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Suzuka, Japan

Matsuura K.,Suzuka Kaisei Hospital | Tomimoto H.,Mie University
Internal Medicine | Year: 2015

We herein describe four cases of patients with Parkinson’s disease who were treated with istradefylline (ISD) in the evening and had severe daytime sleepiness. The time to onset of sleepiness varied between 2 weeks to 3 months. All patients recovered after changing the timing of the ISD dosage from evening to morning. ISD is an A2A receptor antagonist with a caffeine-like arousal effect that may worsen the quality of sleep and thus increase daytime sleepiness. This report provides the first evidence of daytime sleepiness induced by evening ISD treatment. We propose that ISD should therefore only be used in the morning, particularly if taken by professional drivers. © 2015 The Japanese Society of Internal Medicine.

Nishimura A.,Mie University | Sugita M.,Mie University | Kato K.,Mie University | Fukuda A.,Suzuka Kaisei Hospital | And 2 more authors.
International Journal of Sports Physiology and Performance | Year: 2010

Purpose: Recent studies have shown that low-intensity resistance training with vascular occlusion (kaatsu training) induces muscle hypertrophy. A local hypoxic environment facilitates muscle hypertrophy during kaatsu training. We postulated that muscle hypertrophy can be more efficiently induced by placing the entire body in a hypoxic environment to induce muscle hypoxia followed by resistance training. Methods: Fourteen male university students were randomly assigned to hypoxia (Hyp) and normoxia (Norm) groups (n = 7 per group). Each training session proceeded at an exercise intensity of 70% of1 repetition maximum (RM), and comprised four sets of10 repetitions of elbow extension and flexion. Students exercised twice weekly for 6 wk and then muscle hypertrophy was assessed by magnetic resonance imaging and muscle strength was evaluated based on 1RM. Results: Muscle hypertrophy was significantly greater for the Hyp-Ex (exercised flexor of the hypoxia group) than for the Hyp-N (nonexercised flexor of the hypoxia group) or Norm-Ex flexor (P < .05, Bonferroni correction). Muscle hypertrophy was significantly greater for the Hyp-Ex than the Hyp-N extensor. Muscle strength was significantly increased early (by week 3) in the Hyp-Ex, but not in the Norm-Ex group. Conclusion: This study suggests that resistance training under hypoxic conditions improves muscle strength and induces muscle hypertrophy faster than under normoxic conditions, thus representing a promising new training technique. © 2010 Human Kinetics, Inc.

Suzuki H.,Loma Linda University | Hasegawa Y.,Loma Linda University | Kanamaru K.,Suzuka Kaisei Hospital | Zhang J.H.,Loma Linda University
Acta Neurochirurgica, Supplementum | Year: 2011

Background: Mitogen-activated protein kinases (MAPKs) have been implicated in the pathogenesis of cerebral vasospasm after subarachnoid hemorrhage. The goal of this review is to bring together recent diverse data concerning the roles of MAPKs in cerebral vasospasm and to consider the future research. Emphasis Type=«Italic»>Method: A review of publications in the National Library of Medicine and National Institutes of Health database was conducted in August 2009 using specific keyword search terms pertaining to subarachnoid hemorrhage and MAPKs. Findings: There are nine in vitro studies and 17 in vivo studies published. Most of previous studies used MAPK inhibitors or their upstream molecule inhibitors, and showed that MAPK inhibitions prevented vasospasm. The MAPK cascade appears to interact with other signaling molecules, and MAPK may be an important final common pathway for the signaling transduction during cerebral vasospasm. However, the mechanism by which MAPK causes sustained vascular smooth muscle contraction remains unclear. In addition, the role of endogenous MAPK inhibitors, MAPK phosphatases, has not been investigated in cerebral vasospasm. Conclusions: The experimental data support the causative role of MAPK in cerebral vasospasm and warrant further research. © 2011 Springer-Verlag/Wien.

Suzuki H.,Loma Linda University | Hasegawa Y.,Loma Linda University | Kanamaru K.,Suzuka Kaisei Hospital | Zhang J.H.,Loma Linda University
Stroke | Year: 2010

Background and Purpose-: Osteopontin (OPN) is an inducible, multifunctional, extracellular matrix protein that may be protective against blood-brain barrier (BBB) disruption after subarachnoid hemorrhage (SAH). However, the protective mechanisms remain unclear. Methods-: We produced the endovascular perforation model of SAH in rats and studied the time course of OPN induction in brains by Western blotting and immunofluorescence (n=50). Then, 34 rats were randomly assigned to sham (n=3), sham+OPN small interfering RNA (siRNA, n=3), SAH+negative control siRNA (n=14), and SAH+OPN siRNA (n=14) groups, and 109 rats were allocated to sham+vehicle (n=17), sham+recombinant OPN (n=17), SAH+vehicle (n=33), SAH+recombinant OPN (n=31), and SAH+recombinant OPN+l-arginyl-glycyl-l-aspartate motif-containing hexapeptide (n=11) groups. The effects of OPN siRNA or recombinant OPN on BBB disruption and related proteins were studied. Results-: OPN was significantly induced in reactive astrocytes and capillary endothelial cells, peaking at 72 hours after SAH, during the recovery phase of BBB disruption. Blockage of endogenous OPN induction exacerbated BBB disruption and was associated with a reduction of angiopoietin-1 and mitogen-activated protein kinase (MAPK) phosphatase-1 (an endogenous MAPK inhibitor), activation of MAPKs, and induction of vascular endothelial growth factor-A at 72 hours after SAH, whereas recombinant OPN treatment improved it and was associated with MAPK phosphatase-1 induction, MAPK inactivation, and vascular endothelial growth factor-A reduction, which was blocked by l-arginyl-glycyl-l-aspartate motif-containing hexapeptide at 24 hours after SAH. Vascular endothelial growth factor-B and angiopoietin-2 levels were unchanged. Conclusions-: OPN may increase MAPK phosphatase-1 that inactivates MAPKs, upstream and downstream of vascular endothelial growth factor-A, by binding to l-arginyl-glycyl-l-aspartate-dependent integrin receptors, suggesting a novel mechanism of OPN-induced post-SAH BBB protection. © 2010 American Heart Association, Inc.

Suzuki H.,Loma Linda University | Ayer R.,Loma Linda University | Sugawara T.,Loma Linda University | Chen W.,Loma Linda University | And 4 more authors.
Critical Care Medicine | Year: 2010

Objective: Accumulated evidence suggests that the primary cause of poor outcome after subarachnoid hemorrhage is not only cerebral arterial narrowing but also early brain injury. Our objective was to determine the effect of recombinant osteopontin, a pleiotropic extracellular matrix glycoprotein, on early brain injury after subarachnoid hemorrhage in rats. Design: Controlled in vivo laboratory study. Setting: Animal research laboratory. Subjects: One hundred seventy-seven male adult Sprague-Dawley rats weighing 300 to 370 g. Interventions: The endovascular perforation model of subarachnoid hemorrhage was produced. Subarachnoid hemorrhage or sham-operated rats were treated with an equal volume (1 μL) of pre-subarachnoid hemorrhage intracerebroventricular administration of two dosages (0.02 and 0.1 μg) of recombinant osteopontin, albumin, or vehicle. Body weight, neurologic scores, brain edema, and blood-brain barrier disruption were evaluated, and Western blot analyses were performed to determine the effect of recombinant osteopontin on matrix metalloproteinase-9, substrates of matrix metalloproteinase-9 (zona occludens-1, laminin), tissue inhibitor of matrix metalloproteinase-1, inflammation (interleukin-1β), and nuclear factor-κB signaling pathways. Measurements and Main Results: Treatment with recombinant osteopontin prevented a significant loss in body weight, neurologic impairment, brain edema, and blood-brain barrier disruption after subarachnoid hemorrhage. These effects were associated with the deactivation of nuclear factor-κB activity, inhibition of matrix metalloproteinase-9 induction, the maintenance of tissue inhibitor of matrix metalloproteinase-1, the consequent preservation of the cerebral microvessel basal lamina protein laminin, and the tight junction protein zona occludens-1. Conclusions: These results demonstrate that recombinant osteopontin treatment is effective for early brain injury after subarachnoid hemorrhage. Copyright © 2010 by the Society of Critical Care Medicine and Lippincott Williams & Wilkins.

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