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Search Results: 1 - 10 of 319 matches for " Yoshifumi Sonobe "
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GM-CSF increases LPS-induced production of proinflammatory mediators via upregulation of TLR4 and CD14 in murine microglia
Parajuli Bijay,Sonobe Yoshifumi,Kawanokuchi Jun,Doi Yukiko
Journal of Neuroinflammation , 2012, DOI: 10.1186/1742-2094-9-268
Abstract: Background Microglia are resident macrophage-like cells in the central nervous system (CNS) and cause innate immune responses via the LPS receptors, Toll-like receptor (TLR) 4 and CD14, in a variety of neuroinflammatory disorders including bacterial infection, Alzheimer’s disease, and amyotrophic lateral sclerosis. Granulocyte macrophage-colony stimulating factor (GM-CSF) activates microglia and induces inflammatory responses via binding to GM-CSF receptor complex composed of two different subunit GM-CSF receptor α (GM-CSFRα) and common β chain (βc). GM-CSF has been shown to be associated with neuroinflammatory responses in multiple sclerosis and Alzheimer’s disease. However, the mechanisms how GM-CSF promotes neuroinflammation still remain unclear. Methods Microglia were stimulated with 20 ng/ml GM-CSF and the levels of TLR4 and CD14 expression were evaluated by RT-PCR and flowcytometry. LPS binding was analyzed by flowcytometry. GM-CSF receptor complex was analyzed by immunocytechemistry. The levels of IL-1β, IL-6 and TNF-α in culture supernatant of GM-CSF-stimulated microglia and NF-κB nuclear translocation were determined by ELISA. Production of nitric oxide (NO) was measured by the Griess method. The levels of p-ERK1/2, ERK1/2, p-p38 and p38 were assessed by Western blotting. Statistically significant differences between experimental groups were determined by one-way ANOVA followed by Tukey test for multiple comparisons. Results GM-CSF receptor complex was expressed in microglia. GM-CSF enhanced TLR4 and CD14 expressions in microglia and subsequent LPS-binding to the cell surface. In addition, GM-CSF priming increased LPS-induced NF-κB nuclear translocation and production of IL-1β, IL-6, TNF-α and NO by microglia. GM-CSF upregulated the levels of p-ERK1/2 and p-p38, suggesting that induction of TLR4 and CD14 expression by GM-CSF was mediated through ERK1/2 and p38, respectively. Conclusions These results suggest that GM-CSF upregulates TLR4 and CD14 expression in microglia through ERK1/2 and p38, respectively, and thus promotes the LPS receptor-mediated inflammation in the CNS.
Intra-Articular Giant Heterotopic Ossification following Total Knee Arthroplasty for Charcot Arthropathy
Arata Nakajima,Shintaro Tsuge,Yasuchika Aoki,Masato Sonobe,Yoshifumi Shibata,Yu Sasaki,Koichi Nakagawa
Case Reports in Orthopedics , 2013, DOI: 10.1155/2013/472378
Abstract: Although the Charcot arthropathy may be associated with serious complications, total knee arthroplasty (TKA) is the preferred choice of treatment by patients. This case report presents an 80-year-old man with intra-articular giant heterotopic ossification following loosening of femoral and tibial implants and femoral condylar fracture. He had undergone TKA because of Charcot neuropathy seven years ago and had been doing well since. Immediately after a left knee sprain, he became unable to walk. Because he had developed a skin ulcer on his left calf where methicillin-resistant Staphylococcus aureus was detected, we postponed revision surgery until the ulcer was completely healed. While waiting, intra-articular bony fragments grew larger and formed giant heterotopic ossified masses. Eventually, the patient underwent revision surgery, and two major ossified masses were carefully and successfully extirpated. It should be noted that intra-articular heterotopic giant ossification is a significant complication after TKA for neuropathic arthropathy. 1. Introduction Neuropathic arthropathy was described by Jean Martin Charcot (1825–1893) as the progressive destruction of bone and soft tissues in a patient with peripheral neuropathy. Charcot also noted the relationship between syphilis and severe arthropathy in 1868 [1]. Diabetes mellitus is currently the most common cause of Charcot arthropathy, especially of the foot and ankle. The diagnosis of Charcot arthropathy in the knee is rare. However, we can expect the increasing number of diabetic patients living longer due to improvements in medical treatment to show an increasing incidence of neuropathic arthropathy as a late effect of peripheral neuropathy. The optimal treatment for Charcot arthropathy of the knee is controversial. Some investigators [2–4] consider it as an absolute contraindication to total knee arthroplasty (TKA). Recently, however, several studies [5] have shown satisfactory results from TKA. In general, TKA for Charcot arthropathy is associated with high incidence of such serious complications as periprosthetic fractures, aseptic loosening, dislocation of the patella and tibiofemoral joint, and deep infection [6–8]. However, due to excellent functional recovery compared with conservative therapy and arthrodesis, TKA should not be contraindicated. We present a case report of an 80-year-old man with intra-articular, giant, heterotopic ossification and a femoral condylar fracture following loosening of femoral and tibial implants. To date, the occurrence of intra-articular, giant, heterotopic
The neuroprotective effects of milk fat globule-EGF factor 8 against oligomeric amyloid β toxicity
Endong Li, Mariko Noda, Yukiko Doi, Bijay Parajuli, Jun Kawanokuchi, Yoshifumi Sonobe, Hideyuki Takeuchi, Tetsuya Mizuno, Akio Suzumura
Journal of Neuroinflammation , 2012, DOI: 10.1186/1742-2094-9-148
Abstract: The release of MFG-E8 from microglia treated with conditioned medium from neurons exposed to neurotoxic substances, glutamate or oligomeric amyloid β (oAβ) was measured by ELISA. The neuroprotective effects of MFG-E8 and MFG-E8???induced microglial phagocytosis of oAβ were assessed by immunocytochemistry. The effects of MFG-E8 on the production of the anti-oxidative enzyme hemeoxygenase-1 (HO-1) were determined by ELISA and immunocytochemisty.MFG-E8 was induced in microglia treated with conditioned medium from neurons that had been exposed to neurotoxicants, glutamate or oAβ. MFG-E8 significantly attenuated oAβ-induced neuronal cell death in a primary neuron???microglia coculture system. Microglial phagocytosis of oAβ was accelerated by MFG-E8 treatment due to increased CD47 expression in the absence of neurotoxic molecule production, such as tumor necrosis factor-α, nitric oxide, and glutamate. MFG-E8???treated microglia induced nuclear factor E(2)???related factor 2 (Nrf2)???mediated HO-1 production, which also contributed to neuroprotection.These results suggest that microglia release MFG-E8 in response to signals from degenerated neurons and that MFG-E8 protects oAβ-induced neuronal cell death by promoting microglial phagocytic activity and activating the Nrf2-HO-1 pathway. Thus, MFG-E8 may have novel roles as a neuroprotectant in neurodegenerative conditions.
Fingolimod Phosphate Attenuates Oligomeric Amyloid β–Induced Neurotoxicity via Increased Brain-Derived Neurotrophic Factor Expression in Neurons
Yukiko Doi, Hideyuki Takeuchi, Hiroshi Horiuchi, Taketo Hanyu, Jun Kawanokuchi, Shijie Jin, Bijay Parajuli, Yoshifumi Sonobe, Tetsuya Mizuno, Akio Suzumura
PLOS ONE , 2013, DOI: 10.1371/journal.pone.0061988
Abstract: The neurodegenerative processes that underlie Alzheimer's disease are mediated, in part, by soluble oligomeric amyloid β, a neurotoxic protein that inhibits hippocampal long-term potentiation, disrupts synaptic plasticity, and induces the production of reactive oxygen species. Here we show that the sphingosine-1-phosphate (S1P) receptor (S1PR) agonist fingolimod phosphate (FTY720-P)-a new oral drug for multiple sclerosis-protects neurons against oligomeric amyloid β-induced neurotoxicity. We confirmed that primary mouse cortical neurons express all of the S1P receptor subtypes and FTY720-P directly affects the neurons. Treatment with FTY720-P enhanced the expression of brain-derived neurotrophic factor (BDNF) in neurons. Moreover, blocking BDNF-TrkB signaling with a BDNF scavenger, TrkB inhibitor, or ERK1/2 inhibitor almost completely ablated these neuroprotective effects. These results suggested that the neuroprotective effects of FTY720-P are mediated by upregulated neuronal BDNF levels. Therefore, FTY720-P may be a promising therapeutic agent for neurodegenerative diseases, such as Alzheimer's disease.
Sentinel Lymph Node Biopsy as Guidance for Lateral Neck Dissection in Patients with Papillary Thyroid Carcinoma  [PDF]
Yoshifumi Ikeda
Surgical Science (SS) , 2011, DOI: 10.4236/ss.2011.22012
Abstract: Introduction: The surgical management of lateral lymph nodes in differentiated thyroid carcinoma is controversies. Therefore, we analyzed whether sentinel lymph nodes (SLN) biopsy of the first draining nodes in the jugulo-carotid chain is an accurate technique to select patients with true-positive but nonpalpable lymph nodes for selective lateral node dissection. Materials and Methods: From January 2009 to December 2009, 12 patients with solitary papillary carcinoma measuring 2 cm by ultrasonography were included in this study. After the thyroid gland was exposed to avoid injuring the lateral thyroid lymphatic connection, approximately 0.2 ml of 5mg/ml indocyanine green was injected into the parenchyma of upper and lower thyroid gland. Some stained lymph nodes in the jugulo-carotid chain could be identified following the stained lymphatic duct and dissected as the SLN. After that, thyroidectomy with modified neck dissection was performed. Results: The mean tumor size was 22.1 ± 4.6 mm. Identification and biopsy of stained SLN in the ipsilateral jugulo-carotid chain was successful in all 12 cases. In 6 cases, histopathological analysis of SLNs revealed metastases of the papillary thyroid carcinoma. Among them, 2 cases had additional metastatic lymph nodes in the ipsilateral compartment. Of the 6 patients who had negative lymph node metastasis (LNM) in SLNs, all patients had negative LNM in the ipsilateral compartment. Conclusions: The method may be helpful in the detection of true-positive but nonpalpable lymph nodes and may support a decision to perform a selective lateral node dissection in patients with papillary thyroid carcinoma.
Spatial Variations of Soil Respiration in Arid Ecosystems  [PDF]
Gang Liu, Rei Sonobe, Quan Wang
Open Journal of Ecology (OJE) , 2016, DOI: 10.4236/oje.2016.64020
Abstract: Soil respiration releases a major carbon flux back to atmosphere and thus plays an important role in global carbon cycling. Soil respiration is well known for its significant spatial variation in terrestrial ecosystems, especially in fragile ecosystems of arid land, where vegetation is distributed sparsely and the climate changes dramatically. In this study, soil respiration in three typical arid ecosystems: desert ecosystem (DE), desert-farmland transition ecosystem (TE) and farmland ecosystem (FE) in an arid area of northwestern China were studied for their spatial variations in 2012 and 2013. Along with soil respiration (SR), soil surface temperature (ST), soil moisture (SM) and soil electrical conductivity (ECb) were also recorded to investigate the spatial variations and the correlations among them. The results revealed that averaged soil respiration rate was much lower in DE than those in TE and FE. No single factor could adequately explain the variation of soil respiration, except a negative relationship between soil temperature and soil respiration in FE (P < 0.05). Geostatistical analysis showed that the spatial heterogeneity of soil respiration in DE was insignificant but notably in both TE and FE, especially in FE, which was mainly attributed to the different vegetation or soil moisture characteristics in the three ecosystems. The results obtained in this study will help to provide a better understanding on spatial variations of soil respiration and soil properties in arid ecosystems and also on macroscale carbon cycling evaluations.
Blockade of Gap Junction Hemichannel Suppresses Disease Progression in Mouse Models of Amyotrophic Lateral Sclerosis and Alzheimer's Disease
Hideyuki Takeuchi, Hiroyuki Mizoguchi, Yukiko Doi, Shijie Jin, Mariko Noda, Jianfeng Liang, Hua Li, Yan Zhou, Rarami Mori, Satoko Yasuoka, Endong Li, Bijay Parajuli, Jun Kawanokuchi, Yoshifumi Sonobe, Jun Sato, Koji Yamanaka, Gen Sobue, Tetsuya Mizuno, Akio Suzumura
PLOS ONE , 2011, DOI: 10.1371/journal.pone.0021108
Abstract: Background Glutamate released by activated microglia induces excitotoxic neuronal death, which likely contributes to non-cell autonomous neuronal death in neurodegenerative diseases, including amyotrophic lateral sclerosis and Alzheimer's disease. Although both blockade of glutamate receptors and inhibition of microglial activation are the therapeutic candidates for these neurodegenerative diseases, glutamate receptor blockers also perturbed physiological and essential glutamate signals, and inhibitors of microglial activation suppressed both neurotoxic/neuroprotective roles of microglia and hardly affected disease progression. We previously demonstrated that activated microglia release a large amount of glutamate specifically through gap junction hemichannel. Hence, blockade of gap junction hemichannel may be potentially beneficial in treatment of neurodegenerative diseases. Methods and Findings In this study, we generated a novel blood-brain barrier permeable gap junction hemichannel blocker based on glycyrrhetinic acid. We found that pharmacologic blockade of gap junction hemichannel inhibited excessive glutamate release from activated microglia in vitro and in vivo without producing notable toxicity. Blocking gap junction hemichannel significantly suppressed neuronal loss of the spinal cord and extended survival in transgenic mice carrying human superoxide dismutase 1 with G93A or G37R mutation as an amyotrophic lateral sclerosis mouse model. Moreover, blockade of gap junction hemichannel also significantly improved memory impairments without altering amyloid β deposition in double transgenic mice expressing human amyloid precursor protein with K595N and M596L mutations and presenilin 1 with A264E mutation as an Alzheimer's disease mouse model. Conclusions Our results suggest that gap junction hemichannel blockers may represent a new therapeutic strategy to target neurotoxic microglia specifically and prevent microglia-mediated neuronal death in various neurodegenerative diseases.
Argentine Ant Affects Ant-Mimetic Arthropods: Does Argentine Ant Invasion Conserve Colouring Variation of Myrmecomorphic Jumping Spider?  [PDF]
Yoshifumi Touyama, Fuminori Ito
Open Journal of Animal Sciences (OJAS) , 2014, DOI: 10.4236/ojas.2014.43019
Abstract: Argentine ant invasion changed colour-polymorphic composition of ant-mimetic jumping spider Myrmarachne in southwestern Japan. In Argentine ant-free sites, most of Myrmarachne exhibited all-blackish colouration. In Argentine ant-infested sites, on the other hand, blackish morph decreased, and bicoloured (i.e. partly bright-coloured) morphs increased in dominance. Invasive Argentine ant drives away native blackish ants. Disappearance of blackish model ants supposedly led to malfunction of Batesian mimicry of Myrmarachne.
Computation of Greeks Using Binomial Tree  [PDF]
Yoshifumi Muroi, Shintaro Suda
Journal of Mathematical Finance (JMF) , 2017, DOI: 10.4236/jmf.2017.73031
Abstract: This paper proposes a new efficient algorithm for the computation of Greeks for options using the binomial tree. We also show that Greeks for European options introduced in this article are asymptotically equivalent to the discrete version of Malliavin Greeks. This fact enables us to show that our Greeks converge to Malliavin Greeks in the continuous time model. The computation algorithm of Greeks for American options using the binomial tree is also given in this article. There are three advantageous points to use binomial tree approach for the computation of Greeks. First, mathematics is much simpler than using the continuous time Malliavin calculus approach. Second, we can construct a simple algorithm to obtain the Greeks for American options. Third, this algorithm is very efficient because one can compute the price and Greeks (delta, gamma, vega, and rho) at once. In spite of its importance, only a few previous studies on the computation of Greeks for American options exist, because performing sensitivity analysis for the optimal stopping problem is difficult. We believe that our method will become one of the popular ways to compute Greeks for options.
Prediction of Positions of Active Compounds Makes It Possible To Increase Activity in Fragment-Based Drug Development
Yoshifumi Fukunishi
Pharmaceuticals , 2011, DOI: 10.3390/ph4050758
Abstract: We have developed a computational method that predicts the positions of active compounds, making it possible to increase activity as a fragment evolution strategy. We refer to the positions of these compounds as the active position. When an active fragment compound is found, the following lead generation process is performed, primarily to increase activity. In the current method, to predict the location of the active position, hydrogen atoms are replaced by small side chains, generating virtual compounds. These virtual compounds are docked to a target protein, and the docking scores (affinities) are examined. The hydrogen atom that gives the virtual compound with good affinity should correspond to the active position and it should be replaced to generate a lead compound. This method was found to work well, with the prediction of the active position being 2 times more efficient than random synthesis. In the current study, 15 examples of lead generation were examined. The probability of finding active positions among all hydrogen atoms was 26%, and the current method accurately predicted 60% of the active positions.
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