St. Matthew's University

Introduction:Menstrual disorders-including premenstrual syndrome (PMS), premenstrual dysphoric disorder (PMDD), and dysmenorrhea-are highly prevalent among women of reproductive age and are associated with impaired academic performance, psychological distress, and reduced social functioning. Nursing students are particularly vulnerable due to the combined demands of intensive academic schedules and clinical training, yet prevalence estimates and institutional responses remain inconsistent. Methods:A systematic review and meta-analysis were conducted in accordance with PRISMA 2020 guidelines and registered in PROSPERO (CRD420251109363). PubMed, Scopus, Web of Science, CINAHL Ultimate, and APA PsycINFO were searched for studies published between 2016 and 2025. Eligible studies reported prevalence or impact of PMS, PMDD, or dysmenorrhea exclusively in nursing students. The Joanna Briggs Institute checklist for prevalence studies was used for quality appraisal. Random-effects meta-analysis was applied to calculate pooled prevalence estimates, and thematic synthesis was used to evaluate academic, social, and psychosocial impacts, coping strategies, and interventions. Results:Twenty studies involving 5,131 nursing students were included. The pooled prevalence was 62% for PMS, 21% for PMDD (including severe PMS), and 72% for dysmenorrhea, with substantial heterogeneity (I 2 > 80%). Reported impacts included absenteeism, reduced concentration, diminished clinical performance, and impaired quality of life. Coping strategies were largely self-directed, including analgesics, rest, and dietary modifications, while few students accessed formal healthcare or institutional support. Only a limited number of studies evaluated structured interventions such as exercise, yoga, or nutritional supplementation. Conclusion:Menstrual disorders are highly prevalent among nursing students and carry significant academic, social, and psychological consequences. Nursing education programs should integrate routine screening, structured wellness initiatives, and evidence-based interventions to improve student wellbeing, reduce academic disruption, and strengthen workforce preparedness. Systematic Review Registration:https://www.crd.york.ac.uk/PROSPERO/view/CRD420251109363, PROSPERO CRD420251109363.

BackgroundPeptide therapeutics represent an emerging frontier in gerontological medicine, targeting fundamental hallmarks of aging including metabolic dysfunction, telomere attrition, tissue repair impairment, and hormonal decline.ObjectiveTo comprehensively review the mechanisms, clinical applications, evidence base, and safety profiles of therapeutic peptides with demonstrated or potential applications in healthy aging and age-related conditions.MethodsA comprehensive narrative review was conducted through systematic searches of PubMed, Scopus, and regulatory databases (FDA, WADA) from inception through January 2026. Search terms included “peptide therapeutics,” “aging,” “gerontology,” “healthspan,” combined with specific peptide names (tirzepatide, epitalon, GHK-Cu, BPC-157, TB-500, Semax, CJC-1295, ipamorelin, bremelanotide). Peer-reviewed articles, clinical trials, regulatory documents, and preclinical studies were evaluated. A total of 20 primary sources were selected based on relevance, methodological quality, and contribution to understanding peptide mechanisms and clinical outcomes in aging populations.ResultsNine peptides were identified spanning diverse aging interventions: metabolic restoration (tirzepatide), telomere biology (epitalon), dermal regeneration (GHK-Cu), tissue repair (BPC-157, TB-500), neuroprotection (Semax), growth hormone modulation (CJC-1295, ipamorelin), and sexual function (bremelanotide). FDA-approved agents demonstrated robust safety profiles from large-scale trials. Non-approved peptides showed promising preclinical and limited clinical evidence but lack long-term safety data and systematic validation. Significant knowledge gaps include optimal dosing regimens, combination therapy effects, and biomarkers for monitoring efficacy.ConclusionTherapeutic peptides offer mechanistically diverse approaches to multiple aging hallmarks. While FDA-approved agents demonstrate clinical potential, investigational peptides require rigorous validation through well-designed clinical trials to establish safety and efficacy for healthspan extension.

Adult tracheobronchial foreign bodies are uncommon and can be subtle on radiographs, particularly in device-rich environments. An 80-year-old woman with severe heart failure underwent elective implantable cardioverter defibrillator (ICD) placement and had a linear right hilar radiopaque density and right basilar atelectasis/pleural effusion on postoperative portable chest radiography. She was stable on a tracheostomy collar without respiratory distress. Given the appearance and history of home tracheostomy care, a tracheostomy cleaning brush was suspected. Flexible bronchoscopy via the tracheostomy confirmed and retrieved a cleaning brush from the right bronchus intermedius; purulent secretions were irrigated, and there were no complications. The patient remained hemodynamically stable post-procedure. This case illustrates the value of correlating imaging with clinical stability yet proceeding to definitive airway evaluation when suspicion persists, and it highlights tracheostomy-care equipment as a potential source of iatrogenic foreign bodies in adults.

Gut hormones govern appetite and postprandial glucose handling, and both functions deteriorate with age — yet the human literature cannot agree on the direction of the underlying hormonal changes. Incretin secretion is reported both to rise and to fall in older adults; ghrelin to decline, to be unchanged, and to be elevated; and the anorexia of aging is attributed variously to excess satiety signaling and to deficient basal hunger. This mini-review examines these three controversies, identifies the design features that give rise to them, and argues that they are largely reconcilable. Across all three, disputes about magnitude resolve when the outcome measured is instead the fidelity of coupling between nutrient ingestion and hormonal response: elevated GLP-1 coexists with an impaired incretin effect because it is compensation for β-cell failure, not preserved sensing; ghrelin concentrations may be normal while prandial rhythm is abolished; and older adults with low appetite show exaggerated anorexigenic responses despite unchanged subjective appetite. We further note that the human gut-hormone literature and the rapidly advancing rodent literature on age-related intestinal stem cell misdifferentiation have developed in near isolation, and that they currently disagree on whether the aged gut contains more or fewer enteroendocrine cells. Resolving these controversies requires studies that measure hormone concentrations and functional coupling in the same individuals, as well as longitudinal designs that extend beyond incretins.

BackgroundThe aging epigenome is shaped by three mechanistically distinct histone post-translational modifications—acetylation, lactylation, and glycation—each driven by a different metabolic flux: mitochondrial oxidative phosphorylation, glycolytic lactate production, and reactive carbonyl stress, respectively. Understanding their interplay is central to a molecular physiology of epigenetic aging.ScopeThis mini review synthesizes current evidence on the mechanisms of histone acetylation, lactylation, and glycation in aging; their crosstalk and convergence on shared regulatory nodes; and their modulation by environmental, nutritional, and behavioral factors. Key controversies and research gaps are critically appraised.Key FindingsNAD + decline in aging disables the sirtuin deacetylase family, dysregulating the histone acetylation landscape and impairing autophagy, mitochondrial biogenesis, and DNA repair. Histone lactylation, written by p300 at H3K18 and related lysine residues, is context-dependent: physiological pulses during exercise and sleep are adaptive, while chronic accumulation in diabetic microglia drives neuroinflammation via TLR4/NF-κB, and excess in tumor cells enables senescence bypass. Histone glycation by methylglyoxal irreversibly displaces regulatory marks and inactivates sirtuin proteins; pharmacological induction of glyoxalase I and glycation-lowering interventions reduce this burden and extend healthspan. These three axes may converge on a unified metabolic-epigenetic collapse that we propose constitutes the cellular basis of an ‘aging’ metabolic memory.Controversies and GapsLactylation erasers remain uncharacterized; the pro-versus anti-senescence duality of H3K18la is unresolved; and genome-wide histone glycation mapping in human tissues is absent.ConclusionCombinatorial interventions targeting NAD + restoration, modulation of lactylation, and reduction of carbonyl stress offer the most evidence-based approach to slowing metabolic-epigenetic aging.