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Biomedical subjects

A Yoshioka

Publications and source records attributed to A Yoshioka.

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

Effects of one-legged endurance training on femoral arterial and venous size in healthy humans.

The cross-sectional area (CSA) of large-conductance arteries increases in response to endurance training in humans. To determine whether training-induced changes in arterial structure are systemic in nature or, rather, are confined to the arteries supplying exercising muscles, we studied 10 young men who performed one-legged cycle training [80% of one-legged peak O2 uptake (VO2 peak)), 40 min/day, 4 days/wk] for 6 wk and detraining for another 6 wk. There were no significant differences in baseline one-legged VO2 peak) and CSA of the common femoral artery and vein (via B-mode ultrasound) between experimental and control legs. In the experimental leg, one-legged VO2 peak) increased 16% [from 3.0 +/- 0.1 to 3.4 +/- 0.1 (SE) l/min], arterial CSA increased 16% (from 84 +/- 3 to 97 +/- 5 mm2), and venous CSA increased 46% (from 56 +/- 5 to 82 +/- 5 mm2) after endurance training. These changes returned to baseline during detraining. There were no changes in one-legged VO2 peak) and arterial CSA in the control leg, whereas femoral venous CSA in the control leg significantly increased 24% (from 54 +/- 5 to 67 +/- 4 mm2) during training. Changes in femoral arterial and venous CSA in the experimental leg were positively and significantly related to corresponding changes in one-legged VO2 peak) (r = 0.86 and 0.76, respectively), whereas there were no such relations in the control leg (r = 0.10 and 0.17). When stepwise regression analysis was performed, a primary determinant of change in VO2 peak) was change in femoral arterial CSA, explaining approximately 70% of the variability. These results support the hypothesis that the regional increase in blood flow, rather than systemic factors, is associated with the training-induced arterial expansion. Femoral arterial expansion may contribute, at least in part, to improvement in efficiency of blood transport from the heart to exercising muscles and may facilitate achievement of aerobic work capacity.

Adult↗
PubMed2001

Amyotrophic lateral sclerosis associated with sarcoidosis.

We report a rare association of amyotrophic lateral sclerosis (ALS) with incidental pulmonary and muscle sarcoidosis. A 63-year-old woman presented with slowly progressive weakness and atrophy of the extremities starting from the left leg. The biopsy of a small mass in the left gastrocnemius revealed a typical sarcoid nodule. She was treated with corticosteroid for possible sarcoid neuromyopathy. In spite of the treatment, her clinical course was relentlessly progressive and she died of bulbar palsy. Autopsy revealed a loss of motor neurons in the anterior horn, vacuolar degeneration of the lateral funiculus, and noncaseating granulomas in paratracheal lymph nodes and lungs. No granulomatous lesion or cellular infiltration was found in the spinal cord.

Amyotrophic Lateral Sclerosis↗
PubMed2001

Effects of water depth on abdominal [correction of abdominails] aorta and inferior vena cava during standing in water.

During water immersion bradycardia and increase in stroke volume induce by changing in hydrostatic pressure. We hypothesised that the cardiac alterations with immersion are associates with an increase in venous return from lower body. Because the venous return reflects volume of capacitance vein e.g, inferior vena cava. Therefore, we clarified the effects of water immersion on the size in left ventricle, aorta, and vena cava.

Adult↗
PubMed2000

Small GTPase Rab4 regulates Ca2+-induced alpha-granule secretion in platelets.

Upon activation, platelets release many active substances stored in alpha- and dense-core granules. However, the molecular mechanisms governing regulated exocytosis are not yet fully understood. Here, we have established an assay system using permeabilized platelets to analyze the Ca(2+)-induced exocytosis of both types of granules, focusing on RabGTPases. Incubation with Rab GDP dissociation inhibitor, an inhibitory regulator of RabGTPases, reduced membrane-bound RabGTPases extensively, and caused strong inhibition of the Ca(2+)-induced secretion of von Willebrand factor (vWF) stored in alpha-granules, but not that of [(3)H]5-hydroxytryptamine (5-HT) in dense-core granules. Specifically, Rab4 co-fractionated with vWF and P-selectin (an alpha-granule marker) upon separation of platelet organelles by density gradient centrifugation. Incubation of the permeabilized platelets with cell extracts expressing the dominant negative mutant of His-tagged Rab4S22N, but not with those of similar mutant His-Rab3BT36N, inhibited the vWF secretion, whereas neither of the cell extracts affected the [(3)H]5-HT secretion. Importantly, the inhibition of vWF secretion was rescued by depleting the cell extracts of the His-Rab4S22N with nickel beads. Thus, in platelets, the regulatory mechanisms governing alpha- and dense-core granule secretions are distinct, and Rab4 is an essential regulator of the Ca(2+)-induced exocytosis of alpha-granules.

Bacterial Proteins↗
PubMed2000

Segregation of a pure form of spastic paraplegia and NOR insertion into Xq11.2.

A 3-year-old boy, his 7-year-old brother, and a maternal uncle had a pure form of spastic paraplegia and a variant X chromosome with a faintly stained gap at Xq11.2. The mother of the propositus also had the variant X chromosome but was clinically unaffected. Three other unaffected females in the family did not have the variant X chromosome. The gaps in the variant X chromosome from the affected members and the mother were Ag-NOR staining positive, C-banding negative, rDNA FISH analysis positive, and alpha-satellite FISH analysis negative. The gap, therefore, represented an insertion of the nucleolus organizer region (NOR) derived from the short arm of an acrocentric chromosome. The variant X chromosome of the mother was randomly inactivated, as evidenced by BrdU replication analysis of her Epstein-Barr virus-transformed lymphoblastoid cells. Because mutations of the proteolipid protein gene at Xq21 have been responsible for a pure form of spastic paraplegia, this was also investigated but found to be negative in all affected relatives. Summing up these findings, it is proposed that the NOR insertion in the affected members of the family disrupted a hitherto unknown gene for a pure form of spastic paraplegia, situated at Xq11.2, and caused the disorder.

Adult↗
PubMed2000

Factor VIII C2 domain contains the thrombin-binding site responsible for thrombin-catalyzed cleavage at Arg1689.

Thrombin-catalyzed factor VIII activation is an essential positive feedback mechanism regulating intrinsic blood coagulation. A factor VIII human antibody, A-FF, with C2 epitope, exclusively inhibited factor VIII activation and cleavage at Arg(1689) by thrombin. The results suggested that A-FF prevented the interaction of thrombin with factor VIII and that the C2 domain was involved in the interaction with thrombin. We performed direct binding assays using anhydro-thrombin, a catalytically inactive derivative of thrombin in which the active-site serine is converted to dehydroalanine. Intact factor VIII, 80-kDa light chain, 72-kDa light chain, and heavy chain fragments bound dose-dependently to anhydro-thrombin, and the K(d) values were 48, 150, 106, and 180 nm, respectively. The C2 and A2 domains also dose-dependently bound to anhydro-thrombin, and the K(d) values were 440 and 488 nm, respectively. The A1 domain did not bind to anhydro-thrombin. A-FF completely inhibited C2 domain binding to anhydro-thrombin (IC(50), 18 nm), whereas it did not inhibit A2 domain binding. Furthermore, C2-specific affinity purified F(ab)'(2) of A-FF, and the recombinant C2 domain inhibited thrombin cleavage at Arg(1689). Our results indicate that the C2 domain contains the thrombin-binding site responsible for the cleavage at Arg(1689).

Antibodies, Monoclonal↗
PubMed2000

Non-N-methyl-D-aspartate glutamate receptors mediate oxygen--glucose deprivation-induced oligodendroglial injury.

Cells of oligodendroglial lineage are susceptible to oxygen and glucose deprivation. When oligodendrocyte-like cells differentiated from CG-4-immortalized rat O-2A progenitor cells were exposed to hypoxia alone or glucose deprivation alone for 48 h, release of lactate dehydrogenase (LDH) into the culture medium did not increase. However, when cells were deprived of both oxygen and glucose for 6 or 12 h preceding reoxygenation for 2 h, LDH release increased. Adding glucose to the medium protected against cell death and increased lactate production in a concentration-dependent manner. Cell damage induced by deprivation of oxygen and glucose was prevented by calcium-free medium or by non-N-methyl-D-aspartate glutamate receptor (GluR) antagonists, such as 6-cyano-7-nitroquinoxaline-2,3-dione or LY293558, but not by the voltage-dependent calcium channel blocker, nimodipine, or by the N-methyl-D-aspartate GluR antagonist, MK-801. The glutamate concentration in the medium from cells exposed to oxygen-glucose deprivation for 12 h was 49.70+/-3.04 microM/l, which is sufficient to activate GluRs during deprivation of oxygen and glucose. Apoptotic cells detected by terminal deoxynucleotidyl transferase (TdT)-mediated dUTP-biotin nick end-labeling (TUNEL) or Hoechst 33258 staining did not increase in cells exposed to oxygen-glucose deprivation for 12 h and subsequent reoxygenation for 2 h. No DNA laddering was detected by agarose gel electrophoresis from cells exposed to deprivation of oxygen and glucose. Neither acetyl-YVAD-CHO, an inhibitor of caspase-1-like proteases, nor acetyl-DEVD-CHO, an inhibitor of caspase-3-like proteases, prevented oxygen-glucose deprivation-induced injury. Thus, oxygen and glucose deprivation causes calcium-influx-induced necrotic cell damage in cells of oligodendroglial lineage via non-N-methyl-D-aspartate GluR channels.

Animals↗
PubMed2000

An immunohistochemical and ultrastructural study of a follicle-stimulating hormone-secreting gonadotroph adenoma occurring in a 10-year-old girl.

Female gonadotroph adenomas with endocrinological symptoms are uncommon. Six cases of such adenomas have been reported in the literature: two were girls who presented with precocious puberty and four were premenopausal women with accompanying multiple ovarian cysts. We describe here a 10-year-old Japanese girl with a gonadotroph macroadenoma and present detailed morphological findings of the tumor. The patient's chief complaints were nausea, abdominal distention, and abdominal pain. Abdominopelvic ultrasonography and magnetic resonance imaging (MRI) revealed bilateral multiple ovarian cysts. Endocrinological assays showed elevated serum follicle-stimulating hormone (FSH) (33.7 mIU/ml) and estradiol (3840 pg/ml). MRI of the head showed a large pituitary tumor. Two transsphenoidal operations and subsequent radiation therapy were performed. Immunohistochemically, more than half the tumor cells were positive for anti-FSH-beta monoclonal antibody. Ultrastructurally, the tumor cells exhibited a fairly uniform picture of rounded cells. Their nuclei were slightly irregular and contained heterochromatin, and their cytoplasm contained many round, dense core granules, measuring 140-260 nm in diameter, together with well-developed organelles. An in vitro study showed that the tumor cells in primary culture produced FSH (1089.0 mIU/ml). To our knowledge, this is the first immunohistochemical and ultrastructural study of an FSH-secreting gonadotroph adenoma occurring in childhood.

Adenoma↗
PubMed2000

Guillain-Barré syndrome in a child with systemic lupus erythematosus and anti-Ro/SSA and anti-La/SSB autoantibodies.

We report a 9-year follow-up of a girl with systemic lupus erythematosus (SLE) and probable Sjögren's syndrome. At the age of 7 years, the patient developed a chilblain-like eruption with features of SLE, including leucopenia, oral ulcers, positive rheumatoid and antinuclear antibodies and positive anti-dsDNA, anti-Ro/SSA and anti-La/SSB antibodies. At the age of 13 years she developed Guillain-Barré syndrome, which completely resolved with aggressive treatment, including high-dose corticosteroids and the use of plasma exchange followed by intravenous gammaglobulin.

Autoantibodies↗
PubMed2000

Cyclic GMP/cyclic GMP-dependent protein kinase system prevents excitotoxicity in an immortalized oligodendroglial cell line.

Previously, we have demonstrated that excitotoxicity of oligodendrocyte-like cells (OLC), differentiated from immortalized rat O-2A progenitor cells (CG-4 cells), is prevented by cyclic AMP-elevating agents. We now report that some agents that elevate cyclic GMP prevent OLC excitotoxicity. Kainate-induced injury was prevented by cyclic GMP analogues (8-bromo-cyclic GMP and dibutyryl cyclic GMP), a guanylate cyclase activator [atrial natriuretic peptide (ANP)], and phosphodiesterase inhibitors [3-isobutyl-1-methylxanthine (IBMX), ibudilast, propentofylline, and rolipram]. When both forskolin and 8-bromo-cyclic GMP were added, kainate-induced injury was additively prevented. There was a strong positive correlation between suppression of kainate-induced Ca2+ influx and prevention of injury by these chemicals. The measurement of intracellular cyclic AMP and cyclic GMP by radioimmunoassay demonstrated the following: an increase of cyclic GMP with treatment with 8-bromo-cyclic GMP, dibutyryl cyclic GMP, and ANP; an increase of cyclic AMP with treatment with ibudilast and rolipram; and an increase of both cyclic AMP and cyclic GMP with treatment with IBMX and propentofylline. Kainate-induced Ca2+ influx was decreased by 8-(4-chlorophenylthiol)-guanosine-3',5'-monophosphate, an activator of cyclic GMP-dependent protein kinase (PKG), or okadaic acid, an inhibitor of protein phosphatases 1 and 2A. RT-PCR and westem blotting of OLC demonstrated transcription of PKG II gene and translation of PKG Ibeta mRNA, but no translation of PKG Ialpha mRNA. Therefore, we concluded that the cyclic GMP/PKG system prevents OLC excitotoxicity.

Animals↗
PubMed2000

Autoantibody responses to cardiolipin and DNA in infancy: association with lymphocytic panniculitis.

We report an infant with anticardiolipin (aCL) antibodies who presented with erythematous nodular skin lesions and elevated liver enzyme levels. The cutaneous manifestation was histologically lymphocytic lobular panniculitis with vasculitic and hemorrhagic changes. The infant also had low levels of anti-double stranded DNA (dsDNA) and anti-single stranded DNA (ssDNA) antibodies. There were no detectable antibodies to small nuclear ribonucleoproteins including Ro/SSA and La/SSB. His mother was consistently seronegative for any of these antibodies. Without corticosteroid therapy, cutaneous lesions resolved and anticardiolipin antibodies, but not anti-dsDNA and ssDNA antibodies, normalized within 16 months after the onset of the disease. Our patient demonstrated an uncommon presentation of aCL related cutaneous manifestation, the presentation with panniculitis being only the third such patient reported in the literature. Of great interest was the appearance of aCL antibodies and skin lesions during very early infancy.

Adult↗
PubMed2000

Expression of intrapulmonary surfactant apoprotein-A in autopsied lungs: comparative study of cases with or without pulmonary hypoplasia.

To investigate the functional maturity of the lungs of infants with pulmonary hypoplasia, we measured the expression of surfactant apoprotein-A (SP-A) in the autopsied lungs. Autopsied lungs were taken from 16 infants who died at birth or soon after. A lung-to-body weight ratio of less than 1.2% was defined as pulmonary hypoplasia. Eight infants were classified as belonging to the normal group, and eight as belonging to the pulmonary hypoplasia group. Many of the pulmonary hypoplasia group were complicated not only by pulmonary hypoplasia, but also by amniotic fluid volume abnormalities or an anatomical malformation. We measured the expression of SP-A immunologically using murine anti-human SP-A MAb in the autopsied lung tissue, and subjected the tissue to SP-A staining by the direct staining method. The expression of SP-A was assessed as one of four grades: -, +/-, 1+, 2+. The staining intensity of SP-A was high at 1+ or stronger in five infants of the normal group. SP-A expression was significantly reduced, however, in all infants of the pulmonary hypoplasia group except for one infant with normal amniotic fluid volume and relatively mild pulmonary hypoplasia. There was a significant negative correlation between the staining intensity of SP-A and two factors: pulmonary hypoplasia and abnormal amniotic fluid volume (p = 0.039 and p = 0.0063, respectively). In the present study, we demonstrated that SP-A expression was significantly reduced in infants with pulmonary hypoplasia. We speculate that the functional maturity of the lungs of infants with pulmonary hypoplasia is also suppressed.

Autopsy↗
PubMed2000

[Analysis of glomerular anionic charge status in renal biopsy specimens of childhood minimal change nephrotic syndrome using confocal laser scanning microscopy].

Analysis of glomerular anionic charge in human renal biopsy specimens has been restricted previously to staining of sites at the electron microscopic level, which is a product that needs skills and precludes a wide observable area. The introduction of a new tool, confocal laser scanning microscopy together with FITC conjugated poly-L-lysine as a cationic tracer, which demonstrates fixed anionic sites in thin sections from routinely formalin-fixed and paraffin-embedded renal biopsy tissue, has now enabled glomerular charge at light microscopic level. In this method, the patterns of staining in tissue showing minimal change nephrotic syndrome (MCNS) indicate that the intensity of anionic charge in 4 children with heavy proteinuria was significantly less than that in 7 children without proteinuria at remission, supporting previous observations using electron microscopy. Furthermore, staining the serial sections after methylation or saponification revealed that carboxyl components such as sialic acid may be responsible for proteinuria. We anticipate that this method may facilitate the investigation of the participation of charged components in the pathogenesis of MCNS and their role in relation to glomerular proteinuria.

Adolescent↗
PubMed2000

[Two cases of thalamic infarction presenting with "thalamic astasia"].

We report two cases of so-called 'thalamic astasia', associated with thalamic infarction. A 76-year-old-man suddenly noted to fall down to the left side without severe hemiparesis. An MRI showed an infarction in the superolateral portion of the right thalamus. Over eight weeks, his astasia gradually disappeared. A 69-year-old-man suddenly noted inability to stand with loss of balance. He showed mild hemiparesis, hypesthesia and cerebellar signs on the right side. Although right hemiparesis was slight, he was unable to stand by himself. An MRI demonstrated an infarction in the ventrolateral to ventroposterior portion of the left thalamus. Three weeks later, his symptoms except for cerebellar ataxia remarkably disappeared. The overlapped MRI lesions of these two cases were localized in the ventrolateral thalamus, such as Vimi (nucleus ventrointermedii internus), Vci (nucleus ventrocaudalis internus), Cemc (nucleus centralis thalami magnocellularis). These lesions are so-called 'vestibular thalamic nuclei', in which fibers from vestibulocerebellum are terminated. Involvement of the thalamic connectivity explains that two patients noted inability to stand. Thus we concluded that these two patients had thalamic astasia, described by Masdeu and Gorelick.

Aged↗
PubMed2000

Pharmacokinetics, prophylactic effects, and safety of a new recombinant FVIII formulated with sucrose (BAY 14-2222) in Japanese patients with hemophilia A.

A clinical trial of BAY 14-2222, a recombinant factor VIII preparation (rFVIII) manufactured by new purification and formulation processes using sucrose as a stabilizer instead of human serum albumin, was performed in 5 previously treated Japanese patients with severe hemophilia A. In stage I, a single dose of BAY 14-2222 and Kogenate (a currently licensed rFVIII preparation) was administered alternately in the same patients to compare the pharmacokinetics of the 2 compounds using FVIII:C (FVIII clotting activity) as the measure of plasma drug levels. The normalized area under the curve (AUCnorm) and normalized maximal concentration (Cmax,norm) were slightly lower following the administration of BAY 14-2222 than those after the administration of Kogenate (ratio of BAY 14-2222/Kogenate:AUCnorm = 0.88, P = .050; and Cmax,norm = 0.87, P = .041). However, the biological half-life (t1/2) did not differ significantly between the 2 preparations (13.96 +/- 4.18 vs. 13.48 +/- 2.40 hours). The in vivo recovery of FVIII was 67.9 +/- 11.3% after the administration of BAY 14-2222 and 74.4 +/- 5.3% after the administration of Kogenate. In stage II, BAY 14-2222 was administered regularly to the 5 patients with hemophilia at single doses of 20 to 40 IU/kg 3 times weekly for 4 weeks, and its prophylactic effect on bleeding was evaluated. Results indicated that BAY 14-2222 has a good preventive effect on bleeding. Sixty-six infusions were performed in stages I and II of this trial, and no adverse reactions related to BAY 14-2222 were observed. In addition, there were no FVIII inhibitors or antibodies to foreign proteins detected. The trial confirmed that BAY 14-2222 is similar to Kogenate with respect to t1/2 and the in vivo recovery of FVIII:C and that periodic infusions for 4 weeks can be well tolerated. In addition, it was shown that BAY 14-2222 is effective in preventing bleeding. Thus it is expected that BAY 14-2222 will exhibit a hemostatic effect comparable to that of Kogenate in patients with hemophilia A.

Adolescent↗
PubMed2000

An alloantibody recognizing the FVIII A1 domain in a patient with CRM reduced haemophilia A due to deletion of a large portion of the A1 domain DNA sequence.

We report the development of a FVIII inhibitor in a patient with severe, cross reacting material reduced (CRM(R)) haemophilia A. The level of Factor VIII antigen (FVIII:Ag) measured by ELISA using anti-C2 monoclonal and alloantibodies was 1.9 U/dl. This baseline FVIII:Ag level was increased to 8.3 U/dl after administration of DDAVP. The anti-FVIII inhibitor titer was 2.9 Bethesda U/ml. DNA analysis showed a large deletion of the FVIII gene from exon 4 to 7, corresponding to amino acid residues 111-317 included within the A1 domain. The size of the gene deletion was approximately 28 kb. 5' and 3' breakpoints were identified by sequencing in intron 3 and intron 7, respectively. FVIII mRNA was detected in the patient's peripheral lymphocytes and the deletion spanning exon 4 to 7 was confirmed at the RNA level. Immunoprecipitation experiments using 125I labeled A1, A2 and light chain demonstrated that the inhibitor reacted only with the 54 kDa A1 domain. The inhibitor activity was more than 95% neutralized by A1 domain polypeptide. Our findings suggest a close relationship between the inhibitor epitope and the specific gene deletion with regard to the pathogenesis of the inhibitor in this patient.

Adult↗