Search PubMed⌕ Search

Biomedical subjects

K Tashiro

Publications and source records attributed to K Tashiro.

At least 253 records · Page 14Linked to original sources
PubMed1996

Syringomyelia as a cause of body hypertrophy.

BACKGROUND: Among 26 patients with communicating syringomyelia who came to our out-patient clinic from April, 1989, to March, 1995, three (11.5%) had hypertrophy in limbs, hands, or feet. One had crossed hypertrophy. We considered the possibility that syringomyelia caused body hypertrophy. METHODS: We searched MEDLINE for articles which mention body asymmetry or hypertrophy, and examined the findings in our own patients. FINDINGS: The site of hypertrophy in our three patients coincided with the site of the neurological and magnetic resonance imaging findings. In addition, the horizontal and vertical location of the syrinx corresponded with the site of all four hypertrophic limbs. We located ten articles in which a diagnosis of syringomyelia was made, and five in which other diagnoses were made. INTERPRETATION: From studying our patients as well as those previously reported, we speculate that some types of body hypertrophy are due to damage, accompanied by stimulation, of the sympathetic neurons in the ipsilateral lateral horn of the spinal cord. Although there are many causes of hypertrophy, we suggest that the possibility of syringomyelia be investigated in patients with body hypertrophy, especially in those with any accompanying neurological abnormality.

Adult↗
PubMed1996

A 1.6-Mb P1-based physical map of the Down syndrome region on chromosome 21.

The Down syndrome (DS) region on chromosome 21, which is responsible for the main features of DS such as characteristic facial features, a congenital heart defect, and mental retardation, has been defined by molecular analysis of DS patients with partial trisomy 21. The 2. 5-Mb region around the marker D21S55 between D21S17 and ERG in 21q22 is thought to be important, although contributions of other regions cannot be excluded. In this region, we focused on a 1.6-Mb region between a NotI site, LA68 (D21S396, which is mapped distal to D21S17) and ERG, because analysis of a Japanese DS family with partial trisomy 21 revealed that the proximal border of its triplicated region was distal to LA68. We constructed P1 contigs with 46 P1 clones covering more than 95% of the 1.6-Mb region. A high-resolution restriction map using BamHI was also constructed for more detailed analysis. Our P1 contig map supplements other physical maps previously reported and provides useful materials for further analysis including gene isolation and sequencing of the DS region.

Base Sequence↗
PubMed1996

Detection of human T-lymphotropic virus type-I DNA and mRNA in the lymph nodes; using polymerase chain reaction in situ hybridization (PCR/ISH) and reverse transcription (RT-PCR/ISH).

To examine the relationship between human T-lymphotrophic virus type I (HTLV-I) proviral DNA and its expression in the lymph nodes, HTLV-I DNA and tax/rex mRDA were directly amplified by polymerase chain reaction in situ hybridization (PCR/ISH), and reverse transcription (RT)-PCR/ISH [RT-PCR/ISH]. We studied 24 lymph nodes from patients with adult T-cell leukemia/lymphoma (ATLL), incipient ATLL (I-ATLL), and HTLV-I associated lymphadenitis dermatopathic type (HAL-D) and enlarged paracortical type (HAL-EP). In ATLL, 40-60% of the nucleated cells were positive for for HTLV-I proviral DNA by PCR/ISH, while in I-ATLL and HAL, respectively 5-20% and less than 1-5% of cells were positive. The number of mRNA expressing cells was smaller than that of the proviral DNA-positive cells. The mRNA-expressing cells varied in number among the ATLL and I-ATLL cases, while they were only rarely observed in HAL-D and HAL-EP. These results show that HTLV-I infection and activation might increase with malignant transformation of the target T helper cells.

Adult↗
PubMed1996

Complementary DNA cloning and sequencing of rat enteropeptidase and tissue distribution of its mRNA.

A cDNA clone encoding enteropeptidase (EC 3.4.21.9), a key enzyme for the conversion of trypsinogen to trypsin, was isolated from a rat duodenal mucosa cDNA library. Sequences of the 3585 base pair clone predicted that enteropeptidase is synthesized as a single-chain precursor form, proenteropeptidase, consisting of 1058 amino acid residues with an internal signal sequence (51 residues) and is then processed into the mature enzyme consisting of three different peptide chains, i.e., mini, light and heavy chains, not the previously reported two-chain enzyme. The structure of enteropeptidase is relatively conserved among different species and the rat enteropeptidase is 24 and 39 amino acids longer than the porcine and human ones, respectively. Northern blot analysis of rNAs from normal rat tissues revealed that the enteropeptidase mRNA of around 4.4 kb in size was expressed only in the duodenal mucosa, and high proteolytic activity of the enzyme was detected in the proximal small intestine. Additional analysis of the RNAs by RT-PCR revealed that a low level of the mRNA was also expressed in the other parts of the small intestine, i.e., jejunum and ileum. These results indicate that the biosynthesis of enteropeptidase takes place mainly in the proximal small intestine, the duodenum, and the importance of the region in the physiology of intestinal protein digestion regulated by the enzyme is suggested. Furthermore a faint signal of the mRNA was also detected in the stomach, colon and brain in which the existence of trypsin-like serine proteases were reported. The significance of the low level expression of the gene is unclear, but the potential peptide-processing function of the enzyme in these tissues is also suggested.

Amino Acid Sequence↗
PubMed1996

Random suppression of T cells that bear specific T cell receptor V beta sequences in adult T cell leukemia/lymphoma (ATLL) patients at each clinical stage: carrier, smoldering, chronic, and acute.

Human T cell leukemia virus type I (HTLV-I) is associated with adult T cell leukemia/lymphoma (ATLL), which is well known as a T cell malignancy. In order to clarify whether HTLV-I plays a role as a virus-encoded superantigen in the neoplastic process, we examined the TCR V beta families in the peripheral blood at four different clinical stages: carrier, smoldering leukemia, chronic leukemia, and acute leukemia. An increased number of CD4 T cells was found in each of the four clinical stages. However, we found neither uniform specific losses nor uniform clonal expansion of particular TCR V beta gene families in any case from the four clinical stages. However, a suppression of the random TCR V beta families was found. Our data did not therefore directly suggest the existence of a common superantigen model of HTLV-I which induces an increase in CD4 T cells. The random suppression in the TCR V beta repertoire is most likely caused by the influence of HTLV-I neoplastic pathogenesis rather than by virus-encoded superantigens. In the patients with acute leukemia, one or two families of the V beta repertoires were very strongly expressed, while in chronic leukemia, no such repertoire of strong expression was observed. The immunological reaction of the hosts might thus be different between the above described groups.

Acute Disease↗
PubMed1996

Classical Hodgkin and Reed-Sternberg cells demonstrate a non-clonal immature B lymphoid lineage: evidence from a single cell assay and in situ hybridization.

Hodgkin and Reed-Sternberg (H & RS) cells are generally considered to be the neoplastic cells of Hodgkin's disease (HD), however such cells are only found in a minority of the lesions. Recently in a few studies on HD, the clonality of H & RS cells was examined, using a single-cell polymerase chain reaction (PCR) examination. To clarify the lineage and clonality of H & RS cells, we performed single cell PCR and in situ hybridization (ISH), and nine cases of classical HD were thus studied. By ISH, the immunoglobulin J chain, and the kappa and lambda light chain were rarely expressed in the H & RS cells, however, no T-cell markers could be detected. The expression of the recombination activating genes (RAG-1, 2) could be determined in the H & RS cells. We isolated CD30+ H & RS cells, CD3 + T cells and CD20 + B cells from suspended materials using a mechanical sorter. We performed single cell PCR in a sorted individual cell, to amplify the complementarity determining region of the Ig heavy chain (IgH) gene and T-cell receptor gamma chain (TCR gamma) gene. In all cases, TCR gamma could be frequently amplified in the T cells, but was only rarely amplified in the H & RS and B cells. In contrast, the IgH was frequently amplified in the H & RS and B cells, but not in the T cells. In addition, the PCR production of the H & RS cells all showed different lengths. The results therefore support the polyclonal nature and immature B lymphoid cell origin of H & RS cells.

B-Lymphocyte Subsets↗
PubMed1996

Clinical trial of piracetam in patients with myoclonus: nationwide multiinstitution study in Japan. The Myoclonus/Piracetam Study Group.

Sixty patients with disabling myoclonus excluding mainly spinal myoclonus were treated by piracetam as an open-labeled study, and myoclonus score, neurological symptoms, functional disability, and intensity of myoclonus were scored before and after treatment, including a blinded video inspection. Electrophysiological correlation also was investigated before and after treatment. Piracetam was effective in myoclonus, especially that of cortical origin, in both monotherapy and polytherapy. Piracetam also had positive benefits on gait ataxia and convulsions but not on dysarthria, and feeding and hand writing improved much more significantly. Psychologically significant improvement was seen in decreased motivation, sleep disturbance, attention deficit, and depression, all of which might be possibly secondary benefits associated with improvement of myoclonus. There was no positive correlation between clinical and electrophysiological improvement. Tolerance was good, and side effects were transient. However, hematological abnormalities observed in at least two patients in the present study should be kept in mind when relatively large doses of piracetam are administered, especially in combination with other antimyoclonic drugs.

Administration, Oral↗
PubMed1996

Cloning and expression studies of cDNA for a novel Xenopus cadherin (XmN-cadherin), expressed maternally and later neural-specifically in embryogenesis.

From a Xenopus tailbud cDNA library, we obtained the cDNA for a novel cadherin which was named as XmN-cadherin (Xenopus maternally expressed neural cadherin). The cDNA consisted of 3690 bp and encoded 922 amino acid residues. XmN-cadherin preserved five extracellular cadherin motifs, a single transmembrane domain, and a cytoplasmic domain, and was closely related by its sequence to R- and N-cadherin. In the adult frog, XmN-cadherin mRNA was detected strongly in ovary, testis, brain, eye, and kidney, and weakly in stomach, and intestine. In the egg, the mRNA occurred as a maternal mRNA at a relatively high level, and its level became very low by the neurula stage, then increased steadily thereafter. Dissection experiments with 8-cell stage and neurula stage embryos revealed that the maternally inherited mRNA was relatively uniformly distributed within the embryo. By a sharp contrast, whole mount in situ hybridization revealed that the zygotically expressed mRNA occurred almost exclusively in neural tissues such as brain, the anterior part of spinal cord, and the optic and otic vesicles. Thus, XmN-cadherin appears to have at least triple functions; it probably contributes in early embryos to cell-type non-specific cell adhesion, but in post-neurula embryos may be responsible for the development and/or maintenance of anterior neural tissues, and may be used in adult frog for the development and/or maintenance of neural, endodermal and reproductive organs.

Amino Acid Sequence↗
PubMed1996

Central phenotype and related varieties of spinocerebellar ataxia 2 (SCA2): a clinical and genetic study with a pedigree in the Japanese.

The gene for SCA2 has been mapped to chromosome 12q23-q24.1, but the mutant gene remained to be identified. When studying a Japanese family with SCA2, we noted that clinical features and disability varied among patients, with the central feature being progressive ataxia-slow eye movement-hyporeflexia syndrome. Additional symptoms were parkinsonism with minor cerebellar deficits, and severe ataxia with choreoathetosis. Our experience plus related literature documentation indicates that choreoathetosis is not so rare at the advanced stage of the disease, with onset at an early age, and that the variety of SCA2 phenotype depends on age at onset and duration of the disorder.

Adult↗
PubMed1996

Identification of the spinocerebellar ataxia type 2 gene using a direct identification of repeat expansion and cloning technique, DIRECT.

Spinocerebellar ataxia type 2 (SCA2) is an autosomal dominant, neurodegenerative disorder that affects the cerebellum and other areas of the central nervous system. We have devised a novel strategy, the direct identification of repeat expansion and cloning technique (DIRECT), which allows selective detection of expanded CAG repeats and cloning of the genes involved. By applying DIRECT, we identified an expanded CAG repeat of the gene for SCA2. CAG repeats of normal alleles range in size from 15 to 24 repeat units, while those of SCA2 chromosomes are expanded to 35 to 59 repeat units. The SCA2 cDNA is predicted to code for 1,313 amino acids-with the CAG repeats coding for a polyglutamine tract. DIRECT is a robust strategy for identification of pathologically expanded trinucleotide repeats and will dramatically accelerate the search for causative genes of neuropsychiatric diseases caused by trinucleotide repeat expansions.

Amino Acid Sequence↗
PubMed1996

Umbilical vein endothelial cells are an important source of c-kit and stem cell factor which regulate the proliferation of haemopoietic progenitor cells.

The expression and production of c-kit and its ligand, stem cell factor (SCF), in cord blood and neonates were studied. Serum SCF levels were significantly higher in cord blood, neonates aged 1-30 d, and in 4-month-old infants than in the maternal serum (P < 0.01). SCF levels decreased in children from 7 months to 15 years of age (P < 0.01). The serum soluble c-kit levels were significantly higher in cord (P < 0.01) and neonatal blood (P < 0.05) than in the maternal blood. SCF and c-kit levels in placental tissue homogenates and the culture media of decidual cells and trophoblasts were low. To determine the sites of high SCF and c-kit production in cord blood and in early neonates. SCF and c-kit mRNA expression was analysed in various tissues by polymerase chain reaction. High SCF mRNA expression was observed in human umbilical vein endothelial cells (HUVEC). Moderate c-kit mRNA expression was detected in HUVEC, the bone marrow, and cord blood. These findings suggest that endothelial cells mainly produce the SCF in cord blood and in early neonates. To confirm the role of endothelial cells in haemopoiesis, colony-forming assays were performed in the presence of HUVEC culture media, which induced the formation of high numbers of granulocyte and erythroid colonies in cord blood. IL-3, IL-6 and SCF levels were elevated in the media. Our findings suggest that endothelial cells have an important role in the maintenance and proliferation of progenitor cells in neonatal blood via the interaction of c-kit and SCF with other factors. The ex vivo expansion of cord progenitor cells in the presence of endothelial cells needs to be investigated further.

ADP-ribosyl Cyclase↗
PubMed1996

Nodular lymphoid hyperplasia in the lung.

We describe an immunocompetent adult patient presenting with cough and hemoptysis who was found to have a pulmonary mass localized to the right upper lobe. Lobectomy was performed and pathological examination revealed nodular lymphoid hyperplasia (pseudolymphoma) of the bronchus-associated lymphoid tissue.

Aged↗
PubMed1996

Aerosolized and instilled surfactant therapies for acute lung injury caused by intratracheal endotoxin in rats.

OBJECTIVE: To compare the effects of surfactant replacement by aerosol inhalation and bolus instillation on acute lung injury caused by the intratracheal injection of endotoxin in rats. DESIGN: Prospective, randomized study. SETTING: University Laboratory. SUBJECTS: Male Wistar rats weighing 368 +/- 31 (SD) g. INTERVENTIONS: Escherichia coli endotoxin (57 +/- 20 mg/kg) was injected into the tracheas of 36 anesthetized and mechanically ventilated rats (FIO of 1.0). When the PaO2 had decreased to <200 torr (<26.7 kPa), the rats were randomly assigned to one of three groups: a control group (n=12)given no material; a bolus group (n=12) given a modified natural surfactant suspension (100 mg/kg in 2.0 mL/kg saline) by bolus instillation into the trachea; and an aerosol group (n=12) given surfactant aerosolized with an ultra-sonic nebulizer for 60 mins. MEASUREMENTS AND MAIN RESULTS: Bolus instillation transiently decreased the mean blood pressure by approximately 30%. However, aerosol inhalation did not. The PaO2 values of the control group remained <90 torr (<12.0 kPa) until the end of the experiment (180 mins). In contrast, the PaO2 of the bolus group increased to 387 +/- 134 torr (51.6 +/- 17.9 kPa; p<.05 vs. other groups) 15 mins after surfactant replacement, and remained at approximately 400 torr (approximately 53.3 kPa) throughout the experiment. The PaO2 values of the aerosol group increased slowly, peaked at 240 +/- 109 torr (32.0 +/- 14.5 kPa; p<.05 vs. the control group) 60 mins after the start of surfactant replacement, and remained at approximately 200 torr (approximately 26.7 kPa). CONCLUSIONS: Bolus instillation was superior to aerosol inhalation concerning maximum efficacy, the rapid onset of therapeutic effects, and the necessary dose of surfactant. However, aerosol that does not cause hypotension may be of use in the treatment of adult respiratory distress syndrome in patients with circulatory instability.

Aerosols↗
PubMed1996

Serum carnitine and disabling fatigue in multiple sclerosis.

The serum concentrations of total, free and acylcarnitine were compared in 25 patients with multiple sclerosis (MS) and among age- and sex-matched normal controls by the new enzymatic cycling method in order to clarify whether the fatigue in MS might be due to possible carnitine-related fatty acid metabolic abnormalities in the mitochondria of skeletal muscles. Patients with MS were divided into those with and those without excessive fatigue. Levels of total and free carnitine were not significantly different between MS patients and normal controls. Levels of acylcarnitine, whose decrease in chronic fatigue syndrome has been reported, were also similar between MS patients and normal controls. There was no difference in these carnitine levels between MS patients with and without excessive fatigue. We argue that acylcarnitine deficiency and fatty acid metabolic dysfunction in mitochondria are not relevant to the excessive fatigue in patients with MS, and further explanatory investigations are to be sought.

Adult↗
PubMed1996

Immunohistochemical study of hepatic angiomyolipoma.

An immunohistochemical study was performed on nine hepatic angiomyolipomas (AML) found in eight patients. Histologically, the tumors were fundamentally composed of the three heterogeneous tissue components of blood vessels, smooth muscle cells (SMC), and fat cells, although the proportions and distributions were quite variable from tumor to tumor and from area to area in the same tumor. Additionally, cellular pleomorphism and atypia with occasional bizarre giant cells were found in the SMC component. This histologic feature might lead to a mistaken diagnosis of malignant neoplasm, and pathologists should therefore be aware of the broad histologic spectrum of hepatic AML. However, the immunostaining patterns were basically the same in all nine tumors. All tumor components were negative for epithelial membrane antigen (EMA) and for cytokeratin. The spindle-shaped SMC component of the tumor was occasionally positive for vimentin, desmin and alpha-smooth muscle actin, whereas epithelioid SMC were negative for all three. Both the epithelioid and spindle-shaped SMC were occasionally positive for S-100 and neuron-specific enolase. All types of SMC in the tumor, whether spindle, epithelioid, intermediate or pleomorphic SMC, were strongly positive for HMB-45, a melanoma-specific monoclonal antibody. Fat cells were occasionally positive for S-100. Endothelial cells were positive for factor VIII-associated antigen. Among hepatic tumors HMB-45 reactivity is, so far as we know, found exclusively in the SMC of AML, and the HMB-45 reactivity of a hepatic tumor is thus clearly an important piece of information in the diagnosis of AML.

Adult↗
PubMed1996

Clinical features and natural history of spinocerebellar ataxia type 1.

SCA1 is a dominant spinocerebellar ataxia (SCA) and a multi-systemic syndrome caused by abnormal expansion of unstable CAG repeat in a novel gene located on chromosome 6p22-p23. We clinically studied 35 Japanese SCA1 patients who were assumed to have come from a common origin. The age at onset ranged from 15-63 years, and significantly correlated with CAG repeat units of mutant alleles. Ataxia was the initial symptom, and the majority of patients had a similar history of signs and symptoms. Nystagmus was at first minimal, later attenuated, and a slow saccade followed. Limb tendon reflexes were mostly hyperactive and depressed with the development of diffuse amyotrophy. The cardinal feature was ataxia-hyperreflexia-late slow saccade syndrome with terminal amyotrophy. Although the phenotype of SCA1 overlaps with those of other dominant SCAs, some facets of the neurological events differ from either SCA2 with ataxia-hyporeflexia-slow saccade syndrome, or early-onset Machado-Joseph disease with dystonia-bradykinesia-spasticity syndrome.

Adolescent↗