Biomedical subjects

S Takeuchi

Publications and source records attributed to S Takeuchi.

At least 271 records · Page 15Linked to original sources

PubMed1997

TEL is one of the targets for deletion on 12p in many cases of childhood B-lineage acute lymphoblastic leukemia.

Abnormalities of the short arm of chromosome 12 including loss of heterozygosity (LOH) and TEL/AML-1 fusion resulting from a t(12;21)(p13;q22) translocation are frequently observed in childhood acute lymphoblastic leukemia (ALL). We investigated 21 DNA samples of childhood ALL which had LOH at 12p13. Rearrangement of TEL was observed in eight cases and another case showed a homozygous deletion of TEL. Two informative samples with TEL rearrangement had a deletion localized to the 5' region of this gene. The deletion in these two cases includes the helix-loop-helix (HLH) domain. This is consistent with the hypothesis that the normal tel can heterodimerize with the TEL/AML-1 gene product and inhibit the transforming capacity of the chimeric protein. Presumably, loss of the HLH of the normal remaining TEL allele abrogates this tumor suppressor-like function. The case with homozygous deletion of TEL is also consistent with this gene having qualities of a tumor suppressor. One unusual case had T-ALL rather than B-lineage ALL and the leukemic cells had rearrangement of TEL, but they did not have an alteration of the remaining TEL allele suggesting that the etiology of this disease may be different. This analysis further emphasizes the importance of loss of the normal TEL allele in childhood precursor B-lineage ALL.

Blotting, Southern↗

PubMed1997

Homozygous deletions at 9p21 in childhood acute lymphoblastic leukemia detected by microsatellite analysis.

To gain a fuller understanding of the role of deletions of chromosome 9 in the development of childhood acute lymphoblastic leukemia (ALL), we performed detailed deletional mapping of chromosome 9 in 54 primary ALL samples with matched normal DNA using 22 highly polymorphic markers; and this information was combined with our previous data concerning the presence of deletions of CDKN2/INK4A/p16 and CDKN2B/INK4B/p15 in these samples. We have found a very high frequency of loss of heterozygosity (LOH) (31 of 54 cases (57%)) on chromosome arm 9p. As expected, the smallest region of LOH was between D9S1747 and D9S1748 at 9p21, including CDKN2/INK4A/p16, but excluding CDKN2B/INK4B/p15. Homozygous deletions at 9p21 occurred in 23 of 54 (43%) samples (seven of 11 (64%) T-ALL, 16 of 45 (36%) precursor-B ALL). We detected seven cases of homozygous deletions at 9p21 which had not been detected by Southern blot hybridization, showing the power of microsatellite analysis in detecting homozygous deletions. In most cases, homozygous deletions were limited to the region between D9S1747 and CDKN2B/INK4B/p15. We have attempted to determine the mechanism and timing of 9p deletions. Of the 23 samples with homozygous deletions at 9p21, 21 samples had surrounding large LOH. Of the 29 samples with LOH of 9p, homozygous deletion at 9p21 was identified in 22 cases. In addition, six patients have been studied at diagnosis and relapse, all six showed the same 9p21 structure at relapse (normal, three patients; hemizygous deletions, two patients; homozygous deletion, one patient) as their initial presentation. Finally, three patients (homozygous deletion, one patient; hemizygous deletion, two patients) had the IFN-alpha rather than CDKN2/INK4A/p16 deleted. In summary, these data further emphasize the importance of 9p21 loss in the development of childhood ALL.

Carrier Proteins↗

PubMed1997

Microsatellite instability and other molecular abnormalities in childhood acute lymphoblastic leukaemia.

Microsatellite instability (MSI) has been considered to represent the defect of DNA mismatch repair systems and has been implicated in the tumourigenesis of several human malignancies. To investigate the possible presence of microsatellite instability in childhood acute lymphoblastic leukaemia (ALL), we examined 48 primary ALL samples. Instability was determined at 85 different microsatellite loci localized to 12 different chromosome arms. Microsatellite instability was detected in five (10%) samples. Interestingly, the instability was found at chromosomal regions associated with frequent alterations. Two samples had instability at the microsatellite marker within the TEL gene on chromosome arm 12p. Two other samples had instability at a microsatellite marker close to CDKN2/p16 on 9p; one of these samples had a homozygous deletion at 9p21. The fifth sample had instability at the microsatellite marker on 6q, which we have found is a frequent region of loss of heterozygosity in childhood ALL. Taken together, instability was rare in childhood ALL, but was localized to the three most frequently deleted chromosome regions in childhood ALL, suggesting that localized microsatellite instability may identify a fragile chromosomal region which could result in alteration of surrounding target genes and lead to leukaemia.

Blotting, Southern↗

PubMed1997

Microsatellite instability during the progression of acute myelocytic leukaemia.

We studied microsatellite instability (MSI) at the onset and during progression of 17 individuals with acute myelocytic leukaemia (AML). These included two cases of MO, eight with M1 and seven with M4, according to the FAB classification. The DNA from diagnostic, remission and relapsed stages of their disease was analysed at 69 loci. Two MSI were found in the diagnostic and remission phase paired samples (12%), and eight MSI were identified in six of the relapsed phase samples (35%). These results indicate that mismatch repair errors such as MSI are unimportant at the onset of AML, but might have importance during the progression of the disease.

Acute Disease↗

PubMed1997

Adrenergic neurotransmitters and calcium ionophore-induced situs inversus viscerum in Xenopus laevis embryos.

Xenopus laevis embryos at the blastula-early tail bud stage were exposed to norepinephrine or octopamine dissolved in culture saline until they reached the larval stage. The left-right asymmetry of the heart and gut was then examined. We found that these adrenergic neurotransmitters induced situs inversus in the heart and/or gut in up to 35% of tested neurula embryos. Norepinephrine-induced situs inversus was blocked by the alpha-1 adrenergic antagonist prazosin. Furthermore, A23187, a calcium ionophore, also increased the incidence of situs inversus up to 54% when late-neurula embryos were exposed to the solution. A23187 treatment initiated before neural groove formation was less effective. The incidence of situs inversus induced by these reagents decreased towards the control level (2.2%, 25 untreated embryos out of 1127 embryos in total) in embryos past the stage of neural tube closure. In the present experiments we obtained 22 gut-only situs inversus embryos having an inverted gut and a normal heart. In contrast, such embryos were not observed among the 1127 untreated embryos. An adrenergic signal mediated by an increase in intracellular free calcium may be involved in the asymmetrical visceral morphogenesis of Xenopus embryos.

Adrenergic alpha-Agonists↗

PubMed1997

Detection of delayed cerebral vasospasm, after rupture of intracranial aneurysms, by magnetic resonance angiography.

OBJECTIVE: The goal of this study was to assess the value of magnetic resonance angiography (MRA), compared with conventional angiography, in the diagnosis and follow-up monitoring of delayed cerebral vasospasm after subarachnoid hemorrhage resulting from rupture of intracranial aneurysms. METHODS: For 32 patients undergoing examination by both MRA and conventional angiography during the period of risk for vasospasm, on the same day, the frequency and severity of and sequential changes in vasospasm were evaluated. The three-dimensional time-of-flight method was used. MRA was performed three times, i.e., before, during, and after the period of risk for vasospasm. Conventional angiography was performed twice, i.e., at admission and during the period of risk for vasospasm. Vasospasm was assessed at 22 regions of the cerebral arteries, including the bilateral anterior cerebral (A1, A2, and A3 segments), middle cerebral (M1, M2, and M3 segments), internal carotid (C1 and C2 segments), posterior cerebral (P1 and P2 segments), and posterior communicating arteries. RESULTS: Seven patients were excluded because of poor MRA images. Twenty-two of 25 patients (125 arteries) showed vasospasm in conventional angiograms. Nineteen of the 22 patients also showed vasospasm in MRA images; however, 57 arteries (45.6%) were diagnosed as showing vasospasm by MRA, and 59 (47.2%) could not be evaluated because of artifacts. For the remaining three patients (nine arteries, 7.2%), vasospasm could not be detected by MRA. Sequential changes in vasospasm could be well evaluated by MRA. CONCLUSION: MRA could be useful for management of cerebral vasospasm, although it cannot become a practical alternative to conventional angiography.

Adult↗

PubMed1997

Bone-turnover metabolites as clinical markers of bone metastasis in patients with prostatic carcinoma.

BACKGROUND: Candidate markers of prostatic metastases to bone, urinary deoxypyridinoline, serum carboxy-terminal propeptide of type 1 procollagen (P1CP), and pyridinoline cross-linked carboxy-terminal telopeptide of type 1 collagen (1CTP), were measured to evaluate their prognostic efficacy. METHODS: Urinary levels (mean +/- SD) of deoxypyridinoline were measured by a competitive immunoassay, and serum levels of P1CP and 1CTP were measured by radioimmunoassay in 30 patients with benign prostatic hyperplasia, 18 patients with prostatic carcinoma without bone metastases, and 27 patients with prostatic carcinoma and bone metastases. RESULTS: Urinary concentrations of deoxypyridinoline (pmol/micromol creatinine) in patients with prostatic carcinoma and bone metastases (10.4 +/- 7.7) were significantly higher than those in similar patients without bone metastases (4.3 +/- 1.3) and those in patients with benign prostatic hyperplasia (3.8 +/- 1.2). Serum levels of P1CP and 1CTP (ng/mL) in patients with prostatic carcinoma and bone metastases (262.6 +/- 188.7 and 10.3 +/- 9.5, respectively) were significantly higher than those in similar patients without bone metastases (118.1 +/- 30.2 and 4.3 +/- 1.4, respectively) and those in patients with benign prostatic hyperplasia (93.9 +/- 25.1 and 3.3 +/- 1.1, respectively). Serial measurements of urinary deoxypyridinoline and serum P1CP and 1CTP were correlated with a positive response to treatment (reduced measurements) and with the clinical progression of disease (increased measurements) before detection of new bone lesions by bone scintigram. CONCLUSION: Urinary deoxypyridinoline, serum P1CP, and serum 1CTP should be useful markers in confirming and monitoring prostatic carcinoma metastases to bone.

Aged↗

PubMed1997

Intrinsic ureteric involvement by endometriosis: a case report.

Endometriosis occasionally involves the urinary tract, and a ureteral obstruction from this order constitutes a rare variant with serious consequences. Intrinsic ureteric involvement by endometriosis is an exceedingly rare event. This case report describes intrinsic ureteric involvement by endometriosis. The case involved 47-year-old woman, gravida 4, para 2, who had a 4-year history of dysmenorrhea and hypermenorrhea. An intravenous pyelogram showed a right hydronephrosis. She underwent a total abdominal hysterectomy and a right ureteroureterostomy. A pathologic examination revealed complete obstruction of the right ureter by intrinsic intramural endometriosis. We conclude that because ureteral endometriosis, especially intrinsic endometriosis, is usually silent and results in a high rate of renal loss before recognition, physicians should have a hightened awareness of this uncommon but serious manifestation of endometriosis.

Endometriosis↗

PubMed1997

[Analysis of prognosis of bronchopulmonary infectious disease with lung cancer].

Bronchopulmonary infection affects the prognosis of lung cancer patients. Thus, we investigated the relationship between the prognosis of bronchopulmonary infectious diseases and their causative bacteria isolated by transtracheal aspiration (TTA) in lung cancer patients. In the present study, we determined which factor is more predisposing for the outcome of bronchopulmonary infections, the type of causative bacteria or the host nutritional status. A total of 107 lung cancer patients, which consisted of 105 males and 5 females (mean age 67.3 +/- 8.0), were included in this study. The study was conducted from 1981 to 1994. They were classified into the survival group and the deceased group. Causative agents of infection were compared between these 2 groups. S. pneumoniae, alpha-Streptococcus sp., M. catarrhalis, and Neisseria sp. were predominant in organisms isolated from TTA-specimens of lung cancer patients with bronchopulmonary infections, regardless of prognosis. Nutritional status, as determined by serum levels of cholinesterase, albumin, and cholesterol, was poor in the deceased group than in the survival group. These results indicate that the outcome of bronchopulmonary infections in lung cancer patients are affected mainly by the nutritional status of the host.

Aged↗

PubMed1997

Normal S cone electroretinogram b-wave in Oguchi's disease.

AIM: The short wavelength sensitive (S) cone electroretinograms (ERGs) were examined in two patients with Oguchi's disease to study S cone function. METHODS: Ganzfeld colour flashes under bright white background illumination were used to elicit S cone, and mixed long (L) and middle (M) wavelength sensitive cone ERGs. RESULTS: The S cone ERG b-wave was normal with short wavelength stimuli with normal L and M cone responses in both patients. CONCLUSIONS: These ERG results indicate that the S cone system as well as the L and M cone system is not defective in Oguchi's disease, while the S cone responses are not detectable in the complete type of congenital stationary night blindness as reported previously. The results imply that there is a significant difference in the way the S cone system is affected in different forms of stationary night blindness, and that the S cone and rod do not share the same arrestin system.

Adult↗

PubMed1997

Allopurinol reduced hepatic ischemia-reperfusion injury exacerbated by inhalation of high-concentration oxygen in rats.

Exposure to high-concentration oxygen (O2) increases lipid peroxidation of the cellular membrane, leading to tissue injury which may involve hepatic ischemia-reperfusion (I/R) injury. We examined the effects of inhaling high-concentration O2 on hepatic I/R injury with allopurinol, which is a xanthine oxidase inhibitor. Partial hepatic ischemia was performed in rats with or without allopurinol under 21 or 100% O2 inhalation. Levels of lipid peroxide, serum liver enzymes, and hepatocellular oxidative stress in the 100% O2 group were significantly higher than in the 21% O2. Administration of allopurinol significantly inhibited those changes in the 100% O2 group. Severe degeneration of mitochondria were noted in the 100% O2 group, but appeared to be reduced by allopurinol. Results suggest that inhalation of high-concentration O2 during liver surgery may increase lipid peroxidation and exacerbate hepatic I/R injury, but those changes may be prevented by allopurinol.

Alanine Transaminase↗

PubMed1997

Characteristic expression of high molecular mass heat shock protein HSP105 during mouse embryo development.

Expression of 105 k-Da heat shock protein (HSP105) during mouse embryo development was investigated. Although HSP105 was detected scarcely in mouse embryos at gestational day (GD) 8, its level of HSP105 increased markedly in the embryos from GD 9 to 11, and then decreased gradually by GD 14. In contrast, 70 k-Da heat shock cognate protein (HSC70) was detected at constantly high levels in embryo from GD 8 to 17 (before birth). The transient increase in level of HSP105 was observed in most embryonic tissues. Since the levels of HSP105 mRNA was detected at constantly high levels in the embryos between GD 8 and 12, the increased expression of HSP105 at GD 9 to 11 seemed to be regulated at posttranscriptional level. Immunohistochemically, HSP105 as well as HSC70 were localized in the cytoplasm and the nuclei of cells in various mouse embryonic tissues. After treatment of tissue sections with proteinase K, HSP105 but not HSC70 was also found to be localized in condensed cells and condensed bodies which showed the typical characteristics of apoptotic cells and apoptotic bodies at the interdigital regions of limbs. These findings suggest that HSP105 plays important roles during mouse embryo development.

Animals↗

PubMed1997

Detection of Clostridium septicum hemolysin gene by polymerase chain reaction.

A polymerase chain reaction (PCR) was developed for the detection of the hemolysin (alpha toxin) gene of Clostridium septicum. The PCR primers were designed from the sequence of the hemolysin gene and synthesized. A DNA fragment of 270 bp was amplified from 10 strains of C. septicum, but was not from strains of C. chauvoei, C. perfringens, C. novyi, or C. haemolyticum. When the PCR product was digested with Sau3AI, two DNA fragments of the expected 148 bp and 122 bp were recognized. The lowest detectable threshold of PCR for the hemolysin gene was 3.8 x 10(3) cells/ml. The PCR technique may be useful for rapid detection or identification of C. septicum associated with malignant edema.

Animals↗

PubMed1997

Jansen-type metaphyseal chondrodysplasia: analysis of PTH/PTH-related protein receptor messenger RNA by the reverse transcriptase-polymerase chain method.

Jansen-type metaphyseal chondrodysplasia (JMC) has both delayed ossification in long bones and usually hypercalcemia. We report a Japanese male patient with JMC who presented with rachitic signs on radiographs, hypercalcemia (13 mg/dl) and low %TRP at age 3 months (mo). Hypercalcemia was treated from age 3 mo to 11 yr. Progressive widening, splaying and fragmentation of the metaphyses have been recognized on radiographs which resulted in shortened tubular bones and consequent short stature [107 cm (-6.5 SD)] at age 13 yr. Hypercalcemia tended to normalize, and %TRP became normal at age 13 yr. Repeated measurements of serum PTH and PTH-related protein (PTHrP) levels showed that they were low or normal in the face of hypercalcemia and high urine cAMP excretion, which led us to suspect constitutive activation of the PTH/PTHrP receptor. Direct sequencing of PTH/PTHrP receptor complementary DNA from skin fibroblast cells revealed a CAC to CGC transversion yielding a strictly conserved His223 to Arg substitution found in 90% of DNA fragment in the second transmembrane domain of the receptor. This mutation created a restriction site Sphl (G/CATG/C). Direct sequencing of genomic DNA and also restriction enzyme digestion revealed heterozygous transition. The mutation was absent in the parents with normal phenotype. We conclude that both dysplastic bone lesions and calcium homeostasis are age-dependent in JMC, and that the His223-Arg substitution is the same as that found in four Caucasian patients with a similar phenotype irrespective of the ethnic difference, and that the preferential expression of an abnormal allele of the PTH/PTHrP receptor mRNA in skin fibroblast despite heterogygotic transversion in the genomic DNA suggests the importance of allele expression.

Dwarfism↗

PubMed1997

Effect of acquired tolerance to ischemia on focal infarction in gerbils.

The protective effect of prior ischemia on focal cerebral infarction produced by permanent middle cerebral artery (MCA) occlusion was studied in a gerbil model. Forebrain ischemia for 2 and 5 minutes at an interval of 48 hours was used as the prior ischemic insult. Forty-eight hours after the second forebrain ischemia, the MCA was occluded. Progression of ischemic change caused by the MCA occlusion was delayed in the early ischemic period in animals with prior ischemia, as compared to animals without prior ischemia. The mean infarct volume 24 hours after the MCA occlusion was the same in animals with and without prior ischemia. Ischemic tolerance was acquired in this model, but had no effect on the extent of infarction caused by permanent ischemia.

Animals↗

PubMed1997

Histological interaction of cultured endothelial cells and endovascular embolic materials coated with extracellular matrix.

This study was undertaken to evaluate the histological reaction of cultured endothelial cells to endovascular embolic materials in vitro. Endothelial cells were isolated and cultured from a canine carotid artery. Embolic materials (platinum microcoils, polyvinyl alcohol particles, silicon balloons, or silk threads), either in their normal state or after having been coated with type 1 collagen, fibronectin, or laminin, were placed on endothelial cells and cocultured for 6, 12, and 24 hours and 2, 3, 7, 14, and 21 days. The cocultures were investigated histologically using a scanning electron microscope. Endothelial cells were not found on any uncoated embolic materials, even at 21 days. On the materials coated with fibronectin or laminin, endothelial cells began to proliferate in 7 days, covering the materials extensively in 14 days. On the other hand, endothelial cells began to proliferate on the collagen-coated materials in 3 days, covering them extensively in 7 days and reaching confluence with a cobblestone pattern in 21 days. The densities of endothelial cells on collagen-coated materials were much higher than those observed on the materials coated with other extracellular matrices. Future advantages of the clinical use of collagen-coated embolic materials in interventional treatment are discussed.

Animals↗

PubMed1997

Serial changes of hemostasis in aneurysmal subarachnoid hemorrhage with special reference to delayed ischemic neurological deficits.

This study was undertaken to elucidate comprehensively the serial changes occurring in hemostatic systems after aneurysmal subarachnoid hemorrhage (SAH) and thereby to ascertain whether the examination of the integrity of these systems is helpful in predicting delayed ischemic neurological deficits (DINDs). The authors examined 117 patients admitted to the hospital within 24 hours after onset of SAH. Blood samples were collected from each patient on Days 0 (at admission), 3, 6, 14, and 30. A number of hemostatic parameters were examined in these samples, and the relationships between their changes and DINDs were assessed. Eighteen (15.4%) of the patients exhibited DINDs, and their frequency increased as the severity of subarachnoid clotting increased. Also, the frequency of DINDs was significantly higher in the patients with hydrocephalus on initial computerized tomography (CT) scans than in those without hydrocephalus. Regarding the hemostatic parameters at admission, there was no significant difference between the patients with and without DINDs. On Day 3, however, the fibrinogen and D-dimer levels were higher in the patients with than in those without DINDs. The fibrinogen and thrombin-antithrombin complex levels on Day 6 and the D-dimer level on Day 14 in the patients with DINDs were higher than the corresponding levels in those without DINDs. Multivariate analyses revealed that the following variables (in order of importance) were independent predictors of DINDs: the levels of D-dimer on Day 3, fibrinogen on Day 6, and the presence of hydrocephalus on admission. These data indicate that the levels of hemostatic parameters in concert with the CT findings may enable us to predict the appearance of DINDs.

Adult↗

PubMed1997

Insulin-like growth factor-I stimulates proliferation of mouse uterine epithelial cells in primary culture.

Estrogens stimulate proliferation and differentiation of uterine epithelial cells in vivo. Mitogenic action of estrogens may be mediated by growth factors such as insulin-like growth factor-I (IGF-I). This study was designed to determine whether IGF-I and insulin affect proliferation of uterine epithelial cells obtained from 3- to 4-week-old immature female mice in a serum-free culture system. The epithelial cell number on Day 5 in culture was significantly increased by adding IGF-I (10 and 100 ng/ml) or insulin (100 and 1000 ng/ml) to the culture media, indicating that IGF-I is more effective than insulin in inducing the epithelial growth. The epithelial DNA synthesis was significantly stimulated by IGF-I (1 and 10 ng/ml), suggesting that both the epithelial proliferation and their detachment from substratum are stimulated by 1 ng/ml of IGF-I, but that the former is more accelerated than the latter by 10 ng/ml of IGF-I. These results demonstrate that both IGF-I and insulin directly stimulate the growth of uterine epithelial cells, and suggest that insulin may act via IGF-I receptors. IGF-I immunoreactivity was detected in the cytoplasm of the cultured cells, indicating that the cells synthesize IGF-I. Estradiol-17 beta (E2) at lower concentrations (0.001-0.1 nM) tended to increase the number of epithelial cells, while E2 at higher concentrations (1 to 100 nM) did not affect it. It is highly probable that IGF-I produced in endometrial cells induces their proliferation by an autocrine or paracrine mechanism.

Animals↗