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Biomedical subjects

M Abe

Publications and source records attributed to M Abe.

At least 163 records · Page 9Linked to original sources
PubMed2001

[Qualitative features of confabulation in a case with basal forebrain amnesia].

We investigated qualitative features of confabulation in a case with basal forebrain amnesia. A 66-year-old, right-handed woman with a 8th-grade education, was admitted to the Rehabilitation Department of Tohoku University Hospital, Japan, for evaluation and therapy of amnesia. Her previous medical history included hypertension. Nine months before admission, she went to a hospital because of headache and blurred vision. She was diagnosed as suffering from a suprasellar arachnoid cyst and unruptured aneurysm at the anterior communicating artery. Five months later, resection of the cyst and clipping of the aneurysm was performed. After the operation, she became disoriented and amnesic with marked confabulation. On admission to our hospital 3 months later, she was alert and cooperative. Detailed neuropsychological assessment was performed during the next two months. She remained clinically stable throughout her hospitalization. Neurological examination showed no abnormalities. Brain magnetic resonance images revealed lesions in the bilateral orbito-frontal cortices and basal forebrain. Measurement of blood flow with 123I-IMP single photon emission computed tomography showed hypoperfusion in the bilateral frontotemporal regions. We performed systematic investigations to clarify the qualitative features of her confabulations. Her confabulations included many facts she had experienced before, but they were out of context. Each fact was recalled in isolation or associated with erroneous places, persons or times. Her confabulations were never fantastic or momentary in nature, but were consisted with isolated facts. Experimental investigation revealed that she could recognize individual facts (a person, a place, a task and time) in each episode. However, she could not integrate individual facts into an episode. We propose calling this type of confabulation "mosaic confabulation".

Aged↗
PubMed2001

[Clinical application of metabolic bone markers in hematologic malignancies].

Hematologic malignancies such as multiple myeloma, adult T cell leukemia and malignant lymphoma are often complicated with bone lesions and/or hypercalcemia. The abnormal bone metabolism in these diseases are modified by co-existing cachexia, malnutrition, sex hormone deficiency and abnormal parathyroid function or by chemotherapy in a complex manner. Metabolic bone markers are not only clinically useful for evaluation and diagnosis of such bone abnormalities but may also be used to monitor the disease activity itself, particularly in multiple myeloma which almost inevitably involves bone destructive lesions.

English Abstract↗
PubMed2000

Cloning, genomic structure and chromosomal localization of the gene encoding mouse DNA helicase RecQ helicase protein-like 4.

Five members of the RecQ helicase family, RECQL, WRN, BLM, RECQL4 and RECQL5 have been identified in humans. WRN and BLM have been demonstrated to be the responsible genes in Werner and Bloom syndromes, respectively. RECQL4 (RecQ helicase protein-like 4) was identified as a fourth member of the human RecQ helicase family bearing the helicase domain, and it was subsequently shown to be the responsible gene in Rothmund-Thomson syndrome. Here, we isolated mouse RECQL4 and determined the DNA sequence of full-length cDNA as well as the genome organization and chromosome locus. The mouse RECQL4 consists of 3651 base pairs coding 1216 amino acid residues and shares 63.4% of identical and 85.8% of homologous amino acid sequences with human RECQL4. The RECQL4 gene was localized to mouse chromosome 15D3 distal-E1 and rat chromosome 7q34 proximal. They were mapped in the region where the conserved linkage homology has been identified between the two species. Twenty-two exons dispersed over 7 kilo base pairs and all of the acceptor and donor sites for splicing of each exon conformed to the GT/AG rule. Our observations regarding mouse RECQL4 gene will contribute to functional studies on the RECQL4 products.

Adenosine Triphosphatases↗
PubMed2000

Molecular cloning and characterization of a novel gene, CORS26, encoding a putative secretory protein and its possible involvement in skeletal development.

We cloned a novel mouse cDNA, CORS26 (collagenous repeat-containing sequence of 26-kDa protein), encoding a secretory protein by suppression subtractive hybridization between transforming growth factor-beta1-treated and untreated C3H10T1/2 cells. The deduced amino acid sequence of CORS26 consists of 246 amino acids with a secretory signal peptide and contains a collagenous region (Gly-X-Y repeats) at the NH(2) terminus and a complement factor C1q globular domain at the COOH terminus. CORS26 is structurally similar to C1q and to adipocyte-specific protein Acrp30. Transfection analysis suggested that CORS26 is a secretory protein. Northern blot analysis revealed that CORS26 mRNA was present at high levels in rib growth plate cartilage and at moderate levels in kidney of adult mice. CORS26 mRNA was not detected in NIH3T3 cells, BALB/3T3 cells, C3H10T1/2 cells, or osteoblastic MC3T3-E1 cells by reverse transcription-polymerase chain reaction analysis. In situ hybridization of mouse embryos between 13 and 15 days postcoitus revealed relatively high levels of CORS26 mRNA in condensed prechondrocytic cells of cartilage primordia and developing cartilages. However, CORS26 mRNA were undetectable in mature chondrocytes. Furthermore, overexpression of CORS26 enhanced the growth of C3H10T1/2 cells in vitro. The present findings suggest that the CORS26 gene may play an important role in skeletal development.

3T3 Cells↗
PubMed2000

Diastolic fractional flow reserve to assess the functional severity of moderate coronary artery stenoses: comparison with fractional flow reserve and coronary flow velocity reserve.

BACKGROUND: Coronary blood flow occurs mainly during the diastolic phase of each cardiac cycle and is mainly dependent on diastolic driving pressure, especially in the left anterior descending coronary artery (LAD). We hypothesized that calculation of the ratio of the diastolic driving pressure of a stenotic LAD to its normal value, namely diastolic FFR (d-FFR), might provide precise insight into the mechanism of FFR for assessment of the functional severity of the stenosis. We compared d-FFR with FFR, coronary flow reserve (CFR), and exercise myocardial thallium scintigraphy in an lesion of intermediate severity. METHODS AND RESULTS: The study population consisted of 46 consecutive patients with a moderate stenosis in the LAD in whom simultaneous measurements of aortic pressure, left ventricular pressure, and coronary pressure distal to the stenosis were obtained. Coronary flow velocity was successfully measured with a Doppler guidewire in 37 of the 46 patients. Values for FFR, d-FFR, and CFR in the noninvasive test-positive group were significantly lower than those in the negative group. With cutoff values of 0.75, 0.76, and 2.0 for FFR, d-FFR, and CFR, sensitivities were 83.3%, 95.8%, and 88.2% and specificities were 100%, 100%, and 95.0%, respectively. CONCLUSIONS: The close similarity of the sensitivity and specificity of FFR and d-FFR, around almost identical cutoff values (0.75 versus 0.76), confirms the physiological validity of FFR as a clinical standard. In clinical practice, FFR remains the index of choice for assessment of the functional severity of moderate coronary artery stenoses.

Blood Flow Velocity↗
PubMed2000

Expression of DNA-dependent protein kinase catalytic subunit and Ku80 in developing human brains: implication of DNA-repair in neurogenesis.

We investigated expression of DNA-dependent protein kinase catalytic subunit (DNA-PKcs) and Ku80 in developing human brain, both of which have been suggested to be involved in the repair of DNA double-strand break (DSB). Their expressions were well correlated, and the highest immunoreactivity was observed in post-mitotic immature neurons in the cerebral cortex as well as in progenitors in the periventricular germinal layer. The reactivity gradually decreased during development. Our results support the notion that DSB is generated during the ontogeny of the human central nervous system.

Adolescent↗
PubMed2000

Clinical outcomes of orbital irradiation combined with or without systemic high-dose or pulsed corticosteroids for Graves' ophthalmopathy.

PURPOSE: To evaluate the outcomes of orbital irradiation with or without high-dose or pulsed corticosteroids in patients with Graves' ophthalmopathy (GO). METHODS AND MATERIALS: One hundred and twenty-one patients with moderate to severe GO who received orbital irradiation from 1987 to 1997 were retrospectively analyzed. A total dose of 20 Gy in 10 fractions was delivered to the bilateral retrobulbar volume. Eighty-six patients were treated in combination with high-dose or pulsed corticosteroids and irradiation. Univariate and multivariate analyses were performed to assess the prognostic variables. RESULTS: The median follow-up period was 26 months. The overall clinical response was evaluated as excellent in 17 patients (14%), good in 65 (54%), fair in 31 (25%), no response in 7 (6%), and worse in 1 (1%). The best responses were noted for soft-tissue signs, extraocular muscle involvement, and sight loss, while a limited response was noted for proptosis. Multivariate analysis revealed that the use of high-dose corticosteroid or pulsed corticosteroids, female gender, and a shorter duration of ophthalmopathy before radiotherapy were significantly correlated with favorable outcomes. No long-term complications related to radiotherapy were observed. CONCLUSION: Orbital irradiation combined with high-dose or pulsed corticosteroids is an effective treatment for moderate to severe GO, especially in cases with major manifestations of soft-tissue signs, extraocular muscle impairment, or sight loss.

Adolescent↗
PubMed2000

Signal joint formation is also impaired in DNA-dependent protein kinase catalytic subunit knockout cells.

The effort to elucidate the mechanism of V(D)J recombination has given rise to a dispute as to whether DNA-dependent protein kinase catalytic subunit (DNA-PKcs) contributes to signal joint formation (sjf). Observations reported to date are confusing. Analyses using DNA-PKcs-deficient cells could not conclude the requirement of DNA-PKcs for sjf, because sjf can be formed by end-joining activities which are diverse among cells other than those participating in V(D)J recombination. Here, we observed V(D)J recombination in DNA-PKcs knockout cells and showed that both signal and coding joint formation were clearly impaired in the cells. Subsequently, to directly demonstrate the requirement of DNA-PKcs for sjf, we introduced full-length cDNA of DNA-PKcs into the knockout cells. Furthermore, several mutant DNA-PKcs cDNA constructs designed from mutant cell lines (irs-20, V3, murine scid, and SX9) were also introduced into the cells to obtain further evidence indicating the involvement of DNA-PKcs in sjf. We found as a result that the full-length cDNA complemented the aberrant sjf and that the mutant cDNAs constructs also partially complemented it. Lastly, we looked at whether the kinase activity of DNA-PKcs is necessary for sjf and, as a result, demonstrated a close relationship between them. Our observations clearly indicate that the DNA-PKcs controls not only coding joint formation but also the sjf in V(D)J recombination through its kinase activity.

Animals↗
PubMed2000

Lithium lengthens the circadian period of individual suprachiasmatic nucleus neurons.

Lithium treatment lengthens the period of circadian rhythms in most organisms. In the present study, we tested whether lithium acts directly on the mammalian suprachiasmatic nucleus (SCN) to lengthen rhythms of individual neurons. Lithium increased the circadian period of firing rate rhythms of cultured SCN neurons in a concentration-dependent manner. Lithium had no effect on the amplitude of these rhythms, but did affect the period of some cells more than others. The results indicate that lithium acts directly on the SCN to lengthen the free-running period of individual neurons.

Action Potentials↗
PubMed2000

Axonal damage revealed by accumulation of beta-amyloid precursor protein in HTLV-I-associated myelopathy.

We investigated the localization and extent of beta-amyloid precursor protein (APP) immunoreactivity as a sensitive marker for impairment of fast axonal transport in the spinal cords of patients with HTLV-I-associated myelopathy (HAM)/tropical spastic paraparesis (TSP). The results from this study show that APP, used as a marker of early axonal damage in HAM/TSP lesions, is more intensively expressed in areas of active-inflammatory lesions than those of inactive-chronic lesions. The close localization to the areas containing inflammation (activation of macrophage/microglia) is striking and suggests that axonal damage is closely associated with inflammation in active-chronic lesions. Although inflammatory cell infiltration in the central nervous system (CNS) is rarely found in inactive-chronic lesions, a few clusters of APP+ axons are found in the spinal cord white matter in some cases. The presence of APP+ axons without relation to inflammatory cells in inactive-chronic lesions, suggest that soluble neurotoxic factors might induce axonal changes in the CNS of HAM/TSP. The occasional myelinated fibers in the anterior and posterior spinal roots in lower thoracic to lumbar levels had APP+ axons, suggesting that spinal nerve roots can be affected in HAM/TSP, especially in lower thoracic to lumbar levels. Impairment of fast axonal transport may contribute to the development of disability in patients with HAM/TSP.

Aged↗
PubMed2000

Paterno-Buchi photocyclization of 2-siloxyfurans and carbonyl compounds. Notable substituent and carbonyl (Aldehyde vs ketone and singlet- vs triplet-excited state) effects on the regioselectivity (Double-bond selection) in the formation of bicyclic exo-oxetanes

Paterno-Buchi coupling, photochemical [2 + 2] cycloaddition, of carbonyl compounds 2a-f with 2-siloxyfurans 1a-d has been investigated in detail. The stereoselective formations of exo-oxetanes 3 and 4 were observed in high yields. The regioselectivity (double-bond selection, 3 vs 4) was found to be largely dependent upon the carbonyls, the substituents at the furan ring, and the excited state of the carbonyls (singlet vs triplet). The photoreaction of aldehydes 2a-c gave bicyclic exo-oxetanes 3 and 4 at regio-random, independent upon their excited states and the substituents at furan ring. However, the photoreaction of the triplet state of ketones 2d-f was found to give regioselectively exo-oxetanes 4, except for the 4-methyl-2-siloxyfurane 1d case. The singlet-excited state of acetone 2f gave both oxetanes 3 and 4 at regio-random. For the singlet-state photochemistry, the approach direction of the electrophilic oxygen of the excited carbonyls to the furan ring is proposed to be an important factor for the exo-stereoselection. The Griesbeck model can rationalize the regio- and exo-selective formation of oxetanes in the triplet-state photoreaction.

Journal Article↗
PubMed2000

Expression of the 37-kDa laminin binding protein in murine lung tumor cell correlates with tumor angiogenesis.

Expression of the 37-kDa laminin binding protein (37LBP), a precursor protein of the 67-kDa laminin receptor, correlates well with the biological aggressiveness of cancer cells. Previously, we have established murine lung cancer cell lines T11 and T15, in which 37LBP expression was remarkably diminished, and reported that the mean survival time of the T11 and the T15-recipients was significantly prolonged compared with that of the control cell lines (P29 and T42). In the present study, immunohistochemical findings of the tumors demonstrated that the microvessel density in the T11 (28. 1+/-7.2/mm(2)) and in the T15 tumor (29.7+/-6.5/mm(2)) were significantly lower than that observed in P29 (46.3+/-8.7/mm(2)) or in T42 (50.5+/-4.4/mm(2)). Expression of vascular endothelial growth factor (VEGF) was repressed in T11 and T15 compared with its expression in P29 and T42. It was also shown that conditioned media of T11 and T15 cells exhibited significantly reduced proliferation and migration of the capillary endothelial cells. These results suggest that decreased expression of 37LBP in antisense-RNA transfectant may relate to its low tumorigenicity, and that this effect may be partly caused by the diminished tumor angiogenesis of murine lung cancer.

Animals↗
PubMed2000

Medroxyprogesterone acetate inhibits human pancreatic carcinoma cell growth by inducing apoptosis in association with Bcl-2 phosphorylation.

BACKGROUND: A previous study found that medroxyprogesterone acetate (MPA) delayed the in vivo growth of three (AsPC-1, Capan-2, and MiaPaCa-2) of nine human pancreatic carcinoma cell lines transplanted into nude mice (Cancer 1995; 75:1263-72). The current study was undertaken to evaluate the basis for this inhibitor. METHODS: The estrogen receptor (ER) and progesterone receptor (PgR) status in nine human pancreatic carcinoma cell lines, AsPC-1, BxPC-3, Capan-1, Capan-2, Hs-700T, Hs-766T, MiaPaCa-2, PANC-1, and SUIT-2, was assessed using an enzyme immunoassay (EIA). The authors tested the growth inhibitory activity of MPA and the morphologic changes in these nine pancreatic carcinoma cell lines. Cell cycle progression and DNA fragmentation also were evaluated in these cell lines. Immunoblot analysis was used to determine bcl-2 expression and phosphorylation. RESULTS: In the EIA assay, ER was detected in three cell lines (BxPC-3, Capan-2, and MiaPaCa-2), and PgR was also detected in three (AsPC-1, Capan-2, and MiaPaCa-2). Medroxyprogesterone acetate inhibited the growth of three cell lines (AsPC-1, Capan-2, and MiaPaCa-2) with IC50 values ranging from 2.3 x 10(7) to 6.1 x 10(-7) M. In these three responsive cell lines, MPA caused cell detachment and decreased cell density. The nuclei of the MPA-treated cells were condensed and often fragmented. Cell cycle analysis of these three cell lines showed that MPA induced the appearance of a sub-G1 peak, which is characteristic of early apoptotic cells. DNA degradation assay after MPA treatment showed a typical DNA ladder pattern consistent with apoptosis. Immunoblot analysis of MPA-treated cells that overexpressed bcl-2 revealed a pattern consistent with bcl-2 phosphorylation. CONCLUSIONS: Clinically attainable concentrations of MPA can inhibit the growth of some human pancreatic carcinoma cells in vitro by inducing apoptosis, probably through their PgR, in association with the phosphorylation of bcl-2. This agent may be useful for treating patients with pancreatic carcinoma.

Animals↗
PubMed2000

Resetting central and peripheral circadian oscillators in transgenic rats.

In multicellular organisms, circadian oscillators are organized into multitissue systems which function as biological clocks that regulate the activities of the organism in relation to environmental cycles and provide an internal temporal framework. To investigate the organization of a mammalian circadian system, we constructed a transgenic rat line in which luciferase is rhythmically expressed under the control of the mouse Per1 promoter. Light emission from cultured suprachiasmatic nuclei (SCN) of these rats was invariably and robustly rhythmic and persisted for up to 32 days in vitro. Liver, lung, and skeletal muscle also expressed circadian rhythms, which damped after two to seven cycles in vitro. In response to advances and delays of the environmental light cycle, the circadian rhythm of light emission from the SCN shifted more rapidly than did the rhythm of locomotor behavior or the rhythms in peripheral tissues. We hypothesize that a self-sustained circadian pacemaker in the SCN entrains circadian oscillators in the periphery to maintain adaptive phase control, which is temporarily lost following large, abrupt shifts in the environmental light cycle.

Animals↗
PubMed2000

Roles of two VEGF receptors, Flt-1 and KDR, in the signal transduction of VEGF effects in human vascular endothelial cells.

Vascular endothelial growth factor (VEGF) is a principal regulator of vasculogenesis and angiogenesis. VEGF expresses its effects by binding to two VEGF receptors, Flt-1 and KDR. However, properties of Flt-1 and KDR in the signal transduction of VEGF-mediated effects in endothelial cells (ECs) were not entirely clarified. We investigated this issue by using two newly developed blocking monoclonal antibodies (mAbs) against Flt-1 and KDR. VEGF elicits DNA synthesis and cell migration of human umbilical vein endothelial cells (HUVECs). The pattern of inhibition of these effects by two mAbs indicates that DNA synthesis is preferentially mediated by KDR. In contrast, the regulation of cell migration by VEGF appears to be more complicated. Flt-1 regulates cell migration through modulating actin reorganization, which is essential for cell motility. A distinct signal is generated by KDR, which influences cell migration by regulating cell adhesion via the assembly of vinculin in focal adhesion plaque and tyrosine-phosphorylation of focal adhesion kinase (FAK) and paxillin.

3T3 Cells↗