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111.
Yukiko Kato Mao Hagihara Ai Kurumiya Tomoko Takahashi Miki Sakata Yuichi Shibata Hideo Kato Arufumi Shiota Hiroki Watanabe Nobuhiro Asai Yusuke Koizumi Yuka Yamagishi Hiroshige Mikamo 《Journal of infection and chemotherapy》2018,24(1):31-35
Background
Central line-associated bloodstream infections (CLABSIs) are among the most serious complications especially in blood cancer patients. In January 2013, Centers for Disease and Prevention (CDC) introduced a new surveillance definition of mucosal barrier injury-associated laboratory-confirmed bloodstream infection (MBI-LCBI). This study was to determine the impact of MBI-LCBI on CLABSIs and compare the clinical characteristics of MBI versus non-MBI-LCBI cases.Patients and methods
We retrospectively reviewed the records of 250 consecutive patients. They were admitted in department of hematology at Aichi Medical University Hospital. We applied the revised 2013 CLABSI surveillance protocol to all CLABSI cases identified during the 47-months period from May 2012 through June 2016.Results
A total of 44 CLABSIs were identified. The median patient age was 65 years (range, 12 to 89). Among 44 patients, 31 patients were diagnosed as leukemia (70.5%) and 12 patients as lymphoma (27.3%). Six patients underwent bone transplantation for leukemia or myelodysplastic syndrome (13.6%). A total of 20 patients (45.5%) were classified as MBI-LCBI and 24 (54.5%) were classified as non-MBI-LCBI. The primary disease type (P = 0.018), neutropenic within 3 days before CLABSI (MBI-LCBI vs. non-MBI-LCBI: 95.0% vs. 26.3%, P = <0.0001), line(s) removed owing to CLABSI (15.0% vs. 54.2%, P = 0.011) and Gram-negative organisms cultured (70.0% vs. 37.5%, P = 0.004) showed significantly difference between the groups.Conclusion
Our data showed that MBI-LCBI cases account for 45.5% of the CLABSI cases identified in blood cancer patients, and constituted a significant burden to this high-risk patient population. 相似文献112.
Masanori Someya Masakazu Hori Kunihiko Tateoka Kensei Nakata Masaru Takagi Masato Saito Naoki Hirokawa Masato Hareyama Koh-ichi Sakata 《Journal of radiation research》2015,56(1):122-127
In patients undergoing radiotherapy for localized prostate cancer, dose–volume histograms and clinical variables were examined to search for correlations between radiation treatment planning parameters and late rectal bleeding. We analyzed 129 patients with localized prostate cancer who were managed from 2002 to 2010 at our institution. They were treated with 3D conformal radiation therapy (3D-CRT, 70 Gy/35 fractions, 55 patients) or intensity-modulated radiation therapy (IMRT, 76 Gy/38 fractions, 74 patients). All radiation treatment plans were retrospectively reconstructed, dose–volume histograms of the rectum were generated, and the doses delivered to the rectum were calculated. Time to rectal bleeding ranged from 9–53 months, with a median of 18.7 months. Of the 129 patients, 33 patients had Grade 1 bleeding and were treated with steroid suppositories, while 25 patients with Grade 2 bleeding received argon plasma laser coagulation therapy (APC). Three patients with Grade 3 bleeding required both APC and blood transfusion. The 5-year incidence rate of Grade 2 or 3 rectal bleeding was 21.8% for the 3D-CRT group and 21.6% for the IMRT group. Univariate analysis showed significant differences in the average values from V65 to V10 between Grades 0–1 and Grades 2–3. Multivariate analysis demonstrated that patients with V65 ≥ 17% had a significantly increased risk (P = 0.032) of Grade 2 or 3 rectal bleeding. Of the 28 patients of Grade 2 or 3 rectal bleeding, 17 patients (60.7%) were cured by a single session of APC, while the other 11 patients required two sessions. Thus, none of the patients had any further rectal bleeding after the second APC session. 相似文献
113.
Keiichiro Watanabe Ariunzaya Bat-Erdene Hirofumi Tenshin Qu Cui Jumpei Teramachi Masahiro Hiasa Asuka Oda Takeshi Harada Hirokazu Miki Kimiko Sogabe Masahiro Oura Ryohei Sumitani Yukari Mitsui Itsuro Endo Eiji Tanaka Makoto Kawatani Hiroyuki Osada Toshio Matsumoto Masahiro Abe 《Haematologica》2021,106(4):1172
114.
Keisuke Kidoguchi Yasushi Kubota Shun Fujimoto Yasuhisa Sakata Haruna Kizuka-Sano Kyosuke Yamaguchi Hiroshi Ureshino Hiroo Katsuya Toshihiko Ando Motohiro Esaki Shinya Kimura 《Internal medicine (Tokyo, Japan)》2021,60(10):1601
Cronkhite-Canada syndrome (CCS) is a rare polyposis disorder accompanied by alopecia and onychodystrophy. A 63-year-old man with a history of CCS and repeated embolism developed progressive thrombocytopenia and mild anemia. Laboratory testing, a bone marrow examination, and magnetic resonance imaging of the spine resulted in a diagnosis of concurrent aplastic anemia (AA). Paroxysmal nocturnal hemoglobinuria (PNH)-type cells were detected in a peripheral blood specimen. In addition, human leukocyte antigen (HLA) included DRB1*15:01 and DRB1*15:02. Mesalazine was discontinued in consideration of possible drug-induced pancytopenia. Immunosuppressive therapy ameliorated both the gastrointestinal symptoms of CCS and pancytopenia. A common autoimmune abnormality might underlie both CCS and AA. 相似文献
115.
Allahwala Usaid K. Nour Daniel Alsanjari Osama Bhatia Kunwardeep Nagaraja Vinayak Khatri Jaikirshan J. Cockburn James Hildick-Smith David Sakata Yasuhiko Ward Michael Weaver James C. Bhindi Ravinay 《Journal of thrombosis and thrombolysis》2021,51(4):1005-1016
Journal of Thrombosis and Thrombolysis - Acute coronary collateralisation of an infarct-related arterial (IRA) territory may be identified during angiography for ST elevation myocardial infarction... 相似文献
116.
Yasuharu Matsunaga-Lee MD Yasuyuki Egami MD Kohei Ukita MD Akito Kawamura MD Hitoshi Nakamura MD Yutaka Matsuhiro MD Koji Yasumoto MD Masaki Tsuda MD Akihiro Tanaka MD Naotaka Okamoto MD Masamichi Yano MD PhD Ryu Shutta MD Yasushi Sakata MD PhD FACC FESC Masami Nishino MD PhD FACC FESC Jun Tanouchi MD PhD 《Journal of cardiovascular electrophysiology》2021,32(1):58-66
117.
Hyperglycemia increases oxidative stress in various tissues and leads to diabetic cardiovascular complication. Dyslipidemia,
such as an increase in oxidized low-density lipoprotein (LDL), is well recognized in diabetic patients with hyperglycemia.
However, the mechanism by which hyperglycemia causes the increased LDL oxidation remains unclear. Albumin is the most abundant
protein in the circulation, and can function as an antioxidant. Therefore, we examined whether glycoxidative modification
inhibits the antioxidant activity of albumin to LDL oxidation and clarified the mechanism by which this modification may suppress
its antioxidant activity. Human serum albumin (HSA) was incubated in phosphate-buffered saline with and without glucose at
37°C for up to 8 weeks under aerobic conditions (referred to as glycoxidation (goHSA) and oxidation (oHSA), respectively).
Metal chelator-treated, nonoxidative HSA (chHSA) and freshly prepared HSA (fHSA) were used as controls. N
ε-(carboxymethyl)lysine (CML), a glycoxidative product, was determined by enzyme-linked immunosorbent assay. Oxidation was
estimated by measuring the thiols of the HSA molecule. Copper-mediated oxidation of LDL was conducted in the presence or absence
of modified HSAs at 37°C for 6 days. Malondialdehyde and negative charge of LDL were measured. To clarify the mechanism of
reduced antioxidant activity of HSA, we examined firstly the binding activity of modified HSAs to copper, and secondly the
effects of free radical scavengers on the formation of malondialdehyde. CML was formed in goHSA in a time- and concentration-dependent
manner. Both goHSA and oHSA significantly decreased the contents of free thiol groups compared to ch- and fHSAs. The antioxidant
activity of goHSA to LDL oxidation was the lowest among various modified HSAs. The oHSA showed a moderate decrease in antioxidant
activity. The binding activity of go- and oHSAs to copper was lower than that of ch- and fHSAs. The formation of MDA from
LDL oxidation in the presence of goHSA was completely inhibited by Tiron (1,2-dihydroxy-3,5-benzenedisulfonic acid) and superoxide
dismutase. In contrast, catalase and mannitol had no effect. Our results indicate that in vitro glycoxidation of HSA induced
a marked loss of antioxidant activity of this molecule to copper-mediated oxidation of LDL, which may be caused by the generation
of superoxide.
Received: December 17, 2001 / Accepted: June 28, 2002
Acknowledgments The authors thank Drs. Ryoji Nagai and Seikoh Horiuchi (Department of Biochemistry, Kumamoto University School of Medicine,
Kumamoto, Japan) and Drs. Hiroyuki Itabe and Tatsuya Takano (Department of Microbiology and Molecular Pathology, Faculty of
Pharmaceutical Sciences, Teikyo University, Sagamiko, Kanagawa, Japan) for kindly supplying antibodies. We also thank Associate
Professor Takeo Yamaguchi (Department of Chemistry, Faculty of Science, Fukuoka University) for the ESR experiment and Miss
Satoko Nagano for her excellent technical assistance. This work was supported by a Grant-in-Aid from the Ministry of Education,
Science, Sports and Culture of Japan (No. 14570171) and in part by funds from the Central Research Institute of Fukuoka University
(No. 016004).
Correspondence to N. Sakata 相似文献
118.
Shuya Kusumoto Itsuro Jinnai Katsuro Itoh Nobutaka Kawai Tohru Sakata Akira Matsuda Kazunori Tominaga IKUO Murohashi Masami Bessho Kunitake Harashima & Atsuko Heshiki 《British journal of haematology》1996,99(3):649-655
Sixty-one consecutive patients with multiple myeloma were studied with magnetic resonance (MR) imaging of the spine. Sagittal T1-weighted and short inversion time (TI) inversion recovery (STIR) images were obtained. The MR patterns of the bone marrow were classified as diffuse (D) ( n = 26), nodular (N) ( n = 11), D + N ( n = 13) or normal (n) ( n = 11). Abnormal patterns were seen in 50 (82%) of the 61 patients. Correlations were found between the MR imaging patterns and some laboratory findings (WBC, haematocrit, platelet count, serum albumin, and percentage of marrow plasmacytosis). The survival of the patients with abnormal MRI patterns was significantly poorer than that of the patients with normal patterns. However, the survival of patients with a nodular pattern did not differ from those with a normal pattern. The MR imaging pattern of the bone marrow in patients with multiple myeloma is a useful factor in the assessment of prognosis. 相似文献
119.
Sakata Y Chancey AL Divakaran VG Sekiguchi K Sivasubramanian N Mann DL 《Basic research in cardiology》2008,103(1):60-68
The mechanisms that are responsible for the development of myocardial fibrosis in inflammatory cardiomyopathy are unknown.
We have previously generated lines of transgenic mice with cardiac-restricted overexpression of tumor necrosis factor (MHCsTNF
mice), a pro-inflammatory cytokine. The MHCsTNF mice develop a heart failure phenotype that is characterized by progressive
myocardial fibrosis, as well as increased levels transforming growth factor-β (TGF-β)(mRNA and protein. In order to determine
whether TGF-β-mediated signaling was responsible for the myocardial fibrosis observed in the MHCsTNF mice, we treated MHCsTNF
and littermate control mice from 4 to 12 weeks of age with a novel orally available TGF-β receptor antagonist (NP-40208).
At the time of terminal study, myocardial collagen content was determined using the picrosirius red technique, and left ventricular
(LV) systolic and diastolic function were determined using the Langendorff method. Treatment with NP-40208 resulted in a significant
(P < 0.05) 65% decrease in nuclear translocation of Smad 2/3, a significant (P < 0.05), decrease in the heart-weight to body-weight ratio from 6.5 to 5.7, a ∼37% decrease in fibrillar collagen content
(P < 0.01) and a significant (P < 0.05) decrease in the LV chamber stiffness by ∼25% in the MHCsTNF mice when compared to diluent-treated controls. Treatment
with NP-40208 had no discernable effect on LV systolic function, nor any effect on cardiac myocyte size or fetal gene expression
in the MHCsTNF mice. Taken together, these observations suggest that sustained pro-inflammatory signaling in the adult heart
is associated with a pro-fibrotic phenotype that arises, at least in part, from TGF-β-mediated signaling, with resultant activation
of Smad 2/3, leading to increased myocardial fibrosis and increased LV diastolic chamber stiffness.
Returned for 1. revision: 29 August 2007 1. Revision received: 24 September 2007 相似文献
120.
R T Santos E E Sakata P H Yasuda A Wakamatsu C T Kanamura I Candelori C B Pestana V A Alves 《Revista do Instituto de Medicina Tropical de S?o Paulo》1989,31(4):235-241
Tissue damage in leptospirosis has been ascribed to direct effect of the microorganisms and/or their virulence, including products synthetized by leptospires or released during their lysis. This study aimed at chemical extraction of the glycolipoprotein (GLP) from virulent leptospires, production of a rabbit anti-GLP and analysis of its distribution in liver and kidney of inoculated guinea-pigs, sacrificed sequentially from the 1st to 6th day of infection, covering the whole, spectrum of acute leptospirosis. The comparison of GLP expression to local injuries aimed at new pathogenetic data. GLP was detected in liver and kidney in 2 out of 6 guinea-pigs on the 5th day and in all 6 animals on the 6th day of infection. Granular forms were seen in the cytoplasm of macrophages, free in interstitium or adhered to endothelial and parenchymal cell membranes, especially in the most damaged sites. These findings lead us to the hypothesis of GLP as a toxic factor resulting from leptospiral lysis by macrophages. Although it was not proved as a promoter of initial lesions, it seems to be related to the enhancement of tissue damage late in the course of the disease. 相似文献