WordNet

be a contributing factor; "make things factor into a companys profitability"
any of the numbers (or symbols) that form a product when multiplied together
an independent variable in statistics
anything that contributes causally to a result; "a number of factors determined the outcome"
consider as relevant when making a decision; "You must factor in the recent developments" (同)factor in, factor out
resolve into factors; "a quantum computer can factor the number 15" (同)factor in, factor out
an event known to have happened or something known to have existed; "your fears have no basis in fact"; "how much of the story is fact and how much fiction is hard to tell"
a concept whose truth can be proved; "scientific hypotheses are not facts"
a piece of information about circumstances that exist or events that have occurred; "first you must collect all the facts of the case"
a statement or assertion of verified information about something that is the case or has happened; "he supported his argument with an impressive array of facts"
any of various controls or devices for regulating or controlling fluid flow, pressure, temperature, etc.
an official responsible for control and supervision of a particular activity or area of public interest

PrepTutorEJDIC

(…の)『要因』,(…を生み出す)要素《+『in』+『名』(do『ing』)》 / 囲数,約数 / 代理人,《おもに英》仲買人 / =factorize
〈C〉『事実』,実際にある(あった)事 / 〈U〉真相,真実(truth) / 《the~》(法律用語で)犯行
取り締まり人;調整者 / 調整装置

UpToDate Contents

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1. 第V因子ライデンおよび活性化プロテインC抵抗性：臨床症状および診断 factor v leiden and activated protein c resistance clinical manifestations and diagnosis
2. 稀な遺伝性凝固異常 rare inherited coagulation disorders
3. 後天性の凝固因子阻害物質 acquired inhibitors of coagulation
4. 無症候性患者における先天性血栓性素因のスクリーニング screening for inherited thrombophilia in asymptomatic individuals
5. 止血の概要 overview of hemostasis

English Journal

Adipocyte lineages: tracing back the origins of fat.

Sanchez-Gurmaches J1, Guertin DA2.Author information 1Program in Molecular Medicine, University of Massachusetts Medical School, Worcester, MA 01605, USA.2Program in Molecular Medicine, University of Massachusetts Medical School, Worcester, MA 01605, USA. Electronic address: david.guertin@umassmed.edu.AbstractThe obesity epidemic has intensified efforts to understand the mechanisms controlling adipose tissue development. Adipose tissue is generally classified as white adipose tissue (WAT), the major energy storing tissue, or brown adipose tissue (BAT), which mediates non-shivering thermogenesis. It is hypothesized that brite adipocytes (brown in white) may represent a third adipocyte class. The recent realization that brown fat exist in adult humans suggests increasing brown fat energy expenditure could be a therapeutic strategy to combat obesity. To understand adipose tissue development, several groups are tracing the origins of mature adipocytes back to their adult precursor and embryonic ancestors. From these studies emerged a model that brown adipocytes originate from a precursor shared with skeletal muscle that expresses Myf5-Cre, while all white adipocytes originate from a Myf5-negative precursors. While this provided a rational explanation to why BAT is more metabolically favorable than WAT, recent work indicates the situation is more complex because subsets of white adipocytes also arise from Myf5-Cre expressing precursors. Lineage tracing studies further suggest that the vasculature may provide a niche supporting both brown and white adipocyte progenitors; however, the identity of the adipocyte progenitor cell is under debate. Differences in origin between adipocytes could explain metabolic heterogeneity between depots and/or influence body fat patterning particularly in lipodystrophy disorders. Here, we discuss recent insights into adipose tissue origins highlighting lineage-tracing studies in mice, how variations in metabolism or signaling between lineages could affect body fat distribution, and the questions that remain unresolved. This article is part of a Special Issue entitled: Modulation of Adipose Tissue in Health and Disease.
Biochimica et biophysica acta.Biochim Biophys Acta.2014 Mar;1842(3):340-51. doi: 10.1016/j.bbadis.2013.05.027. Epub 2013 Jun 4.
The obesity epidemic has intensified efforts to understand the mechanisms controlling adipose tissue development. Adipose tissue is generally classified as white adipose tissue (WAT), the major energy storing tissue, or brown adipose tissue (BAT), which mediates non-shivering thermogenesis. It is hy
PMID 23747579

Ancestral Myf5 gene activity in periocular connective tissue identifies a subset of fibro/adipogenic progenitors but does not connote a myogenic origin.

Stuelsatz P1, Shearer A1, Yablonka-Reuveni Z2.Author information 1Department of Biological Structure, University of Washington School of Medicine, Seattle, WA 98195, USA.2Department of Biological Structure, University of Washington School of Medicine, Seattle, WA 98195, USA. Electronic address: reuveni@uw.edu.AbstractExtraocular muscles (EOM) represent a unique muscle group that controls eye movements and originates from head mesoderm, while the more typically studied body and limb muscles are somite-derived. Aiming to investigate myogenic progenitors (satellite cells) in EOM versus limb and diaphragm of adult mice, we have been using flow cytometry in combination with myogenic-specific Cre-loxP lineage marking for cell isolation. While analyzing cells from the EOM of mice that harbor Myf5(Cre)-driven GFP expression, we identified in addition to the expected GFP(+) myogenic cells (presumably satellite cells), a second dominant GFP(+) population distinguished as being Sca1(+), non-myogenic, and exhibiting a fibro/adipogenic potential. This unexpected population was not only unique to EOM compared to the other muscles but also specific to the Myf5(Cre)-driven reporter when compared to the MyoD(Cre) driver. Histological studies of periocular tissue preparations demonstrated the presence of Myf5(Cre)-driven GFP(+) cells in connective tissue locations adjacent to the muscle masses, including cells in the vasculature wall. These vasculature-associated GFP(+) cells were further identified as mural cells based on the presence of the specific XLacZ4 transgene. Unlike the EOM satellite cells that originate from a Pax3-negative lineage, these non-myogenic Myf5(Cre)-driven GFP(+) cells appear to be related to cells of a Pax3-expressing origin, presumably derived from the neural crest. In all, our lineage tracing based on multiple reporter lines has demonstrated that regardless of common ancestral expression of Myf5, there is a clear distinction between periocular myogenic and non-myogenic cell lineages according to their mutually exclusive antecedence of MyoD and Pax3 gene activity.
Developmental biology.Dev Biol.2014 Jan 15;385(2):366-79. doi: 10.1016/j.ydbio.2013.08.010. Epub 2013 Aug 19.
Extraocular muscles (EOM) represent a unique muscle group that controls eye movements and originates from head mesoderm, while the more typically studied body and limb muscles are somite-derived. Aiming to investigate myogenic progenitors (satellite cells) in EOM versus limb and diaphragm of adult m
PMID 23969310

Pax3 synergizes with Gli2 and Zic1 in transactivating the Myf5 epaxial somite enhancer.

Himeda CL1, Barro MV, Emerson CP Jr.Author information 1The Departments of Cell and Developmental Biology and Neurology, University of Massachusetts Medical School, Worcester, MA 01655, USA.AbstractBoth Glis, the downstream effectors of hedgehog signaling, and Zic transcription factors are required for Myf5 expression in the epaxial somite. Here we demonstrate a novel synergistic interaction between members of both families and Pax3, a paired-domain transcription factor that is essential for both myogenesis and neural crest development. We show that Pax3 synergizes with both Gli2 and Zic1 in transactivating the Myf5 epaxial somite (ES) enhancer in concert with the Myf5 promoter. This synergy is dependent on conserved functional domains of the proteins, as well as on a novel homeodomain motif in the Myf5 promoter and the essential Gli motif in the ES enhancer. Importantly, overexpression of Zic1 and Pax3 in the 10T1/2 mesodermal cell model results in enrichment of these factors at the endogenous Myf5 locus and induction of Myf5 expression. In our previous work, we showed that by enhancing nuclear translocation of Gli factors, Zics provide spatiotemporal patterning for Gli family members in the epaxial induction of Myf5 expression. Our current study indicates a complementary mechanism in which association with DNA-bound Pax3 strengthens the ability of both Zic1 and Gli2 to transactivate Myf5 in the epaxial somite.
Developmental biology.Dev Biol.2013 Nov 1;383(1):7-14. doi: 10.1016/j.ydbio.2013.09.006. Epub 2013 Sep 10.
Both Glis, the downstream effectors of hedgehog signaling, and Zic transcription factors are required for Myf5 expression in the epaxial somite. Here we demonstrate a novel synergistic interaction between members of both families and Pax3, a paired-domain transcription factor that is essential for b
PMID 24036067

Japanese Journal

Muscle type-specific effect of myostatin deficiency on myogenic regulatory factor expression in adult double-muscled Japanese Shorthorn cattle

MUROYA Susumu,WATANABE Kouichi,HAYASHI Shinichiro,MIYAKE Masato,KONASHI Shigeru,SATO Youichi,TAKAHASHI Manabu,KAWAHATA Shigeki,YOSHIKAWA Yoshisato,ASO Hisashi,CHIKUNI Koichi,YAMAGUCHI Takahiro
Animal science journal 80(6), 678-685, 2009-12-01
NAID 10027887994

MyoD and myogenin mRNA levels after single session of treadmill exercise in rat skeletal muscle

MIYATA TAKUYA,TANAKA SHOJI,TACHINO KATSUHIKO
Journal of physical therapy science 21(1), 81-84, 2009-02-28
[Purpose]: We examined mRNA levels of MyoD and myogenin in rat skeletal muscle after a single session of treadmill running. [Subject]: A total of 26 male Sprague-Dawley rats aged 4 weeks were used in …
NAID 10025401240