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Book ; Thesis: Stabilisation endodontisch behandelter Oberkieferprämolaren durch Insertion von Cerec-Inlays in vitro

Westphal, Christoph

2005

Author's details	vorgelegt von Christoph Westphal
Language	German
Size	69 Bl., Ill., graph. Darst.
Edition	[Mikrofiche-Ausg.]
Publishing country	Germany
Document type	Book ; Thesis
Thesis / German Habilitation thesis	Göttingen, Univ., Diss., 2005
HBZ-ID	HT014887414
Database	Catalogue ZB MED Medicine, Health

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Book ; Audio / Video ; Thesis: Ein Beitrag zur semantischen Modellierung und Analyse von Informationsflüssen in der Produkteigenschaftsabsicherung

Westphal, Christoph

(Fortschritt-Berichte VDI : Reihe 1, Konstruktionstechnik, Maschinenelemente ; 425)

2014

Title variant	Modellierung der Produktabsicherung
Author's details	Christoph Westphal
Series title	Fortschritt-Berichte VDI : Reihe 1, Konstruktionstechnik, Maschinenelemente ; 425
Keywords	Semantisches Netz ; Kraftfahrzeugbau ; Produktentwicklung ; Produkteigenschaft ; Engineering Data Management
Language	German
Size	XI, 164 S., Ill., graph. Darst.
Edition	Als Ms. gedr.
Publisher	VDI-Verl
Publishing place	Düsseldorf
Document type	Book ; Audio / Video ; Thesis
Thesis / German Habilitation thesis	Univ., Diss.--Erlangen-Nürnberg, 2013
ISBN	9783183425013 ; 3183425017
Database	Library catalogue of the German National Library of Science and Technology (TIB), Hannover

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Article ; Online: Combining a High Dose of Metformin With the SIRT1 Activator, SRT1720, Reduces Life Span in Aged Mice Fed a High-Fat Diet.

Palliyaguru, Dushani L / Minor, Robin K / Mitchell, Sarah J / Palacios, Hector H / Licata, Jordan J / Ward, Theresa M / Abulwerdi, Gelareh / Elliott, Peter / Westphal, Christoph / Ellis, James L / Sinclair, David A / Price, Nathan L / Bernier, Michel / de Cabo, Rafael

The journals of gerontology. Series A, Biological sciences and medical sciences

2020 Volume 75, Issue 11, Page(s) 2037–2041

Abstract: SRT1720, a sirtuin1-activator, and metformin (MET), an antidiabetic drug, confer health and life-span benefits when administered individually. It is unclear whether combination of the two compounds could lead to additional benefits. Groups of 56-week-old ...

Abstract	SRT1720, a sirtuin1-activator, and metformin (MET), an antidiabetic drug, confer health and life-span benefits when administered individually. It is unclear whether combination of the two compounds could lead to additional benefits. Groups of 56-week-old C57BL/6J male mice were fed a high-fat diet (HFD) alone or supplemented with either SRT1720 (2 g/kg food), a high dose of MET (1% wt/wt food), or a combination of both. Animals were monitored for survival, body weight, food consumption, body composition, and rotarod performance. Mice treated with MET alone did not have improved longevity, and life span was dramatically reduced by combination of MET with SRT1720. Although all groups of animals were consuming similar amounts of food, mice on MET or MET + SRT1720 showed a sharp reduction in body weight. SRT1720 + MET mice also had lower percent body fat combined with better performance on the rotarod compared to controls. These data suggest that co-treatment of SRT1720 with MET is detrimental to survival at the doses used and, therefore, risk-benefits of combining life-span-extending drugs especially in older populations needs to be systematically evaluated.
MeSH term(s)	Animals ; Body Composition ; Body Weight ; Diet, High-Fat ; Heterocyclic Compounds, 4 or More Rings/administration & dosage ; Heterocyclic Compounds, 4 or More Rings/pharmacology ; Longevity/drug effects ; Male ; Metformin/administration & dosage ; Metformin/pharmacology ; Mice ; Mice, Inbred C57BL ; Models, Animal ; Sirtuin 1
Chemical Substances	Heterocyclic Compounds, 4 or More Rings ; SRT1720 ; Metformin (9100L32L2N) ; Sirt1 protein, mouse (EC 3.5.1.-) ; Sirtuin 1 (EC 3.5.1.-)
Language	English
Publishing date	2020-06-16
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Intramural ; Research Support, Non-U.S. Gov't
ZDB-ID	1223643-3
ISSN	1758-535X ; 1079-5006
ISSN (online)	1758-535X
ISSN	1079-5006
DOI	10.1093/gerona/glaa148
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Article: Fracture resistance of endodontically treated maxillary premolars restored with CAD/CAM ceramic inlays.

Hannig, Christian / Westphal, Christoph / Becker, Klaus / Attin, Thomas

The Journal of prosthetic dentistry

2005 Volume 94, Issue 4, Page(s) 342–349

Abstract: Statement of problem: Endodontically treated posterior teeth are more likely to fracture compared to posterior teeth with vital pulps. Reinforcement with an extracoronal restoration that covers the cusps is the most commonly recommended method for ... ...

Abstract	Statement of problem: Endodontically treated posterior teeth are more likely to fracture compared to posterior teeth with vital pulps. Reinforcement with an extracoronal restoration that covers the cusps is the most commonly recommended method for reducing the risk of fracture. It is not known whether bonded intracoronal restorations without cuspal coverage will reduce the risk of fracture. Purpose: The aim of this in vitro study was to investigate whether reinforcement of endodontically treated premolars with MOD preparations could be achieved by insertion of bonded CAD/CAM ceramic inlays. Material and methods: Forty-five extracted maxillary premolars were equally distributed among 3 groups (END, CER, CTR). In group END (n=15), root canals were enlarged with a rotary NiTi system and obturated with heat-softened gutta-percha around a plastic carrier (Thermafil). After filling of the endodontic access cavities with autopolymerizing composite resin (Luxacore), standardized MOD cavity preparations were made and CAD/CAM ceramic inlays (CEREC) were fabricated and then bonded to the teeth with composite resin (Tetric) and an adhesive system (Syntac Classic). In group CER (n=15), teeth without endodontic treatment were restored with bonded inlays (CEREC). Sound premolars served as controls (group CTR, n=15). Teeth were then thermal cycled (1445 cycles, dwell time: 30 seconds, 5 degrees /55 degrees C). An eccentric load was applied on the buccal incline of the palatal cusp in a universal testing machine until cusp fracture (N). Fracture load was evaluated with the Mann-Whitney test, and type of fracture, with a chi-square analysis (alpha=.05). The type of fracture was determined by visual inspection: type I - supragingival fracture within the palatal cusp; type II - fracture below cemento-enamel junction of palatal cusp; and type III - fracture of palatal cusp and central portion of the tooth exposing the root canal cavity. Results: No significant difference was found among the 3 groups with respect to load required for fracture. Mean fracture load +/- SD was recorded as follows: 291.6 +/- 113.7 N for group END, 363.2 +/- 140.3 N for group CER, and 296.5 +/- 170.5 N for group CTR. Regarding fracture modes, significantly more teeth from group END exhibited fractures of type III and II compared with control specimens. Conclusion: Teeth restored with bonded CAD/CAM ceramic inlays (CEREC) fractured with a significantly higher number of severe fractures compared to the control group.
MeSH term(s)	Bicuspid/physiopathology ; Ceramics/chemistry ; Composite Resins/chemistry ; Computer-Aided Design ; Dental Bonding ; Dental Cavity Preparation/methods ; Dental Enamel/injuries ; Dental Porcelain/chemistry ; Dental Stress Analysis ; Dentin-Bonding Agents/chemistry ; Gutta-Percha/chemistry ; Humans ; Inlays ; Resin Cements/chemistry ; Root Canal Preparation/instrumentation ; Root Canal Therapy ; Stress, Mechanical ; Tooth Cervix/injuries ; Tooth Crown/injuries ; Tooth Fractures/physiopathology ; Tooth, Nonvital/physiopathology
Chemical Substances	Composite Resins ; Dentin-Bonding Agents ; Resin Cements ; Dental Porcelain (12001-21-7) ; Gutta-Percha (9000-32-2)
Language	English
Publishing date	2005-10
Publishing country	United States
Document type	Comparative Study ; Journal Article
ZDB-ID	218157-5
ISSN	1097-6841 ; 0022-3913
ISSN (online)	1097-6841
ISSN	0022-3913
DOI	10.1016/j.prosdent.2005.08.004
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Article ; Online: Pharmacokinetics and tolerability of SRT2104, a first-in-class small molecule activator of SIRT1, after single and repeated oral administration in man.

Hoffmann, Ethan / Wald, Jeff / Lavu, Siva / Roberts, John / Beaumont, Claire / Haddad, Jon / Elliott, Peter / Westphal, Christoph / Jacobson, Eric

British journal of clinical pharmacology

2012 Volume 75, Issue 1, Page(s) 186–196

Abstract: Aim: SRT2104 is a novel, first-in-class, highly selective small molecule activator of the NAD + dependent deacetylase SIRT1. SRT2104 was dosed to healthy male and female volunteers in a series of phase 1 clinical studies that were designed to elucidate ... ...

Abstract	Aim: SRT2104 is a novel, first-in-class, highly selective small molecule activator of the NAD + dependent deacetylase SIRT1. SRT2104 was dosed to healthy male and female volunteers in a series of phase 1 clinical studies that were designed to elucidate tolerability and pharmacokinetics associated with oral dosing to aid in dose selection for subsequent clinical trials. Methods: In the first-in-human study, there was both a single dose phase and 7 day repeat dose phase. Doses used ranged from 0.03 to 3.0 g. A radioactive microtracer study was subsequently conducted to determine systemic clearance, bioavailability and preliminary metabolism, and a crossover study was conducted to determine the effect of gender, formulation and feeding state on SRT2104 pharmacokinetics. Results: SRT2104 was well tolerated in all of these studies, with no serious adverse reactions observed. SRT2104 displayed a dose-dependent, but sub-proportional increase in exposure following single dose and repeated dose administration. Accumulation of three-fold or less occurs after 7 days of repeat dosing. The mean bioavailability was circa 14% and the mean clearance was circa 400 ml min(-1). Although there were no substantial effects on exposure resulting from gender or formulation differences, a notable food effect was observed, manifested as up to four-fold increase in exposure parameters. Conclusions: In the absence of an optimized formulation of SRT2104, the food effect can be used to maximize exposure in future clinical studies. Combined with the good tolerability of all doses demonstrated in these studies, the favourable selectivity profile of SRT2104 allows for the use of this SIRT1 modulator for target validation in the clinic.
MeSH term(s)	Biological Availability ; Dose-Response Relationship, Drug ; Double-Blind Method ; Enzyme Activation ; Female ; Humans ; Imidazoles/administration & dosage ; Imidazoles/adverse effects ; Imidazoles/pharmacokinetics ; Male ; Sirtuin 1/drug effects ; Thiazoles/administration & dosage ; Thiazoles/adverse effects ; Thiazoles/pharmacokinetics
Chemical Substances	Imidazoles ; Thiazoles ; SIRT1 protein, human (EC 3.5.1.-) ; Sirtuin 1 (EC 3.5.1.-)
Language	English
Publishing date	2012-05-22
Publishing country	England
Document type	Clinical Trial, Phase I ; Journal Article ; Randomized Controlled Trial
ZDB-ID	188974-6
ISSN	1365-2125 ; 0306-5251 ; 0264-3774
ISSN (online)	1365-2125
ISSN	0306-5251 ; 0264-3774
DOI	10.1111/j.1365-2125.2012.04340.x
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Article: Ataxia telangiectasia mutated expression and activation in the testis.

Hamer, Geert / Kal, Henk B / Westphal, Christoph H / Ashley, Terry / de Rooij, Dirk G

Biology of reproduction

2004 Volume 70, Issue 4, Page(s) 1206–1212

Abstract: Ionizing radiation (IR) and consequent induction of DNA double-strand breaks (DSBs) causes activation of the protein ataxia telangiectasia mutated (ATM). Normally, ATM is present as inactive dimers; however, in response to DSBs, the ATM dimer partners ... ...

Abstract	Ionizing radiation (IR) and consequent induction of DNA double-strand breaks (DSBs) causes activation of the protein ataxia telangiectasia mutated (ATM). Normally, ATM is present as inactive dimers; however, in response to DSBs, the ATM dimer partners cross-phosphorylate each other on serine 1981, and kinase active ATM monomers are subsequently released. We have studied the presence of both nonphosphorylated as well as active serine 1981 phosphorylated ATM (pS1981-ATM) in the mouse testis. In the nonirradiated testis, ATM was present in spermatogonia and spermatocytes until stage VII of the cycle of the seminiferous epithelium, whereas pS1981-ATM was found only to be present in the sex body of pachytene spermatocytes. In response to IR, ATM became activated by pS1981 cross-phosphorylation in spermatogonia and Sertoli cells. Despite the occurrence of endogenous programmed DSBs during the first meiotic prophase and the presence of ATM in both spermatogonia and spermatocytes, pS1981 phosphorylated ATM did not appear in spermatocytes after treatment with IR. These results show that spermatogonial ATM and ATM in the spermatocytes are differentially regulated. In the mitotically dividing spermatogonia, ATM is activated by cross-phosphorylation, whereas during meiosis nonphosphorylated ATM or differently phosphorylated ATM is already active. ATM has been shown to be present at the synapsed axes of the meiotic chromosomes, and in the ATM knock-out mice spermatogenesis stops at pachytene stage IV of the seminiferous epithelium, indicating that indeed nonphosphorylated ATM is functional during meiosis. Additionally, ATM is constitutively phosphorylated in the sex body where its continued presence remains an enigma.
MeSH term(s)	Animals ; Apoptosis ; Ataxia Telangiectasia Mutated Proteins ; Cell Cycle Proteins ; DNA-Binding Proteins ; Male ; Meiosis ; Mice ; Mice, Inbred Strains ; Mice, Knockout ; Phosphorylation ; Prophase ; Protein-Serine-Threonine Kinases/metabolism ; Protein-Serine-Threonine Kinases/physiology ; Spermatocytes/physiology ; Spermatogonia/physiology ; Testis/metabolism ; Testis/radiation effects ; Tissue Distribution ; Tumor Suppressor Proteins
Chemical Substances	Cell Cycle Proteins ; DNA-Binding Proteins ; Tumor Suppressor Proteins ; Ataxia Telangiectasia Mutated Proteins (EC 2.7.11.1) ; Atm protein, mouse (EC 2.7.11.1) ; Protein-Serine-Threonine Kinases (EC 2.7.11.1)
Language	English
Publishing date	2004-04
Publishing country	United States
Document type	Journal Article ; Research Support, U.S. Gov't, P.H.S.
ZDB-ID	1118-6
ISSN	1529-7268 ; 0006-3363
ISSN (online)	1529-7268
ISSN	0006-3363
DOI	10.1095/biolreprod.103.024950
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Article: Keeping it real with investors.

Dipp, Michelle / Westphal, Christoph / Mirkin, Chad / Baker, James / Harper, Tim / Harris, Charles

Nature biotechnology

2003 Volume 24, Issue 2, Page(s) 133–135

MeSH term(s)	Biotechnology/economics ; Capital Financing/economics ; Entrepreneurship/economics ; Industry/economics ; Investments/economics ; Marketing/economics ; Nanotechnology/economics ; Ownership/economics ; United States
Language	English
Publishing date	2003-02-24
Publishing country	United States
Document type	Journal Article
ZDB-ID	1311932-1
ISSN	1546-1696 ; 1087-0156
ISSN (online)	1546-1696
ISSN	1087-0156
DOI	10.1038/bioent899
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Article ; Online: Sirt1 inhibition promotes in vivo arterial thrombosis and tissue factor expression in stimulated cells.

Breitenstein, Alexander / Stein, Sokrates / Holy, Erik W / Camici, Giovanni G / Lohmann, Christine / Akhmedov, Alexander / Spescha, Remo / Elliott, Peter J / Westphal, Christoph H / Matter, Christian M / Lüscher, Thomas F / Tanner, Felix C

Cardiovascular research

2011 Volume 89, Issue 2, Page(s) 464–472

Abstract: Aims: The mammalian silent information regulator-two 1 (Sirt1) blunts the noxious effects of cardiovascular risk factors such as type 2 diabetes mellitus and obesity. Nevertheless, the role of Sirt1 in regulating the expression of tissue factor (TF), ... ...

Abstract	Aims: The mammalian silent information regulator-two 1 (Sirt1) blunts the noxious effects of cardiovascular risk factors such as type 2 diabetes mellitus and obesity. Nevertheless, the role of Sirt1 in regulating the expression of tissue factor (TF), the key trigger of coagulation, and arterial thrombus formation remains unknown. Methods and results: Human as well as mouse cell lines were used for in vitro experiments, and C57Bl/6 mice for in vivo procedures. Sirt1 inhibition by splitomicin or sirtinol enhanced cytokine-induced endothelial TF protein expression as well as surface activity, while TF pathway inhibitor protein expression did not change. Sirt1 inhibition further enhanced TF mRNA expression, TF promoter activity, and nuclear translocation as well as DNA binding of the p65 subunit of nuclear factor-kappa B (NFκB/p65). Sirt1 siRNA enhanced TF protein and mRNA expression, and this effect was reduced in NFκB/p65(-/-) mouse embryonic fibroblasts reconstituted with non-acetylatable Lys(310)-mutant NFκB/p65. Activation of the mitogen-activated protein kinases p38, c-Jun NH(2)-terminal kinase, and p44/42 (ERK) remained unaffected. In vivo, mice treated with the Sirt1 inhibitor splitomicin exhibited enhanced TF activity in the arterial vessel wall and accelerated carotid artery thrombus formation in a photochemical injury model. Conclusion: We provide pharmacological and genetic evidence that Sirt1 inhibition enhances TF expression and activity by increasing NFκB/p65 activation in human endothelial cells. Furthermore, Sirt1 inhibition induces arterial thrombus formation in vivo. Hence, modulation of Sirt1 may offer novel therapeutic options for targeting thrombosis.
MeSH term(s)	Animals ; Benzamides/pharmacology ; Binding Sites ; Cells, Cultured ; Disease Models, Animal ; Dose-Response Relationship, Drug ; Endothelial Cells/drug effects ; Endothelial Cells/enzymology ; Enzyme Activators ; Genes, Reporter ; Histone Deacetylase Inhibitors/pharmacology ; Humans ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Mitogen-Activated Protein Kinases/metabolism ; Naphthalenes/pharmacology ; Naphthols/pharmacology ; Promoter Regions, Genetic ; Pyrones/pharmacology ; RNA Interference ; RNA, Messenger/metabolism ; Sirtuin 1/antagonists & inhibitors ; Sirtuin 1/deficiency ; Sirtuin 1/genetics ; Sirtuin 1/metabolism ; Stilbenes/pharmacology ; Thromboplastin/genetics ; Thromboplastin/metabolism ; Thrombosis/blood ; Thrombosis/enzymology ; Thrombosis/etiology ; Thrombosis/genetics ; Transcription Factor RelA/deficiency ; Transcription Factor RelA/genetics ; Transcription Factor RelA/metabolism ; Transfection
Chemical Substances	Benzamides ; Enzyme Activators ; Histone Deacetylase Inhibitors ; Naphthalenes ; Naphthols ; Pyrones ; RELA protein, human ; RNA, Messenger ; Rela protein, mouse ; Stilbenes ; Transcription Factor RelA ; sirtinol ; splitomicin (4707-36-2) ; Thromboplastin (9035-58-9) ; Mitogen-Activated Protein Kinases (EC 2.7.11.24) ; SIRT1 protein, human (EC 3.5.1.-) ; Sirt1 protein, mouse (EC 3.5.1.-) ; Sirtuin 1 (EC 3.5.1.-) ; resveratrol (Q369O8926L)
Language	English
Publishing date	2011-02-01
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	80340-6
ISSN	1755-3245 ; 0008-6363
ISSN (online)	1755-3245
ISSN	0008-6363
DOI	10.1093/cvr/cvq339
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Article ; Online: SIRT1 mRNA expression may be associated with energy expenditure and insulin sensitivity.

Rutanen, Jarno / Yaluri, Nagendra / Modi, Shalem / Pihlajamäki, Jussi / Vänttinen, Markku / Itkonen, Paula / Kainulainen, Sakari / Yamamoto, Hiroyasu / Lagouge, Marie / Sinclair, David A / Elliott, Peter / Westphal, Christoph / Auwerx, Johan / Laakso, Markku

Diabetes

2010 Volume 59, Issue 4, Page(s) 829–835

Abstract: Objective: Sirtuin 1 (SIRT1) is implicated in the regulation of mitochondrial function, energy metabolism, and insulin sensitivity in rodents. No studies are available in humans to demonstrate that SIRT1 expression in insulin-sensitive tissues is ... ...

Abstract	Objective: Sirtuin 1 (SIRT1) is implicated in the regulation of mitochondrial function, energy metabolism, and insulin sensitivity in rodents. No studies are available in humans to demonstrate that SIRT1 expression in insulin-sensitive tissues is associated with energy expenditure and insulin sensitivity. Research design and methods: Energy expenditure (EE), insulin sensitivity, and SIRT1 mRNA adipose tissue expression (n = 81) were measured by indirect calorimetry, hyperinsulinemic-euglycemic clamp, and quantitative RT-PCR in 247 nondiabetic offspring of type 2 diabetic patients. Results: High EE during the clamp (r = 0.375, P = 2.8 x 10(-9)) and high DeltaEE (EE during the clamp - EE in the fasting state) (r = 0.602, P = 2.5 x 10(-24)) were associated with high insulin sensitivity. Adipose tissue SIRT1 mRNA expression was significantly associated with EE (r = 0.289, P = 0.010) and with insulin sensitivity (r = 0.334, P = 0.002) during hyperinsulinemic-euglycemic clamp. Furthermore, SIRT1 mRNA expression correlated significantly with the expression of several genes regulating mitochondrial function and energy metabolism (e.g., peroxisome proliferator-activated receptor gamma coactivator-1beta, estrogen-related receptor alpha, nuclear respiratory factor-1, and mitochondrial transcription factor A), and with several genes of the respiratory chain (e.g., including NADH dehydrogenase [ubiquinone] 1alpha subcomplex 2, cytochrome c, cytochrome c oxidase subunit IV, and ATP synthase). Conclusions: Impaired stimulation of EE by insulin and low SIRT1 expression in insulin-sensitive tissues is likely to reflect impaired regulation of mitochondrial function associated with insulin resistance in humans.
MeSH term(s)	Adult ; Animals ; Body Mass Index ; Crosses, Genetic ; Diabetes Mellitus, Type 2/genetics ; Diabetes Mellitus, Type 2/physiopathology ; Energy Metabolism/genetics ; Female ; Gene Expression Regulation ; Glucose Intolerance/genetics ; Humans ; Male ; Mice ; Mice, Inbred BALB C ; Mice, Inbred DBA ; Muscle, Skeletal/physiology ; Muscle, Skeletal/physiopathology ; RNA, Messenger/genetics ; Reference Values ; Sirtuin 1/genetics
Chemical Substances	RNA, Messenger ; SIRT1 protein, human (EC 3.5.1.-) ; Sirt1 protein, mouse (EC 3.5.1.-) ; Sirtuin 1 (EC 3.5.1.-)
Language	English
Publishing date	2010-01-27
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	80085-5
ISSN	1939-327X ; 0012-1797
ISSN (online)	1939-327X
ISSN	0012-1797
DOI	10.2337/db09-1191
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Article ; Online: SRT2104 extends survival of male mice on a standard diet and preserves bone and muscle mass.

Aging cell

2014 Volume 13, Issue 5, Page(s) 787–796

Abstract: Increased expression of SIRT1 extends the lifespan of lower organisms and delays the onset of age-related diseases in mammals. Here, we show that SRT2104, a synthetic small molecule activator of SIRT1, extends both mean and maximal lifespan of mice fed a ...

Abstract	Increased expression of SIRT1 extends the lifespan of lower organisms and delays the onset of age-related diseases in mammals. Here, we show that SRT2104, a synthetic small molecule activator of SIRT1, extends both mean and maximal lifespan of mice fed a standard diet. This is accompanied by improvements in health, including enhanced motor coordination, performance, bone mineral density, and insulin sensitivity associated with higher mitochondrial content and decreased inflammation. Short-term SRT2104 treatment preserves bone and muscle mass in an experimental model of atrophy. These results demonstrate it is possible to design a small molecule that can slow aging and delay multiple age-related diseases in mammals, supporting the therapeutic potential of SIRT1 activators in humans.
MeSH term(s)	Aging ; Animals ; Body Composition ; Body Mass Index ; Bone and Bones/drug effects ; Bone and Bones/metabolism ; Diet ; Heterocyclic Compounds, 2-Ring/pharmacology ; Humans ; Kaplan-Meier Estimate ; Male ; Mice ; Mice, Inbred C57BL ; Survival Analysis
Chemical Substances	Heterocyclic Compounds, 2-Ring ; SRT2104
Language	English
Publishing date	2014-06-16
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Intramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2113083-8
ISSN	1474-9726 ; 1474-9718
ISSN (online)	1474-9726
ISSN	1474-9718
DOI	10.1111/acel.12220
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