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T Shinoe

Publications and source records attributed to T Shinoe.

7 recordsLinked to original sources
PubMed2001

Upregulation of the pro-apoptotic BH3-only peptide harakiri in spinal neurons of amyotrophic lateral sclerosis patients.

DNA fragmentation and activation of caspase-1, implicating involvement of apoptosis, have been reported in the spinal cord of amyotrophic lateral sclerosis (ALS) patients and transgenic mouse models of ALS. Because BH3-only members of the Bcl-2 family have pro-apoptotic activity, we examined the expression of the BH3-only peptide harakiri (Hrk) in the spinal cord of ALS patients. In situ expression of Hrk mRNA and immunoreactivity against the Hrk peptide were verified in the spinal neurons. In the immunoblot analysis, upregulated Hrk protein migrated at 16 kDa. Heterodimerization of Hrk with Bcl-2 was detected by immunoprecipitation, which suggests the competition of Hrk and anti-apoptotic Bcl-2. These findings suggest that Hrk plays a role in apoptotic events in ALS pathogenesis.

Adult↗
PubMed2001

Cyclic AMP regulates the calcium transients released from IP(3)-sensitive stores by activation of rat kappa-opioid receptors expressed in CHO cells.

We analyzed intracellular Ca(2+)and cAMP levels in Chinese hamster ovary cells expressing a cloned rat kappa opioid receptor (CHO-kappa cells). Although expression of kappa(kappa)-opioid receptors was confirmed with a fluorescent dynorphin analog in almost all CHO-kappa cells, the kappa-specific agonists, U50488H or U69593, induced a Ca(2+) transient only in 35% of the cells. The Ca(2+) response occurred in all-or-none fashion and the half-maximal dosage of U50488H (812.1nM) was higher than that (3.2nM) to inhibit forskolin-stimulated cAMP. The kappa-receptors coupled to G(i/o)proteins since pertussis toxin significantly reduced the U50488H actions on intracellular Ca(2+) and cAMP. The Ca(2+) transient originates from IP(3)-sensitive internal stores since the Ca(2+) response was blocked by a PLC inhibitor (U73122) or by thapsigargin depletion of internal stores while removal of extracellular Ca(2+) had no effect. Interestingly, application of dibutyryl cAMP (+ 56.2%) or 8-bromo-cAMP (+ 174.7%) significantly increased the occurrence of U50488H-induced Ca(2+) mobilization while protein kinase A (PKA) inhibitors, Rp-cAMP (-32.3%) or myr-psi PKA (-73.9%) significantly reduced the response. Therefore, it was concluded that cAMP and PKA activity can regulate the Ca(2+) mobilization. These results suggest that the kappa receptor-linked cAMP cascade regulates the occurrence of kappa-opioid-mediated Ca(2+) mobilization.

3,4-Dichloro-N-methyl-N-(2-(1-pyrrolidinyl)-cycloh↗
PubMed2000

A novel function of synapsin II in neurotransmitter release.

Although synapsin has been localized to presynaptic structures, its function remains poorly understood. In the present study, we investigated the presynaptic function of synapsin II using a synaptic vesicle recycling process using synapsin-II-overexpressing NG108-15 cells. Western blot analysis with antibodies for synaptic-vesicle-associated protein indicated that the number of synaptic vesicles was approximately doubled in synapsin II transfectants as reported previously. In differentiated synapsin-II-overexpressing and control cells, the application of high potassium induced strong intracellular calcium elevation along neurites and varicosities after differentiation and a weak calcium rise in the cell bodies. The uptake and release of the fluorescent dye FM1-43 revealed that synaptic vesicle recycling in synapsin-II-transfected cells occurred with the same kinetics in the cell body and neuritic varicosities. Furthermore, the area labeled with FM1-43 fluorescence in the synapsin-II-transfected cells was approximately twice as much as in control cells after stimulation, and ATP released after synaptic vesicle fusion with the plasma membrane in synapsin-II-expressing cells was significantly elevated relative to controls. The number of synaptic vesicles paralleled the amount of transmitter released from the cells leading to the conclusion that the number of releasable synaptic vesicles were increased by synapsin II transfection into NG108-15 cells, suggesting that synapsin II may have a role in the regulation of synaptic vesicle number in presynapse-like structures in NG108-15 cells.

Adenosine Triphosphate↗
PubMed1998

Distal sensory axonopathy after sarin intoxication.

A 51-year-old man inhaled sarin during a terrorist attack on the Tokyo subway system and died 15 months later. Neuropathologic examination revealed marked nerve fiber decrease in the sural nerve, moderate nerve fiber loss in the sciatic nerve, and unremarkable dorsal root ganglia, dorsal roots, and posterior column of the spinal cord. This pathology is consistent with dying-back degeneration of the peripheral nervous system and could represent a late sequela of sarin intoxication.

Fatal Outcome↗
PubMed1996

[Tracheal deformity observed in tracheostomized Duchenne muscular dystrophy patients who can speak with appropriately inflated cuff of tracheal tube].

Respiratory failure occurring during late adolescence is a major cause of death in Duchenne muscular dystrophy (DMD). A number of respiratory assistance techniques including tracheostomy and positive pressure mechanical ventilation have been utilized not only to prolong DMD patients' life but also to improve quality of their life. It is surprising that most of the tracheostomized DMD patients can speak under positive pressure ventilatory assistance. Preserved functions of glosso-pharyngo-laryngeal muscles in these patients presumably make it possible to control the air leak around tracheal tube, which does not necessitate tight inflation of the tube cuff. Recently we noticed that some patients are still able to speak even when the cuff is fully inflated. In order to understand the mechanism of this phenomenon, we visualized the topographical relationship between trachea and the tube cuff using computed tomography by filling the cuff with aqueous contrast medium. We obtained following findings: 1) Trachea is flat and deviated from normal midline position, and 2) the tube cuff is located eccentrically in trachea resulting in compression of one side of the inner wall and leaving open space on the other side. We conclude that the tracheal malposition and deformity underlie this strange phenomenon and tight inflation of the cuff to prevent air leak may result in unfavorable complications in DMD patients.

Adult↗
PubMed1996

[Diameter decrement of abdominal aorta and redistribution of systemic blood flow in non-ambulant Duchenne muscular dystrophy patients].

Cardiomyopathy is a major life-threatening complication in Duchenne muscular dystrophy (DMD). Cardiac output is always low in advanced stage patients. Impaired muscles presumably require extremely low circulation, while blood flow to brain and internal organs is probably maintained. Therefore, the redistribution of systemic circulation must be another important factor which determines whether or not the cardiomyopathy results in fatal heart failure. Although great efforts have been focused on the cardiac function, this problem has seldom attracted attentions. Assuming that diameter of blood vessels reflects blood flow, we measured the diameter of abdominal aorta on CT at four levels: 1) beginning of the abdominal aorta, 2) before and 3) after the branching of renal arteries, 4) before bifurcation of the common iliac arteries. Six bed-ridden DMD patients were compared with 10 ambulant patients suffering from other neurological and non-neurological diseases. We obtained following results. First, the diameter of abdominal aorta is significantly smaller in DMD patients. Second, the decrement is most prominent between before and after the branching of the renal arteries. These results clearly showed predilection of renointestinal circulation at the sacrifice of lower extremities. This narrowing of distal aorta was also observed in Kugelberg-Welander disease and understood as a sequelae of longstanding abolition of lower extremity functions.

Adult↗