Tokushima University / Educator and Researcher Directory --- Minakuchi, Kazuo

Personal Web Page

https://researchmap.jp/read0188849 (researchmap)

Field of Study

○	Pharmacy

Subject of Study

○

Book / Paper

Book:

1.	Takumi Sakurada, Keisuke Ishizawa, Masaki Imanishi, Shoko Fujii, Jumpei Taniguchi, Yuki Izawa-Ishizawa, Licht Miyamoto, Yoshitaka Kihira, Yasumasa Ikeda, Shuhei Tomita, Kazuo Minakuchi, Koichiro Tsuchiya and Toshiaki Tamaki : 腎とフリーラジカル第11集, TOKYO IGAKUSHA, Tokyo, Jan. 2013.
2.	木宿昌俊, 森剛志, 田島壮一郎, 板東篤史, Shinji Abe, Kazuyoshi Kawazoe and Kazuo Minakuchi : 最近の文献情報より新しいがん治療に向けて(2), The Japanese Society of Hospital Pharmacists, Tokyo, Jul. 2007.
3.	小笠原聡子, 桐野靖, 米田良子, 元林有紀, 伊勢夏子, Shinji Abe, Kazuyoshi Kawazoe and Kazuo Minakuchi : 最近の文献情報より脳・精神疾患の最前線(2), The Japanese Society of Hospital Pharmacists, Tokyo, May 2007.
4.	中村敏己, 山下祐紀雄, 西迫寛隆, 下岡幸恵, 西谷典子, Shinji Abe, Kazuyoshi Kawazoe and Kazuo Minakuchi : 最近の文献情報より新しいがん治療に向けて(1), The Japanese Society of Hospital Pharmacists, Tokyo, Mar. 2007.
5.	Shinji Abe, 塩田直青子, 田中裕子, 廣永有沙, 道倉亜実, Kazuyoshi Kawazoe and Kazuo Minakuchi : 最近の文献情報より脳・精神疾患の最前線(1), The Japanese Society of Hospital Pharmacists, Tokyo, Jan. 2007.
6.	Keisuke Ishizawa, Kazuo Minakuchi and 他 : 南山堂医学大辞典改訂19版, NANZANDO Co.,Ltd., Tokyo, Mar. 2006.

Academic Paper (Judged Full Paper):

1.	Takumi Sakurada, Souji Kakiuchi, Soichiro Tajima, Yuya Horinouchi, Naoto Okada, Hirotaka Nishisako, Toshimi Nakamura, Kazuhiko Teraoka, Kazuyoshi Kawazoe, Hiroaki Yanagawa, Yasuhiko Nishioka, Kazuo Minakuchi and Keisuke Ishizawa : Characteristics and risk factors of interstitial lung disease induced by chemotherapy for lung cancer, The Annals of Pharmacotherapy, Vol.49, No.4, 398-404, 2015. (Summary) Drug-induced interstitial lung disease (DILD) is generally a serious adverse effect and almost always necessitates the discontinuation of the offending drug. Cancer pharmacotherapy is strongly associated with DILD, and the risk of DILD has been suggested to be higher in patients with lung cancer because of preexisting pneumonic disease. The aim of this retrospective study was to identify the risk factors and prognostic factors for early death from interstitial lung disease (ILD) induced by chemotherapy for lung cancer. The medical records of 459 patients who underwent chemotherapy for lung cancer between April 2007 and March 2013 were analyzed with regard to patient background and DILD development, initial symptoms, and prognosis. A total of 33 patients (7.2%) developed chemotherapy-induced ILD. The most frequently observed initial symptom was dyspnea (94.3%). Preexisting ILD was identified as a risk factor for DILD (odds ratio [OR] = 5.38; 95% CI = 2.47-11.73; P < 0.01). Among the 33 patients who developed DILD, 10 patients suffered an early death despite steroid therapy. Poor prognostic factors included epidermal growth factor receptor-tyrosine kinase inhibitor (EGFR-TKI) use (OR = 9.26; 95% CI = 1.05-82.0; P < 0.05) and 2 or more prior chemotherapy regimens (OR = 6.95; 95% CI = 1.14-42.3; P < 0.05). Many lung cancer patients have coexisting ILD, and these patients have a high risk of developing chemotherapy-induced ILD. In addition, patients with DILD who underwent EGFR-TKI therapy and 2 or more prior chemotherapy regimens had a higher risk of fatal outcome. (Keyword) Adult / Aged / Aged, 80 and over / Antineoplastic Agents / Female / Humans / Lung Diseases, Interstitial / Lung Neoplasms / Male / Middle Aged / Odds Ratio / Prognosis / Retrospective Studies / Risk Factors (Link to Publication Site) ● Publication site (DOI): 10.1177/1060028014566446 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 25565405 ● Summary page in Scopus @ Elsevier: 2-s2.0-84924872993 (DOI: 10.1177/1060028014566446, PubMed: 25565405, Elsevier: Scopus)
2.	Licht Miyamoto, Yuko Yagi, Aya Hatano, Kazuyoshi Kawazoe, Keisuke Ishizawa, Kazuo Minakuchi, Shuhei Tomita and Koichiro Tsuchiya : Spontaneously hyperactive MEK-Erk pathway mediates paradoxical facilitation of cell proliferation in mild hypoxia, Biochimica et Biophysica Acta (BBA) - General Subjects, Vol.1850, No.4, 640-646, 2015. (Summary) Oxygen is important for common eukaryotic cells to generate ATP. Pathophysiological conditions such as ischemic diseases cause tissue hypoxia. In addition, oxygen availability in deep tissues is supposed to be far lower than surrounding atmosphere even in healthy animals, and the oxygen partial pressures in most normal tissues are estimated to be around 40-50mmHg, so-called mild hypoxia. Recent studies have demonstrated that mild hypoxia has distinct effects on living cells from severe hypoxia. For instance, mild hypoxia was reported to promote cell reprogramming. Although severe hypoxia is known to inhibit cell proliferation, mild hypoxia has been paradoxically demonstrated to increase cell proliferation. However, it has not been clarified by which molecular mechanisms mild hypoxia evokes the discontinuous increment of cell proliferation. We established experimental conditions showing the opposite influences of mild and severe hypoxia on cell proliferation using undifferentiated Caco2 human colon carcinoma cells in order to clarify the underlying molecular mechanism. The basal activity of Erk, which is a typical mediator of mitogenic signals, is spontaneously increased specifically in cells exposed to mild hypoxia, and inhibition of MEK, an upstream kinase of the Erk, completely inhibited the mild hypoxia-induced enhancement of cell proliferation. Spontaneous hyperactivation of the MEK-Erk pathway by mild hypoxia should be the plausible molecular mechanism of the paradoxical promotion of cell proliferation. Our findings will provide clues to the molecular basis of mild hypoxia-evoked phenomena such as cell reprogramming. (Link to Publication Site) ● Publication site (DOI): 10.1016/j.bbagen.2014.12.006 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 25497211 ● Summary page in Scopus @ Elsevier: 2-s2.0-84921044624 (DOI: 10.1016/j.bbagen.2014.12.006, PubMed: 25497211, Elsevier: Scopus)
3.	Takeshi Soeki, Kunihiko Koshiba, Toshiyuki Niki, Kenya Kusunose, Koji Yamaguchi, Hirotsugu Yamada, Tetsuzo Wakatsuki, Michio Shimabukuro, Kazuo Minakuchi, I Kishimoto, Kenji Kangawa and Masataka Sata : Effect of ghrelin on autonomic activity in healthy volunteers., Peptides, Vol.62, 1-5, 2014. (Summary) Ghrelin is a novel growth hormone (GH)-releasing peptide originally isolated from the stomach. Recently, we have shown that ghrelin suppresses cardiac sympathetic activity and prevents early left ventricular remodeling in rats with myocardial infarction. In the present study, we evaluated the effect of ghrelin on autonomic nerve activity in healthy human subjects. An intravenous bolus of human synthetic ghrelin (10g/kg) was administered to 10 healthy men (mean age, 33 years). Holter monitoring assessment was performed before and during 2h after the ghrelin therapy. The standard deviation of normal RR intervals (SDNN), square root of the mean of the sum of the squares of differences between adjacent RR intervals (rMSSD), high-frequency power (HF), and low-frequency power (LF) were analyzed. Blood samples were also obtained before and after the therapy. A single administration of ghrelin decreased both heart rate and blood pressure. Interestingly, ghrelin significantly decreased the LF and LF/HF ratio of heart rate variability and increased the SDNN, rMSSD, and HF. Ghrelin also elicited a marked increase in circulating GH, but not insulin-like growth factor-1. These data suggest that ghrelin might suppress cardiac sympathetic nerve activity and stimulate cardiac parasympathetic nerve activity. (Keyword) Ghrelin / Autonomic nerve activity / Heart rate variability / Electrocardiography / Hemodynamics (Link to Publication Site) ● Publication site (DOI): 10.1016/j.peptides.2014.09.015 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 25265271 ● Search Scopus @ Elsevier (PMID): 25265271 ● Search Scopus @ Elsevier (DOI): 10.1016/j.peptides.2014.09.015 (DOI: 10.1016/j.peptides.2014.09.015, PubMed: 25265271)
4.	Hirofumi Shibata, Kazuyoshi Kawazoe, Shibata Takahiro, Fushitani Shuji, Watanabe Miho, Takagai Tomoko, Nagao Tamiko, Mami Azuma and Kazuo Minakuchi : Investigation of the Cleanliness of Hospital Environmental Surfaces by Adenosine Triphosphate Bioluminescence Assay, Japanese Journal of Infection Prevention and Control, Vol.29, No.6, 417-423, 2014. (Summary) This study evaluated the combined use of adenosine triphosphate (ATP) bioluminescence and microbiological assays for monitoring environmental surfaces in a teaching hospital to develop a method for rapid detection of microbial contamination that could constitute a health risk to patients. ATP bioluminescence assay and microbiological screening were performed of various surfaces of toilet facilities in outpatient wards. In each of the five sites screened, the ATP levels were significantly higher than on a cleaned, disinfected stainless steel surface, indicating that all screened surfaces were "high-touch" surfaces and the surfaces harbored significantly higher levels of certain organic matter. The microbiological assay confirmed that the microbiological contamination had spread throughout the screened sites. The ATP values of the samples positive for microbes occurred in a significantly higher range than those of the samples negative for microbes (p<0.01). However, no linear relationship was established between the ATP values and aerobic colony counts of the screened sites. These results clearly imply that the use of ATP bioluminescence to measure the microbial contamination of an environment yields qualitative rather than quantitative data. In conclusion, ATP monitoring is a rapid and convenient method to assess environmental contamination and persistence of microbes and to monitor the effectiveness of current cleaning practices. (Keyword) hospital environment / environmental surfaces / ATP bioluminescence / microbiological contamination / cleaning procedure / ATP (Link to Publication Site) ● Publication site (DOI): 10.4058/jsei.29.417 (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1390282680274952960 ● Search Scopus @ Elsevier (DOI): 10.4058/jsei.29.417 (DOI: 10.4058/jsei.29.417, CiNii: 1390282680274952960)
5.	Naoto Okada, Takeshi Hanafusa, Takumi Sakurada, Kazuhiko Teraoka, Toshihide Kujime, Masahiro Abe, Yasuo Shinohara, Kazuyoshi Kawazoe and Kazuo Minakuchi : Risk Factors for Early-Onset Peripheral Neuropathy Caused by Vincristine in Patients With a First Administration of R-CHOP or R-CHOP-Like Chemotherapy, Journal of Clinical Medicine Research, Vol.6, No.4, 252-260, 2014. (Summary) Peripheral neuropathy is a well-known side effect of vincristine (VCR), a microtubule inhibitor used for R-CHOP or R-CHOP-like (namely R-CVP and R-THP-COP) regimens. Previous studies have shown that both the total dose of VCR and the number of treatment cycles are related to the incidence of VCR-induced peripheral neuropathy (VIPN). However, VIPN will also occur during the first treatment cycle regardless of the total dose of VCR or number of treatment cycles (early-onset VIPN). There is little information about early-onset VIPN, and it is difficult to predict. The present study's goal was to identify risk factors for early-onset VIPN. We analyzed the case records of patients who had their first administration of an R-CHOP or R-CHOP-like regimen between April 2008 and August 2013 at Tokushima University Hospital in Tokushima, Japan. To identify the risk factors for early-onset VIPN, we performed univariate and multivariate logistic regression analyses. Forty-one patients underwent an R-CHOP or R-CHOP-like regimen for the first time at Tokushima University Hospital between April 2008 and August 2013, and 14 patients had grade 1 or higher early-onset VIPN. A univariate analysis revealed that age, the dose of VCR and the concomitant use of aprepitant appeared to be the risk factors of early-onset VIPN. In our calculation using receiver-operator characteristics curves, the cut-off value for patient age was 65 years and that of the dose of VCR was 1.9 mg. A multivariate analysis revealed that VCR dose ≥ 1.9 mg and the concomitant use of the antiemetic aprepitant were independent risk factors for early-onset VIPN. Our present study showed that the patients who had VCR dose ≥ 1.9 mg and the concomitant use of aprepitant had the risk for early-onset VIPN. This suggests that it is important to use aprepitant in light of the risk of early-onset VIPN and the benefit of aprepitant's antiemetic effect in R-CHOP and R-CHOP-like regimens. (Link to Publication Site) ● Publication site (DOI): 10.14740/jocmr1856w (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 24883150 ● Search Scopus @ Elsevier (PMID): 24883150 ● Search Scopus @ Elsevier (DOI): 10.14740/jocmr1856w (DOI: 10.14740/jocmr1856w, PubMed: 24883150)
6.	Miho Watanabe, Soichiro Tajima, Rumi Katashima, Toshiko Miyamoto, Makiko Yamagami, Kazuo Minakuchi and Hiroaki Yanagawa : Serious adverse events and compensation in registration trials: a review of data from a Japanese university hospital., BMC Research Notes, Vol.7, 245, 2014. (Summary) Clinical trials leading to regulatory approval, or registration trials, play a central role in the development of drugs and medical devices. The contribution of support staff, such as the clinical research coordinator (CRC) and administrative officers, in registration trials is now widely recognized. Attending to serious adverse events is an important duty of the CRC and investigators alike, and managing these complications and compensation constitutes a key responsibility. We retrospectively examined the frequency of serious adverse events and compensation events reported from 2007 through 2011 at Tokushima University Hospital, an academic hospital in rural Japan. We present herein the results of our analysis. Over the five-year period, 284 subjects participating in 106 registration trials experienced a total of 43 serious adverse events, and eight compensation events were documented. Among the serious adverse events, 35 (81.4%) were considered not related to the investigational drug, and 17 (39.5%) resulted in withdrawal of the study drug. Patients with malignant diseases experienced serious adverse events significantly more frequently compared to those with non-malignant diseases (28.3% versus 8.2%, respectively; P < 0.01). The CRC should be vigilant for serious adverse events in oncology clinical trials due to the generally higher frequency of these complications in subjects with malignancy. However, on an individual basis, the CRC may be seldom involved in the process for compensating serious adverse events. Therefore, the CRC's ability to share such experiences may serve as an opportunity for educating clinical trial support staff at the study site as well as those at other sites. However, further study is warranted to determine the role of the clinical trial support staff in optimizing methods for managing adverse events requiring compensation in registration trials. (Tokushima University Institutional Repository) ● Metadata: 114893 (Link to Publication Site) ● Publication site (DOI): 10.1186/1756-0500-7-245 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 24742228 ● Search Scopus @ Elsevier (PMID): 24742228 ● Search Scopus @ Elsevier (DOI): 10.1186/1756-0500-7-245 (Tokushima University Institutional Repository: 114893, DOI: 10.1186/1756-0500-7-245, PubMed: 24742228)
7.	Kensaku Aki, Kazuyoshi Kawazoe, Azusa Izumi, Tomoki Tada, Kazuo Minakuchi and Eiji Hosoi : Direct Determination of ABO Blood Group Genotypes from Whole Blood Using PCR-Amplification of Specific Alleles Method, American Journal of BioScience, Vol.2, 49-55, 2014. (Link to Publication Site) ● Publication site (DOI): 10.11648/j.ajbio.20140202.15 (Link to Search Site for Scientific Articles) ● Search Scopus @ Elsevier (DOI): 10.11648/j.ajbio.20140202.15 (DOI: 10.11648/j.ajbio.20140202.15)
8.	Naoto Okada, Kazuyoshi Kawazoe, Kazuhiko Teraoka, Toshihide Kujime, Masahiro Abe, Yasuo Shinohara and Kazuo Minakuchi : Identification of the Risk Factors Associated with Hypocalcemia Induced by Denosumab, Biological & Pharmaceutical Bulletin, Vol.36, No.10, 1622-1626, 2013. (Summary) Denosumab, a fully human monoclonal antibody that inhibits the receptor activator of nuclear factor-κB ligand, inhibits the activation of osteoclasts. Some clinical trials have shown that denosumab suppresses bone resorption in patients with advanced cancer, but hypocalcemia has been reported as a serious adverse effect after the administration of denosumab. It is difficult to predict hypocalcemia in such cases because the risk factors for denosumab-induced hypocalcemia have not been reported. Accordingly, the aim of the present study was to identify the risk factors for hypocalcemia induced by denosumab. We retrospectively reviewed the records of patients who had received denosumab at Tokushima University Hospital between April 2012 and May 2013. Fifty-three patients were analyzed and eleven patients had hypocalcemia after administration of denosumab. Univariate logistic regression analysis revealed that the patients who had not been administered zoledronic acid before receiving denosumab or had lower creatinine clearance (CCr) appeared to have a higher risk of hypocalcemia (p<0.05). The cut off value of CCr was 50.4 ml/min calculated by receiver-operator characteristics curves. Moreover, multivariate logistic regression analysis revealed that non-administration of zoledronic acid (odds ratio 10.43, p<0.05) and CCr less than 50.0 ml/min (odds ratio 5.90, p<0.05) were independent risk factors for denosumab-induced hypocalcemia. These findings provide useful information regarding the monitoring of hypocalcemia in patients receiving denosumab. (Keyword) denosumab / hypocalcemia / risk factor / zoledronic acid / creatinine clearance (Link to Publication Site) ● Publication site (DOI): 10.1248/bpb.b13-00496 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 23934346 ● CiNii @ National Institute of Informatics (CRID): 1390282679608990592 ● Summary page in Scopus @ Elsevier: 2-s2.0-84887114892 (DOI: 10.1248/bpb.b13-00496, PubMed: 23934346, CiNii: 1390282679608990592, Elsevier: Scopus)
9.	Shinji Abe, Yuki Morita, Mika Kato Kaneko, Masaki Hanibuchi, Yuta Tsujimoto, Hisatsugu Goto, Souji Kakiuchi, Yoshinori Aono, Jun Huang, Seidai Sato, Masatoshi Kishuku, Yuki Taniguchi, Mami Azuma, Kazuyoshi Kawazoe, Yoshitaka Sekido, Seiji Yano, Shin-ichi Akiyama, Saburo Sone, Kazuo Minakuchi, Yukinari Kato and Yasuhiko Nishioka : A novel targeting therapy of malignant mesothelioma using anti-podoplanin antibody, The Journal of Immunology, Vol.190, No.12, 6239-6249, 2013. (Summary) Podoplanin (Aggrus), which is a type I transmembrane sialomucin-like glycoprotein, is highly expressed in malignant pleural mesothelioma (MPM). We previously reported the generation of a rat anti-human podoplanin Ab, NZ-1, which inhibited podoplanin-induced platelet aggregation and hematogenous metastasis. In this study, we examined the antitumor effector functions of NZ-1 and NZ-8, a novel rat-human chimeric Ab generated from NZ-1 including Ab-dependent cellular cytotoxicity (ADCC) and complement-dependent cytotoxicity against MPM in vitro and in vivo. Immunostaining with NZ-1 showed the expression of podoplanin in 73% (11 out of 15) of MPM cell lines and 92% (33 out of 36) of malignant mesothelioma tissues. NZ-1 could induce potent ADCC against podoplanin-positive MPM cells mediated by rat NK (CD161a(+)) cells, but not murine splenocytes or human mononuclear cells. Treatment with NZ-1 significantly reduced the growth of s.c. established tumors of MPM cells (ACC-MESO-4 or podoplanin-transfected MSTO-211H) in SCID mice, only when NZ-1 was administered with rat NK cells. In in vivo imaging, NZ-1 efficiently accumulated to xenograft of MPM, and its accumulation continued for 3 wk after systemic administration. Furthermore, NZ-8 preferentially recognized podoplanin expressing in MPM, but not in normal tissues. NZ-8 could induce higher ADCC mediated by human NK cells and complement-dependent cytotoxicity as compared with NZ-1. Treatment with NZ-8 and human NK cells significantly inhibited the growth of MPM cells in vivo. These results strongly suggest that targeting therapy to podoplanin with therapeutic Abs (i.e., NZ-8) derived from NZ-1 might be useful as a novel immunotherapy against MPM. (Keyword) Animals / Antibodies, Monoclonal / Flow Cytometry / Humans / Immunohistochemistry / Immunotherapy / Male / Membrane Glycoproteins / Mesothelioma / Mice / Mice, SCID / Pleural Neoplasms / Rats / Rats, Wistar / Recombinant Fusion Proteins / Xenograft Model Antitumor Assays (Link to Publication Site) ● Publication site (DOI): 10.4049/jimmunol.1300448 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 23690472 ● Search Scopus @ Elsevier (PMID): 23690472 ● Search Scopus @ Elsevier (DOI): 10.4049/jimmunol.1300448 (DOI: 10.4049/jimmunol.1300448, PubMed: 23690472)
10.	Takumi Sakurada, Keisuke Ishizawa, Masaki Imanishi, Yuki Izawa-Ishizawa, Shoko Fujii, Erika Tominaga, Teppei Tsuneishi, Yuya Horinouchi, Yoshitaka Kihira, Yasumasa Ikeda, Shuhei Tomita, Ken-ichi Aihara, Kazuo Minakuchi, Koichiro Tsuchiya and Toshiaki Tamaki : Nitrosonifedipine ameliorates angiotensin II-induced vascular remodeling via antioxidative effects, Naunyn-Schmiedeberg's Archives of Pharmacology, Vol.386, No.1, 29-39, 2013. (Summary) Nifedipine is unstable under light and decomposes to a stable nitroso analog, nitrosonifedipine (NO-NIF). The ability of NO-NIF to block calcium channels is quite weak compared with that of nifedipine. Recently, we have demonstrated that NO-NIF reacts with unsaturated fatty acid leading to generate NO-NIF radical, which acquires radical scavenging activity. However, the effects of NO-NIF on the pathogenesis related with oxidative stress, such as atherosclerosis and hypertension, are unclear. In this study, we investigated the effects of NO-NIF on angiotensin II (Ang II)-induced vascular remodeling. Ang II-induced thickening and fibrosis of aorta were inhibited by NO-NIF in mice. NO-NIF decreased reactive oxygen species (ROS) in the aorta and urinary 8-hydroxy-20-deoxyguanosine. Ang II-stimulated mRNA expressions of p22(phox), CD68, F4/80, monocyte chemoattractant protein-1, and collagen I in the aorta were inhibited by NO-NIF. Moreover, NO-NIF inhibited Ang II-induced cell migration and proliferation of vascular smooth muscle cells (VSMCs). NO-NIF reduced Ang II-induced ROS to the control level detected by dihydroethidium staining and lucigenin chemiluminescence assay in VSMCs. NO-NIF suppressed phosphorylations of Akt and epidermal growth factor receptor induced by Ang II. However, NO-NIF had no effects on intracellular Ca(2+) increase and protein kinase C-δ phosphorylation induced by Ang II in VSMCs. The electron paramagnetic resonance spectra indicated the continuous generation of NO-NIF radical of reaction with cultured VSMCs. These findings suggest that NO-NIF improves Ang II-induced vascular remodeling via the attenuation of oxidative stress. (Keyword) Angiotensin II / Animals / Antioxidants / Aorta, Thoracic / calcium / Cell Movement / Cell Proliferation / Fibrosis / Male / Mice / Mice, Inbred C57BL / Muscle, Smooth, Vascular / Nifedipine / Nitroso Compounds / oxidative stress / Rats / reactive oxygen species (Link to Publication Site) ● Publication site (DOI): 10.1007/s00210-012-0810-7 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 23149861 ● Summary page in Scopus @ Elsevier: 2-s2.0-84872316103 (DOI: 10.1007/s00210-012-0810-7, PubMed: 23149861, Elsevier: Scopus)
11.	Yasushi Kirino, Masako Sei, Kazuyoshi Kawazoe, Kazuo Minakuchi and Youichi Sato : Plasma dipeptidyl peptidase 4 activity correlates with body mass index and the plasma adiponectin concentration in healthy young people, Endocrine Journal, Vol.59, No.10, 949-953, 2012. (Summary) We previously found that plasma dipeptidyl peptidase 4 (DPP4) activity was associated with the development of obesity, type 2 diabetes, and type 1 diabetes using animal models. In this study, we investigated whether DPP4 activity is correlated with the clinical parameters of obesity and/or diabetes in healthy young subjects. Body mass index (BMI), plasma DPP4 activity, total cholesterol, high density lipoprotein (HDL) cholesterol, triglycerides, fasting blood glucose, adiponectin concentration, and body fat were measured in 165 subjects (110 males and 55 females, age 23.2 ± 2.4 years). In correlation analyses, DPP4 activity displayed strong positive correlations with BMI (p = 5.5 × 10(-5)) and total cholesterol (p = 0.0014), and a negative correlation with the plasma adiponectin concentration (p = 0.013), but not fasting blood glucose. Our findings suggest that plasma DPP4 activity is correlated with the clinical parameters of obesity rather than diabetes in young people. (Link to Publication Site) ● Publication site (DOI): 10.1507/endocrj.EJ12-0158 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 22785237 ● Search Scopus @ Elsevier (PMID): 22785237 ● Search Scopus @ Elsevier (DOI): 10.1507/endocrj.EJ12-0158 (DOI: 10.1507/endocrj.EJ12-0158, PubMed: 22785237)
12.	Masayuki Shono, Mitsuo Kitamura, Ken Konaka, Kazuyoshi Kawazoe and Kazuo Minakuchi : Effects of mechanical pressure on cytoskeleton in human umbilical vein endothelial cells cultured in a newly developed chamber., Journal of Medical Technology, Vol.56, No.7, 803-805, 2012. (Keyword) 血管内皮細胞 / 加圧チャンバー / DAPI染色 / アクチン (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1390002209906676352 (CiNii: 1390002209906676352)
13.	西谷典子, 伏谷秀治, Hirofumi Shibata, 瀧口益史, Kazuyoshi Kawazoe, 吉原新一 and Kazuo Minakuchi : Multiple effects of statins in patients with bacterial infectious diseases, Shikoku Acta Medica, Vol.68, No.1,2, 29-34, 2012. (Summary) Statins, treatments for dyslipidemia, have been reported to possess effects leading to therepair of the vascular endothelium, as well as anti-oxidative and anti-inflammatory effects, and theirclinical usefulness has been focused on. It was also reported in previous clinical research thatbacteremia patients on statins showed a lower mortality compared to those not receiving statins,and atherosclerosis patients on statins showed a significantly lower rate of severe or fatal sepsiscompared to those not receiving them. We conducted a case-control study involving patientshospitalized in Tokushima University Hospital to evaluate the relationship between taking/nottaking statins and bacterial infectious diseases. As a result, there was no relationship betweentaking/not taking statins and the overall patients with bacterial infectious diseases, but sepsispatients on statins showed a significantly lower mortality. The taking of statins was suggested tobe useful for patients with bacterial infectious diseases, particularly males. (Keyword) statin / multiple effect / bacterial infection / sepsis (Tokushima University Institutional Repository) ● Metadata: 97534 (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1050282812440592768 (Tokushima University Institutional Repository: 97534, CiNii: 1050282812440592768)
14.	Kazuyoshi Kawazoe, Kana Ota, Mayuko Okamoto, Youichi Sato and Kazuo Minakuchi : Anti-obesity effects of Schisandra chinensis fruit water extract in rats fed a high-fat diet, Journal of Traditional Medicines, Vol.29, No.3, 143-148, 2012. (Summary) Obesity has become a major public health problem worldwide. To date, many studies on obesity prevention have been performed. In this study, we examined the anti-obesity effects of <I>Schisandra chinensis</I> (Turcz.) Baill. fruit (SC) water extract in rats fed a high-fat diet. We gave the rats high-fat chow including SC water extract for 10 weeks. Although these rats ate the same amount of chow as the high-fat diet group, their weight gain was significantly inhibited compared to that in the high-fat diet group. Moreover, the SC group showed significantly decreased epididymal fat weight and levels of plasma triglycerides, total cholesterol, and leptin compared to the high-fat diet group. In the oral glucose tolerance test (OGTT), the SC group showed lower blood glucose levels than the high-fat diet group 90 min after eating. This is the first study to show that SC water extract has anti-obesity effects. It may be beneficial to drink SC water extract or tea after eating to prevent obesity. (Keyword) traditional medicine / anti-obesity effect / schisandra fruit / epididymal fat / high-calorie diet (Link to Publication Site) ● Publication site (DOI): 10.11339/jtm.29.143 (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1390001205234375424 ● Summary page in Scopus @ Elsevier: 2-s2.0-85024448611 (DOI: 10.11339/jtm.29.143, CiNii: 1390001205234375424, Elsevier: Scopus)
15.	Masayuki Shono, Mitsuo Kitamura, 小中健, Kazuyoshi Kawazoe and Kazuo Minakuchi : Changes in DNA structure in the DPI-induced apoptosis in cultured human HepG2 cells, Journal of Medical Technology, Vol.56, No.3, 331-334, 2012. (Keyword) DPI / HepG2 / apoptosis / DAPI / PI (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1390565159860698496 (CiNii: 1390565159860698496)
16.	Hirofumi Shibata, Nishitani Noriko, Yaohara Sayuri, Naokatu Arakaki, Tomihiko Higuti, Kazuyoshi Kawazoe and Kazuo Minakuchi : Simvastatin represses translocation of Pseudomonas aeruginosa across Madin-Darby canine kidney cell monolayers, The Journal of Medical Investigation : JMI, Vol.59, No.1,2, 186-191, 2012. (Summary) Pseudomonas aeruginosa causes both invasive (bacteremic) and chronic noninvasive infections. An increase in intestinal epithelial permeability is a characteristic of severe sepsis. Alterations in the normal barrier function of the gut mucosa may result in the translocation of microbial cells and products. On the otherhand, it has been demonstrated that statin use is associated with a lower risk of mortality from bloodstream infections. Therefore, we investigated the ability of P. aeruginosa PAO1 to translocate across the Madin-Darby canine kidney (MDCK) cell monolayers in the presence and absence of simvastatin. The bacteria readily translocated across MDCK cell monolayers after 3 h of infection irrespective of the presence or absence of the drug in the medium. However, the bacteria were less able to penetrate the MDCK monolayers in the presence of simvastatin than in its absence. A gentamicin survival assay demonstrated that simvastatin did not affect the bacteria's invasive behavior in the MDCK cells. (Keyword) Animals / Anticholesteremic Agents / Bacterial Translocation / Cell Line / Dogs / Epithelial Cells / Kidney / Pseudomonas Infections / Pseudomonas aeruginosa / Simvastatin (Tokushima University Institutional Repository) ● Metadata: 106020 (Link to Publication Site) ● Publication site (DOI): 10.2152/jmi.59.186 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 22450007 ● Search Scopus @ Elsevier (PMID): 22450007 ● Search Scopus @ Elsevier (DOI): 10.2152/jmi.59.186 (Tokushima University Institutional Repository: 106020, DOI: 10.2152/jmi.59.186, PubMed: 22450007)
17.	Soichiro Tajima, Yasumasa Ikeda, Kaori Sawada, Noriko Yamano, Yuya Horinouchi, Yoshitaka Kihira, Keisuke Ishizawa, Yuki Izawa-Ishizawa, Kazuyoshi Kawazoe, Shuhei Tomita, Kazuo Minakuchi, Koichiro Tsuchiya and Toshiaki Tamaki : Iron reduction by deferoxamine leads to amelioration of adiposity via the regulation of oxidative stress and inflammation in obese and type 2 diabetes KKAy mice., American Journal of Physiology, Endocrinology and Metabolism, Vol.302, No.1, E77-86, 2012. (Summary) Iron is an essential trace metal for most organisms. However, excess iron causes oxidative stress through production of highly toxic hydroxyl radicals via the Fenton/Haber-Weiss reaction. Iron storage in the body is reported to be associated with fat accumulation and type 2 diabetes mellitus. We investigated the role of iron in adiposity by using KKAy mice and obese and diabetic model mice. Eight-week-old KKAy mice were divided into two groups and treated with deferoxamine (DFO), an iron chelator agent, or a vehicle for 2 wk. DFO treatment diminished fat iron concentration and serum ferritin levels in KKAy mice. Fat weight and adipocyte size were reduced significantly in DFO-treated mice compared with vehicle-treated mice. Macrophage infiltration into fat was also decreased in DFO-treated mice compared with vehicle-treated mice. Superoxide production and NADPH oxidase activity in fat, as well as urinary 8-hydroxy-2'-deoxyguanosine excretion, were decreased in KKAy mice after DFO treatment while p22(phox) expression in adipose tissue was diminished in such mice. Ferritin expression in the fat of DFO-treated KKAy mice was decreased. In addition, F4/80-positive cells also presented through both p22(phox) and ferritin expression. The mRNA expression levels of inflammatory cytokines were also reduced in fat tissue of DFO-treated mice. These findings suggest that reduction of iron levels ameliorates adipocyte hypertrophy via suppression of oxidative stress, inflammatory cytokines, and macrophage infiltration, thereby breaking a vicious cycle in obesity. (Keyword) ferrum / oxidative stress / obesity (Link to Publication Site) ● Publication site (DOI): 10.1152/ajpendo.00033.2011 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 21917632 ● Search Scopus @ Elsevier (PMID): 21917632 ● Search Scopus @ Elsevier (DOI): 10.1152/ajpendo.00033.2011 (DOI: 10.1152/ajpendo.00033.2011, PubMed: 21917632)
18.	Yuya Horinouchi, Takumi Sakurada, Toshimi Nakamura, Soichiro Tajima, Hirotaka Nishisako, Shinji Abe, Kazuhiko Teraoka, Toshihide Kujime, Kazuyoshi Kawazoe and Kazuo Minakuchi : Hypertension as a predictive factor of effect of bevacizumab in treatment of colorectal cancer, Journal of the Pharmaceutical Society of Japan, Vol.131, No.8, 1251-1257, 2011. (Summary) Bevacizumab is a monoclonal antibody that targets vascular endothelial growth factor (VEGF) for treatment of metastatic colorectal cancer. Recently, much evidence has suggested that bevacizumab-induced hypertension might be predictive of the effect of bevacizumab. The aim of our study is to retrospectively assess the relationship between the onset of hypertension and the activity of bevacizumab in Japanese metastatic colorectal cancer patients. Between July 2007 and December 2010, 36 patients (median age 66 years; 36-81 years) with metastatic colorectal cancer were assigned to receive bevacizumab in combination with either mFOLFOX6 (5-FU, levofolinate and oxaliplatin) or FOLFIRI (5-FU, levofolinate and irinotecan) at the Tokushima University Hospital. A patient who had increase by >20 mmHg in diastolic blood pressure or had increase to >150/100 mmHg or received antihypertensive treatment was defined as hypertensive. The objective response rate (ORR), disease control rate (DCR) and progression-free survival (PFS) were compared between the hypertensive group (n=10) and non-hypertensive group (n=26). ORR and DCR were 60.0% and 100%, respectively, in the hypertensive group and ORR and DCR were 23.1% and 80.8%, respectively, in the non-hypertensive group. These differences were statistically significant (p<0.05). The median PFS tended to be longer in the hypertensive group (65.0 weeks) than in the non-hypertensive group (40.0 weeks). Our data suggested that bevacizumab-induced hypertension may be predictive of the effect of bevacizumab in Japanese metastatic colorectal cancer patients. (Keyword) Adult / Aged / Aged, 80 and over / Angiogenesis Inhibitors / Antibodies, Monoclonal, Humanized / Antineoplastic Combined Chemotherapy Protocols / Asian Continental Ancestry Group / Bevacizumab / blood pressure / Camptothecin / Colorectal Neoplasms / Disease-Free Survival / Female / Fluorouracil / Forecasting / Humans / hypertension / Leucovorin / Male / Middle Aged / Molecular Targeted Therapy / Organoplatinum Compounds / Retrospective Studies / Treatment Outcome / Vascular Endothelial Growth Factor A (Link to Publication Site) ● Publication site (DOI): 10.1248/yakushi.131.1251 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 21804330 ● CiNii @ National Institute of Informatics (CRID): 1390001206126575616 ● Summary page in Scopus @ Elsevier: 2-s2.0-79961038711 (DOI: 10.1248/yakushi.131.1251, PubMed: 21804330, CiNii: 1390001206126575616, Elsevier: Scopus)
19.	Keisuke Ishizawa, Masanori Yoshizumi, Yoshichika Kawai, Junji Terao, Yoshitaka Kihira, Yasumasa Ikeda, Shuhei Tomita, Kazuo Minakuchi, Koichiro Tsuchiya and Toshiaki Tamaki : Pharmacology in health food: Metabolism of quercetin in vivo and its protective effect against arteriosclerosis, Journal of Pharmacological Sciences, Vol.115, No.4, 466-470, 2011. (Summary) Quercetin, a member of the bioflavonoids family, has been proposed to have anti-atherogenic, anti-inflammatory, and anti-hypertensive properties leading to the beneficial effects against cardiovascular diseases. It was recently demonstrated that quercetin 3-O-β-D-glucuronide (Q3GA) is one of the major quercetin conjugates in human plasma, in which the aglycone could not be detected. Although most of the in vitro pharmacological studies have been carried out using only the quercetin aglycone form, experiments using Q3GA would be important to discover the preventive mechanisms of cardiovascular diseases by quercetin in vivo. Therefore we examined the effects of the chemically synthesized Q3GA, as an in vivo form, on vascular smooth muscle cell (VSMC) disorders related to the progression of arteriosclerosis. Platelet-derived growth factor-induced cell migration and proliferation were inhibited by Q3GA in VSMCs. Q3GA attenuated angiotensin II-induced VSMC hypertrophy via its inhibitory effect on JNK and the AP-1 signaling pathway. Q3GA scavenged 1,1-diphenyl-2-picrylhydrazyl radical measured by the electron paramagnetic resonance method. In addition, immunohistochemical studies with monoclonal antibody 14A2 targeting the Q3GA demonstrated that the positive staining specifically accumulates in human atherosclerotic lesions, but not in the normal aorta. These findings suggest Q3GA would be an active metabolite of quercetin in plasma and may have preventative effects on arteriosclerosis relevant to VSMC disorders. (Keyword) Animals / Antioxidants / Arteriosclerosis / Cell Movement / Cell Proliferation / Drug Evaluation, Preclinical / Free Radicals / Health Food / Humans / Hypertrophy / Muscle, Smooth, Vascular / Quercetin / Signal Transduction (Link to Publication Site) ● Publication site (DOI): 10.1254/jphs.10R38FM (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 21436601 ● Search Scopus @ Elsevier (PMID): 21436601 ● Search Scopus @ Elsevier (DOI): 10.1254/jphs.10R38FM (DOI: 10.1254/jphs.10R38FM, PubMed: 21436601)
20.	Hirotaka Nishisako, Toshitaka Ikehara, Tairoh Shiraishi, Yuki Minami, Ichinose Hiromi Sasaki, Hitoshi Houchi, Kazuyoshi Kawazoe, Kazuo Minakuchi, Mitsuo Kitamura, Masayuki Shono, Kazuo Yoshizaki, Yohsuke Kinouchi and Hiroshi Miyamoto : Effects of a 1.5 T time-varying magnetic field on cell volume regulation of bovine adrenal chromaffin cells in hyposmotic media., The Journal of Medical Investigation : JMI, Vol.58, No.1-2, 95-105, 2011. (Summary) Effects of a time-varying magnetic field on cell volume regulation by hyposmotic stress in cultured bovine adrenal chromaffin cells were examined. Through regulatory volume decrease (RVD), cell volume of chromaffin cells that were incubated in a hypotonic medium initially increased, reached a peak and finally recovered to the initial value. Two hour exposure to a magnetic field and addition of cytochalasin D increased peak value and delayed return to initial value. Intracellular F-actin contents initially decreased but returned to normal levels after 10 sec. Two hour exposure to the magnetic field and addition of cytochalasin D continuously reduced the F-actin content. Results suggest that exposure to the magnetic field stimulated disruption of the actin cytoskeleton and that the disruption delayed the recovery to the volume prior to osmotic stress. (Keyword) Actins / Animals / calcium / Cattle / Cell Size / Cells, Cultured / Chromaffin Cells / Cytochalasin D / Hypotonic Solutions / Magnetics / Osmotic Pressure / Time Factors (Tokushima University Institutional Repository) ● Metadata: 111307 (Link to Publication Site) ● Publication site (DOI): 10.2152/jmi.58.95 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 21372493 ● Search Scopus @ Elsevier (PMID): 21372493 ● Search Scopus @ Elsevier (DOI): 10.2152/jmi.58.95 (Tokushima University Institutional Repository: 111307, DOI: 10.2152/jmi.58.95, PubMed: 21372493)
21.	Naoto Okada, Takenori Yamamoto, Masahiro Watanabe, Yuuya Yoshimura, Eriko Obana, Naoshi Yamazaki, Kazuyoshi Kawazoe, Yasuo Shinohara and Kazuo Minakuchi : Identification of TMEM45B as a protein clearly showing thermal aggregation in SDS-PAGE gels and dissection of its amino acid sequence responsible for this aggregation., Protein Expression and Purification, Vol.77, No.1, 118-123, 2011. (Summary) SDS-PAGE is one of the most powerful experimental techniques used for the separation of proteins, and most proteins are separated according to their molecular size by this technique. However, exceptional proteins showing abnormal behavior in SDS-PAGE gels are known to exist. Thermal aggregation, rarely observed with membrane proteins, is one of the exceptional behaviors of proteins during SDS-PAGE, but detailed characterization of this aggregation has not yet been achieved. In the present study, we found that a putative membrane protein, TMEM45B, very clearly showed properties of thermal aggregation when it was expressed in COS7 cells and subjected to SDS-PAGE. We dissected the region of TMEM45B responsible for this aggregation, and found that of the seven putative transmembrane domains, a region comprising the 4th to 7th ones was essential for the thermal aggregation properties. We also demonstrated that these transmembrane domains, 4th to 7th, of TMEM45B conferred thermal aggregation properties on other proteins, by fusing this amino acid sequence to target proteins. The molecular mechanism causing thermal aggregation by TMEM45B is still uncertain, but TMEM45B could be utilized as a nice model to show clear thermal aggregation in SDS-PAGE gels. (Link to Publication Site) ● Publication site (DOI): 10.1016/j.pep.2011.01.011 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 21277373 ● Search Scopus @ Elsevier (PMID): 21277373 ● Search Scopus @ Elsevier (DOI): 10.1016/j.pep.2011.01.011 (DOI: 10.1016/j.pep.2011.01.011, PubMed: 21277373)
22.	Yasushi Kirino, Youichi Sato, Takayuki Kamimoto, Kazuyoshi Kawazoe and Kazuo Minakuchi : Altered dipeptidyl peptidase 4 activity during the progression of hyperinsulinemic obesity and islet atrophy in spontaneously late-stage type 2 diabetic rats., American Journal of Physiology, Endocrinology and Metabolism, Vol.300, No.2, 372-379, 2011. (Summary) Altered dipeptidyl peptidase-4 (DPP4) activity during the progression of late-stage type 2 diabetes was measured in Otsuka Long-Evans Tokushima fatty (OLETF) rats. Compared with OLETF rats subjected to 30% food restriction, food-satiated OLETF rats exhibited spontaneous hyperphagic obesity, insulin resistance, hyperglycemia, hyperinsulinemia, and increased plasma DPP4 activity during the early phase of the experiment (up to ∼30 wk). Subsequently, their plasma DPP4 activity as well as their body weight, body fat, and plasma insulin concentration declined to control levels during the late phase, resulting in excessive polyuria, proteinuria, dyslipidemia, pancreatic islet atrophy, hypoinsulinemia, and diabetes, which changed from insulin-resistant diabetes to hypoinsulinemic diabetes secondary to progressive islet insufficiency, and their fasting blood glucose level remained high. Since plasma DPP4 activity demonstrated significant positive correlations with body weight and the fasting plasma insulin level but not with the fasting blood glucose level during the late stage of diabetes, body fat and fasting plasma insulin levels may be useful factors for predicting the control of plasma DPP4 activity. In contrast, pancreatic DPP4 activity was significantly increased, and the expression of pancreatic insulin was significantly reduced in late-stage diabetic OLETF rats, suggesting that a relationship exists between the activation of pancreatic DPP4 and insulin depletion in pancreatic islet atrophy. In conclusion, it is suggested that plasma DPP4 activity changes in accordance with the progression of hyperinsulinemic obesity and pancreatic islet atrophy. DPP4 activity may play an important role in insulin homeostasis. (Keyword) Animals / Area Under Curve / Atrophy / Blood Glucose / Body Weight / Diabetes Mellitus, Type 2 / Dipeptidyl Peptidase 4 / Disease Progression / Food Deprivation / Glucose Tolerance Test / Hyperinsulinism / Immunohistochemistry / Insulin / Islets of Langerhans / Male / Obesity / Organ Size / Proteinuria / Rats / Rats, Inbred OLETF / Reverse Transcriptase Polymerase Chain Reaction / Satiation (Link to Publication Site) ● Publication site (DOI): 10.1152/ajpendo.00319.2010 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 21139073 ● Search Scopus @ Elsevier (PMID): 21139073 ● Search Scopus @ Elsevier (DOI): 10.1152/ajpendo.00319.2010 (DOI: 10.1152/ajpendo.00319.2010, PubMed: 21139073)
23.	Youichi Sato, Sakura Kosioka, Yasushi Kirino, Takayuki Kamimoto, Kazuyoshi Kawazoe, Shinji Abe, Kazuo Minakuchi and Yutaka Nakahori : Role of dipeptidyl peptidase IV (DPP4) in the development of dyslipidemia: DPP4 contributes to the steroid metabolism pathway., Life Sciences, Vol.88, No.1-2, 43-49, 2011. (Summary) We previously reported that dipeptidyl peptidase IV (DPP4)-deficient rats were susceptible to dyslipidemia induced by streptozotocin (STZ). Hence, it is suggested that DPP4 is important for lipid metabolism. In this study, to verify the role of DPP4 in the development of dyslipidemia, we carried out a microarray analysis of the livers of STZ-treated wild-type and DPP4-deficient rats and showed that the expression levels of genes involved in metabolic processes (steroid metabolic processes and cellular lipid metabolic processes) were significantly altered by STZ treatment. In the wild-type rats, the expression of hydroxysteroid (17-beta) dehydrogenase 2 (Hsd7b2), which catalyzes sex steroid synthesis from cholesterol, was significantly increased by about 15-fold after STZ treatment; however, it did not change in the DPP4-deficient rats. In the STZ untreated group of DPP4-deficient rats, the expression levels of cytochrome P450, subfamily 51 (Cyp51) and sterol-C4-methyl oxidase-like (Sc4mol), which catalyze intermediate steps in cholesterol synthesis, were significantly elevated compared to those of other groups. Similar results were demonstrated in HuH7-cells after DPP4 overexpression or the addition of human sera containing DPP4. DPP4 is crucial for regulating the expression of factors related to steroid metabolism such as Cyp51, Sc4mol, and Hsd17b2, and DPP4 deficiency or inhibition may cause dyslipidemia. (Keyword) Animals / Cell Line / Cholesterol / Dipeptidyl Peptidase 4 / Dyslipidemias / Estradiol Dehydrogenases / Humans / Lipid Metabolism / Liver / Male / Oligonucleotide Array Sequence Analysis / Rats / Rats, Inbred F344 / Reverse Transcriptase Polymerase Chain Reaction / Sterol 14-Demethylase / Streptozocin (Link to Publication Site) ● Publication site (DOI): 10.1016/j.lfs.2010.10.019 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 21047519 ● Search Scopus @ Elsevier (PMID): 21047519 ● Search Scopus @ Elsevier (DOI): 10.1016/j.lfs.2010.10.019 (DOI: 10.1016/j.lfs.2010.10.019, PubMed: 21047519)
24.	Toshitaka Ikehara, Nishisako Hirotake, Houchi Hitoshi, Kazuyoshi Kawazoe, Kazuo Minakuchi, Yohsuke Kinouchi and Miyamoto Hiroshi : EFFECTS OF EXPOSURE TO TIME-VARYING 1.5 T MAGNETIC FIELD ON VOLUME REGULATION OF BOVINE ADRENAL CHROMAFFIN CELLS, Proceedings of The Bioelectromagnetics Society 32nd Annual Meeting, 37, 2010.
25.	Keisuke Ishizawa, Yuki Izawa-Ishizawa, Narantungalag Dorjsuren, Erika Miki, Yoshitaka Kihira, Yasumasa Ikeda, Shuichi Hamano, Kazuyoshi Kawazoe, Kazuo Minakuchi, Shuhei Tomita, Koichiro Tsuchiya and Toshiaki Tamaki : Angiotensin II receptor blocker attenuates PDGF-induced mesangial cell migration in a receptor-independent manner, Nephrology, Dialysis, Transplantation, Vol.25, No.2, 364-372, 2010. (Summary) Clinical studies have shown that angiotensin II (Ang II) type 1 (AT1) receptor blockers (ARBs) are able to provide renoprotection independent of their blood pressure lowering effects. ARBs also are reported to suppress oxidative stress, inflammation and certain other cellular responses in a receptor-independent manner. We investigated the effects of an ARB, olmesartan, on the cell migration induced by platelet-derived growth factor (PDGF), a major mitogen involved in the pathogenesis of glomerulonephritis in rat mesangial cells (RMCs). Cell migration was determined by a modified Boyden chamber assay. The intracellular signalling pathway was examined by western blotting. AT1 receptor expression was knocked down by small interfering RNAs. The intracellular reactive oxygen species (ROS) was measured by using a fluorescent probe. The O(2)(.-) scavenging activities were studied by the electron paramagnetic resonance-spin trapping method. PDGF-induced cell migration was inhibited by olmesartan in AT1 receptor knockdown RMCs. Olmesartan attenuated big mitogen-activated protein (MAP) kinase 1 (BMK1) and Src activation by PDGF in AT1 receptor knockdown RMCs. PDGF-induced BMK1 activation was suppressed by the Src family tyrosine kinase inhibitors, indicating that Src exists upstream of BMK1. The NADPH oxidase inhibitors inhibited not only PDGF-induced BMK1 and Src activation but also RMC migration. The elevation in ROS generation induced by PDGF was decreased by olmesartan. Olmesartan displayed neither directly ROS scavenging activity nor the inhibition of ROS-mediated intracellular signalling in RMCs. Olmesartan attenuates ROS generation by PDGF, leading to the subsequent inhibition of Src/ BMK1/migration in an AT1 receptor-independent manner in RMCs. (Keyword) Angiotensin II Type 1 Receptor Blockers / Animals / Cell Movement / Cells, Cultured / Imidazoles / Male / Mesangial Cells / Platelet-Derived Growth Factor / Rats / Rats, Sprague-Dawley / Signal Transduction / Tetrazoles (Link to Publication Site) ● Publication site (DOI): 10.1093/ndt/gfp520 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 19812233 ● Search Scopus @ Elsevier (PMID): 19812233 ● Search Scopus @ Elsevier (DOI): 10.1093/ndt/gfp520 (DOI: 10.1093/ndt/gfp520, PubMed: 19812233)
26.	下岡幸恵, 鳥井真由美, 伊勢夏子, Shinji Abe, 島原由美子, Kazuyoshi Kawazoe, Yasuhiro Kuroda, Hitoshi Houchi and Kazuo Minakuchi : Assessment of Pharmacokinetics of Midazolam for Dose Adjustment in Patients Undergoing Brain Hypothemia Therapy, TDM研究, Vol.27, No.1, 33-38, 2010.
27.	Keisuke Ishizawa, Narantungalag Dorjsuren, Yuki Izawa-Ishizawa, Rika Sugimoto, Yasumasa Ikeda, Yoshitaka Kihira, Kazuyoshi Kawazoe, Shuhei Tomita, Koichiro Tsuchiya, Kazuo Minakuchi and Toshiaki Tamaki : Inhibitory effects of adiponectin on platelet-derived growth factor-induced mesangial cell migration, The Journal of Endocrinology, Vol.202, No.2, 309-316, 2009. (Summary) Adiponectin, an adipocyte-derived hormone, has been involved in metabolic syndrome, a known risk factor for the development of chronic kidney disease (CKD). Recent studies have demonstrated that plasma adiponectin levels are elevated when kidney function declines in patients with CKD. Excessive mesangial cell (MC) turnover is one of the important features of CKD. The aim of the present study is to elucidate the effects of adiponectin on platelet-derived growth factor (PDGF)-induced cell migration and intracellular signaling pathways, in cultured rat MCs (RMCs). PDGF-induced RMC migration was significantly inhibited by the pretreatment of adiponectin. Adiponectin alone had no effect on RMC migration. Big mitogen-activated protein (MAP) kinase 1 (BMK1), p38 MAP kinase, and Akt were activated by PDGF stimulation in a time- and concentration-dependent manner in RMC. Adiponectin alone did not affect BMK1, p38 MAP kinase, and Akt phosphorylations in RMC. PDGF-induced BMK1 and p38 MAP kinase phosphorylations were significantly attenuated by the pretreatment of adiponectin in RMCs. On the other hand, the phosphorylation of Akt by PDGF was not diminished by the pretreatment of adiponectin. Adiponectin had no effects on PDGF-receptor autophosphorylation by PDGF. We also confirmed that PDGF-induced RMC migration was significantly suppressed by siBMK1 transfection or SB203580, a p38 MAP kinase inhibitor. From these findings, it is implied that the elevated plasma adiponectin levels in patients with CKD might play a compensatory role aimed at counteracting renal dysfunction related to MC disorders. (Keyword) Adiponectin / Animals / Cell Movement / Cells, Cultured / Dose-Response Relationship, Drug / Enzyme Inhibitors / Glomerular Mesangium / Imidazoles / Male / Mitogen-Activated Protein Kinase 7 / Phosphorylation / Platelet-Derived Growth Factor / Pyridines / RNA, Small Interfering / Rats / Rats, Sprague-Dawley / Recombinant Proteins / p38 Mitogen-Activated Protein Kinases (Link to Publication Site) ● Publication site (DOI): 10.1677/JOE-08-0469 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 19460854 ● Search Scopus @ Elsevier (PMID): 19460854 ● Search Scopus @ Elsevier (DOI): 10.1677/JOE-08-0469 (DOI: 10.1677/JOE-08-0469, PubMed: 19460854)
28.	伏谷秀治, Hirofumi Shibata, Kazuhiko Teraoka, 中村敏己, 西迫寛隆, Kazuyoshi Kawazoe and Kazuo Minakuchi : 抗菌薬，抗がん剤による薬物療法における乳酸菌生菌製剤の併用状況, Japanese Journal of Pharmaceutical Health Care and Sciences, Vol.35, No.5, 360-367, 2009. (Keyword) probiotics / acidophilus biologics / antibiotics / anti-cancer drugs / order entry system / combination (Link to Publication Site) ● Publication site (DOI): 10.5649/jjphcs.35.360 (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1390001204777407104 ● Search Scopus @ Elsevier (DOI): 10.5649/jjphcs.35.360 (DOI: 10.5649/jjphcs.35.360, CiNii: 1390001204777407104)
29.	Kazuyoshi Kawazoe, 坂本久美子, 伏谷秀治, Shinji Abe, 久次米敏秀, Kazuhiko Teraoka and Kazuo Minakuchi : 現役薬剤師を対象とした漢方薬意識調査, Japanese Journal of Pharmaceutical Health Care and Sciences, Vol.35, No.5, 351-359, 2009. (Keyword) questionnaire survey / cluster analysis / Kampo / lifetime education / pharmacist / Tokushima (Link to Publication Site) ● Publication site (DOI): 10.5649/jjphcs.35.351 (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1390282679754118272 ● Search Scopus @ Elsevier (DOI): 10.5649/jjphcs.35.351 (DOI: 10.5649/jjphcs.35.351, CiNii: 1390282679754118272)
30.	Yasushi Kirino, Takayuki Kamimoto, Youichi Sato, Kazuyoshi Kawazoe, Kazuo Minakuchi and Yutaka Nakahori : Increased Plasma Dipeptidyl Peptidase IV (DPP IV) Activity and Decreased DPP IV Activity of Visceral But Not Subcutaneous Adipose Tissue in Impaired Glucose Tolerance Rats Induced by High-Fat or High-Sucrose Diet, Biological & Pharmaceutical Bulletin, Vol.32, No.3, 463-467, 2009. (Summary) Several studies have investigated whether dipeptidyl peptidase IV (DPP IV) activity is correlated to the severity of diabetes; however, it remains unclear. To investigate the roles of DPP IV activity in metabolic abnormalities, impaired glucose tolerance rats were produced using a high-fat (HF) or high-sucrose (HS) diet. HF diet-fed rats obviously exhibited impaired glucose tolerance, with increases in subcutaneous and epididymal fat mass, insulin resistance and dyslipidaemia. In rats fed a HS diet rather than a normal diet, lower body weight and fasting blood glucose were observed temporarily in the early period after HS diet feeding; however, impaired glucose tolerance was evoked to some extent with an increase in epididymal fat mass. Both HF and HS diet-fed rats showed significantly higher plasma DPP IV activity than normal diet-fed rats, in the order of HF diet>HS diet>normal diet. HF and HS diets did not significantly affect DPP IV activity and mRNA expression in the kidney. On the other hand, HF, but not HS, diet caused a significant decrease in DPP IV activity in the liver as compared to the control. Of note, both HF and HS diets caused a significant decrease in DPP IV activity in epididymal fat, even though they did not change DPP IV activity in subcutaneous fat. In conclusion, HF or HS diet-induced impaired glucose tolerance with visceral fat accumulation may be interrelated with increased plasma DPP IV activity and decreased DPP IV activity of visceral but not subcutaneous adipose tissue. (Keyword) Animals / Body Weight / Dietary Fats / Dietary Sucrose / Dipeptidyl Peptidase 4 / Eating / Glucose Intolerance / Glucose Tolerance Test / Intra-Abdominal Fat / Male / Organ Specificity / RNA / Rats / Rats, Inbred F344 / Subcutaneous Fat (Link to Publication Site) ● Publication site (DOI): 10.1248/bpb.32.463 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 19252296 ● Search Scopus @ Elsevier (PMID): 19252296 ● Search Scopus @ Elsevier (DOI): 10.1248/bpb.32.463 (DOI: 10.1248/bpb.32.463, PubMed: 19252296)
31.	Keisuke Ishizawa, Yuki Izawa-Ishizawa, Sachiyo Ohnishi, Yuki Motobayashi, Kazuyoshi Kawazoe, Shuichi Hamano, Koichiro Tsuchiya, Shuhei Tomita, Kazuo Minakuchi and Toshiaki Tamaki : Quercetin Glucuronide Inhibits Cell Migration and Proliferation by Platelet-Derived Growth Factor in Vascular Smooth Muscle Cells, Journal of Pharmacological Sciences, Vol.109, No.2, 257-264, 2009. (Summary) Many epidemiologic studies have reported that dietary flavonoids provide protection against cardiovascular disease. Quercetin, a member of the bioflavonoids family, has been proposed to have anti-inflammatory, anti-atherogenic, and anti-hypertensive properties leading to the beneficial effects against cardiovascular diseases. Recent studies demonstrated that orally administered quercetin appeared in plasma as glucuronide-conjugated forms in rats and humans. Therefore, we examined the effect of chemically synthesized quercetin glucuronide on platelet-derived growth factor (PDGF)-induced cell migration and kinase activation in cultured rat aortic smooth muscle cells (RASMCs). PDGF-induced RASMC migration was inhibited by quercetin 3-O-beta-D-glucuronide (Q3GA). Q3GA also attenuated PDGF-induced cell proliferation in RASMCs. PDGF activated extracellular-signal regulated kinase (ERK) 1/2, c-Jun N-terminal kinase (JNK), p38 mitogen-activated protein (MAP) kinase, and Akt in RASMCs. PDGF-induced JNK and Akt activations were suppressed by Q3GA, whereas ERK1/2 and p38 MAP kinase activations were not affected. We also confirmed that PDGF-induced JNK and Akt activations were inhibited by antioxidants, N-acetylcysteine and diphenyleneiodonium chloride, in RASMCs. These findings suggest Q3GA would be an active metabolite of quercetin in plasma and may possess preventing effects for cardiovascular diseases relevant to vascular smooth muscle cell disorders. (Keyword) Animals / Antioxidants / Cell Movement / Cell Proliferation / Cells, Cultured / Glucuronides / MAP Kinase Kinase 4 / Male / Muscle, Smooth, Vascular / Platelet-Derived Growth Factor / Quercetin / Rats / Rats, Sprague-Dawley (Link to Publication Site) ● Publication site (DOI): 10.1254/jphs.08236FP (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 19202317 ● Search Scopus @ Elsevier (PMID): 19202317 ● Search Scopus @ Elsevier (DOI): 10.1254/jphs.08236FP (DOI: 10.1254/jphs.08236FP, PubMed: 19202317)
32.	Yasushi Kirino, Youichi Sato, Takayuki Kamimoto, Kazuyoshi Kawazoe, Kazuo Minakuchi and Yutaka Nakahori : Interrelationship of dipeptidyl peptidase IV (DPP IV) with the development of diabetes, dyslipidaemia and nephropathy: A streptozotocin-induced model using wild-type and DPP IV-deficient rats, The Journal of Endocrinology, Vol.200, No.1, 53-61, 2009. (Summary) We examined the role of dipeptidyl peptidase IV (DPP4) in the development of diabetes, dyslipidaemia and renal dysfunction induced by streptozotocin (STZ). F344/DuCrlCrlj rats, which lack DPP4 activity, and wild-type rats were treated with STZ. Plasma DPP4 activity and biochemical parameters were measured until 42 days after STZ treatment. At the end of the experiment, renal function and DPP4 expressions of the kidney, liver, pancreas and adipose tissues were determined. Increases in blood glucose, cholesterol and triglycerides were evoked by STZ in both rat strains; however, the onset of hyperglycaemia was delayed in DPP4-deficient rats as compared with wild-type rats. By contrast, more severe dyslipidaemia was observed in DPP4-deficient rats than in wild-type rats after STZ treatment. Plasma DPP4 activity increased progressively with time after STZ treatment in wild-type rats. The kidney of wild-type rats showed decreased DPP4 activity with increased Dpp4 mRNA after STZ treatment. In addition, kidney weight, serum creatinine and excreted amounts of urinary protein, glucose and DPP4 enzyme were enhanced by STZ. DPP4-deficient rats showed increased serum creatinine in accordance with decreased creatinine clearance as compared with wild-type rats after STZ treatment. In conclusion, plasma DPP4 activity increased after STZ treatment, positively correlating to blood glucose. DPP4-deficient rats were resistant to developing diabetes, while susceptible to dyslipidaemia and reduction of glomerular filtration rate by STZ. DPP4 activation may be responsible for hyperglycaemia, lipid metabolism and preservation of renal function. (Keyword) Animals / Cholesterol / Creatinine / Diabetes Mellitus, Experimental / Diabetic Nephropathies / Dipeptidyl Peptidase 4 / Disease Models, Animal / Disease Progression / Dyslipidemias / Gene Expression / Humans / Male / Rats / Rats, Transgenic / Streptozocin (Link to Publication Site) ● Publication site (DOI): 10.1677/JOE-08-0424 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 18931022 ● Search Scopus @ Elsevier (PMID): 18931022 ● Search Scopus @ Elsevier (DOI): 10.1677/JOE-08-0424 (DOI: 10.1677/JOE-08-0424, PubMed: 18931022)
33.	Shinji Abe, Hideki Ohnishi, Koichiro Tsuchiya, Keisuke Ishizawa, Mayumi Torii, Yasuhisa Kanematsu, Kazuyoshi Kawazoe, Kazuo Minakuchi, Masanori Yoshizumi and Toshiaki Tamaki : Calcium and reactive oxygen species mediated Zn²⁺-induced apoptosis in PC12 cells, Journal of Pharmacological Sciences, Vol.102, No.1, 103-111, 2006. (Summary) The release of excessive Zn(2+) from presynaptic boutons into extracellular regions contributes to neuronal apoptotic events, which result in neuronal cell death. However, the mechanisms of Zn(2+)-induced neuronal cell death are still unclear. Therefore, we investigated the dynamics of intracellular Zn(2+), calcium, and reactive oxygen species in PC12 cells. The addition of Zn(2+) produced cell death in a concentration- and time-dependent manner. (45)Ca(2+) influx occurred just after the treatment with Zn(2+), although subsequent hydroxyl radical (()OH) production did not begin until 3 h after Zn(2+) exposure. ()OH production was significantly attenuated in Ca(2+)-free medium or by L-type Ca(2+) channel antagonist treatment, but it was independent of the intracellular Zn(2+) content. Dantrolene treatment had no protective effects against Zn(2+)-induced cell death. Treatment with N-acetyl-L-cysteine blocked ()OH generation and subsequent cell death. These data indicate that Ca(2+) influx and subsequent ()OH production are critical events in Zn(2+)-induced toxicity in PC12 cells. (Keyword) Acetylcysteine / Animals / Apoptosis / Bisbenzimidazole / Calcium / Calcium Channel Blockers / Calcium Channels, L-Type / Calcium Radioisotopes / Cell Survival / Dantrolene / Fluorescent Dyes / Free Radical Scavengers / Hydroxyl Radical / PC12 Cells / Rats / Reactive Oxygen Species / Spectrophotometry, Atomic / Zinc (Link to Publication Site) ● Publication site (DOI): 10.1254/jphs.FP0060342 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 16990703 ● Search Scopus @ Elsevier (PMID): 16990703 ● Search Scopus @ Elsevier (DOI): 10.1254/jphs.FP0060342 (DOI: 10.1254/jphs.FP0060342, PubMed: 16990703)
34.	生田雅子, 会田真規, Keisuke Ishizawa, Kazuo Minakuchi, Koichiro Tsuchiya, Masaru Kihara and Aiko Yamauchi : 徳島大学病院におけるTPN処方設計支援ソフトの使用評価と改良, Japanese Journal of Pharmaceutical Health Care and Sciences, Vol.31, No.4, 279-286, 2005. (Summary) Fluid therapy is a fundamental treatment for almost all inpatients, and nutritional therapy is the most important type of such therapy. Currently, total parenteral nutrition (TPN) is widely used to provide complete nutritional support but 30-40% of TPN recipients are considered to in a malnourished state due to inappropriate TPN prescriptions. Computer-assisted TPN prescription systems are thought to be useful to clinical professionals in solving this problem because they can perform complicated calculations that make it easy to draw up correct TPN prescriptions. So, we made a prototype system for aiding the preparation of TPN prescriptions based on Microsoft^[ !R] EXCEL and it was tested by physicians, pharmacists, dietitians and nurses engaged in TPN therapy at Tokushima University Hospital. We also had them fill out a questionnaire on the system in which they rated it for ease of operation and usefulness according to a scoring system in which 5 indicated full marks. Our Computer-Assisted TPN Prescription System was improved on the basis of the questionnaire results and is now being effectively used by the nutrition support team (NST) in Tokushima University Hospital. (Keyword) computer-assisted TPN prescription system / calculation software / TPN (total parenteral nutrition) / fluid therapy / questionnaire (Link to Publication Site) ● Publication site (DOI): 10.5649/jjphcs.31.279 (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1390282679753550336 ● Search Scopus @ Elsevier (DOI): 10.5649/jjphcs.31.279 (DOI: 10.5649/jjphcs.31.279, CiNii: 1390282679753550336)
35.	Toshitaka Ikehara, Hisao Yamaguchi, Keiko Hosokawa, Hitoshi Houchi, Ki Ho Park, Kazuo Minakuchi, Hideki Kashimoto, Mitsuo Kitamura, Yohsuke Kinouchi, Kazuo Yoshizaki and Hiroshi Miyamoto : Effects of a time-varying strong magnetic field on transient increase in Ca²⁺ release induced by cytosolic Ca²⁺ in cultured pheochromocytoma cells, Biochimica et Biophysica Acta (BBA) - General Subjects, Vol.1724, No.1-2, 8-16, 2005. (Summary) Exposure of pheochromocytoma (PC 12) cells to a time-varying 1.51 T magnetic field inhibited an increase in the intracellular Ca2+ concentration ([Ca2+]i) induced by addition of caffeine to Ca(2+)-free medium. This inhibition occurred after a 15-min exposure and was maintained for at least 2 h. [Ca2+]i sharply increased in cells loaded with cyclic ADP-ribose, and 2-h exposure significantly suppressed the increase. Addition of ATP induced a transient increase in intracellular Ca2+ release mediated by IP3 receptor, and this increase was strongly inhibited by the exposure. Results indicated that the magnetic field exposure strongly inhibited Ca2+ release mediated by both IP3 and ryanodine receptors in PC 12 cells. However, thapsigargin-induced Ca2+ influx (capacitative Ca2+ entry) across the cell membrane was unaffected. The ATP content was maintained at the normal level during the 2-h exposure, suggesting that ATP hydrolysis was unchanged. Therefore, Mg2+ which is known to be released by ATP hydrolysis and inhibit intracellular Ca2+ release may not relate the exposure-caused inhibition. Eddy currents induced in culture medium appear to change cell membrane properties and indirectly inhibit Ca2+ release from endoplasmic reticulum and other Ca2+ stores in PC 12 cells. (Keyword) ryanodine receptor / caffeine / cyclic ADP-ribose / time-varying magnetic field / eddy current (Link to Publication Site) ● Publication site (DOI): 10.1016/j.bbagen.2005.03.008 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 15890451 ● Summary page in Scopus @ Elsevier: 2-s2.0-20444422530 (DOI: 10.1016/j.bbagen.2005.03.008, PubMed: 15890451, Elsevier: Scopus)
36.	Keisuke Ishizawa, Masanori Yoshizumi, Koichiro Tsuchiya, Hitoshi Houchi, Kazuo Minakuchi, Yuki Izawa, Yasuhisa Kanematsu, Shoji Kagami, Masao Hirose and Toshiaki Tamaki : Dual effects of endothelin-1 (1-31): induction of mesangial cell migration and facilitation of monocyte recruitment through monocyte chemoattractant protein-1 production by mesangial cells, Hypertension Research, Vol.27, No.6, 433-440, 2004. (Summary) We previously found that human chymase selectively cleaves big endothelin-1 (ET-1) at the Tyr31-Gly32 bond and produces 31-amino acid endothelins, ET-1 (1-31), without any further degradation products. In this study, we investigated the effect of ET-1 (1-31) on the migration of cultured rat mesangial cells (RMCs) and on cells of the human monocytic cell line, THP-1. In addition, we examined the interaction between RMCs and THP-1 cells using conditioned media from ET-1 (1-31)-stimulated RMCs. ET-1 (1-31) caused an increase in RMC migration in a concentration-dependent manner, and the degree of increase was similar to those by ET-1 and angiotensin II (All). The ET-1 (1-31)-induced increase in RMC migration was inhibited by BQ123, an endothelin ETA receptor antagonist, but not by BQ788, an endothelin ETB receptor antagonist. ET-1 (1-31) alone did not cause significant migration of THP-1 cells. However, significant recruitment of THP-1 cells was observed with conditioned media taken from ET-1 (1-31)-stimulated RMCs. The conditioned media-induced migration of THP-1 cells was inhibited by BQ123, but not by BQ788. Western blotting analysis of the lysate of RMCs revealed that the expression of monocyte chemoattractant protein-1 (MCP-1) protein in RMCs was increased by treatment with ET-1 (1-31). The addition of neutralizing antibody for MCP-1 to the medium inhibited the migration of THP-1 cells induced by conditioned media from ET-1 (1-31)-stimulated RMCs. These findings suggest that ET-1 (1-31) play a role in glomerulonephritis (GN) via dual effects that directly cause the migration of mesangial cells (MCs) and may be responsible for the recruitment of mononuclear cells mediated through the activation of MCs. Since human chymase has been reported to be involved in glomerular disease, ET-1 (1-31) may be among the mediators. (Keyword) Animals / Antibodies / Antihypertensive Agents / Cell Movement / Cells, Cultured / Chemokine CCL2 / Culture Media, Conditioned / Endothelin-1 / Glomerular Mesangium / Peptide Fragments / Peptides, Cyclic / Rats / Rats, Sprague-Dawley (Link to Publication Site) ● Publication site (DOI): 10.1291/hypres.27.433 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 15253109 ● Search Scopus @ Elsevier (PMID): 15253109 ● Search Scopus @ Elsevier (DOI): 10.1291/hypres.27.433 (DOI: 10.1291/hypres.27.433, PubMed: 15253109)
37.	Mami Azuma, Hitoshi Houchi, Hirotaka Nishisako, Keisuke Ishizawa, Koichiro Tsuchiya, Kazuhiko Teraoka, Toshitaka Ikehara, Takenori Kusumi and Kazuo Minakuchi : Inhibitory action of novel arginine derivative on catecholamine secretion evoked by acetylcholine from cultured bovine adrenal chromaffin cells, Journal of Cardiovascular Pharmacology, Vol.42, No.Suppl. 1, S15-S18, 2003. (Summary) A novel product, 4-amino-5-guanidinopentanoic acid 15-[(4-aminobutyl)-3-aminopropylcarbamoyl] pentadecyl ester (Arg-HSA-Spm), was synthesized based on ptilomycalin A, which is one of the extracts from marine sponge. Arg-HSA-Spm contains arginine in its chemical structure. The pharmacological action of Arg-HSA-Spm on catecholamine secretion from cultured bovine adrenal chromaffin cells was examined. Arg-HSA-Spm inhibited catecholamine secretion stimulated by the physiological secretagog acetylcholine. This inhibitory action of Arg-HSA-Spm on catecholamine secretion induced by 10(-4) M acetylcholine was dose-dependent from 10(-8) M to 10(-5) M. In the presence of 3 x 10(-7) M Arg-HSA-Spm, the stimulation of catecholamine secretion observed by increasing acetylcholine up to 10(-3) M did not reach the maximal level observed without Arg-HSA-Spm. Arg-HSA-Spm at 10(-5) M suppressed both the increase in intracellular free Ca2+ level and the influx of 45Ca2+ induced by 10(-4) M acetylcholine. The Arg-HSA-Spm-induced suppression of intracellular free Ca2+ level, the influx of 45Ca2+ and catecholamine secretion were not observed in the presence of extracellular K+ at 56 mM. The results presented in this study suggested that Arg-HSA-Spm may inhibit the influx of extracellular Ca2+ into the cells, probably through its blocking action related to acetylcholine receptors, resulting in the inhibition of catecholamine secretion in adrenal chromaffin cells. (Keyword) Acetylcholine / Adrenal Medulla / Alkaloids / Animals / Arginine / calcium / Calcium Radioisotopes / Carbamates / Catecholamines / Cattle / Cells, Cultured / Chromaffin Cells / Dose-Response Relationship, Drug / Guanidines / Spermidine (Link to Publication Site) ● Publication site (DOI): 10.1097/00005344-200312001-00005 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 14871022 ● Search Scopus @ Elsevier (PMID): 14871022 ● Search Scopus @ Elsevier (DOI): 10.1097/00005344-200312001-00005 (DOI: 10.1097/00005344-200312001-00005, PubMed: 14871022)
38.	福島真理, 鳥井真由美, 胡田順子, Mami Azuma, Eiji Hosoi, 濱野修一, 寺岡和彦, Hitoshi Houchi and Kazuo Minakuchi : シクロオキシゲナーゼII阻害薬のヒト血小板凝集に及ぼす影響, 臨床薬理, Vol.34, No.1, 69-70, 2003.
39.	Yuki Suzaki, Masanori Yoshizumi, Yukio Yamashita, Shinji Abe, Koichiro Tsuchiya, Yumiko Satoh, Yasuhiro Kuroda, Kazuya Horike, Masashi Kano, Yoshio Fukuta, Takashi Kitaichi, Takaki Hori, Yutaka Masuda, Tetsuya Kitagawa, Kazuo Minakuchi and Toshiaki Tamaki : Determination of plasma concentrations of endothelin-1(1-31) and endothelin-1 in healthy subjects and patients with atherosclerosis., Journal of Cardiovascular Pharmacology, Vol.41, No.suppl.1, S83-S87, 2003. (Summary) We previously found that human chymase cleaves big endothelins at the Tyr31-Gly32 bond and produces 31-amino-acid endothelins, endothelins(1-31). Endothelin-1(1-31) has been isolated from a number of human organs, including the heart and lungs. As endothelin-1 has been shown to play a significant role in the paracrine regulation of cardiovascular functions in humans, it is possible that endothelin-1(1-31) may also exhibit biological activity on human tissues. We previously reported that synthetic endothelin-1(1-31) exhibits a number of physiological actions on cultured cells in vitro. In the present study, we investigated the plasma concentrations of endothelin-1(1-31) and endothelin-1 in healthy subjects and compared them with those in patients with cardiovascular diseases. Endothelin-1(1-31) and endothelin-1 in human plasma was measured using a sandwich-enzyme-immunoassay system, which was recently described for measurement of endothelin-1(1-31). The plasma concentrations of endothelin-1(1-31) and endothelin-1 in healthy volunteers were 19.24 +/- 5.70 and 15.54 +/- 4.45 pg/ml (n = 5), respectively. We also measured plasma concentrations of endothelin-1(1-31) and endothelin-1 before and after surgery in patients with abdominal aortic aneurysms. Before surgery, plasma concentrations of endothelin-1(1-31) and endothelin-1 in these patients were higher than those in healthy individuals. After surgery, both endothelin-1(1-31) and endothelin-1 in plasma decreased to levels similar to those of healthy subjects. This suggests that endothelin-1(1-31) may have similar physiological significance to endothelin-1 in patients with atherosclerosis. (Keyword) Adult / Aged / Aortic Aneurysm, Abdominal / Arteriosclerosis / Endothelin-1 / Humans / Male / Middle Aged / Peptide Fragments (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 12688403 ● Search Scopus @ Elsevier (PMID): 12688403 (PubMed: 12688403)
40.	Toshitaka Ikehara, Ki Ho Park, Hisao Yamaguchi, Keiko Hosokawa, Hitoshi Houchi, Mami Azuma, Kazuo Minakuchi, Hideki Kashimoto, Mitsuo Kitamura, Yohsuke Kinouchi, Kazuo Yoshizaki and Hiroshi Miyamoto : Effects of Time-Varying Strong Magnetic Fields on Rerease of Cytosolic Free Ca²⁺ from Intracellular Stores in Cultured Bovine Adrenal Chromaffin Cells, Bioelectromagnetics, Vol.23, No.7, 505-515, 2002. (Summary) This study was made to explain the mechanisms for the effects of exposure to a time varying 1.51 T magnetic field on the intracellular Ca(2+) signaling pathway. The exposure inhibited an increase in intracellular Ca(2+) concentration ([Ca(2+)](i)) in bovine chromaffin cells induced by addition of bradykinin (BK) to a Ca(2+) free medium. The exposure did not change BK induced production of inositol 1,4,5-trisphosphate (IP(3)). [Ca(2+)](i) was markedly increased in IP(3) loaded cells, and this increase was inhibited by the magnetic field exposure. A similar increase in [Ca(2+)](i) by other drugs, which stimulated Ca(2+) release from intracellular Ca(2+) stores, was again inhibited by the same exposure. However, transmembrane Ca(2+) fluxes caused in the presence of thapsigargin were not inhibited by the magnetic field exposure in a Ca(2+) containing medium. Inhibition of the BK induced increase in [Ca(2+)](i) by the exposure for 30 min was mostly recovered 1 h after exposure ended. Our results reveal that the magnetic field exposure inhibits Ca(2+) release from intracellular Ca(2+) stores, but that BK bindings to BK receptors of the cell membrane and intracellular inositol IP(3) production are not influenced. (Keyword) magnetic field / cell physiology (Link to Publication Site) ● Publication site (DOI): 10.1002/bem.10043 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 12224054 ● Summary page in Scopus @ Elsevier: 2-s2.0-0036778437 (DOI: 10.1002/bem.10043, PubMed: 12224054, Elsevier: Scopus)
41.	Keisuke Ishizawa, Masanori Yoshizumi, Koichiro Tsuchiya, Eiko Takishita, Yutaka Nakaya, Kazuhiro Kishi, Yousuke Ebina, Hitoshi Houchi, Kazuo Minakuchi and Toshiaki Tamaki : Effects of losartan in combination with or without exercise on insulin resistance in Otsuka Long-Evans Tokushima Fatty rats., European Journal of Pharmacology, Vol.430, No.2-3, 359-367, 2001. (Summary) Hypertension often complicates type 2 diabetes mellitus, and angiotensin converting enzyme inhibitor treatment has been shown to improve insulin resistance in such cases. However, the effect of angiotensin II type-1 (AT(1)) receptor antagonists on insulin resistance is still controversial. To gain further information on this effect, we examined the effect of losartan on insulin resistance in Otsuka Long-Evans Tokushima Fatty (OLETF) rats, a model of type 2 diabetes mellitus. Losartan administration alone lowered systolic blood pressure, but did not improve oral glucose tolerance test or insulin resistance in OLETF rats. However, the administration of losartan with exercise significantly improved both systolic blood pressure and insulin resistance relative to control OLETF rats. On the other hand, losartan treatment, regardless of exercise, increased glucose uptake in excised soleus muscle and fat cells. To explore the beneficial effect of losartan on skeletal muscle glucose uptake, we examined intracellular signaling of soleus muscle. Although Akt activity and glucose transporter type 4 (GLUT4) expressions were not affected by losartan with or without exercise, extracellular signal-regulated kinase (ERK1/2) and p38 mitogen-activated protein (MAP) kinase activities were increased by both interventions. These results indicate that angiotensin AT(1) receptor antagonist improved local insulin resistance, but not systemic insulin resistance. These findings may explain the controversy over the effect of angiotensin AT(1) receptor antagonists on insulin resistance in clinical use. The enhancing effect of angiotensin AT(1) receptor antagonist on skeletal muscle glucose uptake may be attributable to MAP kinase activation or other mechanisms rather than phosphatidylinositol 3-kinase activation. (Keyword) Adipocytes / Animals / Antihypertensive Agents / Blood Glucose / Blood Pressure / Blotting, Western / Body Weight / Deoxyglucose / Diabetes Mellitus, Type 2 / Enzyme Activation / Glucose / Glucose Tolerance Test / Glucose Transporter Type 4 / Heart Rate / Insulin / Insulin Resistance / JNK Mitogen-Activated Protein Kinases / Losartan / Male / Mitogen-Activated Protein Kinase 1 / Mitogen-Activated Protein Kinase 3 / Mitogen-Activated Protein Kinases / Monosaccharide Transport Proteins / Muscle Proteins / Muscle, Skeletal / Phosphorylation / Physical Conditioning, Animal / Protein-Serine-Threonine Kinases / Proto-Oncogene Proteins / Proto-Oncogene Proteins c-akt / Rats / Rats, Inbred OLETF / p38 Mitogen-Activated Protein Kinases (Link to Publication Site) ● Publication site (DOI): 10.1016/S0014-2999(01)01405-4 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 11711055 ● Summary page in Scopus @ Elsevier: 2-s2.0-0035798388 (DOI: 10.1016/S0014-2999(01)01405-4, PubMed: 11711055, Elsevier: Scopus)
42.	Yuichi Ozawa, Hitoshi Houchi, Kazuhiko Teraoka, Mami Azuma, Takehiro Kamimura, Masanori Yoshizumi, Koichiro Tsuchiya, Toshiaki Tamaki and Kazuo Minakuchi : Long-term regulation of catecholamine formation by ouabain in cultured bovine adrenal cromaffin cells., Journal of Cardiovascular Pharmacology, Vol.36, No.suppl.2, S15-S18, 2000. (Summary) The long-term effects of ouabain, an inhibitor of Na+/K+ -ATPase, on catecholamine formation in cultured bovine adrenal chromaffin cells were examined. The increase in [14C]catecholamine formation from [14C]tyrosine induced by ouabain was dependent on incubation time, and its maximal effect was observed after incubation for 8 h. The stimulatory effect of ouabain was concentration dependent (10-300 nM), causing maximal stimulation at 300 nM. The formation of [14C]catecholamines induced by ouabain was not increased by incubation with [14C]DOPA instead of [14C]tyrosine. Ouabain-induced [14C]catecholamine formation was influenced by decreases in extracellular Ca2+ concentration, but not by the presence of cycloheximide or actinomycin D. These results suggested that ouabain stimulates continuous activation of hydroxylation of tyrosine through a Ca2+ -dependent mechanism in cultured bovine adrenal chromaffin cells. (Keyword) Animals / Calcium / Catecholamines / Cattle / Cells, Cultured / Chromaffin Cells / Enzyme Inhibitors / Ouabain / Sodium-Potassium-Exchanging ATPase / Tyrosine / Tyrosine 3-Monooxygenase (Link to Publication Site) ● Publication site (DOI): 10.1097/00005344-200000006-00005 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 11206714 ● Summary page in Scopus @ Elsevier: 2-s2.0-0034480287 (DOI: 10.1097/00005344-200000006-00005, PubMed: 11206714, Elsevier: Scopus)
43.	Ozawa Yuichi, Masanori Yoshizumi, Yasushi Fukuta, Daisuke Inui, Koichiro Tsuchiya, Hitoshi Houchi, Toshiaki Tamaki and Kazuo Minakuchi : Dopamine Clearance During Dopamine Infusion in Infants and Children After Cardiac Surgery, Journal of Cardiovascular Pharmacology, Vol.34, No.Supplement 4, S85-S89, 1999.
44.	Takabumi Umeda, Mami Azuma, Hitoshi Houchi, Toshitaka Ikehara, Fumiaki Shono, Masanori Yoshizumi, Toshiaki Tamaki and Kazuo Minakuchi : Stimulatory effect of enkephalines on calcium efflux from bovine adrenal chromaffin cells in culture., Life Sciences, Vol.65, No.21, PL247-252, 1999.
45.	Hitoshi Houchi, Mami Azuma, Masanori Yoshizumi, Toshiaki Tamaki and Kazuo Minakuchi : Possible role of bradykinin on stimulus-secretion coupling in adrenal chromaffin cells, The Journal of Medical Investigation : JMI, Vol.46, No.1-2, 1-9, 1999. (Summary) Nonapeptide bradykinin is known to be a central nervous system neurotransmitter and to play a role in regulation of neuronal function. However, few details are known of the function of its peptide on stimulus-secretion coupling in neuronal cells. In this article, the role of bradykinin on catecholamine biosynthesis, secretion and Ca2+ movement in adrenal chromaffin cells as a model for catecholamine-containing neurons are examined. Bradykinin receptors are classified as B1 and B2 receptor subtypes. These receptors are present on the adrenal chromaffin cell membrane. Bradykinin increases the influx of Ca2+ and the turnover of phosphoinositide through the stimulation of bradykinin B2 receptor. The secretion of catecholamine from the cells is initiated by the raise of [Ca2+]i. An increase in [Ca2+]i and production of diacylglycerol stimulate the activation of calcium-dependent protein kinases. These kinases stimulate the activation of tyrosine hydroxylase, a rate-limiting enzyme in the biosynthesis of catecholamine. Otherwise, bradykinin increases Ca2+ efflux from the cells through the stimulation of the bradykinin-B2 receptor. This action may be explained by an extracellular Na(+)-dependent mechanism, probably through acceleration of Na+/Ca2+ exchange. It is interesting that bradykinin, which stimulates the biosynthesis and secretion of catecholamine in adrenal chromaffin cells, plays a role in the termination of calcium-signal transduction through the stimulation of Ca2+ efflux from the cells. (Keyword) Bradykinin / Catecholamine / Biosynthesis / Secretion / calcium (Tokushima University Institutional Repository) ● Metadata: 22088 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 10408151 ● Search Scopus @ Elsevier (PMID): 10408151 (Tokushima University Institutional Repository: 22088, PubMed: 10408151)
46.	Koichiro Tsuchiya, Jiang Jin-Jie, Masanori Yoshizumi, Toshiaki Tamaki, Hitoshi Houchi, Kazuo Minakuchi, Kenji Fukuzawa and P.Mason Ronald : Nitric oxide-forming reactions of the water-soluble nitric oxide spin-trapping agent, MGD., Free Rad. Biol. Med., Vol.27, 347-355, 1999.
47.	Yuichi Ozawa, Masanori Yoshizumi, Daisuke Inui, Koichiro Tsuchiya, Hitoshi Houchi, Toshiaki Tamaki and Kazuo Minakuchi : Plasma levels of free and sulfoconjugated catecholamines in patients with atherosclerosis., Biological & Pharmaceutical Bulletin, Vol.22, 657-659, 1999.
48.	Hitoshi Houchi, Masanori Yoshizumi, Koichiro Tsuchiya, Masao Hirose, Tetsuya Kitagawa, Toshihida Kujime, Eiji Shimizu, Yasuharu Niwa, Kazuo Minakuchi and Toshiaki Tamaki : Endothelin-1 stimulates sodium-dependent calcium efflux from bovine adrenal chromaffin cells in culture., British Journal of Pharmacology, Vol.125, No.1, 55-60, 1998.
49.	Toshiataka Ikehara, Park Ho Ki, Hitoshi Houchi, Keiko Hosokawa, Masayuki Shono, Kazuo Minakuchi, Toshiaki Tamaki, Yohsuke Kinouchi, Kazuo Yoshizaki and Hiroshi Miyamoto : Effects of a time-varying strong magnetic field on transient increase in cytosolic free-Ca²⁺ induced by bradykinin in cultured bovine adrenal chromaffin cells., FEBS Letters, Vol.435, 229-232, 1998.
50.	Masanori Yoshizumi, Tetsuya Kitagawa, Yuichi Ozawa, Kasutoshi Tano, Koichiro Tsuchiya, Hitoshi Houchi, Kazuo Minakuchi and Toshiaki Tamaki : Changes in plasma free and sulfoconjugated catecholamines during the perioperative period of cardiac surgery:Effect of continuous infusion of dopamine., Biological & Pharmaceutical Bulletin, Vol.21, 787-791, 1998.
51.	Masanori Yoshizumi, Hitoshi Houchi, Yasuo Ishimura, Masao HIrose, Tetsuya Kitagawa, Koichiro Tsustiya, Kazuo Minakuchi and Toshiaki Tamaki : Effect of evodiamine on catecholamine secretion from bovine adrenal medulla., The Journal of Medical Investigation : JMI, Vol.44, No.1,2, 79-82, 1997. (Summary) The effect of evodiamine on catecholamine secretion from bovine adrenal medulla was investigated. Evodiamine, a bioactive component isolated from dry unripened fruit of Evodia rutaecarpa Bentham, was found to stimulate the secretion of catecholamine from perfused bovine adrenal medulla at a concentration of 10 microM and its effect persisted for at least 30 min. This stimulatory effect of evodiamine was abolished by omission of Ca2+ from the perfusion fluid. Evodiamine (0.1-10 microM) markedly enhanced the secretion of catecholamine from the adrenal medulla induced by acetylcholine (100 microM or high K+(56 mM). The secretion of catecholamine was promptly enhanced by acetylcholine or high K+, but returned to the control level on treatment for 20 min. However, when evodiamine was added to the perfusion fluid after acetylcholine or high K+ stimulation for 10 min, the secretion of catecholamine again increased greatly. These results indicate that evodiamine not only stimulated the secretion of catecholamine from bovine adrenal medulla but also reversed insensitivity of these cells to acetylcholine or high K+ stimulation. (Keyword) Adrenal Medulla / Animals / Catecholamines / Cattle / Plant Extracts / Quinazolines / Vasodilator Agents (Tokushima University Institutional Repository) ● Metadata: 111645 (Link to Search Site for Scientific Articles) ● PubMed @ National Institutes of Health, US National Library of Medicine (PMID): 9395722 ● Search Scopus @ Elsevier (PMID): 9395722 (Tokushima University Institutional Repository: 111645, PubMed: 9395722)
52.	Hitoshi Houchi, Masanori Yoshizumi, Kazuo Minakuchi, Yasuko Ishimura, Kyoji Morita, Toshiaki Tamaki and Motoo Oka : Potentiation of histamine-induced catecholamine secretion by ouabain in cultured bovine adrenal chromaffin cells is dependent on calcium and sodium influx., Life Sciences, Vol.60, No.23, 2051-2058, 1997.
53.	Kazuo Minakuchi, Hitoshi Houchi, Masanori Yoshizumi, Yasuko Ishimura, Kyoji Morita, Masumitsu Takasugi, Motoo Oka and Toshiaki Tamaki : Serotonin increases Na⁺-dependent Ca²⁺ efflux from bovin sdrenal chromaffin cells in culture., Neuroscience Letters, Vol.223, 17-20, 1997.
54.	Masanori Yoshizumi, Hitoshi Houchi, T Tuchiya, Kazuo Minakuchi, Kazuya Horike, Tetsuya Kitagawa, Itsuo Katoh and Toshiaki Tamaki : Atrial natriuretic peptide stimulates Na⁺-dependent Ca²⁺ effulux from freshly isolated adult rat cardiomyocytes., FEBS Letters, Vol.419, No.2,3, 255-258, 1997.
55.	Masahiro Nomura, Masanori Yoshizumi, 石村泰子, Yutaka Masuda, Kazuo Minakuchi, Yutaka Nakaya, 大内武, 加藤逸夫, 岡源郎, 日比野敏行, 三好由貴子, Tetsuzo Wakatsuki, 大木崇 and Susumu Ito : マラソン前後における血中遊離型および硫酸抱合型カテコラミンの変動, Heart, Vol.25, No.Suppl 2, 97-99, 1993. (Link to Publication Site) ● Publication site (DOI): 10.11281/shinzo1969.25.Supplement2_97 (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1390001205485924224 ● Search Scopus @ Elsevier (DOI): 10.11281/shinzo1969.25.Supplement2_97 (DOI: 10.11281/shinzo1969.25.Supplement2_97, CiNii: 1390001205485924224)
56.	Masanori Yoshizumi, Yutaka Nakaya, Toshiyuki Hibino, Masahiro Nomura, Kazuo Minakuchi, Tetsuya Kitagawa, Itsuo Katoh, Takeshi Ohuchi and Motoo Oka : Changes in plasma free and sulfoconjugated catecholamines before and after acute physical exercise:Experimental and clinical studies., Life Sciences, Vol.51, No.3, 227-234, 1992.

Academic Paper (Unrefereed Paper):

1.	Kazuyoshi Kawazoe, 伏谷秀治, Yoshiki Kashiwada, Hisako Sasaki, Yuka Ohmichi, Shinichirou Kurimoto, 篠崎陽介, 柴山恵美子, 関田倫彦, 金子礼, Yoshihiro Suyama, Sawa Takagishi, 中野芙佐子, Ai Hirata, Yuki Miyazaki, Souichirou Tajima, Takumi Sakurada, 中川博之, 田岡寛之, 足立麻美, Takahiro Shibata, Naoto Okada, 継岡知美, 淵上美由紀, Ken Konaka, 今林潔, 今林優佳, Yoshihisa Takaishi and Kazuo Minakuchi : つるぎ町一宇地区の民間薬調査, 阿波学会紀要, No.57, 89-98, 2011.
2.	Kazuo Minakuchi, Amamiya Michiko, Otsubo Kenji, Oguchi Tosho, Kase Yasuko, Kadobayashi Muneo, Kawakatsu Kazuo, Kazuyoshi Kawazoe, Kihira Kenji, Kyotani Shojiro, Genma Takahide, Yutaka Nishioka, Hayakari Makoto, Hiraga Hajime and Miyahsita Seiichiro : 病院薬剤部・薬局の整備，構造，機能基準の改定に関する研究(最終報告), Journal of Japnese Society of Hospital Pharmacists, Vol.45, No.8, 1001-1004, 2009.
3.	Kazuyoshi Kawazoe and Kazuo Minakuchi : NSAIDSがアスピリンの抗血小板作用に与える影響の検討, 治療学, Vol.41, No.12, 95-98, 2007.
4.	Kazuyoshi Kawazoe, 伏谷秀治, Yoshiki Kashiwada, Naonobu Tanaka, Mamoru Okasaka, Shunsuke Ishida, Takanori Kamakura, Masatoshi Satou, Chika Hashida, 西迫寛隆, 田島壮一郎, 森剛志, 鈴木恭子, Waka Hashida, Emiko Heya, 高田千絵, 遠藤友香, 金尚永, Hiroyuki Taoka, Kazuya Nishimura, Yoshihisa Takaishi and Kazuo Minakuchi : 三好市東祖谷地区の民間薬調査, 阿波学会紀要, No.53, 87-98, 2007.
5.	Yuki Minami, Toshitaka Ikehara, Keiko Hosokawa, Hisao Yamaguchi, Keisuke Ishizawa, Masayuki Shono, Kazuyoshi Kawazoe, Kazuo Minakuchi, Kazuo Yoshizaki, Yohsuke Kinouchi and Hiroshi Miyamoto : Effect of time-varying magnetic field on cell volume regulation of adrenal chromaffin cells, The Journal of Japan Biomagnetism and Bioelectromagnetics Society, Vol.19, No.1, 156-157, 2006.

Academic Letter:

1.	庄野文章, Yasuhiko Nishioka, Ichiro Shimizu, Seiki Tashiro, 濱佳子, Susumu Ito and Kazuo Minakuchi : Surveillance and the Approach for the Proper Use of Antibiotics at Tokushima University Hospital, Japanese Journal of Pharmaceutical Health Care and Sciences, Vol.29, No.5, 611-615, 2003. (Summary) The working committee for the proper use of antibiotics was organized at Tokushima University Hospital in March 2002, and the institutional guidelines for the selection and use of antibiotics were established. The infection control team (ICT) also started monitoring the use of particular antibiotics, including third- and fourthgeneration cephalosporins, calbapenems and anti-MRSA antibiotics, and reported on their use in August 2002. To assess these activities, we examined the status of antibiotic use for injections and compared our findings with the previous data. The results were as follows : 1) the reports required were presented in 47% of the total antibiotics used ; 2) after starting the surveillance, the use of the third- and fourth-generation cephalosporins and calbapenems shifted to the first- and second-generation drugs, while the use of anti-MRSA drugs clearly decreased ; 3) these changes resulted in a savings of more than two million yen in medical expenditures in a month. These results suggest that closely monitoring the use of antibiotics may thus be beneficial not only for promoting the proper use of antibiotics but also for reducing overall medical costs. (Keyword) antibiotics / anti-MRSA antibiotics / proper use / ICT (Link to Publication Site) ● Publication site (DOI): 10.5649/jjphcs.29.611 (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1390282679752865920 ● Search Scopus @ Elsevier (DOI): 10.5649/jjphcs.29.611 (DOI: 10.5649/jjphcs.29.611, CiNii: 1390282679752865920)

Review, Commentary:

1.	櫻田巧, Keisuke Ishizawa, Masaki Imanishi, 藤井聖子, 谷口順平, Yuki Izawa-Ishizawa, Licht Miyamoto, Yoshitaka Kihira, Yasumasa Ikeda, Shuhei Tomita, Kazuo Minakuchi, Koichiro Tsuchiya and Toshiaki Tamaki : Nitrosonifedipineはangiotensin IIによるマウス血管リモデリングを抑制する, 腎とフリーラジカル, Vol.11, 78-81, Jan. 2013.
2.	Keisuke Ishizawa, Kazuo Minakuchi and Toshiaki Tamaki : 医療人としての薬剤師育成教育の実践, Medicine and Drug Journal, Vol.43, No.3, 871-874, Mar. 2007.
3.	Keisuke Ishizawa and Kazuo Minakuchi : 栄養管理における薬剤師の役割, 調剤と情報, Vol.11, No.1, 95-100, Jan. 2005.
4.	Keisuke Ishizawa and Kazuo Minakuchi : 大学病院におけるNST活動と薬剤師, 薬事新報, Vol.2332, 902-905, Oct. 2004.
5.	Keisuke Ishizawa, Hitoshi Houchi and Kazuo Minakuchi : 大学病院における栄養支援チーム(NST)と薬剤師, Journal of Japnese Society of Hospital Pharmacists, Vol.40, No.10, 1245-1248, Oct. 2004. (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1573950401508262400 (CiNii: 1573950401508262400)
6.	Yasuhiko Nishioka, 中川達夫, Kazuo Minakuchi and Saburo Sone : 難治性固形癌に対する癌抗原ペプチドパルス樹状細胞を用いた癌ワクチン療法 - トランスレーショナルリサーチとしての展開 -, Shikoku Acta Medica, Vol.59, No.6, 280-286, Dec. 2003. (Tokushima University Institutional Repository) ● Metadata: 39620 (Tokushima University Institutional Repository: 39620)
7.	Yoshihiro Takegawa, 森健一, Kazuo Minakuchi and 清水寛 : Education of Oriental medicine at The University of Tokushima School of Medicine, Shikoku Acta Medica, Vol.59, No.1-2, 74-78, Apr. 2003. (Keyword) lecture of traditional Oriental medicine / medical students / curriculum (Tokushima University Institutional Repository) ● Metadata: 110591 (Tokushima University Institutional Repository: 110591)
8.	Yasuhiko Nishioka, 中川達夫, Kazuo Minakuchi and Saburo Sone : 難治性固形癌に対する癌抗原ペプチドパルス樹上細胞を用いた癌ワクチン療法ートランスレーショナルリサーチとしての展開ー, Shikoku Acta Medica, Vol.69, No.6, 280-286, 2003.

Proceeding of International Conference:

1.	Naoto Okada, Kazuyoshi Kawazoe, Kazuhiko Teraoka, Kujime Toshihide and Kazuo Minakuchi : Evaluation of risk factors for hypocalcemia induced by denosumab, 48th ASHP Midyear Clinical Meeting, Orlando, Dec. 2013.
2.	Yuya Horinouchi, Fiona A. Summers, Marilyn Ehrenshaft, Hitoshi Houchi, Toshiaki Tamaki, Kazuo Minakuchi and Ronald P. Mason : Cytotoxity evaluation of environmental chemicals via free radical detection using newly technique immuno-spin trapping, In-Cell Western and confocal microscopy, 49th Congress of the European Societies of Toxicology (EUROTOX), Sep. 2013.
3.	Takumi Sakurada, K. Miyako, Yuya Horinouchi, Kazuhiko Teraoka, T. Kujime, Kazuyoshi Kawazoe, Hitoshi Houchi, Toshiaki Tamaki and Kazuo Minakuchi : NITROSONIFEDIPINE, A PHOTODEGRADATION PRODUCT OF NIFEDIPINE, SUPPRESS THE PROGRESSION OF DIABETIC NEPHROPATHY WITH THE ENDOTHELIAL DYSFUNCTION, 11th EACPT Congress, Aug. 2013.
4.	Fushitani Shuji, Hirofumi Shibata, Shibata Takahiro, Kazuyoshi Kawazoe and Kazuo Minakuchi : Involvement of outpatients as a source of supply in nosocomial transmission of MRSA, 13th Asia-Pacific Congress of Clinical Microbiology and Infection (Abstract book), 289, Beijing, Oct. 2012.
5.	Yasuhiko Nishioka, Shinji Abe, Yuki Morita, Mika K Kaneko, Masaki Hanibuchi, Hisatsugu Goto, Souji Kakiuchi, Yoshinori Aono, Jun Huang, Atsushi Mitsuhashi, Seidai Sato, Kazuo Minakuchi and Yukinari Kato : Antitumor effects of anti-podoplanin antibody NZ-1 against malignant mesothelioma, 14th International Biennial Congress of the Metastasis Research Society, Brisbane, Sep. 2012.
6.	Konaka Ken, Moriyama Kouta, Sue Kazuyoshi, Mizoguchi Tetsuya, Masayuki Shono, Kazuyoshi Kawazoe and Kazuo Minakuchi : Effect of kakkonto on a vascular endothelial model (HUVEC), 24th FAPA Congress 2012, Denpasar, Jul. 2012.
7.	Yasuhiko Nishioka, Shinji Abe, Mika K Kaneko, Yoshinori Aono, Jun Huang, Hisatsugu Goto, Masatoshi Kishuku, Masaki Hanibuchi, Saburo Sone, Kazuo Minakuchi and Yukinari Kato : Antitumor effects of anti-podoplanin antibody NZ-1 against malignant mesothelioma via ADCC, ATS 2012 International Conference, San Francisco, May 2012.
8.	Ikuta Kenji, Ise Natsuko, Shimooka Yukie, Katagiri Yuki, Shinji Abe, Kazuhiko Teraoka, Kujime Toshihide, Kazuyoshi Kawazoe and Kazuo Minakuchi : Pharmaceutical and economical role of clinical phamacist in emergency and critical care medicine, 46th ASHP Midyear Clinical Meeting and Exhibition, New Orleans, Dec. 2011.
9.	Masaki Hanibuchi, Shinji Abe, Masatoshi Kishuku, Souji Kakiuchi, Kazuyoshi Kawazoe, Kazuo Minakuchi, Mika K. Kaneko, Yukinari Kato and Yasuhiko Nishioka : Targeted therapy for mesothelioma using anti-podoplanin antibody NZ-1 via ADCC, 5th EORTC-NCI-ASCO Annual Meeting on 'Molecular Markers in Cancer', Brussels, Belgium, Oct. 2011.
10.	Soichiro Tajima, Yasumasa Ikeda, Noriko Yamano, Koichiro Tsuchiya, Yuki Izawa-Ishizawa, Yoshitaka Kihira, Keisuke Ishizawa, Kazuyoshi Kawazoe, Shuhei Tomita, Kazuo Minakuchi and Toshiaki Tamaki : Inhibition of Adipocyte Hypertrophy by Deferoxiamine Diabetic KKAy mice, High Blood Pressure Research Scientific Sessions 2011 Scientific Sessions, Orlando, Sep. 2011.
11.	Yuya Horinouchi, Takumi Sakurada, Toshimi Nakmura, Tsuyoshi Mori, Ken Konaka, Soichiro Tajima, Shinji Abe, Kazuhiko Teraoka, Toshihide Kujime, Kazuyoshi Kawazoe, Hitoshi Houchi and Kazuo Minakuchi : Correlation between development of hypertension and efficay in metastatic colorectal cancer patients treated with bevacizumab, Abstracts of 10th Congress of the Europian Association for Clinical Pharmacology and Therapeutics, Vol.109, No.S1, 57, Budapest, Jun. 2011.
12.	Soichiro Tajima, Yasumasa Ikeda, Noriko Yamano, Koichiro Tsuchiya, Yoshitaka Kihira, Keisuke Ishizawa, Kazuyoshi Kawazoe, Shuhei Tomita, Kazuo Minakuchi and Toshiaki Tamaki : IRON DERIVATION AMELIORATES GLUCOSE TOLERANCE THROUGH REDUCTION OF OXIDATIVE STRESS AND INFLAMMATION IN DIABETIC KKAY MICE, 2010 American Physiological Society Conference Inflammation, Immunity and Cardiovascular Disease, Aug. 2010.
13.	Soichiro Tajima, Yasumasa Ikeda, Yoshitaka Kihira, Keisuke Ishizawa, Kazuyoshi Kawazoe, Shuhei Tomita, Kazuo Minakuchi, Toshiaki Tamaki and Koichiro Tsuchiya : Deferoxamine, an iron chelator, promotes angiogenesis after ischemic hind limb through Akt-eNOS-dependent pathway, The 6th International Conference on the Biology, Chemistry, and Therapeutic Applications of Nitric Oxide, Jun. 2010.
14.	Souichiro Tajima, Yasumasa Ikeda, Yoshitaka Kihira, Keisuke Ishizawa, Kazuyoshi Kawazoe, Shuhei Tomita, Kazuo Minakuchi, Toshiaki Tamaki and Koichiro Tsuchiya : Deferoxamine, an iron chelator, promotes angiogenesis after ischemic hind limb through Akt-eNOS-dependent pathway, The 6th International Conference on the Biology, Chemistry, and Therapeutic Applications of Nitric Oxide, Kyoto, Apr. 2010.
15.	Takeshi Mori, Nishisako Hirotaka, Nakamura Toshimi, Yuya Horinouchi, Sakurada Takumi, Shinji Abe, Kazuhiko Teraoka, Kujime Toshihide, Kazuyoshi Kawazoe and Kazuo Minakuchi : Prediction of adverse effects based on cluster analysis by demography and clinical factor in the outpatients treated with cancer chemotherapy, 15th Anniversary Congress of EAHP, Niece, Mar. 2010.
16.	Kirino Yasushi, Kazuhiko Teraoka, Kujime Toshihide, Kazuyoshi Kawazoe, Tetsuro Ohmori and Kazuo Minakuchi : Analysis of body weight gain in patients treated with the second-generation antipsychotic drugs in Tokushima University Hospital, 15th Anniversary Congress of EAHP, Niece, Mar. 2010.
17.	Nishisako Hirotaka, Mori Takeshi, Mori Toshimi, Kirino Yasushi, Miki Yukiyo, Abe Shinji, Kazuyoshi Kawazoe and Kazuo Minakuchi : Adverse effect monitoring in the ourpatients under anticancer chemotherapy: Prediction of adverse effects by demography and clinical factor of the patients by means of cluster analysis., 44th ASHP Midyear Clincal Meeting & Exhibition, Las Vegas, Dec. 2009.
18.	Shuji Fushitani, Hirofumi Shibata, Takahiro Shibata, Takafumi Umeda, Kazuyoshi Kawazoe, Fumiaki Shono and Kazuo Minakuchi : Profiles and distribution of airborne fungi in Tokushima University Hospital, The 4th International Congress of the Asia Pacific Society of Infection Control, Macau, Jul. 2009.
19.	Kawano Wataru, Hirofumi Shibata, Hikichi Kaori, Masanori Higuti, Kazuyoshi Kawazoe, Kazuo Minakuchi and Tomihiko Higuti : Antiviral Effect of Octyl Gallate, 11th Western Pacific Congress on Chemotherapy and Infectious Diseases, 0, Taipei, Dec. 2008.
20.	Yuya Horinouchi, Koichiro Tsuchiya, 石澤啓介, 田島壮一郎, 元林有紀, 山口邦久, 川添和義, Kazuo Minakuchi and Toshiaki Tamaki : Endothelial cell protective activity of nitorosonifedipine, Biomedical Redox Navigation (EPR2008), Fukuoka, Sep. 2008.
21.	Koichiro Tsuchiya, Soichiro Tajima, Mai Hamamoto, Hideki Ohnishi, Yuki Motobayashi, Yuya Horinouchi, Kunihisa Yamaguchi, Keisuke Ishizawa, Kazuyoshi Kawazoe, Kazuo Minakuchi and Toshiaki Tamaki : Effect of angiotensin II on iron (II) turnover in HGEC, Biomedical Redox Navigation (EPR2008), Fukuoka, Sep. 2008.
22.	Yuya Horinouchi, Koichiro Tsuchiya, Keisuke Ishizawa, Soichiro Tajima, Yuki Motobayashi, Kunihisa Yamaguchi, Kazuyoshi Kawazoe, Kazuo Minakuchi and Toshiaki Tamaki : Endotherial cell protective activity of nitrosonifedipine, Biomedical Redox Navigation (EPR2008), Fukuoka, Sep. 2008.
23.	Yuki Motobayashi, Keisuke Ishizawa, Yuki Izawa-Ishizawa, Sakiko Orino, Dorjsuren Narantungalag, Kunihisa Yamaguchi, Kazuo Minakuchi and Toshiaki Tamaki : Inhibitory effects of adiponectin on cell migration induced by insulin-like growth factor-1 in vascular smooth muscle cells, The IXth World Conference on Clinical Pharmacology and Therapeutics, Québec City, Jul. 2008.
24.	Toshitaka Ikehara, Shiraishi Tairho, Nishisako Hirotaka, Hisao Yamaguchi, Mitsuo Kitamura, Masayuki Shono, Kazuo Yoshizaki, Kazuyoshi Kawazoe, Kazuo Minakuchi, Yohsuke Kinouchi and Hiroshi Miyamoto : EFFECTS OF TIME-VARYING MAGNETIC FIELD ON REGULATORY VOLUME DECREASE IN BOVINE ADRENAL CHROMAFFIN CELLS, The Bioelectromagnetics Society 30th Annual Meeting, 368-369, San Diego, Jan. 2008.
25.	Toshitaka Ikehara, Nishisako Hirotaka, Shiraishi Tairoh, Hisao Yamaguchi, Masayuki Shono, Mitsuo Kitamura, Kazuyoshi Kawazoe, Kazuo Minakuchi, Kazuo Yoshizaki, Yohsuke Kinouchi and Hiroshi Miyamoto : Effects of a time-varying magnetic field on bovine adrenal chromaffin cells., Proceedings of the International Symposium on Biological and Physiological Engineering /The 22nd SICE Symposium on Biological and Physiological Engineering, 117-118, Harbin, Jan. 2008.
26.	Yasushi Kirino, Toshimi Nakamura, Hirotaka Nishisako, Natsuko Ise, Keisuke Ishizawa, Toshihide Kujime, Kazuhiko Teraoka, Kazuyoshi Kawazoe and Kazuo Minakuchi : Dosase adjustment and monitoring the side effects of the anticancer drug in Tokushima University Dental Hospital, 42nd ASHP Midyear Clinical Meeting & Exhibition, Las Vegas, Dec. 2007.
27.	Toshitaka Ikehara, Yuki Minami, Shiota Naoko, Hisao Yamaguchi, Masayuki Shono, Mitsuo Kitamura, Kazuyoshi Kawazoe, Kazuo Minakuchi, Kazuo Yoshizaki, Yohsuke Kinouchi and Hiroshi Miyamoto : EFFECTS OF A TIME-VARYING MAGNETIC FIELD ON CELL VOLUME REGULATION OF CULTURED BOVINE ADRENAL CHROMAFFIN CELLS, Abstract Book The Bioelectromaginetics Society 29th Annual Meeting, 375-376, Kanazawa, Jun. 2007.
28.	Shinji Abe, Shimooka Yukie, Kujime Toshihide, Kazuhiko Teraoka, Kazuyoshi Kawazoe and Kazuo Minakuchi : A sinple method for prevention of adverse effects in double filtration plasmapheresis (DFPP), Pharmaceutical Sciences World Congress 2007, Amsterdam, Apr. 2007.
29.	Keisuke Ishizawa, Rika Sugimoto, Yuki Izawa, Koichiro Tsuchiya, Kazuo Minakuchi and Toshiaki Tamaki : The inhibitory effect of adiponectin on migration and proliferation induced by PDGF in rat mesangial cells, 38th ASN annual meeting, Philadelphia, Nov. 2005.
30.	Keisuke Ishizawa, Rika Sugimoto, Yuki Izawa, Kazuo Minakuchi, Koichiro Tsuchiya and Toshiaki Tamaki : Adiponectin inhibits PDGF-induced migration and proliferation in rat mesangial cells, 第10回アディポサイエンス研究会シンポジウム(第10回記念国際シンポジウム), Osaka, Aug. 2005.
31.	Hitoshi Houchi, Mami Azuma, M. Torii, T. Umeda, M. Mizuta, K. Teraoka and Kazuo Minakuchi : Inhibitory action of cilostazol, A phosphodiesterase inhibitor, on catecholamine secretion from cultured bovine adrenal chromaffin cells, Society for Neuroscience 34th Annual Meeting, San Diego, Oct. 2004.

Proceeding of Domestic Conference:

1.	Ken Konaka, 森剛志, Takahiro Shibata, 西迫寛隆, 中村敏己, Kazuhiko Teraoka, Kazuyoshi Kawazoe and Kazuo Minakuchi : バニツムマブによる低マグネシウム血症の発現状況と治療成功期間に関する検討, 第26回日本医療薬学会年会要旨集, 386, Sep. 2014.
2.	石田俊介, 前田和輝, 伏谷秀治, 渡邉美穂, Kazuhiko Teraoka, Kazuyoshi Kawazoe and Kazuo Minakuchi : 徳島大学病院薬剤部におけるかなりツール作成による副作用情報収集の効率化, 第25回日本医療薬学会年会要旨集, 258, Sep. 2014.
3.	Naoto Okada, Takeshi Hanafusa, Kazuhiko Teraoka, 中村敏己, Kazuyoshi Kawazoe and Kazuo Minakuchi : R-CHOP療法及びR-CHOP-like療法におけるビンクリスチン誘発早期末梢神経障害の危険因子の同定, 第24回日本医療薬学会年会要旨集, 181, Sep. 2014.
4.	櫻田巧, 田島壮一郎, Souji Kakiuchi, Yuya Horinouchi, Kazuhiko Teraoka, 久次米敏秀, Kazuyoshi Kawazoe, Yasuhiko Nishioka and Kazuo Minakuchi : ペメトレキセド治療における皮疹に対するデキサメタゾン投与量の検討, 日本薬学会第134年会, Mar. 2014.
5.	伏谷秀治, Kazuhiko Teraoka, Kazuyoshi Kawazoe, 桐野靖, 石田俊介 and Kazuo Minakuchi : ハイリスク薬チェックにおけるファイルメーカーProの活用, 日本薬学会第134年会, Mar. 2014.
6.	Takeshi Hanafusa, Kazuyoshi Sue, Kohta Moriyama, Ken Konaka, Naoto Okada, Kazuyoshi Kawazoe and Kazuo Minakuchi : 加味逍遙散及び芍薬甘草湯がpaclitaxelによる末梢神経障害モデル細胞に与える影響, 日本薬学会第134年会, Mar. 2014.
7.	Shinji Abe, 木宿昌俊, Mari Nakase, Chiemi Sato, Hirofumi Shibata, Kazuyoshi Kawazoe, Mami Azuma, Yasuhiko Nishioka and Kazuo Minakuchi : 悪性胸膜中皮腫移植マウスに対するNZ-1およびラットNK細胞併用投与の抗腫瘍効果, 日本薬学会第134年会, Mar. 2014.
8.	Ken Konaka, Takeshi Hanafusa, Kohta Moriyama, 西迫寛隆, Naoto Okada, Masayuki Shono, Kazuyoshi Kawazoe and Kazuo Minakuchi : 血管内皮細胞におけるビンカロイドの細胞障害に対するエフェドラの影響, 日本薬学会第134年会, Mar. 2014.
9.	牧原汐里, 宮﨑渚, 多田智紀, 大星航, 松本直貴, Kazuyoshi Kawazoe, Kazuo Minakuchi, Kensaku Aki and Eiji Hosoi : 巨核球系分化誘導細胞を用いた抗血小板薬の評価, 第37回徳島県医学検査学会, Dec. 2013.
10.	柴田高洋, Naoto Okada, 伏谷秀治, Hirofumi Shibata, Mami Azuma, Kazuyoshi Kawazoe and Kazuo Minakuchi : MRSA院内伝播の要因としての外来患者の可能性について, 第52回日本薬学会・日本薬剤師会・日本病院薬剤師会中国四国支部学術大会, Oct. 2013.
11.	Naoto Okada, Kazuyoshi Kawazoe, Kazuhiko Teraoka, 久次米敏秀 and Kazuo Minakuchi : デノスマブによる低カルシウム血症の発現リスクを予測する因子の検討, 第52回日本薬学会・日本薬剤師会・日本病院薬剤師会中国四国支部学術大会, Oct. 2013.
12.	Ken Konaka, Takahiro Shibata, 森剛志, 中村敏己, 西迫寛隆, Naoto Okada, 久次米敏秀, Kazuhiko Teraoka, Kazuyoshi Kawazoe and Kazuo Minakuchi : 当院におけるホスアプレピタントによる血管痛への取り組み, 第52回日本薬学会・日本薬剤師会・日本病院薬剤師会中国四国支部学術大会, Oct. 2013.
13.	Naoki Matsumoto, Tomoki Tada, Kensaku Aki, Wataru Ohboshi, 廣瀬政雄, Naoto Okada, Kazuyoshi Kawazoe, Eiji Hosoi and Kazuo Minakuchi : ヒト巨核球系細胞株CMKを用いた血小板機能に及ぼす各種薬剤評価の検討, 第52回日本薬学会・日本薬剤師会・日本病院薬剤師会中国四国支部学術大会, Oct. 2013.
14.	Kazuyoshi Sue, Kohta Moriyama, Takeshi Hanafusa, Ken Konaka, Naoto Okada, Kazuyoshi Kawazoe and Kazuo Minakuchi : 漢方製剤のPC12細胞神経突起進展に及ぼす影響, 第52回日本薬学会・日本薬剤師会・日本病院薬剤師会中国四国支部学術大会, Oct. 2013.
15.	Takuya Mikami, Youichi Sato, Kohta Moriyama, Kohsuke Miyataka, Naoto Okada, Kazuyoshi Kawazoe and Kazuo Minakuchi : 高脂肪食ラットに及ぼすリンゴ酸の影響, 第52回日本薬学会・日本薬剤師会・日本病院薬剤師会中国四国支部学術大会, Oct. 2013.
16.	佐藤友香, 小林小春, Mari Nakase, Chiemi Sato, Shinji Abe, Hirofumi Shibata, 溝口徹也, Kazuhiko Teraoka, 久次米敏秀, Kazuyoshi Kawazoe, Kazuo Minakuchi and Mami Azuma : 実務実習におけるセーフティマネジメント教材の作成と検討∼薬学実務実習生の調剤ミスをなくすために∼, 第52回日本薬学会・日本薬剤師会・日本病院薬剤師会中国四国支部学術大会, Oct. 2013.
17.	Naoto Okada, 森剛志, Ken Konaka, Kazuyoshi Kawazoe, Kazuhiko Teraoka, 久次米敏秀 and Kazuo Minakuchi : デスノマブによる低カルシウム血症の発現に関与する因子の探索, 第23回医療薬学会年会, Sep. 2013.
18.	多田智紀, 松本直貴, Kensaku Aki, 大星航, Kazuyoshi Kawazoe, Kazuo Minakuchi and Eiji Hosoi : 巨核球系培養細胞を用いた抗血小板薬アスピリンの薬剤評価の検討, 第8回日本臨床検査学教育学会学術大会, Aug. 2013.
19.	Naoto Okada, 河野渉, Kazuhiko Teraoka, 久次米敏秀, Kazuyoshi Kawazoe and Kazuo Minakuchi : Efficacy of the prophylactic administration for hypocalcemia induced by denosumab, 日本薬学会第133年会, Mar. 2013.
20.	石田俊介, 伏谷秀治, Kazuhiko Teraoka, 久次米敏秀, Kazuyoshi Kawazoe and Kazuo Minakuchi : Structure of management tool with status of use for proper usage of antibiotics, 日本薬学会第133年会, Mar. 2013.
21.	Shinji Abe, Yuki Taniguchi, Masatoshi Kishuku, Mari Nakase, Hirofumi Shibata, Kazuyoshi Kawazoe, Mami Azuma, Yasuhiko Nishioka and Kazuo Minakuchi : Selectivity of new anti-podoplanin antibody against malignant pleural mesothelioma, 日本薬学会第133年会, Mar. 2013.
22.	田島壮一郎, Yasumasa Ikeda, Koichiro Tsuchiya, Yuya Horinouchi, Takumi Sakurada, Yoshitaka Kihira, Yuki Izawa-Ishizawa, Keisuke Ishizawa, Kazuyoshi Kawazoe, Kazuo Minakuchi and Toshiaki Tamaki : The influence of angiotensin II on duodenal iron absorption, 第86回日本薬理学会年会, Mar. 2013.
23.	田島壮一郎, Yasumasa Ikeda, Hideaki Enomoto, Yuki Izawa-Ishizawa, Yoshitaka Kihira, Keisuke Ishizawa, Koichiro Tsuchiya, Kazuo Minakuchi and Toshiaki Tamaki : 鉄制限食によってdb/dbマウスの糖尿病性腎症進展は抑制される, 第42回日本心脈管作動物質学会, Feb. 2013.
24.	Masayuki Shono, Mitsuo Kitamura, 小中健, Kazuyoshi Kawazoe and Kazuo Minakuchi : 開発培養チャンバーを用いた物理的圧迫によるHUVEC細胞骨格変化の影響, 第246回徳島医学会学術集会, Feb. 2013.
25.	Naoto Okada, Takenori Yamamoto, 渡邊政博, 吉村勇哉, Eriko Obana, Naoshi Yamazaki, Kazuyoshi Kawazoe, Yasuo Shinohara and Kazuo Minakuchi : 機能未知タンパク質TMEM45Bの熱凝集に関与するアミノ酸配列の同定, 第85回生化学会, Dec. 2012.
26.	堀家由貴, 谷井菜緒子, 多田智紀, 泉あずさ, 松本直貴, Kazuyoshi Kawazoe, Kazuo Minakuchi, Kensaku Aki and Eiji Hosoi : 巨核球系培養細胞を用いた薬剤評価の検討, 第36回徳島県医学検査学会, Dec. 2012.
27.	谷井菜緒子, 堀家由貴, 泉あずさ, 多田智紀, 松本直貴, Kazuyoshi Kawazoe, Kazuo Minakuchi, Kensaku Aki and Eiji Hosoi : 長期ストレス状態における免疫系への影響, 第36回徳島県医学検査学会, Dec. 2012.
28.	田島壮一郎, 櫻田巧, Souji Kakiuchi, 上松卓, Rumi Katashima, Kazuhiko Teraoka, 久次米敏秀, Kazuyoshi Kawazoe, Yasuhiko Nishioka, Hiroaki Yanagawa and Kazuo Minakuchi : UGT1A1遺伝子のヘテロ接合体(6または28)を持つイリノテカン投与患者における治療安全性ならびに継続性に関する検討, 第33回日本臨床薬理学会年会, Nov. 2012.
29.	Risa Sahara, Aki Murakami, Naoto Okada, Kazuyoshi Kawazoe and Kazuo Minakuchi : ヒト腸管上皮細胞において生薬抽出物がCYP3A4の安定性に与える影響, 第51回日本薬学会・日本薬剤師会・日本病院薬剤師会中国四国支部学術大会, Nov. 2012.
30.	Kohta Moriyama, Kazuyoshi Sue, Ken Konaka, Masayuki Shono, Kazuyoshi Kawazoe and Kazuo Minakuchi : 葛根湯が血管内皮細胞のCa濃度に与える影響, 第51回日本薬学会・日本薬剤師会・日本病院薬剤師会中国四国支部学術大会, Nov. 2012.
31.	小中健, 森剛志, 柴田高洋, 中村敏己, Kazuhiko Teraoka, 久次米敏秀, Kazuyoshi Kawazoe and Kazuo Minakuchi : 肺がんにおけるタキサン系抗がん剤に誘発された末梢神経障害に対するプレガバリンの使用実績と有効性の評価, 第51回日本薬学会・日本薬剤師会・日本病院薬剤師会中国四国支部学術大会, Nov. 2012.
32.	田島壮一郎, Shinji Abe, Hiroaki Yanagawa, 大和志保, 天羽亜美, 明石晃代, 高井繁美, 宮本登志子, 渡邊美穂, 伏谷秀治, Kazuhiko Teraoka, 久次米敏秀, Kazuyoshi Kawazoe, Mami Azuma and Kazuo Minakuchi : 薬学生実務実習における臨床研究・治験教育の導入と評価, 第51回日本薬学会・日本薬剤師会・日本病院薬剤師会中国四国支部学術大会, Nov. 2012.
33.	Shinji Abe, 伊勢夏子, 生田賢治, Naoto Okada, Mari Nakase, Hirofumi Shibata, Kazuyoshi Kawazoe, Mami Azuma and Kazuo Minakuchi : 病院実務実習における救急・集中治療領域での徳島大学薬学部教員の取り組み, 第51回日本薬学会・日本薬剤師会・日本病院薬剤師会中国四国支部学術大会, Nov. 2012.
34.	Yuki Taniguchi, Shinji Abe, Masatoshi Kishuku, Mami Azuma, Kazuyoshi Kawazoe, Yasuhiko Nishioka and Kazuo Minakuchi : ADCCを介したヒトキメラ型抗ポドプラニン抗体の悪性胸膜中皮腫に対する抗腫瘍効果の検討, 第51回日本薬学会・日本薬剤師会・日本病院薬剤師会中国四国支部学術大会, Nov. 2012.
35.	Masaki Hanibuchi, Shinji Abe, Yukinari Kato, Mika Kaneko, Masatoshi Kishuku, Kazuyoshi Kawazoe, Jun Huang, Atsushi Mitsuhashi, Kazuo Minakuchi and Yasuhiko Nishioka : 抗ポドプラニン抗体NZ-1の悪性胸膜中皮腫に対する抗体依存性細胞障害活性と抗腫瘍効果, 第53回日本肺癌学会総会, Nov. 2012.
36.	Shinji Abe, 伊勢夏子, 生田賢治, Naoto Okada, Ryoko Satoyoshi, Hirofumi Shibata, Kazuyoshi Kawazoe, Mami Azuma and Kazuo Minakuchi : 薬学部教員による救急・集中治療領域における実務実習指導の取り組み, 第22回日本医療薬学会, Oct. 2012.
37.	Yasuhiko Nishioka, Shinji Abe, Masatoshi Kishuku, Kazuyoshi Kawazoe, Jun Huang, Masaki Hanibuchi, Kazuo Minakuchi, Saburo Sone and Yukinari Kato : 悪性胸膜中皮腫に対するラット-ヒトキメラ型抗ポドプラニン抗体NZ-8の抗腫瘍効果, 第71回日本癌学会学術総会, Sep. 2012.
38.	田島壮一郎, Yasumasa Ikeda, Koichiro Tsuchiya, Yuya Horinouchi, 櫻田巧, Yoshitaka Kihira, Yuki Izawa-Ishizawa, Keisuke Ishizawa, Kazuyoshi Kawazoe, Shuhei Tomita, Kazuo Minakuchi and Toshiaki Tamaki : 十二指腸からの鉄吸収に対するAngiotensinⅡの影響, 第36回日本鉄バイオサイエンス学会学術集会, Sep. 2012.
39.	Kato Yukinari, Shinji Abe, Kazuo Minakuchi and Yasuhiko Nishioka : ヒトキメラ型抗ポドプラニン抗体による転移抑制機序の解明, 第16回日本がん分子標的治療学会学術集会, Jun. 2012.
40.	Yasuhiko Nishioka, Shinji Abe, Yukinari Kato, Masatoshi Kishuku, Kazuyoshi Kawazoe, Jun Huang, Masaki Hanibuchi, Kazuo Minakuchi and Saburo Sone : 悪性胸膜中皮腫に対するヒトキメラ型抗ポドプラニン抗体NZ-8の抗腫瘍効果, 第16回日本がん分子標的治療学会学術集会, Jun. 2012.
41.	Shinji Abe, Yukinari Kato, Mika Kaneko, Masatoshi Kisyuku, Kazuyoshi Kawazoe, Mami Azuma, Kazuo Minakuchi, Saburo Sone and Yasuhiko Nishioka : 悪性胸膜中皮腫に対する抗ポドプラニン抗体NZ-1の抗腫瘍効果に関する検討, 第52回日本呼吸器学会学術講演会, Apr. 2012.
42.	Jun Huang, Shinji Abe, Yuki Morita, Shuji Ozaki, Masatoshi Kishuku, Kazuo Minakuchi, Masaki Hanibuchi, Toshio Matsumoto, Saburo Sone and Yasuhiko Nishioka : Antibody-dependent cellular cytotoxicity against mesothelioma cells mediated by anti-HM 1.24 antibodies, 第52回日本呼吸器学会学術講演会, Apr. 2012.
43.	Ken Konaka, Aki Murakami, Tomoshi Koyama, 西迫寛隆, Masayuki Shono, Naoto Okada, Kazuyoshi Kawazoe and Kazuo Minakuchi : Effect of kakkonto in endothelial cell, 日本薬学会第132年会, Mar. 2012.
44.	Shinji Abe, Yuki Taniguchi, Masatoshi Kishuku, Ryoko Satoyoshi, Kazuyoshi Kawazoe, Mami Azuma, Yasuhiko Nishioka and Kazuo Minakuchi : Expression of the new tumor antigen OFA-iLRP in lung cancer, 日本薬学会第132年会, Mar. 2012.
45.	足立麻美, 桐野靖, 伏谷秀治, Kazuyoshi Kawazoe and Kazuo Minakuchi : The pharmaceutical management of the antibiotic -appropriate use of linezolid-, 日本薬学会第132年会, Feb. 2012.
46.	柴田高洋, 伏谷秀治, Hirofumi Shibata, 長尾多美子, Kazuyoshi Kawazoe and Kazuo Minakuchi : 当大学病院における注射薬搬送カートのATP拭き取り調査と細菌調査, 第27回日本環境感染学会総会抄録集, Vol.27 Supplement, 318, Feb. 2012.
47.	岸田真季, 倍味宏行, 山本歩実, 曽根淳美, 足立麻衣, 泉あずさ, Kensaku Aki, Naoki Matsumoto, Kazuyoshi Kawazoe, Kazuo Minakuchi and Eiji Hosoi : 精油による自律神経系及び免疫系への影響, 第35回徳島県医学検査学会, Dec. 2011.
48.	山本歩実, 岸田真季, 倍味宏行, 足立麻衣, 曽根淳美, 泉あずさ, Kensaku Aki, 松本直貴, Kazuyoshi Kawazoe, Kazuo Minakuchi and Eiji Hosoi : 血小板機能に及ぼす各種薬剤作用の血液培養細胞を用いた解析, 第35回徳島県医学検査学会, Dec. 2011.
49.	Naoto Okada, Takenori Yamamoto, 渡邊政博, 吉村勇哉, Eriko Obana, Naoshi Yamazaki, Kazuyoshi Kawazoe, Kazuo Minakuchi and Yasuo Shinohara : 機能未同定のタンパク質TMEM45Bに見られた熱凝集と熱凝集を引き起こすアミノ酸領域の同定, 第33回生体膜と薬物の相互作用シンポジウム, Nov. 2011.
50.	Yuya Horinouchi, 中村敏己, Takumi Sakurada, 森剛志, Ken Konaka, 三木幸代, 田島壮一郎, Shinji Abe, Kazuhiko Teraoka, 久次米敏秀, Kazuyoshi Kawazoe and Kazuo Minakuchi : ベバシズマブ投与大腸がん患者における早期高血圧の効果予測因子としての意義, 第50回日本薬学会・日本薬剤師会・日本病院薬剤師会中国四国支部学術大会, Nov. 2011.
51.	柴田高洋, 伏谷秀治, 中川博之, 長尾多美子, Hirofumi Shibata, Kazuyoshi Kawazoe and Kazuo Minakuchi : 院内感染制御を目的とした注射薬搬送カートのATP拭き取り調査と細菌調査, 第50回日本薬学会・日本薬剤師会・日本病院薬剤師会中国四国支部学術大会, Nov. 2011.
52.	Naoto Okada, 廣瀬由記子, 溝口徹也, Kazuhiko Teraoka, 久次米敏秀, Kazuyoshi Kawazoe and Kazuo Minakuchi : サリドマイド及びレナリドマイド服用患者に対する薬剤師の介入, 第50回日本薬学会・日本薬剤師会・日本病院薬剤師会中国四国支部学術大会, Nov. 2011.
53.	八木祐子, Koichiro Tsuchiya, Masayuki Shono, Kazuyoshi Kawazoe and Kazuo Minakuchi : ヒト結腸癌由来Caco-2細胞における抗癌剤耐性に及ぼす酸素分圧の影響, 第50回日本薬学会・日本薬剤師会・日本病院薬剤師会中国四国支部学術大会, Nov. 2011.
54.	Shinji Abe, Yuki Taniguchi, Masatoshi Kishuku, 加藤幸成, Kazuyoshi Kawazoe, Mami Azuma, Yasuhiko Nishioka and Kazuo Minakuchi : ポドプラニンを標的とした悪性胸膜中皮腫に対する新規抗体療法の検討, 第50回日本薬学会・日本薬剤師会・日本病院薬剤師会中国四国支部学術大会, Nov. 2011.
55.	Jumpei Taniguchi, Keisuke Ishizawa, Masaki Imanishi, Yoshitaka Kihira, Yasumasa Ikeda, Kazuyoshi Kawazoe, Koichiro Tsuchiya, Kazuo Minakuchi, Toshiaki Tamaki and Shuhei Tomita : 血管平滑筋細胞のhypoxia-inducible factor-1αはangiotensinⅡ誘発血管リモデリングの形成に関与する, 第50回日本薬学会・日本薬剤師会・日本病院薬剤師会中国四国支部学術大会, Nov. 2011.
56.	Takumi Sakurada, Keisuke Ishizawa, Masaki Imanishi, Jumpei Taniguchi, Shoko Fujii, Asami Nuno, Yuta Suzuki, Licht Miyamoto, Yoshitaka Kihira, Koichiro Tsuchiya, Kazuyoshi Kawazoe, Kazuo Minakuchi and Toshiaki Tamaki : マウス血管リモデリングに対するnitrosonifedipineの抑制効果, 第50回日本薬学会・日本薬剤師会・日本病院薬剤師会中国四国支部学術大会, Nov. 2011.
57.	Ken Konaka, Aya Miyatani, Masayuki Shono, Naoto Okada, Kazuyoshi Kawazoe and Kazuo Minakuchi : 正常ヒト臍帯静脈内皮細胞(HUVEC)に対する漢方薬成分の影響, 第50回日本薬学会・日本薬剤師会・日本病院薬剤師会中国四国支部学術大会, Nov. 2011.
58.	Mayuko Okamoto, Youichi Sato, Takuya Mikami, Kazuyoshi Kawazoe and Kazuo Minakuchi : 五味子水抽出物の新規生理活性に関する研究, 第50回日本薬学会・日本薬剤師会・日本病院薬剤師会中国四国支部学術大会, Nov. 2011.
59.	Aya Miyatani, Ken Konaka, Masayuki Shono, 西迫寛隆, Kazuyoshi Kawazoe and Kazuo Minakuchi : ウシ副腎髄質クロマフィン細胞に対する葛根湯構成生薬の影響, 第50回日本薬学会・日本薬剤師会・日本病院薬剤師会中国四国支部学術大会, Nov. 2011.
60.	伊勢夏子, 下岡幸恵, 生田賢治, Kazuhiko Teraoka, 久次米敏秀, Kazuyoshi Kawazoe and Kazuo Minakuchi : 持続的血液濾過透析施行患者に対するテイコプラニンの投与設計, 第5回日本腎と薬剤研究会学術大会, Sep. 2011.
61.	田島壮一郎, Yasumasa Ikeda, Koichiro Tsuchiya, Noriko Yamano, Yuya Horinouchi, Takumi Sakurada, Yoshitaka Kihira, Yuki Izawa-Ishizawa, Keisuke Ishizawa, Kazuyoshi Kawazoe, Shuhei Tomita, Kazuo Minakuchi and Toshiaki Tamaki : 肥満の脂肪組織における鉄の役割, 第35回日本鉄バイオサイエンス学会学術集会, Sep. 2011.
62.	Naoto Okada, 廣瀬由記子, 溝口徹也, Kazuhiko Teraoka, 久次米敏秀, Kazuyoshi Kawazoe and Kazuo Minakuchi : サリドマイド及びレナリドマイドにおける副作用モニタリングの重要性, 医療薬学フォーラム2011/第19回クリニカルファーマシーシンポジウム, Jul. 2011.
63.	Jumpei Taniguchi, Keisuke Ishizawa, Masaki Imanishi, Yoshitaka Kihira, Yasumasa Ikeda, 久次米敏秀, Kazuyoshi Kawazoe, Koichiro Tsuchiya, Kazuo Minakuchi, Toshiaki Tamaki and Shuhei Tomita : 動脈硬化におけるhypoxia-inducible factor-1αの新規治療標的分子としての可能性, 医療薬学フォーラム2011/第19回クリニカルファーマシーシンポジウム, Jul. 2011.
64.	田島壮一郎, Yasumasa Ikeda, Koichiro Tsuchiya, Yuya Horinouchi, Noriko Yamano, Yoshitaka Kihira, Keisuke Ishizawa, Kazuyoshi Kawazoe, Shuhei Tomita, Kazuo Minakuchi and Toshiaki Tamaki : ヒト腎糸球体血管内皮細胞において細胞内遊離鉄はangiotensin ⅡによるICAM-1の発現を増強する, 第54回日本腎臓学会学術集会, Jun. 2011.
65.	Masaki Imanishi, Keisuke Ishizawa, Takumi Sakurada, 富永えりか, Yuya Horinouchi, Jumpei Taniguchi, Shoko Fujii, Yoshitaka Kihira, Yasumasa Ikeda, Shuhei Tomita, Kazuo Minakuchi, Koichiro Tsuchiya and Toshiaki Tamaki : Nitrosonifedipineによる血管リモデリング抑制効果の検討, 日本薬学会第131回年会, Mar. 2011.
66.	Naoto Okada, Takenori Yamamoto, 渡邊政博, 吉村勇哉, Naoshi Yamazaki, Yasuo Shinohara and Kazuo Minakuchi : TMEM45Bのthermal aggregationに関与するアミノ酸配列の同定, 日本薬学会第131年会, Mar. 2011.
67.	Yuya Horinouchi, Koichiro Tsuchiya, 田島壮一郎, Yoshitaka Kihira, Yasumasa Ikeda, Keisuke Ishizawa, Shuhei Tomita, Kazuyoshi Kawazoe, Toshiaki Tamaki and Kazuo Minakuchi : Nitrosonifedipine の細胞保護効果に関する検討, 日本薬学会第131年会, Mar. 2011.
68.	Shinji Abe, Kazuhiko Teraoka, 久次米敏秀, Kazuyoshi Kawazoe and Kazuo Minakuchi : 徳島大学病院における病院実務実習カリキュラムとその成果, 日本薬学会第131年会, Mar. 2011.
69.	田島壮一郎, Kazuhiko Teraoka, Rumi Katashima, 宮本登志子, Kazuyoshi Kawazoe, 久次米敏秀, Naomi Morita, Kazuo Minakuchi, Masafumi Harada and Hiroaki Yanagawa : 自主臨床研究におけるCRC の役割 ―放射性薬剤の品質試験について―, 日本薬学会第131年会, Mar. 2011.
70.	西谷典子, 伏谷秀治, Kazuyoshi Kawazoe, 瀧口益史, Kazuo Minakuchi and 吉原新 : 肺炎および敗血症患者におけるスタチン服用の有無と予後の関連性, 日本薬学会第131年会, Mar. 2011.
71.	Miho Watanabe, Hirofumi Shibata, 伏谷秀治, Kazuyoshi Kawazoe and Kazuo Minakuchi : 病院施設のATP拭き取り検査と細菌汚染状況調査, 第26回日本環境感染学会総会, Feb. 2011.
72.	田島壮一郎, Yasumasa Ikeda, Koichiro Tsuchiya, Noriko Yamano, Yuya Horinouchi, Yoshitaka Kihira, Keisuke Ishizawa, Kazuyoshi Kawazoe, Shuhei Tomita, Kazuo Minakuchi and Toshiaki Tamaki : 鉄除去は脂肪肥大を抑制して糖尿病を改善する, 第40回日本心脈管作動物質学会, Feb. 2011.
73.	田島壮一郎, Yasumasa Ikeda, Koichiro Tsuchiya, Noriko Yamano, Yuya Horinouchi, Yoshitaka Kihira, Keisuke Ishizawa, Kazuyoshi Kawazoe, Shuhei Tomita, Kazuo Minakuchi and Toshiaki Tamaki : 鉄除去は脂肪肥大を抑制して糖尿病を改善する, 第40回日本心脈管作動物質学会, Feb. 2011.
74.	猪井紅美子, 平田有紀奈, Kensaku Aki, 曽根淳美, 足立麻衣, Eiji Hosoi, Kazuyoshi Kawazoe and Kazuo Minakuchi : ストレス条件下における免疫パラメータの変動, 第34回徳島県医学検査学会, Dec. 2010.
75.	平田有紀奈, 猪井紅美子, Kensaku Aki, 足立麻衣, 曽根淳美, Eiji Hosoi, 谷口友紀, Kazuyoshi Kawazoe and Kazuo Minakuchi : 血小板モデル細胞を用いた薬剤評価測定系の確立, 第34回徳島県医学検査学会, Dec. 2010.
76.	Chieko Okumura, Mayumi Sugimura, Shinji Abe, 米田良子, 上村卓広, 溝口徹也, Kazuhiko Teraoka, 久次米敏秀, Kazuyoshi Kawazoe, Kazuo Minakuchi, Mami Azuma and Yoshihisa Takaishi : 「病院実務実習」における指導薬剤師と薬学部実務家教員の連携, 第31回徳島大学薬学部卒後教育公開講座, Dec. 2010.
77.	Keisuke Ishizawa, 中西智子, Hirofumi Shibata, Shinji Abe, Mayumi Sugimura, Chieko Okumura, Yoshiyuki Yoshimura, Youichi Sato, Naokatu Arakaki, Kazuyoshi Kawazoe, Mami Azuma, Koichiro Tsuchiya, Aiko Yamauchi, Tetsuo Yamazaki and Kazuo Minakuchi : 徳島大学における薬学部・薬剤部連携による病院実務実習の実践, 第20回日本医療薬学会年会, Nov. 2010.
78.	西迫寛隆, 米田良子, 上村卓広, 溝口徹也, Shinji Abe, Kazuhiko Teraoka, 久次米敏秀, Kazuyoshi Kawazoe and Kazuo Minakuchi : 徳島大学病院におけるオピオイド製剤使用状況調査と適正使用における薬剤師の働き, 第20回日本医療薬学会年会, Nov. 2010.
79.	Yuya Horinouchi, 櫻田巧, 中村敏己, 森剛志, 小中健, 三木幸代, 田島壮一郎, 西迫寛隆, Shinji Abe, Kazuyoshi Kawazoe and Kazuo Minakuchi : 血圧上昇を指標としたベバシツマブ投与結腸・直腸がん患者の効果予測に関する検討, 第20回日本医療薬学会年会, Nov. 2010.
80.	渡邉美穂, Hirofumi Shibata, 上松卓, 伏谷秀治, Shinji Abe, Kazuyoshi Kawazoe, Tetsuo Yamazaki and Kazuo Minakuchi : 病院施設のATP拭き取り検査と細菌汚染状況調査, 第49回日本薬学会・日本薬剤師会・日本病院薬剤師会中国四国支部学術大会, Nov. 2010.
81.	Yuya Horinouchi, 櫻田巧, 中村敏己, Tsuyoshi Mori, 小中健, 三木幸代, 田島壮一郎, 西迫寛隆, Shinji Abe, Kazuhiko Teraoka, 久次米敏秀, Kazuyoshi Kawazoe and Kazuo Minakuchi : 分子標的治療薬ベバシズマブによる血圧上昇について ∼発現状況調査ならびに効果予測の検討∼, 第49回日本薬学会・日本薬剤師会・日本病院薬剤師会中国四国支部学術大会, Nov. 2010.
82.	太田佳那, Youichi Sato, 岡本茉佑子, Shinji Abe, ASHRAF ABDEL AZIM EWIS, Masako Sei, Kazuyoshi Kawazoe and Kazuo Minakuchi : 五味子水抽出物の新規作用に関する検討, 第49回日本薬学会・日本薬剤師会・日本病院薬剤師会中国四国支部学術大会, Nov. 2010.
83.	大上知妃呂, 佐原理沙, 田島壮一郎, Shinji Abe, Kazuyoshi Kawazoe and Kazuo Minakuchi : ヒト腸管上皮細胞における薬物代謝酵素CYP3A4 に対する生薬の影響, 第49回日本薬学会・日本薬剤師会・日本病院薬剤師会中国四国支部学術大会, Nov. 2010.
84.	木宿昌俊, Shinji Abe, 森田結貴, Kazuhiko Teraoka, 久次米敏秀, Yasuhiko Nishioka, Kazuyoshi Kawazoe, Saburo Sone and Kazuo Minakuchi : 成熟樹状細胞由来sVEGFR-1 の腫瘍血管新生に及ぼす影響, 第49回日本薬学会・日本薬剤師会・日本病院薬剤師会中国四国支部学術大会, Nov. 2010.
85.	森田結貴, Shinji Abe, 木宿昌俊, Yasuhiko Nishioka, Kazuyoshi Kawazoe, Saburo Sone and Kazuo Minakuchi : HM1.24 を標的とした悪性胸膜中皮腫に対する抗体療法の開発, 第49回日本薬学会・日本薬剤師会・日本病院薬剤師会中国四国支部学術大会, Nov. 2010.
86.	富永えりか, Keisuke Ishizawa, Masaki Imanishi, 櫻田巧, 谷口順平, 藤井聖子, Yuya Horinouchi, Yoshitaka Kihira, Shinji Abe, Kazuyoshi Kawazoe, Koichiro Tsuchiya, Toshiaki Tamaki and Kazuo Minakuchi : アンジオテンシンII による血管リモデリングに対するニトロソニフェジピンの影響, 第49回日本薬学会・日本薬剤師会・日本病院薬剤師会中国四国支部学術大会, Nov. 2010.
87.	下岡幸恵, 生田賢治, 伊勢夏子, Shinji Abe, Kazuhiko Teraoka, 久次米敏秀, Kazuyoshi Kawazoe and Kazuo Minakuchi : 集学治療病棟専任薬剤師によるテイコプラニン処方設計へのリアルタイム血中濃度測定を介した薬学的支援, 第4回日本腎と薬剤研究会学術大会2010, Oct. 2010.
88.	田島壮一郎, Yasumasa Ikeda, Koichiro Tsuchiya, Noriko Yamano, Yuya Horinouchi, Yoshitaka Kihira, Keisuke Ishizawa, Kazuyoshi Kawazoe, Shuhei Tomita, Kazuo Minakuchi and Toshiaki Tamaki : 2型糖尿病モデルマウスに対する鉄キレート剤による糖尿病改善効果の検討, 第34回日本鉄バイオサイエンス学会学術集会, Sep. 2010.
89.	Toshitaka Ikehara, 西迫寛隆, 白石泰郎, Kazuyoshi Kawazoe, Kazuo Minakuchi, Mitsuo Kitamura, 庄野正行, Kazuo Yoshizaki, Yohsuke Kinouchi and Hiroshi Miyamoto : Effects of time-varying magnetic field on cell volume regulation of bovine adrenal chromaffin cells in hyposmotic medium., 第87回日本生理学会大会, May 2010.
90.	柴田高博, Hirofumi Shibata, 伏谷秀治, 渡邉美穂, Mami Azuma, 庄野文章 and Kazuo Minakuchi : 病院環境における浮遊真菌の実態調査, 日本薬学会第130年会, Mar. 2010.
91.	田島壮一郎, Yasumasa Ikeda, Koichiro Tsuchiya, Yuya Horinouchi, 櫻田巧, Yoshitaka Kihira, Keisuke Ishizawa, Kazuyoshi Kawazoe, Shuhei Tomita, Kazuo Minakuchi and Toshiaki Tamaki : KK-Ay マウスにおける鉄キレート剤Deferoxamineによる糖尿病病態改善効果の検討, 第83回日本薬理学会, Mar. 2010.
92.	Keisuke Ishizawa, Kazuyoshi Kawazoe, Mami Azuma, Koichiro Tsuchiya, Aiko Yamauchi, Tetsuo Yamazaki, Kazuo Minakuchi, 智子中西, Hirofumi Shibata, Shinji Abe, Mayumi Sugimura, Chieko Okumura, Yoshiyuki Yoshimura, Youichi Sato and Naokatu Arakaki : P1-571 徳島大学における薬学部・薬剤部連携による病院実務実習の実践(一般演題ポスター発表,薬学教育(実務実習),臨床から学び臨床へと還元する医療薬学), The Annual Meeting of Japanese Society of Pharmaceutical Health Care and Sciences, Vol.20, No.0, 382, 2010. (Link to Search Site for Scientific Articles) ● CiNii @ National Institute of Informatics (CRID): 1390845713041900800 (CiNii: 1390845713041900800)
93.	Toshitaka Ikehara, Hirotaka Nishisako, Tairoh Shiraishi, Kazuyoshi Kawazoe, Kazuo Minakuchi, Mitsuo Kitamura, Masayuki Shono, Kazuo Yoshizaki, Yohsuke Kinouchi and Hiroshi Miyamoto : Effects of time-varying magnetic field on cell volume regulation of bovine adrenal chromaffin cells in hyposmotic medium, The Journal of Physiological Sciences, Vol.60, No.Supplement 1, S106, 2010.
94.	仁木朋加, 足立麻衣, Kensaku Aki, Eiji Hosoi, 真部裕一, Kazuyoshi Kawazoe and Kazuo Minakuchi : ヒト血小板機能に及ぼすバルプロ酸Naによる抑制機構の検討2 ∼カルモジュリン(CaM)系への作用∼, 第33回徳島県医学検査学会, Dec. 2009.
95.	足立麻衣, 仁木朋加, Kensaku Aki, Eiji Hosoi, 真部裕一, Kazuyoshi Kawazoe and Kazuo Minakuchi : ヒト血小板機能に及ぼすバルプロ酸Naによる抑制機構の検討1∼プロテインキナーゼC(PKC)系への作用∼, 第33回徳島県医学検査学会, Dec. 2009.
96.	富永えりか, Keisuke Ishizawa, 櫻田巧, 今西正樹, 谷口順平, Kazuyoshi Kawazoe, Yoshitaka Kihira, Yasumasa Ikeda, Shuhei Tomita, Koichiro Tsuchiya, Kazuo Minakuchi and Toshiaki Tamaki : Angiotensin IIによる血管平滑筋細胞遊走に対するnifedipine代謝物の影響, 第30回日本臨床薬理学会年会, Dec. 2009.
97.	真部裕一, Kensaku Aki, Kazuyoshi Kawazoe, Kazuo Minakuchi and Eiji Hosoi : バルプロ酸Naのヒト血小板機能に対する抑制作用, 第54回日本輸血·細胞治療学会中国·四国地方会, Nov. 2009.
98.	柴田高洋, Hirofumi Shibata, 伏谷秀治, 渡邉美穂, Kazuyoshi Kawazoe, 庄野文章, Kazuo Minakuchi and Naokatu Arakaki : 徳島大学病院病棟における浮遊真菌調査について, 第48回日本薬学会・日本薬剤師会・日本病院薬剤師会中国四国支部学術大会, Nov. 2009.
99.	八百原さゆり, 西谷典子, Kazuyoshi Kawazoe, Kazuo Minakuchi, Naokatu Arakaki and Hirofumi Shibata : スタチン系薬剤が緑膿菌のトランスロケーションに及ぼす影響, 第48回日本薬学会・日本薬剤師会・日本病院薬剤師会中国四国支部学術大会, Nov. 2009.
100.	森剛志, 西迫寛隆, 中村敏己, 三木幸代, Yuya Horinouchi, 櫻田巧, Shinji Abe, Kazuhiko Teraoka, 久次米敏秀, Kazuyoshi Kawazoe and Kazuo Minakuchi : 外来乳がん化学療法におけるクラスター解析を用いた副作用予測の試み, 第48回日本薬学会・日本薬剤師会・日本病院薬剤師会中国四国支部学術大会, Nov. 2009.
101.	Shinji Abe, Yasuhiko Nishioka, 木宿昌俊, 中野沙織, 森田結貴, Kazuhiko Teraoka, 久次米敏秀, Kazuyoshi Kawazoe, Saburo Sone and Kazuo Minakuchi : 特異的癌抗原MAGE-3を標的とした癌免疫療法の検討, 第48回日本薬学会・日本薬剤師会・日本病院薬剤師会中国四国支部学術大会, Nov. 2009.
102.	真部裕一, Kazuyoshi Kawazoe, Shinji Abe, Kazuo Minakuchi, 安藝健作 and Eiji Hosoi : バルプロ酸ナトリウムによる血小板凝集抑制メカニズムについての検討, 第48回日本薬学会・日本薬剤師会・日本病院薬剤師会中国四国支部学術大会, Nov. 2009.
103.	下岡幸恵, 生田賢治, 上村卓広, Shinji Abe, Kazuhiko Teraoka, 久次米敏秀, Kazuyoshi Kawazoe and Kazuo Minakuchi : 集学治療病棟専任薬剤師による薬剤管理業務, 第48回日本薬学会・日本薬剤師会・日本病院薬剤師会中国四国支部学術大会, Nov. 2009.
104.	元林有紀, 野口悠高, 梅田貴文, Kazuhiko Teraoka, 久次米敏秀, Kazuyoshi Kawazoe and Kazuo Minakuchi : 糖尿病性網膜症患者に対する服薬指導 ∼ベバシズマブ使用患者を中心に∼, 第48回日本薬学会・日本薬剤師会・日本病院薬剤師会中国四国支部学術大会, Nov. 2009.
105.	桐野靖, Kazuhiko Teraoka, 久次米敏秀, Kazuyoshi Kawazoe, Tetsuro Ohmori and Kazuo Minakuchi : 徳島大学病院における非定型抗精神病薬の体重増加についての解析, 第48回日本薬学会・日本薬剤師会・日本病院薬剤師会中国四国支部学術大会, Nov. 2009.
106.	富永えりか, Keisuke Ishizawa, 櫻田巧, 今西正樹, 谷口順平, 山﨑有希子, Yoshitaka Kihira, Kazuyoshi Kawazoe, Koichiro Tsuchiya, Kazuo Minakuchi and Toshiaki Tamaki : ニフェジピン代謝物はアンジオテンシンⅡ誘発血管平滑筋細胞遊走を抑制する, 第48回日本薬学会・日本薬剤師会・日本病院薬剤師会中国四国支部学術大会, Nov. 2009.
107.	山﨑有希子, Keisuke Ishizawa, 富永えりか, 谷口順平, 櫻田巧, Kazuyoshi Kawazoe, Koichiro Tsuchiya, Toshiaki Tamaki and Kazuo Minakuchi : アンジオテンシンⅡによる血管平滑筋細胞遊走・増殖における細胞内鉄の関与, 第48回日本薬学会・日本薬剤師会・日本病院薬剤師会中国四国支部学術大会, Nov. 2009.
108.	腰岡桜, Youichi Sato, 桐野靖, 紙本尚幸, Shinji Abe, Kazuyoshi Kawazoe, Yutaka Nakahori and Kazuo Minakuchi : DPP4欠損ラットを用いた1型糖尿病誘発モデルにおける脂質代謝異常発症のメカニズム解明, 第48回日本薬学会・日本薬剤師会・日本病院薬剤師会中国四国支部学術大会, Nov. 2009.
109.	阿部有里子, 宮谷綾, 西迫寛隆, Shinji Abe, Kazuyoshi Kawazoe and Kazuo Minakuchi : ウシ副腎髄質クロマフィン細胞の漢方薬成分に対する応答, 第48回日本薬学会・日本薬剤師会・日本病院薬剤師会中国四国支部学術大会, Nov. 2009.
110.	平松由佳子, 阿古目健志, Shinji Abe, Kazuyoshi Kawazoe, Junji Terao and Kazuo Minakuchi : 漢方薬の品質変化と剤型との関連性, 第48回日本薬学会・日本薬剤師会・日本病院薬剤師会中国四国支部学術大会, Nov. 2009.
111.	中野沙織, Shinji Abe, 森田結貴, 木宿昌俊, Yasuhiko Nishioka, Kazuyoshi Kawazoe, Saburo Sone and Kazuo Minakuchi : 新規癌抗原OFA-iLRPを標的とした肺癌に対する免疫療法の開発, 第48回日本薬学会・日本薬剤師会・日本病院薬剤師会中国四国支部学術大会, Nov. 2009.
112.	東谷香奈, 大上知妃呂, 野口悠高, Shinji Abe, Kazuyoshi Kawazoe and Kazuo Minakuchi : Caco-2細胞に発現したCYP3A4に及ぼす生薬抽出物の影響, 第48回日本薬学会・日本薬剤師会・日本病院薬剤師会中国四国支部学術大会, Nov. 2009.
113.	阿部有里子, 宮谷綾, 西迫寛隆, Kazuyoshi Kawazoe and Kazuo Minakuchi : ウシ副腎髄質クロマフィン細胞に対する葛根湯の影響, 第26回和漢医薬学会学術大会, Vol.26, No.Supplement, 100, Aug. 2009.
114.	Harumi Hinode, Mami Azuma, 菊石美也子, 伏谷秀治, Kazuyoshi Kawazoe and Kazuo Minakuchi : 「徳島大学薬学部病院実務実習テキスト」の作成とその活用についての調査, 日本薬学会129年会, 0, Mar. 2009.
115.	山口佳津騎, 福岡憲泰, 鈴木聖, 谷久美子, 田中裕章, 元木貴大, 朝倉正登, 新田正道, Kazuyoshi Kawazoe and Kazuo Minakuchi : 薬学部学生のがん治療に対する意識調査, 日本薬学会129年会, 0, Mar. 2009.
116.	田島壮一郎, Koichiro Tsuchiya, 濱本磨以, Yuya Horinouchi, Shuhei Tomita, Keisuke Ishizawa, Kazuyoshi Kawazoe, Toshiaki Tamaki and Kazuo Minakuchi : Angiotensin IIによるヒト腎糸球体血管内皮細胞(HGEC)内における鉄動態の検討, 日本薬学会129年会, Mar. 2009.
117.	伏谷秀治, Hirofumi Shibata, 柴田高洋, Kazuyoshi Kawazoe, 安倍正博, Shinji Abe, Tomihiko Higuti, 庄野文章 and Kazuo Minakuchi : 徳島大学病院病棟における環境中の浮遊真菌調査について, 第24回日本環境感染学会総会, Feb. 2009.
118.	Tatsuya Okada, Tomiaki Morikawa, Yuu Tamaki, Masato Tagi, Kazuyoshi Kawazoe, 伏谷秀治, Kazuo Minakuchi and Hiroki Moriguchi : 薬品の使用履歴に基づいた薬品情報配信システムの構築と評価, 医療情報学連合大会論文集28回, Nov. 2008.
119.	廣永有沙, Keisuke Ishizawa, 山崎有希子, 野瀬文乃, Kazuyoshi Kawazoe, Toshiaki Tamaki and Kazuo Minakuchi : オルメサルタンはPDGF誘導メサンギウム細胞遊走をAT1受容体非依存的に抑制する, 第47回日本薬学会・日本薬剤師会・日本病院薬剤師会中国四国支部学術大会, 189, Nov. 2008.
120.	田中亜紀, 香川恵子, Kazuyoshi Kawazoe, Takeshi Nikawa, Junji Terao and Kazuo Minakuchi : 栄養学的指標に基づく漢方薬の医薬品としての品質評価, 第47回日本薬学会・日本薬剤師会・日本病院薬剤師会中国四国支部学術大会, 164, Nov. 2008.
121.	河野渉, 引地香織, Hirofumi Shibata, Shinji Abe, Kazuyoshi Kawazoe, Kazuo Minakuchi and Tomihiko Higuti : 銀翹散のin vitro抗インフルエンザウイルス活性につて, 第47回日本薬学会・日本薬剤師会・日本病院薬剤師会中国四国支部学術大会, 97, Nov. 2008.
122.	白石泰郎, 西迫寛隆, Toshitaka Ikehara, Shinji Abe, Kazuyoshi Kawazoe and Kazuo Minakuchi : ウシ副腎髄質クロマフィン細胞におけるアクチンと細胞容積調節機能に及ぼす変動磁界の影響, 第47回日本薬学会・日本薬剤師会・日本病院薬剤師会中国四国支部学術大会, 84, Nov. 2008.
123.	紙本尚幸, 桐野靖, 腰岡桜, Youichi Sato, Shinji Abe, Kazuyoshi Kawazoe, Kazuo Minakuchi and Yutaka Nakahori : ストレプトゾトシン誘発糖尿病ラットモデルにおけるDipptidyl pdptidase 4と脂質代謝異常の関連性について, 第47回日本薬学会・日本薬剤師会・日本病院薬剤師会中国四国支部学術大会, 83, Nov. 2008.
124.	Mami Azuma, Harumi Hinode, 三木あかね, Kazuhiko Teraoka, 久次米敏秀, Kazuyoshi Kawazoe and Kazuo Minakuchi : 学生の体験に基づくリスクマネージメント実習の試み, 第18回日本医療薬学会年会, 276, Sep. 2008.
125.	Kazuhiko Teraoka, 中村敏己, 梅田貴文, 久次米敏秀, Kazuyoshi Kawazoe and Kazuo Minakuchi : 調剤インシデント発生状況から見た調剤過誤防止対策の評価, 第18回日本医療薬学会年会, 273, Sep. 2008.
126.	Kazuyoshi Kawazoe, 坂本久美子, 伏谷秀治 and Kazuo Minakuchi : 現役薬剤師に対する漢方薬意識調査, 第18回日本医療薬学会年会, 275, Sep. 2008.
127.	柴田高洋, Hirofumi Shibata, 伏谷秀治, Kazuyoshi Kawazoe, 阿倍正博, Tomihiko Higuti, Kazuo Minakuchi and 庄野文章 : 徳島大学病院病棟内における浮遊菌調査, 第18回日本医療薬学会年会, 246, Sep. 2008.
128.	白石泰郎, 藤原智弘, Kazuyoshi Kawazoe, 西迫寛隆 and Kazuo Minakuchi : 抗がん剤の細胞毒性を抑制する漢方薬の探索研究, 日本薬学会年会, Mar. 2008.
129.	紙本尚幸, 桐野靖, Youichi Sato, Kazuyoshi Kawazoe, Kazuo Minakuchi and Yutaka Nakahori : 高カロリー食付加動物モデルを用いた，血中dipeptidyl peptidase 4(DPP4)活性と肥満ならびに耐糖能異常との関連性について, 日本薬学会年会, Mar. 2008.
130.	田中亜紀, Kazuyoshi Kawazoe, Takeshi Nikawa, Junji Terao and Kazuo Minakuchi : 栄養学的指標に基づく漢方薬の評価研究, 日本薬学会年会, Mar. 2008.
131.	森剛志, 中村敏己, 西迫寛隆, 三木幸代, 山口美代子, 梅田貴文, Mami Azuma, Kazuhiko Teraoka, Kazuyoshi Kawazoe and Kazuo Minakuchi : 外来がん化学療法における副作用の集積・解析・フィードバック, 第25回徳島大学薬学部卒後教育公開講座, Dec. 2007.
132.	田中麻衣, 板東美和, Eiji Hosoi, 道倉亜実, Kazuyoshi Kawazoe, Kazuo Minakuchi and 芳地一 : ヒト血小板機能に及ぼすバルプロ酸ナトリウムの影響, 第31回徳島県医学検査学会, Dec. 2007.
133.	Kazuyoshi Kawazoe, 川内陽子, 伏谷秀治, Tomiaki Morikawa, Tatsuya Okada, Hiroki Moriguchi and Kazuo Minakuchi : ホームページを利用したオンデマンド型院内医薬品情報配信システムの構築と評価, 第27回医療情報学連合大会論文集, 1142-1143, Nov. 2007.
134.	Kazuyoshi Kawazoe, Kazuo Minakuchi and Minoru Irahara : 健康食品，漢方薬，そして薬, 第46回日本薬学会・日本薬剤師会・日本病院薬剤師会中国四国支部学術大会, 31, Nov. 2007.
135.	道倉亜実, Shinji Abe, 沼田ちえ, 田中麻衣, Miwa Bando, Eiji Hosoi, Kazuyoshi Kawazoe, Hitoshi Houchi and Kazuo Minakuchi : ヒト血小板機能に及ぼす抗てんかん剤の影響, 第46回日本薬学会・日本薬剤師会・日本病院薬剤師会中国四国支部学術大会, 158, Nov. 2007.
136.	Shinji Abe, 木宿昌俊, Yasuhiko Nishioka, 中村敏己, 西迫寛隆, Kazuhiko Teraoka, 久次米敏秀, Kazuyoshi Kawazoe, Saburo Sone and Kazuo Minakuchi : 肺癌に対する腫瘍特異的免疫療法の検討, 第46回日本薬学会・日本薬剤師会・日本病院薬剤師会中国四国支部学術大会, 148, Nov. 2007.
137.	西迫寛隆, Toshitaka Ikehara, Kazuyoshi Kawazoe and Kazuo Minakuchi : ウシ副腎髄質クロマフィン細胞におけるアクチンと細胞容積調節機能に及ぼす変動磁界の影響, 第46回日本薬学会・日本薬剤師会・日本病院薬剤師会中国四国支部学術大会, 119, Nov. 2007.
138.	西迫寛隆, 中村敏己, 三木幸代, 山口美代子, 森剛志, 梅田貴文, Mami Azuma, Kazuhiko Teraoka, Kazuyoshi Kawazoe and Kazuo Minakuchi : 外来がん化学療法における副作用の集積・解析に基づいたレジメン別パンフレットの改善, 第17回日本医療薬学会年会, Sep. 2007.
139.	下岡幸恵, 鳥井真由美, 伏谷秀治, Harutaka Yamaguchi, Shinji Abe, Kazuyoshi Kawazoe, Masaji Nishimura and Kazuo Minakuchi : 腎機能障害患者におけるテイコプラニン連日投与方法に関する検討, The Japanese Journal of Therapeutic Drug Monitoring, Vol.24, No.3, s123, Jul. 2007.
140.	溝口徹也, 伏谷秀治, 鳥井真由美, 下岡幸恵, 森剛志, Kazuyoshi Kawazoe and Kazuo Minakuchi : リネゾリド適応追加による抗MRSA薬使用状況の変化, 医療薬学フォーラム2007, 278, Jul. 2007.
141.	中村敏己, 西迫寛隆, 森剛志, 田島壮一郎, 梅田貴文, 寺岡和彦, Kazuyoshi Kawazoe and Kazuo Minakuchi : 全診療科を対象としたレジメン管理とチェックシステムの構築, 医療薬学フォーラム2007, 158, Jul. 2007.
142.	山下由起, Miwa Bando, Eiji Hosoi, 白潟朋美, 道倉亜実, Kazuyoshi Kawazoe, Kazuo Minakuchi, 芳地一 and 廣瀬政雄 : ヒト血小板機能に及ぼす一般用医薬品 (イブプロフェン)の影響について, 第30回徳島県医学検査学会, Dec. 2006.
143.	杉豪介, 小林憲司, 沼谷ちえ, Miwa Bando, Eiji Hosoi, 白潟朋美, 道倉亜実, Kazuyoshi Kawazoe, Kazuo Minakuchi, 芳地一 and 廣瀬政雄 : フローサイトメトリー法による血小板表面抗原の解析2∼アスピリン・シロスタゾール・イブプロフェンの血小板活性抑制効果について∼, 第30回徳島県医学検査学会, Dec. 2006.
144.	小林憲司, 杉豪介, 沼谷ちえ, Miwa Bando, Eiji Hosoi, 白潟朋美, 道倉亜実, Kazuyoshi Kawazoe, Kazuo Minakuchi, 芳地一 and 廣瀬政雄 : フローサイトメトリー法による血小板表面抗原の解析1∼血小板活性化マーカーの検出法について∼, 第30回徳島県医学検査学会, Dec. 2006.
145.	Shinji Abe, 久次米敏秀, 寺岡和彦, Kazuyoshi Kawazoe and Kazuo Minakuchi : 米国における薬剤師育成の現状, 第45回日本薬学会・日本病院薬剤師会中国四国支部学術大会, 204, Oct. 2006.
146.	白潟朋美, 道倉亜実, Shinji Abe, 沼田ちえ, 杉豪介, 田中麻衣, Miwa Bando, Eiji Hosoi, Kazuyoshi Kawazoe, Hitoshi Houchi and Kazuo Minakuchi : ヒト活性化血小板における抗血小板薬の効果, 第45回日本薬学会・日本病院薬剤師会中国四国支部学術大会, 138, Oct. 2006.
147.	黒川ふみ, Shinji Abe, 鳥井真由美, 濱野修一, Kazuyoshi Kawazoe, Hitoshi Houchi and Kazuo Minakuchi : アスピリンとNSAIDs併用における相互作用 ∼ヒト血小板凝集能に及ぼす影響∼, 第45回日本薬学会・日本病院薬剤師会中国四国支部学術大会, 138, Oct. 2006.
148.	松村敏彦, 宮本由加里, 黒川ふみ, Shinji Abe, 榊原啓之, Keisuke Ishizawa, Koichiro Tsuchiya, 清水寛, Junji Terao, Toshiaki Tamaki, Kazuyoshi Kawazoe and Kazuo Minakuchi : ラット強制水泳試験における漢方薬の抗うつ作用の検討, 第45回日本薬学会・日本病院薬剤師会中国四国支部学術大会, 125, Oct. 2006.
149.	平広範, Keisuke Ishizawa, 廣永有沙, Kazuyoshi Kawazoe, Toshiaki Tamaki and Kazuo Minakuchi : 血管内皮細胞障害におけるアンジオテンシンII受容体拮抗薬の保護効果, 第45回日本薬学会・日本病院薬剤師会中国四国支部学術大会, 102, Oct. 2006.
150.	南有紀, 塩田直青子, Toshitaka Ikehara, 庄野正行, Keisuke Ishizawa, Kazuo Yoshizaki, Yohsuke Kinouchi, Shinji Abe, Hitoshi Houchi, Kazuyoshi Kawazoe and Kazuo Minakuchi : ウシ副腎髄質細胞の容積変化に及ぼす変動磁界の影響, 第45回日本薬学会・日本病院薬剤師会中国四国支部学術大会, 76, Oct. 2006.
151.	白潟朋美, 道倉亜実, Shinji Abe, 沼谷ちえ, 杉豪介, 田中麻衣, 坂東美和, Eiji Hosoi, Hitoshi Houchi, Kazuyoshi Kawazoe and Kazuo Minakuchi : ヒト活性化血小板における抗血小板薬の効果, 日本薬学会・日本病院薬剤師会第45回中国四国支部学術大会, Oct. 2006.
152.	中村敏己, Mami Azuma, 梅田貴文, 西迫寛隆, 桐野靖, 寺岡和彦, 久次米敏秀, Kazuyoshi Kawazoe and Kazuo Minakuchi : がん化学療法チームによるセーフティマネジメント, 第16回日本医療薬学会年会, Oct. 2006.
153.	Kazuyoshi Kawazoe, 松村敏彦, 黒川ふみ, 榊原啓之, Keisuke Ishizawa, Koichiro Tsuchiya, 清水寛, Junji Terao, Toshiaki Tamaki and Kazuo Minakuchi : ラット強制水泳試験による漢方薬の抗うつ作用評価, 第109回日本薬理学会近畿部会, 30, Jun. 2006.
154.	安田裕美, Miwa Bando, Eiji Hosoi, 井上めぐみ, 白潟朋美, Keisuke Ishizawa, Kazuyoshi Kawazoe, Kazuo Minakuchi and 芳地一 : ヒト活性化血小板における抗血小板薬の効果, 第29回徳島県医学検査学会抄録集, 27, Dec. 2005.
155.	西迫寛隆, Keisuke Ishizawa, 溝口徹也, 桐野靖, Shinji Abe, Kazuyoshi Kawazoe and Kazuo Minakuchi : 結核病棟薬剤管理指導におけるワークシートの活用とNSTとの連携, 第44回日本薬学会・日本病院薬剤師会中国四国支部学術大会, 190, Nov. 2005.
156.	富永樹, 黒川ふみ, Keisuke Ishizawa, 鳥井真由美, 大山真由美, 胡田順子, 濱野修一, Kazuyoshi Kawazoe, Hitoshi Houchi and Kazuo Minakuchi : アスピリンと非ステロイド性消炎鎮痛薬のヒト血小板凝集能へ及ぼす併用効果, 第44回日本薬学会・日本病院薬剤師会中国四国支部学術大会, 136, Nov. 2005.
157.	三木智重子, Keisuke Ishizawa, 松村敏彦, 木宿昌俊, Kazuyoshi Kawazoe and Kazuo Minakuchi : アルドステロンはBig MAP kinase 1 (BMK1)活性化を介してラット平滑筋細胞を増殖させる, 第44回日本薬学会・日本病院薬剤師会中国四国支部学術大会, 115, Nov. 2005.
158.	Hiromi Sasaki, 南有紀, Toshitaka Ikehara, 細川敬子, Hisao Yamaguchi, Kazuo Yoshizaki, Yohsuke Kinouchi, Keisuke Ishizawa, Kazuyoshi Kawazoe, Hitoshi Houchi and Kazuo Minakuchi : 牛副腎髄質由来細胞内の一過性Ca²⁺増加機構に対する磁界の影響, 第44回日本薬学会・日本病院薬剤師会中国四国支部学術大会, 126, Nov. 2005.
159.	井上めぐみ, 白潟朋美, Keisuke Ishizawa, Kazuyoshi Kawazoe, 安田裕美, 板東美和, Eiji Hosoi, Hitoshi Houchi and Kazuo Minakuchi : 抗血小板薬におけるヒト血小板内Ca²⁺濃度の変動と凝集の抑制, 第44回日本薬学会・日本病院薬剤師会中国四国支部学術大会, 124, Nov. 2005.
160.	杉本理香, Keisuke Ishizawa, 平広範, 勝部紗和子, 桐野靖, Kazuyoshi Kawazoe and Kazuo Minakuchi : ラットメサンギウム細胞の遊走および増殖に対するアディポネクチンの作用とそのメカニズム, 第44回日本薬学会・日本病院薬剤師会中国四国支部学術大会, 124, Nov. 2005.
161.	河野美代, Mami Azuma, 田村祥祐, 加地充, 井上信裕, 元木宏, 玉田正夫, Kazuo Minakuchi and 南博 : 新体制薬局実務実習に向けての徳島県薬剤師会の取り組み, 第38回日本薬剤師会学術大会, Oct. 2005.
162.	生田雅子, 石澤啓介, Kazuo Minakuchi, Koichiro Tsuchiya, Aiko Yamauchi and Masaru Kihara : 徳島大学病院におけるTPN処方設計支援ソフトの使用評価と改良, 日本薬学会第124年会, Mar. 2004.
163.	大久保美佐緒, 河野美代, Mami Azuma, 寺岡和彦, 芳地一, Kazuo Minakuchi, 田村祥祐, 仁木稔, 元木宏, 玉田正夫, Aiko Yamauchi, Yoshiharu Takiguchi, Masaru Kihara and 原谷明 : 薬学部学生の薬局実務実習についての意識調査∼薬局薬剤師および学生の立場から∼, 第36回日本薬剤師会学術大会, Oct. 2003.
164.	Yasuhiko Nishioka, 中川達夫, Hiroaki Yanagawa, Kazuo Minakuchi and Saburo Sone : 難治性固形癌に対するMAGE-3ペプチドパルス成熟樹状細胞を用いた癌免疫療法の第I相臨床試験, 第3回トランスレーショナルリサーチワークショップ, Sep. 2003.
165.	Aiko Yamauchi, Yoshiharu Takiguchi, 雅之横田, Masaru Kihara, 久次米俊秀, 寺岡和彦, Kazuo Minakuchi and 高杉益充 : 徳島大学大学院薬学研究科医療薬学専攻における初年度臨床薬学実習の評価, 日本薬学会第118年会, Mar. 1998.
166.	合田真規, Aiko Yamauchi, Masaru Kihara, Koichiro Tsuchiya and Kazuo Minakuchi : 徳島大·医·病院におけるIVH処方設計支援ソフトを使用してみて, 第36回日本薬学会·日本病院薬剤師会学術大会中国四国支部大会, Nov. 1997.

Et cetera, Workshop:

1.	Kazuo Minakuchi and Keisuke Ishizawa : Interview 薬剤業務の周辺, カレントファーマシー, Vol.22, 5-6, Dec. 2004.
2.	Kazuo Minakuchi and Keisuke Ishizawa : 適切な栄養療法をサポートする NSTにおける薬剤師の役割, GSKファーマシストジャーナル, Vol.7, 4-6, Nov. 2004.

Report:

1.	Kazuo Minakuchi, Hiroki Moriguchi, Hitoshi Houchi and Takafumi Katayama : 徳島大学病院における医療情報の電子化状況について, 医薬品等医療技術リスク評価研究事業平成15年度研究報告, Mar. 2004. (Keyword) Electric Medical Record / Hospital Information System

Grants-in-Aid for Scientific Research (KAKEN Grants Database @ NII.ac.jp)

Pharmacokinetics of sedative medicine during brain hypothermia therapy and its proper use (Project/Area Number: 16590113 )
Physiological Role of Calcium Efflux from Neuronal Cells and Its Regulation by Drugs (Project/Area Number: 10672150 )
Search by Researcher Number (30284326)

Professor Emeritus : Minakuchi, Kazuo

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Grants-in-Aid for Scientific Research (KAKEN Grants Database @ NII.ac.jp)