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Yokukansan Inhibits Neuronal Death during ER Stress by Regulating the Unfolded Protein Response
Toru Hiratsuka,Shinsuke Matsuzaki,Shingo Miyata,Mitsuhiro Kinoshita,Kazuaki Kakehi,Shinji Nishida,Taiichi Katayama,Masaya Tohyama
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0013280
Abstract: Recently, several studies have reported Yokukansan (Tsumura TJ-54), a traditional Japanese medicine, as a potential new drug for the treatment of Alzheimer's disease (AD). Endoplasmic reticulum (ER) stress is known to play an important role in the pathogenesis of AD, particularly in neuronal death. Therefore, we examined the effect of Yokukansan on ER stress-induced neurotoxicity and on familial AD-linked presenilin-1 mutation-associated cell death.
Breast Surgery with Application of Doughnut Mastopexy Lumpectomy Technique  [PDF]
Kyoichi Matsuzaki
Modern Plastic Surgery (MPS) , 2012, DOI: 10.4236/mps.2012.24022
Abstract: Purpose: Doughnut mastopexy lumpectomy (DML) is a breast resection technique in which a tissue segment is removed and the breast reshaped through a doughnut-shaped de-epithelialized periareolar area. In this study, we attempted to determine whether the DML technique could be useful for other types of breast surgery, in addition to breast cancer lumpectomy. Methods: This study examined a total of 4 patients who underwent the DML technique and were followed up for at least 1 year postoperatively. One patient underwent phyllodes tumor resection, 1 patient underwent removal of a siliconoma, and 2 patients underwent breast reduction mammaplasty. Results: This method enabled en-bloc removal of a large tissue mass or large foreign body that could not be removed through a short periareolar incision. The surgical method of this study enabled the extent of de-epithelialization to be changed according to the size and location of the mass to be excised; good cosmetic results were also obtained. In addition, the surgical method enabled the facile excision of tumors and foreign materials. Conclusions: The DML technique is a useful surgical method that is applicable to other breast surgeries, in addition to breast cancer surgery.
Usefulness of Free Nipple-Areola Complex Graft for Nipple Malposition after Nipple Sparing Mastectomy  [PDF]
Kyoichi Matsuzaki
Modern Plastic Surgery (MPS) , 2012, DOI: 10.4236/mps.2012.24021
Abstract: Purpose: This article identifies the advantage and disadvantage of a free nipple areola complex graft (FNACG) for nipple malposition which resulted from tissue-expander insertion and subsequently replaced with an implant after nipple sparing mastectomy (NSM). Methods: The subjects were three such patients treated using FNACG and who were followed up for at least one year postoperatively. The surgical outcome was assessed for symmetry of nipple-areola position, graft take, depigmentation, and shrinkage. Results: In all patients, the graft was accurately transferred to a position to achieve symmetry with the unaffected breast, and there was complete graft take in the areola by simple surgical design and techniques. No depigmentation of the areola was observed. The size of the areola was almost unchanged after grafting in two patients, but areolar shrinkage occurred in one other patient. There was complete graft take in the nipple in one patient and no depigmentation of the nipple was observed. Necrosis occurred at the tip of the nipple in two other patients. These patients had depigmentation, and the height of nipples decreased in proportion to the level of necrosis. Conclusion: FNACG can be a useful method if its advantages and disadvantages are well considered.
TRAP1 Controls Mitochondrial Fusion/Fission Balance through Drp1 and Mff Expression
Hironori Takamura, Yoshihisa Koyama, Shinsuke Matsuzaki, Kohei Yamada, Tsuyoshi Hattori, Shingo Miyata, Kana Takemoto, Masaya Tohyama, Taiichi Katayama
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0051912
Abstract: Mitochondria are dynamic organelles that change in response to extracellular stimuli. These changes are essential for normal mitochondrial/cellular function and are controlled by a tight balance between two antagonistic pathways that promote fusion and fission. Although some molecules have been identified to mediate the mitochondrial fusion and fission process, the underlying mechanisms remain unclear. Tumor necrosis factor receptor-associated protein 1 (TRAP1) is a mitochondrial molecule that regulates a variety of mitochondrial functions. Here, we examined the role of TRAP1 in the regulation of morphology. Stable TRAP1 knockdown cells showed abnormal mitochondrial morphology, and we observed significant decreases in dynamin-related protein 1 (Drp1) and mitochondrial fission factor (Mff), mitochondrial fission proteins. Similar results were obtained by transient knockdown of TRAP1 in two different cell lines, SH-SY5Y neuroblastoma cells and KNS-42 glioma cells. However, TRAP1 knockdown did not affect expression levels of fusion proteins. The reduction in Drp1 and Mff protein levels was rescued following treatment with the proteasome inhibitor MG132. These results suggest that TRAP1 regulates the expression of fission proteins and controls mitochondrial fusion/fission, which affects mitochondrial/cellular function.
Government Expenditure Financing in the Money-in-the-Production-Function Model  [PDF]
Akihiko Kaneko, Daisuke Matsuzaki
Theoretical Economics Letters (TEL) , 2018, DOI: 10.4236/tel.2018.82008
Abstract: In this study, we consider a scenario in which the government resorts to an income and inflation tax to finance its expenditures in the money-in-the-production-function model. We show that a financing shift from the inflation tax to the income tax increases the real money holdings-to-capital ratio because the accumulation of capital is less favorable than holding money. We also find that a country’s economic growth rate is maximized if all government expenditures are financed through an income tax. For welfare maximization, the government should set the income tax rate higher than the growth maximizing tax rate and reimburse the excess revenue using money contraction.
Increased Stathmin1 Expression in the Dentate Gyrus of Mice Causes Abnormal Axonal Arborizations
Kohei Yamada,Shinsuke Matsuzaki,Tsuyoshi Hattori,Ryusuke Kuwahara,Manabu Taniguchi,Hitoshi Hashimoto,Norihito Shintani,Akemichi Baba,Natsuko Kumamoto,Kazuo Yamada,Takeo Yoshikawa,Taiichi Katayama,Masaya Tohyama
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0008596
Abstract: Pituitary adenylate cyclase-activating polypeptide (PACAP) is involved in multiple brain functions. To clarify the cause of abnormal behavior in PACAP deficient-mice, we attempted the identification of genes whose expression was altered in the dentate gyrus of PACAP-deficient mice using the differential display method. Expression of stathmin1 was up-regulated in the dentate gyrus at both the mRNA and protein levels. PACAP stimulation inhibited stathmin1 expression in PC12 cells, while increased stathmin1expression in neurons of the subgranular zone and in primary cultured hippocampal neurons induced abnormal arborization of axons. We also investigated the pathways involved in PACAP deficiency. Ascl1 binds to E10 box of the stathmin1 promoter and increases stathmin1 expression. Inhibitory bHLH proteins (Hes1 and Id3) were rapidly up-regulated by PACAP stimulation, and Hes1 could suppress Ascl1 expression and Id3 could inhibit Ascl1 signaling. We also detected an increase of stathmin1 expression in the brains of schizophrenic patients. These results suggest that up-regulation of stathmin1 in the dentate gyrus, secondary to PACAP deficiency, may create abnormal neuronal circuits that cause abnormal behavior.
Dysbindin Regulates the Transcriptional Level of Myristoylated Alanine-Rich Protein Kinase C Substrate via the Interaction with NF-YB in Mice Brain
Hiroaki Okuda,Ryusuke Kuwahara,Shinsuke Matsuzaki,Shingo Miyata,Natsuko Kumamoto,Tsuyoshi Hattori,Shoko Shimizu,Kohei Yamada,Keisuke Kawamoto,Ryota Hashimoto,Masatoshi Takeda,Taiichi Katayama,Masaya Tohyama
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0008773
Abstract: An accumulating body of evidence suggests that Dtnbp1 (Dysbindin) is a key susceptibility gene for schizophrenia. Using the yeast-two-hybrid screening system, we examined the candidate proteins interacting with Dysbindin and revealed one of these candidates to be the transcription factor NF-YB.
Reduced Rate of Neural Differentiation in the Dentate Gyrus of Adult Dysbindin Null (Sandy) Mouse
Naomi Nihonmatsu-Kikuchi,Ryota Hashimoto,Satoko Hattori,Shinsuke Matsuzaki,Takiko Shinozaki,Haruka Miura,Shigeru Ohota,Masaya Tohyama,Masatoshi Takeda,Yoshitaka Tatebayashi
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0015886
Abstract: Genetic variations in the gene encoding dysbindin has consistently been associated with schizophrenia and bipolar disorder, although little is known about the neural functions carried out by dysbindin. To gain some insight into this area, we took advantage of the readily available dysbindin-null mouse sandy (sdy?/?) and studied hippocampal neurogenesis using thymidine analogue bromodeoxuridine (BrdU). No significant differences were found in the proliferation (4 hours) or survival (1, 4 and 8 weeks after the last BrdU injection) of progenitors in the subgranular regions of the dentate gyrus between sdy?/? and sdy+/+ (control) mice. However, 4 weeks after the last BrdU injection, a significant reduction was observed in the ratio of neuronal differentiation in sdy?/? when compared to that of sdy+/+ (sdy+/+ = 87.0±5.3% vs. sdy?/? = 71.3±8.3%, p = 0.01). These findings suggest that dysbindin plays a role during differentiation process in the adult hippocampal neurogenesis and that its deficit may negatively affect neurogenesis-related functions such as cognition and mood.
bFGF Regulates PI3-Kinase-Rac1-JNK Pathway and Promotes Fibroblast Migration in Wound Healing
Shigeyuki Kanazawa,Toshihiro Fujiwara,Shinsuke Matsuzaki,Kenta Shingaki,Manabu Taniguchi,Shingo Miyata,Masaya Tohyama,Yasuo Sakai,Kenji Yano,Ko Hosokawa,Tateki Kubo
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0012228
Abstract: Fibroblast proliferation and migration play important roles in wound healing. bFGF is known to promote both fibroblast proliferation and migration during the process of wound healing. However, the signal transduction of bFGF-induced fibroblast migration is still unclear, because bFGF can affect both proliferation and migration. Herein, we investigated the effect of bFGF on fibroblast migration regardless of its effect on fibroblast proliferation. We noticed involvement of the small GTPases of the Rho family, PI3-kinase, and JNK. bFGF activated RhoA, Rac1, PI3-kinase, and JNK in cultured fibroblasts. Inhibition of RhoA did not block bFGF-induced fibroblast migration, whereas inhibition of Rac1, PI3-kinase, or JNK blocked the fibroblast migration significantly. PI3-kinase-inhibited cells down-regulated the activities of Rac1 and JNK, and Rac1-inhibited cells down-regulated JNK activity, suggesting that PI3-kinase is upstream of Rac1 and that JNK is downstream of Rac1. Thus, we concluded that PI3-kinase, Rac1, and JNK were essential for bFGF-induced fibroblast migration, which is a novel pathway of bFGF-induced cell migration.
The dual origin of the peripheral olfactory system: placode and neural crest
Hiroyuki Katoh, Shinsuke Shibata, Kimiko Fukuda, Momoka Sato, Etsuko Satoh, Narihito Nagoshi, Takeo Minematsu, Yumi Matsuzaki, Chihiro Akazawa, Yoshiaki Toyama, Masaya Nakamura, Hideyuki Okano
Molecular Brain , 2011, DOI: 10.1186/1756-6606-4-34
Abstract: Examination of these transgenic mice revealed GFP-positive cells in the OE, demonstrating that NC-derived cells give rise to OE cells with morphologic and antigenic properties identical to placode-derived cells. OECs were also positive for GFP, confirming their NC origin. Cell lineage tracing studies performed in chick embryos confirmed the migration of NC cells into the OE. Furthermore, spheres cultured from the dissociated cells of the olfactory mucosa demonstrated self-renewal and trilineage differentiation capacities (neurons, glial cells, and myofibroblasts), demonstrating the presence of NC progenitors in the olfactory mucosa.Our data demonstrates that the NC plays a larger role in the development of the olfactory system than previously believed, and suggests that NC-derived cells may in part be responsible for the remarkable capacity of the OE for neurogenesis and regeneration.The sensory organs of the vertebrate head derive from two embryological structures, the sensory placodes and the cranial neural crest (NC), which arise from the border between neural and non-neural ectoderms on the lateral edge of the neural plate and contribute to the formation of the peripheral sensory nervous system in an intricate relationship during cranial development. Placodes are discrete areas of thickened non-neural epithelium that form in characteristic positions in the head of vertebrate embryos and give rise to the paired sensory organs, including the olfactory system. The NC is a multipotent population of migratory cells unique to the vertebrate embryo that delaminate from the neural epithelium and migrate throughout the embryo to give rise to a wide variety of cell types [1,2].The olfactory organ has been shown to arise from a combination of the olfactory placode and cranial NC cells, with the olfactory placode giving rise to the olfactory sensory neurons and supporting cells of the olfactory epithelium (OE) [3-5], and the NC contributing to the structural elements of the
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