segunda-feira, 27 de agosto de 2012

Importantes vídeos sobre a glicação AGEs





Convido você visitante a assistir estes 3 vídeos abaixo do youtube sobre AGEs, como pode ser observado são 2 pesquisadores com experiência em AGEs que discorrem sobre o assunto.

http://www.youtube.com/watch?v=tYLC63zVf6Q

Vincent Monnier: AGEs as Markers of 

Microvascular Disease in Type I Diabetes

June 15th, 2012
Case Western Reserve University's Wolstein Research Building Auditorium


http://www.youtube.com/watch?v=Lrnc6q0MVyI

Hot Topic in Biochemistry:

Transcriptional control of glyoxalase 1

by nrf2 by Paul Thornalley



Webcast of the presentation entitled 'Transcriptional control of glyoxalase 1 by nrf2 provides a stress-responsive defence against dicarbonyl glycation' given by Paul Thornalley (University of Warwick, UK), presented at the Biochemical Society Hot Topic Event in December 2011.

http://www.youtube.com/watch?v=lnGK0auyj1Y

SENS5 - Increased damage to proteins in ageing

 SENS Foundation 2011 - http://www.sens.org

The Fifth SENS conference - Paul Thornalley

Increased damage to proteins in ageing -- wear and tear potentially avoidable by extending preventive maintenance of life's essential machinery 

Authors: 
P.J. Thornalley, N. Rabbani
University of Warwick


Proteins undergo continual spontaneous modifications in physiological systems leading to change in their structure and function. This increases with age. Proteins are modified by glycation, oxidation and nitration leading to formation of glycation, oxidation and nitration adducts residues in proteins -- including formation of non-disulfide crosslinks. Damaged proteins undergo proteolysis to form glycated, oxidised and nitrated amino acids or free adducts that are then metabolised or excreted. Protein damage adduct residues and free adducts may be robustly quantified by stable isotopic dilution analysis tandem mass spectrometry. Data of protein damage is now being combined to produce refined dynamic, multi-compartmental mathematical models of in-life protein damage. Accumulation of protein damage in ageing, that is, increased steady-state levels of damaged proteins occurs as a consequence of: (i) increased rates of protein damage -- linked to increased rate of damaging agent formation and decreased anti-glycation and oxidant defences, (ii) decreased rates of repair of damaged proteins, and (iii) decreased rates of proteolysis of damaged proteins. Oxidative and non-oxidative mechanisms are involved. Antistress gene transcriptional responses also decline with age leaving the proteome particularly vulnerable in periods of oxidative, metabolic and lipogenic stress. Healthy ageing has been achieved in transgenic animals through manipulation of oxidative and non-oxidative mechanisms. Healthy ageing may be available for people through dietary supplements which prevent decline in expression in adulthood of a battery of genes protective against multi-modal stresses. Such interventions are designed to maintain vascular, metabolic, skeleto-muscular and other aspects of health, in part, through preventing increased flux of damage to proteins and increased steady-state levels of damaged proteins.

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