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Search Results: 1 - 10 of 125 matches for " Akitoshi Ishizaka "
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Deregulation of histone lysine methyltransferases contributes to oncogenic transformation of human bronchoepithelial cells
Hideo Watanabe, Kenzo Soejima, Hiroyuki Yasuda, Ichiro Kawada, Ichiro Nakachi, Satoshi Yoda, Katsuhiko Naoki, Akitoshi Ishizaka
Cancer Cell International , 2008, DOI: 10.1186/1475-2867-8-15
Abstract: We observed differential HKMT expression in a lung cancer model in which normal human bronchial epithelial (NHBE) cells expressing telomerase, SV40 large T antigen, and Ras were immortal, formed colonies in soft agar, and expressed specific HKMTs for H3 lysine 9 and 27 residues but not for H3 lysine 4 residue. Modifications in the H3 tails affect the binding of proteins to the histone tails and regulate protein function and the position of lysine methylation marks a gene to be either activated or repressed. In the present study, suppression by siRNA of HKMTs (EZH2, G9A, SETDB1 and SUV39H1) that are over-expressed in immortalized and transformed cells lead to reduced cell proliferation and much less anchorage-independent colony growth. We also found that the suppression of H3-K9, G9A and SUV39H1 induced apoptosis and the suppression of H3-K27, EZH2 caused G1 arrest.Our results indicate the potential of these HKMTs in addition to the other targets for epigenetics such as DNMTs and HDACs to be interesting therapeutic targets.Alterations in the processing of the genetic information in carcinogenesis result from stable genetic mutations involving tumor suppressor genes, oncogenes and DNA stability genes as well as from potentially reversible epigenetic changes leading to modifications in gene function [1,2]. It is well established that epigenetic modifications of nucleosomal histones are central to proper gene expression and aberrant DNA methylation of genes play an important role in tumor progression. However, still relatively little is known about histone modifications, especially methylation, with respect to tumorigenesis. The N-terminus of histone tails is modified by amino-acid phosphorylation, acetylation or methylation to form a code for specifying downstream events and consequently a certain chromatin structure. Tens of histone lysine methyltransferases (HKMTs) have been identified and histone lysine methylation is now considered to be a critical regulator of tra
Macrophage derived chemokine (CCL22), thymus and activation-regulated chemokine (CCL17), and CCR4 in idiopathic pulmonary fibrosis
Yurika Yogo, Seitaro Fujishima, Takashi Inoue, Fumitake Saito, Takayuki Shiomi, Kazuhiro Yamaguchi, Akitoshi Ishizaka
Respiratory Research , 2009, DOI: 10.1186/1465-9921-10-80
Abstract: We examined the expression of CCR4, a specific receptor for CCL22 and CCL17, in bronchoalveolar lavage (BAL) fluid cells, as well as the levels of CCL22 and CCL17, to elucidate their pathophysiological roles in pulmonary fibrosis. We also studied their immunohistochemical localization.BAL fluid CCL22 and CCL17 levels were significantly higher in patients with IPF than those with collagen vascular diseases and healthy volunteers, and there was a significant correlation between the levels of CCL22 and CCL17 in patients with IPF. CCL22 levels in the BAL fluid did not correlate with the total cell numbers, alveolar lymphocytes, or macrophages in BAL fluid. However, the CCL22 levels significantly correlated with the numbers of CCR4-expressing alveolar macrophages. By immunohistochemical and immunofluorescence analysis, localization of CCL22 and CCR4 to CD68-positive alveolar macrophages as well as that of CCL17 to hyperplastic epithelial cells were shown. Clinically, CCL22 BAL fluid levels inversely correlated with DLco/VA values in IPF patients.We speculated that locally overexpressed CCL22 may induce lung dysfunction through recruitment and activation of CCR4-positive alveolar macrophages.Idiopathic pulmonary fibrosis (IPF), also called usual interstitial pneumonia (UIP) on histological basis, is a chronically progressive interstitial lung disease of unknown etiology, characterized by diffuse interstitial inflammation, fibroblast proliferation with accelerated remodeling of extracellular matrix, and hyperplasia of type II epithelial cells. The prognosis for IPF patients is poor with a median survival of 3-5 years [1-3]. Although several agents such as glucocorticoids, immunosuppressants and pirfenidone, have been administered to IPF patients, less than 30% patients show objective evidence of improvement, and there is no established treatment that certainly improves their outcomes [2-4]. The key pathogenic mechanisms of pulmonary fibrosis are still ill defined, but it i
Effects of long-term low-dose oxygen supplementation on the epithelial function, collagen metabolism and interstitial fibrogenesis in the guinea pig lung
Takuya Aoki, Fumihiro Yamasawa, Takeo Kawashiro, Tetsuichi Shibata, Akitoshi Ishizaka, Tetsuya Urano, Yasumasa Okada
Respiratory Research , 2008, DOI: 10.1186/1465-9921-9-37
Abstract: Guinea pigs (n = 159) were exposed to either 21% or 40% oxygen for a maximum of 16 weeks, and to 90% oxygen for a maximum of 120 hours. Clearance of inhaled technetium-labeled diethylene triamine pentaacetate (Tc-DTPA) and bronchoalveolar lavage fluid-to-serum ratio (BAL/Serum) of albumin (ALB) were used as markers of epithelial permeability. Lung wet-to-dry weight ratio (W/D) was measured to evaluate pulmonary edema, and types I and III collagenolytic activities and hydroxyproline content in the lung were analyzed as indices of collagen metabolism. Pulmonary fibrotic state was evaluated by histological quantification of fibrous tissue area stained with aniline blue.The clearance of Tc-DTPA was higher with 2 week exposure to 40% oxygen, while BAL/Serum Alb and W/D did not differ between the 40% and 21% groups. In the 40% oxygen group, type I collagenolytic activities at 2 and 4 weeks and type III collagenolytic activity at 2 weeks were increased. Hydroxyproline and fibrous tissue area were also increased at 2 weeks. No discernible injury was histologically observed in the 40% group, while progressive alveolar damage was observed in the 90% group.These results indicate that epithelial function is damaged, collagen metabolism is affected, and both breakdown of collagen fibrils and fibrogenesis are transiently induced even with low-dose 40% oxygen exposure. However, these changes are successfully compensated even with continuous exposure to low-dose oxygen. We conclude that long-term low-dose oxygen exposure does not significantly induce permanent lung injury in guinea pigs.Chronic obstructive pulmonary disease (COPD) has been expected to become a major cause of morbidity and mortality worldwide [1-3]. The patient population receiving long-term oxygen therapy has been increasing with rising morbidity of COPD. Although oxygen supplementation is indispensable in the management of hypoxemia in patients with various respiratory disorders such as COPD, high-dose oxygen inev
Acute lung inflammation and ventilator-induced lung injury caused by ATP via the P2Y receptors: an experimental study
Hiroki Matsuyama, Fumimasa Amaya, Soshi Hashimoto, Hiroshi Ueno, Satoru Beppu, Mitsuhiko Mizuta, Nobuaki Shime, Akitoshi Ishizaka, Satoru Hashimoto
Respiratory Research , 2008, DOI: 10.1186/1465-9921-9-79
Abstract: The effects of intratracheal ATP on lung permeability, edema or lung inflammation were assessed by measurements of the lung wet-to-dry weight ratio and lung permeability index, immunohistochemistry and expression of key cytokines by real-time polymerase chain reaction. The ATP concentration in broncho-alveolar lavage (BAL) fluid from mice mechanically ventilated was measured by luciferin-luciferase assay. The suppressive effects of a P2 receptor antagonist on ventilator-induced lung inflammation were also examined.ATP induced inflammatory reactions in the lung mainly via the ATP-P2Y receptor system. These reactions were alleviated by the co-administration of a specific P2 receptor antagonist. Mechanical ventilation with a large tidal volume caused lung inflammation and increased the ATP concentration in BAL fluid. P2 receptor antagonism partially mitigated the inflammatory effects of large tidal volume ventilation.Our observations suggest that the ATP-P2Y receptor system is partially involved in the pathogenesis of ventilator-induced lung injury.Acute lung injury and acute respiratory distress syndrome are major causes of acute respiratory failure, and are characterized by pulmonary edema, neutrophil infiltration with hemorrhage and increased production of inflammatory mediators [1]. Although mechanical ventilation is indispensable for the survival of critically ill patients presenting with acute lung injury (ALI)/acute respiratory distress syndrome (ARDS) [2], clinical trials have shown that improperly delivered mechanical ventilation may worsen or cause lung injury [3]. Lungs exposed to ineffective ventilator settings often develop diffuse alveolar injury [4], pulmonary edema [5] and activation of inflammatory cells [6]. The development of ventilator-induced lung injury (VILI) has been closely related to an increased production of pro-inflammatory cytokines [7], and to the leakage of inflammatory mediators into the systemic circulation [8]. Ventilation with a smal
Paper-Based Affect Misattribution Procedure for Implicit Measurement  [PDF]
Kazuo Mori, Akitoshi Uchida
Psychology (PSYCH) , 2015, DOI: 10.4236/psych.2015.612149
Abstract: The Affect Misattribution Procedure (AMP) (Payne et al., 2005) can measure implicit attitudes based on a conceptually different procedure from the Implicit Association Test (IAT) (Greenwald et al., 1998). We aim to improve the administrative advantage of the AMP by converting it into a paper-based performance test so that it can collect massive data easily without using a computer for each examinee. We conduct three Paper-based AMP experiments to achieve the typical AMP results with large effect sizes (Study 1), obtain sufficient reliability by the test-retest method (Study 2), and find a similar phenomenon of the disappearance of misattribution when participants evaluate the primes consciously prior to the target evaluation (Study 3).
Protective role of vascular endothelial growth factor in endotoxin-induced acute lung injury in mice
Hidefumi Koh, Sadatomo Tasaka, Naoki Hasegawa, Wakako Yamada, Mie Shimizu, Morio Nakamura, Makoto Yonemaru, Eiji Ikeda, Yoshiyuki Adachi, Seitaro Fujishima, Kazuhiro Yamaguchi, Akitoshi Ishizaka
Respiratory Research , 2007, DOI: 10.1186/1465-9921-8-60
Abstract: To evaluate the role of VEGF in the pathogenesis of acute lung injury, we first evaluated the effects of exogenous VEGF and VEGF blockade using monoclonal antibody on LPS-induced lung injury in mice. Using the lung specimens, we performed TUNEL staining to detect apoptotic cells and immunostaining to evaluate the expression of apoptosis-associated molecules, including caspase-3, Bax, apoptosis inducing factor (AIF), and cytochrome C. As a parameter of endothelial permeability, we measured the albumin transferred across human pulmonary artery endothelial cell (HPAEC) monolayers cultured on porous filters with various concentrations of VEGF. The effect of VEGF on apoptosis HPAECs was also examined by TUNEL staining and active caspase-3 immunoassay.Exogenous VEGF significantly decreased LPS-induced extravascular albumin leakage and edema formation. Treatment with anti-VEGF antibody significantly enhanced lung edema formation and neutrophil emigration after intratracheal LPS administration, whereas extravascular albumin leakage was not significantly changed by VEGF blockade. In lung pathology, pretreatment with VEGF significantly decreased the numbers of TUNEL positive cells and those with positive immunostaining of the pro-apoptotic molecules examined. VEGF attenuated the increases in the permeability of the HPAEC monolayer and the apoptosis of HPAECs induced by TNF-α and LPS. In addition, VEGF significantly reduced the levels of TNF-α- and LPS-induced active caspase-3 in HPAEC lysates.These results suggest that VEGF suppresses the apoptosis induced by inflammatory stimuli and functions as a protective factor against acute lung injury.Vascular endothelial growth factor (VEGF) was originally discovered as a vascular permeability factor in guinea pig skin, and is a mitogen that regulates endothelial cell differentiation, angiogenesis, and the maintenance of existing vessels [1-4]. VEGF is involved in the pathogenesis of rheumatoid arthritis, diabetic retinopathy, and tum
Intratracheal synthetic CpG oligodeoxynucleotide causes acute lung injury with systemic inflammatory response
Sadatomo Tasaka, Hirofumi Kamata, Keisuke Miyamoto, Yasushi Nakano, Hiromi Shinoda, Yoshifumi Kimizuka, Hiroshi Fujiwara, Naoki Hasegawa, Seitaro Fujishima, Taku Miyasho, Akitoshi Ishizaka
Respiratory Research , 2009, DOI: 10.1186/1465-9921-10-84
Abstract: Acute respiratory distress syndrome (ARDS), which is the most severe form of acute lung injury (ALI), is a critical illness with high mortality. ALI/ARDS may occur in association with direct lung injury, including pneumonia, aspiration of gastric contents, and inhalation of noxious gas, or indirect lung injury, such as sepsis, blood transfusions and shock. Among the various predisposing factors, severe pneumonia is one of the most common causes [1]. Intratracheal administration of endotoxin (lipopolysaccharide; LPS), which is a cell wall component of gram-negative bacteria, has been extensively used as an experimental model of ALI/ARDS following severe pneumonia [2]. However, the roles of other bacterial components, such as genomic DNA, in the development of lung injury and systemic inflammatory response remain to be determined.The bacterial genome, compared to vertebrate DNA, contains a higher frequency of unmethylated cytosine-phosphate-guanine (CpG) dinucleotides. Small oligodeoxynucleotides (ODN) with unmethylated CpG dinucleotides (CpG-ODN) are able to mimic the immunostimulatory activity of bacterial DNA since bacterial DNA and synthetic ODN share similar base sequences and bind to the same receptor system [3-5].Toll-like receptors (TLRs) have been shown to play an essential role in the activation of innate immunity by recognizing specific patterns of microbial components [6]. Among the TLRs, TLR9 recognizes bacterial or viral DNA, although it is now known that TLR9 also recognizes unmethylated CpG-containing DNA sequences, including those of mammalian origin and synthetic ODN [4,7]. In the lung, constitutive expression of TLR9 has been detected in endothelial cells and macrophages [8,9]. It was reported that intraperitoneal or intratracheal administration of CpG-ODN causes lung inflammation [10-12]. However, little is known regarding the lung permeability changes, time course of the cytokine levels, and systemic effects of intratracheal CpG-ODN challenge.In t
A High-Level Synthesis Technology Using C Source Code Analysis
Akitoshi Matsuda
International Journal of Image Processing and Visual Communication , 2012, DOI: ijipvcv1i205
Abstract: Recently, in the development of complex embedded systems, a model-based design approach has attracted considerable attention. We propose a high-level synthesis method involving C-based design that pays attention to efficient development of hardware design in complex embedded systems. By modeling the C source code, the structure is visualized, and this makes it easier for third parties to understand it. In this design flow, if the entire structure can be visualized, the system-level C source code can be optimized, resulting in an improvement in design quality and a shortening of the design cycle. The optimization of system-level C source code is more efficient compared to co-design and co-verification in hardware and software. Therefore, system-level C source code visualization and optimization is proposed to facilitate consistent hardware design in this paper. Experimental results indicate that our technique improves circuit performance by as much as 9.6% and reduces the circuit area by up to 10% in hardware design.
Influence of difference in knee alignment on site of pain and psychological state after long-distance walking
Akitoshi Sogabe
Physical Activity Review , 2013,
Abstract: Background and Study Aim: In this study, focusing on the individual difference in thecharacteristics of the knee joint, which plays an important role in weight bearing during walking, we examined the relationship between difference in knee alignment and pain in the legs during walking andeffect of the pain on the psychological state of exercise performers. Material/Methods: A total of 40 subjects, including 25 healthy men and 15 women were recruited to this study. Knee alignment was classified according to the intercondylar and intermalleolar distances by increments of 2.0 cm. After walking (85km) on day 3 of the 5-day event, subjects were required to answer a questionnaire asking where in the leg they had pain. The psychological state of each subject was assessed by performing the Profile of Mood States (POMS) after they had rested after walking on each of days 1, 2 and 3 of the 5-day event. Results: The following sites exhibited significant differences in the number and incidence of injury between groups: the anterior side of lower leg (p <0.05), posterior side of lower leg (p <0.01), ankle joint (p <0.05) and sole of foot (p <0.01). In the genu valgum group, the score for factor V(:Vigor)decreased by 4.0 points between days 1 to 3: 18.1 ± 4.6 points on day 1 and 14.1 ± 7.6 points on day 3, with a significant difference between days 1 and 3. Conclusions: When performing an exercise thatplaces load on the legs, such as walking, one should consider the risk of injury by measuring the individual’s knee alignment before commencing the exercise.
Differential Recursion and Differentially Algebraic Functions
Akitoshi Kawamura
Computer Science , 2007, DOI: 10.1145/1507244.1507252
Abstract: Moore introduced a class of real-valued "recursive" functions by analogy with Kleene's formulation of the standard recursive functions. While his concise definition inspired a new line of research on analog computation, it contains some technical inaccuracies. Focusing on his "primitive recursive" functions, we pin down what is problematic and discuss possible attempts to remove the ambiguity regarding the behavior of the differential recursion operator on partial functions. It turns out that in any case the purported relation to differentially algebraic functions, and hence to Shannon's model of analog computation, fails.
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