Occupational Carpal Tunnel Syndrome: a scoping review of causes, mechanisms, diagnosis, and intervention strategies.

Carpal Tunnel Syndrome (CTS) has traditionally been viewed as a specialized medical condition. However, its escalating prevalence among professionals across a multitude of industries has sparked substantial interest in recent years. This review aims to delve into CTS as an occupational disease, focusing on its epidemiological patterns, risk factors, symptoms, and management options, particularly emphasizing its relevance in professional environments. The complex interaction of anatomical, biomechanical, and pathophysiological factors that contribute to the development of CTS in different work settings underlines the critical role of ergonomic measures, prompt clinical identification, and tailored treatment plans in reducing its effects. Nevertheless, the challenges presented by existing research, including diverse methodologies and definitions, highlight the need for more unified protocols to thoroughly understand and tackle this issue. There's a pressing demand for more in-depth research into the epidemiology of CTS, its injury mechanisms, and the potential role of targeted medicine. Moreover, recognizing CTS's wider ramifications beyond personal health is essential. The economic burden associated with CTS-related healthcare costs, productivity losses, and compensation claims can significantly impact both businesses and the broader society. Therefore, initiatives aimed at preventing CTS through workplace interventions, education, and early intervention programs not only benefit the affected individuals but also contribute to the overall well-being of the workforce and economic productivity. By fostering a collaborative approach among healthcare professionals, employers, policymakers, and other stakeholders, we can strive towards creating safer and healthier work environments while effectively managing the challenges posed by CTS in occupational settings.

A Preclinical Systematic Review and Meta-Analysis of Behavior Testing in Mice Models of Ischemic Stroke.

Stroke remains one of the most important causes of death and disability. Preclinical research is a powerful tool for understanding the molecular and cellular response to stroke. However, a lack of standardization in animal evaluation does not always ensure reproducible results. In the present study, we wanted to identify the best strategy for evaluating animal behavior post-experimental stroke. As such, a meta-analysis was made, evaluating behavioral tests done on male C57BL/6 mice subjected to stroke or sham surgery. Overall, fifty-six studies were included. Our results suggest that different types of tests should be used depending on the post-stroke period one needs to analyze. In the hyper-acute, post-stroke period, the best quantifier will be animal examination scoring, as it is a fast and inexpensive way to identify differences between groups. When evaluating stoke mice in the acute phase, a mix of animal examination and motor tests that focus on movement asymmetry (foot-fault and cylinder testing) seem to have the best chance of picking up differences between groups. Complex tasks (the rotarod test and Morris water maze) should be used within the chronic phase to evaluate differences between the late-subacute and chronic phases.

Effects of Acute Sepsis on Cellular Dynamics and Amyloid Formation in a Mouse Model of Alzheimer's Disease.

Our objective was to investigate how sepsis influences cellular dynamics and amyloid formation before and after plaque formation. As such, APP-mice were subjected to a polymicrobial abdominal infection resulting in sepsis at 2 (EarlySepsis) and 4 (LateSepsis) months of age. Behavior was tested before sepsis and at 5 months of age. We could not detect any short-term memory or exploration behavior alterations in APP-mice that were subjected to Early or LateSepsis. Immunohistochemical analysis revealed a lower area of NeuN+ and Iba1+ signal in the cortex of Late compared with EarlySepsis animals (p = 0.016 and p = 0.01), with an increased astrogliosis in LateSepsis animals compared with WT-Sepsis (p = 0.0028), EarlySepsis (p = 0.0032) and the APP-Sham animals (p = 0.048). LateSepsis animals had larger areas of amyloid compared with both EarlySepsis (p = 0.0018) and APP-Sham animals (p = 0.0024). Regardless of the analyzed markers, we were not able to detect any cellular difference at the hippocampal level between groups. We were able to detect an increased inflammatory response around hippocampal plaques in LateSepsis compared with APP-Sham animals (p = 0.0003) and a decrease of AQP4 signal far from Sma+ vessels. We were able to show experimentally that an acute sepsis event before the onset of plaque formation has a minimal effect; however, it could have a major impact after its onset.

Heterogeneity in the Number of Astrocytes in the Central Nervous System after Peritonitis.

Sepsis remains a major medical emergency that describes the body's systemic immune response to an infectious process and can lead to end-stage organ dysfunction and death. Clinical studies have introduced the concept of sepsis associated encephalopathy, which seems to have a plethora of cellular and molecular triggers starting from systemic inflammatory cytokines, blood-brain barrier (BBB) rupture, microscopic brain injury, altered cerebral circulation, neurotransmission, or even metabolic dysfunction. The purpose of our study is to reproduce the sepsis model previously described using the cecal ligature and puncture (CLP), and to take a closer look to the acute modifications that occur on cellular level when it comes to the brain-blood-barrier of the mice with systemic inflammation. After a rapid systemic response to peritonitis, we show a heterogeneity in astrocytic response within different cortical structures; hippocampus having the longest change in the number of GFAP+cells, while no difference was seen in the number of cortical astrocytes. With even more increasing roles of astrocytes in different pathologies, the relation between sepsis and astrocytes could prove a valuable in discovering new therapy in sepsis.

Different Age Related Neurological and Cardiac Effects of Verapamil on a Transgenic Mouse Model of Alzheimer's Disease.

Dementias are the third cause of the disability-adjusted life-years (DALYs) worldwide with Alzheimer's (AD) having the highest prevalence. Despite ample research in the field, therapeutic options are limited. However, with the increase in lifespan, a larger number of AD patients will receive other medication for the evermore-increased number of comorbidities that such patients face. The purpose of this study was to evaluate the neurological and cardiac effects of verapamil, on C57BL/6J-TgN (Thy1-APPKM670/671NL; Thy1-PS1L166P (APP) mice. The daily administration of 3.5mg/kg of verapamil for 28 days revealed different effects on young and aged APP mice. While young animals showed less anxiety and improved short-term memory with minimal cardiac effects (an increase in the duration of ventricular depolarization), aged ones did not present behavioral improvements, but with a decrease in the duration of ventricular depolarizing. Repolarization effects of verapamil were similar in young and aged animals, except for the duration of the ST segment that was longer in aged animals. Considering our results, the use of calcium blockers in AD patients should take into consideration the stage of the disease, as different effects could be seen at different stages of AD, in our model.

Caloric restriction stabilizes body weight and accelerates behavioral recovery in aged rats after focal ischemia.

Obesity and hyperinsulinemia are risk factors for stroke. We tested the hypothesis that caloric restriction, which reduces the incidence of age-related obesity and metabolic syndrome, may represent an efficient and cost-effective strategy for preventing stroke and its devastating consequences. To this end, we placed aged, obese Sprague-Dawley aged rats on a calorie-restricted diet for 8 weeks prior to the experimental infarction. Stroke in this animal model caused a progressive decrease in weight that reached a minimum at day 6 for the young rats, and at day 10 for the aged, ad libitum-fed rats. However, in aged animals that were calorie-restricted prior to stroke, body weight did not decrease after stroke, but we noted accelerated body weight gain shortly thereafter starting at day 5 poststroke. Moreover, calorie-restricted aged animals showed improved behavioral recovery in tasks requiring complex sensorimotor skills, or in tasks requiring cutaneous sensitivity and sensorimotor integration or spatial memory. Likewise, calorie-restricted aged rats showed significant poststroke increases in serum glucose, insulin, and IGF1 levels, as well as CR-specific changes in the expression of gene transcripts involved in glycogen metabolism, IGF signaling, apoptosis, arteriogenesis, and hypoxia. In conclusion, our study shows that recovery from stroke is enhanced in aged rats by a dietary regimen that reduces body weight prior to infarct.

Autophagy in aging and disease.

Autophagy is a catabolic degradation system used to destroy and recycle the unnecessary or damaged components of a cell. Autophagy is present at a basal level in all mammals and is regulated by some conditions, such as oxidative stress, starvation or hypoxia. In aged tissues, increased but also decreased expression of autophagy-specific proteins, Beclin 1, LC3, Atg5 and Atg7 has been reported. Likewise, it could be shown that the lifespan of yeast, nematodes and flies is prolonged by pharmacologically stimulated autophagy using exogenous administered spermidine. Autophagy is potentially implicated in acute lung injury and sepsis, two main causes of morbidity and mortality worldwide. Finally, a quite recent study supports the hypothesis that autophagy might be useful in vascular disease prevention by stimulating cholesterol efflux, which leads to inhibition of necrotic core formation and lipid accumulation. Since autophagy is also implicated in neuro-protection, in Alzheimer's and Huntington's disease animal models and many others normal and pathological states, including immunity, diabetes mellitus, different kind of tumors, colorectal cancer, different inflammations, lung diseases, neurodegenerative diseases, autophagy is of interest to many biomedical researchers.