- 遺伝性の
WordNet
- capable of being inherited; "inheritable traits such as eye color"; "an inheritable title" (同)heritable
- not inheritable (同)nonheritable
PrepTutorEJDIC
- (財産など)相続できる / (病気・性格が)遺伝性の
- 世襲の,親譲りの / 遺伝的な,遺伝性の
UpToDate Contents
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- 1. エルドハイム・チェスター病 erdheim chester disease
- 2. アスリートにおける心電図異常および伝導障害 electrocardiographic abnormalities and conduction disturbances in athletes
- 3. 胎児水腫の生後ケア postnatal care of hydrops fetalis
- 4. 脳卒中の二次予防：危険因子の低減 secondary prevention of stroke risk factor reduction
- 5. 小児における急性呼吸困難の緊急評価 emergent evaluation of acute respiratory compromise in children
English Journal
- Murine models of hepatitis C: What can we look forward to?
- von Schaewen M1, Ploss A2.Author information 1Department of Molecular Biology, Princeton University, 110 Lewis Thomas Laboratory, Washington Road, Princeton, NJ 08544, United States.2Department of Molecular Biology, Princeton University, 110 Lewis Thomas Laboratory, Washington Road, Princeton, NJ 08544, United States. Electronic address: aploss@princeton.edu.AbstractThe study of interactions between hepatitis C virus (HCV) with its mammalian host, along with the development of more effective therapeutics and vaccines has been delayed by the lack of a suitable small animal model. HCV readily infects only humans and chimpanzees, which poses logistic, economic and ethical challenges with analyzing HCV infection in vivo. Progress has been made in understanding the determinants that dictate HCV's narrow host range providing a blueprint for constructing a mouse model with inheritable susceptibility to HCV infection. Indeed, genetically humanized mice were generated that support viral uptake, replication and production of infectious virions - albeit at low levels. These efforts are complemented with attempts to select for viral variants that are inherently more capable of replicating in non-human species. In parallel, engraftment of relevant human tissues into improved xenorecipients is being continuously refined. Incorporating advances in stem-cell-biology and tissue engineering may allow the generation of patient-specific humanized mice. Construction of such mouse "avatars" may allow analyzing functionally patient-specific differences with respect to susceptibility to infection, disease progression and responses to treatment. In this review, we discuss the three, before mentioned approaches to overcome current species barriers and generate a small animal model for HCV infection, i.e. genetic modification of mice to increase their susceptibility to the virus; genetic modification of HCV, to increase its pathogenicity for mice; and the introduction of human liver and immune cells into immunodeficient mice, to create "humanized" mice. Although in the foreseeable future there will not be a single model that perfectly mimics the natural course of HCV in humans there is reason for optimism. The spectrum of murine animal models for hepatitis C provides a broad arsenal for analyzing the disease. These models may play an important role by prioritizing vaccine candidates and possibly refining combination anti-viral drug therapies. This article forms part of a symposium in Anti-viral Research on "Hepatitis C: next steps toward global eradication."
- Antiviral research.Antiviral Res.2014 Apr;104:15-22. doi: 10.1016/j.antiviral.2014.01.007. Epub 2014 Jan 24.
- The study of interactions between hepatitis C virus (HCV) with its mammalian host, along with the development of more effective therapeutics and vaccines has been delayed by the lack of a suitable small animal model. HCV readily infects only humans and chimpanzees, which poses logistic, economic and
- PMID 24462693
- Cardiac channelopathy testing in 274 ethnically diverse sudden unexplained deaths.
- Wang D1, Shah KR1, Um SY1, Eng LS1, Zhou B1, Lin Y1, Mitchell AA2, Nicaj L3, Prinz M4, McDonald TV5, Sampson BA3, Tang Y6.Author information 1Molecular Genetics Laboratory, New York City Office of Chief Medical Examiner, New York, NY 10016, United States.2Forensic Biology Department, New York City Office of Chief Medical Examiner, New York, NY 10016, United States.3Forensic Pathology Department, New York City Office of Chief Medical Examiner, New York, NY 10016, United States.4Formerly Forensic Biology Department, New York City Office of Chief Medical Examiner, New York, NY 10016, United States.5Departments of Medicine (Cardiology) & Molecular Pharmacology, Albert Einstein College of Medicine, 1300 Morris Park Ave. Bronx, NY 10461, United States.6Molecular Genetics Laboratory, New York City Office of Chief Medical Examiner, New York, NY 10016, United States. Electronic address: ytang@ocme.nyc.gov.AbstractSudden unexplained deaths (SUD) in apparently healthy individuals, for which the causes of deaths remained undetermined after comprehensive forensic investigations and autopsy, present vexing challenges to medical examiners and coroners. Cardiac channelopathies, a group of inheritable diseases that primarily affect heart rhythm by altering the cardiac conduction system, have been known as one of the likely causes of SUD. Adhering to the recommendations of including molecular diagnostics of cardiac channelopathies in SUD investigation, the Molecular Genetics Laboratory of the New York City (NYC) Office of Chief Medical Examiner (OCME) has been routinely testing for six major channelopathy genes (KCNQ1, KCNH2, SCN5A, KCNE1, KCNE2, and RyR2) since 2008. Presented here are the results of cardiac channelopathy testing in 274 well-characterized autopsy negative SUD cases, all with thorough medicolegal death investigation including complete autopsy by NYC OCME between 2008 and 2012. The cohort consisted of 141 infants (92.9% younger than six-month old) and 133 non-infants (78.2% were between 19 and 58 years old). Among the ethnically diverse cohort, African American infants had the highest risks of SUD, and African American non-infants died at significantly younger age (23.7 years old, mean age-at-death) than those of other ethnicities (30.3 years old, mean age-at-death). A total of 22 previously classified cardiac channelopathy-associated variants and 24 novel putative channelopathy-associated variants were detected among the infants (13.5%) and non-infants (19.5%). Most channelopathy-associated variants involved the SCN5A gene (68.4% in infants, 50% in non-infants). We believe this is the first study assessing the role of cardiac channelopathy genes in a large and demographically diverse SUD population drawn from a single urban medical examiner's office in the United States. Our study supports that molecular testing for cardiac channelopathy is a valuable tool in SUD investigations and provides helpful information to medical examiners/coroners seeking cause of death in SUD as well as potentially life-saving information to surviving family members.
- Forensic science international.Forensic Sci Int.2014 Apr;237:90-9. doi: 10.1016/j.forsciint.2014.01.014. Epub 2014 Feb 15.
- Sudden unexplained deaths (SUD) in apparently healthy individuals, for which the causes of deaths remained undetermined after comprehensive forensic investigations and autopsy, present vexing challenges to medical examiners and coroners. Cardiac channelopathies, a group of inheritable diseases that
- PMID 24631775
- Genome-wide parent-of-origin DNA methylation analysis reveals the intricacies of human imprinting and suggests a germline methylation-independent mechanism of establishment.
- Court F1, Tayama C, Romanelli V, Martin-Trujillo A, Iglesias-Platas I, Okamura K, Sugahara N, Simón C, Moore H, Harness JV, Keirstead H, Sanchez-Mut JV, Kaneki E, Lapunzina P, Soejima H, Wake N, Esteller M, Ogata T, Hata K, Nakabayashi K, Monk D.Author information 1Imprinting and Cancer Group, Cancer Epigenetic and Biology Program, Institut d'Investigació Biomedica de Bellvitge, Hospital Duran i Reynals, 08908 Barcelona, Spain;AbstractDifferential methylation between the two alleles of a gene has been observed in imprinted regions, where the methylation of one allele occurs on a parent-of-origin basis, the inactive X-chromosome in females, and at those loci whose methylation is driven by genetic variants. We have extensively characterized imprinted methylation in a substantial range of normal human tissues, reciprocal genome-wide uniparental disomies, and hydatidiform moles, using a combination of whole-genome bisulfite sequencing and high-density methylation microarrays. This approach allowed us to define methylation profiles at known imprinted domains at base-pair resolution, as well as to identify 21 novel loci harboring parent-of-origin methylation, 15 of which are restricted to the placenta. We observe that the extent of imprinted differentially methylated regions (DMRs) is extremely similar between tissues, with the exception of the placenta. This extra-embryonic tissue often adopts a different methylation profile compared to somatic tissues. Further, we profiled all imprinted DMRs in sperm and embryonic stem cells derived from parthenogenetically activated oocytes, individual blastomeres, and blastocysts, in order to identify primary DMRs and reveal the extent of reprogramming during preimplantation development. Intriguingly, we find that in contrast to ubiquitous imprints, the majority of placenta-specific imprinted DMRs are unmethylated in sperm and all human embryonic stem cells. Therefore, placental-specific imprinting provides evidence for an inheritable epigenetic state that is independent of DNA methylation and the existence of a novel imprinting mechanism at these loci.
- Genome research.Genome Res.2014 Apr;24(4):554-69. doi: 10.1101/gr.164913.113. Epub 2014 Jan 8.
- Differential methylation between the two alleles of a gene has been observed in imprinted regions, where the methylation of one allele occurs on a parent-of-origin basis, the inactive X-chromosome in females, and at those loci whose methylation is driven by genetic variants. We have extensively char
- PMID 24402520
Japanese Journal
- Availability of brachymorphic mice as undersulfated animals
- 名古屋文理大学紀要 15, 45-53, 2015-03-31
- NAID 110009921522
- 濃厚な家族歴を有し，稀な胆管拡張形態を呈した膵・胆管合流異常の1例
- 日本小児外科学会雑誌 51(7), 1186-1189, 2015
- NAID 130005114218
- Contribution of Cardiac Sodium Channel β-Subunit Variants to Brugada Syndrome
- Circulation Journal 79(10), 2118-2129, 2015
- NAID 130005099851
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- in·her·it·a·ble (ĭn-hĕr′ĭ-tə-bəl) adj. 1. Capable of being inherited: inheritable traits; inheritable property. 2. Having the right to inherit or the capability of inheriting: an inheritable heir. in·her′it·a·bil′i·ty n. inheritable (ɪnˈhɛrɪtəbəl) adj 1. ...
- inheritableとは。意味や和訳。[形]1 〈財産・権利・称号が〉相続可能な，世襲的な；〈体質・性質が〉遺伝する.2 相続権を有する.in・hèr・it・a・bíl・i・ty[名] in・her・it・a・ble・ly[副] - goo英和辞書は14万項目以上を収録し、発音、音声 ...
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★リンクテーブル★
| リンク元 | 「hereditary」「heritable」「遺伝性」「inherited」 |
| 拡張検索 | 「inheritable character」 |
「hereditary」
- adj.
- 遺伝性の、遺伝の
「heritable」
- 遺伝性の、遺伝的な
「遺伝性」
「inherited」
- 遺伝性の