Search

Background: Over the past few decades, the scientific community has recognized the impact of physical activity on health and performance. In parallel, researchers have been actively exploring novel methodologies to analyze the physiological and metabolic responses to exercise. Fourier transform infrared spectroscopy has emerged as a powerful tool in this effort, offering the potential to provide unique insights into exercise-related changes at the molecular level., Objective: The primary goal of this systematic review is to confirm the viability of utilizing Fourier transform infrared spectroscopy for the analysis of the biochemical changes associated with physical exercise and its potential applications., Methods: This systematic review adhered to PRISMA (Preferred Reporting Items for Systematic Reviews and Meta-Analyses) guidelines and examined studies employing Fourier transform infrared spectroscopy to analyze exercise and physical activity, focusing on a biological sample collection and spectral analysis. Four databases (PubMed, SPORTDiscus, Web of Science, and Scopus) were searched, and inclusion criteria encompassed original English-language studies involving human participants aged 18-50 years, a biological sample collection (urine, saliva, and blood), and the use of Fourier transform infrared spectroscopy. The studies were analyzed considering the type of exercise or sport that was investigated, and also the type of spectral analysis conducted., Results: The review encompassed 15 studies that demonstrated the versatility of Fourier transform infrared spectroscopy in assessing various aspects of exercise, including metabolism, cardiovascular responses, and muscular fatigue. The largest study evaluated 57 athletes from several different sports. On average, almost all the studies were performed with around 20 athletes. Notably, the technique's holistic approach allows for a comprehensive analysis of the complex network of metabolites and proteins within the human body. Data analysis methodologies, particularly when coupled with machine learning, show great potential for advancing the field of sports science., Conclusions: Fourier transform infrared spectroscopy emerges as a promising tool for monitoring and enhancing the performance of high-level athletes, preventing overtraining or even over-reaching, and assessing metabolism. Its accuracy, efficiency, and affordability also make it a candidate for broader applications in assessing the health and fitness of the general population. Future research should explore its applicability across diverse exercise modalities and demographic groups, aiming to prescribe exercise plans that consider a multitude of parameters for larger, more intricate exercise cohorts., Clinical Trial Registration: The study protocol was registered in the International Prospective Register of Systematic Reviews (PROSPERO) under the ID number CRD42023441965., Competing Interests: Declarations. Funding: This study is primarily funded by Fundación MAPFRE (Ayuda Investigacion Ignacio H. Larramendi). Funding was also provided by COMPETE 2020—Operational Programme for Competitiveness and Internationalisation and Portuguese national funds via FCT—Fundação para a Ciência e a Tecnologia, 2021.06848.BD, 2022.10099.BD, UIDB/04539/2020, UIDP/04539/2020, and LA/P/0058/2020, DL57/2016/CP1448/CT0027. Conflicts of Interest: Pedro Afonso Valente, Sandra I. Mota, Ana Teixeira, Elisabete Ferreiro, Hugo Sarmento, Inês Cipriano, João R. Campos, Luís Rama, and Paulo J. Oliveira have no conflicts of interest that are directly relevant to the content of this article. Ethics Approval: Not applicable. Consent to Participate: Not applicable. Consent for Publication: Not applicable. Availability of Data and Material: Not applicable. Code Availability: Not applicable. Authors’ Contributions: The authors’ contributions were made following the CRediT (Contributor Roles Taxonomy). PO: conceptualization and supervision, funding acquisition, validation and writing (review and editing); LR: supervision and project administration; PV: conceptualization, data curation, formal analysis, funding acquisition, methodology, writing the original draft, visualization; SM: formal analysis, supervision, validation, visualization and writing (review and editing); AT: supervision; EF: funding acquisition, project administration, visualization, writing (review and editing); IC: data curation, validation, methodology; HS: conceptualization, data curation, methodology, validation; JC: validation, writing (review and editing). All authors read and approved the final version., (© 2024. The Author(s).)

Introduction: Cardiac surgery-associated acute kidney injury (CSA-AKI) is a well-known complication that increases morbidity and mortality rates. The objective of this study was to reduce CSA-AKI through nephrologist intervention in patients awaiting cardiac surgery., Methods: We performed a single center, open-label, randomized clinical trial including 380 patients who underwent scheduled cardiac surgery at the Hospital de Bellvitge between July 2015 and October 2019. A total of 184 patients were evaluated by the same Nephrologist one month before the surgery to minimize the risk factors for AKI. In addition to assessments at the outpatient clinic, we also collected clinical data during hospitalization and during the first year., Results: Despite the intervention, no differences were observed between the groups in the incidence of CSA-AKI (intervention group 26.37% vs. standard of care 25.13%, p=0.874), mortality (3.91% vs. 3.59%, p=0.999), length of Intensive Care Unit (ICU) stay (10 days [7.00;15.0] for both groups, p=0.347), or renal function after one year of follow-up (estimated glomerular filtration rate (eGFR) by CKD-EPI: 74.5 ml/min (standard deviation 20.6) vs 76.7 (20.8) ml/min, respectively, p=0.364). A reduction in the need for blood transfusion was observed in the intervention group, although the difference was not statistically significant (37.22% vs. 45.03%, p =0.155)., Conclusion: In this clinical trial, nephrologist intervention in the entire population on the cardiac surgery waiting list did not show a nephroprotective benefit., Clinical Trial Registration: ClinicalTrials.gov, identifier (NCT02643745)., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2024 Codina, Oliveras, Ferreiro, Rovira, Coloma, Lloberas, Melilli, Hueso, Sbraga, Boza, Vazquez, Pérez-Fernández, Sabater, Cruzado and Montero.)

Alzheimer's disease (AD) is characterized by the deposition in the brain of senile plaques composed of amyloid-β peptides (Aβs) that increase inflammation. An endogenous peptide derived from the insulin-like growth factor (IGF)-I, glycine-proline-glutamate (GPE), has IGF-I-sensitizing and neuroprotective actions. Here, we examined the effects of GPE on Aβ levels and hippocampal inflammation generated by the intracerebroventricular infusion of Aβ25-35 for 2 weeks (300 pmol/day) in ovariectomized rats and the signaling-related pathways and levels of Aβ-degrading enzymes associated with these GPE-related effects. GPE prevented the Aβ-induced increase in the phosphorylation of p38 mitogen-activated protein kinase and the reduction in activation of signal transducer and activator of transcription 3, insulin receptor substrate-1, and Akt, as well as on interleukin (IL)-2 and IL-13 levels in the hippocampus. The functionality of somatostatin, measured as the percentage of inhibition of adenylate cyclase activity and the levels of insulin-degrading enzyme, was also preserved by GPE co-treatment. These findings indicate that GPE co-administration may protect from Aβ insult by changing hippocampal cytokine content and somatostatin functionality through regulation of leptin- and IGF-I-signaling pathways that could influence the reduction in Aβ levels through modulation of levels and/or activity of Aβ proteases.

The global population over 60 years old is projected to reach 1.5 billion by 2050. Understanding age-related disorders and gender-specificities is crucial for a healthy aging. Reliable age-related biomarkers are needed, preferentially obtained through non-invasive methods. Urine-derived stem cells (UDSCs) can be easily obtained, although a detailed bioenergetic characterization, according to the donor aging, remain unexplored. UDSCs were isolated from young and elderly adult women (22-35 and 70-94 years old, respectively). Surprisingly, UDSCs from elderly subjects exhibited significantly higher maximal oxygen consumption and bioenergetic health index than those from younger individuals, evaluated through oxygen consumption rate. Exploratory data analysis methods were applied to engineer a minimal subset of features for the classification and stratification of UDSCs. Additionally, RNAseq of UDSCs was performed to identify age-related transcriptional changes. Transcriptional analysis revealed downregulation of genes related to glucuronidation and estrogen metabolism, and upregulation of inflammation-related genes in UDSCs from elderly individuals. This study demonstrates unexpected differences in the UDSCs' OCR between young and elderly individuals, revealing improved bioenergetics in concurrent with an aged-like transcriptome signature. UDSCs offer a non-invasive model for studying age-related changes, holding promise for aging research and therapeutic studies., Competing Interests: Conflict of Interest The authors declare no conflict of interest., (Copyright © 2024 The Authors. Published by Elsevier B.V. All rights reserved.)

Amyotrophic lateral sclerosis (ALS) is a devastating neurodegenerative disease characterized by the progressive loss of motor neurons, for which current treatment options are limited. Recent studies have shed light on the role of mitochondria in ALS pathogenesis, making them an attractive therapeutic intervention target. This review contains a very comprehensive critical description of the involvement of mitochondria and mitochondria-mediated mechanisms in ALS. The review covers several key areas related to mitochondria in ALS, including impaired mitochondrial function, mitochondrial bioenergetics, reactive oxygen species, metabolic processes and energy metabolism, mitochondrial dynamics, turnover, autophagy and mitophagy, impaired mitochondrial transport, and apoptosis. This review also highlights preclinical and clinical studies that have investigated various mitochondria-targeted therapies for ALS treatment. These include strategies to improve mitochondrial function, such as the use of dichloroacetate, ketogenic and high-fat diets, acetyl-carnitine, and mitochondria-targeted antioxidants. Additionally, antiapoptotic agents, like the mPTP-targeting agents minocycline and rasagiline, are discussed. The paper aims to contribute to the identification of effective mitochondria-targeted therapies for ALS treatment by synthesizing the current understanding of the role of mitochondria in ALS pathogenesis and reviewing potential convergent therapeutic interventions. The complex interplay between mitochondria and the pathogenic mechanisms of ALS holds promise for the development of novel treatment strategies to combat this devastating disease.