Seed priming with gas plasma-activated water in Ethiopia's "orphan" crop tef (Eragrostis tef).

MAIN CONCLUSION: Seed priming with gas plasma-activated water results in an increased ageing resilience in Eragrostis tef grains compared to a conventional hydropriming protocol. Tef (Eragrostis tef) is a cereal grass and a major staple crop of Ethiopia and Eritrea. Despite its significant importance in terms of production, consumption, and cash crop value, tef has been understudied and its productivity is low. In this study, tef grains have undergone different priming treatments to enhance seed vigour and seedling performance. A conventional hydropriming and a novel additive priming technology with gas plasma-activated water (GPAW) have been used and tef grains were then subjected to germination performance assays and accelerated ageing. Tef priming increases the germination speed and vigour of the grains. Priming with GPAW retained the seed storage potential after ageing, therefore, presenting an innovative environmental-friendly seed technology with the prospect to address variable weather conditions and ultimately food insecurity. Seed technology opens new possibilities to increase productivity of tef crop farming to achieve a secure and resilient tef food system and economic growth in Ethiopia by sustainable intensification of agriculture beyond breeding.

A genome-wide association study uncovers a ZmRap2.7-ZCN9/ZCN10 module to regulate ABA signalling and seed vigour in maize.

Seed vigour, including rapid, uniform germination and robust seedling establishment under various field conditions, is becoming an increasingly essential agronomic trait for achieving high yield in crops. However, little is known about this important seed quality trait. In this study, we performed a genome-wide association study to identify a key transcription factor ZmRap2.7, which regulates seed vigour through transcriptionally repressing expressions of three ABA signalling genes ZmPYL3, ZmPP2C and ZmABI5 and two phosphatidylethanolamine-binding genes ZCN9 and ZCN10. In addition, ZCN9 and ZCN10 proteins could interact with ZmPYL3, ZmPP2C and ZmABI5 proteins, and loss-of-function of ZmRap2.7 and overexpression of ZCN9 and ZCN10 reduced ABA sensitivity and seed vigour, suggesting a complex regulatory network for regulation of ABA signalling mediated seed vigour. Finally, we showed that four SNPs in ZmRap2.7 coding region influenced its transcriptionally binding activity to the downstream gene promoters. Together with previously identified functional variants within and surrounding ZmRap2.7, we concluded that the distinct allelic variations of ZmRap2.7 were obtained independently during maize domestication and improvement, and responded separately for the diversities of seed vigour, flowering time and brace root development. These results provide novel genes, a new regulatory network and an evolutional mechanism for understanding the molecular mechanism of seed vigour.

Nano zinc oxide mediated resuscitation of aged Cajanus cajan via modulating aquaporin, cell cycle regulatory genes and hormonal responses.

KEY MESSAGE: Nanoparticle pretreatment improved the health of aged Cajanus cajan seeds viz., regulation of redox status, gene expression, and restoration of hormonal homeostasis. Ageing deteriorates the quality of seeds by lowering their vigor and viability, and terminating with loss of germination. These days, nanotechnology has been seen to revolutionize the agricultural sectors, and particularly nano zinc oxide (nZnO) has gained considerable interests due to its distinctive properties. The aim of the present work was to decipher the possibilities of using nZnO to rejuvenate accelerated aged (AA) seeds of Cajanus cajan. Both chemically (CnZnO) and green (GnZnO; synthesized using Moringa oleifera) fabricated nZnOs were characterized via standard techniques to interpret their purity, size, and shape. Experimental results revealed erratic germination with a decline in viability and membrane stability as outcomes of reactive oxygen intermediate (ROI) buildup in AA seeds. Application of nZnO substantially rebated the accrual of ROI, along with enhanced production of antioxidants, α-amylase activity, total sugar, protein and DNA content. Higher level of zinc was assessed qualitatively/ histologically and quantitatively in nZnO pulsed AA seeds, supporting germination without inducing toxicity. Meantime, augmentation in the gibberellic acid with a simultaneous reduction in the abscisic acid level were noted in nZnO invigorated seeds than that determined in the AA seeds, suggesting possible involvement of ROI in hormonal signalling. Furthermore, nZnO-subjected AA seeds unveiled differential expression of aquaporins and cell cycle regulatory genes. Summarizing, among CnZnO and GnZnO, later one holds better potential for a revival of AA seeds of Cajanus cajan by providing considerable tolerance against ageing-associated deterioration via recouping the cellular redox homeostasis, hormonal signaling, and alteration in expression patterns of aquaporin and cell cycle regulatory genes.

Persistent accelerated epigenetic ageing in a longitudinal cohort of vertically infected HIV-positive adolescents.

We have previously shown accelerated ageing in adolescents perinatally infected with HIV (PHIV +), based on discrepancies between epigenetic and chronological age. The current study examines follow-up longitudinal patterns of epigenetic ageing and the association of epigenetic ageing with cognition as well as whole brain structure changes in PHIV + and healthy controls enrolled in the Cape Town Adolescent Antiretroviral Cohort Study (CTAAC). The Illumina EPIC array was used to generate blood DNA methylation data from 60 PHIV + adolescents and 36 age-matched controls aged 9-12 years old at baseline and again at a 36-month follow-up. Epigenetic clock software estimated two measures of epigenetic age acceleration: extrinsic epigenetic accelerated ageing (EEAA) and age acceleration difference (AAD) at both time points. At follow-up, each participant completed neuropsychological testing, structural magnetic resonance imaging, and diffusion tensor imaging. At follow-up, PHIV infection remains associated with increased EEAA and AAD. Accelerated epigenetic ageing remained positively associated with viral load and negatively associated with CD4 ratio. EEAA was positively associated with whole brain grey matter volume and alterations in whole brain white matter integrity. AAD and EEAA were not associated with cognitive function within the PHIV + group. Measures of epigenetic ageing, as detected in DNA methylation patterns, remain increased in PHIV + adolescents across a 36-month period. Associations between epigenetic ageing measures, viral biomarkers, and alterations in brain micro- and macrostructure also persist at 36-month follow-up. Further study should determine if epigenetic age acceleration is associated with cognitive functional changes due to brain alterations in later life.

Effect of titanium dioxide nanocoating on the colour stability of room temperature vulcanizing maxillofacial silicone-an invitro study.

OBJECTIVE: The aim of this in vitro study was to evaluate the effect of an oxide nanocoating to prevent colour degradation of maxillofacial silicone elastomers following accelerated ageing. MATERIAL AND METHODS: Specimens (N = 40) of specified dimensions were fabricated in Factor II room temperature vulcanizing (RTV) silicone and processed according to the manufacturer's instructions. Two groups were classified with 20 specimens each. Specimens in the first group were coated with titanium dioxide (TiO2) by atomic layer deposition technology. The colour stability test was conducted with a UV-VIS spectrometer (Schimadzu) for both titanium dioxide nanocoated and uncoated specimen groups after subjecting them to accelerated ageing. It was analysed using the CIE L*a*b method. RESULTS: The average colour change was highest for uncoated specimens (2.868), and the average colour change for titanium dioxide-coated specimens was significantly low (1.774). The average colour change of uncoated specimens (2.868) was close to the acceptable threshold value (3), and that of coated specimens (1.774) was far below the acceptable threshold (3). CONCLUSIONS: The colour change that occurred in titanium dioxide nanocoated specimens following accelerated ageing was significantly lower than that in the uncoated group, showing that the TiO2 nanocoating was effective in reducing the colour degradation of silicone elastomers. CLINICAL RELEVANCE: Maxillofacial prostheses fabricated from silicone elastomers go through undesirable colour degradation over time. The development of a scientific technique that retards the colour deterioration of silicone prostheses would be of great clinical significance.

Dental anxiety and ageing anxiety: Moderated mediation roles of Oral Health-Related Quality of Life and subjective accelerated ageing.

BACKGROUND: Oral health and its relation to ageing is an important topic often neglected among geriatric populations. Proper oral rehabilitation may aid in alleviating mental health burdens in such populations. OBJECTIVES: The present study aimed to explore the association between dental anxiety and ageing anxiety, with regard to the interplay of Oral Health-Related Quality of Life (OHRQoL) as mediator and subjective accelerated ageing as a moderator. METHODS: A total of 577 participants with mean age 72.78 years (SD = 3.832, range = 68-87) were recruited via a survey company in Israel. They completed a self-report battery of questionnaires about dental anxiety, OHRQoL, subjective accelerated ageing and ageing anxiety, along with their informed consent. RESULTS: The findings revealed that dental anxiety was positively associated with ageing anxiety (direct effect), and that OHRQoL mediated the link between dental anxiety and ageing anxiety (indirect effect). Additionally, subjective accelerated ageing moderated the positive link between dental anxiety and OHRQoL, as well as the positive link between OHRQoL and ageing anxiety. CONCLUSIONS: The results provide insight for the roles of OHRQoL and subjective accelerated ageing among older adults between dental anxiety and ageing anxiety. Tailoring oral rehabilitation interventions that focus on these factors are warranted to improve older adults' dental health.

Assessment of the Prediction Power of Forced Ageing Methodology on Lager Beer Aldehyde Evolution during Maritime Transportation.

The globalisation of the beer market forces brewers to have methodologies that rapidly evaluate the evolution of beer flavour stability. Commonly used forced ageing methods have limitations since temperature and transportation conditions (temperature, vibrations, long-distance travel, and other factors) impact beer quality. This study assessed the prediction power of a forced ageing methodology on the evolution of aldehydes during maritime transportation across four sample groups (maritime transport, storage simulation, and three ageing periods: 7, 21, and 28 days at 37 °C), which differed in their bottle-opening system (either crown cap or ring pull cap). The results revealed that forced ageing up to 28 days could estimate the evolution of phenylacetaldehyde, 3-methylbutanal, 2-methylpropanal, and hexanal during maritime transport. In contrast, the benzaldehyde content was consistently underestimated, on average, 0.8 times lower. In general, the ageing conditions significantly favoured the formation or liberation from a bound state, up to 2.2 times higher, of trans-2-nonenal, acetaldehyde, and 5-hydroximethylfurfural in comparison to the levels registered on exportation simulation beers. Moreover, forced-aged beers with ring pull caps developed quantifiable levels of nonanal and increased phenylacetaldehyde, benzaldehyde, and acetaldehyde content over time. Moreover, thermal stress induced a continuous increase in the extent of beer staling, up to seven times higher, in most samples.

In vivo stress reporters as early biomarkers of the cellular changes associated with progeria.

Age-related diseases account for a high proportion of the total global burden of disease. Despite recent advances in understanding their molecular basis, there is a lack of suitable early biomarkers to test selected compounds and accelerate their translation to clinical trials. We have investigated the utility of in vivo stress reporter systems as surrogate early biomarkers of the degenerative disease progression. We hypothesized that cellular stress observed in models of human degenerative disease preceded overt cellular damage and at the same time will identify potential cytoprotective pathways. To test this hypothesis, we generated novel accelerated ageing (progeria) reporter mice by crossing the LmnaG609G mice into our oxidative stress/inflammation (Hmox1) and DNA damage (p21) stress reporter models. Histological analysis of reporter expression demonstrated a time-dependent and tissue-specific activation of the reporters in tissues directly associated with Progeria, including smooth muscle cells, the vasculature and gastrointestinal tract. Importantly, reporter expression was detected prior to any perceptible deleterious phenotype. Reporter expression can therefore be used as an early marker of progeria pathogenesis and to test therapeutic interventions. This work also demonstrates the potential to use stress reporter approaches to study and find new treatments for other degenerative diseases.

Spontaneous Synthesis of [FeII (Atrz)3 ]SO4 and its Analogues Through Accelerated Ageing: New Insights from Small-Scale Reactions.

Accelerated ageing reactions that take place between two solid materials on contact in the absence of added solvent have been used to synthesize two spin-crossover-active 1D coordination polymers and one of their Cu(II) analogues. The hygroscopy of the ligands and the relative humidity of the reaction chamber have been shown to be particularly important factors in the rate of reaction. Small-scale reactions between a few individual crystals have allowed observation of deliquescence of the 4-aminotriazole ligand at high humidity. The metal salt does not dissolve, and the ligand diffuses into the crystal of the metal salt during the reaction. In the case of the Cu analogue, the formation of the product causes the crystal of the metal salt to deform with the formation of pseudocrystals, which have a fibrous structure.

Physical capability in a rural birth cohort at the age of 52: association with early environmental, nutritional, and developmental factors.

INTRODUCTION: Midlife physical capability (PC) is associated with developmental factors in the populations of economically developed countries. As far as we know, there is no information for rural populations of low- and middle-income countries. The aim of the study was to investigate the influence of pre- and postnatal factors on midlife objective measures of PC in a 1966-67 birth cohort from a Mexican rural community. The hypothesis was that adverse developmental conditions are associated with low midlife PC. METHODS: In 1966-67, a birth cohort of all children from a poor Mexican rural community was assembled. Data on family socioeconomic status (SES), parental health and nutritional status, birth weight, postnatal growth and feeding patterns were registered. In 2018, out of the 336 cohort members, 118 were living in the community, and eighty-two of them underwent a comprehensive clinical evaluation. The evaluation included grip strength, gait velocity and chair-stand PC tests. In multivariable linear models, PC tests were the dependent variables, and prenatal, birth and postnatal factors were the independent variables. Adjustment for confounding was made with adult anthropometric, body composition, clinical and ageing status variables. RESULTS: Independent of adult health status and other ageing indicators, lower PC was associated with family organization and SES, parental nutritional status, birth weight, infant postnatal growth velocity, and weaning time. These results indicate that adverse family and environmental conditions that are prevalent in poor rural communities are associated with low midlife PC.

Crosstalk among DNA Damage, Mitochondrial Dysfunction, Impaired Mitophagy, Stem Cell Attrition, and Senescence in the Accelerated Ageing Disorder Werner Syndrome.

Werner syndrome (WS) is an accelerated ageing disease caused by multiple mutations in the gene encoding the Werner DNA helicase (WRN). The major clinical features of WS include wrinkles, grey hair, osteoporosis, and metabolic phenomena such as atherosclerosis, diabetes, and fatty liver, and resemble those seen in normal ageing, but occur earlier, in middle age. Defective DNA repair resulting from mutations in WRN explain the majority of the clinical features of WS, but the underlying mechanisms driving the larger metabolic dysfunction remain elusive. Recent studies in animal models of WS and in WS patient cells and blood samples suggest the involvement of impaired mitophagy, NAD+ depletion, and accumulation of damaged mitochondria in metabolic dysfunction. This mini-review summarizes recent progress in the understanding of the molecular mechanisms of metabolic dysfunction in WS, with the involvement of DNA damage, mitochondrial dysfunction, mitophagy reduction, stem cell impairment, and senescence. Future studies on NAD+ and mitophagy may shed light on potential therapeutic strategies for the WS patients.

Systemic transplantation of adult multipotent stem cells prevents articular cartilage degeneration in a mouse model of accelerated ageing.

BACKGROUND: Osteoarthritis (OA) is one of the most prevalent joint diseases of advanced age and is a leading cause of disability worldwide. Ageing is a major risk factor for the articular cartilage (AC) degeneration that leads to OA, and the age-related decline in regenerative capacity accelerates OA progression. Here we demonstrate that systemic transplantation of a unique population of adult multipotent muscle-derived stem/progenitor cells (MDSPCs), isolated from young wild-type mice, into Zmpste24-/- mice (a model of Hutchinson-Gilford progeria syndrome, a condition marked by accelerated ageing), prevents ageing-related homeostatic decline of AC. RESULTS: MDSPC treatment inhibited expression of cartilage-degrading factors such as pro-inflammatory cytokines and extracellular matrix-proteinases, whereas pro-regenerative markers associated with cartilage mechanical support and tensile strength, cartilage resilience, chondrocyte proliferation and differentiation, and cartilage growth, were increased. Notably, MDSPC transplantation also increased the expression level of genes known for their key roles in immunomodulation, autophagy, stress resistance, pro-longevity, and telomere protection. Our findings also indicate that MDSPC transplantation increased proteoglycan content by regulating chondrocyte proliferation. CONCLUSIONS: Together, these findings demonstrate the ability of systemically transplanted young MDSPCs to preserve a healthy homeostasis and promote tissue regeneration at the molecular and tissue level in progeroid AC. These results highlight the therapeutic potential of systemically delivered multipotent adult stem cells to prevent age-associated AC degeneration.

Targeting Stem Cells in Chronic Inflammatory Diseases.

Mesenchymal stem cell (MSC) dysfunction is a serious complication in ageing and age-related inflammatory diseases such as type 2 diabetes mellitus. Inflammation and oxidative stress-induced cellular senescence alter the immunomodulatory ability of MSCs and hamper their pro-regenerative function, which in turn leads to an increase in disease severity, maladaptive tissue damage and the development of comorbidities. Targeting stem/progenitor cells to restore their function and/or protect them against impairment could thus improve healing outcomes and significantly enhance the quality of life for diabetic patients. This review discusses the dysregulation of MSCs' immunomodulatory capacity in the context of diabetes mellitus and focuses on intervention strategies aimed at MSC rejuvenation. Research pertaining to the potential therapeutic use of either pharmacological agents (NFкB antagonists), natural products (phytomedicine) or biological agents (exosomes, probiotics) to improve MSC function is discussed and an overview of the most pertinent methodological considerations given. Based on in vitro studies, numerous anti-inflammatory agents, antioxidants and biological agents show tremendous potential to revitalise MSCs. An integrated systems approach and a thorough understanding of complete disease pathology are however required to identify feasible candidates for in vivo targeting of MSCs.

Towards the Functional Ageing of Electrically Conductive and Sensing Textiles: A Review.

Electronic textiles (e-textiles) have become more and more important in daily life and attracted increased attention of the scientific community over the last decade. This interdisciplinary field of interest ranges from material science, over chemistry, physics, electrical engineering, information technology to textile design. Numerous applications can already be found in sports, safety, healthcare, etc. Throughout the life of service, e-textiles undergo several exposures, e.g., mechanical stress, chemical corrosion, etc., that cause aging and functional losses in the materials. The review provides a broad and critical overview on the functional ageing of electronic textiles on different levels from fibres to fabrics. The main objective is to review possible aging mechanisms and elaborate the effect of aging on (electrical) performances of e-textiles. The review also provides an overview on different laboratory methods for the investigation on accelerated functional ageing. Finally, we try to build a model of cumulative fatigue damage theory for modelling the change of e-textile properties in their lifetime.

A roadmap to build a phenotypic metric of ageing: insights from the Baltimore Longitudinal Study of Aging.

Over the past three decades, considerable effort has been dedicated to quantifying the pace of ageing yet identifying the most essential metrics of ageing remains challenging due to lack of comprehensive measurements and heterogeneity of the ageing processes. Most of the previously proposed metrics of ageing have been emerged from cross-sectional associations with chronological age and predictive accuracy of mortality, thus lacking a conceptual model of functional or phenotypic domains. Further, such models may be biased by selective attrition and are unable to address underlying biological constructs contributing to functional markers of age-related decline. Using longitudinal data from the Baltimore Longitudinal Study of Aging (BLSA), we propose a conceptual framework to identify metrics of ageing that may capture the hierarchical and temporal relationships between functional ageing, phenotypic ageing and biological ageing based on four hypothesized domains: body composition, energy regulation, homeostatic mechanisms and neurodegeneration/neuroplasticity. We explored the longitudinal trajectories of key variables within these phenotypes using linear mixed-effects models and more than 10 years of data. Understanding the longitudinal trajectories across these domains in the BLSA provides a reference for researchers, informs future refinement of the phenotypic ageing framework and establishes a solid foundation for future models of biological ageing.

Identification of novel seed longevity genes related to oxidative stress and seed coat by genome-wide association studies and reverse genetics.

Seed longevity is a polygenic trait of relevance for agriculture and for understanding the effect of environment on the ageing of biological systems. In order to identify novel longevity genes, we have phenotyped the natural variation of 270 ecotypes of the model plant, Arabidopsis thaliana, for natural ageing and for three accelerated ageing methods. Genome-wide analysis, using publicly available single-nucleotide polymorphisms (SNPs) data sets, identified multiple genomic regions associated with variation in seed longevity. Reverse genetics of 20 candidate genes in Columbia ecotype resulted in seven genes positive for seed longevity (PSAD1, SSLEA, SSTPR, DHAR1, CYP86A8, MYB47 and SPCH) and five negative ones (RBOHD, RBOHE, RBOHF, KNAT7 and SEP3). In this uniform genetic background, natural and accelerated ageing methods provided similar results for seed-longevity in knock-out mutants. The NADPH oxidases (RBOHs), the dehydroascorbate reductase (DHAR1) and the photosystem I subunit (PSAD1) highlight the important role of oxidative stress on seed ageing. The cytochrome P-450 hydroxylase, CYP86A8, and the transcription factors, MYB47, KNAT7 and SEP3, support the protecting role of the seed coat during seed ageing.

DNA methylation-based measures of accelerated biological ageing and the risk of dementia in the oldest-old: a study of the Lothian Birth Cohort 1921.

BACKGROUND: Previous studies have demonstrated an association between DNA methylation-based measures of accelerated ageing and age-related health outcomes and mortality. As a disease closely associated with advancing age, we hypothesized that DNA methylation-based measures of accelerated ageing might be associated with risk for dementia. This study therefore aimed to examine the association between four recognised measures of age acceleration and subsequent dementia. METHODS: Study subjects (n = 488) were members of the Lothian Birth Cohort 1921. Dementia case ascertainment used data from death certificates, electronic hospital records, and clinical reviews. Venous blood samples were taken at baseline, at age 79 years. DNA methylation and measures of epigenetic age were calculated in accordance with Horvath's epigenetic clock tutorial, using the online calculator (https://dnamage.genetics.ucla.edu/). From these values, four measures of accelerated ageing were calculated: extrinsic epigenetic age acceleration (EEAA), intrinsic epigenetic age acceleration (IEAA), AgeAccelPheno and AgeAccelGrim. Competing risk regression models - with death as a competing risk - were performed to examine the association between each measure of accelerated ageing and incident dementia. APOE ɛ4 status, sex, age, smoking status, history of cardiovascular disease, cerebrovascular disease, hypertension, and diabetes were included as covariates. RESULTS: None of the multivariate models revealed a positive association between increased epigenetic age acceleration and dementia risk. Across all included models, never-smoking increased risk for dementia (HR 1.69 [1.06, 2.71], p = 0.03), and having no APOE ɛ4 alleles reduced risk for dementia (HR 0.44 [0.29, 0.67], p < 0.001). CONCLUSIONS: The present study did not demonstrate any consistent association between DNA methylation-based measures of accelerated ageing and dementia in subjects aged over 79 years. Further, larger studies - including separate analyses of dementia subtypes - are required to further investigate the potential association between DNA methylation-based measures of accelerated ageing and dementia.

Accelerated ageing profile in inflammatory arthritis is unique and tissue compartment specific.

Rheumatoid arthritis is prevalent in more than 1% of the global population, with the highest occurrence between ages 35 and 50, which places a huge burden on the economy. Drug discovery for the prevention of this chronic disease is; therefore, a priority. It is known that subclinical progression of many chronic non-communicable diseases is exacerbated via accelerated ageing, a pro-inflammatory phenotype shift. However, rheumatoid arthritis additionally has significant humoral immune activation, inflammatory signalling-and thus the accelerated ageing profile-may differ from other chronic inflammatory diseases. The current study simulated inflammatory arthritis onset in a collagen-induced arthritis (CIA) rodent model, to characterise the redox and inflammatory profile at the onset of clinical symptoms, in different tissues, in the presence and absence of preventative antioxidant treatment. The data illustrate that an increased free radical level are evident already very early on in RA disease progression. Furthermore, oxidative stress seems to somewhat precede a significant pro-inflammatory state, perhaps due to humoral immune activation. Our data across different compartments further suggest that the compensatory increase in endogenous antioxidant activity is gradually exhausted at a different pace, with the liver showing the first signs of oxidant damage, even before significant evidence exist in circulation. The current data further suggest that preventative antioxidant intervention may have a sparing effect on endogenous antioxidant mechanisms and preserve telomere length to delay disease progression-or at least the accelerated ageing known to exacerbate RA symptoms-although it did not seem to have a significant direct effect on the autoimmune activity.

Seed life span and food security.

Much is known about the inter-specific distribution of life span in a wide diversity of vertebrates and in adult plants, but not for seeds, yet the functional trait seed life span underpins global agriculture, plant species conservation and seed persistence in the soil. We sourced data for five storage conditions (soil seed bank; high temperature - high humidity accelerated ageing; temperate, cooler, open storage; cool, dry, refrigerator; and cold, dry, freezer); and analysed the distribution of orthodox seed life span amongst crop and wild species. In all cases, whether for maximum known in situ life span in the soil seed bank (417 species), or for half-lives (P50s) ex situ (732 species), the distribution is right-skewed. The finding that seeds of > 50% of species are likely to have life spans ≤ 20% of the longest recorded under the same conditions has implications for future research on the evolution of seed traits and gene bank collections management.

'Obesageing': Linking obesity & ageing.

Obesity is one of the leading causes of preventable mortalities in many parts of the globe. The rise in geriatric population due to better treatment opportunities has also emerged as a major public health challenge. Both of these health challenges have impacted developed as well as developing countries. Obesity is attributed as a powerful risk factor of a variety of health problems such as cardiovascular diseases, hypertension, type 2 diabetes, dementia, neuropsychiatric diseases and many more. On the other hand, ageing is a natural process involving a gradual decline in physiological functions and is associated with similar co-morbidities as obesity. This review discusses about the commonalities (termed as 'Obesageing') between the pathological phenomenon of obesity and normal physiological process of ageing. A unique rodent model of obesageing has been developed (WNIN/Ob) that has characteristics of morbid obesity as well as premature ageing. Such a novel animal model would facilitate the understanding of the complex interplay of different mechanisms that are common to obesity and ageing and help to devise strategies in future to tackle the growing burden of obesity and ageing.