is exactly adjacent to exon 16 and exon 17 encoding the beta A4 protein, would probably occur very rarely in the CNS and that the splicing of L-APP might already be regulated in the embryonic stage.

Amyloid beta-Protein Precursor↗
PubMed1993

A missense mutation in the proteolipid protein gene responsible for Pelizaeus-Merzbacher disease in a Japanese family.

We investigated the proteolipid protein (PLP) gene of two boys in a Japanese family with Pelizaeus-Merzbacher disease (PMD), an X-linked neurologic disorder characterized by dysmyelination in the central nervous system (CNS). The patients showed similar clinical signs from birth and autopsy on the elder brother confirmed a connatal type of PMD. Direct sequencing of the PLP gene and PLP mRNAs from the brain of the PMD patient revealed a G to T transition in exon V of the PLP gene, which leads to a glycine to cysteine substitution at residue 220. Allele-specific oligonucleotide hybridization revealed that this mutation was also present in his brother, but was absent in 100 X chromosomes of normal Japanese individuals. Northern blot analysis showed that the mRNA levels of PLP and myelin basic protein, two major myelin proteins produced by oligodendrocytes, were much reduced in the PMD brain, hence, there was a specific loss of oligodendrocytes. It seems likely that the substitution is responsible for PMD (connatal type) in this particular family and causes oligodendrocytes death in the CNS.

Adolescent↗
PubMed1993

Developments in diagnosis for prion diseases.

The protease resistant isoform of prion protein (PrP) is a diagnostic marker of spongiform encephalopathies in humans and animals. Immunoblotting is a sensitive method but requires either fresh or frozen, unfixed materials. Immunohistochemistry using formalin-fixed, paraffin-embedded materials is now also considered to be sensitive and comparable to immunoblotting after various treatments, especially using the hydrolytic autoclaving method on tissue sections before staining. The advantage of this method is that it can be applied to routine pathology materials or long preserved materials. The kuru plaque-type deposition of PrP suggests abnormalities of the PrP gene, while synaptic-type deposition suggests either sporadic CJD or particular familial CJD. PrP gene abnormalities are thus related to PrP deposition and modify clinical symptoms and their progression. A PrP gene analysis can be done using either preclinical, clinical or post-mortem materials.

Genes, Viral↗
PubMed1993

The rat central nervous system expresses Alzheimer's amyloid precursor protein APP695, but not APP677 (L-APP form).

A novel splicing form of beta A4 amyloid precursor protein (APP) lacking exon 15, corresponding to 18 residues, was first reported in leukocytes and then in ubiquitous organs. To determine which APP molecules (APP695, APP751, or APP770) either with (N-APP) or without (L-APP; leukocyte-derived APP) exon 15 were expressed in various organs, we investigated the alternative splicing at exon 15 in the rat brain, kidney, heart, and testis by a PCR analysis of reverse-transcribed RNA and Southern blot analysis. Regarding APP695 without exons 7 and 8, L-APP was either seldom or never expressed in the brain, whereas both N- and L-APP were expressed in other organs. On the other hand, regarding APP751/770 containing exon 7, which codes for the Kunitz-type serine protease inhibitor domain, both N- and L-APP were expressed in all the organs examined, including the brain. These results suggest that a particular alternative regulation system related to exon 15 might be present in only APP695 of the brain and influence the proteolytic processing of APP.

Alzheimer Disease↗
PubMed1993

The effects of synthetic alpha-human atrial natriuretic peptide (alpha-hANP) on the overall baroreflex system in anesthetized mongrel dogs.

The effects of alpha-hANP (0.3 micrograms/kg body weight/min) on the baroreflex system were studied in anesthetized dogs according to three different protocols. In the first protocol, the effects of alpha-hANP on an open-loop gain (G(AP)) of the overall baroreflex system and a gain (GHR) of the baroreflex heart rate control system during quick mild hemorrhage and blood infusion were studied. G(AP) was decreased from 7.6 +/- 0.6 to 2.8 +/- 0.5 by alpha-hANP with hemorrhage. G(AP) decreased 7.4 +/- 0.8 to 2.9 +/- 0.4 by alpha-hANP with blood infusion. G(AP) was restored nearly to the control levels one hour after alpha-hANP administration. GHR did not change by alpha-hANP administration. In the second and third protocol, a site of action of alpha-hANP was analysed. alpha-hANP inhibited the responses of systemic vascular resistance to quick mild hemorrhage and blood infusion, but did not affect the responses of cardiac output to quick mild hemorrhage and blood infusion in the second protocol. After carotid sinus denervation and vagotomy, alpha-hANP inhibited an arterial pressure responses to phenylephrine and nitroglycerin bolus injection in the third protocol. These findings suggest that alpha-hANP has mainly an effect on the peripheral vascular system to decrease its responsiveness, resulting in a decrease in G(AP).

Anesthesia↗
PubMed1993

Accumulation of abnormal prion protein in mice infected with Creutzfeldt-Jakob disease via intraperitoneal route: a sequential study.

We immunohistochemically studied the location of abnormal prion protein in the central nervous system and visceral organs at the clinical and preclinical stages of mice infected with Creutzfeldt-Jakob disease via intraperitoneal route. Abnormal prion protein was diffusely distributed in the central nervous system. The sequential study showed that its stainings were first detected 120 days after inoculation, were found in all mice after 180 days, and were the most intense and widespread after 270 days. There was no restricted involvement at the early stages nor rostrally dominant distribution of the stainings that had been found in mice infected via intracerebral route. Abnormal prion protein was also located in the follicular dendritic cells in the spleen, lymph nodes, intestinal Peyer's patch, and thymus. Its stainings were first detected in the spleen, lymph nodes, and Peyer's patch 14 or 30 days after inoculation. In the thymus, however, the stainings were first detected after 210 days in the germinal centers formed in the medulla.

Animals↗