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Human aging results in a variety of changes to skeletal muscle. Sarcopenia is the age-associated loss of muscle mass and is one of the main contributors to musculoskeletal impairments in the elderly. Previous research has demonstrated that resistance training can attenuate skeletal muscle function deficits in older adults, however few articles have focused on the effects of resistance training on functional mobility. The purpose of this systematic review was to 1) present the current state of literature regarding the effects of resistance training on functional mobility outcomes for older adults with skeletal muscle function deficits and 2) provide clinicians with practical guidelines that can be used with seniors during resistance training, or to encourage exercise. We set forth evidence that resistance training can attenuate age-related changes in functional mobility, including improvements in gait speed, static and dynamic balance, and fall risk reduction. Older adults should be encouraged to participate in progressive resistance training activities, and should be admonished to move along a continuum of exercise from immobility, toward the recommended daily amounts of activity.

Introduction The growing demographic presence of the transgender (TGD) population has sparked an increase in clinical investigations focusing on the impacts of gender-affirming hormone therapy (GAHT) in adults with gender dysphoria. Despite this surge in studies, there remains a significant gap in the literature regarding the health status of older TGD individuals. This review aims to assess prevalent pathological conditions within the TGD population, specifically concentrating on aging-related diseases investigated to date. Methods A systematic search across Embase Ovid, Scopus, PubMed, Cochrane Library, and Web of Science databases was conducted to identify articles reporting on the aging process in TGD individuals. Methodological quality was evaluated using Newcastle–Ottawa Scale (NOS) scores. Results Initial database searches yielded 12,688 studies, which were refined to 18 through elimination of duplicates and title/abstract review. Following a comprehensive appraisal, nine studies were included in the systematic review. These articles, published between 2017 and 2023, involved a total of 5403 participants. The evidence indicates a noteworthy percentage of the TGD population being at risk for cardiovascular diseases, experiencing depression or disability, and demonstrating hesitancy toward major recommended screening programs. Conclusions Limited studies on older TGD individuals highlight not only an organic risk of chronic diseases but also a cognitive/psychiatric risk that should not be underestimated. Further research is imperative to deepen our understanding of the pathophysiological mechanisms involved in the health challenges faced by older TGD individuals.

One of the pathogenetic hypotheses of delirium is the “neuroinflammatory theory” with consequent neurotoxicity of brain connectivity networks. Micronutrients may play a significant role in the prevention of neuroinflammation. This systematic review addresses the role of micronutrients in the development of delirium in older populations. The EBSCO, Cochrane, PubMed, and Web of Science databases were searched for articles on delirium and micronutrients. The methodological quality of the studies included in the review was evaluated with the Newcastle-Ottawa Scales for observational studies and for case-control studies. 1326 papers were identified from the searches, 7 of which met the inclusion criteria (see section 2.3). All the papers included were written in English. Delirium was predominantly secondary to post-operative dysfunction or acute medical conditions. By altering the production of neurotransmitters resulting in an imbalance, and by reducing their immunomodulatory role with a consequent increase in inflammatory oxidative stress, micronutrient deficiency seems to be associated with an increased incidence of delirium. This review supports the existence of an association between micronutrient deficiency (i.e. cobalamin, thiamine, and vitamin D) and an increased incidence of delirium, with a greater prevalence in hospitalized patients.

Transportin 3 (TNPO3) is a nuclear carrier for serine/arginine-rich proteins which are essential for mRNA splicing and metabolism. Mutations in the TNPO3 gene result in a protein with an extended C-terminal domain, leading to the onset of LGMDD2, a rare form of limb girdle muscular dystrophy. To investigate the role of TNPO3 in skeletal muscle and the pathogenic mechanism underlying LGMDD2, we develped both in vitro and in vivo models of the disease. The in vitro model was established using the C2C12 cell line, transfected with plasmids encoding either the wild-type (WT) or mutated (MUT) human TNPO3 (hTNPO3). For the in vivo model, we microinjected zebrafish ( Danio rerio ) embryos with mRNAs encoding WT or MUT hTNPO3. We analyzed the expression patterns of myogenesis-related genes, muscle-specific genes, myomiRNA and genes strictly related to the disease. These analyses were complemented by protein expression studies, morphological assessments in both models, and behavioral assays to validate the LGMDD2 zebrafish model. Our results demonstrate a key role for TNPO3 in regulating myogenesis in both models and reveal that the TNPO3 mutation disrupts normal myogenic commitment, supporting its contribution to LGMDD2 pathogenesis. Overall, this study represents a significant advance in understanding the role of TNPO3 in skeletal muscle biology and the molecular basis of LGMDD2.

An abnormal structural form of glycogen (with less branching points or amylopectin-like polysaccharide) called polyglucosan (PG) may accumulate in various tissues such as striated and smooth muscles, brain, nerve, liver and skin, and cause a group of nine different genetic disorders manifesting with a variety of clinical phenotypes that affect mainly the nervous system (Lafora disease, adult PG body disease), the heart (glycogen storage disease type XV, hypertrophic cardiomyopathy type 6, PG body myopathy type 1) and the skeletal muscle (glycogen storage disease type IV, glycogen storage disease type VII, PG body myopathy type 2), depending on the organs which are mostly affected by the PG aggregates. The pathological feature of PG storage in tissues is a hallmark of these disorders. Whole-genome sequencing has allowed to obtain a diagnosis in a large number of patients with a previously unrecognized disorder. We describe the clinical, pathological and molecular features of these genetic disorders, for many of which the pathological mechanisms underlying the corresponding mutant gene have been investigated and, at least in part, understood.

Background/Objectives: Persons with Parkinson’s disease (PD) are at elevated risk of falling due to deficits in postural control, lower limb strength, and sensory integration. While community-based boxing programs (CBPs) have shown promise in improving strength and balance, their feasibility and potential role in addressing fall risk remain unclear. This preliminary, prospective cohort study explored the feasibility of a CBP enhanced with individualized balance training tailored to somatosensory deficits and explored early indications of potential impact on fall risk and related outcomes. Methods: Twenty individuals with mild-to-moderate PD participated in a 12-week exercise program consisting of group-based boxing, functional circuit training, and one-on-one balance training based on the Modified Clinical Test of Sensory Interaction in Balance. Self-reported falls were collected at baseline and 3 months post-intervention. Secondary outcomes included standard measures of balance, gait, and functional mobility. Results: Participants demonstrated significant improvements in balance and functional mobility including the Timed Up and Go (F(2, 40.85) = 24.83, p < 0.001, η2 = 0.580), Five Times Sit-to-Stand Test (F(2, 78.13) = 50.22, p < 0.001, η2 = 0.736), and Berg Balance Scale (F(2, 193.39) = 12.72, p < 0.001, η2 = 0.414), among others. 4 participants experienced a decrease in falls, 2 experienced an increase, and the remainder had no change. Conclusions: These preliminary findings suggest that integrating individualized balance training with a CBP is feasible and may positively influence functional mobility and balance in persons with PD. However, effects on fall reduction remain inconclusive. These results should be interpreted as exploratory and used to inform the design of future structured clinical trials.

Recognized since antiquity, gout is still a relevant pathology with rising prevalence and incidence. This study aims to assess the reference accuracy in journal articles mentioning the early use of the word ‘gout’. Specifically, it investigates whether the term was indeed coined in the 13th century by the Dominican monk Randolphus of Bocking, as widely believed. Several historical sources in their original Latin were consulted to test the hypothesis of literary mentions predating Randolphus of Bocking’s description. At the same time, biomedical articles spanning the last two decades were perused using specific keywords in different combinations to determine the accuracy level of references related to the earliest use of the word ‘gout’. The results showed that several biomedical publications wrongly ascribed the origin of the word ‘gout’ to Randolphus of Bocking. Indeed, various texts predate his mention by many years. In particular, gutta, the Latin word used to indicate a host of rheumatological conditions including gout, is recorded as early as the 10th century in a biography dedicated to the martyred nun Saint Wiborada of St. Gall. Written by Swiss monks between AD 960 and 963, this text should be regarded as containing the earliest known adoption of the word. For this reason, scholars should now avoid quoting Randolph of Bocking’s description as the first use of the word ‘gout’ in Western literature.

This work presents the results of a geomatic survey conducted on the Anatomical Machines within the Sansevero Chapel in Naples, Italy. These anatomical artifacts have the unique characteristics of being upright standing skeletons with nearly intact circulatory systems. Previous research revealed that the intricate vascular systems, once believed to be natural, are instead elaborate reconstructions made using materials such as beeswax and dyes.In response to the lack of metric data of these models, a series of geomatic surveys has been conducted to create the Machines’ 3D models. This study discusses the theoretical and practical challenges associated with surveying these complex and fragile artifacts, emphasising the need for accurate extraction techniques to overcome the limitations imposed by the wooden cases in which they are encased. Two distinct approaches were used: a photogrammetric reconstruction and a laser scanning survey to overcome some logistical difficulties encountered. Despite the challenges, the 3D models' analysis gave satisfactory results.This work addresses the palaeopathological and anatomical questions related to the Anatomical Machines by leveraging non-invasive geomatic methodologies, shedding light on the complexities of surveying historically significant artifacts and aiming at further establishing a valuable foundation for improving these modelling techniques.

Identifying lifestyle strategies and allied neurobiological mechanisms that reduce aging-related motor impairment is imperative, given the accelerating number of retirees and increased life expectancy. A physically active lifestyle prior to old age can reduce risk of debilitating motor decline. However, if exercise is initiated after motor decline has begun in the lifespan, it is unknown if aging itself may impose a limit on exercise efficacy to decelerate further aging-related motor decline. In Brown-Norway/Fischer 344 F1 hybrid (BNF) rats, locomotor activity begins to decrease in middle age (12-18 months). One mechanism of aging-related motor decline may be decreased expression of GDNF family receptor, GFRα-1, which is decreased in substantia nigra (SN) between 12 and 30 months old. Moderate exercise, beginning at 18 months old, increases nigral GFRα-1 and tyrosine hydroxylase (TH) expression within 2 months. In aged rats, replenishing aging-related loss of GFRα-1 in SN increases TH in SN alone and locomotor activity. A moderate exercise regimen was initiated in sedentary male BNF rats in a longitudinal study to evaluate if exercise could attenuate aging-related motor decline when initiated at two different ages in the latter half of the lifespan (18 or 24 months old). Motor decline was reversed in the 18-, but not 24-month-old, cohort. However, exercise efficacy in the 18-month-old group was reduced as the rats reached 27 months old. GFRα-1 expression was not increased in either cohort. These studies suggest exercise can decelerate motor decline when begun in the latter half of the lifespan, but its efficacy may be limited by age of initiation. Decreased plasticity of GFRα-1 expression following exercise may limit its efficacy to reverse motor decline.

A high incidence of relapses following induction chemotherapy is a major hindrance to patient survival in acute myelogenous leukemia (AML). There is strong evidence that activation of the phosphoinositide 3 kinase (PI3K)/Akt signaling network plays a significant role in rendering AML blasts drug resistant. An important mechanism underlying drug resistance is represented by overexpression of membrane drug transporters such as multidrug resistance-associated protein 1 (MRP1) or 170-kDa P-glycoprotein (P-gp). Here, we present evidence that MRP1, but not P-gp, expression is under the control of the PI3K/Akt axis in AML blasts. We observed a highly significant correlation between levels of phosphorylated Akt and MRP1 expression in AML cells. Furthermore, incubation of AML blasts with wortmannin, a PI3K pharmacological inhibitor, resulted in lower levels of phosphorylated Akt, downregulated MRP1 expression, and decreased Rhodamine 123 extrusion in an in vitro functional dye efflux assay. We also demonstrate that wortmannin-dependent PI3K/Akt inhibition upregulated p53 protein levels in most AML cases, and this correlated with diminished MRP1 expression and enhanced phosphorylation of murine double minute 2 (MDM2). Taken together, these data suggest that PI3K/Akt activation may lead to the development of chemoresistance in AML blasts through a mechanism involving a p53-dependent suppression of MRP1 expression.