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991.
Ikuno T Enomoto S Yamamoto K Sakamoto T 《Kyobu geka. The Japanese journal of thoracic surgery》2011,64(5):370-374
Left ventricular pseudoaneurysm is a rare complication of myocardial infarction. However, the risk of rupture and heart failure are high, especially in a case of rapidly expanding aneurysm. As for left ventricular pseudoaneurysm, the risk of operation is high, and the long-term results are not good. We experienced 2 cases The 1st case was lost due to methicillin-resistant Staphylococcus aureus (MRSA) pneumonia The 2nd case is alive and has been free from heart failure for 3 years. The early diagnosis and surgery is necessary for a pseudoaneurysm. 相似文献
992.
Purpose
Tumors expressing high levels of CYP3A4 are likely to have a poor treatment response to docetaxel (DOC), which is metabolized by CYP3A4. Tissue samples of recurrent breast cancer are sometimes hard to obtain just before treatment because the tumor is often difficult to access. Using immunohistochemistry, we measured CYP3A4 expression in primary lesions and compared their treatment responses to DOC with those of recurrent breast cancer lesions. 相似文献993.
Enomoto T Furuya Y Tomimori Y Mori K Miyazaki J Yasuda H 《Journal of bone and mineral metabolism》2011,29(4):414-421
Hypercalcemia is a significant complication of certain human malignancies that is primarily caused by the release of calcium
from bone due to marked bone resorption by osteoclast activation. Osteoclast differentiation and activation is mediated by
receptor activator of NF-κB ligand (RANKL). Transgenic mice overexpressing murine soluble RANKL (sRANKL) that we generated
previously exhibited severe osteoporosis accompanied with enhanced osteoclastogenesis, but never exhibited hypercalcemia.
To analyze the relationship between serum concentration of sRANKL and hypercalcemia and generate a simple and quick hypercalcemia
model, an adenovirus vector harboring murine sRANKL cDNA (Ad-sRANKL) was injected i.p. into male C57BL/6 mice. Sera were collected
to measure the levels of sRANKL, calcium and biochemical markers of bone turnover. Food intake and body weight were measured
every 3 or 4 days. All the mice were killed 2 weeks after the injection, and femurs were collected to measure bone structure
and bone mineral density (BMD). Serum sRANKL and calcium increased, peaking on day 7. Food intake and body weight significantly
declined on day 7. These results indicated that the mice had anorexia as a symptom of hypercalcemia. Increases in bone resorption
and formation markers with a marked decrease in BMD were observed on day 14. These results reflect accelerated bone formation
following activation of osteoclasts, indicating coupling between bone formation and resorption. In conclusion, a new murine
model of hypercalcemia with anorexia was established by overexpressing sRANKL. This model would be useful for studies of hypercalcemia
and coupling between bone formation and resorption. 相似文献
994.
995.
Naoto Takahashi Yoshihiro Kameoka Hiroyuki Tagawa Naohito Fujishima Hirobumi Saitoh Makoto Hirokawa Kenichi Sawada Toshiaki Yoshioka Katsuhiko Enomoto 《Journal of infection and chemotherapy》2011,17(6):858-862
Stenotrophomonas maltophilia is increasingly emerging as a multiresistant pathogen in the hospital environment. In immunosuppressed patients, this bacterium may cause severe infections associated with sepsis and multiple organ dysfunction. We report on a 57-year-old woman treated with intensive chemotherapy for non-Hodgkin lymphoma who developed severe neutropenia, hemorrhagic pneumonia, and acute respiratory failure, which led to her death within 36 h of onset of pneumonia. Postmortem examination revealed bilateral extensive intraalveolar hemorrhage associated with severe infection by the gram-negative bacterium Stenotrophomonas maltophilia. In vitro susceptibility testing showed resistance to carbapenem, cephalosporines and aminoglycosides, but sensitivity to minocycline, ciprofloxacin, levofloxacin, and trimethoprim/sulfamethoxazole (cotrimoxazole). Early diagnosis and adequate antibiotic treatment were difficult, as the clinical course was rapid and fulminant, and this bacterium is resistant to multiple antibiotics. To improve prognosis in such cases, it will be necessary to develop an effective prophylactic strategy for high-risk patients. 相似文献
996.
997.
Shinya Matsuzaki Takayuki Enomoto Satoshi Serada Kiyoshi Yoshino Shushi Nagamori Akiko Morimoto Takuhei Yokoyama Ayako Kim Toshihiro Kimura Yutaka Ueda Masami Fujita Minoru Fujimoto Yoshikatsu Kanai Tadashi Kimura Tetsuji Naka 《International journal of cancer. Journal international du cancer》2014,134(8):1796-1809
Although platinum drugs are often used for the chemotherapy of human cancers, platinum resistance is a major issue and may preclude their use in some cases. We recently reported that enhanced expression of Annexin A4 (Anx A4) increases chemoresistance to carboplatin through increased extracellular efflux of the drug. However, the precise mechanisms underlying that chemoresistance and the relationship of Anx A4 to platinum resistance in vivo remain unclear. In this report, the in vitro mechanism of platinum resistance induced by Anx A4 was investigated in endometrial carcinoma cells (HEC1 cells) with low expression of Anx A4. Forced expression of Anx A4 in HEC1 cells resulted in chemoresistance to platinum drugs. In addition, HEC1 control cells were compared with Anx A4‐overexpressing HEC1 cells in xenografted mice. Significantly greater chemoresistance to cisplatin was observed in vivo in Anx A4‐overexpressing xenografted mice. Immunofluorescence analysis revealed that exposure to platinum drugs induced relocation of Anx A4 from the cytoplasm to the cellular membrane, where it became colocalized with ATP7A, a copper transporter also well known as a mechanism of platinum efflux. ATP7A expression suppressed by small interfering RNA had no effect on HEC1 control cells in terms of chemosensitivity to platinum drugs. However, suppression of ATP7A in Anx A4‐overexpressing platinum‐resistant cells improved chemosensitivity to platinum drugs (but not to 5‐fluorouracil) to a level comparable to that of control cells. These results indicate that enhanced expression of Anx A4 confers platinum resistance by promoting efflux of platinum drugs via ATP7A. 相似文献
998.
Y Akashi T Oda Y Ohara R Miyamoto T Kurokawa S Hashimoto T Enomoto K Yamada M Satake N Ohkohchi 《British journal of cancer》2014,110(6):1481-1487
Background:
Impaired drug transport is an important factor that reduces the efficacy of anticancer agents against pancreatic cancer. Here, we report a novel combination chemotherapy using gemcitabine (GEM) and internalised-RGD (iRGD) peptide, which enhances tumour-specific drug penetration by binding neuropilin-1 (NRP1) receptor.Methods:
A total of five pancreatic cancer murine models (two cell line-based xenografts (CXs) and three tumour grafts (TGs)) were treated with either GEM (100 mg kg−1, q3d × 4) alone or GEM plus iRGD peptide (8 μmol kg−1). Evaluation of NRP1 expression in xenografts and 48 clinical cancer specimens was performed by immunohistochemistry (IHC).Results:
We identified a subset of pancreatic cancer models that showed NRP1 overexpression sensitive to iRGD co-administration. Treatment with GEM plus iRGD peptide resulted in a significant tumour reduction compared with GEM monotherapy in CXs, but not remarkable in TGs. Potential targets of iRGD were characterised as cases showing NRP1 overexpression (IHC-2+/3+), and these accounted for 45.8% of the clinical specimens.Conclusions:
Internalised RGD peptide enhances the effects of co-administered drugs in pancreatic cancer models, its efficacy is however only appreciable in those employing cell lines. Therefore, the clinical application needs to be given careful consideration. 相似文献999.
1000.
Atsushi Enomoto Takemichi Fukasawa Nobuhiko Takamatsu Michihiko Ito Akinori Morita Yoshio Hosoi Kiyoshi Miyagawa 《European journal of cancer (Oxford, England : 1990)》2013,49(16):3547-3558
The ansamycin-based HSP90 inhibitor 17-AAG (17-allylamino-17-demethoxygeldanamycin) combats tumors and has been shown to modulate cellular sensitivity to radiation, prompting researchers to use 17-AAG as a radiosensitizer. 17-AAG causes the degradation of several oncogenic and signaling proteins. We previously demonstrated that oxidative stress activates serine/threonine kinase 38 (STK38), a member of the protein kinase A (PKA)/PKG/PKC-like family. In the present study, we investigated how 17-AAG affects STK38 expression, and evaluated STK38’s role in the regulation of radiosensitivity. We found that 17-AAG depleted cellular STK38 and reduced STK38’s kinase activity. Importantly, 17-AAG downregulated the stk38 gene expression. Deletion analysis and site-directed mutagenesis experiments demonstrated that Sp1 was required for the stk38 promoter activity. Treatment with 17-AAG inhibited Sp1’s binding to the stk38 promoter by decreasing the amount of Sp1 and knocking down Sp1 reduced STK38 expression. Moreover, 17-AAG treatment or STK38 knockdown enhanced the radiosensitivity of HeLa cells. Our data provide a novel mechanism, mediated by stk38 downregulation, by which 17-AAG radiosensitizes cells. 相似文献