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BMJ Military Health Jul 2023Traumatic injury is one of the leading causes of death worldwide, and despite significant improvements in patient care, survival in the most severely injured patients...
INTRODUCTION
Traumatic injury is one of the leading causes of death worldwide, and despite significant improvements in patient care, survival in the most severely injured patients remains unchanged. There is a crucial need for innovative approaches to improve trauma patient outcomes; this is particularly pertinent in remote or austere environments with prolonged evacuation times to definitive care. Studies suggest that maintenance of cellular homeostasis is a critical component of optimal trauma patient management, and as the cell powerhouse, it is likely that mitochondria play a pivotal role. As a result, therapies that optimise mitochondrial function could be an important future target for the treatment of critically ill trauma patients.
METHODS
A systematic review of the literature was undertaken in accordance with the Preferred Reporting Items for Systematic Reviews and Meta-Analyses protocol to determine the potential role of mitochondria in traumatic injury and haemorrhagic shock (HS) and to identify current evidence for mitochondrial optimisation therapies in trauma. Articles were included if they assessed a mitochondrial targeted therapy in comparison to a control group, used a model of traumatic injury and HS and reported a method to assess mitochondrial function.
RESULTS
The search returned 918 articles with 37 relevant studies relating to mitochondrial optimisation identified. Included studies exploring a range of therapies with potential utility in traumatic injury and HS. Therapies were categorised into the key mitochondrial pathways impacted following traumatic injury and HS: ATP levels, cell death, oxidative stress and reactive oxygen species.
CONCLUSION
This systematic review provides an overview of the key cellular functions of the mitochondria following traumatic injury and HS and identifies why mitochondrial optimisation could be a viable and valuable target in optimising outcome in severely injured patients in the future.
PubMed: 37491136
DOI: 10.1136/military-2023-002427 -
Environmental Research Nov 2023Photothermal therapy (PTT) is an emerging non-invasive method used in cancer treatment. In PTT, near-infrared laser light is absorbed by a chromophore and converted into... (Review)
Review
Photothermal therapy (PTT) is an emerging non-invasive method used in cancer treatment. In PTT, near-infrared laser light is absorbed by a chromophore and converted into heat within the tumor tissue. PTT for cancer usually combines a variety of interactive plasmonic nanomaterials with laser irradiation. PTT enjoys PT agents with high conversion efficiency to convert light into heat to destroy malignant tissue. In this review, published studies concerned with the use of nanoparticles (NPs) in PTT were collected by a systematic and comprehensive search of PubMed, Cochrane, Embase, and Scopus databases. Gold, silver and iron NPs were the most frequent choice in PTT. The use of surface modified NPs allowed selective delivery and led to a precise controlled increase in the local temperature. The presence of NPs during PTT can increase the reactive generation of oxygen species, damage the DNA and mitochondria, leading to cancer cell death mainly via apoptosis. Many studies recently used core-shell metal NPs, and the effects of the polymer coating or ligands targeted to specific cellular receptors in order to increase PTT efficiency were often reported. The effective parameters (NP type, size, concentration, coated polymers or attached ligands, exposure conditions, cell line or type, and cell death mechanisms) were investigated individually. With the advances in chemical synthesis technology, NPs with different shapes, sizes, and coatings can be prepared with desirable properties, to achieve multimodal cancer treatment with precision and specificity.
PubMed: 37487920
DOI: 10.1016/j.envres.2023.116526 -
Molecular & Cellular Proteomics : MCP Aug 2023Osteoarthritis (OA) is the most prevalent rheumatic pathology. However, OA is not simply a process of wear and tear affecting articular cartilage but rather a disease of...
Osteoarthritis (OA) is the most prevalent rheumatic pathology. However, OA is not simply a process of wear and tear affecting articular cartilage but rather a disease of the entire joint. One of the most common locations of OA is the knee. Knee tissues have been studied using molecular strategies, generating a large amount of complex data. As one of the goals of the Rheumatic and Autoimmune Diseases initiative of the Human Proteome Project, we applied a text-mining strategy to publicly available literature to collect relevant information and generate a systematically organized overview of the proteins most closely related to the different knee components. To this end, the PubPular literature-mining software was employed to identify protein-topic relationships and extract the most frequently cited proteins associated with the different knee joint components and OA. The text-mining approach searched over eight million articles in PubMed up to November 2022. Proteins associated with the six most representative knee components (articular cartilage, subchondral bone, synovial membrane, synovial fluid, meniscus, and cruciate ligament) were retrieved and ranked by their relevance to the tissue and OA. Gene ontology analyses showed the biological functions of these proteins. This study provided a systematic and prioritized description of knee-component proteins most frequently cited as associated with OA. The study also explored the relationship of these proteins to OA and identified the processes most relevant to proper knee function and OA pathophysiology.
Topics: Humans; Cartilage, Articular; Knee Joint; Osteoarthritis, Knee
PubMed: 37356495
DOI: 10.1016/j.mcpro.2023.100606 -
Neurochemical Research Aug 2023Peripheral neuropathies caused by the peripheral nervous system (PNS) damage can occur due to trauma and other disorders. They present as altered sensation, weakness,... (Meta-Analysis)
Meta-Analysis Review
Peripheral neuropathies caused by the peripheral nervous system (PNS) damage can occur due to trauma and other disorders. They present as altered sensation, weakness, autonomic symptoms, and debilitating pain syndrome with a wide range of clinical signs. Acetyl-L-Carnitine (ALCAR) is a biological compound with essential roles in mitochondrial oxidative metabolism and anti-oxidant effects that protects mitochondria from oxidative damage and inhibits apoptosis caused by mitochondrial damage. This study is a systematic review and meta-analysis of the effects of ALCAR on peripheral nerve injuries. This review examines studies on treating traumatic peripheral neuropathies in which ALCAR is administered to rats with sciatic nerve injury with an appropriate control group. The articles were divided based on the mode of ALCAR administration. If one method was used in more than one article, their results were entered in the "Revman5.4" software and were meta-analyzed. Studies were selected from 1994 to 2018 on rats with varying physical injuries to their sciatic nerves. In one study, ALCAR was provided to rats in their drinking water, while in other studies, ALCAR was injected intra-peritoneally. Different mechanisms of ALCAR actions have been suggested in this study, but the underpinnings of the neuroprotective effects of ALCAR are still unclear. Further studies are mandatory to clarify the actual mechanisms of the neuroprotective activity of ALCAR. Based on the results of existing studies, ALCAR effectively increases the tolerance threshold of thermal and mechanical stimuli, reduces latency, and reduces apoptosis; finally, adjusting the dose and duration of administration may increase the dose and duration axon diameter.
Topics: Animals; Rats; Acetylcarnitine; Nerve Regeneration; Peripheral Nerve Injuries; Sciatic Nerve
PubMed: 37037995
DOI: 10.1007/s11064-023-03911-1 -
European Child & Adolescent Psychiatry Jun 2024The global prevalence of attention-deficit/hyperactivity disorder (ADHD) is estimated to be between 6% and 7% in children worldwide. The pathophysiology of this... (Review)
Review
The global prevalence of attention-deficit/hyperactivity disorder (ADHD) is estimated to be between 6% and 7% in children worldwide. The pathophysiology of this heterogeneous neurodevelopmental disorder remains unknown. Mitochondrial dysfunction has been proposed as a possible contributing factor to the etiology of ADHD. There is limited literature available to help our understanding of this hypothesis, and thus we conducted a systematic review of the number and quality of studies pertaining to mitochondrial genetic alterations in ADHD. A systematic search was conducted in the relevant databases Medline (PubMed) and Embase up to March 2021. Inclusion criteria included randomized control trials, cross-sectional studies, and case-control studies. This search resulted in a total of 507 articles that emerged from the search criteria. Of these results, 10 primary research articles were selected for in depth review based on the inclusion and exclusion criteria. These studies all reported on mitochondrial genetic variation in ADHD cases such as increased copy number, single-nucleotide polymorphisms, and haplogroup associations. This initial review of the experimental literature suggests mitochondrial genetic variation, in both the mitochondrial DNA and nuclear-encoded mitochondrial genes, may indeed contribute to ADHD pathophysiology. The studies reviewed here provide promising evidence for future research to further examine the mitochondrial genetics contributing to ADHD pathophysiology. We suggest that expansion of investigations into mitochondrial mechanisms may have potential to inform new treatment options for ADHD.
Topics: Humans; Attention Deficit Disorder with Hyperactivity; DNA, Mitochondrial; Genetic Variation; Mitochondria; Child; Polymorphism, Single Nucleotide
PubMed: 35796884
DOI: 10.1007/s00787-022-02030-6