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Search Results: 1 - 10 of 2117 matches for " Koichi Hasegawa "
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Genetic and Cellular Characterization of Caenorhabditis elegans Mutants Abnormal in the Regulation of Many Phase II Enzymes
Koichi Hasegawa,Johji Miwa
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0011194
Abstract: The phase II detoxification enzymes execute a major protective role against xenobiotics as well as endogenous toxicants. To understand how xenobiotics regulate phase II enzyme expression, acrylamide was selected as a model xenobiotic chemical, as it induces a large number and a variety of phase II enzymes, including numerous glutathione S-transferases (GSTs) in Caenorhabditis elegans.
Measurement of the Wheelchair-Operating Time Spent by Stroke Patients Using a New Triaxial Accelerometer System  [PDF]
Yoshino Terui, Takanobu Shioya, Koichi Hasegawa, Eriko Suto, Atsuyoshi Kawagoshi, Masahiro Satake, Sachie Sawamura, Shunichi Sakata
Open Journal of Therapy and Rehabilitation (OJTR) , 2014, DOI: 10.4236/ojtr.2014.24020
Abstract: Purpose: We investigated the validity of a triaxial accelerometer system for measuring the time spent lying down, sitting, standing, walking, and operating a wheelchair by control subjects and stroke patients in a convalescence ward. Methods: Physical activities were measured using a new triaxial accelerometer system (A-MES; Activity Monitoring and Evaluation System) that consists of two sensors, a station, and analytical software used with a personal computer. In Experiment 1, the times that the healthy subjects (n = 12) spent operating a wheelchair, lying down, sitting, standing, and walking were measured both by the A-MES and by videotaping (video time). In Experiment 2, the amounts of time spent by the stroke patients not able to walk without support (n = 30) as they were lying down, sitting, standing, walking, and operating a wheelchair were measured by the A-MES. Results: The time spent operating a wheelchair measured with the A-MES was significantly correlated with the video time in the healthy subjects. The stroke patients’ average times (minutes) of total, operating a wheelchair, lying down, sitting, standing, and walking were 601.0 ± 18.1, 57.1 ± 28.8, 265.0 ± 86.3, 263.3 ± 60.6, 7.8 ± 7.0, and 7.7 ± 6.0, respectively. Conclusions: The A-MES accurately evaluated the stroke patients’ time spent operating a wheelchair. The stroke patients’ mean time spent operating a wheelchair over the course of one day was 57.1 ± 28.8 min in a Center for Rehabilitation.
Allyl Isothiocyanate that Induces GST and UGT Expression Confers Oxidative Stress Resistance on C. elegans, as Demonstrated by Nematode Biosensor
Koichi Hasegawa,Satsuki Miwa,Kaname Tsutsumiuchi,Johji Miwa
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0009267
Abstract: Electrophilic xenobiotics and endogenous products from oxidative stresses induce the glutathione S-transferases (GSTs), which form a large family within the phase II enzymes over both animal and plant kingdoms. The GSTs thus induced in turn detoxify these external as well as internal stresses. Because these stresses are often linked to ageing and damage to health, the induction of phase II enzymes without causing adverse effects would be beneficial in slowing down ageing and keeping healthy conditions.
Churg-Strauss Syndrome with Necrosis of Toe Tips
Acta Medica Okayama , 2011,
Abstract: Churg-Strauss syndrome (CSS) is a granulomatous necrotizing vasculitis of unknown etiology associated with bronchial asthma. Despite affecting small to medium-sized vessels, necrosis of the digits due to vasculitis is extremely rare. We report a case of CSS with necrosis of the toe tips. A 37-year-old woman with asthma, who had been diagnosed with CSS 2 years ago, was admitted to our hospital with an exacerbation of CSS. The patient had a high grade fever and complained of abdominal pain and numbness of the lower extremities. Blood examination revealed marked eosinophilia. The fever pattern, abdominal pain and blood eosinophilia showed improvement by combination treatment with prednisolone and cyclophosphamide. However, the color of her right toe tips changed, and necrosis finally resulted despite antithrombotic therapy. Arteriography showed narrowing of the dorsalis pedis artery and of the more peripheral arteries of her right leg. Stump plasty with negative pressure dressing therapy for the toe tips, but not amputation, was done to preserve the leg function. While numbness of the extremities remained, no recurrence of necrosis was seen. Clinicians need to be aware that rare complications of CSS, including necrosis of the digits, can occur.
Antagonistic Interplay between Necdin and Bmi1 Controls Proliferation of Neural Precursor Cells in the Embryonic Mouse Neocortex
Ryohei Minamide, Kazushiro Fujiwara, Koichi Hasegawa, Kazuaki Yoshikawa
PLOS ONE , 2014, DOI: 10.1371/journal.pone.0084460
Abstract: Neural precursor cells (NPCs) in the neocortex exhibit a high proliferation capacity during early embryonic development and give rise to cortical projection neurons after maturation. Necdin, a mammal-specific MAGE (melanoma antigen) family protein that possesses anti-mitotic and pro-survival activities, is expressed abundantly in postmitotic neurons and moderately in tissue-specific stem cells or progenitors. Necdin interacts with E2F transcription factors and suppresses E2F1-dependent transcriptional activation of the cyclin-dependent kinase Cdk1 gene. Here we show that necdin serves as a suppressor of NPC proliferation in the embryonic neocortex. Necdin is moderately expressed in the ventricular zone of mouse embryonic neocortex, in which proliferative cell populations are significantly increased in necdin-null mice. In the neocortex of necdin-null embryos, expression of Cdk1 and Sox2, a stem cell marker, is significantly increased, whereas expression of p16, a cyclin-dependent kinase inhibitor, is markedly diminished. Cdk1 and p16 expression levels are also significantly increased and decreased, respectively, in primary NPCs prepared from necdin-null embryos. Intriguingly, necdin interacts directly with Bmi1, a Polycomb group protein that suppresses p16 expression and promotes NPC proliferation. In HEK293A cells transfected with luciferase reporter constructs, necdin relieves Bmi1-dependent repression of p16 promoter activity, whereas Bmi1 counteracts necdin-mediated repression of E2F1-dependent Cdk1 promoter activity. In lentivirus-infected primary NPCs, necdin overexpression increases p16 expression, suppresses Cdk1 expression, and inhibits NPC proliferation, whereas Bmi1 overexpression suppresses p16 expression, increases Cdk1 expression, and promotes NPC proliferation. Our data suggest that embryonic NPC proliferation in the neocortex is regulated by the antagonistic interplay between necdin and Bmi1.
Necdin Promotes Ubiquitin-Dependent Degradation of PIAS1 SUMO E3 Ligase
Ibrahim Gur, Kazushiro Fujiwara, Koichi Hasegawa, Kazuaki Yoshikawa
PLOS ONE , 2014, DOI: 10.1371/journal.pone.0099503
Abstract: Necdin, a pleiotropic protein that promotes differentiation and survival of mammalian neurons, is a member of MAGE (melanoma antigen) family proteins that share a highly conserved MAGE homology domain. Several MAGE proteins interact with ubiquitin E3 ligases and modulate their activities. However, it remains unknown whether MAGE family proteins interact with SUMO (small ubiquitin-like modifier) E3 ligases such as PIAS (protein inhibitor of activated STAT) family, Nsmce2/Mms21 and Cbx4/Pc2. In the present study, we examined whether necdin interacts with these SUMO E3 ligases. Co-immunoprecipitation analysis revealed that necdin, MAGED1, MAGEF1 and MAGEL2 bound to PIAS1 but not to Nsmce2 or Cbx4. These SUMO E3 ligases bound to MAGEA1 but failed to interact with necdin-like 2/MAGEG1. Necdin bound to PIAS1 central domains that are highly conserved among PIAS family proteins and suppressed PIAS1-dependent sumoylation of the substrates STAT1 and PML (promyelocytic leukemia protein). Remarkably, necdin promoted degradation of PIAS1 via the ubiquitin-proteasome pathway. In transfected HEK293A cells, amino- and carboxyl-terminally truncated mutants of PIAS1 bound to necdin but failed to undergo necdin-dependent ubiquitination. Both PIAS1 and necdin were associated with the nuclear matrix, where the PIAS1 terminal deletion mutants failed to localize, implying that the nuclear matrix is indispensable for necdin-dependent ubiquitination of PIAS1. Our data suggest that necdin suppresses PIAS1 both by inhibiting SUMO E3 ligase activity and by promoting ubiquitin-dependent degradation.
A Human T Lymphotropic Virus Type 1 Carrier Coinfected with Mycobacterium intracellulare and Pneumocystis jirovecii with a Characteristic Compositional Change of Bone Marrow Cells  [PDF]
Sayaka Uda, Shinsuke Shiotsu, Ayaka Omura, Ryosuke Hamashima, Akihiro Yoshimura, Naoko Kurisu, Tomoya Sagawa, Koichi Hasegawa, Tatsuya Yuba, Chieko Takumi, Seiko Ono, Noriya Hiraoka, Noriya Hiraoka
Open Journal of Respiratory Diseases (OJRD) , 2017, DOI: 10.4236/ojrd.2017.73011
Abstract: Human T lymphotropic virus type 1 (HTLV-1) is endemic in the southern part of Japan. Infection of the virus can cause adult T cell leukemia/lymphoma (ATL), while most infected individuals remain in a carrier state for a long period of time. Although rare cases of carriers, like ATL patients, who developed opportunistic infections, have been reported, hematological changes of carriers who are prone to opportunistic infections have not been well defined. Here, we present a case of an HTLV-1 carrier who developed Mycobacterium intracellulare infection and Pneumocystis jirovecii pneumonia (PcP) simultaneously. Flow cytometric analysis of bone marrow cells revealed an aberrant compositional change similar to that in ATL patients. This suggests the presence of a pre-ATL state prior to the development of ATL, which is notable in terms of underlying cellular immunodeficiency.
Structural Characterization of Neutral and Acidic Glycolipids from Thermus thermophilus HB8
Yasuo Suda, Fumiaki Okazaki, Yushi Hasegawa, Seiji Adachi, Koichi Fukase, Susumu Kokubo, Seiki Kuramitsu, Shoichi Kusumoto
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0035067
Abstract: The structural characterization of glycolipids from Thermus thermophilus HB8 was performed in this study. Two neutral and one acidic glycolipids were extracted and purified by the modified TLC-blotting method, after which their chemical structures were determined by chemical composition analysis, mass spectrometry (MS) and nuclear magnetic resonance (NMR) spectroscopy. The structure of one of the neutral glycolipids, NGL-A, was Galp(α1-6)GlcpNacyl(β1-2)Glcp(α1-)acyl2Gro, and the other, NGL-C, was Galf(β1-2)Galp(α1-6)GlcpNacyl(β1-2)Glcp(α1-)acyl2Gro. The structure of NGL-C was identical to that reported previously [Oshima, M. and Ariga, T. (1976) FEBS Lett. 64, 440]. Both neutral glycolipids shared a common structural unit found in the Thermus species. The acyl groups found in NGL-A and NGL-C, iso-type pentadecanoxy and heptadecanoxy fatty acid, were also the same as those found in this species. In contrast, the acidic glycolipid, AGL-B, possessed the structure of N-(((GlcpNAc(α1-)acyl2Gro)P-2)GroA)alkylamine. The alkyl group in AGL-B was an iso-type heptadecanyl, suggesting that the iso-type structure of the long alkyl chain is responsible for the thermal stability of the bacteria.
Necdin Controls Proliferation of White Adipocyte Progenitor Cells
Kazushiro Fujiwara, Koichi Hasegawa, Tsuyoshi Ohkumo, Hiroyuki Miyoshi, Yu-Hua Tseng, Kazuaki Yoshikawa
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0030948
Abstract: White adipose tissues are composed mainly of white fat cells (adipocytes), which play a key role in energy storage and metabolism. White adipocytes are terminally differentiated postmitotic cells and arise from their progenitor cells (preadipocytes) or mesenchymal stem cells residing in white adipose tissues. Thus, white adipocyte number is most likely controlled by the rate of preadipocyte proliferation, which may contribute to the etiology of obesity. However, little is known about the molecular mechanisms that regulate preadipocyte proliferation during adipose tissue development. Necdin, which is expressed predominantly in postmitotic neurons, is a pleiotropic protein that possesses anti-mitotic and pro-survival activities. Here we show that necdin functions as an intrinsic regulator of white preadipocyte proliferation in developing adipose tissues. Necdin is expressed in early preadipocytes or mesenchymal stem cells residing in the stromal compartment of white adipose tissues in juvenile mice. Lentivirus-mediated knockdown of endogenous necdin expression in vivo in adipose tissues markedly increases fat mass in juvenile mice fed a high-fat diet until adulthood. Furthermore, necdin-null mutant mice exhibit a greater expansion of adipose tissues due to adipocyte hyperplasia than wild-type mice when fed the high-fat diet during the juvenile and adult periods. Adipose stromal-vascular cells prepared from necdin-null mice differentiate in vitro into a significantly larger number of adipocytes in response to adipogenic inducers than those from wild-type mice. These results suggest that necdin prevents excessive preadipocyte proliferation induced by adipogenic stimulation to control white adipocyte number during adipose tissue development.
Features of hepatocellular carcinoma in cases with autoimmune hepatitis and primary biliary cirrhosis
Takuya Watanabe, Kenji Soga, Haruka Hirono, Katsuhiko Hasegawa, Koichi Shibasaki, Hirokazu Kawai, Yutaka Aoyagi
World Journal of Gastroenterology , 2009,
Abstract: AIM: To characterize the clinical features of hepatocellular carcinoma (HCC) associated with autoimmune liver disease, we critically evaluated the literature on HCC associated with autoimmune hepatitis (AIH) and primary biliary cirrhosis (PBC).METHODS: A systematic review of the literature was conducted using the Japana Centra Revuo Medicina database which produced 38 cases of HCC with AIH (AIH-series) and 50 cases of HCC with PBC (PBC-series). We compared the clinical features of these two sets of patients with the general Japanese HCC population.RESULTS: On average, HCC was more common in men than in women with AIH or PBC. While many patients underwent chemolipiodolization (CL) or transcatheter arterial embolization (TAE) (AIH-series: P = 0.048 (vs operation), P = 0.018 (vs RFA, PEIT); PBC-series: P = 0.027 (vs RFA, PEIT), others refused therapeutic interventions [AIH-series: P = 0.038 (vs RFA, PEIT); PBC-series: P = 0.003 (vs RFA, PEIT)]. Liver failure was the primary cause of death among patients in this study, followed by tumor rupture. The survival interval between diagnosis and death was fairly short, averaging 14 ± 12 mo in AIH patients and 8.4 ± 14 mo in PBC patients.CONCLUSION: We demonstrated common clinical features among Japanese cases of HCC arising from AIH and PBC.
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