Acute vocal cord paralysis in hereditary neuropathy with liability to pressure palsies.
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Acute Disease↗
Biomedical subjects
T Wada
Publications and source records attributed to T Wada.
A point mutation in a cadherin gene, Cdh23, causes deafness in a novel mutant, Waltzer mouse niigata.
A novel mouse model for human nonsyndromic hearing loss, Waltzer niigata (v(ngt)), is found and subjected to positional cloning analysis. Genome-wide scan of 1648 backcross mice maps v(ngt) to the D10Mit258 locus near Waltzer (v). Recombination breakpoints are positioned on a physical map consisting of 13 BACs relative to the flanking markers in the vicinity of v(ngt). Allelism test done in parallel shows that v(ngt) and v are allelic. Sequence analysis reveals one-base deletion in the cDNA encoding a cadherin-related protein, Cdh23, mutation of which is recently reported in v mutants. The frame-shift change, producing a truncated protein of 51 amino acids, is ascribed to a base-substitution of G to A in the acceptor site of splicing junction which is predicted to cause one-base shift of the splicing position.
Animals↗
Regulation of oligodendrocyte development.
Oligodendrocytes are myelinating cells in the central nervous system. Recent studies demonstrated that oligodendrocyte progenitor cells are generated from a restricted region in the ventricular zone. In the rodent spinal cord, progenitor cells appear from narrow and bilateral longitudinal columns in the ventral ventricular zone, and then migrate dorsally. This ventral-specific appearance of oligodendrocyte progenitors may be controlled along the dorso-ventral axis in the spinal cord by extrinsic signals secreted from both the dorsal and ventral cords. The combined action of the Notch signaling pathway and a basic helix-loop-helix class of transcription factors may modulate this early specification of spinal oligodendrocytes and also be involved in multiple steps of oligodendrocyte differentiation.
Animals↗
Differential expression of three sialidase genes in rat development.
Mammalian sialidases have been reported to give a great influence on a number of cellular functions including cell differentiation and cell growth by removal of sialic acids from glycoproteins and gangliosides. To understand the roles of the sialidases during development, we investigated expression pattern of three types of sialidase in developing rat brain and liver. For this purpose we cloned a new membrane-associated sialidase cDNA from rat brain. The cDNA encodes 418 amino acids containing three ASP-boxes characteristic of sialidases and the major transcript of 3.5 kb is highly expressed in brain and cardiac muscle but low in liver. Competitive polymerase chain reaction methods were developed to evaluate the mRNA level together with activity assays in comparison with cytosolic and lysosomal sialidases previously obtained. The results indicate that the expression of individual sialidase genes is spatiotemporally controlled with distinct roles in determining the concentration and components of sialo-glycoconjugates during development.
Amino Acid Sequence↗
Syntheses and redox properties of bis(hydroxoruthenium) complexes with quinone and bipyridine ligands. Water-oxidation catalysis.
The novel bridging ligand 1,8-bis(2,2':6',2"-terpyridyl)anthracene (btpyan) is synthesized by three reactions from 1,8-diformylanthracene to connect two [Ru(L)(OH)]+ units (L = 3,6-di-tert-butyl-1,2-benzoquinone (3,6-tBu2qui) and 2,2'-bipyridine (bpy)). An addition of tBuOK (2.0 equiv) to a methanolic solution of [RuII2(OH)2(3,6-tBu2qui)2(btpyan)](SbF6)2 ([1](SbF6)2) results in the generation of [RuII2(O)2(3,6-tBu2sq)2(btpyan)]0 (3,6-tBu2sq = 3,6-di-tert-butyl-1,2-semiquinone) due to the reduction of quinone coupled with the dissociation of the hydroxo protons. The resultant complex [RuII2(O)2(3,6-tBu2sq)2(btpyan)]0 undergoes ligand-localized oxidation at E1/2 = +0.40 V (vs Ag/AgCl) to give [RuII2(O)2(3,6-tBu2qui)2(btpyan)]2+ in MeOH solution. Furthermore, metal-localized oxidation of [RuII2(O)2(3,6-tBu2qui)2(btpyan)]2+ at Ep = +1.2 V in CF3CH2OH/ether or water gives [RuIII2(O)2(3,6-tBu2qui)2(btpyan)]4+, which catalyzes water oxidation. Controlled-potential electrolysis of [1](SbF6)2 at +1.70 V in the presence of H2O in CF3CH2OH evolves dioxygen with a current efficiency of 91% (21 turnovers). The turnover number of O2 evolution increases to 33,500 when the electrolysis is conducted in water (pH 4.0) by using a [1](SbF6)2-modified ITO electrode. On the other hand, the analogous complex [RuII2(OH)2(bpy)2(btpyan)](SbF6)2 ([2](SbF6)2) shows neither dissociation of the hydroxo protons, even in the presence of a large excess of tBuOK, nor activity for the oxidation of H2O under similar conditions.
Journal Article↗
Molecular recognition studies on supramolecular systems. 32. Molecular recognition of dyes by organoselenium-bridged bis(beta-cyclodextrin)s.
A series of novel bis(beta-cyclodextrin)s tethered with organoselenium linkers, i.e., 6,6'-(o-phenylene-diseleno)-bridged bis(beta-cyclodextrin) (2), 6,6'-[2,2'-diselenobis(benzoyloxy)]-bridged bis(beta-cyclodextrin) (3), and 6,6'-[2,2'-diselenobis[2-(benzoylamino)ethylamino]]-bridged bis(beta-cyclodextrin) (4), were synthesized from beta-cyclodextrin (1). The inclusion complexation behavior of 1-4 with some dyes, such as 8-anilinonaphthalenesulfonate (ANS), Brilliant Green, Crystal Violet, Tropaeolin OO, Auramine O, and Methyl Orange, was investigated in aqueous phosphate buffer solution (pH 7.20) at 25 degrees C by UV-vis, fluorescence, and circular dichroism spectrometry, as well as fluorescence lifetime measurements. The complex stability constants (Ks) and Gibbs free energy changes (delta Go) for the stoichiometric 1:1 inclusion complexation of 1-4 with the dyes were obtained by the spectrophotometric or spectropolarimetric titrations. The bis(beta-cyclodextrin)s 2-4 showed much higher affinities toward these guest dyes than native beta-cyclodextrin 1 with fairly good molecular selectivities. The cooperative binding abilities of these bis(beta-cyclodextrin)s are discussed from the viewpoints of size/shape-fit interaction, induced-fit concept, and multiple recognition mechanism.
Journal Article↗
Fluorometric studies on inclusion complexation of L/D-tryptophan by beta-cyclodextrin 6-O-pyridinecarboxylates.
Novel beta-cyclodextrin (beta-CD) derivatives, bearing a nicotinic or isonicotinic moiety, have been synthesized by a convenient method in 21 and 25% yields, respectively. The stability constants (K) and Gibbs free energy changes (-DeltaG degrees ) for the inclusion complexation of beta-cyclodextrin 6-O-mono(3-pyridinecarboxylate) (1), 6-O-mono(4-pyridinecarboxylate) (2), and 6-O-monobenzoate (3) with L- and D-tryptophan have been determined by spectrofluorome try in aqueous buffer solution (pH = 7.20) at 25.0 degrees C. All of the modifications dramatically enhanced the original K for beta-CD by a factor of 30-280 and interestingly switched the original enantiomer preference for L- to D-tryptophan, thus affording the inverted enantio-selectivities of K(L)/K(D) = 2.5 for beta-CD and K(D)/K(L) = 1.2-2.1 for the modified CDs 1-3. These results are discussed from the viewpoints of the size-fit and geometrical complementary relationship between the host and guest.
Carboxylic Acids↗
Left ventricular free wall rupture possibly induced by coronary spasm. Surgical repair in the emergency room.
A 68-year-old woman complained of chest discomfort after a traffic accident in which she driving hit a child. At about twenty-five minutes later, she went into sudden cardiogenic shock due to acute myocardial infarction caused by non-occlusive intracoronary thrombosis without significant organic coronary stenosis and without any sign of extraluminal contrast pooling on coronary angiography. She was transported to our emergency room by ambulance because of cardiac tamponade caused by a left ventricular free wall rupture following the acute myocardial infarction. On arrival, she was near cardio-pulmonary arrest on intraaortic balloon pumping. We performed emergency open cardiac massage and pericardiotomy. The hairline perforation responsible for the blowout-type left ventricular free wall rupture was successfully closed with Teflon-reinforced sutures. In conclusion, it was strongly suspected that the present case of left ventricular free wall rupture was caused by acute myocardial infarction due to intracoronary thrombosis following coronary spasm without significant organic coronary stenosis or rupture of atheromatous plaque.
Aged↗
Myofascial flap without skin for intra-oral reconstruction. 1: Animal studies.
BACKGROUND: Although myofascial flaps are already used clinically in intra-oral reconstruction, the source and process of epithelialization remain unclear. METHODS: The process of epithelialization of grafted myofascia in the oral cavity was investigated using the latissimus dorsi muscle of Wistar strain rats. RESULTS: The use of myofascial tissue to fill in defects may maintain the space by preventing shrinkage and contracture of the wound, and this myofascial tissue may induce regeneration of the mucosal epithelium. Myofascia itself did not have the potential to epithelialize. Epithelialization progressed gradually along the surface of the granulated myofascia from the surrounding incised mucosal margin of the recipient site to the central portion. Immunohistochemical staining showed that keratinocyte growth factor-expressing cells were found mainly in the granulated myofascia. Within the study period, regenerated epithelium with orthokeratosis consisting of stratified squamous cells was thin and had scanty rete pegs, but it was similar to normal epithelium. CONCLUSION: Grafted myofascia in the oral cavity may play a space-making role, and induce regeneration of the mucosal epithelium, associated with the production of keratinocyte growth factor.
Animals↗
Myofascial flap without skin for intra-oral reconstruction. 2: Clinical studies.
BACKGROUND: Based on the results of our animal experiment, we evaluated the clinical usefulness of myofascial graft materials in the reconstruction of intra-oral soft-tissue defects. METHODS: An axial-pattern or random-pattern myofascial flap was grafted to reconstruct oral soft-tissue defects caused by tumor resection in ten patients. A pectoralis major myofascial flap was employed in four patients, and a platysma myofascial flap was employed in six patients. RESULTS: All flaps survived, and epithelialization progressed gradually from the surrounding incised mucosal margin. Cicatricial contracture of the wound seemed to be mild and the regenerated mucosa was more flexible than skin. Because the myofascial tissue had only raw surfaces, the handling of the flaps in the oral cavity was very flexible. Moreover, cosmetically unsatisfactory scar formation and dysfunction at the donor site were mild. CONCLUSION: We feel that the myofascial graft procedure is a very useful option for the reconstruction of intra-oral soft-tissue defects, and will soon become a common procedure. We refer to this procedure as the "biological-guided mucosa regeneration (BGMR)" technique.
Adult↗
Oral etoposide following combination chemotherapy and radiation therapy in a patient with advanced adult neuroblastoma led to long survival.
Although neuroblastoma is a common tumor of early childhood, it is rare in adults. In spite of the poor prognosis of advanced neuroblastoma in adults, there is still no effective treatment for this condition in adults. Here we report that oral etoposide salvage chemotherapy was able to prolong the survival of an adult patient with advanced neuroblastoma. A 26-year-old man had advanced neuroblastoma that was resistant to combination intravenous chemotherapy and radiation therapy. He was then treated with oral etoposide, at a dose of 50 mg daily for 5 days in a 21-day course. Toxicity was very mild and he was followed as an outpatient while he received 76 courses of this oral etoposide salvage chemotherapy. Seventy months after diagnosis, this patient is still alive and has no new distant metastases.
Administration, Oral↗
SH2-containing inositol phosphatase 2 negatively regulates insulin-induced glycogen synthesis in L6 myotubes.
AIMS/HYPOTHESIS: PI(3,4,5)P3 produced by PI3-kinase seems to be a key mediator for insulin's metabolic actions. We have recently cloned rat SHIP2 cDNA which is abundantly expressed in target tissues of insulin. Here, we clarify the role of SHIP2 possessing 5'-phosphatase activity toward PI(3,4,5)P3 in insulin signalling in the skeletal muscle. METHODS: The role of SHIP2 in insulin-induced glycogen synthesis was studied by expressing wild-type (WT)-SHIP2 and a 5'-phosphatase defective (Delta IP)-SHIP2 into L6 myotubes by means of adenovirus mediated gene transfer. RESULTS: The early events of insulin signalling including tyrosine phosphorylation of the insulin receptor and IRS-1, IRS-1 association with the p85 subunit, and PI3-kinase activity were not affected by expression of WT- and Delta IP-SHIP2. Although PI(3,4,5)P3 and PI(3,4)P2 are known to possibly activate a downstream molecule of PI3-kinase Akt in vitro, overexpression of WT-SHIP2 inhibited insulin-induced phosphorylation and activation of Akt. Conversely, Akt activity was increased by expression of Delta IP-SHIP2. GSK3 beta located downstream of Akt is an important molecule to further transmit insulin signal for glycogen synthesis in skeletal muscles. In accordance with the results of Akt, insulin-induced phosphorylation and inactivation of GSK3 beta, subsequent activation of glycogen synthase and glycogen synthesis were decreased by expression of WT-SHIP2, whereas these events were increased by expression of Delta IP-SHIP2. CONCLUSION/INTERPRETATION: Our results indicate that SHIP2 plays a negative regulatory role via the 5'-phosphatase activity in insulin signalling, and that PI(3,4,5)P3 rather than PI(3,4)P2 is important for in vivo regulation of insulin-induced Akt activation leading to glycogen synthesis in L6 myotubes.
Adenoviridae↗
Horse-related injuries in a thoroughbred stabling area in Japan.
To investigate the demographic details and patterns of injuries related to horse handling, we reviewed 637 horse-related injuries in 581 stable- or stud-workers in a representative area of thoroughbred stabling in Japan. We found that (1) injuries occurred most frequently in a group of a relatively young workers, with a seasonal variation; (2) the principal mechanism of injury was kicks, which accounted for 39.2% of all injuries, including 11 serious and one lethal visceral injuries; (3) the upper half of the body was more frequently involved than the lower half; and (4) the peripheral bones (hand and foot) and the ribs accounted for more than half of 148 fractures. These findings are distinct from those in horse-riding injuries reported in the literature and emphasize the importance in developing preventive strategies specifically for workers in horse stables.
Accidents, Occupational↗
Prevention and detection of spinal cord injury during thoracic and thoracoabdominal aortic repairs.
BACKGROUND: Spinal cord injury is a most dreaded and unpredictable complication. In this study, based on our experimental results in dogs and early clinical results, we reviewed the incidence of paraplegia and the detection of spinal cord injury. METHODS: Eighty-two patients who underwent elective surgical repair of the descending thoracic and thoracoabdominal aorta over 17 years were subjects for this study. Sixty-two patients were male and 20 were female. Their mean age was 61.6 years (range, 17 to 81 years). Monitoring somatosensory evoked potentials (SEP) and measurement of mean distal aortic pressure and cerebrospinal fluid pressure were performed perioperatively. RESULTS: Sixty patients had no ischemic change in SEP. In 17 patients with significant ischemic changes of SEP, SEP recovered by increasing spinal cord perfusion pressure to more than 40 mm Hg. Two patients with complete loss of SEP experienced paraplegia. One patient had delayed paraplegia. CONCLUSIONS: These results strongly suggest that SEP, mean distal aortic pressure, cerebrospinal fluid pressure should be monitored during aortic cross-clamping. Maintaining spinal cord perfusion pressure at more than 40 mm Hg by increasing mean distal aortic pressure or withdrawal of cerebrospinal fluid is valuable for preventing paraplegia.
Adolescent↗
Abdominal wall haematoma in an adolescent javelin thrower.
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Abdominal Muscles↗
Glucosamine enhances platelet-derived growth factor-induced DNA synthesis via phosphatidylinositol 3-kinase pathway in rat aortic smooth muscle cells.
Vascular smooth muscle cells play a key role in the development of atherosclerosis. Culture of vascular smooth muscle A10 cells with high glucose for 4 weeks enhanced platelet-derived growth factor (PDGF)-induced BrdU incorporation. Since a long period of high glucose incubation was required for the effect, and it was inhibited by co-incubation with azaserine, the role of hexosamine biosynthesis in the development of atherosclerosis in diabetes was studied in A10 cells. Addition of glucosamine to the culture media enhanced PDGF-stimulated BrdU incorporation, and PDGF-induced tyrosine phosphorylation of the PDGF beta-receptor was increased by glucosamine treatment. Of the subsequent intracellular signaling pathways, PDGF-induced PDGF beta-receptor association with PLC gamma was not affected, whereas tyrosine phosphorylation of Shc, subsequent association of Shc with Grb2, and MAP kinase activation were relatively decreased. In contrast, PDGF-induced PDGF beta-receptor association with the p85 regulatory subunit of PI3-kinase and PI3-kinase activation were increased by 20% (P<0.01) and 36% (P<0.01), respectively. The intracellular signaling molecules responsible for the glucosamine effect were further examined using pharmacological inhibitors. Pretreatment with PLC inhibitor (U73122) had negligible effects, and MEK1 inhibitor (PD98059) showed only a slight inhibitory effect on the PDGF-induced BrdU incorporation. In contrast, pretreatment with PI3-kinase inhibitor (LY294002) significantly inhibited glucosamine enhancement of PDGF-induced BrdU incorporation. These findings suggest that glucosamine is involved in the development of atherosclerosis by enhancing PDGF-induced mitogenesis specifically via the PI3-kinase pathway.
Adaptor Proteins, Signal Transducing↗
UT841 purified from sea urchin (Toxopneustes pileolus) venom inhibits time-dependent (45)Ca(2+) uptake in crude synaptosome fraction from chick brain.
To clarify the mechanism by which the toxic abstract from Toxopneustes pileolus inhibits time-dependent (Time-dep.) Ca(2+) uptake in crude synaptosome fraction, the effective component from pedicellarial venom of the sea urchin was purified. The crude extracts were purified by a series of steps including ion exchange (DEAE-sephadex-A25 gel), gel filtration (with Superdex-2000 and Superdex-peptide columns) and reversed-phase chromatography (Sephasil-C18 column). The effective component that inhibited Time-dep. 45Ca(2+) uptake was purified and named UT841. Its IC(50) was determined to be lower than 35ng/ml. UT841 is an acidic protein with an apparent molecular weight of about 18,000. The N-terminal sequence (40 amino acids) was almost identical to that of Contractin A (a protein purified from the same kind of venom which induces smooth muscle contraction). Even though it is unclear whether or not UT841 is Contractin A, Ca(2+) mobilization in nerve cells was shown to be influenced by UT841. This investigation also revealed that a donor of nitric oxide, arachidonic acid and an inhibitor of phospholipase C selectively inhibit Time-dep. (45)Ca(2+) uptake. These results suggest that UT841 purified from sea urchin venom may affect Time-dep. (45)Ca(2+) uptake through the metabolism of some lipids and nitric oxide.
Amino Acid Sequence↗
Dose-dependent augmentation effect of bromocriptine in a case with refractory depression.
1. A 52-year-old female with refractory depression had not responded to various treatments including electroconvulsive therapy and augmentation therapy with lithium or triiodothyronine. 2. Addition of bromocriptine 2.5-5 mg/day to imipramine improved her depressive symptoms. However, when the dose was increased to 15 mg/day to treat residual depressive symptoms, her clinical status deteriorated and returned to the original level. The dose reduction to 5mg/day again improved her depressive symptoms. 3. This report confirms the augmentation effect of bromocriptine for refractory depression. It also suggests that there is dose-dependency in this effect.
Bromocriptine↗