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Biomedical subjects

A Sakai

Publications and source records attributed to A Sakai.

At least 55 records · Page 3Linked to original sources
PubMed2001

[Evaluation of peripheral facial nerve palsy with R 2 wave latency in blink reflex].

Electrically elicited blink reflexes were investigated in 60 patients with peripheral facial nerve palsy. The purpose of this study was to evaluate the utility of analysis of R 2 wave in blink reflex as a prognostic indicator for the patients with facial palsy. The patients treated by stellate ganglion block were classified into three groups: Group I scored more than 90 points (full score is 100 points) within 2 weeks, Group II scored more than 90 points over 2 weeks, and Group III scored less than 90 points. The examinations were performed at the first visit, and 2, 4, 6 weeks after the onset of facial palsy. Latencies of ipsilateral and contralateral R 2 wave were measured by electrical stimulation on both side. There were significant differences of R 2 latency between ipsilateral and contralateral side in each of the three groups at the first visit. In Group II, contralateral R 2 latency obtained by stimulation of the paralytic side was prolonged significantly. In Group III, the ipsilateral R 2 wave was not observed. The results of this study indicate that measurement of the R 2 latency of blink reflex is useful in judging the severity of the peripheral facial nerve palsy. The R 2 latencies obtained by stimulation of ipsilateral and contralateral side should be used as one of the parameters for evaluation of the prognosis of patients with peripheral facial nerve palsy.

Adult↗
PubMed2001

Changes in trabecular bone turnover and bone marrow cell development in tail-suspended mice.

Skeletal unloading induces trabecular bone loss in loaded bones. The tail-suspended mouse model simulates conditions associated with lack of mechanical stress such as space flight for the loaded bones. In such a model, the tail supports the body weight. The forelimbs are normally loaded and the movement of its hindlimbs is free without weight bearing. Histomorphometric analyses of the murine tibiae of the elevated hindlimbs show that trabecular bone volume rapidly diminishes within one week and stabilizes at that level in the subsequent week of tail suspension. Two-week reloading after one-week unloading completely restores trabecular bone volume, but this does not happen after two-week unloading. Unloading for one or two weeks significantly reduces bone formation rate and increases both the osteoclast surface and number compared with age-matched ground control mice. Subsequent reloading restores reduced bone formation and suppresses increased bone resorption. In bone marrow cell cultures, the numbers of alkaline phosphatase (ALP)-positive colony-forming units-fibroblastic (CFU-f) and mineralized nodules are significantly reduced, but the numbers of adherent marrow cells and total CFU-f are unaltered after tail suspension. On the other hand, subsequent reloading increases the number of adherent marrow cells. Unloading for one week significantly increases the number of tartrate-resistant acid phosphatase (TRAP)- positive multinucleated cells compared with the control level. Our data demonstrate that tail suspension in mice reduces trabecular bone formation, enhances bone resorption, and is closely associated with the formation of mineralized nodules and TRAP-positive multinucleated cells in bone marrow cultures obtained from tibiae. Two-week reloading restores bone volume reduced after one-week unloading, but does not after two-week unloading. The tail-suspended model provides a unique opportunity to evaluate the physiological and cellular mechanisms of the skeletal response to unloading and reloading.

Journal Article↗
PubMed2000

HD-PTP: A novel protein tyrosine phosphatase gene on human chromosome 3p21.3.

A human cDNA encoding a novel protein tyrosine phosphatase has been isolated. The phosphatase has unique features in its domain structure: a "Zn-hand" domain containing several SH3-binding motifs, a tyrosine phosphatase domain, a C-terminal PEST motif, and an N-terminal domain similar to yeast BRO1, an apoptosis-related mammalian AIP1 and to a RHO-binding protein, Rhophilin. The gene is located at chromosome 3p21.3, an area frequently deleted in many types of cancer, especially within the functionally defined narrow region. The gene may be a human homolog of the rat PTP-TD14 gene reported by others, which can suppress H-ras-mediated transformation. We identified a hemizygous missense mutation in a lung cancer cell line. Thus, the phosphatase gene may be a candidate for one of the tumor suppressor genes located on 3p21.3.

Amino Acid Sequence↗
PubMed2000

Detection of differentially expressed genes in lymphomas using cDNA arrays: identification of clusterin as a new diagnostic marker for anaplastic large-cell lymphomas.

This study reports the first use of gene array technology for the identification of a tumor-specific marker in lymphoid neoplasms. The differential gene expression of 31 hematopoietic cell lines, representing most major lymphoma subgroups of B- and T-cell origin, was assessed by hybridizing labeled complementary DNA to Atlas human expression arrays containing 588 genes. Genes known to be specific for B, T, or myelomonocytic lineages were appropriately identified in the arrays, validating the general utility of this approach. One gene, clusterin, not previously known to be expressed in lymphoid neoplasms, was specifically found in all 4 anaplastic large-cell lymphoma (ALCL) cell lines, but not in any of the 27 remaining tumor lines. Using a monoclonal antibody against clusterin, its differential expression was confirmed by Western blotting and immunohistochemistry. A total of 198 primary lymphomas (representing most major lymphoma subtypes), including 36 cases of systemic ALCL, were surveyed for clusterin expression by immunohistochemistry and Western blotting. All of the 36 ALCL cases marked for clusterin, with most cases showing moderate to strong staining in the majority of neoplastic cells. Clusterin expression was not related to expression of anaplastic lymphoma kinase-1. With 2 exceptions, none of the remaining 162 non-ALCL cases marked with the clusterin antibody, including Hodgkin disease and primary cutaneous ALCL. In reactive lymphoid tissues, only follicular dendritic cells and fibroblastic reticular cells exhibited staining. Clusterin is a highly conserved glycoprotein implicated in intercellular and cell matrix interactions, regulation of the complement system, lipid transport, stress responses, and apoptosis. Although its function in ALCL is unknown, the unique expression of clusterin within this category of lymphoma provides an additional marker for the diagnosis of ALCL. This study illustrates the enormous potential of gene array technologies for diagnostic marker discovery. (Blood. 2000;96:398-404)

Biomarkers, Tumor↗
PubMed2000

Orexin-induced food intake involves neuropeptide Y pathway.

Orexins (orexin-A and -B) are recently identified neuropeptides, which are thought to be implicated in the regulation of feeding behavior. We used a NPY-Y1 receptor specific antagonist, BIBO3304, to examine whether NPY is involved in orexin-induced feeding behavior. Intracerebroventricular administration of orexin-A (10 nmol) induced food intake in rats (food intake for 3 h; vehicle 0.3+/-0.2 g vs. orexin-A 10 nmol, 4.0+/-0.5 g, n=4). Orexin-induced feeding behavior was partially inhibited by prior administration of BIBO3304 (3 h food intake: orexin-A 10 nmol, 4.0+/-0.5 g vs. BIBO3304 (60 microgram) + orexin-A 10 nmol, 2.2+/-0.2 g, n=4). A low dose of BIBO3304 (30 microgram) did not show a significant inhibitory effect. BIBO3457, an inactive enantiomer, used as a negative control, did not show any inhibitory effect on orexin-A-induced feeding behavior. Fos expression was observed in NPY-containing neurons in the arcuate nucleus 1 h after orexin-A (10 nmol) was administered intracerebroventricularly (control 0.3+/-0.08%, orexin-A 10.2+/-0.8%, n=5 rats/group). These observations suggest that NPY is involved in orexin-induced feeding behavior. However, BIBO3304 did not completely abolish the effect of orexin-A. These results suggest that orexin-A elicits feeding behavior partially via the NPY pathway. The NPY system could be the one of downstream pathways by which orexin-A induces feeding behavior. Another pathway may also be involved in orexin-A-induced feeding behavior, because BIBO3304 did not completely abolish orexin-A-induced feeding behavior.

Animals↗
PubMed2000

Analysis of expressed immunoglobulin heavy chain genes in familial B-CLL.

In this study, we wished to determine whether familial chronic lymphocytic leukemia of B-cell phenotype (CLL) shares with sporadic B-CLL the same immunoglobulin (Ig) heavy chain variable region (VH) gene usage and occurrence of somatic mutation, to gain insight into the pathogenetic relatedness of these epidemiologically distinct forms of CLL. We therefore analyzed the expressed Ig heavy chain genes in 23 cases (11 families) of familial CLL, and compared these results with data previously reported for sporadic CLL. In addition, we assessed the relationship of the occurrence of somatic mutation to several clinical and phenotypic features. The distribution of V genes among these cases was similar to that observed in sporadic CLL: VH3 > VH1 > VH4. Thirteen of the 23 cases (57%) showed germ line VH gene sequences, whereas somatic mutations were detected in 10 cases (43%). The average mutation frequency of these latter 10 cases of was 6.7% (ranging from 1.7% to 8.8%), and evidence of antigen selection was noted in 6. Intraclonal variation, followed by clonal evolution and the appearance of a second clone over a 20-year period was observed in 1 case, suggesting that mutations can continue to accumulate after neoplastic transformation. The presence of somatic mutations correlated with age at presentation, low white blood cell (WBC) count, and low fluorescence intensity of surface CD5, and the potential significance of these relationships is discussed. Our data indicate that familial and sporadic B-CLL display a similar pattern of immunoglobulin gene usage and frequency of somatic mutation, and are consistent with a common ontogeny and immunogenetic origin for these 2 epidemiologically distinct forms of CLL. (Blood. 2000;95:1413-1419)

Adult↗
PubMed2000

Infective endocarditis affecting both systemic and pulmonary circulations predisposed by a ventricular septal defect.

A 39-year-old woman was admitted to our hospital presenting persisting fever. An echocardiographic examination showed severe aortic and mitral valve regurgitation with moderate tricuspid regurgitation. Small left-to-right shunt through the ventricular septal defect was identified. Vegetation was also detected on the tricuspid, mitral, and aortic valves. At one month after admission, the patient showed sudden onset of headache and abdominal pain. A computed tomographic scan demonstrated cerebral and splenic infarction. A pulmonary perfusion scintigram demonstrated perfusion defects in left-S1 and right-S6 regions. At 4 months after admission, as operation was performed. The aortic valve was replaced with a #23 mm CarboMedics prosthesis and the mitral valve with a #29 mm Carbo Medics prosthesis. Tricuspid valve plasty was performed, with closure of He laceration and perforation of the anterior leaflet combined with a commissuroplasty, according to Kay's method. Ventricular septal defect was closed with a bovine pericardial patch. She was discharged at 19 days after the operation, and is leading a good life. Pervasion of the organism seemed to be initiated from the mitral valve which was conveyed by the blood stream to the aortic valve, and to the tricuspid valve through the ventricula septal defect. Left heart evaluation may be important in cases with infective endocarditis and ventricula septal defect.

Adult↗
PubMed2000

Isolation, characterization, and chromosomal mapping of an ftsZ gene from the unicellular primitive red alga Cyanidium caldarium RK-1.

The FtsZ protein is involved in eukaryote plastid division, but there is little information on its involvement in the plastid-dividing apparatus. To investigate the relationship between FtsZ and the plastid-dividing ring, the ftsZ gene was isolated from the unicellular primitive red alga Cyanidium caldarium RK-1. Comparison of several prokaryotic and eukaryotic FtsZ proteins shows that there are six highly conserved domains in the core region of FtsZ. To determine the chromosomal location of ftsZ, we first determined the electrophoretic karyotype of C. caldarium RK-1. Southern-hybridization analysis combined with CHEF revealed the chromosomes on which the ftsZ gene exist. Northern-hybridization analysis indicated that the C. caldarium RK-1 ftsZ gene is transcribed as a 1.9-kb molecule, and that the transcripts specifically accumulate just before plastid division. Phylogenetic analysis indicated that C. caldarium RK-1 and other eukaryotic ftsZ genes are the descendants of cyanobacterial ftsZ genes, supporting the current agreement that FtsZ is involved in plastid division.

Algal Proteins↗
PubMed2000

A putative mitochondrial ftsZ gene is present in the unicellular primitive red alga Cyanidioschyzon merolae.

Two ftsZ homologues were isolated from the unicellular primitive red alga Cyanidioschyzon merolae (CmftsZ1 and CmftsZ2). Phylogenetic analysis revealed that CmftsZ1 is most closely related to the ftsZ genes of alpha-Proteobacteria, suggesting that it is a mitochondrial-type ftsZ gene, whereas CmftsZ2 is most closely related to the ftsZ genes of cyanobacteria, suggesting that it is a plastid-type ftsZ gene. Southern analysis indicates that CmftsZ1 and CmftsZ2 are both single-copy genes located on chromosome XIV in the C. merolae genome. Northern analysis revealed that both CmftsZ1 and CmftsZ2 are transcribed, and accumulate specifically before cell and organelle division. The results of Western analysis suggest that CmFtsZ1 is localized in mitochondria.

Amino Acid Sequence↗
PubMed2000

Development of a new instrument to measure oxygen saturation and total hemoglobin volume in local skin by near-infrared spectroscopy and its clinical application.

The oxygen saturation (StO2) and total hemoglobin volume in cutaneous blood are closely related to cutaneous metabolism and are important factors in determining the skin color. Most conventional apparatuses for the measurement of cutaneous metabolism have been designed to evaluate qualitative changes in the oxyhemoglobin volume, deoxyhemoglobin volume, and their sum (total Hb volume) relative to their baseline values. In this study, we developed an instrument for non-invasive evaluation of individual and regional differences in StO2 and Hb volume, a system unaffected by melanin (Kao PSA system model III), and examined the validity of its application. First, changes in StO2 and total Hb volume in the antebrachial region during venous occlusion and devascularization by compression of the brachial region were evaluated. Changes in total Hb volume following venous occlusion were found to reflect the cutaneous blood flow. Also, StO2 was considered to reflect the state of oxygen consumption by the skin, because it was markedly reduced during devascularization. Next, the subjects were exposed to graded hypobaric conditions, and the relationships among StO2, arterial blood oxygen saturation (SaO2), and venous blood oxygen saturation (SvO2) were studied. StO2 showed significant positive correlations with SaO2 (r=0.811, P<0.001) and SvO2 (r=0.966, P<0.001), and its correlation with SvO2 was particularly strong. Therefore, StO2 was found to be closely dependent on SvO2. Lastly, StO2, total Hb volume, and other parameters were measured in healthy women (aged 20-69 years), and their regional differences and age-associated changes were evaluated. These regional differences (angle of mouth > cheek > forehead) and age-associated decreases in StO2 are considered to be caused by the age-associated decreases in the cutaneous blood flow.

Adult↗
PubMed2000

The effect of "living high-training low" on physical performance in rats.

In this research, we hypothesized that, in rats, adaptation to high altitude (2500 m) plus training at low altitude (610 m), "living high-training low", improves physical performance at low altitude more than living and training at low altitude (610 m). Rats were divided into four groups: (1) living at low altitude (LL, n=12), (2) living and training at low altitude (LLTL, n=13), (3) living at high altitude (LH, n=12), (4) living at high altitude and training at low altitude (LHTL, n=13). The program for living at high altitude involved raising rats under hypobaric hypoxia (equivalent to 2500 m), and the training program consisted of running on a treadmill at low altitude. All groups were raised at each altitude and trained to run at 35 m/min for 40 min/day, 6 days/week for 6 weeks. During this program, we measured heart rates both at rest and during exercise, and performed running-time trials. The mean heart rate during exercise was lower in groups with training than in groups without training, and the groups receiving training could run longer than the untrained groups. The LHTL group especially showed the lowest mean heart rate during exercise and the longest running time among all groups. After 6 weeks of the training program, all rats had a catheter implanted into the carotid artery, and the mean systemic arterial pressure was continuously measured during treadmill running. The rate of increase of this pressure as the running intensity increased was lower in groups with training than in groups without training, especially in the LHTL group. Finally, we anesthetized all the rats and extracted both the right and left ventricles, and the triceps surae and liver. Training increased the weight of the left ventricle, triceps surae, and liver. The increase in weight of the left ventricle and triceps surae was higher in the LHTL group than in the LLTL group in particular. It appeared that living high-training low may be an effective strategy to improve performance ability at low altitude.

Acclimatization↗
PubMed2000

Matrix metalloproteinase-9 and tensile strength of fetal membranes in uncomplicated labor.

OBJECTIVE: To analyze the relation between tensile strength and levels of matrix metalloproteinase-9, tissue inhibitor of metalloproteinase-1, and tissue inhibitor of metalloproteinase-2 at a number of sites in human fetal membranes. METHODS: Tensile strengths of fetal membranes from five women who delivered vaginally at term were measured by the method of modified force application. A piece of membrane at each measured site was then dissected, and the levels of matrix metalloproteinase-9, tissue inhibitor of metalloproteinase-1, and tissue inhibitor of metalloproteinase-2 were measured by sandwich enzyme immunoassay. The relationship between tensile strength and enzyme levels was evaluated by Scheffé F test at a total of 81 sites on the five membranes. RESULTS: The mean tensile strength of the membranes was 45.3 +/- 19.8 (mean +/- standard deviation) mmHg/0.3 mm(2) (n = 81). When the measured sites were divided according to tensile strength into four groups (<25, 25-49, 50-74, and >/=75 mmHg/0.3 mm(2)), the level of matrix metalloproteinase-9 (0.72 +/- 0.82 nmol/g protein, n = 12) in the less than 25 mmHg/0.3 mm(2) group was significantly higher than the other groups (0.35 +/- 0.22, 0.28 +/- 0.15, and 0.15 +/- 0.08 nmol/g protein; n = 39, 23, and 7, respectively). The significance level was still higher when the molar ratio of matrix metalloproteinase-9 to tissue inhibitor of metalloproteinase-1 was used for comparison. CONCLUSION: An increased molar ratio of matrix metalloproteinase-9 to tissue inhibitor of metalloproteinase-1 might be related to decreased tensile strength of human fetal membranes in uncomplicated labor.

Extraembryonic Membranes↗
PubMed2000

Dislocation propagation in GaN films formed by epitaxial lateral overgrowth

We have investigated by scanning electron microscopy (SEM) and transmission electron microscopy (TEM) the relationship between surface morphological evolution and dislocation propagation in GaN films formed by epitaxial lateral overgrowth (ELO) in hydride vapour phase epitaxy. The SEM observations revealed that step and terrace structures were formed on (0001) surfaces of the films both in the earlier and the later stages of growth, suggesting the occurrence of step-flow growth during ELO. Bending dislocations with laterally propagated segments were frequently observed in the ELO films and their morphology led to a reduction in threading dislocation density in the film surface regions. Systematic TEM observations were performed to reveal the detailed structure of the bending dislocations. Comparison between the SEM and the TEM results showed that the lateral propagation of the dislocation was closely related to the appearance of the [1101) facets. A mechanism for dislocation propagation is discussed that explains the observed dislocation structure and surface step morphology.

Journal Article↗
PubMed2000

Analyses of oxidative DNA damage and its repair activity in the livers of 3'-methyl-4-dimethylaminoazobenzene-treated rodents.

We measured the levels of 8-hydroxyguanine (8-OH-Gua) and its repair activity in the livers of the Donryu rat, the carcinogen-resistant DRH rat, and the ddy mouse, which were fed a 0.06% 3'-methyl-4-dimethylaminoazobenzene (3'-MeDAB)-containing diet. In a short-term rat experiment (maximum 2 months), 3'-MeDAB did not increase the 8-OH-Gua levels in the livers of the two rat strains, although it significantly increased the repair activity in only the Donryu rat liver at 1 and 2 months. After long-term 3'-MeDAB administration to the ddy mouse (8 months), the levels of 8-OH-Gua and its repair activity were increased in the liver by 3.6-fold and 1.6-fold, respectively. These experiments suggest that 3'-MeDAB increases 8-OH-Gua generation in rodent liver DNA and the 8-OH-Gua repair assay is a reliable marker of cellular oxidative stress induced by carcinogens.

Animals↗
PubMed2000

Plasma lactate concentration and muscle blood flow during dynamic exercise with negative-pressure breathing.

This study assessed the hypothesis that increasing cardiac filling pressure (CFP) would enhance contracting muscle blood flow (MBF) by stretching cardiopulmonary baroreceptors and attenuate the increase in plasma lactate concentration ([Lac(-)](p)) during dynamic exercise. Continuous negative-pressure breathing (CNPB) (-15 cmH(2)O) was used to increase the CFP by accelerating the venous return to the heart. In the first series of experiments, 10 men performed a graded exercise seated on a cycle ergometer with (N1) and without CNPB (C1). The increase in [Lac(-)](p) for N1 was attenuated at 60%, 90%, and 100% of maximal exercise intensity compared with that in C1 (P < 0.001). Also, the increases in mean arterial pressure (MAP) and plasma catecholamine concentrations were attenuated in N1 compared with those in C1 throughout the graded exercise (P < 0.05). However, heart rate and pulse pressure were not significantly influenced by CNPB. Second, we studied the impact of CNPB on forearm MBF during a rhythmic handgrip exercise in 5 of the 10 subjects. Forearm MBF was measured immediately after cessation of the exercise by venous occlusion plethysmography at rest, 30%, 50%, and 70% of maximal work load (WL(max)) with (N2) and without CNPB (C2). Forearm MBF and vascular conductance for both trials increased with the increase in intensity, but forearm skin blood flow measured by laser-Doppler flowmetry remained unchanged. MBF and vascular conductance in N2, however, increased more than in C2 at every intensity (P < 0.01) except for MBF at 70% WL(max), whereas the increase in MAP for N2 was attenuated compared with that in C2 (P < 0.05). Thus augmented active muscle vasodilation occurred in N2 with a lower increase in MAP compared with that in C2. These findings suggest that the stretch of intrathoracic baroreceptors, such as cardiopulmonary mechanoreceptors, by CNPB increased MBF by suppressing sympathetic nerve activity. The attenuation of the increase in [Lac(-)](p) might be caused, at least partially, by the increased MBF.

Adult↗
PubMed2000

Antemortem evaluation for magnetic resonance imaging of the equine flexor tendon.

In this study antemortem evaluation of equine flexor tendons--the superficial digital flexor tendon and the deep digital flexor tendon--using magnetic resonance (MR) images was performed. Postmortem flexor tendons were used to prepare the slice positions, coil and body positions for MR imaging. It was possible by this method to take antemortem MR images of equine limbs that distinguished features as well as postmortem images described in previous studies. The total time of antemortem scanning was about 40 min. This study is the first to report antemortem MR images in horses.

Anesthesia, Inhalation↗