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and Toshio SATOH*** * Kyorin University, School of Medicine ... *, Atsuo YANAGISAWA*, Kyozo ISHIKAWA*, Satoshi MINEO**, Hitoshi MATSUMOTO***, ...doi:10.5650/jos1956.38.184 fatcat:rn2rsvunffaunengm3dkbuvdou
Longterm results after corrective surgery for patients with congenital heart disease and Down syndromedoi:10.11281/shinzo1969.25.7_761 fatcat:q3cautj6mnawjng7h7m34v7vpy
A 51-year-old female with an ependymal cyst in the left occipital lobe presented with headache, vomiting, dizziness, and right incomplete homonymous hemianopsia. Following a cyst-ventricular communication and cyst-peritoneal shunting procedure, the visual field loss improved markedly. On the basis of the visual field symptoms, computed tomographic findings, and intraoperative observa tions, the cyst was considered to have developed in the vicinity of the body and posterior horn of the leftdoi:10.2176/nmc.29.417 pmid:2477743 fatcat:y42f4nsjung6zgjiqp6bo73iqm
more »... al ventricle, extending to the left occipital lobe.
Hitoshi Matsumoto • Toshio Satoh* hyaluronidaseは,高 等 動 物 の 各 種 臓 のlysosomc,睾 丸,皮 膚 を は じめ と す る さ ま ざ ま な 場 所 に 存 在 す る 生 体 膜 成 分hyaluronic acidの 加 水 分 解 酵 素 で あ る1).hy- aluronidaseは,通 常 不 活 性 で あ り,Ca2 ...doi:10.2492/jsir1981.4.4_437 fatcat:tsvlfrzo4bfyhkqxosj7g7knu4
How to reference In order to correctly reference this scholarly work, feel free to copy and paste the following: Yasuyuki Satoh, Hisakazu Nakamura, Hitoshi Katayama and Hirokazu Nishitani (2009). ...doi:10.5772/6512 fatcat:j2g65vkxuvdrpn7hror2fevehq
Normal human mammaryepithelial cells (HMEC) isolated from surgically resected breast tissues were cultured under serum-free conditions using MCDB170 medium. With the increase in the number of passages, in particular after the 5th passage, the number of enlarged, flattened and vacuolated cells increased while cell proliferation decreased. The senescent cells occasionally had keratohyaline granules in the cytoplasm and were positive in immunohistochemistry for keratinizing squamousdoi:10.1247/csf.18.315 fatcat:llvpg4h4lnhepni6vlmbv4krz4
more »... ificcytokeratin 10. When HMEC were cultured between floating double-layered collagen gels, the cells lost growth activity, showed marked stratification, and became positive for carcinoembryonic antigen (CEA). The stratified cells underwent squamous differentiation and tonofilament bundles appeared around the nuclei. The stratification and squamousdifferentiation of HMECwere observed within seven days after transfer to the three-dimensional culture, regardless of the number of passages. These results indicate that the HMEC in vitro ultimately differentiate into squamous epithelia and also that there is a close relationship between the squamous-type differentiation and the loss of cell proliferation.
Japanese Journal of Oral & Maxillofacial Surgery
CREB3L3 is involved in fatty acid oxidation and ketogenesis in a mutual manner with PPARα. To evaluate relative contribution, a combination of knockout and transgenic mice was investigated. On a ketogenic-diet (KD) that highlights capability of hepatic ketogenesis, Creb3l3 −/− mice exhibited reduction of expression of genes for fatty oxidation and ketogenesis comparable to Ppara −/− mice. Most of the genes were further suppressed in double knockout mice indicating independent contribution ofdoi:10.1038/srep39182 pmid:27982131 pmcid:PMC5159891 fatcat:lmuak2gssjdopbw6kgpo232mjy
more »... atic CREB3L3. During fasting, dependency of ketogenesis on CREB3L3 is lesser extents than Ppara −/− mice suggesting importance of adipose PPARα for supply of FFA and hyperlipidemia in Creb3l3 −/− mice. In conclusion CREB3L3 plays a crucial role in hepatic adaptation to energy starvation via two pathways: direct related gene regulation and an auto-loop activation of PPARα. Furthermore, as KD-fed Creb3l3 −/− mice exhibited severe fatty liver, activating inflammation, CREB3L3 could be a therapeutic target for NAFLD. The common characteristics of metabolic disorders, such as obesity, diabetes, cardiovascular diseases, and fatty liver, impair nutrient homeostasis, which is tightly regulated by balancing energy production (e.g. ketogenesis, gluconeogenesis, and lipid synthesis) with energy utilization (e.g. lipid oxidation). As fasting progresses, metabolic substrates stored in white adipose tissue (WAT) are released into the circulation as glycerol and free fatty acids (FFA) and transported into the liver. The liver then adapts by increasing β -oxidation, which converts fatty acids into acetyl coenzyme A (acetyl-coA), and by increasing ketogenesis, which converts the resulting acetyl-CoA into ketone bodies. The first ketone body formed from acetyl-CoA is acetoacetate (Acac), which can generate acetone via non-enzymatic decarboxylation, as well as β -OH butyrate in a reaction catalysed by D-β -hydroxybutryate dehydrogenase (BDH1). The rate of conversion from acetyl-CoA to these ketone bodies is limited by hydroxymethylglutaryl CoA synthase 2 (HMGCS2), which converts acetoacetyl-CoA to HMG-CoA. The production of ketone bodies as an alternative energy source is crucial for maintaining energy homeostasis during fasting, as they are used as the main energy source for peripheral tissue, particularly the brain. The fatty acid oxidation process consists of three pathways: peroxisomal β -oxidation, mitochondrial β -oxidation, and ω -oxidation in the endoplasmic reticulum (ER). Although the substrate spectra of mitochondrial and peroxisomal β -oxidation partly overlap, an important distinction is that the mitochondria catalyse the β -oxidation of the bulk of the short (< C8), medium (C8-C12), and long (C14-C20) chain fatty acids (LCFAs), whereas β -oxidation in the peroxisomes preferentially shortens very long chain fatty acids (> C20) to LCFAs, which can then be further oxidized in the mitochondria. FA transport across the mitochondrial membrane is triggered by carnitine palmitoyltransferase 1a, liver (CPT1a) and carnitine palmitoyltransferase 1b, muscle (CPT1b), which are localized in the mitochondrial membrane. The activation of peroxisome proliferator-activated receptor α (PPARα ) by fatty acids promotes hepatic fatty acid oxidation and ketogenesis. Several genes are directly regulated by PPARα in the liver, including those encoding acyl-CoA oxidase (Acox1) 1 , which is involved in the peroxisomal β -oxidation of fatty acids; Cpt1a 2,3 , which transports fatty acids across the outer mitochondrial membrane; and HMGCS2 2-4 . Consequently, mice that lack PPARα accumulate copious amounts of hepatic triglycerides (TG) and become hypoketonaemic and hypoglycaemic during fasting and starvation 5-7 . cAMP responsive element-binding protein 3-like 3 (CREB3L3) is a basic, liver-specific leucine zipper transcription factor belonging to the CREB/ATF family 8 . Under ER stress, CREB3L3 traffics to the Golgi apparatus where site 1 and 2 proteases cleave its amino-terminal portion to induce the expression of genes that are responsible for the systemic inflammatory response 9 . Creb3l3 expression is induced in fasted or insulin-resistant states, resulting in the accumulation of the nuclear form of CREB3L3 10 , which activates hepatic gluconeogenic genes, including phosphoenolpyruvate carboxykinase 1 (Pck1) and glucose-6-phosphatase (G6pc) 11 . Creb3l3 deletion causes a defect in TG lipolysis in the blood, with Creb3l3 −/− mice exhibiting hypertriglyceridaemia as a result of inefficient catalysis of TG clearance by lipoprotein lipase (LPL); this is due to a reduction in the expression of the LPL coactivators Apolipoprotein c2 (Apoc2), Apoa4, and Apoa5, and upregulation of the LPL inhibitor Apoc3 12,13 . Thus, the defective expression of the enzymes that are required for lipolysis and lipid transport in the liver of Creb3l3 −/− mice may explain why mice that are fed either an atherogenic high-fat diet or normal chow exhibit hypertriglyceridaemia, reduced fat mass, body-weight gain, and massive steatosis 12 . When fed a methionine-choline-deficient diet or ketogenic diet, the deficiency of Creb3l3 also develops hepatic steatosis 14,15 . FGF21, a unique member of the FGF family with hormone-like actions 16 , is a key mediator of starvation that regulates lipolysis in WAT and increases fatty acid oxidation and ketogenesis in the liver 17,18 . There is some controversy over the effects of FGF21 on ketogenesis. Hotta et al. 19 reported that FGF21 regulates lipolysis in WAT but is not required for ketogenesis and TG clearance in the liver, but Badman et al. 20 showed that the adaptation to ketogenesis is impaired in Fgf21 −/− mice. FGF21 has been shown to have therapeutic effects on obesity-related metabolic disturbances, such as insulin resistance, diabetes, and hypertriglyceridaemia in ob/ob mice, diet-induced obese mice, and diabetic monkeys 21, 22 . Fgf21 expression is regulated by PPARα , which plays a key role in lipid oxidation, and is induced by fasting or ketogenic diet (KD) consumption 17,18 . CREB3L3 and PPARα are activated in an auto-loop manner in response to starvation and, in turn, synergistically activate Fgf21 expression 23,24 . Therefore, it is believed that these molecules have overlapping functions. In this study, we examined the role of CREB3L3 in energy metabolism during fasting by comparing Creb3l3 −/− , Ppara −/− , and Creb3l3 −/− Ppara −/− mice.
A structure involving the absolute configuration of acinetobactin (1b) was clarified. It was reconfirmed that preacinetobactin (1a) produced 1b by a rearrangement reaction.doi:10.1248/cpb.58.1552 pmid:21048355 fatcat:qzecgxcg65cinh6jeidlkv3jl4
研 究 鼻 粘 膜 の ヒ ス タ ミ ンH2レ セ プ タ ー 佐 藤 成 彦 ・島 田 均 ・馬 場 廣 太 郎 Histamine H2 Receptors in Nasal Mucosa Shigehiko Satoh, Hitoshi Shimada and Kohtaro Baba (Dokkyo University) Nasal mucous membrane is a pathogenic ...doi:10.5631/jibirin.87.1281 fatcat:gapq2vhfpvedhe6gtgtr4shd3e
The pathogenicity of coagulase-negative Staphylococci (CNS) in aural infectious diseases is controversial. To determine the contribution of CNS to the development of aural infectious diseases, bacteriological studies of otorrhea obtained from patients with otitis externa, acute otitis media, chronic otitis media and tympanostomy tube complications were performed. Six species and 49 CNS including 22 S. simulans, 14 S. epidermidis, 9 S. capitis, 2 S. auricularis, one S. hominis and one S. sciuridoi:10.5631/jibirin.86.189 fatcat:qcgnjfmd2fajfmudsdoqd2t3tm
more »... ere isolated from the 48 otorrheas, and 21 of them were isolated without any other bacteria. Some CNS were resistant to a variety of antimicrobial drugs and had 3-lactamase. This study indicates that some CNS may induce inflammatory processes directly by a parasite-host relationship, and/or indirectly by inactivating antimicrobial drugs.
Conventional plastic teeth (CV teeth) are inferior to porcelain teeth in maintaining an adequate esthetic appearance with wear and discoloration, and thus have a shorter period of durability. Recently, high-strength plastic teeth (HS teeth) have been developed and applied to overcome the wear problems of CV teeth. Since HS teeth made of hard resin are still susceptible to staining with pigments, it has been observed that the esthetics of removable partial dentures made from such plastic teethdoi:10.2334/josnusd1959.35.192 fatcat:ryqah574zrdenhgbcjk6vda5he
more »... e gradually impaired in many patients. To investigate the susceptibility of HS teeth to pigments, we conducted an in vitro study by immersing three types of artificial teeth in three coloring liquids. It was found that the HS teeth tended to be less susceptible to the test pigments than the CV teeth to various degrees. In contrast, they showed markedly stronger susceptibility to the pigments than porcelain teeth. For all three artificial tooth types, daily tooth cleaning with an ultrasonic vibrator had a tendency to reduce the coloration in comparison with their counterparts without ultrasonic cleaning.
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