Nobuaki Egashira

Fukuoka University, Fukuoka-shi, Fukuoka-ken, Japan

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Publications (161)426.2 Total impact

  • [Show abstract] [Hide abstract]
    ABSTRACT: Oxaliplatin is a key drug in the treatment of colorectal cancer, but it causes acute and chronic neuropathies in patients. Amitriptyline has widely been used in patients with painful neuropathy. In this study, we investigated the effect of amitriptyline on the oxaliplatin-induced neuropathy in rats. Repeated administration of amitriptyline (5 and 10 mg/kg, p.o., once a day) reduced the oxaliplatin-induced mechanical allodynia but not cold hyperalgesia and reversed the oxaliplatin-induced increase in the expression of NR2B protein and mRNA in rat spinal cord. These results suggest that amitriptyline is useful for the treatment of oxaliplatin-induced neuropathy clinically.
    Journal of Pharmacological Sciences 03/2012; 118(4):547-51. · 2.11 Impact Factor
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    ABSTRACT: Vancomycin chloride (VCM), a glycopeptide antibiotic, is widely used for the therapy of infections caused by methicillin-resistant Staphylococcus aureus. However, nephrotoxicity is a major adverse effect in VCM therapy. In this study, we investigated the cellular mechanisms underlying VCM-induced renal tubular cell injury in cultured LLC-PK1 cells. VCM induced a concentration- and time-dependent cell injury in LLC-PK1 cells. VCM caused increases in the numbers of annexin V-positive/PI-negative cells and TUNEL-positive cells, indicating the involvement of apoptotic cell death in VCM-induced renal cell injury. The VCM-induced apoptosis was accompanied by the activation of caspase-9 and caspase-3/7 and reversed by inhibitors of these caspases. Moreover, VCM caused an increase in intracellular reactive oxygen species production and mitochondrial membrane depolarization, which were reversed by vitamin E. In addition, mitochondrial complex I activity was inhibited by VCM as well as by the complex I inhibitor rotenone, and rotenone mimicked the VCM-induced LLC-PK1 cell injury. These findings suggest that VCM causes apoptotic cell death in LLC-PK1 cells by enhancing mitochondrial superoxide production leading to mitochondrial membrane depolarization followed by the caspase activities. Moreover, mitochondrial complex I may play an important role in superoxide production and renal tubular cell apoptosis induced by VCM.
    Free Radical Biology and Medicine 03/2012; 52(9):1865-73. · 5.27 Impact Factor
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    ABSTRACT: Epirubicin, an anthracycline antitumor drug, often causes vascular injury such as vascular pain, phlebitis, and necrotizing vasculitis. However, an effective prevention for the epirubicin-induced vascular injury has not been established. The purpose of this study is to identify the mechanisms of cell injury induced by epirubicin in porcine aorta endothelial cells (PAECs). PAECs were exposed to epirubicin for 10 min followed by further incubation without epirubicin. The exposure to epirubicin (3-30 μM) decreased the cell viability concentration and time dependently. Epirubicin increased the activity of caspase-3/7, apoptotic cells, and intracellular lipid peroxide levels, and also induced depolarization of mitochondrial membranes. These intracellular events were reversed by glutathione (GSH) and N-acetylcysteine (NAC), while epirubicin rather increased intracellular GSH slightly and L-buthionine-(S,R)-sulfoximine, a specific inhibitor of GSH synthesis, had no effect on the epirubicin-induced cell injury. The epirubicin-induced cell injury and increase of caspase-3/7 activity were also attenuated by p38 mitogen-activated protein kinase (MAPK) inhibitors, SB203580 and PD169316. Moreover, epirubicin significantly enhanced the phosphorylation of p38 MAPK, and these effects were attenuated by GSH and NAC. In contrast, a c-Jun N-terminal kinase inhibitor SP600125, an extracellular signal-regulated kinase inhibitor PD98059, and a p53 inhibitor pifithrin α did not affect the epirubicin-induced cell injury and increase of caspase-3/7 activity. These results indicate that an activation of p38 MAPK by oxidative stress is involved in the epirubicin-induced endothelial cell injury.
    Free Radical Biology and Medicine 02/2012; 52(8):1285-93. · 5.27 Impact Factor
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    ABSTRACT: Oxaliplatin is an important drug used in the treatment of colorectal cancer. However, it frequently causes severe acute and chronic peripheral neuropathies. We recently reported that repeated administration of oxaliplatin induced cold hyperalgesia in the early phase and mechanical allodynia in the late phase in rats, and that oxalate derived from oxaliplatin is involved in the cold hyperalgesia. In the present study, we examined the effects of Ca²⁺ channel blockers on oxaliplatin-induced cold hyperalgesia in rats. Cold hyperalgesia was assessed by the acetone test. Oxaliplatin (4 mg/kg), sodium oxalate (1.3 mg/kg) or vehicle was injected i.p. on days 1 and 2. Ca²⁺ (diltiazem, nifedipine and ethosuximide) and Na⁺ (mexiletine) channel blockers were administered p.o. simultaneously with oxaliplatin or oxalate on days 1 and 2. Oxaliplatin (4 mg/kg) induced cold hyperalgesia and increased in the transient receptor potential melastatin 8 (TRPM8) mRNA levels in the dorsal root ganglia (DRG). Furthermore, oxalate (1.3 mg/kg) significantly induced the increase in TRPM8 protein in the DRG. Treatment with oxaliplatin and oxalate (500 μM for each) also increased the TRPM8 mRNA levels and induced Ca²⁺ influx and nuclear factor of activated T-cell (NFAT) nuclear translocation in cultured DRG cells. These changes induced by oxalate were inhibited by nifedipine, diltiazem and mexiletine. Interestingly, co-administration with nifedipine, diltiazem or mexiletine prevented the oxaliplatin-induced cold hyperalgesia and increase in the TRPM8 mRNA levels in the DRG. These data suggest that the L type Ca²⁺ channels/NFAT/TRPM8 pathway is a downstream mediator for oxaliplatin-induced cold hyperalgesia, and that Ca²⁺ channel blockers have prophylactic potential for acute neuropathy.
    Molecular Pain 01/2012; 8:7. · 3.53 Impact Factor
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    ABSTRACT: We examined the role of 5-hydroxytryptamine(2C) (5-HT(2C)) receptors in marble-burying behavior in mice. When administered alone, the selective 5-HT(2C) agonist WAY161503 (3 mg/kg) inhibited marble-burying behavior. Moreover, the selective 5-HT(2C) antagonist SB242084 (3 mg/kg) reversed the inhibition of marble-burying behavior by 2,5-dimethoxy-4-iodoamphetamine (DOI) (1 mg/kg) or WAY161503 (3 mg/kg). Similarly, SB242084 (1 mg/kg) reversed the inhibition of marble-burying behavior by fluvoxamine (30 mg/kg) or paroxetine (3 mg/kg). These results suggest that 5-HT(2C) receptors play a role in marble-burying behavior in mice.
    Biological & Pharmaceutical Bulletin 01/2012; 35(3):376-9. · 1.85 Impact Factor
  • Iryo Yakugaku (Japanese Journal of Pharmaceutical Health Care and Sciences). 01/2012; 38(4):211-219.
  • Iryo Yakugaku (Japanese Journal of Pharmaceutical Health Care and Sciences). 01/2012; 38(6):350-358.
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    ABSTRACT: Oxaliplatin is a key drug in the treatment of colorectal cancer, but it causes acute and chronic neuropathies in patients. Goshajinkigan (GJG) is a Kampo medicine that is used for the treatments of several neurological symptoms including pain and numbness. More recently, GJG has been reported to prevent the oxaliplatin-induced peripheral neuropathy in clinical studies. No experimental study, however, has been conducted to date to determine the effect of GJG on pain behaviour in a rat model of oxaliplatin-induced neuropathy. Moreover, the impact on the anti-tumour effect of oxaliplatin remains unknown. In the present study, we examined the effects of GJG on the peripheral neuropathy and anti-tumour activity of oxaliplatin in rodents. Repeated administration of oxaliplatin caused cold hyperalgesia from days 3 to 37 and mechanical allodynia from days 21 to 28. Repeated administration of GJG prevented the oxaliplatin-induced cold hyperalgesia but not mechanical allodynia and axonal degeneration in rat sciatic nerve. Single administration of GJG reduced both cold hyperalgesia and mechanical allodynia after the development of neuropathy. In addition, GJG did not affect the anti-tumour effect of oxaliplatin in the tumour cells or tumour cells-implanted mice. These results suggest that GJG relieves the oxaliplatin-induced cold hyperalgesia and mechanical allodynia without affecting anti-tumour activity of oxaliplatin, and, therefore, may be useful for the oxaliplatin-induced neuropathy in clinical practice.
    European journal of cancer (Oxford, England: 1990) 09/2011; 48(9):1407-13. · 4.12 Impact Factor
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    ABSTRACT: Anticancer drugs are classified as vesicant, irritant, and nonvesicant drugs on the basis of frequency of their vascular disorder. In this study, we compared the injuring effects of three typical anticancer drugs of each class on porcine aorta endothelial cells (PAECs). The concentration inducing 50% cell viability inhibition was lower in the order of vesicant, irritant, and nonvesicant drugs. These results suggest that injuring effects of anticancer drugs on PAECs may be relevant as an indicator of frequency of their vascular disorder, and that this experimental model may be useful for the study of vascular disorder.
    Journal of Pharmacological Sciences 09/2011; 117(2):125-8. · 2.11 Impact Factor
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    ABSTRACT: Nanoparticle albumin-bound paclitaxel (nab-paclitaxel) is delivered to tumors and increases antitumor activity compared with solvent-based paclitaxel. However, in a clinical trial, higher and lower rates of peripheral neuropathy and neutropenia were observed. In this study, we compared the effects of nab-paclitaxel and standard paclitaxel on pain behaviors in rats. Repeated administration of nab-paclitaxel dose-dependently induced both mechanical and cold allodynia, and the effects of nab-paclitaxel on pain behaviors tended to be stronger than that of standard paclitaxel at the doses used clinically. These results suggest that closer attention must be paid to the neuropathy when administering nab-paclitaxel in clinical settings.
    Journal of Pharmacological Sciences 09/2011; 117(2):116-20. · 2.11 Impact Factor
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    ABSTRACT: Cannabis is a widely used illicit substance. ∆(9)-Tetrahydrocannabinol (THC), the major psychoactive component of cannabis, is known to induce cognitive deficits that closely resemble the impairment observed in schizophrenic patients. We previously reported that THC (6 mg/kg) impairs spatial memory in the eight-arm radial maze, and that this memory disturbance was reversed by the cannabinoid CB(1) receptor antagonist rimonabant (0.1 mg/kg), suggesting that the effect of THC is mediated through cannabinoid CB(1) receptors. The present study was designed to examine the possible involvement of opioid receptors in the THC-induced impairment of spatial memory. The effects of treatment with the nonselective opioid receptor antagonist naloxone (0.3 and 1 mg/kg), the μ-opioid receptor antagonist β-funaltrexamine (0.3 and 1 mg/kg), the δ-opioid receptor antagonist naltrindole (1 and 3 mg/kg), and the κ-opioid receptor antagonist nor-binaltorphimine (0.03 and 0.1 mg/kg) on the impairment of spatial memory induced by THC were evaluated using the eight-arm radial maze. The nonselective opioid receptor antagonist naloxone, the μ-opioid receptor antagonist β-funaltrexamine, and the κ-opioid receptor antagonist nor-binaltorphimine, but not the δ-opioid receptor antagonist naltrindole, attenuated THC-induced cognitive deficits, suggesting an involvement of μ- and κ-opioid receptors in this behavioral response. These results demonstrate that the endogenous opioid system is involved in the regulation of the acute short-term and working memory deficits induced by cannabis.
    Psychopharmacology 08/2011; 219(4):1111-8. · 3.99 Impact Factor
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    ABSTRACT: The intravenous injection of vinorelbine often causes venous irritation such as erythema, injection site pain, and phlebitis. The purpose of the present study was to investigate the risk factor associated with the vinorelbine-induced venous irritation and to establish a suitable administration method of vinorelbine. We analyzed the risk factor associated with venous irritation in 63 patients administered vinorelbine from April 2006 to September 2008. We subsequently changed the regimen of vinorelbine and examined the incidence of venous irritation in 24 patients administered vinorelbine from October 2008 to March 2010. A multivariate logistic regression analysis revealed that the dose of vinorelbine (≥ 40 mg) was a significant predictor for venous irritation (adjusted odds ratio = 4.39; 95% confidence intervals, 1.33-14.49; p = 0.015). Moreover, the grade of venous irritation in patients administered vinorelbine at the doses of ≥ 40 mg was significantly higher than that in patients administered vinorelbine at the doses of <40 mg (p = 0.011). Based on this result, we altered the volume of normal saline for vinorelbine dissolution from 50 to 100 mL. After the change of regimen, the grade of venous irritation induce by vinorelbine was significantly decreased (p = 0.034), although the incidence was not significantly changed (46.0% versus 33.3%). The change of regimen of vinorelbine based on the analysis significantly decreased the grade of venous irritation. Pharmacists can contribute to the management for the vinorelbine-induced venous irritation.
    Supportive Care in Cancer 07/2011; 20(7):1549-53. · 2.09 Impact Factor
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    ABSTRACT: In the present study, we investigated the effect of the Kampo medicine Yokukansan (YKS) on pentobarbital-induced sleep in group-housed and socially isolated mice. Socially isolated mice showed shorter sleeping time than the group-housed mice. YKS (300 mg/kg, p.o.) prolonged the pentobarbital-induced sleeping time in socially isolated mice without affecting pentobarbital sleep in group-housed mice. The prolongation of sleeping time by YKS was reversed by bicuculline (3 mg/kg, i.p.) and flumazenil (3 mg/kg, i.p.), but not WAY100635. These findings suggest that the GABA(A)-benzodiazepine receptor complex, but not 5-HT(1A) receptors, is involved in the reversal effect of YKS on the decrease of pentobarbital sleep by social isolation.
    Journal of Pharmacological Sciences 07/2011; 116(3):316-20. · 2.11 Impact Factor
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    ABSTRACT: We previously reported that systemic administration of the endocannabinoid anandamide inhibited the head-twitches induced by the hallucinogenic drug 2,5-dimethoxy-4-iodoamphetamine (DOI) in mice, which is mediated via the activation of 5-HT(2A) receptors. Endocannabinoid and glutamatergic systems have been suggested to modulate the function of 5-HT(2A) receptors. In the present study, we further investigated the role of endocannabinoid and glutamatergic systems in DOI-induced head-twitch response in mice. An anandamide transport inhibitor AM404 (0.3-3mg/kg, i.p.), a fatty acid amide hydrolase inhibitor URB597 (0.1-10mg/kg, i.p.), a glutamate release inhibitor riluzole (0.3 and 1mg/kg, i.p.), a natural glutamate analog l-glutamylethylamide (theanine, 1 and 3mg/kg, p.o.) and an α-amino-3-hydroxy-5-methyl-4-isoxazolepropionate (AMPA) receptor antagonist NBQX (0.01-0.3mg/kg, i.p.) significantly inhibited DOI-induced head-twitch response. The AMPA receptor positive modulator aniracetam (30 or 100mg/kg, p.o.) reversed inhibition of head-twitch response by NBQX and URB597. These findings indicated that endocannabinoid and glutamatergic systems participate in the mechanism of action of DOI to induce head-twitch response.
    Pharmacology Biochemistry and Behavior 07/2011; 99(1):52-8. · 2.82 Impact Factor
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    ABSTRACT: Emesis is the most feared side effect in patients who are undergoing cancer chemotherapy. In particular, cisplatin causes severe acute and delayed emesis. Although early vomiting is well controlled by 5-hydroxytryptamine 3 (5-HT(3)) receptor antagonists, delayed-phase vomiting is not sufficiently controlled. Substance P is thought to be involved in the development of emesis, and tachykinin NK(1) receptor antagonists can inhibit delayed vomiting. We previously have reported that substance P is involved in the paclitaxel-induced hypersensitivity reaction in rats, and anti-allergic agent pemirolast reduces these reactions via inhibition of substance P release. In the present study, we investigated the effect of pemirolast on cisplatin-induced kaolin intake, which is an index of nausea/vomiting in the rat. Cisplatin (5 mg/kg, i.p.) induced kaolin intake and reduced normal feed intake from days 1 to 5 after injection. Cisplatin-induced kaolin intake was significantly reduced by co-administration of ondansetron (2 mg/kg, i.p.), a 5-HT(3) receptor antagonist, and dexamethasone (2 mg/kg, i.p.) from days 1 to 5. Similarly, pemirolast (10 mg/kg, p.o.) and the tachykinin NK(1) receptor antagonist aprepitant (10 and 30 mg/kg, p.o.) significantly reduced cisplatin-induced kaolin intake on days 3 and 4. Moreover, pemirolast at the same dose significantly reversed the cisplatin-induced increase in the cerebrospinal fluid level of substance P in rats. These results suggest that substance P is involved in cisplatin-induced kaolin intake in rats, and pemirolast reduces kaolin intake by inhibition of substance P release.
    European journal of pharmacology 07/2011; 661(1-3):57-62. · 2.59 Impact Factor
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    ABSTRACT: Epirubicin is an antitumor drug, particularly used in the treatment of the breast cancer. The peripheral intravenous infusion of epirubicin frequently causes venous irritation such as, erythema, injection site pain, and phlebitis. The purpose of the present study was to investigate the risk factor associated with the epirubicin-induced venous irritation and to establish a suitable administration method of epirubicin. The phlebitis scores (Visual Infusion Phlebitis score) were evaluated retrospectively using the collected nursing record. We analyzed the risk factor associated with venous irritation in 97 patients administered with epirubicin from December 2004 to September 2008. We subsequently changed the regimen of epirubicin and examined the incidence of venous irritation in 26 patients administered with epirubicin from August 2009 to March 2010. The phlebitis scores were significantly higher in the patients treated with ready-to-use solution compared with lyophilized powder (P = 0.04). Based on this result, we switched the formulation of epirubicin to lyophilized powder. After the intervention, the phlebitis scores were significantly decreased (P = 0.003). An ordinal logistic regression analysis revealed that use of ready-to-use solution was a significant predictor for venous irritation (odds ratio = 3.70; 95%, confidence intervals, 1.29-11.45; P = 0.02). The use of ready-to-use solution was a risk factor for epirubicin-induced venous irritation. The change of formulation by pharmacist intervention decreased the risk of venous irritation.
    Supportive Care in Cancer 04/2011; 20(5):951-5. · 2.09 Impact Factor
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    ABSTRACT: Oxaliplatin is a key drug for colorectal cancer, but it causes acute peripheral neuropathy (triggered by cold) and chronic neuropathy (sensory and motor neuropathy) in patients. Neurotropin, a non-protein extract from the inflamed rabbit skin inoculated with vaccinia virus, has been used to treat various chronic pains. In the present study, we investigated the effect of neurotropin on the oxaliplatin-induced neuropathy in rats. Repeated administration of oxaliplatin caused cold hyperalgesia from Day 5 to Day 29 and mechanical allodynia from Day 15 to Day 47. Repeated administration of neurotropin relieved the oxaliplatin-induced mechanical allodynia but not cold hyperalgesia, and inhibited the oxaliplatin-induced axonal degeneration in rat sciatic nerve. Neurotropin also inhibited the oxaliplatin-induced neurite degeneration in cultured pheochromocytoma 12 (PC12) and rat dorsal root ganglion (DRG) cells. On the other hand, neurotropin did not affect the oxaliplatin-induced cell injury in rat DRG cells. These results suggest that repeated administration of neurotropin relieves the oxaliplatin-induced mechanical allodynia by inhibiting the axonal degeneration and it is useful for the treatment of oxaliplatin-induced neuropathy clinically.
    European journal of pain (London, England) 04/2011; 15(4):344-50. · 3.37 Impact Factor
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    ABSTRACT: The painful peripheral neuropathy occurring frequently during chemotherapy with paclitaxel or oxaliplatin is one of their dose-limiting factors. We reported previously that substance P is involved in the pathogenesis of pulmonary hypersensitivity reaction to paclitaxel in rats, and an antiallergic agent pemirolast reverses this reaction via the blockade of release of substance P. In the present study, we investigated the involvement of substance P in paclitaxel-induced peripheral neuropathy compared with that by oxaliplatin. In von Frey and acetone tests in rats repeated administration of paclitaxel (6 mg/kg i.p., once a week for 4 weeks) or oxaliplatin (4 mg/kg i.p., twice a week for 4 weeks) induced both mechanical allodynia and cold hyperalgesia. Paclitaxel-induced peripheral neuropathy was reversed primarily by the acute administration of pemirolast (0.1 and 1 mg/kg p.o.). Moreover, coadministration of the receptor antagonists neurokinin 1 [N-acetyl-l-tryptophan 3,5-bis(trifluoromethyl)benzylester (L-732,138), 100 μg/body i.t.] and neurokinin 2 [5-fluoro-3-[2-[4-methoxy-4-[[(R)-phenylsulphinyl]methyl]-1-piperidinyl]ethyl]-1H-indole (GR159897), 100 μg/body i.t.] strongly reversed paclitaxel-induced neuropathy. On the other hand, oxaliplatin-induced peripheral neuropathy was not reversed by pemirolast. In the in vitro study using cultured adult rat dorsal root ganglion neurons paclitaxel (1000 ng/ml) significantly increased the release of substance P, and pemirolast (100 and 1000 nM) significantly inhibited this increase of substance P release. Oxaliplatin, by contrast, did not increase the release of substance P. These results suggest that substance P is involved in paclitaxel-induced neuropathy, and the mechanism of its action is clearly different from that of oxaliplatin.
    Journal of Pharmacology and Experimental Therapeutics 03/2011; 337(1):226-35. · 3.89 Impact Factor
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    ABSTRACT: Oxaliplatin is a platinum-based chemotherapy drug characterized by the development of acute and chronic peripheral neuropathies. The chronic neuropathy is a dose-limiting toxicity. We previously reported that repeated administration of oxaliplatin induced cold hyperalgesia in the early phase and mechanical allodynia in the late phase in rats. In the present study, we investigated the involvement of NR2B-containing N-methyl-D-aspartate (NMDA) receptors in oxaliplatin-induced mechanical allodynia in rats. Repeated administration of oxaliplatin (4 mg/kg, i.p., twice a week) caused mechanical allodynia in the fourth week, which was reversed by intrathecal injection of MK-801 (10 nmol) and memantine (1 μmol), NMDA receptor antagonists. Similarly, selective NR2B antagonists Ro25-6981 (300 nmol, i.t.) and ifenprodil (50 mg/kg, p.o.) significantly attenuated the oxaliplatin-induced pain behavior. In addition, the expression of NR2B protein and mRNA in the rat spinal cord was increased by oxaliplatin on Day 25 (late phase) but not on Day 5 (early phase). Moreover, we examined the involvement of nitric oxide synthase (NOS) as a downstream target of NMDA receptor. L-NAME, a non-selective NOS inhibitor, and 7-nitroindazole, a neuronal NOS (nNOS) inhibitor, significantly suppressed the oxaliplatin-induced pain behavior. The intensity of NADPH diaphorase staining, a histochemical marker for NOS, in the superficial layer of spinal dorsal horn was obviously increased by oxaliplatin, and this increased intensity was reversed by intrathecal injection of Ro25-6981. These results indicated that spinal NR2B-containing NMDA receptors are involved in the oxaliplatin-induced mechanical allodynia.
    Molecular Pain 01/2011; 7:8. · 3.53 Impact Factor
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    ABSTRACT: Although S-1 is frequently used in cancer chemotherapy, the drug interaction with warfarin, an anticoagulant agent, is not fully paid attention. In the present study, we investigated retrospectively the timing of expression of blood coagulation abnormality in nine patients treated with warfarin and S-1 concomitantly. In five patients, the dose of warfarin was reduced or interrupted after concomitant use of S-1. The International Normalized Ratio (INR) was significantly increased after combination with S-1 compared with the former value. In all patients, the INR was increased in three weeks after combination with S-1. On the other hand, serum creatinine, aspartate aminotransferase, alanine aminotransferase or serum albumin was not different before and after combination with S-1. These results suggest that the careful monitoring of the blood coagulation ability is necessary in all patients receiving warfarin and S-1 concomitantly.
    Yakugaku zasshi journal of the Pharmaceutical Society of Japan 07/2010; 130(7):955-60. · 0.31 Impact Factor

Publication Stats

2k Citations
426.20 Total Impact Points

Institutions

  • 2000–2012
    • Fukuoka University
      • • Faculty of Pharmaceutical Sciences
      • • Department of Psychiatry
      Fukuoka-shi, Fukuoka-ken, Japan
  • 2008–2010
    • Kyushu University
      • Faculty of Medical Sciences
      Fukuoka-shi, Fukuoka-ken, Japan
  • 2009
    • Gifu University Hospital
      Gihu, Gifu, Japan
  • 2006–2009
    • St.Mary's Hospital (Fukuoka - Japan)
      Hukuoka, Fukuoka, Japan
    • University of Toronto
      • Tanz Centre for Research in Neurodegenerative Diseases
      Toronto, Ontario, Canada
  • 2007–2008
    • Azabu University
      • School of Veterinary Medicine
      Japan
  • 2002–2007
    • Pamukkale University
      • • Department of Internal Medicine
      • • Faculty of Medicine
      Denisli, Denizli, Turkey
  • 2005–2006
    • Miyazaki University
      • Department of Obstetrics and Gynecology
      Миядзаки, Miyazaki, Japan