Endogenous Stress Research Articles

Correlation between preoperative frailty and postoperative delirium in elderly patients undergoing hip arthroplasty.

Postoperative delirium (POD) refers to acute brain dysfunction occurring within 7 days after operation or before discharge. Frailty refers to the state that the body's physiological reserve is insufficient, so that the compensative capacity to endogenous and exogenous stress stimuli decreases. The purpose of this study is to explore the association of preoperative frailty (PF) with POD in elderly patients undergoing hip arthroplasty. Totally 228 elderly patients (age ≥ 65 years) who received elective hip arthroplasty in the Ningbo No. 6 Hospital between December 2021 and June 2022 were enrolled. One day before surgery, the frailty phenotype scale was adopted for evaluation of patients' frailty. On the 1st-3rd day after operation, the confusion assessment method was adopted for evaluation of delirium, and the patients were grouped into a POD group and non-POD group. Logistic regression was conducted to analyze the correlation between PF and POD. Among the patients, the incidence of PF was 30.70% (70/228), and the incidence of delirium within 3 days after operation was 25.88% (59/228). According to binary logistic regression analysis, PF, age, hypertension, diabetes mellitus, and preoperative sleep disorder were independent risk factors for POD in elderly patients undergoing hip arthroplasty (all P < .05). PF is a crucial risk factor for POD in elderly patients undergoing hip arthroplasty.

The efficacy of non-invasive brain stimulation in the treatment of children and adolescents with Anorexia Nervosa: study protocol of a randomized, double blind, placebo-controlled trial

BackgroundCurrent psychological and pharmacological treatments for Anorexia Nervosa (AN) provide only moderate effective support, and there is an urgent need for research to improve therapies, especially in developing age. Non-invasive brain stimulation has suggested to have the potential to reducing AN symptomatology, via targeting brain alterations, such as hyperactivity of right prefrontal cortex (PFC). We suppose that transcranial direct current stimulation (tDCS) to the PFC may be effective in children and adolescents with AN.MethodsWe will conduct a randomized, double blind, add-on, placebo-controlled trial to investigate the efficacy of tDCS treatment on clinical improvement. We will also investigate brain mechanisms and biomarkers changes acting in AN after tDCS treatment. Eighty children or adolescent with AN (age range 10–18 years) will undergo treatment-as-usual including psychiatric, nutritional and psychological support, plus tDCS treatment (active or sham) to PFC (F3 anode/F4 cathode), for six weeks, delivered three times a week. Psychological, neurophysiological and physiological measures will be collected at baseline and at the end of treatment. Participants will be followed-up one, three, six months and one year after the end of treatment. Psychological measures will include parent- and self-report questionnaires on AN symptomatology and other psychopathological symptoms. Neurophysiological measures will include transcranial magnetic stimulation (TMS) with electroencephalography and paired pulse TMS and repetitive TMS to investigate changes in PFC connectivity, reactivity and plasticity after treatment. Physiological measures will include changes in the functioning of the endogenous stress response system, body mass index (BMI) and nutritional state.DiscussionWe expect that tDCS treatment to improve clinical outcome by reducing the symptoms of AN assessed as changes in Eating Disorder Risk composite score of the Eating Disorder Inventory-3. We also expect that at baseline there will be differences between the right and left hemisphere in some electrophysiological measures and that such differences will be reduced after tDCS treatment. Finally, we expect a reduction of endogenous stress response and an improvement in BMI and nutritional status after tDCS treatment. This project would provide scientific foundation for new treatment perspectives in AN in developmental age, as well as insight into brain mechanisms acting in AN and its recovery.Trial registration The study was registered at ClinicalTrials.gov (ID: NCT05674266) and ethical approval for the study was granted by the local research ethics committee (process number 763_OPBG_2014).

Ribonucleic Acid-Mediated Control of Protein Translation Under Stress.

Significance: The need of cells to constantly respond to endogenous and exogenous stress has necessitated the evolution of pathways to counter the deleterious effects of stress and to restore cellular homeostasis. The inability to activate a timely and adequate response can lead to disease and is a hallmark of aging. Besides protein-coding genes, cells contain a plethora of noncoding regulatory elements that allow cells to respond rapidly and efficiently to external stimuli by activating highly specific and tightly controlled mechanisms. Many of these programs converge on the regulation of translation, one of the most energy-consuming processes in cells. Recent Advances: The noncoding dimension of translational regulation includes short and long noncoding ribonucleic acids (ncRNAs), as well as messenger RNA features, such as the sequence and modification status of the 5' and 3' untranslated regions (UTRs), that do not change the amino acid sequence of the produced protein. Critical Issues: In this review, we discuss the regulatory role of the nonprotein-coding components of translation under stress, particularly oxidative stress. We conclude that the regulation of translation through ncRNAs, UTRs, and nucleotide modifications is emerging as a critical component of the stress response. Future Directions: Further areas of study using long-read sequencing technologies will be discussed. Antioxid. Redox Signal. 39, 374-389.

Strategic mistakes

To study the equilibrium implications of decision frictions, we introduce a new class of control costs in continuum-player, continuum-action games in which agents interact via an aggregate of the actions of others. The costs that we study accommodate a rich class of decision frictions, including ex post misoptimization, imperfect ex ante planning, cognitive constraints that depend endogenously on the behavior of others, and consideration sets. We provide primitive conditions such that equilibria exist, are unique, are efficient, and feature monotone comparative statics for action distributions, aggregates, and the size of agents' mistakes. We apply the model to make robust equilibrium predictions in a monetary business-cycle model of price-setting with planning frictions and a model of consumption and savings during a liquidity trap when endogenous stress worsens decisions.

Examination of stress–turnover relationship through perceived employee's exploitation at workplace

PurposeIn the purview of stress–turnover relationship, the present study aims to explore the endogenous and exogenous aspects of stress and employees' turnover intentions. Further, it also intends to evaluate the mediating role of perceived employee's exploitation between stressors and employee turnover intentions. For that matter, antecedents of stressors were identified and classified into endogenous and exogenous stressors: endogenous stressors relate to the employees' negative psychological contact within an organization and exogenous stressors are various macro-economic factors which have a considerable influence on employees' workplace behavior.Design/methodology/approachFor the purpose of this study, this study choses private school teachers as respondents working in the economically depressed state of India. Thus, data for the present study has been collected from 628 private school teachers of J&amp;K (India) which were randomly selected. In order to ensure valid and reliable statistical inferences from the study, data collected has been validated using confirmatory factor analysis and hypothesis testing has been carried out through structural equation modeling.FindingsIt was found that both types of stressors were contributing negatively toward employee's psychological state resulting in undesirable employee organizational relationships manifested as turnover intentions among employees. Moreover, perceived employee's exploitation was found to intensify the relationship of employee turnover as a dependent variable regressed on endogenous, exogenous and occupational stress by fully mediating the stress–turnover intricacies.Research limitations/implicationsThe implications of the study include the identification of employees' stressor needs in order to gauge the understanding of the mechanism by which employees react to their environment and develop attitudes toward their jobs. The present study includes a small sample size obtained from private educational institutions only. Therefore, there is a need to take a geographically diverse sample that is inevitable for universal inferences and validity.Originality/valueVery little research has been conducted to explore endogenous, exogenous and unique stressors such as economic stress and perceived external opportunities which constitute the overall stress. Moreover, to the best of the authors’ knowledge, this is the first study which tests the model empirically that examines the effect of stress–turnover relationship through perceived employee's exploitation in the teaching and educational sector.

Accelerated -Rule-Out of acute Myocardial Infarction using prehospital copeptin and in-hospital troponin: The AROMI study.

The present acute myocardial infarction (AMI) rule-out strategies are challenged by the late temporal release of cardiac troponin. Copeptin is a non-specific biomarker of endogenous stress and rises early in AMI, covering the early period where troponin is still normal. An accelerated dual-marker rule-out strategy combining prehospital copeptin and in-hospital high-sensitivity troponin T could reduce length of hospital stay and thus the burden on the health care systems worldwide. The AROMI trial aimed to evaluate if the accelerated dual-marker rule-out strategy could safely reduce length of stay in patients discharged after early rule-out of AMI. Patients with suspected AMI transported to hospital by ambulance were randomized 1:1 to either accelerated rule-out using copeptin measured in a prehospital blood sample and high-sensitivity troponin T measured at arrival to hospital or to standard rule-out using a 0 h/3 h rule-out strategy. The AROMI study included 4351 patients with suspected AMI. The accelerated dual-marker rule-out strategy reduced mean length of stay by 0.9 h (95% confidence interval 0.7-1.1 h) in patients discharged after rule-out of AMI and was non-inferior regarding 30-day major adverse cardiac events when compared to standard rule-out (absolute risk difference -0.4%, 95% confidence interval -2.5 to 1.7; P-value for non-inferiority = 0.013). Accelerated dual marker rule-out of AMI, using a combination of prehospital copeptin and first in-hospital high-sensitivity troponin T, reduces length of hospital stay without increasing the rate of 30-day major adverse cardiac events as compared to using a 0 h/3 h rule-out strategy.

UBQLN1 deficiency mediates telomere shortening and IPF through interacting with RPA1.

Premature telomere shortening is a known factor correlated to idiopathic pulmonary fibrosis (IPF) occurrence, which is a chronic, progressive, age-related disease with high mortality. The etiology of IPF is still unknown. Here, we found that UBQLN1 plays a key role in telomere length maintenance and is potentially relevant to IPF. UBQLN1 involves in DNA replication by interacting with RPA1 and shuttling it off from the replication fork. The deficiency of UBQLN1 retains RPA1 at replication fork, hinders replication and thus causes cell cycle arrest and genome instability. Especially at telomere regions of the genome, where more endogenous replication stress exists because of G rich sequences, UBQLN1 depletion leads to rapid telomere shortening in HeLa cells. It revealed that UBQLN1 depletion also shortens telomere length at mouse lung and accelerates mouse lung fibrosis. In addition, the UBQLN1 expression level in IPF patients is downregulated and correlated to poor prognosis. Altogether, these results uncover a new role of UBQLN1 in ensuring DNA replication and maintaining telomere stability, which may shed light on IPF pathogenesis and prevention.

Mitigation of endogenous oxidative stress and improving growth, hemato-biochemical parameters, and reproductive performance of Zaraibi goat bucks by dietary supplementation with Chlorella vulgaris or/and vitamin C

This study was conducted to explore the effects of dietary inclusion of Chlorella vulgaris (CV) or/and vitamin C (VC) on growth, hemato-biochemical parameters, oxidative and antioxidant status, reproductive hormones, and semen quality variables, and scrotal-testicular dimensions of Zaraibi goat bucks. Twenty sexually mature bucks (41.49 ± 0.91 kg BW) were randomly divided into 4 groups (5 bucks/group). The control group was fed the control diet, while the other three groups received a diet supplemented with VC (2 g/animal /day), CV (5 g/animal/day), and CV plus VC (the same levels), respectively, for 8 weeks (treatment period), and then semen was collected for 8 weeks. Results showed that dietary supplementation with CV-VC combination significantly increased the final body weight, weight gain, packed cell volume, hemoglobin, red blood cells, white blood cells, and lymphocytes; elevated serum total protein, globulin, testosterone, estradiol, superoxide dismutase, glutathione peroxidase with a significant reduction in Malondialdehyde in serum and seminal plasma. Also, the CV-VC combination significantly improved the ejaculate volume, total sperm output, sperm concentration, and live sperm, and reduced reaction time and sperm abnormality of bucks. Either CV or VC given separately or in combination, at the chosen levels, had no detrimental effects on animal physiological responses with normal hepatic and renal functions. Therefore, the CV-VC combination could be safely utilized as a dietary supplement in buck’s diets to improve antioxidant defenses, scavenge free radicals, and potentiate buck’s reproductive activities under normal conditions.

Functional Additives in a Selected European Sea Bass (Dicentrarchus labrax) Genotype: Effects on the Stress Response and Gill Antioxidant Response to Hydrogen Peroxide (H2O2) Treatment.

Functional ingredients have profiled as suitable candidates for reinforcing the fish antioxidant response and stress tolerance. In addition, selective breeding strategies have also demonstrated a correlation between fish growth performance and susceptibility to stressful culture conditions as a key component in species domestication processes. The aim of the present study is to evaluate the ability of a selected high-growth genotype of 300 days post-hatch European sea bass (Dicentrarchus labrax) juveniles to use different functional additives as endogenous antioxidant capacity and stress resistance boosters when supplemented in low fish meal (FM) and fish oil (FO) diets. Three isoenergetic and isonitrogenous diets (10% FM/6% FO) were supplemented with 200 ppm of a blend of garlic and Labiatae plant oils (PHYTO0.02), 1000 ppm of a mixture of citrus flavonoids and Asteraceae and Labiatae plant essential oils (PHYTO0.1) or 5000 ppm of galactomannan-oligosaccharides (GMOS0.5). A reference diet was void of supplementation. The fish were fed the experimental diets for 72 days and subjected to a H2O2 exposure oxidative stress challenge. The fish stress response was evaluated through measuring the circulating plasma cortisol levels and the fish gill antioxidant response by the relative gene expression analysis of nfΚβ2, il-1b, hif-1a, nd5, cyb, cox, sod, cat, gpx, tnf-1α and caspase 9. After the oxidative stress challenge, the genotype origin determined the capacity of the recovery of basal cortisol levels after an acute stress response, presenting GS fish with a better pattern of recovery. All functional diets induced a significant upregulation of cat gill gene expression levels compared to fish fed the control diet, regardless of the fish genotype. Altogether, suggesting an increased capacity of the growth selected European sea bass genotype to cope with the potential negative side-effects associated to an H2O2 bath exposure.

Comprehensive analysis of nanoplastic effects on growth phenotype, nanoplastic accumulation, oxidative stress response, gene expression, and metabolite accumulation in multiple strawberry cultivars

Nanoplastics (NPs) have emerged as a novel environmental threat due to their potential impacts on both animals and plants. Currently, research on the ecotoxicity of NPs has mainly focused on marine aquatic organisms and freshwater algae, with very limited investigations conducted on horticultural plants. This study examined the effects of varying concentrations (0, 1, 10, 50 mg·L−1) of polystyrene NPs (PS-NPs) on strawberry growth. The findings revealed that low concentrations of PS-NPs stimulated strawberry growth, whereas high concentrations impeded it. Notably, diverse strawberry cultivars displayed considerable differences in their sensitivity to PS-NP exposure. Laser scanning confocal microscopy confirmed the absorption of PS-NPs by strawberry roots, with variations in PS-NP accumulation observed across different cultivars. Comparative transcriptomics analysis suggested that the differential expression of genes responsible for calcium ion transport played a significant role in the observed intervarietal differences in PS-NP accumulation among strawberry cultivars. Furthermore, distinct variations in endogenous oxidative responses were observed in different strawberry cultivars under PS-NP treatment. Further analysis indicated that the down-regulation of peroxidase (POD) gene expression and terpenoid compounds accumulation were responsible for heightened endogenous oxidative stress observed in certain strawberry cultivars under PS-NP treatment. Transcriptomic and metabolomic analyses were performed on six strawberry cultivars to investigate their response to PS-NPs in terms of endogenous gene expression and metabolite accumulation. The results identified one commonly up-regulated gene (wall-associated receptor kinase-like) and sixteen commonly down-regulated genes associated with lipid metabolism and carbohydrate metabolism. In addition, a significant reduction in fatty acid metabolite accumulation was observed in the six strawberry cultivars under PS-NP treatment. These findings have significant implications for understanding the effects of NPs on strawberry growth, metabolism, and antioxidant responses, as well as identifying marker genes for monitoring and evaluating the impact of NP pollution on strawberry.

Role of melatonin as a protective antioxidant in the amelioration of oxidative stress mediated tissue injury: a new vision for futuristic medicine

Melatonin (N-acetyl-5-methoxy tryptamine) is ubiquitous in almost every creature; diatoms, bacteria, plants, and animals. During thecourse of organic evolution, melatonin (a pineal secretory product in vertebrates and mammals, including humans) never changed itsstructure and thus remain conserved as an ancient molecule in nature. Since discovery of the antioxidant properties of melatonin byDr. Dun-Xian Tan in 1993, its antioxidative efficacy in various situations of oxidative stress in plants, animals and humans has been wellestablished. It is clear that melatonin has evolved much earlier than other antioxidants. Ischaemic heart disease (IHD) and consequential myocardial infarction (MI) is a health problem of global concern and its ubiquitous prevalence is increasing worldwide annually. The involvement of oxidative stress in myocardial ischemia has long been recognized around the globe. Moreover, the prescribed medicines for cardiac tissue well-being sometimes became detrimental for gastric epithelium. Though endogenous gastric melatonin plays a protective role in offering protection to the entire gastric system, stress-mediated challenged melatonin level brings about threats to the gastric system. Mitigation of oxidative stress in the myocardium and gastric system as well, by antioxidants, may play an effective role in protection and the results of our studies carried out through several years have revealed that melatonin offers extensive protection toward the said systems when subjected to stress by physiological as well as synthetic molecules. Further, we have extrapolated our studies to check whether its protective action is extended toward erythrocytes, the first exposed cellular system to various exogenous and endogenous stressors. Moreover, melatonin was also found to exhibit cardio-protection when ISO aggravated high-fat diet-induced oxidative stress-mediated myocardial onslaught. Our studies revealed the association of a unique pathway in cardio-protection by melatonin. These findings further strengthen the role of melatonin as a cardio-protective antioxidant with no or minimal side effects, recognized globally and having immense future therapeutic relevance

Spatial mapping of the DNA adducts in cancer

DNA adducts and strand breaks are induced by various exogenous and endogenous agents. Accumulation of DNA damage is implicated in many disease processes, including cancer, aging, and neurodegeneration. The continuous acquisition of DNA damage from exogenous and endogenous stressors coupled with defects in DNA repair pathways contribute to the accumulation of DNA damage within the genome and genomic instability. While mutational burden offers some insight into the level of DNA damage a cell may have experienced and subsequently repaired, it does not quantify DNA adducts and strand breaks. Mutational burden also infers the identity of the DNA damage. With advances in DNA adduct detection and quantification methods, there is an opportunity to identify DNA adducts driving mutagenesis and correlate with a known exposome. However, most DNA adduct detection methods require isolation or separation of the DNA and its adducts from the context of the nuclei. Mass spectrometry, comet assays, and other techniques precisely quantify lesion types but lose the nuclear context and even tissue context of the DNA damage. The growth in spatial analysis technologies offers a novel opportunity to leverage DNA damage detection with nuclear and tissue context. However, we lack a wealth of techniques capable of detecting DNA damage in situ. Here, we review the limited existing in situ DNA damage detection methods and examine their potential to offer spatial analysis of DNA adducts in tumors or other tissues. We also offer a perspective on the need for spatial analysis of DNA damage in situ and highlight Repair Assisted Damage Detection (RADD) as an in situ DNA adduct technique with the potential to integrate with spatial analysis and the challenges to be addressed.

Oxidative stress drives mutagenesis through transcription-coupled repair in bacteria

In bacteria, mutations lead to the evolution of antibiotic resistance, which is one of the main public health problems of the twenty-first century. Therefore, determining which cellular processes most frequently contribute to mutagenesis, especially in cells that have not been exposed to exogenous DNA damage, is critical. Here, we show that endogenous oxidative stress is a key driver of mutagenesis and the subsequent development of antibiotic resistance. This is the case for all classes of antibiotics and highly divergent species tested, including patient-derived strains. We show that the transcription-coupled repair pathway, which uses the nucleotide excision repair proteins (TC-NER), is responsible for endogenous oxidative stress-dependent mutagenesis and subsequent evolution. This suggests that a majority of mutations arise through transcription-associated processes rather than the replication fork. In addition to determining that the NER proteins play a critical role in mutagenesis and evolution, we also identify the DNA polymerases responsible for this process. Our data strongly suggest that cooperation between three different mutagenic DNA polymerases, likely at the last step of TC-NER, is responsible for mutagenesis and evolution. Overall, our work identifies a highly conserved pathway that drives mutagenesis due to endogenous oxidative stress, which has broad implications for all diseases of evolution, including antibiotic resistance development.

The Role of Oxidative Stress and Cellular Senescence in the Pathogenesis of Metabolic Associated Fatty Liver Disease and Related Hepatocellular Carcinoma.

Hepatocellular carcinoma (HCC) represents a worryingly increasing cause of malignancy-related mortality, while Metabolic Associated Fatty Liver Disease (MAFLD) is going to become its most common cause in the next decade. Understanding the complex underlying pathophysiology of MAFLD-related HCC can provide opportunities for successful targeted therapies. Of particular interest in this sequela of hepatopathology is cellular senescence, a complex process characterised by cellular cycle arrest initiated by a variety of endogenous and exogenous cell stressors. A key biological process in establishing and maintaining senescence is oxidative stress, which is present in multiple cellular compartments of steatotic hepatocytes. Oxidative stress-induced cellular senescence can change hepatocyte function and metabolism, and alter, in a paracrine manner, the hepatic microenvironment, enabling disease progression from simple steatosis to inflammation and fibrosis, as well as HCC. The duration of senescence and the cell types it affects can tilt the scale from a tumour-protective self-restricting phenotype to the creator of an oncogenic hepatic milieu. A deeper understanding of the mechanism of the disease can guide the selection of the most appropriate senotherapeutic agent, as well as the optimal timing and cell type targeting for effectively combating HCC.

Mechanisms of epithelial growth and development in the zebrafish intestine.

The intestinal epithelium is a complex tissue monolayer composed of regionally and functionally specialized intestinal epithelial cells. Given epithelial exposure to harsh and varied luminal conditions, epithelial cells continuously regenerate to sustain the barrier against environmental factors, including microbial invaders. Multipotent intestinal stem cells are essential to epithelial regenerative capacity, generating a programed mixture of absorptive and secretory cell types. Mechanisms of epithelial growth and differentiation in response to endogenous or external stressors remain under investigation. In this review, we highlight the zebrafish, Danio rerio, as a potent model of intestinal epithelial development and function. We describe epithelial composition and key regulators of epithelial renewal to promote the zebrafish as an investigative tool to study epithelial development and growth. We also highlight areas for discovery, particularly in the context of stress-dependent regulation of epithelial function.

Alkaloids as Natural NRF2 Inhibitors: Chemoprevention and Cytotoxic Action in Cancer.

Being a controller of cytoprotective actions, inflammation, and mitochondrial function through participating in the regulation of multiple genes in response to stress-inducing endogenous or exogenous stressors, the transcription factor Nuclear Factor Erythroid 2-Related Factor 2 (NRF2) is considered the main cellular defense mechanism to maintain redox balance at cellular and tissue level. While a transient activation of NRF2 protects normal cells under oxidative stress, the hyperactivation of NRF2 in cancer cells may help them to survive and to adapt under oxidative stress. This can be detrimental and related to cancer progression and chemotherapy resistance. Therefore, inhibition of NRF2 activity may be an effective approach for sensitizing cancer cells to anticancer therapy. In this review, we examine alkaloids as NRF2 inhibitors from natural origin, their effects on cancer therapy, and/or as sensitizers of cancer cells to anticancer chemotherapeutics, and their potential clinical applications. Alkaloids, as inhibitor of the NRF2/KEAP1 signaling pathway, can have direct (berberine, evodiamine, and diterpenic aconitine types of alkaloids) or indirect (trigonelline) therapeutic/preventive effects. The network linking alkaloid action with oxidative stress and NRF2 modulation may result in an increased NRF2 synthesis, nuclear translocation, as well in a downstream impact on the synthesis of endogenous antioxidants, effects strongly presumed to be the mechanism of action of alkaloids in inducing cancer cell death or promoting sensitivity of cancer cells to chemotherapeutic agents. In this regard, the identification of additional alkaloids targeting the NRF2 pathway is desirable and the information arising from clinical trials will reveal the potential of these compounds as a promising target for anticancer therapy.

The Impact of Alcohol Consumption and Oral Microbiota on Upper Aerodigestive Tract Carcinomas: A Pilot Study.

Alcohol consumption is associated with oxidative stress and an increased risk of carcinoma of the upper aero-digestive tract (UADT). Recently, it has been found that some microorganisms in the human oral cavity may locally metabolize ethanol, forming acetaldehyde, a carcinogenic metabolite of alcohol. In a cohort of patients first visited for UADT cancers, we estimated their alcohol consumption by measuring Ethyl Glucuronide/EtG (a long-lasting metabolite of ethanol) in the hair and carbohydrate-deficient transferrin/CDT (short-term index of alcohol intake) in the serum. Moreover, we analyzed, by culture-based methods, the presence of Neisseria subflava, Streptococcus mitis, Candida albicans, and glabrata (microorganisms generating acetaldehyde) in the oral cavity. According to the EtG values, we correlated drinking alcohol with endogenous oxidative stress and the investigated microorganism's presence. We found that 55% of heavy drinkers presented microorganisms generating acetaldehyde locally. Moreover, we found that the presence of oral acetaldehyde-producing bacteria correlates with increased oxidative stress compared to patients without such bacteria. As for the study of alcohol dehydrogenase gene polymorphisms (the enzyme that transforms alcohol to acetaldehyde), we found that only the "CGTCGTCCC" haplotype was more frequent in the general population than in carcinoma patients. This pilot study suggests the importance of estimating alcohol consumption (EtG), the presence of bacteria producing acetaldehyde, and oxidative stress as risk factors for the onset of oral carcinomas.

Social and Ecological Impacts of Fire to Coastal Fisheries: A Study of the Kenai River Fishery (Alaska,USA)

AbstractIn a rapidly changing environment where fires are becoming more frequent and severe, scientists and managers need information and tools to enhance understanding of the numerous ways in which fire can affect fisheries. We used Ostrom's social–ecological systems framework to structure the development and refinement of fuzzy cognitive maps with stakeholders across the Kenai River fishery in Alaska, USA. The process yielded a model characterizing the structure and function of the Kenai River fishery. The model was then used to guide interviews with stakeholders focused on the effects of the 2019 Swan Lake Fire. We identified seven direct pathways through which fire can affect the social and ecological components of a coastal fishery. We also used the model to guide a targeted literature review to further explore how fire can affect the components of the Kenai River fishery. This synthesis of information allowed us to develop a more complete understanding of the impacts of fire on the fishery—an understanding informed by input from local stakeholders (via our interviews) and relevant scientific and management literature (via our literature review). Lastly, we used the model to assess the fishery's vulnerability to fire. We discuss how early run Chinook SalmonOncorhynchus tshawytschaconstitute a highly vulnerable component of the system and have the greatest potential to impact the fishery as a whole through a chain of negative social and ecological interactions. This final step illustrates how the model can be used to assess the vulnerability of system components to specific threats. The model of the Kenai River fishery provides an empirically grounded and easily understood visual representation of the complex dynamics affecting coastal fisheries. As such, it can be used to structure discussions among managers and stakeholders, organize our understanding of how fire affects fisheries, and assess vulnerabilities to endogenous and exogenous stressors.

Insights into inactivation and response mechanisms of sublethal Listeria monocytogenes treated by cold plasma with joint transcriptomics and metabolomics

The aim of the current study is to elucidate the inactivation and molecular response pattern of sublethal Listeria monocytogenes to cold plasma mediated two-pronged oxidative microenvironments from a high-throughput multi-omics perspective. First joint transcriptomics and metabolomics analyses revealed that significantly expressed genes and metabolites were mainly involved in enhanced transmembrane transport and Fe2+/Cu+ efflux, amino acids limitation, cytoplasmic pH homeostasis, reconfiguration of central carbon metabolism flux and energy conservation strategy, which triggered the surge of intracellular endogenous oxidative stress and finally mediated bacterial ferroptosis and pathogenicity attenuation. Typical antioxidant systems such as the TrxR-Trx system and common antioxidant genes (e.g. sodA, katA, ahpC, trxA, spxA) were inhibited, and the more prominent antioxidant pathways include methionine metabolism, pentose phosphate pathway and glutathione metabolism as well as the DNA repair systems. Therefore, our work confirmed from the transcriptional and metabolic as well as physiological levels that cold plasma-mediated intracellular oxidative stress induced big perturbations in pathways as a driving force for the inactivation and pathogenicity attenuation of L. monocytogenes.

Skin aging from mechanisms to interventions: focusing on dermal aging.

Skin aging is a multifaceted process that involves intrinsic and extrinsic mechanisms that lead to various structural and physiological changes in the skin. Intrinsic aging is associated with programmed aging and cellular senescence, which are caused by endogenous oxidative stress and cellular damage. Extrinsic aging is the result of environmental factors, such as ultraviolet (UV) radiation and pollution, and leads to the production of reactive oxygen species, ultimately causing DNA damage and cellular dysfunction. In aged skin, senescent cells accumulate and contribute to the degradation of the extracellular matrix, which further contributes to the aging process. To combat the symptoms of aging, various topical agents and clinical procedures such as chemical peels, injectables, and energy-based devices have been developed. These procedures address different symptoms of aging, but to devise an effective anti-aging treatment protocol, it is essential to thoroughly understand the mechanisms of skin aging. This review provides an overview of the mechanisms of skin aging and their significance in the development of anti-aging treatments.