2th Wednesday session "Telomeres and cancer" begins by introducing Zhenyu JU project "Telomere dysfunction and stem cell aging" So, it's not surprised that telomere dysfunction represents as one of the molecular mechanisms in order to limit adult stem function.It is supposed that it is possible to rejuvenate the aging stem cells bydeletion DNA damage checkpoints. Also it has been found that telomere dysfunction induce alteration systemic environmental factors contribute to the impared lymphopoiesis and decline stem cell functionality. However the ntES and iPS cells applying can rejuvenate the somatic cells from aged telomere dysfunctuion.
The next delegate Haroldo SIlva (SENS Research Foundation, USA) spoke about ALT (Alternative Lengthening of Telomeres)
according to cancer cells, especially 10-15percent of cancer cells characterized by the ALT presence but the the main problem in order to use ALT therapies is a lack of assays that are reliable to high- content screens.(HTS). However the OncoSENS team has made a great work in order to making some of these key ALT assays compatimble with HTS formatIn that way it seems to achieve more success according to ALT-based anti-cancer development. By shutting down bo4th ALT- and telomerase- based pathways in cancers will move move thefield forward realizing the goal of a complete eradication in exciting age-related disease. Rigton Lentz(Georgetown University, USA) concluded the session and reportedabout clinicaldata on the use of the of blood filtration in order to reduce the levels of these receptors below the tumor protective threshold and by the way to destroy and clean even advanced metastatic cancers. The 4th session - Combination persistent viruses was opened by Charles Cao project "Nanoparticle- based artificial RNA silencing machinery forr antiviral therapy".It was shown an nontoxic specifically designed nanozyme for the treatment of hepatitis C virus can easily cleave HCV RNA in a sequence spesific manner.It is a great promise to use such creation as a useful tool for functional genomics. Then Paul Lenher (Cambridge University, UK) reported about a novel therapetutic target for latent human cytomegalovirus infection.Finally,
Todd RIder (Massachusetts Institute of Technology, USA) told about the "Panacea broad-spectrum antiviral therapeutics" .So the group of scientists developed Double-stranded RNA Activated Caspase Oligomerizer (DRACO) approach which selectively induces apoptosis in cells containing viral dsDNA and rapidly killing infected cells without any toxic effect to the uninfected cells. The next associated with short talks, cell senescene and anergy.Gregory Chin (SENS Research Foundation, USA)opened tis talk on the traningfuture SENS Researchers education. Lia GInaldi(University of L'Aquila, Italy) told about the link between osteoporosis and the iflammatory immune profile characterising immunosenescence. Alexandra Stolzing reported about in vitro derived microglia transplation opportunities in order to treat an age-related neurodegenerative Alzheimer's disease. It is found that senescene microglia accumulate in AD causing inflammation, neuonal damage and that's why seems to be attractive target for replacement therapies.John Sedivy from Brown University, USA discussed about "Chromatin and epigenetic dynamics in senescene phenotypes". He developed a the hypothesis that that the "loosening" of our endogenous genomic parasites, the RTEs(retrotransposable elements, is an important unexplored molecular aging process that can potentionally occur in most of our tissue. Jan van Deursen (Mayo Clinic, USA) spoke about stem and progenitor cell senescene in aging..So, his scientific group discovered mutant mice with low amountsof the mitotic checkpoint protein BubR1 accumulate large amounts of p16Ink4a positevely senescent cells in eye, skeletal muscles and fat at a young age.By genetic inactivation of p16Ink4a or drug-induced apoptosis we get an ability to delay premature aging.The next session posed an exiting topic associated with disruptive medicine. Richard Barker from CASMI, UK represented the he collarobation between Oxford University and University College London and the translation research research processes from bench to clinic. Sam Parnia observed the topic about redefining and reversing death - the prospect for new restricitation techniques to allow patients to make a full recovery even after multiple hours spent clinically "dead".
Finally the 7th Wednesday session emphasized delegate's attention to the cardiovascular aging. So,Elizabeth Corder (Matrix Genomics, USA) reported about her group's finding on the relantionship between SNPs region of the human telomerase and the incidence of coronary artery disease. After that David Spiegel from the Yale University reported about chemical andbiological approaches to understanding advanced glycatio end-products (AGEs). Brian O'Nuallian closed this sessin by introducing the innate and vaccin-generated antibodies against transtyretin amyloids.discussed the role aoamyloids relatively Alzheimer's disease and diabetes. It is known that amyloid diseases are incurable and it is needed an non-invasive diagnostics.So in order to this the antibodies were created allowing to both recognise and directly catalyse the breakdown of toxic amyloid assemblies.
The next delegate Haroldo SIlva (SENS Research Foundation, USA) spoke about ALT (Alternative Lengthening of Telomeres)
according to cancer cells, especially 10-15percent of cancer cells characterized by the ALT presence but the the main problem in order to use ALT therapies is a lack of assays that are reliable to high- content screens.(HTS). However the OncoSENS team has made a great work in order to making some of these key ALT assays compatimble with HTS formatIn that way it seems to achieve more success according to ALT-based anti-cancer development. By shutting down bo4th ALT- and telomerase- based pathways in cancers will move move thefield forward realizing the goal of a complete eradication in exciting age-related disease. Rigton Lentz(Georgetown University, USA) concluded the session and reportedabout clinicaldata on the use of the of blood filtration in order to reduce the levels of these receptors below the tumor protective threshold and by the way to destroy and clean even advanced metastatic cancers. The 4th session - Combination persistent viruses was opened by Charles Cao project "Nanoparticle- based artificial RNA silencing machinery forr antiviral therapy".It was shown an nontoxic specifically designed nanozyme for the treatment of hepatitis C virus can easily cleave HCV RNA in a sequence spesific manner.It is a great promise to use such creation as a useful tool for functional genomics. Then Paul Lenher (Cambridge University, UK) reported about a novel therapetutic target for latent human cytomegalovirus infection.Finally,
Todd RIder (Massachusetts Institute of Technology, USA) told about the "Panacea broad-spectrum antiviral therapeutics" .So the group of scientists developed Double-stranded RNA Activated Caspase Oligomerizer (DRACO) approach which selectively induces apoptosis in cells containing viral dsDNA and rapidly killing infected cells without any toxic effect to the uninfected cells. The next associated with short talks, cell senescene and anergy.Gregory Chin (SENS Research Foundation, USA)opened tis talk on the traningfuture SENS Researchers education. Lia GInaldi(University of L'Aquila, Italy) told about the link between osteoporosis and the iflammatory immune profile characterising immunosenescence. Alexandra Stolzing reported about in vitro derived microglia transplation opportunities in order to treat an age-related neurodegenerative Alzheimer's disease. It is found that senescene microglia accumulate in AD causing inflammation, neuonal damage and that's why seems to be attractive target for replacement therapies.John Sedivy from Brown University, USA discussed about "Chromatin and epigenetic dynamics in senescene phenotypes". He developed a the hypothesis that that the "loosening" of our endogenous genomic parasites, the RTEs(retrotransposable elements, is an important unexplored molecular aging process that can potentionally occur in most of our tissue. Jan van Deursen (Mayo Clinic, USA) spoke about stem and progenitor cell senescene in aging..So, his scientific group discovered mutant mice with low amountsof the mitotic checkpoint protein BubR1 accumulate large amounts of p16Ink4a positevely senescent cells in eye, skeletal muscles and fat at a young age.By genetic inactivation of p16Ink4a or drug-induced apoptosis we get an ability to delay premature aging.The next session posed an exiting topic associated with disruptive medicine. Richard Barker from CASMI, UK represented the he collarobation between Oxford University and University College London and the translation research research processes from bench to clinic. Sam Parnia observed the topic about redefining and reversing death - the prospect for new restricitation techniques to allow patients to make a full recovery even after multiple hours spent clinically "dead".
Finally the 7th Wednesday session emphasized delegate's attention to the cardiovascular aging. So,Elizabeth Corder (Matrix Genomics, USA) reported about her group's finding on the relantionship between SNPs region of the human telomerase and the incidence of coronary artery disease. After that David Spiegel from the Yale University reported about chemical andbiological approaches to understanding advanced glycatio end-products (AGEs). Brian O'Nuallian closed this sessin by introducing the innate and vaccin-generated antibodies against transtyretin amyloids.discussed the role aoamyloids relatively Alzheimer's disease and diabetes. It is known that amyloid diseases are incurable and it is needed an non-invasive diagnostics.So in order to this the antibodies were created allowing to both recognise and directly catalyse the breakdown of toxic amyloid assemblies.
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