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A Takeda

Publications and source records attributed to A Takeda.

At least 19 recordsLinked to original sources
PubMed1998

Evaluation of portal pressure by splenic perfusion measurement using dynamic CT.

OBJECTIVE: The purposes of this study were to determine if splenic perfusion measurements obtained using dynamic CT are useful in the evaluation of portal hypertension. MATERIALS AND METHODS: Forty-four patients with chronic liver disease (29 men and 15 women, 49-81 years old) and 38 control subjects (17 men and 21 women, 21-79 years old) underwent dynamic CT of the spleen. Regions of interest were drawn on images of the spleen and aorta, and splenic perfusion was calculated by dividing the peak gradient of the splenic time-attenuation curve by the peak aortic CT measurement increase. In 11 patients with chronic liver disease and three patients with normal livers, we measured the wedged hepatic vein pressure (WHVP) of the right or right accessory hepatic vein to estimate portal vein pressure. RESULTS: Splenic perfusion was less in patients with chronic liver disease (0.894 +/- 0.324 ml/min) than in the control group (1.299 +/- 0.429 ml/min; p < .0001). We found a significant negative correlation between splenic perfusion and WHVP (r = .741; p = .0024). CONCLUSION: A significant decrease in splenic perfusion in patients with chronic liver disease negatively correlated with WHVP. Measurement of splenic perfusion may be useful in the evaluation of portal hypertension.

Aged↗
PubMed1997

Universal skew of T cell receptor (TCR) V beta usage for Crohn's disease (CrD).

It would be of clear interest and importance to identify T cell populations which correlate with the initiation of some T cell-mediated diseases; however, it is difficult to observe the initial response of T cells in these diseases because of modification due to immunosuppressive treatment. We investigated T cell receptor (TCR) V beta usage in both affected and unaffected mucosa from 16 patients with active Crohn's disease (CrD), undergoing nutritional therapy without any immunomodulatory medications. Semiquantitative reverse transcriptase-polymerase chain reaction showed increased expression of V beta 12 and 13 in the entire mucosa of CrD but not in the controls. This was confirmed by introducing a random cloning method. Such skewing was observed primarily in CD4+ lamina propria lymphocytes. DNA sequence analysis demonstrated a striking clonal expansion of V beta 12 T cells, but the dominant clones were not identical in the patients. These findings suggest the importance of superantigen as well as specific T cell response in the pathogenesis of CrD.

Adult↗
PubMed1997

Tau immunoreactivity in glial cytoplasmic inclusions in multiple system atrophy.

In order to clarify the manner and significance of tau expression in glial cytoplasmic inclusions (GCIs), ubiquitinated oligodendroglial abnormal structures in multiple system atrophy (MSA), an immunohistochemical study was carried out in the lesions of the pontine nuclei of 10 cases of MSA using antibodies against various epitope locations of tau protein. As a result, tau-2 was constantly but weakly positive in ubiquitinated GCIs in each case (from 28.6 to 66.7%). However, tau-2-immunoreactivity in GCIs was not correlated to the density of ubiquitin-positive GCIs or preserved pontine neurons. Antibodies against tau proteins of N-terminal or C-terminal failed to label GCIs, although a few number of GCIs were occasionally positive for tau-1 after dephosphorylation. In comparison with the knowledge on tau-immunoreactivity of coiled bodies (CBs) in oligodendroglia in progressive supranuclear palsy (PSP) or corticobasal degeneration, GCIs are quite different from CBs which have a wide range of epitope location of tau proteins, including N-terminal and C-terminal. This study suggests that expression of tau proteins in GCIs is not related to the essential neurodegenerative process in MSA but induced by non-specific stress in oligodendroglia, unlike CB in various 'tau diseases' such as PSP.

Aged↗
PubMed1997

Change of zinc distribution in rat brain with increasing age.

Zinc (Zn) accumulation in the brain of rats of various ages was studied to look into the significance of Zn for the development and function of the brain. The Zn concentration of the cerebral hemisphere was relatively low in 1- to 11-day-old rats. The Zn concentration of the cerebellum gradually increased after birth and reached nearly a plateau at 11 days old. At 48 weeks old, the Zn concentrations of the cerebral cortex and hippocampus formation were approximately twice that of the cerebral hemisphere at the early stage after birth and significantly higher than that of the cerebellum. When 65ZnCl2 was injected into two groups of rats at 5 days and 48 weeks old for comparison, 65Zn distribution in the brain of the former group was higher than that of the latter. In the neonatal rats, the highest concentration of 65Zn was found in the cerebellum, followed by the hippocampus formation, a Zn-containing neuron-rich region. In the adult rats, the highest concentration of 65Zn was found in the CA3 and dentate gyrus of the hippocampus formation. At 48 weeks, 65Zn distribution in the cerebellum was relatively low and at about the same level as in the cerebral cortex. These results suggest that Zn is highly demanded by the cerebellum, which develops rapidly after birth. The increase in Zn concentration with increasing age may reflect the Zn requirement for functioning as an neuromodulator as well as for brain development.

Aging↗
PubMed1997

Zinc distribution in the brain of Nagase analbuminemic rat and enlargement of the ventricular system.

65ZnCl2 was intravenously injected into Nagase analbuminemic rats (NAR), which have a genetical mutation affecting albumin mRNA processing and lack serum albumin, to test the hypothesis that albumin is necessary for zinc (Zn) transport into the brain. One hour after injection, 65Zn was largely concentrated in the choroid plexus of NAR as well as normal parental Sprague-Dawley rats (SDR). Six days after injection, in both groups, the 65Zn concentration in the choroid plexus decreased, with increases in other brain regions. The finding that there was no significant difference in brain distribution of 65Zn between NAR and SDR suggests that Zn transport into the brain and its distribution through the blood-cerebrospinal fluid barrier as well as the blood-brain barrier are not dependent on serum albumin. A most interesting observation was that the cerebral ventricles were considerably enlarged in NAR.

Animals↗
PubMed1997

Immunohistochemical localization of advanced glycation end products, pentosidine, and carboxymethyllysine in lipofuscin pigments of Alzheimer's disease and aged neurons.

Lipofuscins are intracellular fluorescent pigments accumulating in the central nervous system (CNS) with aging and degenerative processes such as Alzheimer's disease (AD). Although they are thought to be lipid peroxidation products derived from malondialdehyde, their biogenesis remains controversial. We further characterize the chemical nature of lipofuscins in brain tissues from AD patients and normal aged subjects. Advanced glycation end products (AGEs), pentosidine and carboxymethyllysine (CML), were identified by appropriate specific antibodies. They have physicochemical properties similar to those of lipofuscin and also increase with aging. Pentosidine and CML were identified in the neuronal perikarya and the extraneuroperikaryal deposits of both the AD and aged brain. Pentosidine, but not CML, was present in the fiber-like structure within the neuropil and the core of classical senile plaque. In the brain of young subjects without CNS disease, pentosidine and CML staining was faint. Pentosidine and CML co-localized with lipofuscin pigments in the neuronal perikarya of both the AD and aged brain. We demonstrate for the first time that lipofuscin is constituted not only of lipid peroxidation products but also from glycation products which may be the origin of fluorescent pigments. Lipofuscins should thus be considered as fluorescent pigments generated by lipid- and sugar-derived Schiff base-protein polymers.

Adolescent↗
PubMed1997

Tumor cell growth is inhibited by suppressing metallothionein-I synthesis.

The effect of metallothionein (MT)-I antisense oligodeoxynucleotide (ODN) on the growth of three kinds of tumor cells was studied, since MTs may be involved in cell growth. When MT-I antisense ODN was added to leukemia P388 cells, cell growth was inhibited in a manner dependent on the dose and incubation time. MT-I antisense ODN was also inhibitory for other tumor cell lines, i.e. Ehrlich carcinoma and sarcoma 180. A significant decrease in the level of MT, but not of Zn, was observed in MT-I antisense ODN-treated cells. On the other hand, control ODN did not inhibit the cell growth appreciably. These results indicate that MT-I expression may be necessary for the growth and survival of these tumor cells.

Animals↗
PubMed1997

Neuronal inclusions in the dentate fascia in patients with multiple system atrophy.

Ubiquitin-immunoreactive neuronal inclusions in the granular cells in the dentate fascia (UNIDs) of patients with multiple system atrophy (MSA) were examined for immunohistochemical and ultrastructural characterization especially in comparison with those which were recently reported for amyotrophic lateral sclerosis with dementia (ALS-D). Eight of 23 MSA patients had UNIDs which were also identified by Gallyas-Braak impregnation but immunonegative for other antibodies including against tau, neurofilaments, and alphaB crystallin. Ultrastructurally, loosely aggregated fibrils without limiting membrane located around the nucleus, which was confirmed by the results of ubiquitin-immunoelectron microscopy. The formation of UNIDs in MSA and ALS-D was suggested to be caused by different types of degeneration because UNIDs in MSA differ from these in ALS-D in terms of their stainability by Gallyas-Braak impregnation and ultrastructurally. In this study hippocampal involvement in MSA differing from ALS-D was clarified.

Aged↗
PubMed1997

Zinc transport in the rat olfactory system.

To study zinc (Zn) mobility in the rat olfactory tract, brain distribution of 65Zn after injection into the olfactory bulb or amygdaloid nuclei was analyzed by autoradiography. Twenty-four hours after 65Zn injection into the olfactory bulb, 65Zn was distributed in the ipsilateral piriform cortex, amygdaloid nuclei and the anterior commissure. Moreover, in the case of injection of a higher level of 65Zn into the olfactory bulb, 65Zn was distributed in the ipsilateral entorhinal cortex in addition to the above regions. Twenty-four hours after 65Zn injection into the amygdaloid nuclei, 65Zn was distributed in the ipsilateral piriform and entorhinal cortex. These results suggest that Zn is intraneuronally transported along the olfactory tract. Zn may be taken up by the piriform neurons after release from the secondary olfactory neuron terminals and transported to the entorhinal area.

Amygdala↗
PubMed1997

CD45-associated protein is a lymphocyte-specific membrane protein expressed in two distinct forms.

CD45-AP is a recently identified CD45-associated protein. The two proteins interact specifically through their respective transmembrane segments. Northern hybridization analysis of CD45+ T lymphocytes and their CD45- variants demonstrated that the production of CD45-AP and CD45 mRNA is regulated independently. On the other hand, Western blotting analysis indicated that the CD45-AP protein has a shorter half-life in the absence of CD45 in three out of four variants. Similar analysis of various types of leukocytes demonstrated that CD45-AP is expressed in T, B, and pre-B cells, but not in plasma cells or cells of the monocyte/macrophage lineage. Two forms of CD45-AP mRNA exist in all types of CD45-AP-expressing lymphocytes analyzed. One form corresponds to the previously reported CD45-AP cDNA and the other form encodes an additional 12 amino acids at the N terminus. The two CD45-AP proteins are identical in their capacity for specific binding to CD45, but employ different mechanisms for endoplasmic reticulum membrane translocation.

Amino Acid Sequence↗
PubMed1997

Preferential binding with Escherichia coli hsp60 of antibodies prevalent in sera from patients with rheumatoid arthritis.

One hundred thirty-two patients with various connective tissue disorders, including 60 with rheumatoid arthritis (RA), had antibodies against human as well as Escherichia coli hsp60 in titers significantly higher than those of normal controls. There was a correlation between titers of antibody to human hsp60 and those to E. coli hsp60. Levels of antibodies against human and E. coli hsp60 were lower in joint fluids than in sera, indicating little production of antibodies in the joint. Antibodies affinity-purified with E. coli hsp60 bound strongly with the homologous hsp60, but weakly with human hsp60. However, antibodies affinity-purified with human hsp60 bound comparably with both E. coli hsp60 and human hsp60. Antibodies affinity-purified with Mycobacterium tuberculosis hsp65 bound to human hsp60 with a reactivity similar to the reactivity of those affinity-purified with human hsp60. The reactivity to the three hsp60 species was lost when sera were absorbed with E. coli hsp60, while the reactivity to E. coli hsp60 remained after extensive absorption with M. tuberculosis hsp65 or human hsp60. These results indicate that anti-hsp60 antibodies in patients with RA and other connective tissue disorders are raised by infection with intestinal microorganisms such as E. coli. They may represent another example of autoimmune responses triggered by antigenic mimicry of host proteins to microbes and suggest that the reactivity of antibodies from RA patients with M. tuberculosis hsp65 might have been a cross-reaction with the E. coli homologue.

Antibodies↗
PubMed1997

Different pathophysiology of cardiac hypertrophy in hypertension and hypertrophic cardiomyopathy.

In order to investigate differences in the pathophysiology of cardiac hypertrophy between patients with arterial hypertension and hypertrophic cardiomyopathy, DNA synthesis by cardiac myocytes and the effects of an angiotensin-converting enzyme inhibitor were examined in these two groups of patients. DNA synthesis and the cell cycle were investigated by flow cytometry using autopsy materials from patients with hypertension and hypertrophic cardiomyopathy. The hypertension group (n=10) included four men and six women aged 61+/-10 years (heart weight: 470+/-79 g, mean+/-s.d.); the cardiomyopathic group (n=10) included eight men and two women aged 61+/-23 years (heart weight: 615+/-211 g). The percentage of cells in G2M phase of the cell cycle was significantly decreased in the myocardium from patients with hypertrophic cardiomyopathy compared with that from hypertensive patients (cardiomyopathy v hypertension: 1.1+/-0.6 v 7.7+/-2.6%, mean+/-s.d.). Captopril, an angiotensin-converting enzyme inhibitor, was administered for 12 months to patients with hypertension (n=20) and hypertrophic cardiomyopathy (n=15). Regression of cardiac hypertrophy was assessed by echocardiography. Long-term administration of captopril achieved regression of cardiac hypertrophy in the hypertensive patients, but not in the patients with hypertrophic cardiomyopathy. In the hypertensive patients, the left ventricular mass was 234+/-9 g before treatment and 198+/-26 g after treatment (mean+/-s.d., P<0. 01). In cardiomyopathic patients, on the other hand, there was no significant difference of left ventricular mass after treatment (before v after, 305+/-85 v 285+/-90 g, mean+/-s.d.). These results suggest that the mechanism of cardiac hypertrophy differs between patients with hypertension and hypertrophic cardiomyopathy.

Aged↗
PubMed1997

Microsatellite polymorphism in the human heme oxygenase-1 gene promoter and its application in association studies with Alzheimer and Parkinson disease.

Oxidative stress has been suggested to be involved in the pathogenesis of neurodegenerative diseases, such as Alzheimer disease (AD) and Parkinson disease (PD). Heme oxygenase-1 (HO-1), a key enzyme in heme catabolism, also functions as an antioxidant enzyme. Here, we show that a (GT)n repeat in the human HO-1 gene promoter region is highly polymorphic, although no particular alleles are associated with AD or PD. This newly identified genetic marker should allow us to study the possible involvement of HO-1 in certain human diseases.

Adult↗
PubMed1997

Abnormal cyanide metabolism in uraemic patients.

BACKGROUND: We previously investigated the factors involved in uraemic neuropathy in patients undergoing regular haemodialysis and found a significant relationship between the severity of vibration sensation impairment and the patients' smoking habits. The administration of methylcobalamin markedly improved the severity of uraemic neuropathy in terms of vibration perception thresholds. We presumed that abnormal cyanide metabolism is involved in the development of uraemic neuropathy. METHODS: Serum levels of thiocyanate (SCN-), the detoxication product of cyanide, were determined in 12 patients with preterminal chronic renal failure (PCRF), 30 patients undergoing regular haemodialysis (HD patients), and 13 healthy volunteers as a control group. Nine of the 30 HD patients were smokers. In addition, in 10 HD patients without smoking habits and 10 non-smoking healthy volunteers, the proportion of each vitamin B12 analogue in total vitamin B12 was estimated. RESULTS: The mean serum SCN- level of the 12 PCRF patients (5.1 +/- 1.5 micrograms/ml) was significantly higher than that of the control (2.8 +/- 0.9 micrograms/ml) (P < 0.01). The mean SCN- level before haemodialysis in the 21 non-smoking HD patients was identical to that in the PCRF group, whereas the level in the nine smoking HD patients (7.2 +/- 1.8 micrograms/ml) significantly higher than that in the non-smoking subgroup (P < 0.01). In 16 HD patients with methylcobalamin treatment, serum SCN- levels were lower than in those without methylcobalamin treatment (4.5 +/- 0.5 micrograms/ml in non-smoking subgroup, P < 0.05). And in the methylcobalamin-treated subgroup (n = 5), the proportion of each vitamin B12 analogue in total vitamin B12 was normal. In the untreated subgroup (n = 5), the proportion of cyanocobalamin fraction (10.5 +/- 2.6%) was as high as the level in Leber's disease patients, while the proportion of methylcobalamin fraction was low. And the serum cyanocobalamin level was higher in the treated subgroup. CONCLUSION: In uraemic patients, cyanide detoxication capability is impaired because of a reduced SCN- clearance, and increased cyanocobalamin synthesis indicates elevation of cyanide pool, which would be related to the development of uraemic neuropathy. Methylcobalamin was considered to be utilized in cyanide detoxication process via cyanocobalamin synthesis.

Adult↗
PubMed1997

Central facial weakness due to medial medullary infarction: the course of facial corticobulbar fibres.

Two patients are reported with contralateral hemiparesis including a face of supranuclear type, caused by an infarct of the unilateral ventromedial part of the upper medulla. Data from these patients support the hypothesis that part of the corticobulbar fibres supplying the lower facial muscles descend ipsilaterally in the ventromedial part of the upper medulla and then, after decussation, ascend rostrally to the contralateral facial nucleus.

Adult↗
PubMed1997

Hydrometrocolpos with ectopic vaginal opening to the bladder. A case report.

A case of hydrometrocolpos with vaginal opening to the bladder is presented. A newborn female presented abdominal distention and postaxial polydactyly at birth. Clinical investigation revealed hydrometrocolpos, precocious puberty, urogenital sinus and other multiple malformations. The vagina was open to the bladder with a small orifice. Vaginal pull-through surgery and closure of the communication was performed. Over a hundred cases of hydrometrocolpos have been reported previously. However, we could not find a case of hydrometrocolpos with vaginal opening to the bladder among them.

Female↗
PubMed1997

Association of interleukin 6 release from endothelial cells and pulmonary hypertension in SLE.

OBJECTIVE: To investigate how sera from 37 patients with systemic lupus erythematosus (SLE) stimulate interleukin (IL) 6 release from IL-1beta pretreated endothelial cells and compare these effects to those of sera from 16 normal controls. METHODS: Endothelial cells pretreated 18 h with IL-1beta (5 U/ml) were incubated 2 h with sera diluted 10-fold with phosphate buffered saline (PBS). IL-6 concentrations in endothelial culture supernatants collected after incubation were measured by ELISA. RESULTS: Compared with PBS, sera from controls and 24 patients with SLE suppressed IL-6 release from IL-1beta pretreated cells. However, sera from 13 patients with SLE augmented IL-6 release. Of note, sera from 5 patients with pulmonary hypertension induced the highest level of IL-6 release. IgG from control sera suppressed IL-6 release, whereas F(ab')2 did not. Both IgG and F(ab')2 from the sera of patients with SLE with pulmonary hypertension augmented IL-6 release from IL-1beta pretreated cells. CONCLUSION: IgG antiendothelial cell antibodies from patients with SLE may be associated with the pathogenesis of SLE and pulmonary hypertension.

Adolescent↗