Search Results (833)

Post-traumatic stress disorder (PTSD) is a chronic mental health condition resulting from exposure to traumatic events. It is associated with long-term neurobiological changes and disturbances in emotional regulation. Understanding the sociodemographic profiles, biomarkers, and emotional control in patients with PTSD helps to better comprehend the impact of the disorder on the body and its clinical course. An analysis of biomarkers such as Interleukin-18 (IL-18), Inositol-Requiring Enzyme 1 (IRE1), Phosphorylated Extracellular Signal-Regulated Kinase (pERK), and Activating Transcription Factor–6 (ATF-6) in PTSD patients with varying durations of illness (≤5 years and >5 years) and a control group without PTSD revealed significant differences. Patients with recently diagnosed PTSD (≤5 years) showed markedly elevated levels of inflammatory and cellular stress markers, indicating an intense neuroinflammatory response during the acute phase of the disorder. In the chronic PTSD group (>5 years), the levels of these biomarkers were lower than in the recently diagnosed group, but still significantly higher than in the control group. An opposite trend was observed regarding the suppression of negative emotions, as measured by the Courtauld Emotional Control Scale (CECS): individuals with chronic PTSD exhibited a significantly greater suppression of anger, depression, and anxiety than those with recent PTSD or healthy controls. Correlations between biomarkers were strongest in individuals with chronic PTSD, suggesting a persistent neuroinflammatory dysfunction. However, the relationships between biomarkers and emotional suppression varied depending on the stage of PTSD. These findings highlight the critical role of PTSD duration in shaping the neurobiological and emotional mechanisms of the disorder, which may have important implications for therapeutic strategies and patient monitoring. Full article

Hydrogen-rich water (HRW) has shown neuroprotective effects in acute brain injury, but its role in chronic radiation-induced brain injury (RIBI) remains unclear. This study investigated the long-term efficacy of HRW in mitigating cognitive impairment and neuronal damage caused by chronic RIBI. Fifty male Sprague Dawley rats were randomly divided into five groups: control, irradiation (IR), IR with memantine, IR with HRW, and IR with combined treatment. All but the control group received 20 Gy whole-brain X-ray irradiation, followed by daily interventions for 60 days. Behavioral assessments, histopathological analyses, oxidative stress measurements, ¹⁸F-FDG PET/CT imaging, transcriptomic sequencing, RT-qPCR, Western blot, and serum ELISA were performed. HRW significantly improved anxiety-like behavior, memory, and learning performance compared to the IR group. Histological results revealed that HRW reduced neuronal swelling, degeneration, and loss and enhanced dendritic spine density and neurogenesis. PET/CT imaging showed increased hippocampal glucose uptake in the IR group, which was alleviated by HRW treatment. Transcriptomic and molecular analyses indicated that HRW modulated key genes and proteins, including CD44, CD74, SPP1, and Wnt1, potentially through the MIF, Wnt, and SPP1 signaling pathways. Serum CD44 levels were also lower in treated rats, suggesting its potential as a biomarker for chronic RIBI. These findings demonstrate that HRW can alleviate chronic RIBI by preserving neuronal structure, reducing inflammation, and enhancing neuroplasticity, supporting its potential as a therapeutic strategy for radiation-induced cognitive impairment. Full article

This story began half a century ago with the discovery of an unusually high presence of tryptophan (Trp, W) in transthyretin (TTR), one of the three carrier proteins of thyroid hormones. With the Trp-rich retinol-binding protein (RBP), TTR forms a plasma complex implicated in the delivery of retinoid compounds to body tissues. W has the lowest concentration among all AAs involved in the sequencing of human body proteins. The present review proposes molecular maps focusing on the ratio of W/AA residues found in the sequence of proteins involved in immune events, allowing us to ascribe the guidance of inflammatory processes as fully under the influence of W. Under the control of cytokine stimulation, plasma biomarkers of protein nutritional status work in concert with major acute-phase reactants (APRs) and with carrier proteins to release, in a free and active form, their W and hormonal ligands, interacting to generate hot spots affecting the course of acute stress disorders. The prognostic inflammatory and nutritional index (PINI) scoring formula contributes to identifying the respective roles played by each of the components prevailing during the progression of the disease. Glucagon demonstrates ambivalent properties, remaining passive under steady-state conditions while displaying stronger effects after cytokine activation. In developing countries, inappropriate weaning periods lead to toddlers eating W-deficient cereals as a staple, causing a dramatic reduction in the levels of W-rich biomarkers in plasma, constituting a novel nutritional deficiency at the global scale. Appropriate counseling should be set up using W implementations to cover the weaning period and extended until school age. In adult and elderly subjects, the helpful immune protections provided by W may be hindered by the surge in harmful catabolites with the occurrence of chronic complications, which can have a significant public health impact but lack the uncontrolled surges in PINI observed in young infants and teenagers. Biomarkers of neurodegenerative and neoplastic disorders measured in elderly patients indicate the slow-moving elevation of APRs due to rampant degradation processes. Full article

Background: Stress hyperglycemia (SH), a transient elevation in blood glucose levels during acute stress such as stroke, has been increasingly recognized as a critical determinant of clinical outcomes. This review aims to evaluate the association between SH and clinical outcomes across different stroke subtypes and its role as a prognostic indicator. Methods: The current literature review was conducted through a comprehensive literature search of PubMed, Scopus, and Web of Science electronic databases. Initial title and abstract screening was conducted by two independent reviewers depending on the relevance to the topic of interest. Final study inclusion was based on the clinical relevance and agreement between reviewers. Results: Current evidence links SH with higher stroke severity (Higher national institutes of health stroke scale (NIHSS)), larger infarct volumes, increased risk of hemorrhagic transformation, and worse functional recovery (Lower modified rankin scale (mRS)), especially in ischemic stroke. In hemorrhagic stroke, SH is associated with hematoma expansion, perihematomal edema, and worsening neurological function. Although SH has been shown to be a reliable stroke outcome predictor, there is no scientific consensus regarding the most reliable measurement method. The use of absolute blood glucose values may not accurately reflect SH, particularly in diabetic patients, where chronic baseline hyperglycemia complicates interpretation. This underscores the necessity for individualized assessment rather than a uniform interpretation. Clinically, the early detection of SH may provide enhanced monitoring and supportive care; however, rigorous glucose management remains contentious due to the risk of hypoglycemia. Conclusions: This review synthesizes evidence from recent studies and supports SH as a prognostic marker of both short- and long-term adverse outcomes in stroke patients. Further research is warranted to evaluate the efficacy of targeted glycemic treatments on such outcomes. Full article

The zebrafish (Danio rerio) has emerged as a powerful model organism for investigating the mechanisms of post-traumatic stress disorder (PTSD), offering unique advantages in translational relevance, genetic trackability, and cost-effectiveness. As a logical continuation of our recent systematic review, this manuscript critically examines the spectrum of experimental strategies used to model PTSD in zebrafish, with a focus on the comparative efficacy and validity of acute, chronic, and complex stress paradigms. Among these, 14–15-day chronic unpredictable stress (CUS/UCS) protocols are identified as the gold standard, reliably inducing core PTSD-like phenotypes—such as anxiety-like behavior, cortisol dysregulation, and neuroinflammatory gene activation. We discuss the influence of environmental, developmental, and genetic factors on stress responses, and highlight the importance of standardized behavioral and molecular endpoints for model validation. While alternative paradigms—including acute, social, pharmacological, and predator-based models—offer mechanistic insights, their translational relevance remains limited without further refinement. We conclude by outlining future directions for zebrafish-based PTSD research, emphasizing the need for protocol harmonization, integration of multi-modal readouts, and exploration of individual variability to enhance the translational value of this model system. Full article

Background and Clinical Significance: Spontaneous renal hematoma, also known as Wunderlich syndrome (WS), is a rare disease characterized by the acute onset of spontaneous renal hemorrhage into the subcapsular, perirenal, and/or pararenal spaces without a history of prior trauma. WS can be a life-threatening condition due to hemorrhagic shock; consequently, prompt diagnosis and a therapeutic approach are essential for favorable outcomes. Treatment ranges from conservative management to surgical intervention. The most common etiologies are neoplasms and vascular diseases, but WS can also be observed in patients undergoing hemodialysis. In patients with end-stage renal disease (ESRD), especially those on hemodialysis, acquired cystic kidney disease and renal cell carcinoma are among the primary causes of WS. Although less common, WS can develop in dialysis patients even in the absence of traditional (primary) risk factors. In general, patients with chronic kidney disease (CKD) have a paradoxical hemostatic profile, likely explaining their higher tendency to bleed, so WS can occur without existing predisposing factors. The multifactorial pathogenesis in these patients includes functional platelet abnormalities, intimal arterial fibrosis, chronic inflammation, and oxidative stress associated with ESRD. The use of hemodialysis-related antithrombotic medications could serve as another contributing factor increasing the risk of bleeding. Case Presentation: We present a case report of a 62-year-old male on chronic dialysis who developed sudden right-sided lumbar pain and hematuria during dialysis without evidence of prior trauma. Imaging revealed a large subcapsular hematoma of the right kidney. Further investigations did not reveal additional risk factors in this instance; however, his routinely used hemodialysis-related antithrombotic medications were potentially a contributing factor. Despite conservative treatment, his condition worsened, and the hematoma enlarged, requiring emergency nephrectomy. Postoperatively, his condition gradually improved. Conclusions: This case highlights the importance of considering WS in hemodialysis patients, even without the presence of traditional risk factors, as well as including WS in the differential diagnosis of acute abdominal pain. Full article

Background/Objectives: There is evidence concerning herbal medicines and plant-based compounds, including Lamiaceae species, as putative senolytic agents; however, there are only a few reports on Ocimum americanum properties using rat models. The aim of this study was to investigate the neuroprotective effects and potential modes of action of Ocimum americanum L. using ex vivo and in vivo assays to assess the effects of OAEE on hippocampal tissue from young adult and late middle-aged Wistar rats, with a focus on oxidative stress, cholinesterase activity, and neuroinflammatory markers. Methods: Ocimum americanum ethanol extract (OAEE) was incubated with hippocampal slices of young adult and late middle-aged male Wistar rats exposed to H₂O₂; an acute treatment with OAEE was evaluated in aversive memory performance and neurochemical parameters, such as hippocampal cellular oxidative state, and anticholinesterase activity, and a diet supplementation of OAEE were evaluated on several hippocampal biochemical parameters, such as oxidative state, anticholinesterase activity, and neuroinflammatory parameters in young adult and late middle-aged male rats. Results: OAEE reversed the H₂O₂-induced impaired cellular viability in hippocampal slices from young adult rats, as well as protected hippocampal slices against H₂O₂-induced damage in both young adult and late middle-aged Wistar rats, indicating its neuroprotective action. Chronic dietary OAEE supplementation reduced aging-induced increases in reactive species and lipid peroxidation levels in the hippocampus. Indeed, this supplementation reduced the TNF-α content in hippocampus from both ages, and IL-1β levels in young adult rats. Conclusions: The antioxidant actions of OAEE here observed, preventing the lipoperoxidation, as well as its anti-neuroinflammatory effect, might be related to neuroprotective effect. Our findings add evidence to support the idea of the potential use of Ocimum americanum as a nutraceutical or functional food in the aging process. Full article

The study of metabolic abnormalities regarding mitochondrial respiration and energy production has significantly advanced our understanding of cell biology and molecular mechanisms underlying cardiovascular diseases (CVDs). Mitochondria provide 90% of the energy required for maintaining normal cardiac function and are central to heart bioenergetics. During the initial phase of heart failure, mitochondrial number and function progressively decline, causing a decrease in oxidative metabolism and increased glucose uptake and glycolysis, leading to ATP depletion and bioenergetic starvation, finally contributing to overt heart failure. Compromised mitochondrial bioenergetics is associated with vascular damage in hypertension, vascular remodeling in pulmonary hypertension and acute cardiovascular events. Thus, mitochondrial dysfunction, leading to impaired ATP production, excessive ROS generation, the opening of mitochondrial permeability transition pores and the activation of apoptotic and necrotic pathways, is revealed as a typical feature of common CVDs. Molecules able to positively modulate cellular metabolism by improving mitochondrial bioenergetics and energy metabolism and inhibiting oxidative stress production are expected to exert beneficial protective effects in the heart and vasculature. This review discusses recent advances in cardiovascular research through the study of cellular bioenergetics in both chronic and acute CVDs. Emerging therapeutic strategies, specifically targeting metabolic modulators, mitochondrial function and quality control, are discussed. Full article

Background/Objectives: Inflammatory bowel disease (IBD) is a chronic gastrointestinal disorder marked by relapsing episodes of gastrointestinal inflammation, potentially causing severe symptoms. These unpredictable acute episodes, paired with chronic disabilities, such as fatigue and malabsorption, and extensive pharmacological and surgical treatments, can severely impact patients’ quality of life. This study aimed to assess which aspects of the patients’ lives IBD impacts, and how IBD patients perceive their disease. Methods: All IBD patients who had an appointment in our tertiary centre from 10 October 2022 to 21 February 2023, were invited to complete anonymous questionnaires. The questionnaires used were IBDQ-32, WPAI, and IBD Disk, all designed specifically to assess the IBD patients’ quality of life. Results: The questionnaires were completed by a total of 159 participants, 51% of whom were males, 47.9% who had UC, and 49.4% who had been or were currently treated with biologics. There was no statistically significant difference in the answers from patients with CD compared to UC, as well as those treated with conventional therapies compared to those with advanced options. Most of them considered their health to be good, but only a few (12.8%) claimed, with absolute certainty, that their health was at the level of healthy individuals, and only 13 (8.3%) claimed their health was excellent. A total of 95 (60.1%) participants expressed at least minor limitations when performing strenuous activities, but lighter forms of activities were not affected as much by the disease. A significant portion (48.7%) of the participants believed they were exposed to more stress than others, and their current pharmacological therapy was the cause of fear in 26.5%. A total of 119 (75.3%) participants believed that the disease affected their lives at least mildly during remission. Conclusions: Our study showed that IBD patients have diminished quality of life, not only in the periods of active disease but also during clinical remission. The decline in quality of life was not solely attributed to physical symptoms, as previously thought. Other factors, such as mental health issues, were found to impact quality of life as well. We firmly believe that restoring quality of life should be emphasised in guidelines as one of the most important therapeutic goals. Full article

Background: Sarcopenia is a syndrome associated with aging, characterized by a progressive decline in skeletal muscle mass and function. Its onset compromises the health and longevity of older adults by increasing susceptibility to falls, fractures, and various comorbid conditions, thereby diminishing quality of life and capacity for independent living. Accumulating evidence indicates that moderate-intensity aerobic exercise is an effective strategy for promoting overall health in older adults and exerts a beneficial effect that mitigates age-related sarcopenia. However, the underlying molecular mechanisms through which exercise confers these protective effects remain incompletely understood. Methods: In this study, we established a naturally aging mouse model to investigate the effects of a 16-week treadmill-based aerobic exercise regimen on skeletal muscle physiology. Results: Results showed that aerobic exercise mitigated age-related declines in muscle mass and function, enhanced markers associated with protein synthesis, reduced oxidative stress, and modulated the expression of genes and proteins implicated in mitochondrial quality control. Notably, a single session of aerobic exercise acutely elevated circulating levels of β-hydroxybutyrate (β-HB) and upregulated the expression of BDH1, HCAR2, and PPARG in the skeletal muscle, suggesting a possible role of β-HB–related signaling in exercise-induced muscle adaptations. However, although these findings support the beneficial effects of aerobic exercise on skeletal muscle aging, further investigation is warranted to elucidate the causal relationships and to characterize the chronic signaling mechanisms involved. Conclusions: This study offers preliminary insights into how aerobic exercise may modulate mitochondrial quality control and β-HB–associated signaling pathways during aging. Full article

Acute heart failure (AHF) is a clinical syndrome characterized by the sudden onset or rapid worsening of heart failure signs and symptoms, frequently triggered by myocardial ischemia, pressure overload, or cardiotoxic injury. A central component of its pathophysiology is the activation of intracellular signal transduction cascades that translate extracellular stress into cellular responses. Among these, the mitogen-activated protein kinase (MAPK) pathways have received considerable attention due to their roles in mediating inflammation, apoptosis, hypertrophy, and adverse cardiac remodeling. The canonical MAPK cascades—including extracellular signal-regulated kinases (ERK1/2), p38 MAPK, and c-Jun N-terminal kinases (JNK)—are activated by upstream stimuli such as angiotensin II (Ang II), aldosterone, endothelin-1 (ET-1), and sustained catecholamine release. Additionally, emerging evidence highlights the role of receptor-mediated signaling, cellular stress, and myeloid cell-driven coagulation events in linking MAPK activation to fibrotic remodeling following myocardial infarction. The phosphatidylinositol 3-kinase (PI3K)/Akt signaling cascade plays a central role in regulating cardiomyocyte survival, hypertrophy, energy metabolism, and inflammation. Activation of the PI3K/Akt pathway has been shown to confer cardioprotective effects by enhancing anti-apoptotic and pro-survival signaling; however, aberrant or sustained activation may contribute to maladaptive remodeling and progressive cardiac dysfunction. In the context of AHF, understanding the dual role of this pathway is crucial, as it functions both as a marker of compensatory adaptation and as a potential therapeutic target. Recent reviews and preclinical studies have linked PI3K/Akt activation with reduced myocardial apoptosis and attenuation of pro-inflammatory cascades that exacerbate heart failure. Among the multiple signaling pathways involved, glycogen synthase kinase-3β (GSK-3β) has emerged as a key regulator of apoptosis, inflammation, metabolic homeostasis, and cardiac remodeling. Recent studies underscore its dual function as both a negative regulator of pathological hypertrophy and a modulator of cell survival, making it a compelling therapeutic candidate in acute cardiac settings. While earlier investigations focused primarily on chronic heart failure and long-term remodeling, growing evidence now supports a critical role for GSK-3β dysregulation in acute myocardial stress and injury. This comprehensive review discusses recent advances in our understanding of the MAPK signaling pathway, the PI3K/Akt cascade, and GSK-3β activity in AHF, with a particular emphasis on mechanistic insights, preclinical models, and emerging therapeutic targets. Full article

Background/Objectives: Hypertension is a major contributor to cardiovascular diseases and is often intensified by psychological stress, which can also affect bone metabolism. Although both conditions independently compromise bone health, their combined impact—particularly under acute and chronic stress—remains unclear. This pilot study aimed to assess the effects of such stressors on bone structure in spontaneously hypertensive rats (SHRs). Methods: Forty male rats, both normotensive and SHRs, were randomly assigned to control, acute stress, or chronic stress groups. Acute stress involves a single 2 h physical restraint. Chronic stress was induced over 10 days using alternating stressors: agitation, forced swimming, physical restraint, cold exposure, and water deprivation. Tibial bones were analyzed by microcomputed tomography (micro-CT), and histology was performed using Hematoxylin and Eosin and Masson’s Trichrome stains. Results: Micro-CT showed increased trabecular bone volume in normotensive rats under chronic stress, whereas SHRs displayed impaired remodeling under both stress types. Histological analysis revealed preserved connective tissue overall but evident changes in growth plate structure among stressed rats. SHRs exhibited exacerbated trabecular formation and cartilage abnormalities, including necrotic zones. Conclusions: Both acute and chronic stress, especially in the context of hypertension, negatively affect bone remodeling and maturation. Despite the absence of overt inflammation, structural bone changes were evident, indicating potential long-term risks. These findings highlight the importance of further studies on stress–hypertension interactions in bone health as well as the exploration of therapeutic approaches to mitigate skeletal damage under such conditions. Full article

Background: The phenomenon of fear of movement is called kinesiophobia. Kinesiophobia is a significant factor that complicates the treatment process. Fear of movement and physical activity is a risk factor for the transformation of acute pain into chronic pain. Therefore, the assessment of the level of kinesiophobia is a prognostic factor for disability and mental stress, thus having a significant impact on the quality of life of people with lower back pain. One of the psychometric diagnostic tools for assessing the level of kinesiophobia is the Kinesiophobia Causes Scale (KCS). The aim of the study was to assess the reliability of the KCS test used in people suffering from chronic nonspecific lower back pain (nsLBP). Methods: The study included a group of 112 people suffering from chronic nsLBP. The subjects completed the same Polish version of the KCS questionnaire 4 weeks apart. Results: Good internal consistency was recorded for both domains—the biological and psychological one—as well as the general KCS index (Cronbach’s alpha index α from 0.8 to 0.9). Reliability was excellent for both domains (95% CI of ICC_3.1 biological domain: 0.86–0.93 and for psychological domain: 0.92–0.96) and for the total score of the Kinesiophobia Causes Scale (95% CI of ICC_3.1: 0.91–0.93). Conclusions: These results indicate very good measurement reliability of the Polish version of the KCS questionnaire among people suffering from chronic nsLBP. Full article

(1) Background: Physiological responses, such as heart rate and heart rate variability, have been increasingly utilized to monitor, detect, and predict mental stress. This review summarizes and synthesizes previous studies which analyzed the impact of mental stress on heart activity as well as mathematical, statistical, and visualization methods employed in such analyses. (2) Methods: A total of 119 articles were reviewed following the Systematic Reviews and Meta-Analyses extension for Scoping Reviews (PRISMA-ScR) guidelines. Non-English documents, studies not related to mental stress, and publications on machine learning techniques were excluded. Only peer-reviewed journals and conference proceedings were considered. (3) Results: The studies revealed that heart activities and behaviors changed during stressful events. The majority of the studies utilized descriptive statistical tests, including t-tests, analysis of variance (ANOVA), and correlation analysis, to assess the statistical significance between stress and non-stress events. However, most of them were performed in controlled laboratory settings. (4) Conclusions: Heart activity shows promise as an indicator for detecting stress events. This review highlights the application of time series techniques, such as autoregressive integrated moving average (ARIMA), detrended fluctuation analysis, and autocorrelation plots, to study heart rate rhythm or patterns associated with mental stress. These models analyze physiological data over time and may help in understanding acute and chronic cardiovascular responses to stress. Full article

Background/Objectives: The establishment of early gut microbiota is crucial for host health. Lactoferrin (LF), which is present in breast milk, positively impacts gut microbiota composition. However, the effect of lactation LF on the establishment and composition of early gut microbiota in different disease models in adulthood remains unclear. Methods: Lactation-LF-deficient mice were established using systemically LF–knocked-out maternal mice. This study assessed the maturity of the gut microbiota in LF feeding-deficient mice in relation to age and changes in the gut microbiota in adult high-fat diet (HFD)-induced obesity, dextran sodium sulfate (DSS)-induced acute colitis, and chronic unpredictable mild stress (CUMS)-induced depression models. Results: Compared to LF intake during lactation, LF deficiency during lactation increased the abundance of potentially pathogenic bacteria in the gut, resulting in abnormal microbial maturation. LF intake during lactation aggravated gut microbiota dysbiosis induced via HFD, DSS, and CUMS in adulthood and may change the function of Enterorhabdus, GCA-900066575, Peptococcus, Tuzzerella, Akkermansia, and Desulfovibrio. Comparing the different models revealed that bacteria that were jointly upregulated via HFD and DSS exhibited increased levels of inflammation and oxidation. LF deficiency during lactation may weaken the association between an HFD and inflammatory bowel disease (IBD). The changing trends in many gut microbes caused by DSS and HFD were opposite to those that changed with age. Conclusions: Lactoferrin deficiency increases the abundance of potential pathogens and disrupts microbial maturation. This lack of LF exacerbates dysbiosis in models of obesity, colitis, and depression. Regulating the gut microbiota according to the rules of microbial succession during the maturation process of gut microbiota may improve gut microbiota dysbiosis in patients with obesity and IBD. Full article