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Journal of Biophotonics Dec 2019Visible light synchronizes the human biological clock in the suprachiasmatic nuclei of the hypothalamus to the solar 24-hour cycle. Short wavelengths, perceived as blue... (Review)
Review
Visible light synchronizes the human biological clock in the suprachiasmatic nuclei of the hypothalamus to the solar 24-hour cycle. Short wavelengths, perceived as blue color, are the strongest synchronizing agent for the circadian system that keeps most biological and psychological rhythms internally synchronized. Circadian rhythm is important for optimum function of organisms and circadian sleep-wake disruptions or chronic misalignment often may lead to psychiatric and neurodegenerative illness. The beneficial effect on circadian synchronization, sleep quality, mood, and cognitive performance depends not only on the light spectral composition but also on the timing of exposure and its intensity. Exposure to blue light during the day is important to suppress melatonin secretion, the hormone that is produced by the pineal gland and plays crucial role in circadian rhythm entrainment. While the exposure to blue is important for keeping organism's wellbeing, alertness, and cognitive performance during the day, chronic exposure to low-intensity blue light directly before bedtime, may have serious implications on sleep quality, circadian phase and cycle durations. This rises inevitably the need for solutions to improve wellbeing, alertness, and cognitive performance in today's modern society where exposure to blue light emitting devices is ever increasing.
Topics: Aging; Behavior; Circadian Rhythm; Color; Humans; Light; Retina
PubMed: 31433569
DOI: 10.1002/jbio.201900102 -
Biochimica Et Biophysica Acta. Reviews... Sep 2023Cell death is a fundamental physiological process that occurs in all organisms and is crucial to each organism's evolution, ability to maintain a stable internal... (Review)
Review
Cell death is a fundamental physiological process that occurs in all organisms and is crucial to each organism's evolution, ability to maintain a stable internal environment, and the development of multiple organ systems. Disulfidptosis is a new mode of cell death that is triggered when cells with high expression of solute carrier family 7 member 11 (SLC7A11) are exposed to glucose starvation to initiate the process of cell death. The disulfidptosis mechanism is a programmed cell death mode that triggers cell death through reduction-oxidation (REDOX) reactions and disulfur bond formation. In disulfidptosis, disulfur bonds play a crucial role and cause the protein in the cell to undergo conformational changes, eventually leading to cell death. This mode of cell death has unique characteristics and regulatory mechanisms in comparison with other modes of cell death. In recent years, an increasing number of studies have shown that the disulfidptosis mechanism plays a key role in the occurrence and development of a variety of diseases. For example, cancer, cardiovascular diseases, neurodegenerative diseases, and liver diseases are all closely related to cell disulfidptosis mechanisms. Therefore, it is of paramount clinical significance to conduct in-depth research regarding this mechanism. This review summarizes the research progress on the disulfidptosis mechanism, including its discovery history, regulatory mechanism, related proteins, and signaling pathways. Potential applications of the disulfidptosis mechanism in disease therapy and future research directions are also discussed. This mechanism represents another subversive discovery after ferroptosis, and provides both a fresh perspective and an innovative strategy for the treatment of cancer, as well as inspiration for the treatment of other diseases.
Topics: Humans; Cell Death; Apoptosis; Cardiovascular Diseases; Clinical Relevance; Biology
PubMed: 37451411
DOI: 10.1016/j.bbcan.2023.188955 -
The Bone & Joint Journal Nov 2022Periprosthetic joint infection (PJI) remains an extremely challenging complication. We have focused on this issue more over the last decade than previously, but there...
Periprosthetic joint infection (PJI) remains an extremely challenging complication. We have focused on this issue more over the last decade than previously, but there are still many unanswered questions. We now have a workable definition that everyone should align to, but we need to continue to focus on identifying the organisms involved. Surgical strategies are evolving and care is becoming more patient-centred. There are some good studies under way. There are, however, still numerous problems to resolve, and the challenge of PJI remains a major one for the orthopaedic community. This annotation provides some up-to-date thoughts about where we are, and the way forward. There is still scope for plenty of research in this area.Cite this article: 2022;104-B(11):1193-1195.
Topics: Humans; Prosthesis-Related Infections; Arthroplasty, Replacement, Hip; Synovial Fluid; Arthroplasty, Replacement, Knee; Biomarkers; Arthritis, Infectious; Sensitivity and Specificity
PubMed: 36317347
DOI: 10.1302/0301-620X.104B11.BJJ-2022-0944 -
Experimental Gerontology Apr 2020Aging is characterized by a progressive decline in the normal physiological functions of an organism, ultimately leading to mortality. Nicotinamide adenine dinucleotide... (Review)
Review
Aging is characterized by a progressive decline in the normal physiological functions of an organism, ultimately leading to mortality. Nicotinamide adenine dinucleotide (NAD) is an essential cofactor that plays a critical role in mitochondrial energy production as well as many enzymatic redox reactions. Age-associated decline in NAD is implicated as a driving factor in several categories of age-associated disease, including metabolic and neurodegenerative disease, as well as deficiency in the mechanisms of cellular defense against oxidative stress. The kynurenine metabolic pathway is the sole de novo NAD biosynthetic pathway, generating NAD from ingested tryptophan. Altered kynurenine pathway activity is associated with both aging and a variety of age-associated diseases. Kynurenine pathway interventions can extend lifespan in both fruit flies and nematodes, and altered NAD metabolism represents one potential mediating mechanism. Recent studies demonstrate that supplementation with NAD or NAD-precursors increase longevity and promote healthy aging in fruit flies, nematodes, and mice. NAD levels and the intrinsic relationship to mitochondrial function have been widely studied in the context of aging. Mitochondrial function and dynamics have both been implicated in longevity determination in a range of organisms from yeast to humans, at least in part due to their intimate link to regulating an organism's cellular energy economy and capacity to resist oxidative stress. Recent findings support the idea that complex communication between the mitochondria and the nucleus orchestrates a series of events and stress responses involving mitophagy, mitochondrial number, mitochondrial unfolded protein response (UPR), and mitochondria fission and fusion events. In this review, we discuss how mitochondrial morphological changes and dynamics operate during aging, and how altered metabolism of tryptophan to NAD through the kynurenine pathway interacts with these processes.
Topics: Aging; Animals; Brain; Humans; Kynurenine; Longevity; Metabolic Networks and Pathways; Mice; Mitochondria; Mitophagy; NAD; Neurodegenerative Diseases; Oxidation-Reduction; Oxidative Stress; Tryptophan
PubMed: 31954874
DOI: 10.1016/j.exger.2020.110841 -
Pediatric Annals Sep 2019The incidence of septic arthritis among children in developed countries is estimated to be 4 to 10 cases per 100,000 children per year, peaking at about age 3 years. The... (Review)
Review
The incidence of septic arthritis among children in developed countries is estimated to be 4 to 10 cases per 100,000 children per year, peaking at about age 3 years. The most common causative organism is Staphylococcus aureus, although the microbiology varies by age. Prompt diagnosis and treatment is critical to prevent long-term sequelae. Empiric therapy should target the most likely causative organism(s) and total duration generally falls between 10 days and 4 weeks depending on clinical course, patient age, and organism. A short intravenous course is sufficient in most cases. Unusual and alternate causes of arthritis should be considered in special cases. [Pediatr Ann. 2019;48(9):e354-e359.].
Topics: Adolescent; Anti-Bacterial Agents; Arthritis, Infectious; Child; Child, Preschool; Drug Administration Schedule; Humans; Infant; Infant, Newborn; Injections, Intravenous; Staphylococcal Infections
PubMed: 31505009
DOI: 10.3928/19382359-20190816-02