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At least 19 recordsLinked to original sources
PubMed1979

Relationship between actinic damage and chronologic aging in keratinocyte cultures of human skin.

The relationship of actinically-induced "premature aging" to chronological aging was studied in paired keratinocyte cultures obtained from the habitually sun-exposed (lateral) and nonexposed (medial) aspects of the arm of 5 male donors, aged 41 to 80 yr. In all cases, the number of cell generations in vitro was greater for cultures derived from sun-exposed skin, and this discrepancy increased with donor age and the severity of clinical aging changes. Hence, chronic sun exposure does accelerate aging in human skin by at least one previously established in vitro criterion: it decreased the lifespan of cultured keratinocytes. Plating efficiency was 11- to 32-fold higher for keratinocytes from chronically sun-exposed skin than nonexposed controls, perhaps reflecting the recognized carcinogenic potential of actinic radiation. Keratinocyte cultures appear to be as amenable to gerontologic studies as the already widely used human fibroblast cultures.

Adult↗
PubMed1979

Weight and skeletal maturation - a study of radiological and chronological age in an anorexia nervosa population.

The carpal bones of 18 anorexia nervosa patients were radiographed and the X-ray age assessed by 2 different standard methods. The study demonstrates that skeletal development in anorexia nervosa patients is delayed such that there is no association between radiological assessment of age and chronological age. It is strongly suggested that bony development actually ceases when body weight falls sufficiently to stop menstruation. There was a highly significant (P = 0.001) linear relationship between radiological age and the sum of the age of onset of the illness plus any period(s) of re-feeding. Weight gain seems to re-kindle the bone maturing mechanisms: the role of weight thresholds and associated hormone activity being discussed. The findings of this study strongly support the existing evidence that the anorexia nervosa patient is biologically and psychologically immature.

Adolescent↗
PubMed1976

Growth of the second metacarpal according to chronological age and skeletal maturation.

In relation to chronological age and skeletal maturation, the growth of the second metacarpal is discussed based on radiographs of the right hand and wrist in 499 male and 424 female Japanese aged 1 to 18 years. When plotted against age, bone length and width present the general growth pattern of Scammon, the adolescent spurt occurring at about 13 years in the males and 11 years in the females, and the mean values are significantly larger in the males than in the females at age 15 years for length, and age 13 years for width, and later. The growth curves of both sexes are almost parallel to each other for bone length plotted against skeletal maturation. Bone width progresses in parallel in males and females until about adolescence, whereafter there is a more rapid increase in growth in the males than in the females. The mean values for length and width are almost always significantly greater in the males than in the females. The width/length index decreases rapidly until a certain period, the minimum value being at about ten years or a maturity corresponding to that age, and then increase slightly again to reach an equilibrium state on the basis of both age and skeletal maturation. At any given age, the mean values are always greater in the males than in the females. However, according to skeletal maturation, the sex differences are steadily significant at and after the skeletal maturity corresponding to about 12 years in the males and 10 years in the females.

Adolescent↗
PubMed1979

A brief note on a preliminary study of life satisfaction for male university faculty of differing chronological ages.

Male faculty of a large southeastern university were surveyed in order to determine the relationship between life satisfaction and chronological age for a relatively homogeneous population. It was found that satisfaction increased linearly with age for this group. However, the relationship was so slight it was suggested that differences in chronological age did not account for a meaningful amount of the variance in life satisfaction. This is consistent with results obtained for larger segments of the population. Suggestions for further research are provided.

Adult↗
PubMed2026

The effects of tildrakizumab in the epigenetic aging deviation of psoriasis: A 52-week open-label study.

BACKGROUND: While biologic therapies targeting interleukin-23 control cutaneous inflammation in psoriasis, their impact on epigenetic aging has not been previously demonstrated. OBJECTIVES: To evaluate the effects of tildrakizumab treatment in the epigenetic aging deviation of moderate-to severe psoriasis. METHODS: In an open-label 52-week clinical trial, 20 adults with psoriasis were treated with tildrakizumab-asmn 100 mg injections until week 28. Ten age-matched controls without psoriasis were enrolled. Genome-wide DNA methylation was profiled in peripheral blood leukocyte DNA (MethylationEPICv2.0, Illumina) to calculate epigenetic aging clocks predictive of all-cause-mortality, phenotypic age, chronological age, pace of aging, and telomere length. Epigenetic age deviation was calculated as the residuals against chronological age. RESULTS: Psoriasis patients had increased epigenetic age deviation in clocks predictive of mortality: PCGrimAge (P = .008), cytosine-phosphate-guanine (CpG) PTPCGrimAge3 (P = .019), CpGPTGrimAge3 (P = .019), GrimAge2 (P = .049). PCGrimAge was reversed by 0.3 years (week 28, P = .005) and 0.5 years (week 52, P = .04) after the use of tildrakizumab-asmn. The pace of aging was increased in psoriasis patients: DunedinPACE (P = .049). LIMITATIONS: Pilot study (small sample size). CONCLUSIONS: Psoriasis patients presented accelerated epigenetic aging in mortality-predictive clocks. Treatment with tildrakizumab-asmn (interleukin-23 inhibition) showed partial reversal of those clocks in 28 weeks. (Funded by Sun Pharmaceutical Industries, Inc; ClinicalTrials.gov number, NCT05110313).

DNA methylation clocks↗
PubMed1979

Pharmacokinetic properties of netilmicin in newborn infants.

Netilmicin and gentamicin susceptibilities of 258 gram-negative organisms and 25 strains of Staphylococcus aureus were nearly identical. The pharmacokinetic properties of netilmicin were evaluated in 101 newborn infants and related to birth weight, gestational age, chronological age, and route of administration. Mean peak serum concentrations of 5.6 to 6.9 and 7.8 to 8.4 mug/ml were observed 30 min after 3- and 4-mg/kg doses, respectively, were given intramuscularly. The peak concentrations were directly related to gestational age. The average serum half-life values varied from 3.4 to 4.7 h and in general were inversely related to birth weight, gestational age, and postnatal age. The pharmacokinetics of netilmicin in 10 infants were similar after intramuscular and intravenous administration. A comparative study of netilmicin and gentamicin in seven neonates revealed greater variability in serum concentrations of gentamicin and a shorter half-life for netilmicin. There was evidence of accumulation of netilmicin in 12 low-birth weight, premature infants who received 4-mg/kg doses for an average of 6.4 days. Serum and urine levels of netilmicin were measured up to 11 days after discontinuation of the drug. These data are well characterized by a two-compartment model. Additional studies of efficacy and long-term toxicity of netilmicin in neonates are necessary.

Bacteria↗
PubMed1977

Clinical pharmacology of methicillin in neonates.

The pharmacokinetic properties of methicillin were investigated in 59 newborn infants. Concentrations of methicillin in serum were approximately 58 and 80 microng/ml at one hour after 25 and 50 mg/kg doses, respectively. The average serum half-life values ranged from one to three hours and were inversely correlated with birth weight and chronologic age. The half-life values, volumes of distribution, and plasma clearances of methicillin are shown in relationship to gestational age and chronologic age. A dosage of 25 mg/kg is recommended for therapy of most neonatal staphylococcal diseases; the frequency of administration is altered on the basis of birth weight and chronologic age.

Birth Weight↗
PubMed2025

Multiomic clocks to predict phenotypic age in mice.

Biological age refers to a person's overall health in aging, as distinct from their chronological age. Diverse measures of biological age, referred to as "clocks," have been developed in recent years and enable risk assessments and an estimation of the efficacy of longevity interventions in animals and humans. Although most clocks are trained to predict chronological age, clocks have been developed to predict more complex composite biological age outcomes, at least in humans. These composite outcomes can be made up of a combination of phenotypic data, chronological age, and disease or mortality risk. Here, we develop the first such composite biological age measure for mice: the mouse phenotypic age model (Mouse PhenoAge). This outcome is based on frailty measures, complete blood counts, and mortality risk in a longitudinally assessed cohort of male and female C57BL/6 mice. We then develop clocks to predict Mouse PhenoAge, based on multiomic models using metabolomic and DNA methylation data. Our models accurately predict Mouse PhenoAge, and residuals of the models are associated with remaining lifespan, even for mice of the same chronological age. These methods offer novel ways to accurately predict mortality in laboratory mice, thus reducing the need for lengthy and costly survival studies.

Animals↗
PubMed2026

Metabolomic ageing across mental and behavioural disorders.

BACKGROUND: Individuals with mental disorders face excess morbidity and premature mortality. Accelerated ageing has been proposed as a contributing mechanism but population-scale evidence across diverse diagnoses is limited. OBJECTIVE: To examine whether metabolomic ageing differs across mental disorders and whether associations vary by sex, age group and genetic liability. METHODS: Using plasma metabolomic profiles from UK Biobank participants, we applied a metabolomic ageing clock (MileAge) to estimate disorder-specific differences between metabolite-predicted and chronological age. Mental disorders were ascertained from health records and self-reported physician diagnoses. We analysed nine diagnostic groups and 45 individual disorders and assessed sex and age group differences and associations with polygenic scores. FINDINGS: Among 225&#x2009;212 participants (54% female; mean age 56.97), 38&#x2009;524 had a diagnosis preceding baseline. Substance use, psychotic, affective and neurotic disorders were associated with a metabolite-predicted age older than chronological age, largest for psychosis (&#x3b2;=0.556, 95% CI 0.250 to 0.861, p<0.001). Obsessive-compulsive and eating disorders were associated with a metabolite-predicted age younger than chronological age. Several associations were stronger in males and in individuals aged <65 years. Higher genetic liability to depression, autism and attention-deficit/hyperactivity disorder predicted an older metabolomic age (&#x3b2; range=0.020&#x2009;to 0.047), whereas polygenic scores for psychosis and tobacco use disorder predicted a younger metabolomic age (&#x3b2; range=-0.023&#x2009;to -0.040). For obsessive-compulsive disorder and anorexia nervosa, clinical and genetic associations indicated younger metabolomic ageing. CONCLUSIONS: Metabolomic ageing in mental disorders is heterogeneous. While many disorders are associated with an older biological age, some are linked to a younger biological age. Divergence between genetic liability and clinical phenotypes suggests that non-genetic factors shape biological ageing differences. CLINICAL IMPLICATIONS: Biological age should not be assumed to uniformly exceed chronological age across mental disorders. Sex and age-specific approaches could improve understanding of biological ageing processes in psychiatry.

Humans↗
PubMed1979

Body composition in hypopituitary dwarfs before and during human growth hormone therapy.

The clinical characteristics and body composition of eight hypopituitary dwarfs (10.2-21.6 yr) were analyzed before and after 6 and 12 mo of growth hormone therapy. 2 IU 3 times/wk. Before treatment, growth rate was 1.8 +/- 0.7 cm/yr, height age was 2.0-12.8 yr less, and bone age 2.0-11.1 yr less than chronologic age. Total body water (TBW), lean body mass (LBM), extracellular water (ECW), and intracellular water (ICW) were below normal for chronologic age, but normal for height. Muscle mass (MM) was below normal for age and height. During HGH therapy, growth rate was 7.1 +/- 1.6 cm/yr in the first 6 mo and 7.8 +/- 1.4 cm/yr during the next 6 mo; the ratio of change in height age to change in chronologic age was greater than or equal to 1.0 in all patients and the ratio of change in bone age to change in height age was 1.2 in one patient and less than or equal to 1.0 in the others. TBW, LBM, ECW, and ICW increased according to height increments; however, MM increased at a faster rate than expected from the height gains. Also, a relative or absolute loss of total body fat was recorded during the first 6 mo of therapy. It is suggested (1) that among the body composition parameters studied, muscle mass is the tissue most closely reflecting the lack of HGH and also its therapeutic benefits and (2) evaluation of body composition in hypopituitary dwarfs in response to HGH therapy shows striking changes not reflected by the determination of stature or weight alone.

Adolescent↗
PubMed1975

Prediction of adult height from height, bone age, and occurrence of menarche, at ages 4 to 16 with allowance for midparent height.

Multiple regression equations for predicting the adult height of boys and girls from height and bone age at ages 4 and upwards are presented. There is a separate equation for each half year of chronological age; and for pre- and postmenarcheal girls at ages 11 to 14. These are based on longitudinal data from 116 boys and 95 girls of the Harpenden Growth Study and the London group of the International Children's Centre longitudinal study. The bone age used is the revised version of the Tanner-Whitehouse standards, omitting the score for carpal bones (RUS age, TW 2 system). Boys aged 4 to 12 are predicted in 95% of instances to within plus or minus 7 cm of true height, and at ages 13 and 14 to within plus or minus 6 cm. Girls ages 4 to 11 are predicted to within plus or minus 6 cm; premenarcheal girls aged 12 and 13 to within plus or minus 5 and plus or minus 4 cm, respectively; and postmenarcheal girls aged 12 and 13 to within plus or minus 4 and plus or minus 3 cm, respectively. Prediction can be somewhat imporved by allowing for midparent height. One-third of the amount that midparent height differs from mean midparent height is added or subtracted. An alternative system of equations which are based on initial classification by bone age rather than chronological age is given. These have about the same accuracy as the equations based on initial classification by chronological age, but allowance for bone age retardation is less. It is not clear which system is preferable. The equations probably apply to girls complaining of tall stature and boys or girls complaining of shortness and needing reassurance as to normality. In clearly pathological children, such as those with endocrinopathies, they do not apply.

Adolescent↗
PubMed2026

Epigenetic aging of colorectal mucosa in cancer development.

BACKGROUND: The past decade has seen the development of epigenetic models of aging that accurately estimate chronological age and predict disease incidence and mortality. These estimates are modulated by lifestyle and environmental factors linked to carcinogenesis, but to date this has primarily been studied in blood. METHODS: We examined epigenetic aging in normal colonic tissue (n&#x2009;=&#x2009;96), adjacent mucosa (n&#x2009;=&#x2009;245) and tumors (n&#x2009;=&#x2009;208), using models trained on age (Horvath, Hannum, Zhang), mortality (PhenoAge, GrimAge), aging rate (DunedinPACE), cellular mitotic history (EpiTOC, epiTOC2, miAGe), and telomere length (DNAmTL). RESULTS: The Horvath model was the most accurate estimator of chronological age in normal colonic mucosa, with high correlation (r&#x2009;>&#x2009;0.70) between the Horvath, Hannum, Zhang, PhenoAge and GrimAge models, and between mitotic clocks (r&#x2009;>&#x2009;0.94). All models showed similar performance in normal tissue and adjacent mucosa, but substantially more variation in estimates in tumors. Significant differences in age acceleration were present between normal and adjacent mucosa by six models (Hannum, Zhang, PhenoAge, EpiTOC, epiTOC2 and miAge), while tumors showed highly significant differences by all models. Age acceleration differed by region of the colon, with varying patterns by model type. Physical activity (PhenoAge), smoking history (GrimAge), and alcohol consumption (Horvath, mitotic clocks) were associated with epigenetic aging in adjacent mucosa, while smoking history, smoking intensity, and alcohol consumption were associated with DNAmTL in tumors. CONCLUSIONS: Our study reveals an impact of tissue type, region, and lifestyle factors on epigenetic aging, but also highlights significant heterogeneity between models and the need for careful consideration within study design.

DNA methylation↗
PubMed2026

Identifying biomarkers of accelerated ageing in cancer patients from routine clinical data.

INTRODUCTION: Cancer and ageing have a bidirectional relationship: age is the strongest risk factor for cancer, and cancer and treatments can accelerate ageing. Therefore, biological age can differ from chronological age; biomarkers are needed to stratify interventions to minimise accelerated ageing. METHODS: PhenoAge was calculated from routine blood test results of patients attending a Geriatric Oncology clinic. PhenoAgeAccel was the residual from a regression of PhenoAge against age. RESULTS: Data were available for 173 patients (62% male). Mean PhenoAge was higher than age (84.3 (12.6) vs 76.2 (7.24), p&#x202f;<&#x202f;0.001), though the two were correlated (r&#x202f;=&#x202f;0.579, p&#x202f;<&#x202f;0.001). Unlike age, PhenoAge and PhenoAgeAccel were associated with one-year mortality (PhenoAge OR=1.083, 95% CI: 1.038-1.136; PhenoAgeAccel OR=1.096, 95% CI: 1.047-1.155). PhenoAge correlated with Clinical Frailty Score and Timed Up and Go (CFS: Rs=0.31, p&#x202f;<&#x202f;0.001; TUG: Rs=0.25, p&#x202f;<&#x202f;0.005); there were no correlations with age. PhenoAgeAccel correlated with the number of CGA interventions made (Rs=0.17, p&#x202f;<&#x202f;0.05), unlike age and PhenoAge. Patients with diabetes mellitus had a higher PhenoAgeAccel compared to those without (3.40 vs -1.71, p&#x202f;=&#x202f;0.002). In patients receiving systemic anti-cancer treatment, patients with PhenoAgeAccel calculated pre-treatment had less age acceleration than those with PhenoAgeAccel calculated post-treatment, both overall (2.18 vs -2.87; p&#x202f;=&#x202f;0.048) and in matched samples (n&#x202f;=&#x202f;21, 7.76 vs -2.87, p&#x202f;<&#x202f;0.001). CONCLUSIONS: PhenoAgeAccel is a greater predictor of risk than chronological age in older people with cancer. This makes it a promising biomarker to stratify patients for holistic geriatric assessment, dose reductions, or future geroprotective measures which could be integrated within electronic healthcare record systems.

Humans↗
PubMed2026

Sex-specific biological aging clocks across organs and omics.

Sex differentially shapes aging, neurodevelopment and neurodegenerative diseases such as Alzheimer's disease (AD). However, most biological aging clocks (artificial intelligence-predicted age minus chronological age) were trained on sex-pooled samples and implicitly assume sex invariance.Here we developed 38 sex-specific biological aging clocks across 15 organ systems. We first demonstrate the importance of sex-stratified training for constructing sex-specific healthy normative references and then reveal marked divergence between female and male clocks. Key genetic parameters and Mendelian randomization results indicate that organ-specific aging liability and its relationships to cardiometabolic, endocrine and mental traits are configured differently in females and males. Proteomic analyses identify distinct, organ-resolved synaptic, immune, vascular and metabolic networks that differentially track female and male biological aging. In longitudinal survival analyses, sex-specific clocks predict whole-body systemic diseases and all-cause mortality in a sex-dependent and organ-dependent manner. Further analyses reveal sex-dependent associations between the brain aging clock and cognitive decline trajectory during a preclinical AD clinical trial. Sex-stratified clocks may offer distinct value by defining biological age against sex-appropriate normative references and revealing sex-dependent genetic, molecular and clinical signatures that pooled models may obscure. Meanwhile, sex-pooled and sex-interaction approaches remain valuable, as human aging and disease also share fundamental biological similarities between females and males. Together, these findings reveal sex-specific biological aging signatures in aging, AD and systemic health, highlighting the need for explicitly sex-stratified modeling approaches.

Journal Article↗
PubMed1977

Skeletal maturity of the hand and wrist in Japanese children in Sapporo by the TW2 method.

Skeletal maturity of Japanese children aged 6--18 years in Sapporo was compared with that of Japanese children in Toko, as well as with that of British children, by the TW2 method. In Sapporo children, the mean skeletal age was in advance of the chronological age after ages 12 years in boys and 10 years in girls. The ages at which the skeletal age preceded the chronological age occurred earlier in the children in Tokyo than in Sapporo. The hand and wrist bones completed maturation about the same age in both Japanese and British children. Somatometric and radiological results agreed exactly.

Adolescent↗
PubMed2024

Racial and regional disparities in the risk of noncommunicable disease between sub-Saharan black and European white patients.

OBJECTIVES: Greater vulnerability of Black vs. White individuals to cardiovascular disease (CVD) and chronic kidney disease (CKD) is well charted in the United States, but studies involving sub-Saharan blacks are scarce. METHODS: Baseline data (2021-2024) were collected in 168 sub-Saharan Blacks and 93 European Whites in an ongoing clinical trial (NCT04299529), using standardized patient selection criteria. Data included clinical and biochemical risk factors, ECG and echocardiographic traits, Framingham CVD risk, CKD grades (KDIGO 2024), self-assessed symptoms (WHO questionnaire), and urinary proteomic profiles predictive of left ventricular dysfunction (LVD) and CKD, HF1, and CKD273, respectively. Racial comparisons rested on unadjusted and multivariable-adjusted analyses. RESULTS: Despite being younger (60.4 vs. 68.3&#x200a;years), blacks had a worse risk profile, as evidenced by higher diabetes prevalence, higher BMI, faster heart rate, unfavourable serum cholesterol fractions, lower estimated glomerular filtration rate, microalbuminuria, and sedentary lifestyle. This resulted in blacks having higher 10-year CVD risk, higher heart age (index of vascular ageing with chronological age as reference), and a worse CKD grades. In both races, CKD273 increased with CKD grade, but CKD273 and HF1 were not different by race. These observations were robust in subgroup and adjusted analyses. CONCLUSION: This study did not differentiate host (genetic, molecular, and pathogenic) from environmental drivers of disease. Nonetheless, the findings call for a multipronged and comprehensive implementation of innovative health policies in sub-Saharan countries. Education, research, empowerment of stakeholders, and international learned societies connecting experts from a wide array of disciplines should vigorously sustain this effort.

Humans↗