aging-us

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Aging-US: Aging Model From Retired Sled Dogs

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Aging-US: Treating Alzheimer’s Disease as a Systems Network Disorder

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mTOR-Driven Aging and Rapamycin with Mikhail Blagosklonny and Dennis Mangan

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Aging-US: Hyperbaric Oxygen Therapy, Telomeres, and Immunosenescence

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Aging-US: Hyperbaric Oxygen Therapy Alleviates Vascular Dysfunction and ...

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Aging-US: TGF-beta and Oxytocin Reversed to Reverse Aging

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Aging-US: DNA Markers Distinguish Sarcopenia from Frailty

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Aging-US: Senescent Cells and Inflamm-Aging

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Aging-US: Cellular Senescence in Lymphoid Organs and Immunosenescence

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Aging-US: COVID-19 Mortality in Children

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Aging-US: Shorter Telomeres in Patients With Severe COVID-19

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Aging-US: Reversal of Cognitive Decline in Alzheimer's Disease

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Aging-US: Knockdown of Disease Specific Proteins APP, Tau, SOD1 G93A and...

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Aging-US published "Identification of RNA binding protein interacting with circular RNA and hub candidate network for hepatocellular carcinoma" which reported that 17 DERBPs, which were commonly dysregulated in HCC from The Clinical Proteomic Tumor Analysis Consortium, The Cancer Genome Atlas and International Cancer Genome Consortium projects, were utilized to construct the RBP-circRNA network.

Additionally, gene set enrichment analysis showed that dysregulated TARDBP might be involved in some pathways related to the HCC pathogenesis.

Therefore, a hub RBP-circRNA network was generated based on TARDBP.

RNA immunoprecipitation and RNA pull-down confirmed that hsa_circ_0004913 binds to TARDBP.

These findings, published in Aging-US, indicated a certain RBP-circRNA regulatory network potentially involved in the pathogenesis of HCC, which provides novel insights into the mechanism of study and biomarker identification for HCC.

Dr. Yuhan Chen from The Southern Medical University said, "Hepatocellular carcinoma (HCC) is most common types of primary liver cancer."

Previous studies have demonstrated that circRNAs can act as sponges of RNA binding protein, in the meantime RBPs are also able to participate in back-splicing. Therefore, the interaction with RBPs can be also regarded as a crucial element to explore functions of circRNAs.

However, there are very few studies related to the effects of RBP-circRNA interactions on HCC, which requires more exploration.

In this study, the authors screened out the differently expressed circRNA in HCC cases from Gene Expression Omnibus database and predicted the RBPs binding to DEcircRNA.

After evaluating the expression level of RBPs in HCC from The Clinical Proteomic Tumor Analysis Consortium, International Cancer Genome Consortium and The Cancer Genome Atlas projects, they utilized 17 common DERBPs to construct the RBP-circRNA regulatory network in HCC.

These findings indicated that certain RBP-circRNA networks may be closely related to HCC, which provides ideas for the mechanism of study for HCC.

The Chen Research Team concluded in their Aging-US Research Output, "we identified some DERBPs interacting with circRNAs and generated RBP-circRNA regulatory networks for HCC. Among the DERBPs, high TARDBP expression was corelated with high grade, advanced stage and low macrophage fraction of HCC. We also constructed the hub RBP-circRNA network based on TARDBP and confirmed that hsa_circ_0004913 could bind to TARDBP, which may provide new clues for HCC mechanism study. However, there are also some limitations in our study. First, we only used TCGA, ICGC and CPTAC projects for analysis and little data resulted in only one RBP with prognostic significance, which may lead to the loss of some potential functional RBPs. Second, we didn’t classify samples according to the etiology and these identified circRNAs and RBPs may not be representative in HCC with different etiologies. Moreover, the number of HCC cases with circRNA data included in this study is relatively small. Due to our current lack of HCC samples and no survival information of HCC with circRNA expression profiles in GEO, we could not verify the expression and assess the prognostic value of circRNAs for HCC. In summary, our results indicated that some RBP-circRNA networks take a potential part in the pathogenesis of HCC and provide a new perspective for further mechanism study and biomarker development of HCC."

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DOI - https://doi.org/10.18632/aging.203139

Full Text - https://www.aging-us.com/article/203139/text

Correspondence to: Yuhan Chen email: cspnr1@126.com

Keywords: hepatocellular carcinoma, autophagy, progression, miR-513b-5p, PIK3R3

About Aging-US

Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research as well as topics beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, cancer, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR among others), and approaches to modulating these signaling pathways.

To learn more about Aging-US, please visit http://www.Aging-US.com or connect with @AgingJrnl

Aging-US is published by Impact Journals, LLC please visit http://www.ImpactJournals.com or connect with @ImpactJrnls

Media Contact 18009220957x105 MEDIA@IMPACTJOURNALS.COM

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Aging-US testimonial from Dr. Kara Fitzgerald ND IFMCP with The Institute for Functional Medicine in Federal Way Washington USA talking about their experience publishing “Potential reversal of epigenetic age using a diet and lifestyle intervention: a pilot randomized clinical trial” READ MORE: A groundbreaking clinical trial shows we can reduce biological age (as measured by the Horvath 2013 DNAmAge clock) by more than three years in only eight weeks with diet and lifestyle through balancing DNA methylation. A first-of-its-kind, peer-reviewed study provides scientific evidence that lifestyle and diet changes can deliver immediate and rapid reduction of our biological age. Since aging is the primary driver of chronic disease, this reduction has the power to help us live better, longer. The study, released on April 12, utilized a randomized controlled clinical trial conducted among 43 healthy adult males between the ages of 50-72. The 8-week treatment program included diet, sleep, exercise and relaxation guidance, and supplemental probiotics and phytonutrients, resulting in a statistically significant reduction of biological age–over three years younger, compared to controls. The study was independently conducted by the Helfgott Research Institute, with laboratory assistance from Yale University Center for Genome Analysis, and the results independently analyzed at McGill University and the National University of Natural Medicine. The study’s lead author, Kara Fitzgerald ND IFMCP, stated that “the combined intervention program was designed to target a specific biological mechanism called DNA methylation, and in particular the DNA methylation patterns that have been identified as highly predictive of biological age. We suspect that this focus was the reason for its remarkable impact. These early results appear to be consistent with, and greatly extend, the very few existing studies that have so far examined the potential for biological age reversal. And it is unique in its use of a safe, non-pharmaceutical dietary and lifestyle program, control group, and the extent of the age reduction. We are currently enrolling participants for a larger study which we expect will corroborate these findings.“ Leading epigeneticist Moshe Szyf PhD of McGill University and co-author on the study adds, “The uniqueness of Dr Fitzgerald approach is that her trial devised a natural but mechanistic driven strategy to target the methylation system of our body. This study provides the first insight into the possibility of using natural alterations to target epigenetic processes and improve our well being and perhaps even longevity and lifespan.” DNA methylation patterns have become a leading means by which scientists evaluate and track biological aging, a term used to describe the accumulation of damage and loss of function to our cells, tissues and organs. This damage is what drives diseases of aging. “What is extremely exciting,” commented Dr. Fitzgerald, “is that food and lifestyle practices, including specific nutrients and food compounds known to selectively alter DNA methylation, are able to have such an impact on those DNA methylation patterns we know predict aging and age-related disease. I believe that this, together with new possibilities for us all to measure and track our DNA methylation age, will provide significant new opportunities for both scientists and consumers.“ ### To read the study: https://www.aging-us.com/article/202913 For background information on aging and DNA methylation: https://www.drkarafitzgerald.com/2021/04/13/biological-aging-and-methylation/ For press/interviews contact: media@drkarafitzgerald.com About Aging-US Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research as well as topics beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, cancer, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR among others), and approaches to modulating these signaling pathways. To learn more about Aging-US, please visit http://www.Aging-US.com or connect with @AgingJrnl Aging-US is published by Impact Journals, LLC please visit http://www.ImpactJournals.com or connect with @ImpactJrnls Media Contact 18009220957×105 MEDIA@IMPACTJOURNALS.COM Original Sourcehttps://www.aging-us.com/news_room/three-years-younger-in-just-eight-weeks-a-new-study-suggests-yes Related Journal Articlehttp://dx.doi.org/10.18632/aging.202913

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Aging-US testimonial from Dr. Kara Fitzgerald ND IFMCP with The Institute for Functional Medicine in Federal Way Washington USA talking about their experience publishing "Potential reversal of epigenetic age using a diet and lifestyle intervention: a pilot randomized clinical trial" READ MORE: A groundbreaking clinical trial shows we can reduce biological age (as measured by the Horvath 2013 DNAmAge clock) by more than three years in only eight weeks with diet and lifestyle through balancing DNA methylation. A first-of-its-kind, peer-reviewed study provides scientific evidence that lifestyle and diet changes can deliver immediate and rapid reduction of our biological age. Since aging is the primary driver of chronic disease, this reduction has the power to help us live better, longer. The study, released on April 12, utilized a randomized controlled clinical trial conducted among 43 healthy adult males between the ages of 50-72. The 8-week treatment program included diet, sleep, exercise and relaxation guidance, and supplemental probiotics and phytonutrients, resulting in a statistically significant reduction of biological age–over three years younger, compared to controls. The study was independently conducted by the Helfgott Research Institute, with laboratory assistance from Yale University Center for Genome Analysis, and the results independently analyzed at McGill University and the National University of Natural Medicine. The study’s lead author, Kara Fitzgerald ND IFMCP, stated that “the combined intervention program was designed to target a specific biological mechanism called DNA methylation, and in particular the DNA methylation patterns that have been identified as highly predictive of biological age. We suspect that this focus was the reason for its remarkable impact. These early results appear to be consistent with, and greatly extend, the very few existing studies that have so far examined the potential for biological age reversal. And it is unique in its use of a safe, non-pharmaceutical dietary and lifestyle program, control group, and the extent of the age reduction. We are currently enrolling participants for a larger study which we expect will corroborate these findings.“ Leading epigeneticist Moshe Szyf PhD of McGill University and co-author on the study adds, “The uniqueness of Dr Fitzgerald approach is that her trial devised a natural but mechanistic driven strategy to target the methylation system of our body. This study provides the first insight into the possibility of using natural alterations to target epigenetic processes and improve our well being and perhaps even longevity and lifespan.” DNA methylation patterns have become a leading means by which scientists evaluate and track biological aging, a term used to describe the accumulation of damage and loss of function to our cells, tissues and organs. This damage is what drives diseases of aging. “What is extremely exciting,” commented Dr. Fitzgerald, “is that food and lifestyle practices, including specific nutrients and food compounds known to selectively alter DNA methylation, are able to have such an impact on those DNA methylation patterns we know predict aging and age-related disease. I believe that this, together with new possibilities for us all to measure and track our DNA methylation age, will provide significant new opportunities for both scientists and consumers.“ ### To read the study: https://www.aging-us.com/article/202913 For background information on aging and DNA methylation: https://www.drkarafitzgerald.com/2021/04/13/biological-aging-and-methylation/ For press/interviews contact: media@drkarafitzgerald.com About Aging-US Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research as well as topics beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, cancer, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR among others), and approaches to modulating these signaling pathways. To learn more about Aging-US, please visit http://www.Aging-US.com or connect with @AgingJrnl Aging-US is published by Impact Journals, LLC please visit http://www.ImpactJournals.com or connect with @ImpactJrnls Media Contact 18009220957×105 MEDIA@IMPACTJOURNALS.COM Original Source https://www.aging-us.com/news_room/three-years-younger-in-just-eight-weeks-a-new-study-suggests-yes Related Journal Article http://dx.doi.org/10.18632/aging.202913 

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Aging-US: Glial Senescence in Brainstem Causes Sympathetic Overactivity