内在性活性化物質、内在性活性化因子、内因性活性化物質

WordNet

of or resembling an endogen
derived or originating internally (同)endogenic
(biology) any agency bringing about activation; a molecule that increases the activity of an enzyme or a protein that increases the production of a gene product in DNA transcription

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(生物が)内部から成長する,内性の,内因性の

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1. 止血の概要 overview of hemostasis
2. 外傷に伴う凝固障害 coagulopathy associated with trauma
3. 内科患者における静脈血栓塞栓症の予防 prevention of venous thromboembolic disease in medical patients
4. カンジダ属に起因する内因性眼内炎の治療 treatment of endogenous endophthalmitis due to candida species
5. 真性多血症の臨床症状および診断 clinical manifestations and diagnosis of polycythemia vera

English Journal

Genome-Wide Association Study for Circulating Tissue Plasminogen Activator Levels and Functional Follow-Up Implicates Endothelial STXBP5 and STX2.

Huang J1, Huffman JE, Yamkauchi M, Trompet S, Asselbergs FW, Sabater-Lleal M, Trégouët DA, Chen WM, Smith NL, Kleber ME, Shin SY, Becker DM, Tang W, Dehghan A, Johnson AD, Truong V, Folkersen L, Yang Q, Oudot-Mellkah T, Buckley BM, Moore JH, Williams FM, Campbell H, Silbernagel G, Vitart V, Rudan I, Tofler GH, Navis GJ, Destefano A, Wright AF, Chen MH, de Craen AJ, Worrall BB, Rudnicka AR, Rumley A, Bookman EB, Psaty BM, Chen F, Keene KL, Franco OH, Böhm BO, Uitterlinden AG, Carter AM, Jukema JW, Sattar N, Bis JC, Ikram MA; Cohorts for Heart and Aging Research in Genome Epidemiology (CHARGE) Consortium Neurology Working Group, Sale MM, McKnight B, Fornage M, Ford I, Taylor K, Slagboom PE, McArdle WL, Hsu FC, Franco-Cereceda A, Goodall AH, Yanek LR, Furie KL, Cushman M, Hofman A, Witteman JC, Folsom AR, Basu S, Matijevic N, van Gilst WH, Wilson JF, Westendorp RG, Kathiresan S, Reilly MP; CARDIoGRAM Consortium, Tracy RP, Polasek O, Winkelmann BR, Grant PJ, Hillege HL, Cambien F, Stott DJ, Lowe GD, Spector TD, Meigs JB, Marz W, Eriksson P, Becker LC, Morange PE, Soranzo N, Williams SM, Hayward C, van der Harst P, Hamsten A, Lowenstein CJ, Strachan DP, O'Donnell CJ; CHARGE Consortium Hemostatic Factor Working Group.Author information 1From National Heart, Lung, and Blood Institute's Framingham Heart Study, Framingham, MA (J.H., A.D.J., C.J.O.); Division of Intramural Research, National Heart, Lung, and Blood Institute, Bethesda, MD (J.H., A.D.J., C.J.O.); MRC Human Genetics Unit, Institute of Genetics and Molecular Medicine, Western General Hospital, Edinburgh, Scotland, United Kingdom (J.E.H., V.V., A.F.W., C.H.); The Aab Cardiovascular Research Institute, Department of Medicine, University of Rochester School of Medicine and Dentistry, Rochester, NY (M.Y., C.J.L.); Departments of Cardiology (S.T., J.W.J.), Gerontology and Geriatrics (S.T., A.J.M.d.C., R.G.J.W.), and Molecular Epidemiology (P.E.S.), Leiden University Medical Center, the Netherlands; Department of Cardiology, Division of Heart and Lungs, University Medical Center Utrecht, Utrecht, the Netherlands (F.W.A.); Durrer Center for Cardiogenetic Research, ICIN-Netherlands Heart Institute, Utrecht, the Netherlands (F.W.A.); Institute of Cardiovascular Science, Faculty of Population Health Sciences, University College London, London, United Kingdom (F.W.A.); Cardiovascular Genetics and Genomics Group, Atherosclerosis Research Unit, Department of Medicine (M.S.-L., L.F., P.E., A.H.), Karolinska Institutet, Karolinska University Hospital, Solna, Stockholm, Sweden; INSERM UMRS 937, Pierre et Marie Curie University, Paris, France (D.-A.T., V.T., T.O.M., F.C.); ICAN Institute for Cardiometabolism and Nutrion, Paris, France (D.-A.T., V.T., F.C.); Departments of Public Health Sciences (W.M.C., B.B.W., F.C.) and Biochemistry and Molecular Genetics (M.M.S.), Center for Public Health Genomics, University of Virginia, Charlottesville, VA; Departments of Epidemiology (N.L.S., B.M.P., B.M.), Medicine (B.M.P., J.C.B.), and Health Services (B.M.P.), University of Washington, Seattle, WA; Group Health Research Institute, Group Health Cooperative, Seattle, WA (N.L.S., B.M.P.); Seattle Epidemiologic Research and Information Center, VA Office of Research andAbstractOBJECTIVE: Tissue plasminogen activator (tPA), a serine protease, catalyzes the conversion of plasminogen to plasmin, the major enzyme responsible for endogenous fibrinolysis. In some populations, elevated plasma levels of tPA have been associated with myocardial infarction and other cardiovascular diseases. We conducted a meta-analysis of genome-wide association studies to identify novel correlates of circulating levels of tPA.
Arteriosclerosis, thrombosis, and vascular biology.Arterioscler Thromb Vasc Biol.2014 May;34(5):1093-101. doi: 10.1161/ATVBAHA.113.302088. Epub 2014 Feb 27.
OBJECTIVE: Tissue plasminogen activator (tPA), a serine protease, catalyzes the conversion of plasminogen to plasmin, the major enzyme responsible for endogenous fibrinolysis. In some populations, elevated plasma levels of tPA have been associated with myocardial infarction and other cardiovascular
PMID 24578379

Tranexamic acid as adjunct therapy to bypassing agents in haemophilia A patients with inhibitors.

Tran HT1, Sørensen B, Rea CJ, Bjørnsen S, Ueland T, Pripp AH, Tjønnfjord GE, Holme PA.Author information 1Research Institute of Internal Medicine, Oslo University Hospital, Rikshospitalet, Oslo, Norway; Institute of Clinical Medicine, University of Oslo, Oslo, Norway; Department of Haematology, Oslo University Hospital, Rikshospitalet, Oslo, Norway.AbstractHaemophilia patients with inhibitors require bypassing agents (BPA) like activated prothrombin complex concentrate (aPCC) and recombinant activated factor VII (rFVIIa) to control bleeds. Adjunct tranexamic acid (TXA) may improve haemostasis. The objective of this study was to investigate safety and haemostatic effect of TXA given in combination with BPA. Healthy volunteers (N = 5) and haemophilia inhibitor patients (N = 6) were enrolled in a prospective case crossover design. Controls were treated with TXA 20 mg kg(-1) orally (O.R.) Patients were treated with aPCC 75 IU kg(-1) intravenous (I.V.) on day 1 followed by TXA 20 mg kg(-1) O.R. combined with aPCC 75 IU kg(-1) I.V. on day 2. A 14-day washout occurred before crossover to rFVIIa 90 μg kg(-1) I.V. ±TXA. Safety evaluation and blood sampling processes were performed at baseline, 15, 30, 60, 120, 180 and 240 min post treatment. Primary outcome was maximum clot firmness (MCF) evaluated by whole blood thromboelastometry using a TF + tissue plasminogen activator-based assay. Healthy controls showed a 20-fold increase in MCF following TXA. Adjunct TXA to aPCC or rFVIIa induced a significant increase in MCF (P < 0.0001) reaching levels indistinguishable from healthy controls treated with TXA (P > 0.05). Infusion of aPCC or rFVIIa alone induced only 3-10 fold increase in MCF from baseline, with a decline in MCF starting after 60-120 min. TXA did not increase the endogenous thrombin potential. No clinical or laboratory signs of thromboembolic events, disseminated intravascular coagulation, or hypercoagulability were observed. Combination of aPCC or rFVIIa with TXA normalizes clot stability in haemophilia patients with inhibitor as compared to healthy controls. No clinical or laboratory adverse events were observed.
Haemophilia : the official journal of the World Federation of Hemophilia.Haemophilia.2014 May;20(3):369-75. doi: 10.1111/hae.12318. Epub 2013 Nov 19.
Haemophilia patients with inhibitors require bypassing agents (BPA) like activated prothrombin complex concentrate (aPCC) and recombinant activated factor VII (rFVIIa) to control bleeds. Adjunct tranexamic acid (TXA) may improve haemostasis. The objective of this study was to investigate safety and
PMID 24251535

Dynamics and reproductive effects of complement factors in the spontaneous abortion model of CBA/J×DBA/2 mice.

Takeshita A1, Kusakabe KT2, Hiyama M3, Kuniyoshi N3, Kondo T1, Kano K3, Kiso Y3, Okada T1.Author information 1Department of Integrated Structural Biosciences, Division of Veterinary Science, Graduate School of Life and Environmental Science, Osaka Prefecture University, Osaka 598-8531, Japan.2Laboratory of Basic Veterinary Science, The United Graduate School of Veterinary Science, Yamaguchi University, Yamaguchi 753-8515, Japan. Electronic address: kusakabe@yamaguchi-u.ac.jp.3Laboratory of Basic Veterinary Science, The United Graduate School of Veterinary Science, Yamaguchi University, Yamaguchi 753-8515, Japan.AbstractThe complement system is one component of innate immunity that could participate in fetal loss. We have already reported that adipsin, a complement activator in the alternative pathway, is stably expressed in the placenta and that an increase in this expression is related to spontaneous abortion. However, complement inhibitor Crry was concurrently expressed in the placenta, and the role of complement factors during pregnancy was not clear. In the present study, we examined the endogenous regulation of complement factors in placenta and serum by using another model mouse for spontaneous abortion and studied the effect of exogenous complement disruption on pregnancy. Compared to control mice, the CBA/J×DBA/2 model mice had higher expression levels of adipsin in the placenta and serum. Adipsin and complement C3 were localized in the metrial gland and labyrinth regions, and both positive reactive ranges were limited in the maternal blood current in normal implantation sites. These results suggest that extrauterine adipsin hematogenously reaches the placenta, activates complement C3, and promotes destruction of the feto-maternal barrier in aborted implantation sites. Crry was consistently expressed in the placenta and serum and reduced in the resorption sites of CBA/J×DBA/2 mice as compared to normal sites. Injection of recombinant adipsin increased the resorption rate and changed the expression of Th-type cytokines toward a Th1 bias. The present study indicates that adipsin could induce the fetal loss that accompanies the Th1 bias and may be a crucial cause of spontaneous abortion. In addition, the local expression of Crry prevents complement activation in placenta in response to a systemic increase of adipsin.
Immunobiology.Immunobiology.2014 May;219(5):385-91. doi: 10.1016/j.imbio.2014.01.001. Epub 2014 Jan 10.
The complement system is one component of innate immunity that could participate in fetal loss. We have already reported that adipsin, a complement activator in the alternative pathway, is stably expressed in the placenta and that an increase in this expression is related to spontaneous abortion. Ho
PMID 24576554

Japanese Journal

Generation of α1,3-galactosyltransferase and cytidine monophospho-N-acetylneuraminic acid hydroxylase gene double-knockout pigs

MIYAGAWA Shuji,MATSUNARI Hitomi,WATANABE Masahito,NAKANO Kazuaki,UMEYAMA Kazuhiro,SAKAI Rieko,TAKAYANAGI Shuko,TAKEISHI Toki,FUKUDA Tooru,YASHIMA Sayaka,MAEDA Akira,EGUCHI Hiroshi,OKUYAMA Hiroomi,NAGAYA Masaki,NAGASHIMA Hiroshi
Journal of Reproduction and Development advpub(0), 2015
… Zinc-finger nucleases (ZFNs) and transcription activator-like effector nucleases (TALENs) are new tools for producing gene knockout (KO) animals. … The current study reports produced genetically modified pigs, in which two endogenous genes were knocked out. …
NAID 130005088822

Effects of miR-9 and Tetramethylpyrazine on Activation of Hepatic Stellate Cells

Li Shan-Gao,Zhou Jun,Zhong Ji-Hong [他],Cao Hai-Jun,Zhu Ling,Liu Jun,Hu Hua-Jun,Lv Bin
Biological and Pharmaceutical Bulletin 38(3), 396-401, 2015
… Downstream factors that may be affected by miR-9 such as leptin, α-smooth muscle actin (SMA), and collagen I, as well as phosphorylation levels of Janus kinase 1 (JAK1)/signal transducer and activator of transcription 3 (STAT3) were investigated at the protein level. …
NAID 130004872271

人工酵素によるゲノム編集工学とその応用，可能性

野村渉
薬学雑誌. 乙号 135(3), 405-414, 2015
… The recent development of new platforms using transcription activator-like effector (TALE) proteins or the clustered regularly interspaced short palindromic repeats/CRISPR-associated protein (CRISPR/Cas) system has expanded the range of possibilities for genome-editing technologies. … The development of artificial ZFPs has greatly increased the feasibility of manipulating endogenous gene functions through transcriptional control and gene modification. …
NAID 130004756508