WordNet
- aware or knowing; "a witting tool of the Communists"
- with full knowledge and deliberation; "he wittingly deleted the references" (同)knowingly
- not aware or knowing; "an unwitting subject in an experiment"
- without knowledge or intention; "he unwittingly deleted the references" (同)inadvertently, unknowingly
PrepTutorEJDIC
- (行為などが)意識して行われた,故意の
- 承知で,わざと
- 知らず知らずの,無意識の
Wikipedia preview
出典(authority):フリー百科事典『ウィキペディア(Wikipedia)』「2016/04/26 13:31:18」(JST)
[Wiki en表示]
Witting is a popular Germanic surname.
Etymology
"Witting" is thought to be a patronymic surname, derive the Old English personal name Hwit, meaning "the white one".[1]
Notable people
- Alexander Witting (1861–1946), German mathematician
- Amy Witting (1918–2001), Australian novelist and poet
- Richard Witting (1856–1923), Prussian politician and financier
- Rolf Witting (1879–1944), Minister of Foreign Affairs (Finland) 1940–1943
References
- ^ "Witting Family Crest and History". House of Names.
English Journal
- Ultrahigh resolution mass spectrometry-based metabolic characterization reveals cerebellum as a disturbed region in two animal models.
- Lin S, Kanawati B, Liu L, Witting M, Li M, Huang J, Schmitt-Kopplin P, Cai Z.Author information Department of Chemistry, Hong Kong Baptist University, Hong Kong SAR, China.AbstractIn the previous reports about cognitive dysfunction, cerebellum was thought to be a less affected tissue by genetic or environmental alterations in comparison to other tissues in the brain including hippocampus under the same conditions. In this work, we investigated two types of metabolomic alterations inside the cerebellum tissue. The first one addressed the differences in the metabolomics profiles between Transgenic (Tg) CRND8 of Alzheimer's disease mice and non-transgenic (non-Tg) littermates. The second one addressed the metabolic differences between wild type mice exposed to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) and wild type mice which are not exposed to this toxic compound. For these two investigations, ultrahigh resolution Fourier transform ion cyclotron resonance mass spectrometry (FT-ICR/MS) was implemented. As a result, the significant changes of each comparison were tentatively annotated by the high mass accuracy generated from the measurements in the negative ion mode. The biosynthesis of amino acids was also enhanced pronouncedly, and perturbation of purine metabolism was also observed in Tg mice compared to non-Tg littermates. In another animal model, the reduced levels of amino acids were found whereas the intermediate levels in purine metabolism and fatty acids including fatty acid conjugated metabolites were elevated in cerebellar tissues of mice exposed to TCDD compared to control group. Collectively, it was demonstrated that FT-ICR/MS was a powerful tool for interpretation of the elemental compositions of the peaks, revealing that the metabolic perturbations in cerebellar tissues of mice were induced by either genetic manipulation or environmental factor. Therefore, the non-targeted approach, alternatively, provides various metabolic phenotypes for the systems-level mirror of the complex etiology of neurotoxicity in the cerebellum.
- Talanta.Talanta.2014 Jan 15;118:45-53. doi: 10.1016/j.talanta.2013.09.019. Epub 2013 Oct 5.
- In the previous reports about cognitive dysfunction, cerebellum was thought to be a less affected tissue by genetic or environmental alterations in comparison to other tissues in the brain including hippocampus under the same conditions. In this work, we investigated two types of metabolomic alterat
- PMID 24274269
- The smoking-associated oxidant hypothiocyanous acid induces endothelial nitric oxide synthase dysfunction.
- Talib J, Kwan J, Suryo Rahmanto A, Witting PK, Davies MJ.Author information ‡Discipline of Pathology, School of Medical Sciences, University of Sydney, Sydney, NSW 2006, Australia.AbstractSmokers have an elevated risk of cardiovascular disease but the origin(s) of this increased risk are incompletely defined. Considerable evidence supports an accumulation of the oxidant-generating enzyme MPO (myeloperoxidase) in the inflamed artery wall, and smokers have high levels of SCN-, a preferred MPO substrate, with this resulting in HOSCN (hypothiocyanous acid) formation. We hypothesized that this thiol-specific oxidant may target the Zn2+-thiol cluster of eNOS (endothelial nitric oxide synthase), resulting in enzyme dysfunction and reduced formation of the critical signalling molecule NO•. Decreased NO• bioavailability is an early and critical event in atherogenesis, and HOSCN-mediated damage to eNOS may contribute to smoking-associated disease. In the present study it is shown that exposure of isolated eNOS to HOSCN or MPO/H2O2/SCN- decreased active dimeric eNOS levels, and increased inactive monomer and Zn2+ release, compared with controls, HOCl (hypochlorous acid)- or MPO/H2O2/Cl--treated samples. eNOS activity was increasingly compromised by MPO/H2O2/Cl- with increasing SCN- concentrations. Exposure of HCAEC (human coronary artery endothelial cell) lysates to pre-formed HOSCN, or MPO/H2O2/Cl- with increasing SCN-, increased eNOS monomerization and Zn2+ release, and decreased activity. Intact HCAECs exposed to HOCl and HOSCN had decreased eNOS activity and NO2-/NO3- formation (products of NO• decomposition), and increased free Zn2+. Exposure of isolated rat aortic rings to HOSCN resulted in thiol loss, and decreased eNOS activity and cGMP levels. Overall these data indicate that high SCN- levels, as seen in smokers, can increase HOSCN formation and enhance eNOS dysfunction in human endothelial cells, with this potentially contributing to increased atherogenesis in smokers.
- The Biochemical journal.Biochem J.2014 Jan 1;457(1):89-97. doi: 10.1042/BJ20131135.
- Smokers have an elevated risk of cardiovascular disease but the origin(s) of this increased risk are incompletely defined. Considerable evidence supports an accumulation of the oxidant-generating enzyme MPO (myeloperoxidase) in the inflamed artery wall, and smokers have high levels of SCN-, a prefer
- PMID 24112082
- Phenotype of htgA (mbiA), a recently evolved orphan gene of Escherichia coli and Shigella, completely overlapping in antisense to yaaW.
- Fellner L, Bechtel N, Witting MA, Simon S, Schmitt-Kopplin P, Keim D, Scherer S, Neuhaus K.Author information Lehrstuhl für Mikrobielle Ökologie, Wissenschaftszentrum Weihenstephan, Technische Universität München, Freising, Germany.AbstractOverlapping embedded genes, such as htgA/yaaW, are assumed to be rare in prokaryotes. In Escherichia coli O157:H7, gfp fusions of both promoter regions revealed activity and transcription start sites could be determined for both genes. Both htgA and yaaW were inactivated strand specifically by introducing a stop codon. Both mutants exhibited differential phenotypes in biofilm formation and metabolite levels in a nontargeted analysis, suggesting that both are functional despite YaaW but not HtgA could be expressed. While yaaW is distributed all over the Gammaproteobacteria, an overlapping htgA-like sequence is restricted to the Escherichia-Klebsiella clade. Full-length htgA is only present in Escherichia and Shigella, and htgA showed evidence for purifying selection. Thus, htgA is an interesting case of a lineage-specific, nonessential and young orphan gene.
- FEMS microbiology letters.FEMS Microbiol Lett.2014 Jan;350(1):57-64. doi: 10.1111/1574-6968.12288. Epub 2013 Oct 17.
- Overlapping embedded genes, such as htgA/yaaW, are assumed to be rare in prokaryotes. In Escherichia coli O157:H7, gfp fusions of both promoter regions revealed activity and transcription start sites could be determined for both genes. Both htgA and yaaW were inactivated strand specifically by intro
- PMID 24111745
Japanese Journal
- Selection-delayed population dynamics in baleen whales and beyond
- Selection-delayed population dynamics in baleen whales and beyond
- <1,2>-WITTING REARRANGEMENT OF AROMATIC HETEROCYCLES
- Yang Jingyue,Wangweerawong Apiwat,Dudley Gregory B.
- Heterocycles : an international journal for reviews and communications in heterocyclic chemistry 85(7), 1603-1606, 2012-07-01
- NAID 40019365150
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