Aging-US

BUFFALO, NY- September 20, 2023 – A new research paper was published in Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science) Volume 15, Issue 17, entitled, “Development of a DNA damage-induced senescence model in osteoarthritic chondrocytes.” Senescent cells (SnCs) have been described to accumulate in osteoarthritis (OA) joint tissues in response to injury, thereby participating in OA development and progression. However, clinical therapeutic approaches targeting SnCs using senolysis, although promising in preclinical OA models, have not yet proven their efficacy in patients with knee OA. This pitfall may be due to the lack of understanding of the mechanisms underlying chondrocyte senescence. In their new study, researchers Mélina Georget, Anaïs Defois, Romain Guiho, Nina Bon, Sophie Allain, Cécile Boyer, Boris Halgand, Denis Waast, Gaël Grimandi, Alban Fouasson-Chailloux, Jérôme Guicheux, and Claire Vinatier from Nantes Université aimed to generate models of chondrocyte senescence. “In this context, our study aims to develop in vitro models of chondrocyte senescence by investigating the ability of etoposide and IL-1β treatments to produce a reliable chondrocyte senescent model.” This study used etoposide, to induce DNA damage-related senescence or chronic exposure to IL-1β to entail inflammation-related senescence in human OA chondrocytes. Several hallmarks of cellular senescence, such as cell cycle arrest, expression of cyclin-dependent kinase inhibitors, DNA damages, and senescence-associated secretory profile were evaluated. Chronic exposure to IL-1β induces only partial expression of senescence markers and does not allow us to conclude on its ability to induce senescence in chondrocytes. On the other hand, etoposide treatment reliably induces DNA damage-related senescence in human articular chondrocytes evidenced by loss of proliferative capacity, DNA damage accumulation, and expression of some SASP components. “Etoposide-induced senescence model may help investigate the initiation of cellular senescence in chondrocytes, and provide a useful model to develop therapeutic approaches to target senescence in OA.” DOI - https://doi.org/10.18632/aging.204881 Corresponding author - Claire Vinatier - claire.vinatier@univ-nantes.fr Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.204881 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords - aging, senescence, osteoarthritis, etoposide, chondrocytes About Aging-US Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways. Please visit our website at https://www.Aging-US.com​​ and connect with us: SoundCloud - https://soundcloud.com/Aging-Us Facebook - https://www.facebook.com/AgingUS/ X - https://twitter.com/AgingJrnl Instagram - https://www.instagram.com/agingjrnl/ YouTube - https://www.youtube.com/@AgingJournal LinkedIn - https://www.linkedin.com/company/aging/ Pinterest - https://www.pinterest.com/AgingUS/ Media Contact 18009220957 MEDIA@IMPACTJOURNALS.COM

A new priority research paper was published on the cover of Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science) Volume 15, Issue 17, entitled, “Fail-tests of DNA methylation clocks, and development of a noise barometer for measuring epigenetic pressure of aging and disease.” In this new study, researchers Xiaoyue Mei, Joshua Blanchard, Connor Luellen, Michael J. Conboy, and Irina M. Conboy from the University of California, Berkeley, show that Elastic Net (EN) DNA methylation (DNAme) clocks have low accuracy of predictions for individuals of the same age and a low resolution between healthy and disease cohorts; caveats inherent in applying linear model to non-linear processes. “We found that change in methylation of cytosines with age is, interestingly, not the determinant for their selection into the clocks.” Moreover, an EN clock’s selected cytosines change when non-clock cytosines are removed from the training data; as expected from optimization in a machine learning (ML) context, but inconsistently with the identification of health markers in a biological context. To address these limitations, the researchers moved from predictions to measurement of biological age, focusing on the cytosines that on average remain invariable in their methylation through lifespan, postulated to be homeostatically vital. They established that dysregulation of such cytosines, measured as the sums of standard deviations of their methylation values, quantifies biological noise, which in their hypothesis is a biomarker of aging and disease. “We term this approach a ‘noise barometer’ - the pressure of aging and disease on an organism.” These noise-detecting cytosines are particularly important as sums of SD on the entire 450K DNAme array data yield a random pattern through chronology. Testing how many cytosines of the 450K arrays become noisier with age, the team found that the paradigm of DNAme noise as a biomarker of aging and disease remarkably manifests in ~1/4 of the total. In that large set even the cytosines that have on average constant methylation through age show increased SDs and can be used as noise detectors of the barometer. DOI - https://doi.org/10.18632/aging.205046 Corresponding author - Irina M. Conboy - iconboy@berkeley.edu Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.205046 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords - aging, DNA methylation, epigenetics, clocks’ fail-test, biological noise About Aging-US Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways. Please visit our website at https://www.Aging-US.com​​ and connect with us: SoundCloud - https://soundcloud.com/Aging-Us Facebook - https://www.facebook.com/AgingUS/ Twitter - https://twitter.com/AgingJrnl Instagram - https://www.instagram.com/agingjrnl/ YouTube - https://www.youtube.com/@AgingJournal LinkedIn - https://www.linkedin.com/company/aging/ Pinterest - https://www.pinterest.com/AgingUS/ Media Contact 18009220957 MEDIA@IMPACTJOURNALS.COM

In the realm of cancer research, one persistent trend has emerged — the incidence of invasive melanoma rises steadily with advancing age. While this insidious disease remains rare in children and adolescents, it progressively asserts its presence as individuals grow older. The connection between age and melanoma incidence persists around the world, albeit with varying rates in different countries. Australia has the highest melanoma rates in the world. According to the Melanoma Institute Australia, every 30 minutes an Australian is diagnosed with melanoma and every 6 hours an Australian dies from it. Thankfully, research is making a difference. In the last decade, the 5-year overall survival rate for advanced melanoma has increased from less than 10% to more than 50%. In 2011, melanoma was Australia’s 7th most deadly cancer. In 2021, melanoma was Australia’s 11th most deadly cancer. In a new editorial paper, researchers John F. Thompson and Gabrielle J. Williams from the Melanoma Institute Australia at The University of Sydney discuss the intricacies of how age influences different varieties of melanoma incidence, prognosis and treatment. On August 17, 2023, their editorial was published in Aging’s Volume 15, Issue 16, entitled, “The effect of age on melanoma incidence and prognosis.” Full blog - https://aging-us.org/2023/09/the-impact-of-age-on-melanoma-insights-from-recent-research/ Paper DOI - https://doi.org/10.18632/aging.204653 Corresponding author - John F. Thompson - john.thompson@melanoma.org.au Video short - https://www.youtube.com/watch?v=V0wwfLEJGW0 Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.204653 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords - aging, melanoma, incidence, age, prognosis About Aging-US Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways. Please visit our website at https://www.Aging-US.com​​ and connect with us: SoundCloud - https://soundcloud.com/Aging-Us Facebook - https://www.facebook.com/AgingUS/ X - https://twitter.com/AgingJrnl Instagram - https://www.instagram.com/agingjrnl/ YouTube - https://www.youtube.com/@AgingJournal LinkedIn - https://www.linkedin.com/company/aging/ Pinterest - https://www.pinterest.com/AgingUS/ Media Contact 18009220957 MEDIA@IMPACTJOURNALS.COM

A new editorial paper was published in Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science) Volume 15, Issue 16, entitled, “Microvascular contributions to white matter injury in Alzheimer’s disease.” In their new editorial, researchers Zsolt Bagi, Larry S. Sherman and Stephen A. Back from Augusta University discuss mechanisms of cognitive impairment and dementia. Impairments in cognitive and executive function of presumed cerebral microvascular origin are important and recently recognized neuropathological manifestations of vascular contributions to cognitive impairment and dementia (VCID). It has been long known that hypertensive cerebrovascular disease also involves a spectrum of subcortical small vessel diseases, such as arteriolosclerosis and lipohyalinosis of small penetrating arterioles, which contribute to progressive injury of periventricular, frontal and parietal white matter (WM). “However, until recently, recognition of the role of WM injury during aging and the progression of Alzheimer disease and related dementias (AD/ADRD) was very limited.” Despite growing interest in VCID and AD/ADRD, there have been few studies of mechanistic links between subcortical small vessel disease, WM injury and cognitive decline. Even though WM constitutes >80% of the human cerebral hemispheres, a PubMed search of AD and WM injury yielded only 381 articles (including reviews) vs. 193,303 articles for AD alone. Notably, 50% of diagnosed AD patients have mixed vascular and AD pathology. Hence, there is a critical need to explore connections between AD, WM injury and cerebral small vessel disease to define mechanisms and diagnostic features of mixed vascular and AD neuropathological change (ADNC). “To provide rigorous access to human WM lesions, we recently developed a unique rapid autopsy brain procurement protocol using specimens donated by participants in the Adult Changes in Thought (ACT) study, a prospective, population-based study of aging and incident dementia among men and women in Seattle, Washington [5].” DOI - https://doi.org/10.18632/aging.204997 Corresponding author - Zsolt Bagi - zbagi@augusta.edu Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.204997 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords - aging, cerebrovascular, neuropathology, vasodilation, parenchymal, arteriole About Aging-US Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways. Please visit our website at https://www.Aging-US.com​​ and connect with us: SoundCloud - https://soundcloud.com/Aging-Us Facebook - https://www.facebook.com/AgingUS/ Twitter - https://twitter.com/AgingJrnl Instagram - https://www.instagram.com/agingjrnl/ YouTube - https://www.youtube.com/@AgingJournal LinkedIn - https://www.linkedin.com/company/aging/ Pinterest - https://www.pinterest.com/AgingUS/ Media Contact 18009220957 MEDIA@IMPACTJOURNALS.COM

A new research paper was published in Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science) Volume 15, Issue 16, entitled, “Copy number variation as a tool for implementing pregnancy as an aging model.” Copy number variations (CNV) are a major contributor to genome variability. CNVs have been linked to aging and other degradable phenotypes such as pregnancy physiology. In this new study, researchers Mariana Andrawus, Lital Sharvit, Noga Touitou, Batia Lerrer, Haim Y. Cohen, and Gil Atzmon from University of Haifa and Bar-Ilan University used CNVs from pregnant mice to demonstrate how pregnancy can be used as a model of aging. “We hypothesize that pregnancy can serve as a model for aging by demonstrating similar biomarkers, pathologies, and genetic and epigenetic effects [3]. To test this hypothesis, we designed a study that assesses CNVs associated with human longevity (unpublished results) in pregnancy.” Candidate CNVs were selected by applying case-control analysis in human centenarians compared with control groups. These CNVs were aligned with the mouse genome and their copy variation was assessed using qRT-PCR in liver and blood tissue samples from pregnant mice throughout pregnancy (baseline; first, second, and third trimester; post-partum). Eight of the ten selected CNVs demonstrated a significant decline/increase trend throughout the pregnancy followed by opposite direction soon after delivery in the liver and blood of the mouse tissues. Furthermore, significant differential expression was detected among the candidate CNVs’ close vicinity genes (APA2A, LSS, RBDHF1, PLAAT1, and SCL17A2), but not in the WSCD2 gene. Establishing a genetic link between longevity and pregnancy is a significant step toward implementing the pregnancy process as a model for aging. These results in pregnant mice highlight the mechanism and similarities between pregnancy and aging. “Investigating the mechanisms that cause such rejuvenation after labor could change our aging treatment paradigm.” DOI - https://doi.org/10.18632/aging.204936 Corresponding author - Gil Atzmon - gatzmon@univ.haifa.ac.il Video short - https://www.youtube.com/watch?v=82466m-S-tU Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.204936 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords - aging, pregnancy, copy number variation, gene expression About Aging-US Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways. Please visit our website at https://www.Aging-US.com​​ and connect with us: SoundCloud - https://soundcloud.com/Aging-Us Facebook - https://www.facebook.com/AgingUS/ Twitter - https://twitter.com/AgingJrnl Instagram - https://www.instagram.com/agingjrnl/ YouTube - https://www.youtube.com/@AgingJournal LinkedIn - https://www.linkedin.com/company/aging/ Pinterest - https://www.pinterest.com/AgingUS/ Media Contact 18009220957 MEDIA@IMPACTJOURNALS.COM

A new research paper was published in Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science) Volume 15, Issue 16, entitled, “Reorganization of pancreas circadian transcriptome with aging.” The evolutionarily conserved circadian system allows organisms to synchronize internal processes with 24-h cycling environmental timing cues, ensuring optimal adaptation. Like other organs, the pancreas function is under circadian control. Recent evidence suggests that aging by itself is associated with altered circadian homeostasis in different tissues which could affect the organ’s resiliency to aging-related pathologies. Pancreas pathologies of either endocrine or exocrine components are age-related. Whether pancreas circadian transcriptome output is affected by age is still unknown. In their new study, researchers Deepak Sharma, Caitlin R. Wessel, Mahboobeh Mahdavinia, Fabian Preuss, and Faraz Bishehsari from Rush University and University of Wisconsin-Parkside profiled the impact of age on the pancreatic transcriptome over a full circadian cycle and elucidated a circadian transcriptome reorganization of pancreas by aging. “Here we carried out a 24-h circadian transcriptomic analysis of pancreas from male mice at young and old ages.” The researchers defined a comprehensive circadian transcriptome landscape and identified biological pathways that are reflective of aging pancreas. Additionally, analysis of the pancreatic microenvironment revealed novel mechanistic insights into the fibroblast-mediated regulation of rhythmicity in aged pancreas. The team suggests that the circadian transcriptome in aging pancreas re-organizes in response to age-specific signals from the cellular microenvironment, primarily modulated by fibroblasts. “Our study highlights gain of rhythms in the extrinsic cellular pathways in the aged pancreas and extends a potential role to fibroblast-associated mechanisms.” DOI - https://doi.org/10.18632/aging.204929 Corresponding author - Faraz Bishehsari - Faraz_Bishehsari@rush.edu Video short - https://www.youtube.com/watch?v=dhHK8udB1eg Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.204929 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords - aging, circadian rhythms, RNA transcriptomics, pancreas About Aging-US Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways. Please visit our website at https://www.Aging-US.com​​ and connect with us: SoundCloud - https://soundcloud.com/Aging-Us Facebook - https://www.facebook.com/AgingUS/ Twitter - https://twitter.com/AgingJrnl Instagram - https://www.instagram.com/agingjrnl/ YouTube - https://www.youtube.com/@AgingJournal LinkedIn - https://www.linkedin.com/company/aging/ Pinterest - https://www.pinterest.com/AgingUS/ Media Contact 18009220957 MEDIA@IMPACTJOURNALS.COM

A new research paper was published on the cover of Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science) Volume 15, Issue 16, entitled, “Dectin-1 stimulation promotes a distinct inflammatory signature in the setting of HIV-infection and aging.” Dectin-1 is an innate immune receptor that recognizes and binds β-1, 3/1, 6 glucans on fungi. In this new study, researchers Archit Kumar, Jiawei Wang, Allen Esterly, Chris Radcliffe, Haowen Zhou, Brent Vander Wyk, Heather G. Allore, Sui Tsang, Lydia Barakat, Subhasis Mohanty, Hongyu Zhao, Albert C. Shaw, and Heidi J. Zapata evaluated Dectin-1 function in myeloid cells in a cohort of HIV-positive and HIV-negative young and older adults. “The HIV-positive and HIV-negative groups were comparable in age and gender distribution, incidence of comorbidities such as diabetes, metabolic syndrome, cardiovascular disease and pulmonary disease.” Stimulation of monocytes with β-D-glucans induced a pro-inflammatory phenotype in monocytes of HIV-infected individuals that was characterized by increased levels of IL-12, TNF-α, and IL-6, with some age-associated cytokine increases also noted. Dendritic cells showed a striking HIV-associated increase in IFN-α production. These increases in cytokine production paralleled increases in Dectin-1 surface expression in both monocytes and dendritic cells that were noted with both HIV and aging. Differential gene expression analysis showed that HIV-positive older adults had a distinct gene signature compared to other cohorts characterized by a robust TNF-α and coagulation response (increased at baseline), a persistent IFN-α and IFN-γ response, and an activated dendritic cell signature/M1 macrophage signature upon Dectin-1 stimulation. Dectin-1 stimulation induced a strong upregulation of MTORC1 signaling in all cohorts, although increased in the HIV-Older cohort (stimulation and baseline). In sum, this study demonstrates that the HIV Aging population has a distinct immune signature in response to Dectin-1 stimulation. This signature may contribute to the pro-inflammatory environment that is associated with HIV and aging. “Overall, this study demonstrates that age, HIV-infection and co-morbidities can alter the individual immune response. In particular our study showed a unique immune signature in the setting of both HIV and aging in response to Dectin-1 stimulation.” DOI - https://doi.org/10.18632/aging.204927 Corresponding author - Heidi J. Zapata - heidi.zapata@yale.edu Video short - https://www.youtube.com/watch?v=MpMBDvv0dDI Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.204927 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords - aging, immune response, innate immune cells, HIV-infection, dectin-1 About Aging-US Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways. Please visit our website at https://www.Aging-US.com​​ and connect with us: SoundCloud - https://soundcloud.com/Aging-Us Facebook - https://www.facebook.com/AgingUS/ Twitter - https://twitter.com/AgingJrnl Instagram - https://www.instagram.com/agingjrnl/ YouTube - https://www.youtube.com/@AgingJournal LinkedIn - https://www.linkedin.com/company/aging/ Pinterest - https://www.pinterest.com/AgingUS/ Media Contact 18009220957 MEDIA@IMPACTJOURNALS.COM

A new editorial paper was published in Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science) Volume 15, Issue 15, entitled, “Epigenetic aging in oocytes.” Aging-related phenotypes span many different tissues and cell types, and start to occur at different ages - a different typical age for every cell type. In their new editorial, researchers Peera Wasserzug-Pash and Michael Klutstein from The Hebrew University of Jerusalem discuss one of the earliest occurring aging events in the human body, which is the beginning of female reproductive aging and deterioration. The clinical cut-off for advanced maternal age (AMA), a condition associated with poor reproductive outcomes, is 35 years old. “The early onset of reproductive aging poses a significant challenge to clinicians since a global consistent increase in maternal age at first birth has occurred in recent decades, effectively shortening the available time window for reproduction [1].” As the rate of patients with advanced maternal age rises, and with it, the number of patients in fertility clinics, so does the necessity for a fundamental understanding of the reproductive aging process. In recent years, it has been established that there is a substantial dominating influence of oocyte quality loss on age-related fertility decline. This is best demonstrated by the rise in IVF success rates in reproductively aged women when they receive an egg donation from a younger woman. Oocyte quality loss is characterized by diminished cellular function and an increased occurrence of chromosomal nondisjunctions. “Our recent publication [4] addresses the question of additional, epigenetic mechanisms that lead to the occurrence of age-related oocyte quality loss.” DOI - https://doi.org/10.18632/aging.204976 Corresponding author - Michael Klutstein - michaelk@ekmd.huji.ac.il Video short - https://www.youtube.com/watch?v=KHOVKKaJykY&t=45s Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.204976 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords - aging, oocytes, heterochromatin, epigenetics, maturation About Aging-US Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways. Please visit our website at https://www.Aging-US.com​​ and connect with us: SoundCloud - https://soundcloud.com/Aging-Us Facebook - https://www.facebook.com/AgingUS/ Twitter - https://twitter.com/AgingJrnl Instagram - https://www.instagram.com/agingjrnl/ YouTube - https://www.youtube.com/@AgingJournal LinkedIn - https://www.linkedin.com/company/aging/ Pinterest - https://www.pinterest.com/AgingUS/ Media Contact 18009220957 MEDIA@IMPACTJOURNALS.COM

The lacrimal gland, found in the upper outer part of the eye’s hollow area, is an important gland that makes tears to protect the eye from infections. It’s split into two parts: one near the inside of the eyelid that can be seen when the eyelid is flipped, and another part with ducts lower in the eye that connects to its counterpart. In their fully functioning status, these ducts release fluid onto the surface of the eye. As humans age (especially women), the lacrimal gland gradually becomes infiltrated by aberrant immune cells and can ultimately lead to an uncomfortable condition known as dry eye disease. “Burning and redness in the eyes, grittiness and blurry vision make life miserable and currently, eye drops with a variety of lubricant components and in the most severe cases, immunosuppressors, are the only therapies approved for this disease.” In a well-written new editorial paper, researchers Claudia M. Trujillo-Vargas and Cintia S. de Paiva from the Department of Ophthalmology at Baylor College of Medicine artfully discuss their recent studies which shed light on the immune system’s role in dry eye disease. On August 11, 2023, their editorial was published in Aging’s Volume 15, Issue 15, entitled, “Our search of immune invaders in the aged lacrimal gland.” Full blog - https://aging-us.org/2023/08/dry-eyes-it-may-be-immune-infiltration-in-aging-lacrimal-glands/ Paper DOI - https://doi.org/10.18632/aging.204651 Corresponding author - Cintia S. de Paiva - cintiadp@bcm.edu Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.204651 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords - aging, lacrimal gland, ectopic lymphoid structures, immune invasion About Aging-US Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways. Please visit our website at https://www.Aging-US.com​​ and connect with us: SoundCloud - https://soundcloud.com/Aging-Us Facebook - https://www.facebook.com/AgingUS/ Twitter - https://twitter.com/AgingJrnl Instagram - https://www.instagram.com/agingjrnl/ YouTube - https://www.youtube.com/@AgingJournal LinkedIn - https://www.linkedin.com/company/aging/ Pinterest - https://www.pinterest.com/AgingUS/ Media Contact 18009220957 MEDIA@IMPACTJOURNALS.COM

A new research paper was published in Aging (Aging-US) Volume 15, Issue 15, entitled, “Cardiovascular events and death after catheter ablation in very old patients with nonvalvular atrial fibrillation.” Catheter ablation of atrial fibrillation (AF) is recommended for selected older patients. However, the preventive effects of AF ablation on cardiovascular events and death remain unclear, especially in older patients. In this new study, researchers Keisuke Okawa, Satoshi Taya, Takeshi Morimoto, Ryu Tsushima, Yuya Sudo, Ai Sakamoto, Eisuke Saito, Masahiro Sogo, Masatomo Ozaki, and Masahiko Takahashi from Kagawa Prefectural Central Hospital and Hyogo Medical University aimed to investigate the impact of AF ablation on the incidence of cardiovascular events and death in very old nonvalvular AF (NVAF) patients. “We conducted a prospective cohort study of consecutive patients with NVAF aged ≥80 years and using direct oral anticoagulants (DOACs).” The researchers defined cardiovascular events as acute heart failure (AHF), strokes and systemic embolisms (SSEs), acute coronary syndrome (ACS), and sudden cardiac death (SCD) and cardiovascular death as AHF/SSE/ACS-related death and SCD. They compared the 3-year incidence of cardiovascular events and death between the patients who underwent AF ablation (Ablation group) and those who received medical therapy only (Medication group). Among the 782 NVAF patients using DOACs, propensity score matching provided 208 patients in each group. The Ablation group had a significantly lower 3-year incidence of cardiovascular events and death than the Medication group: cardiovascular events, 24 (13.2%) vs. 43 (23.3%), log-rank P = 0.009 and hazard ratio (HR) 0.52 (95% confidence interval (CI) 0.32–0.86) and cardiovascular deaths, 5 (3.0%) vs. 15 (7.8%), log-rank P = 0.019 and HR 0.32 (95% CI 0.16–0.88). “In very old NVAF patients using DOACs, those who underwent AF ablation had a lower incidence of both cardiovascular events and death than those who received medical therapy only.” DOI - https://doi.org/10.18632/aging.204952 Corresponding author - Keisuke Okawa - k-ookawa@chp-kagawa.jp Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.204952 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords - aging, atrial fibrillation, catheter ablation, cardiovascular event, cardiovascular death, very old patient About Aging-US Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways. Please visit our website at https://www.Aging-US.com​​ and connect with us: SoundCloud - https://soundcloud.com/Aging-Us Facebook - https://www.facebook.com/AgingUS/ Twitter - https://twitter.com/AgingJrnl Instagram - https://www.instagram.com/agingjrnl/ YouTube - https://www.youtube.com/@AgingJournal LinkedIn - https://www.linkedin.com/company/aging/ Pinterest - https://www.pinterest.com/AgingUS/ Media Contact 18009220957 MEDIA@IMPACTJOURNALS.COM