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retinol
ريتينُول
Ultimo aggiornamento 2018-05-23
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retinol binding protein
بروتين رابط للرّيِتينول
Ultimo aggiornamento 2022-10-19
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retinol-binding protein
بروتين ٌ رابط للرّيِتينول
Ultimo aggiornamento 1970-01-01
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retinol is one of the animal forms of vitamin a.
الريتينول هو أحد الأشكال الحيوانية لفيتامين a .
Ultimo aggiornamento 2016-03-03
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c/ unit of vitamin a is re (retinol equivalents).
(ج) وحدة فيتامين ألف هي المكافئ من (الريتينول).
Ultimo aggiornamento 2016-12-01
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ttr is a serum and cerebrospinal fluid carrier of t4 and retinol.
والترانزثايريتين هو مصل وسائل نخاعي شوكي يعمل كناقل لهرمون الثيروكسين وفيتامين الرتنول.
Ultimo aggiornamento 2016-12-01
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fractional excretion of sodium (fena), retinol-binding protein
الإفراغ الجزئي للصوديوم (fena)، والـ retinol-binding protein.
Ultimo aggiornamento 2013-07-02
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fractional excretion of sodium (fe na ), retinol-binding protein
الإفراغ الجزئي للصوديوم ( fe na )، والـ retinol-binding protein .
Ultimo aggiornamento 2013-07-03
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vitamin-a deficiency - low retinol levels in blood (percentages)
نقص فيتامين ألف - مستويات الشبكية المنخفضة في الدم (نسب مئوية)
Ultimo aggiornamento 2016-12-01
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vitamin a, 50, 000iu, capsule/tablet, oral, water missible, retinol
فيتامين أ، ٥٠، ٠٠٠وحدة دولية، كبسولة/قرص، عن طريق الفم ، ممتزج بالماء، ريتانول
Ultimo aggiornamento 2019-08-06
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palmitate is attached to the alcohol form of vitamin a, retinol, to make vitamin a stable in milk.
توصل البالميتات إلى الشكل الكحولي للفيتامين ألف، ("retinol")، وذلك لجعل فيتامين ألف مستقرًا في الحليب.
Ultimo aggiornamento 2016-03-03
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Attenzione: contiene formattazione HTML nascosta
reduced fitness of offspring in birds as well as reduced retinol concentrations in polar bears is associated with beta-hch and hchs levels.
ويرتبط انخفاض لياقة النسل لدى الطيور وكذلك انخفاض تركيزات الريتينول (فيتامين أ) لدى الدببة القطبية بمستويات بيتا - hch، وايسومرات hch.
Ultimo aggiornamento 2016-12-02
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monitoring data on effects in svalbard polar bears revealed a significant negative correlation between retinol and hchs (amap, 2004).
وقد كشفت بيانات الرصد على التأثيرات في دببة سفالبارد القطبية عن وجود ترابط سلبي مهم بين الريتينول وبوليمرات سداسي كلور حلقي الهكسان (amap، 2004).
Ultimo aggiornamento 2016-12-02
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retinol is essential as it is required in reproduction, embryonic and foetal development, as well as in vision, growth, differentiation and tissue maintenance.
والريتينول ضروري حيث أنه لازم للتكاثر، ولنمو الأجنة غير المُخَلَقة والمُخَلقَة وكذلك من حيث الإبصار والنمو وتنوع الأنسجة والمحافظة عليها.
Ultimo aggiornamento 2016-12-02
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monitoring data on effects in svalbard polar bears revealed that there is a significant negative correlation between retinol and hchs (amap, 2004).
وقد كشفت بيانات الرصد على التأثيرات في دببة سفالبارد القطبية عن وجود ترابط سلبي مهم بين الريتينول وبوليمرات hch (amap، 2004).
Ultimo aggiornamento 2016-12-02
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39. since 1998, the ministry of health has pursued a strategy of distributing vitamin a capsules to target groups, in order to limit or reduce the prevalence of serum retinol deficiency.
39- ما تزال وزارة الصحة منذ 1998 تتبع استراتيجية خاصة للحد أو لإنقاص نسبة انتشار نقص ريتينول المصل بتوزيع كبسولات الفيتامين a للفئات المستهدفة وهي:
Ultimo aggiornamento 2016-12-01
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monitoring data on arctic polar bears revealed a negative correlation with retinol concentrations and hchs, which may impact a wide range of biological functions (amap, 2004).
وكشفت بيانات الرصد عن الدببة القطبية الشمالية ترابطاً سلبياً مع تركّزات الرتينول وأيزومرات (hch)، مما قد يؤثّر في طائفة واسعة من الوظائف الأحيائية (البيولوجية) (amap, 2004).
Ultimo aggiornamento 2016-12-02
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leukodepletion on pump using leukocyte-reducing filters may attenuate glomerular and tubular injury.this has been shown to lower the levels of microalbumin and retinol-binding protein indexed to creatinine. 72
قد يُساعد استعمال فلتر الكريات البيض أثناء التروية خارج الجسم على التخفيف من أذيّة الكُبب والأنابيب الكلوية.
Ultimo aggiornamento 2013-08-17
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besity-associated insulin resistance, with consideration of their role in an integrated physiological framework. finally, increasing recognition of the integrated nature of metabolic physiology has sparked investigation of mecha- nisms of insulin resistance that involve crosstalk between insulin-responsive tissues. inflammatory signaling has emerged as a key paracrine/endocrine driver of insulin re- sistance; for example, activated adipose tissue macrophages have been strongly linked to metabolic dysfunction (331, 446, 594). the mechanisms by which inflammation pro- motes insulin resistance are under intense investigation. ad- ditionally, the last two decades have yielded the identifica- tion of dozens of endogenous circulating bioactive peptide hormones with putative effects on insulin sensitivity and have also revealed that circulating branched-chain amino acids may be a predictive biomarker of insulin resistance (577). rather than providing a catalog entry for each of these circulating factors, section vii focuses on those with established mechanistic links to cellular mechanisms of in- sulin action and resistance: retinol binding protein-4 (rbp4), adiponectin, fetuin-a, and fibroblast growth factor 21 (fgf21). in offering this review, we hope that our comprehensive treatment of both insulin action and inaction presents a unified framework for understanding the physiology of this critically important signaling axis in health and disease and that it provides context for future discoveries that will fa- cilitate the prevention and treatment of t2d. we attempt to develop such a unified summary in section viii. ii. direct insulin action a. proximal insulin signaling: the insulin receptor and its direct substrates insulin exerts all of its known physiological effects by bind- ing to the insulin receptor (insr) on the plasma membrane of target cells (297). insr is a heterotetrameric receptor tyrosine kinase formed from two extracellular subunits, which bind insulin, and two membrane-spanning - sub- units, each of which contains a tyrosine kinase domain (343). there are two insr isoforms, a and b, but the b isoform is much more specific for insulin; is the primary isoform expressed in differentiated liver, muscle, and wat; and is thus thought to mediate most metabolic effects of insulin (44). the a isoform, differentiated by the splicing out of exon 11, is expressed highly in fetal development, when its high affinity for igf-2 is particularly useful (44). insr has two insulin binding sites but exhibits negative cooperativity, meaning that insulin binding at one site de- creases insulin binding affinity in the other site (186). thus available evidence indicates that at physiological concentra- tions, one insulin molecule binds and activates one insr (186, 343). the induced conformational change in the - subunit relieves cis-autoinhibition in the kinase activation loop and permits trans-autophosphorylation of the activa- tion loop tyrosines tyr1162, tyr1158, and tyr1163, in that order (344, 889). the - subunit, thus activated by tris- phosphorylation, undergoes further tyrosine phosphoryla- tion on residues including tyr972 in the juxtamembrane region; these additional events are important for recruit- ment of insr substrates (941). signaling events down- stream of insr activation can be grossly functionally di- vided into mitogenic and metabolic signals. the mitogenic signals primarily involve activation of the mitogen-acti- vated protein kinase (mapk) pathway common to many receptor tyrosine kinases; this signaling axis has been re- viewed extensively (41, 400, 535, 616). the insulin concen- trations necessary to stimulate metabolic responses are lower than those needed for mitogenic responses; this rela- tionship is reversed for the igf-1 receptor (41). this review focuses on the insr-activated pathways that regulate me- tabolism. in all cell types, activated insr initiates downstream met- abolic signaling by first recruiting phosphotyrosine-binding scaffold proteins, which in turn activate downstream effec- tors (figure 1) (826). this is in contrast to many other receptor tyrosine kinases, which phosphorylate cytoplasmic substrates directly. the recruitment of diverse phosphoty- rosine-binding proteins to insr permits early ramification of insulin signaling to activate multiple functional modules. insr can engage several phosphotyrosine-binding pro- teins. shc interacts through its phosphotyrosine-binding (ptb) domain with insr ptyr972 (343). sh2b1, sh2b2/ aps, grb10, and grb14 interact through their src homol- ogy 2 (sh2) domains with the activated, tris-phosphory- lated insr activation loop (190, 343). these substrates can serve critical regulatory functions (190, 343). for example, grb10 phosphorylation and stabilization by mtorc1, which is itself activated by insulin signaling, provides feed- back inhibition of insr activity (339). other insr sub- strates, such as grb2 and shc, are involved in the mito- genic arm of insulin signaling (41), while sh2b2/aps helps to initiate the metabolic insulin response, at least in some cell types (471). attenuation of this proximal phosphoty- rosine-based insulin signaling is carried out in part by re- ceptor internalization and dephosphorylation. one key reg- ulator of insr internalization is ceacam1, which is itself an insr substrate (568, 660). insr dephosphorylation is performed by protein tyrosine phosphatases (ptpases), es- pecially ptp1b. however, this attenuation likely occurs with a time delay, after insr internalization (808). imme- diately after activation, insr inhibits ptp1b activity by activating nad(p)h oxidase 4 (nox4). nox4-derived h2o2 in turn inhibits ptp1b activity, providing feedfor- ward amplification in the early phase of insulin signaling (515, 921).
Ultimo aggiornamento 2021-04-14
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