Decline In Physiological Function Research Articles

The influence of nutrition on brain aging: A Comprehensive Review

Purpose: Aging is characterized by a progressive decline in physiological functions, including those of the brain. As individuals age, cognitive and emotional functionalities are subject to change, Consequently, it is essential to consider both cognitive abilities and emotional functioning when examining the effects of aging on the brain. Objectives: The objective is to synthesize current scientific evidence on the relationship between nutrition and brain aging, with a specific focus on cognitive abilities as a measure of brain function. Methodology: A systematic review was conducted on nine studies. The PRISMA statement standards were adhered to in this systematic review. Findings: The findings showed how important it is for people to change their diets to prevent the onset and progression of various comorbidities and to encourage healthy aging. The findings of the study included in this Comprehensive review indicate that good aging and a higher quality of life may be achieved by abstaining from bad behaviors, particularly those related to food. Conclusions: The current body of study indicates a relationship between nutrition and brain aging, but additional studies are necessary to expand our understanding of these complex interactions and to develop clear dietary recommendations to support cognitive health across the lifespan.

Enhanced recovery after surgery (ERAS) improves outcomes in elderly patients undergoing short-level lumbar fusion surgery: a retrospective study of 333 cases

BackgroundDegenerative lumbar disease significantly impairs the quality of life in elderly individuals, with short-segment lumbar degenerative disease being particularly prevalent. When conservative treatment proves ineffective, surgical intervention becomes the optimal choice for managing lumbar disease. The implementation of Enhanced Recovery After Surgery (ERAS) in spinal surgery has been progressively refined, leading to greater patient benefits. However, age and the associated decline in physiological function remain critical factors influencing surgical decision-making. Currently, there is a paucity of research focused on elderly patients undergoing lumbar fusion surgery to substantiate that advanced age does not diminish the benefits derived from ERAS in this demographic.MethodsThis is a retrospective cohort study of prospectively collected data. Patients who underwent short-segment (1 or 2 segments) transforaminal lumbar interbody fusion (TLIF) under the care of the same surgical team at our institution were recruited, and divided into no-ERAS-elder, ERAS-elder, and ERAS-younger groups. Subsequently, time to physiological function recovery and other outcomes were compared.ResultsThe outcomes of the ERAS-elder group (n = 113) and the no-ERAS-elder group (n = 120) were compared. The overall physiological function recovery was significantly faster (6.71 ± 2.6 days vs. 8.6 ± 2.67 days, p = 0.01) in the ERAS-elder group. Next, the outcomes of the ERAS-elder group (n = 113) were compared with those of the ERAS-younger group (n = 100), and no significant difference in total physiological function recovery was found between the two groups (6.71 ± 2.6 days vs. 6.14 ± 1.63 days, p = 0.252).ConclusionsThis study shows that the implementation of the ERAS program can effectively shorten the recovery time of physiological function in elderly patients after short-segment lumbar surgery, reduce the incidence of some complications, alleviate pain, and significantly shorten the length of hospital stay. ERAS enables elderly patients to achieve outcomes comparable to those of younger patients.

Genomic instability and genetic heterogeneity in aging: insights from clonal hematopoiesis (CHIP), monoclonal gammopathy (MGUS), and monoclonal B-cell lymphocytosis (MBL).

Aging is a multifaceted process characterized by a gradual decline in physiological function and increased susceptibility to a range of chronic diseases. Among the molecular and cellular mechanisms driving aging, genomic instability is a fundamental hallmark, contributing to increased mutation load and genetic heterogeneity within cellular populations. This review explores the role of genomic instability and genetic heterogeneity in aging in the hematopoietic system, with a particular focus on clonal hematopoiesis of indeterminate potential (CHIP), monoclonal gammopathy of undetermined significance (MGUS), and monoclonal B-cell lymphocytosis (MBL) as biomarkers. CHIP involves the clonal expansion of hematopoietic stem cells with somatic mutations. In contrast, MGUS is characterized by the presence of clonal plasma cells producing monoclonal immunoglobulins, while MBL is characterized by clonal proliferation of B cells. These conditions are prevalent in the aging population and serve as measurable indicators of underlying genomic instability. Studying these entities offers valuable insights into the mechanisms by which somatic mutations accumulate and drive clonal evolution in the hematopoietic system, providing a deeper understanding of how aging impacts cellular and tissue homeostasis. In summary, the hematopoietic system serves as a powerful model for investigating the interplay between genomic instability and aging. Incorporating age-related hematological conditions into aging research, alongside other biomarkers such as epigenetic clocks, can enhance the precision and predictive power of biological age assessments. These biomarkers provide a comprehensive view of the aging process, facilitating the early detection of age-related diseases and hopefully enabling personalized healthcare strategies.

Sirtuin 3 drives sex-specific responses to age-related changes in mouse embryonic fibroblasts

The aging process is a complex phenomenon characterised by a gradual decline in physiological functions and an increased susceptibility to age-related diseases. An important factor in aging is mitochondrial dysfunction, which leads to an accumulation of cellular damage over time. Mitochondrial Sirtuin 3 (Sirt3), an important regulator of energy metabolism, plays a central role in maintaining mitochondrial function. Loss of Sirt3 can lead to reduced energy levels and an impaired ability to repair cellular damage, a hallmark of the aging process. In this study we investigated the impact of Sirt3 loss on mitochondrial function, metabolic responses and cellular aging processes in male and female mouse embryonic fibroblasts (MEF) exposed to etoposide-induced DNA damage, which is commonly associated with cellular dysfunction and senescence. We found that Sirt3 contributes to the sex-specific metabolic response to etoposide treatment. While male MEF exhibited minimal damage suggesting potential prior adaptation to stress due to Sirt3 loss, female MEF lacking Sirt3 experienced higher vulnerability to genotoxic stress, implying a pivotal role of Sirt3 in their resistance to such challenges. These findings offer potential insights into therapeutic strategies targeting Sirt3- and sex-specific signalling pathways in diseases associated with DNA damage that play a critical role in the aging process.

The impact of mind-body exercise on the quality of life in older adults: the chain mediation effect of perceived social support and psychological resilience.

With the intensification of the global aging trend, there is a contradiction between the extended lifespan and the decline of physiological functions among the older adult. It has become a global consensus to focus on and improve the quality of life for the older adult. Mind-body exercises (Tai Chi, Ba Duan Jin, Yi Jin Jing) play a crucial role in promoting the quality of life for older adults, but the mechanisms and mediating effects are not yet clear. This study examines the impact of mind-body exercises (Tai Chi, Ba Duan Jin, Yi Jin Jing) on the quality of life in older adults, with a particular focus on exploring the chain mediating effects of perceived social support and psychological resilience. This study is a cross-sectional study that surveyed 1,087 older adults participating in mind-body exercises (Tai Chi, Ba Duan Jin, Yi Jin Jing) in 13 districts of Beijing, China, from March 25 to May 3, 2024. The Physical Activity Rating Scale (PARS-3), the World Health Organization Quality of Life Scale (WHOQOL-BREF), the Perceived Social Support Scale (PSSS), and the Connor-Davidson Resilience Scale (CD-RISC) were used to measure mind-body exercise, perceived social support, psychological resilience, and quality of life, respectively. Data were statistically analyzed using SPSS 26.0, and mediation effects were tested and effect analysis was conducted through structural equation modeling (AMOS) and the Bootstrap method. The study results show that mind-body exercises (Tai Chi, Ba Duan Jin, Yi Jin Jing) are significantly and positively correlated with the quality of life in older adults (r = 0.549, p < 0.01). The path coefficients for the relationships mind-body exercise → perceived social support (β = 0.46, p < 0.001) → psychological resilience (β = 0.20, p < 0.001) → quality of life in older adults (β = 0.39, p < 0.001) are significant, indicating that perceived social support and psychological resilience have a chain mediating effect between mind-body exercise and the quality of life in older adults. Mind-body exercises not only improve the quality of life for older adults but also indirectly enhance it by strengthening perceived social support and psychological resilience. This study provides significant reference for developing health intervention strategies targeted at older adults, suggesting that promoting mind-body exercises can improve their sense of perceived social support and psychological resilience, thereby increasing their quality of life.

The impact of social partners: investigating mixed-strain housing effects on aging in female mice.

Aging is a multifaceted process characterized by the gradual decline of physiological functions and can be modulated by various internal and external factors. While social interactions have been shown to affect behaviors and physiology in different species, the impact of social partners on aging-related phenotypes and lifespan in mice remains understudied. To address this question, we investigated various aging-related traits and lifespan in two mouse strains, C57BL/6J and BALB/c, under two different housing conditions: mixed-strain and same-strain housing. Analyses using a Generalized Linear Model revealed significant differences between the two strains in several phenotypes, including metabolic, anxiety-like, and electrocardiographic traits. However, surprisingly, housing conditions did not significantly affect most of the examined parameters, including overall lifespan. Only 3 out of 25 traits-body weight change in a metabolic cage, running wheel activity, and survival days of a quartiles of mice with middle lifespans-were influenced by housing conditions in a strain-dependent manner. Together, our study suggested a minimal influence of co-housing with social partners from different genetic backgrounds on aging-related phenotypes. This result demonstrates the feasibility of mixed housing for mouse husbandry and, more importantly, provides valuable insights for future research on the social influences on the aging process in mice.

The vicious cycle of frailty and pain: a two-sided causal relationship revealed.

The decline in physiological functions in the older people is frequently accompanied with pain and frailty, yet the causal connection between frailty and pain remains uncertain. In this study, we utilized a two-sample Mendelian randomization (MR) approach to investigate the potential causal association between frailty and pain. Two-sample bidirectional MR was conducted using summary data from genome-wide association studies to examine the potential causal relationship between frailty (defined by the frailty index and frailty phenotype) and pain. Summary genome wide association statistics were extracted from populations of European ancestry. We also investigated the causal relationship between frailty and site-specific pain, including joint pain, limb pain, thoracic spine pain and low back pain. Causal effects were estimated using the inverse variance weighting method. Sensitivity analyses were performed to validate the robustness of the results. Genetic predisposition to frailty was associated with an increased risk of pain (frailty phenotype odds ratio [OR]: 1.73; P = 3.54 × 10-6, frailty index OR: 1.36; P = 2.43 × 10-4). Meanwhile, individuals with a genetic inclination toward pain had a higher risk of developing frailty. Regarding site-specific pain, genetic prediction of the frailty phenotype increased the occurrence risk of joint pain, limb pain and low back pain. Reverse MR analysis further showed that limb pain and low back pain were associated with an increased risk of frailty occurrence. This study presented evidence supporting a bidirectional causal relationship between frailty and pain. We highlighted the significance of addressing pain to prevent frailty and recommend the inclusion of pain assessment in the evaluation system for frailty.

Oxidative stress and aging: synergies for age related diseases.

Aging is characterized by a progressive decline in physiological function and underlies several disabilities, including the increased sensitivity of cells and tissues to undergo pathological oxidative stress. In recent years, efforts have been made to better understand the relationship between age and oxidative stress and further develop therapeutic strategies to minimize the impact of both events on age-related diseases. In this work, we review the impact of the oxidant and antioxidant systems during aging and disease development and discuss the crosstalk of oxidative stress and other aging processes, with a focus on studies conducted in elderly populations.

Integrating Machine Learning with Multi-Omics Technologies in Geroscience: Towards Personalized Medicine.

Aging is a fundamental biological process characterized by a progressive decline in physiological functions and an increased susceptibility to diseases. Understanding aging at the molecular level is crucial for developing interventions that could delay or reverse its effects. This review explores the integration of machine learning (ML) with multi-omics technologies-including genomics, transcriptomics, epigenomics, proteomics, and metabolomics-in studying the molecular hallmarks of aging to develop personalized medicine interventions. These hallmarks include genomic instability, telomere attrition, epigenetic alterations, loss of proteostasis, disabled macroautophagy, deregulated nutrient sensing, mitochondrial dysfunction, cellular senescence, stem cell exhaustion, altered intercellular communication, chronic inflammation, and dysbiosis. Using ML to analyze big and complex datasets helps uncover detailed molecular interactions and pathways that play a role in aging. The advances of ML can facilitate the discovery of biomarkers and therapeutic targets, offering insights into personalized anti-aging strategies. With these developments, the future points toward a better understanding of the aging process, aiming ultimately to promote healthy aging and extend life expectancy.

Evaluating the Effects of Long-Term Exposure to Fine Particulate Matter (PM2.5) on Depressive Mood among Korean Older Adults Using Multilevel Analysis.

The harmful effects of particulate matter (PM) are amplified in older adults, who experience a decline in physiological function, reducing their ability to expel and detoxify inhaled PM. Moreover, older adults may be more vulnerable to fine particulate toxicity due to underlying medical conditions. We assessed the effects of long-term exposure to fine particulate matter (PM2.5) on depressive mood (DM) in adults aged > 65 yr using community-based data. In the 2017, Korean Community Health Survey (KCHS) data, data of PM2.5 and community factors were constructed based on participants who responded to DM in a sample of 67,802 individuals. To evaluate the effect of PM2.5 on DM among older adults, a multilevel regression model was constructed using individual-(KCHS) and community-level data (PM2.5, green area per capita, urban area, social welfare budget, health, and social business). For PM2.5, an independent variable, quartiles were used to classify regions according to concentration. A positive correlation was found between PM2.5 and DM of older adults. Compared to Q1, the odds ratio increased to 1.15 (95% CI 0.76-1.74) in Q2, 1.55 (95% CI 1.02-2.35) in Q3, and 1.60 (95% CI 1.16-2.20) in Q4. DM may increase in older individuals living in areas with high PM2.5. Systematic mental health management is required for older individuals residing in such areas.

Beyond the genome: protecting the proteome may be the key to preventing skin aging.

Skin aging is associated with a progressive decline in physiological functions, skin cancers and, ultimately, death. It may be categorized as intrinsic or extrinsic, whereby intrinsic aging is attributed to chronological and genetic factors. At the molecular level, skin aging involves changes in protein conformation and function. The skin proteome changes constantly, mainly through carbonylation; an irreversible phenomenon leading to protein accumulation as toxic aggregates that impair cellular physiology and accelerate skin aging. This review details the central role of proteostasis during skin aging and why proteome protection may be a promising approach in mitigating skin aging. A comprehensive literature review of 87 articles focusing on the proteome, proteostasis, proteotoxicity, protein carbonylation, and the impact of the damaged proteome on aging, and in particular skin aging, was conducted. Skin aging is associated with deficiencies in the repair mechanisms of DNA, transcriptional control, mitochondrial function, cell cycle control, apoptosis, cellular metabolism, changes in hormonal levels secondary to toxicity of damaged proteins, and cell-to-cell communication for tissue homeostasis, which are largely controlled by proteins. In this context, a damaged proteome that leads to the loss of proteostasis may be considered as the first step in tissue aging. There is growing evidence that a healthy proteome plays a central role in skin and in maintaining healthy tissues, thus slowing down the process of skin aging. Hence, protecting the proteome against oxidative or other damage may be an appropriate strategy to prevent and delay skin aging.

Glycosylation in aging and neurodegenerative diseases.

Aging, a complex biological process, involves the progressive decline of physiological functions across various systems, leading to increased susceptibility to neurodegenerative diseases. In society, demographic aging imposes significant economic and social burdens due to these conditions. This review specifically examines the association of protein glycosylation with aging and neurodegenerative diseases. Glycosylation, a critical post-translational modification, influences numerous aspects of protein function that are pivotal in aging and the pathophysiology of diseases such as Alzheimer's disease, Parkinson's disease, and other neurodegenerative conditions. We highlight the alterations in glycosylation patterns observed during aging, their implications in the onset and progression of neurodegenerative diseases, and the potential of glycosylation profiles as biomarkers for early detection, prognosis, and monitoring of these age-associated conditions, and delve into the mechanisms of glycosylation. Furthermore, this review explores their role in regulating protein function and mediating critical biological interactions in these diseases. By examining the changes in glycosylation profiles associated with each part, this review underscores the potential of glycosylation research as a tool to enhance our understanding of aging and its related diseases.

The long noncoding RNA (LINC-RBE) expression in testicular cells is associated with aging of the rat.

Long noncoding RNAs (lncRNAs) are important regulatory biomolecules responsible for many cellular processes. The aging of mammals is manifested by a slow and gradual decline of physiological functions after adulthood, progressively resulting in age-related diseases. Testis comprises different cell-types with defined functions for producing haploid gametes and androgens in males, contributing gene-pool to the next generation with genetic variations to species for evolutionary advantage. The LINC-RBE (long intergenic noncoding-rat brain expressed) RNA showed highest expression in the Leydig cells, responsible for steroidogenesis and production of testosterone; higher expression in primary spermatocytes (pachytene cells), responsible for generation of haploid gametes and high expression in Sertoli cells, the nursing cells of the testes. Testes of immature (4-weeks), adult (16- and 44-weeks), and nearly-old (70-weeks) rats showed low, high, and again low levels of expression, respectively. This along with the nuclear-cytoplasmic localization of LINC-RBE RNA showed age-related expression and function. Thus, expression of LINC-RBE is involved in the molecular physiology of testes, especially Leydig cells, primary spermatocytes, and Sertoli cells. The decline in its expression correlates with diminishing reproductive function of the testes during aging of the rat.

The Effect of Omega-3 Fatty Acid Supplementation and Exercise on Locomotor Activity, Exploratory Activity, and Anxiety-Like Behavior in Adult and Aged Rats.

Aging is an inevitable and complex biological process that is associated with a gradual decline in physiological functions and a higher disease susceptibility. Omega-3 fatty acids, particularly docosahexaenoic acid, play a crucial role in maintaining brain health and their deficiency is linked to age-related cognitive decline. Combining omega-3-rich diets with exercise may enhance cognitive function more effectively, as both share overlapping neurobiological and physiological effects. This study aimed to evaluate the effect of exercise and omega-3 fatty acid (FA) supplementation in two different doses (160 mg/kg and 320 mg/kg) on anxiety-like behavior and cognitive abilities in both adult and aged rats. Male Wistar rats (4-5- and 23-24-month-old) were randomly divided into seven groups: 3-week control supplemented with placebo without exercise, low-dose omega-3 FAs, high-dose omega-3 FAs, 7-week control supplemented with placebo without exercise, exercise-only, low-dose omega-3 FAs with exercise, and high-dose omega-3 FAs with exercise. The administered oil contained omega-3 FAs with DHA:EPA in a ratio of 1.5:1. Our results indicate that aging negatively impacts the locomotor and exploratory activity of rats. In adult rats, a low dose of omega-3 FAs reduces locomotor activity when combined with exercise while high dose of omega-3 FAs reduces anxiety-like behavior and improves recognition memory when combined with exercise. The combination of omega-3 FAs and exercise had varying impacts on behavior, suggesting a need for further research in this area to fully understand their therapeutic efficacy in the context of cognitive changes associated with aging.

Towards Healthy Longevity: Comprehensive Insights from Molecular Targets and Biomarkers to Biological Clocks.

Aging is a complex and time-dependent decline in physiological function that affects most organisms, leading to increased risk of age-related diseases. Investigating the molecular underpinnings of aging is crucial to identify geroprotectors, precisely quantify biological age, and propose healthy longevity approaches. This review explores pathways that are currently being investigated as intervention targets and aging biomarkers spanning molecular, cellular, and systemic dimensions. Interventions that target these hallmarks may ameliorate the aging process, with some progressing to clinical trials. Biomarkers of these hallmarks are used to estimate biological aging and risk of aging-associated disease. Utilizing aging biomarkers, biological aging clocks can be constructed that predict a state of abnormal aging, age-related diseases, and increased mortality. Biological age estimation can therefore provide the basis for a fine-grained risk stratification by predicting all-cause mortality well ahead of the onset of specific diseases, thus offering a window for intervention. Yet, despite technological advancements, challenges persist due to individual variability and the dynamic nature of these biomarkers. Addressing this requires longitudinal studies for robust biomarker identification. Overall, utilizing the hallmarks of aging to discover new drug targets and develop new biomarkers opens new frontiers in medicine. Prospects involve multi-omics integration, machine learning, and personalized approaches for targeted interventions, promising a healthier aging population.

Kegiatan Penapisan Status Gizi Pada Kelompok Lanjut Usia Di Gereja ST. Fransiskus Asisi

Aging is associated with a gradual decline in physiological function, impacting multiple organ systems and reducing resistance to physical, cognitive, and mental stress. Adequate nutrition is critical for elderly people's health and quality of life. However, elderly people are susceptible to nutritional problems, including weight loss, decreased muscle mass (sarcopenia), and weakness. Decreased physical activity, hormonal changes, and metabolic adjustments influence these changes. The elderly population receiving treatment in institutions and hospitals has a significantly higher prevalence of malnutrition. This activity uses the Plan-Do-Check-Act (PDCA) framework to screen the nutritional status of the elderly using the Mini Nutritional Assessment (MNA) questionnaire. Activities were held at St. Fransiskus Assisi, Jakarta which included 35 participants. It was found that 10 people (27.78%) were at risk of experiencing malnutrition and 6 people (16.67%) experienced malnutrition. Early nutritional screening using the MNA questionnaire is essential to detect and prevent complications related to malnutrition in the elderly, thereby improving individual health outcomes and quality of life.

Aging and Autophagy: Roles in Musculoskeletal System Injury.

Aging is a multifactorial process that ultimately leads to a decline in physiological function and a consequent reduction in the health span, and quality of life in elderly population. In musculoskeletal diseases, aging is often associated with a gradual loss of skeletal muscle mass and strength, resulting in reduced functional capacity and an increased risk of chronic metabolic diseases, leading to impaired function and increased mortality. Autophagy is a highly conserved physiological process by which cells, under the regulation of autophagy-related genes, degrade their own organelles and large molecules by lysosomal degradation. This process is unique to eukaryotic cells and is a strict regulator of homeostasis, the maintenance of energy and substance balance. Autophagy plays an important role in a wide range of physiological and pathological processes such as cell homeostasis, aging, immunity, tumorigenesis and neurodegenerative diseases. On the one hand, under mild stress conditions, autophagy mediates the restoration of homeostasis and proliferation, reduction of the rate of aging and delay of the aging process. On the other hand, under more intense stress conditions, an inadequate suppression of autophagy can lead to cellular aging. Conversely, autophagy activity decreases during aging. Due to the interrelationship between aging and autophagy, limited literature exists on this topic. Therefore, the objective of this review is to summarize the current concepts on aging and autophagy in the musculoskeletal system. The aim is to better understand the mechanisms of age-related changes in bone, joint and muscle, as well as the interaction relationship between autophagy and aging. Its goal is to provide a comprehensive perspective for the improvement of diseases of the musculoskeletal system.

PARG Protein Regulation Roles in Drosophila Longevity Control.

Aging, marked by a gradual decline in physiological function and heightened vulnerability to age-related diseases, remains a complex biological process with multifaceted regulatory mechanisms. Our study elucidates the critical role of poly(ADP-ribose) glycohydrolase (PARG), responsible for catabolizing poly(ADP-ribose) (pADPr) in the aging process by modulating the expression of age-related genes in Drosophila melanogaster. Specifically, we uncover the regulatory function of the uncharacterized PARG C-terminal domain in controlling PARG activity. Flies lacking this domain exhibit a significantly reduced lifespan compared to wild-type counterparts. Furthermore, we observe progressive dysregulation of age-related gene expression during aging, accelerated in the absence of PARG activity, culminating in a premature aging phenotype. Our findings reveal the critical involvement of the pADPr pathway as a key player in the aging process, highlighting its potential as a therapeutic target for mitigating age-related effects.

Validation of Hospital Frailty Risk Score in Heart Failure

Background: Frailty is prevalent in older people and results from age-related decline in physiological function and reserve. The objective of this study was to validate the Hospital Frailty Risk Score (HFRS) in predicting outcomes and hospitalisation usage in older hospitalised heart failure (HF) patients. Methods: This study was a retrospective review of electronic medical records. Patients aged ≥65 years admitted with HF to a Singapore tertiary hospital between 1 January 2021 and 30 April 2021 were included. Patients were identified as HF patients in the value-driven care pathway and using ICD codes for HF. They were categorised into low risk (&lt;5), intermediate risk (5–15) and high risk (&gt;15) of frailty using the HFRS. Results: A total of 208 older patients with HF were included (mean age 79.4 years; 50.5% males). Using the HFRS, 35.1% were deemed at low risk, 46.2% at intermediate risk and 18.8% at high risk of frailty. Those at high risk of frailty were older than those at low risk (mean age 84.8 versus 76.5 years, respectively; p&lt;0.001). Women had a higher risk of frailty than men. Univariate analyses showed longer length of stay (LOS) and higher 30-, 90- and 365-day mortality in those at high frailty risk. In multivariate analyses, HFRS was associated with long LOS, 90-day and 1-year mortality. Dementia, acute MI and renal disease were more common in high-risk patients. Comparing HFRS with the Charlson Comorbidity Index (CCI), HFRS was a better predictor of long LOS, mortality at 30, 90, 1 year and 30-day readmission than CCI. HFRS alone was a better predictor than combining the HFRS and CCI. Conclusion: Older patients with higher HFRS have increased healthcare utilisation, including longer LOS and higher mortality.

P01 Remodelling of the dermoepidermal junction occurs in intrinsically aged Far East Asian skin without significant epidermal atrophy

Abstract Introduction and aims Ageing is characterized by a gradual decline in physiological function and is influenced by both intrinsic genetic and extrinsic lifestyle and environmental factors. However, much of our knowledge of cutaneous ageing comes from the study of White populations. We have previously shown that the organization of young healthy skin is ethnicity-dependent and that altered epidermal morphology in White volunteers correlates with loss of biomechanical function in the skin. In this study, we used epidermal morphometry to determine whether parameters associated with intrinsic skin ageing in White skin are also observed in Far East Asian skin. Methods Archival skin samples were obtained from the Asian Skin Biobank [young (3–21 years), N = 38, 37 male samples (Chinese, n = 16; Malay, n = 16; other Far East, n = 6); aged (61–86 years), N = 7, one male sample (Chinese, n = 6; Malay, n = 1)] and stained with haematoxylin and eosin prior to image analysis for dermoepidermal junction (DEJ) convolution and measurement of epidermal thickness. Weigert’s resorcin-fuchsin stain was used to ensure samples were photoprotected. Results Weigert’s resorcin-fuchsin stain revealed that all samples were photoprotected, with no evidence of solar elastosis. We next compared whether geographic ancestry of our local Far East Asian population impacted epidermal morphology in young skin; neither DEJ convolution nor epidermal thickness were impacted by geographic ancestry. However, a significant flattening of the DEJ was observed between young and aged samples (P &amp;lt; 0.01). Interestingly, no significant difference in epidermal thickness was observed as a function of age. Conclusions While intrinsically aged Asian skin undergoes the same flattening of the DEJ that is seen in White populations, epidermal thickness does not significantly alter; this is in stark contrast to intrinsically aged White skin, where epidermal atrophy is observed. Hence, the trajectory of intrinsic cutaneous ageing may be ethnicity-dependent, providing further evidence that studies of skin from different ethnicities are necessary.