There have been numerous attempts to establish a correlation between obesity and stress, inflammatory, and dysmetabolism biomarkers in children and adolescents. Here, we performed a meta-analysis of existing studies to shed light on the elusive correlations of childhood and adolescent obesity with physiological indicators of stress, inflammation, and metabolism before and after lifestyle interventions. Observational studies, meta-analyses, narrative and systematic reviews were excluded. From a total of 53 articles, 11 were selected according to specific criteria. The biomarkers examined were circulating glucose, insulin, HDL, LDL, triglycerides, adiponectin, leptin, CRP, TNF-alpha, interleukin (IL)-6, systolic and diastolic blood pressure, and HOMA-IR. All analyses were performed using IBM SPSS Statistics Version 28.0.1.0 (142). The current meta-analysis provides evidence of a beneficial effect of a lifestyle intervention and/or drugs in children and adolescents living with obesity or overweight, consistent with a significant reduction in body fat—but not in BMI or waist circumference—an increase in circulating adiponectin and/or a reduction in serum insulin levels and diastolic blood pressure, and a trend towards a reduction of circulating leptin and glucose levels, as well as of the HOMA-IR. This meta-analysis indicates that lifestyle interventions could reduce overweight-/obesity-associated systemic inflammation and dysmetabolism even without an apparent decrease in BMI.

Medical technology has made significant advances in the 21^st century and, at present, medicine makes use of information technology, telecommunications, and state-of-the-art engineering to provide the best possible healthcare services. Electronic sensors provide health practitioners with the ability to constantly monitor their patients’ health, to streamlines a number of medical processes, and to increase patients' access to health services. Mobile phones also empower patients and play a major role in their health's monitoring. The use of cybernetics technology can now help patients overcome even serious disabilities, enabling many disabled patients to live their lives similarly to their non-disabled fellow men through the use of artificial organs and implants. All these advances have paved the way for a more personalized type of healthcare that provides individualized solutions to each patient. Once a number of hurdles are overcome, medical technology will bring forth a new era of more precise and enabling medicine.

Aging is a complex biological process characterized by the progressive accumulation of cellular and molecular damage, leading to functional decline and increased susceptibility to age-related diseases. Central to this process is cellular senescence, a state of irreversible cell cycle arrest that acts as both a protective mechanism against tumorigenesis and a contributor to tissue degeneration. Herein, we explore the genetic and molecular mechanisms underlying aging, with a focus on telomere dynamics, the Klotho gene, angiotensin-converting enzyme (ACE), and the NF-κB pathway. Telomeres, which serve as protective caps at chromosome ends, shorten with each cell division, leading to replicative senescence, while the enzyme telomerase plays a pivotal role in maintaining telomere length and cellular longevity. The Klotho gene encoding for an aging suppressor influences insulin/IGF-1 signaling and has antioxidant properties that protect against oxidative stress. ACE, through its dual role in regulating blood pressure and degrading amyloid-beta, impacts longevity and age-related pathologies. The NF-κB pathway drives chronic inflammation or “inflammaging,” contributing to the onset of age-related diseases. Understanding these pathways offers promising avenues for therapeutic interventions to extend health span and lifespan. Targeting mechanisms such as telomerase activation, Klotho supplementation, ACE inhibition, and NF-κB modulation hold potential for combating the detrimental effects of aging and promoting healthier aging in the population.

The evolutionary conserved Notch signaling pathway functions as a mediator of direct cell–cell communication between neighboring cells during development. Notch plays a crucial role in various fundamental biological processes in a wide range of tissues. Accordingly, the aberrant signaling of this pathway underlies multiple genetic pathologies such as developmental syndromes, congenital disorders, neurodegenerative diseases, and cancer. Over the last two decades, significant data have shown that the Notch signaling pathway displays a significant function in the mature brains of vertebrates and invertebrates beyond neuronal development and specification during embryonic development. Neuronal connection, synaptic plasticity, learning, and memory appear to be regulated by this pathway. Specific mutations in human Notch family proteins have been linked to several neurodegenerative diseases including Alzheimer’s disease, CADASIL, and ischemic injury. Neurodegenerative diseases are incurable disorders of the central nervous system that cause the progressive degeneration and/or death of brain nerve cells, affecting both mental function and movement (ataxia). There is currently a lot of study being conducted to better understand the molecular mechanisms by which Notch plays an essential role in the mature brain. In this study, an in silico analysis of polymorphisms and mutations in human Notch family members that lead to neurodegenerative diseases was performed in order to investigate the correlations among Notch family proteins and neurodegenerative diseases. Particular emphasis was placed on the study of mutations in the Notch3 protein and the structure analysis of the mutant Notch3 protein that leads to the manifestation of the CADASIL syndrome in order to spot possible conserved mutations and interpret the effect of these mutations in the Notch3 protein structure. Conserved mutations of cysteine residues may be candidate pharmacological targets for the potential therapy of CADASIL syndrome.

Continuous genomic surveillance of influenza virus is critical for monitoring viral evolution, detecting emerging variants, and informing vaccine strain selection. While partial-gene Sanger sequencing has traditionally underpinned national surveillance programs, whole-genome sequencing (WGS) enables simultaneous characterization of all eight genomic segments, providing resolution not achievable through conventional approaches. This is the first published, systematic, whole-genome-based influenza surveillance study reported from Greece. We sequenced and characterized influenza viruses circulating in Southern Greece (S. Greece) during two consecutive influenza seasons, 2024–2025 and 2025–2026, using Oxford Nanopore Technologies (ONT) sequencing. A total of 40 samples were analyzed, with complete or near-complete genome assembly achieved in the vast majority of them. During 2024–2025, co-circulation of A(H1N1)pdm09 (subclades C.1.9.3 and D.3.1), A(H3N2) (subclades J.1.1 and J.2.2), and B/Victoria (C.5 subclades, predominantly C.5.7) influenza viruses was confirmed, with the detection of an oseltamivir-resistant H1N1 variant carrying NA H275Y as a clinically significant finding. Extension of surveillance into 2025–2026 revealed a complete inter-seasonal lineage transition in A(H1N1)pdm09 from subclade C.1.9.3 to D.3.1/D.3.1.1, and the rapid emergence and geographic dissemination of A(H3N2) subclade K across multiple regions of Southern Greece. Phylogenetic analysis characterized the HA subclade composition across the two seasons and positioned the Greek strains within the European and global context. Sequences of subclade K strains from S. Greece were phylogenetically concordant with the updated 2026–2027 vaccine strains, in line with ECDC and WHO surveillance data. Whole-genome analysis confirmed the absence of virulence-associated polymerase markers in all isolates with fully assembled polymerase segments, and identified conserved internal segment substitution patterns co-segregating with circulating subclades. These findings provide the first published whole-genome evolutionary dataset for influenza in Southern Greece, contributing insight into subtype and clade-level evolutionary dynamics and demonstrating the public health value of sustained genomic surveillance at a national reference laboratory level.