Biological Mechanisms Research Articles

High temporal-resolution transcriptome landscape reveals the biological process and regulatory genes of melanin deposition in breast muscle of Silkie chickens during embryonic development

BackgroundAbnormal deposition of melanin in skeletal muscle is an interesting phenomenon and the Silkie is the most typical example. Melanin deposition involves multiple steps such as neural crest cell migration, melanocyte differentiation, melanosome assembly and melanin biosynthesis, which have already occurred during the embryonic stage of Silkies. However, there is no comprehensive understanding of the dynamic changes in the biological processes and regulatory mechanism underlying melanin deposition in skeletal muscle during chicken embryonic development.ResultsIn this study, high-performance liquid chromatography (HPLC) was used to accurately measure the melanin content in breast muscle across 13 embryonic time points. There was no melanin in breast muscle on embryonic day 8 (E08) to E10, a trace amount of melanin on E11 to E16 and a large amount of melanin on E17 to E21. According to melanin content and deposition pattern, the melanin deposition process in breast muscle was further divided into five stages, including E08 to E10, E11 to E14, E15 to E16, E17 to E18, and E19 to E21. High temporal-resolution transcriptome analysis was performed in the breast muscle of Silkies across 13 embryonic time points. The protein-coding genes (PCGs) and transcriptional factors (TFs) significantly specifically expressed at these five stages were identified. Among these stage-specific genes, stage-specific DEGs between Silkies and Wenchang chickens without melanosis were further screened at each stage. During E08 to E10, three stage-specific DEGs and one stage-specific TF act on neural crest cell migration and melanocyte stem cell differentiation. During E17 to E21, nine stage-specific DEGs and one stage-specific TF act on melanosome assembly and melanin biosynthesis. During E19 to E21, one stage-specific DEG enhances melanin biosynthesis. These stage-specific DEGs and TFs all affect the final melanin content of breast muscle.ConclusionsThis study reveals the critical stage of melanin deposition in breast muscle during the embryonic development, and identified the biological processes and functional genes at each stage. This study provides novel insights into the biological process and regulatory mechanism of melanin deposition in skeletal muscle and provides a reference for breeding Silkies with high muscle melanin content.

Integrative analysis of the expression profile and prognostic values of SENP gene family in hepatocellular carcinoma

IntroductionHepatocellular carcinoma (HCC) stands as the fourth leading cause of cancer-related deaths worldwide. SUMO-specific peptidases, known as SENPs, emerge as critical players, regulating tumorigenesis and progression of numerous cancer types. Despite this, the specific impact of SENPs in HCC remains unclear. Hence, our study aimed to reveal the immune and prognostic implications of SENPs in HCC.MethodsThe gene expression of SENP in various cancers was examined using open-access databases including TCGA, GTEx, and CPTAC. In order to investigate the prognostic potential of the SENP family, Kaplan–Meier analysis was used. To clarify the underlying biological mechanisms, gene set enrichment analysis (GSEA) was carried out. cBioPortal database was used to evaluate genetic mutation profiles. For insight into the relationship between SENP genes and tumor immunity, various algorithms were used.ResultsOur findings showed that SENP1, SENP2, SENP3, SENP5, SENP6, and SENP7 expression levels were significantly higher in HCC tumor tissues compared to normal tissues. In HCC patients, elevated SENP1 and SENP5 expression has been associated with tumor development and poor outcomes. Our immune infiltration patterns results also showed significant correlations between SENP5 expression and neutrophil (cor = 0.346, p < 0.001), myeloid dendritic cell (cor = 0.491, p < 0.001), macrophage (cor = 0.465, p < 0.001), and memory B cell (cor = 0.336, p < 0.001) infiltration in HCC, whereas SENP1 expression was associated with none of these infiltrations.ConclusionsThe prognostic and immunogenetic value of SENP1 and SENP5 in HCC was demonstrated in this study. Therefore, these two genes have the potential to function as separate prognostic biomarkers and offer promise as immunotherapeutic targets in the fight against HCC.

Cambridge Neoadjuvant Cancer of the Prostate (CANCAP03): A Window Study into the Effects of Olaparib ± Degarelix in Primary Prostate Cancer.

The purpose was to investigate combined PARP and androgen inhibition in primary prostate cancer and understand the biological mechanisms underlying clinical efficacy, especially in the absence of mutations in homologous recombination (HR) repair pathways. The primary objective was to measure PARP inhibition, and the secondary objectives were to assess safety and feasibility. Participants received olaparib for 2 weeks before prostatectomy and were randomly assigned or not assigned (1:1) to degarelix. We analyzed diagnostic biopsy and radical prostatectomy samples for PARylated protein expression using IHC. Exploratory analyses included tumor gene sequencing, mutation analysis, and RNA sequencing (RNA-seq) using both bulk and single-cell RNA-seq performed on pretreatment and posttreatment tissues. PARylated protein expression was significantly reduced in both cohorts, with no drug-related delays in radical prostatectomy. The gene set enrichment analysis identified distinct treatment response signatures related to olaparib in both cohorts and showed downregulation of androgen response genes after olaparib + degarelix treatment.Transcript profiling revealed an upregulation of the p53 hallmark, which was more pronounced with the combination treatment. Canonical cell-cycle progression hallmarks, including E2F targets and the G2-M checkpoint, were suppressed across all cases, correlating with a HR-deficient transcriptional signature. Single-nuclear RNA-seq indicated a greater increase in inflammatory response pathway activity within tumor epithelia after combination treatment. Transcriptomic analysis identified common hallmark alterations reflecting the combined impact of PARP inhibitor and androgen blockade on cell-cycle progression. We observed a shared phenotypic response to combination therapy across prostate cancers without known HR repair gene alterations. This suggests alternative mechanisms rather than antiandrogen-induced HR deficiency.

Could the HALP score indicate poor prognosis in colorectal cancer patients?

Colorectal cancer (CRC) is a major health problem worldwide. According to estimates for the year 2030, cancer will be the number one cause of death for both genders. CRC is the third most common type of cancer and the second most common cause of cancer-related deaths. Various parameters are needed to provide information about the course and prognosis of the disease. The study included 103 patients diagnosed with CRC between 2017 and 2023. The patients' HALP scores were retrospectively analyzed together with clinical data. The relationship between survival times, disease stage, and treatment response was examined. The obtained data showed that low HALP scores were associated with worse overall survival. Although the HALP score cut-off value was found to be different in various studies conducted on benign or malignant diseases, a low HALP score indicates a poor prognosis. In our study, a HALP score below 23 was found to be associated with low overall survival. This study suggests that a low HALP score is associated with poor prognosis and could serve as a valuable prognostic marker in the clinical management of CRC patients. However, certain limitations must be considered. While albumin is a marker of systemic inflammation and nutritional status, its specificity is limited in acute and chronic inflammatory conditions, which may impact the prognostic value of the HALP score. Further investigation into the biological mechanisms underlying this relationship and the potential of the HALP score in predicting treatment response would enhance its clinical applicability.

Revisiting the Open Vein Hypothesis to Reduce the Postthrombotic Syndrome: Implications for Multidisciplinary Care and Research: A Scientific Statement From the American Heart Association.

The "open vein hypothesis" postulates that early thrombus clearance and restoration of venous blood flow may prevent postthrombotic syndrome after proximal deep vein thrombosis. Since its proposal several decades ago, new insights from basic and clinical studies have motivated a re-evaluation and refinement of this hypothesis. According to data from these studies, susceptibility to postthrombotic syndrome occurs as a result of differences in genetic composition, thrombophilic conditions, predilection to inflammation and fibrosis, endogenous fibrinolytic capability, timing of s ymptom presentation and treatment initiation, and efficacy of antithrombotic therapy. Although initial restoration of an open vein appears to be beneficial for selected patient groups, freedom from postthrombotic syndrome is more likely in the setting of long-term venous patency, reduced recurrent thrombotic episodes, and reduced perithrombotic (eg, vein wall and valve) inflammation. These underlying biological mechanisms need further elucidation, with a long-term goal of personalizing treatment by mapping the individuals' clinical presentation with their underlying risk factors and assessing time-dependent biological processes that occur as a clinical venous thrombosis resolves. This scientific statement (1) highlights historical fundamentals of the open vein hypothesis and then showcases new research insights into the pathophysiological factors driving postthrombotic syndrome; (2) discusses advantages and disadvantages of imaging modalities for deep vein thrombosis used in clinical practice, including the potential to depict thrombus chronicity and status of vein wall injury; (3) proposes measures to develop integrated multidisciplinary care for deep vein thrombosis focused on the reduction of postthrombotic syndrome; and (4) identifies priority areas and questions for further research.

Suppressed DNA repair capacity in flight attendants after air travel

Elevated cancer risk and compromised reproductive health have been well documented in flight attendants (FA), but the etiology remains unknown. Many studies using cell and animal models suggest that air travel related exposures might plausibly explain the adverse health outcomes observed in flight crew, but our understanding of the underlying biological mechanisms is incomplete. During air travel, FA are constantly exposed to complex mixtures of mutagens in the flight cabin that may contribute to genomic instability by inducing DNA damage and interfering with DNA repair. Defects in DNA repair capacity (DRC) have been associated with risk of cancer and other diseases. To explore our hypothesis that alterations in DNA damage and repair in FA are related to flight travel, we conducted a pilot study of FA’s DNA damage and assess global DNA repair efficiency pre and post flight. We collected venous blood samples from nine FA before and after flight. Differential blood cell counts were carried out to assess immune responses and functional assays were performed to assess the DNA damage response. The CometChip assay was employed to quantify baseline DNA damage and repair kinetics for DNA damage induced by X-rays. Fluorescence multiplex based host cell reactivation (FM-HCR) assays were utilized to assess DRC in five major DNA repair pathways. Our findings revealed a significant increase in lymphocyte counts as well as diminished repair of ionizing radiation induced DNA damage and excision of 8oxoG:C lesions in after flight samples. Our results illustrate the potential for using biological samples to identify molecular mechanisms that may implicate impaired genomic stability and altered immune responses in the etiology of excess cancer in FAs.

CTE in Athletes: Understanding the Long-Term Effects of Repetitive Head Injuries

Introduction and PurposeChronic traumatic encephalopathy (CTE) is a progressive neurodegenerative disease linked to repeated head injuries such as concussions and sub-concussive impacts [19]. Initially observed in retired boxers with behavioral and cognitive symptoms, it was called “punch-drunk syndrome” [3,9,16]. CTE is mostly found in athletes from contact sports (e.g., football, boxing, hockey, rugby) and in military personnel [1,3,9,13,19]. While most reported cases involve male athletes, anyone exposed to repetitive head injury (RHI) is at risk [2,10,13]. Due to increasing awareness of its long-term effects on brain health, CTE is now a critical topic in sports medicine, neurology, and public health. Material and MethodsA literature review was conducted using PubMed, focusing on studies published up to the end of 2023. Keywords included: “CTE in athletes,” “repetitive head impacts,” “tau protein,” “encephalopathy,” and “CTE.” Studies were selected based on their focus on long-term effects of RHI, CTE pathology, and prevention strategies. ResultsThe review highlights the connection between repeated brain trauma and CTE in athletes. Ongoing research aims to uncover its biological mechanisms and develop early diagnostic tools and targeted treatments. Long-term studies tracking athletes are vital for identifying causes and modifiable risk factors. ConclusionsCTE illustrates the complex link between repeated head trauma and brain health decline. While progress has been made, diagnosis, treatment, and prevention remain difficult. Continued research and collaboration among clinicians, researchers, sports organizations, and policymakers are essential to reduce risks and protect athlete well-being.

Modeling the PAX5P80R Mutation Reveals HIF2α Activation as a Common Feature and Therapeutic Target in B-Cell Acute Lymphoblastic Leukemia.

The transcription factor PAX5 is a major target of genetic alterations in human B-cell precursor acute lymphoblastic leukemia (B-ALL). Among the alterations, the P80R mutation affecting the DNA-binding domain represents the most frequent PAX5 point mutation in B-ALL. In contrast to other somatic PAX5 mutations, PAX5P80R defines a distinct B-ALL subtype characterized by a unique transcriptional program. Here, we aimed to develop a model to elucidate the mechanism by which PAX5P80R perturbs normal B-cell differentiation and the oncogenic relays involved in PAX5P80R-driven malignant progression. A retroviral complementation approach of Pax5-deficient murine fetal liver cells demonstrated at the functional and molecular levels that PAX5P80R failed to rescue definitive B-cell commitment but maintained the repression of T-cell development. Moreover, PAX5P80R eventually led to clonal B-ALL transformation after transplantation through the acquisition of secondary mutations in genes involved in the JAK/STAT and RAS/MAPK pathways. Finally, transcriptomic analyses combined with pharmacological investigation revealed ectopic activation of HIF2α as a common feature of B-ALL and identified acriflavine as a potent drug against B-ALL. Hence, this study provides a strategy to model the multistep process of B-ALL and sheds light on the biological mechanism by which the PAX5P80R mutation leads to leukemia.

A Vertically‐Stacked Optoelectronic Sensor for Localized Hemodynamics Monitoring

AbstractOptoelectronic sensors are widely used as they monitor important biosignals in real‐time, many times in non‐invasive ways by making use of the degree of light absorption through live tissues. In many of the applications, the optoelectronic sensors in a small form factor with attachable or insertable forms enable understanding the critically important biological states and mechanisms, including localized activities in very complex biological environments, such as in the brain. In this report, an optoelectronic sensor is presented, built by vertically integrating two different micro light emitting diodes (microLEDs) next to a photodetector with a predetermined interoptode distance in attachable or insertable forms. Both of the optical simulations and experimental results validate the designs and capabilities of the approach, by demonstrating the sensors on a human finger, around femoral vessels in a mouse model, and in mouse brains to monitor optogenetically‐induced localized hemodynamics.

Intimate partner violence and stress-related disorders: from epigenomics to resilience

Intimate Partner Violence (IPV) is a major public health problem to be addressed with innovative and interconnecting strategies for ensuring the psychophysical health of the surviving woman. According to the World Health Organization, 27% of women worldwide have experienced physical and sexual IPV in their lifetime. Most of the studies on gender-based violence focus on short-term effects, while long-term effects are often marginally included even though they represent the most serious and complex consequences. The molecular mechanisms underlying stress-related disorders in IPV victims are multiple and include dysregulation of the hypothalamic-pituitary-adrenal axis, inflammatory response, epigenetic modifications, neurotransmitter imbalances, structural changes in the brain, and oxidative stress. This review aims to explore the long-term health consequences of intimate partner violence (IPV), emphasizing the biological and psychological mechanisms underlying stress-related disorders and resilience. By integrating findings from epigenetics, microbiome research, and artificial intelligence (AI)-based data analysis, we highlight novel strategies for mitigating IPV-related trauma and improving recovery pathways. Genome-wide environment interaction studies, enhanced by AI-assisted data analysis, offer a promising public health approach for identifying factors that contribute to stress-related disorders and those that promote resilience, thus guiding more effective prevention and intervention strategies.

Dementia with Lewy bodies and Parkinson disease dementia - the same or different and is it important?

Biological definitions of neurological diseases are now becoming a reality, although still in the research phase. This development will recategorize neurological diseases, providing objective diagnostics and the promise of therapeutics that target biological mechanisms - similar to the strategy that has proven successful in tumours and other conditions. In this Perspective article, we discuss this development for dementias with dominant Lewy pathology, as the availability of biological assays for this pathology has sparked new interest in a single disease diagnosis for all individuals positive for α-synuclein. On the basis of current evidence, we argue that an α-synuclein assay alone is unlikely to be a specific criterion for a spectrum of clinical syndromes with Lewy pathology or a definitive diagnostic marker for Lewy body dementia. We advocate that one biological assay will not reflect the complex spatiotemporal features of brain pathology. Diverse sequential mechanisms underpin the highly heterogeneous phenotypes and clinicopathological processes of Lewy body dementias. Disease modification, if possible, will be most effective when it targets the early underlying mechanisms, especially those leading to aggressive phenotypes.

The Functional Impact of the Noncoding SNP rs3741442 on Orofacial Clefting.

Orofacial cleft (OFC) is a common congenital anomaly in humans with variable birth prevalence in different ethnic groups. Although genome-wide association studies (GWAS) have identified single nucleotide polymorphisms (SNPs) associated with nonsyndromic OFC (nsOFC), understanding of the underlying biological mechanisms of causative SNPs and genes in nsOFC remains limited. Here, we report that the noncoding SNP, rs3741442, has an expression quantitative trait locus (eQTL) effect on epithelial genes associated with periderm differentiation. Using a combination of epigenetic markers and in silico analysis, we prioritized the intergenic SNP rs3741442 as a potential causal factor in nsOFC. The risk allele of rs3741442 is prevalent in East Asian populations, and its presence in CRISPR-edited cells leads to reduced expression of neighboring KRT18 and EIF4B. The transcription factor SP1 differentially binds the risk versus nonrisk alleles of rs3741442. Alongside this cis-eQTL impact, rs3741442 has a trans-eQTL effect on the epithelial gene TP63 that is associated with syndromic forms of OFC and psoriasis. These findings provide insights into the mechanism by which an intergenic SNP can affect palatogenesis through the modulation of gene expression.

Circulating Cytokines Mediate the Protective Effect of Physical Activity on Cardiovascular Diseases: A Mendelian Randomization Mediation Analysis

Cardiovascular diseases (CVDs) represent a major public health concern globally, being one of the leading causes of illness and death across populations. While physical activity is widely recognized as a protective factor against these diseases, the exact biological mechanisms that explain this relationship are still not fully understood. This study utilized a two-sample Mendelian randomization (MR) method to investigate the potential role of circulating cytokines in mediating the effects of physical activity on major CVD outcomes, including coronary artery disease (CAD), heart failure (HF), and ischemic heart disease (IHD). Our primary MR analysis revealed an inverse association between physical activity and IHD risk. Moreover, a two-step MR mediation approach identified IL10RB (Interleukin-10 receptor subunit beta) as an intermediate mediator, explaining about 6.65% of the observed contribution of physical activity to IHD. These results indicate that physical activity may mitigate CVD risk through modulation of immune pathways, particularly via IL10RB signaling. Our findings underscore the significance of cytokine networks in mediating the cardiovascular benefits of exercise and suggest potential therapeutic strategies for CVD risk reduction through immune system modulation.

How Sports Make Kids Feel Better

Can sports make a difference in how you feel? We studied this question in 4,000 children in Rotterdam, the Netherlands. We found that children who played sports had fewer emotional problems, such as worrying or feeling sad. Curious to find out why, we explored various mechanisms that might explain how sports can affect mental health. Overall, we identified that self-esteem, which is how you perceive and feel about yourself, was the primary way that sports participation might help prevent or reduce emotional issues and concerns. In simpler terms, playing sports can boost your self-esteem, which in turn helps you deal with emotional problems and worries. We also explored biological mechanisms (for example, brain size) and behavioral mechanisms (for example, sleep quality), but these did not explain the link between sports and mental health. Overall, the study showed that playing sports can potentially help young people feel better about themselves and boost their moods.

Genomics of schizophrenia, bipolar disorder and major depressive disorder.

Schizophrenia, bipolar disorder and major depressive disorder - which are the most common adult disorders requiring psychiatric care - contribute substantially to premature mortality and morbidity globally. Treatments for these disorders are suboptimal, there are no diagnostic pathologies or biomarkers and their pathophysiologies are poorly understood. Novel therapeutic and diagnostic approaches are thus badly needed. Given the high heritability of psychiatric disorders, psychiatry has potentially much to gain from the application of genomics to identify molecular risk mechanisms and to improve diagnosis. Recent large-scale, genome-wide association studies and sequencing studies, together with advances in functional genomics, have begun to illuminate the genetic architectures of schizophrenia, bipolar disorder and major depressive disorder and to identify potential biological mechanisms. Genomic findings also point to the aetiological relationships between different diagnoses and to the relationships between adult psychiatric disorders and childhood neurodevelopmental conditions.

Endocrine Disruptors and Their Impact on Quality of Life: A Literature Review.

Endocrine-disrupting chemicals (EDCs) are widespread environmental contaminants that interfere with hormonal regulation, affecting metabolism, reproduction, neurodevelopment, and overall health. This review presents an overview of recent evidence on the health effects and biological mechanisms of EDCs, with a focus on their impact on hormonal balance and quality of life. An integrative literature review was conducted using 28 peer-reviewed articles published between 2020 and 2025, retrieved from databases such as PubMed, Scopus, and ScienceDirect. The selected studies explored the physiological and pathological effects of EDCs in humans. Compounds, such as bisphenol A, phthalates, and polychlorinated biphenyls (PCBs), can mimic or block hormones, disrupt endocrine signaling pathways, and bioaccumulate in tissues. Exposure, especially during critical developmental windows, is linked to metabolic disorders, infertility, neurodevelopmental delays, and hormone-sensitive cancers. Common exposure sources include food, air, household dust, water, and personal care products. Key mechanisms of action involve receptor binding interference, oxidative stress, and epigenetic alterations. EDCs pose a significant and growing threat to public health, warranting urgent regulatory measures, increased public awareness, and continued research to mitigate long-term health consequences.

The Impact of Anabolic Androgenic Steroids on Organ Failure in Bodybuilders - a Review of Actual Literature

Anabolic-Androgenic Steroids (AAS), despite their therapeutic applications in the management of selected medical conditions, are increasingly being misused for non-medical purposes—particularly among bodybuilders and individuals seeking to enhance their physique. This review article examines the impact of chronic AAS administration on the functionality of selected human organs and physiological systems. Based on current clinical and preclinical evidence, the biological mechanisms of AAS action are discussed, with particular emphasis on their affinity for androgen receptors and modulation of intracellular signaling pathways. The paper presents robust evidence of the adverse effects associated with AAS use, including cardiomyopathies, renal dysfunction, neuropsychiatric disorders (notably increased aggression and depressive symptoms), hepatotoxicity, and metabolic disturbances. Special attention is given to the potential mechanisms underlying AAS-induced toxicity, as well as the reversibility of the observed pathological alterations. The findings underscore the necessity for intensified health education and systematic monitoring of individuals using AAS, due to the elevated risk of irreversible, multisystem complications.

Anti-Obesity Medications and the Risk of Obesity-Related Cancers in Older Women: A Propensity Score Matching Analysis of 2007–2015 SEER-Medicare Data

Background/Objectives: The increasing prevalence of obesity has led to a growing interest in anti-obesity medications (AOMs). While these medications have shown promise in aiding weight loss, their potential impact on reducing obesity-related cancers (ORCs) incidence remains poorly understood, particularly among women over 65 years of age. This study examined the association between the use of AOMs and the risk of ORCs in this population. Methods: A retrospective cohort study was conducted using 2007–2015 SEER-Medicare data, including 10,830 women aged ≥65 years in a 1:2 propensity-score matching design. The primary exposure was AOM use, with additional analyses focused specifically on phentermine and liraglutide exposure. Conditional multivariable Cox proportional hazards models were conducted. Results: We found an inverse association between the use of AOMs and the risk of ORCs (aHR: 0.78; 95% CI: 0.73–0.84; p &lt; 0.001). Similar findings were observed in cancer-specific sites analysis, advanced-stage ORCs (aHR: 0.76; 95% CI: 0.65–0.89; p &lt; 0.001), breast (aHR: 0.84; 95% CI: 0.77–0.91; p &lt; 0.001), colorectal (aHR: 0.82; 95% CI: 0.71–0.96; p = 0.010), and advanced-stage colorectal cancers (aHR: 0.71; 95% CI: 0.54–0.91; p &lt; 0.001). In secondary analyses, phentermine was inversely associated with the risk of ORCs, breast, and endometrial cancers, but no associations with liraglutide were observed. Conclusions: The use of AOMs, including phentermine, was inversely associated with ORCs and some cancer-specific sites in a cohort of older women. Further prospective studies are warranted to validate these findings among women of different age groups and to identify the underlying biological mechanisms.

Tryptophan-induced transcriptomic changes in the European Seabass are highly dependent on neuroendocrine-immune conditions

In European seabass (Dicentrarchus labrax), dietary tryptophan (TRP) surplus has a notable modulatory effect on the hypothalamic–pituitary–interrenal axis under chronic stress and acute inflammation, affecting cortisol levels and neuroendocrine- and immune-related gene expression. A transcriptomic approach (RNA-seq) was applied to head-kidney samples of fish submitted to confinement stress and/or acute inflammation to uncover the biological mechanisms behind these effects. Undisturbed seabass fed dietary TRP supplementation showed an up-regulation of various innate immune functions, contrasting previous studies which indicated mainly a TRP regulatory role. Upon bacterial injection, TRP-fed fish showed a transcriptomic profile similar to their counterparts fed on control diet, indicating TRP’s inability to modulate immune mechanisms under bacterial challenge. Under confinement stress, TRP-fed fish exhibited a molecular profile similar to unstressed control fish, highlighting TRP’s role in mitigating stress. However, combining dietary TRP supplementation with confinement stress and immune stimulation by bacterial inoculation resulted in a unique molecular profile. Stressed fish fed TRP did not show the restorative effect of immune stimulation on carbohydrate metabolism and showed downregulated genes related to glycolysis and glycogenolysis. Additionally, transcription upregulation in these fish after bacterial injection included terms related to serine and steroid metabolism (carboxyl ester lipase 2), indicating tryptophan-induced changes in lipid mobilization in the head-kidney, potentially affecting cortisol synthesis and other hormones.

Sleep impact on obesity – literature review

Purpose: The aim of this literature review is to analyze existing studies on the relationship between sleep and obesity, with a focus on how sleep quality, duration, and circadian rhythm disruptions influence obesity development. It also identifies biological mechanisms, such as changes in appetite-regulating hormones, and evaluates the effectiveness of sleep-related interventions in obesity prevention and treatment. Methodology: A systematic review of scientific literature was conducted, including clinical trials, cohort studies, and meta-analyses from the last 10 years. The review examined various populations and age groups, focusing on the impact of sleep duration, quality, and circadian rhythm disturbances on obesity. Findings: Results consistently show that poor sleep quality and short sleep duration (&lt;6 hours) are associated with higher BMI, increased waist circumference, and visceral fat. Sleep disturbances impact hormones like ghrelin and leptin, promoting overeating. Circadian disruptions from shift work or social jetlag further contribute to abdominal fat. Sleep improvement interventions have shown promising effects on weight reduction, though long-term impact requires more study. Conclusions: This review highlights the important role of sleep in obesity development. Poor sleep duration and quality, along with circadian misalignment, are linked to weight gain and metabolic dysfunction. While sleep-targeted interventions show potential for improving metabolic health and aiding weight loss, further research is needed to fully understand underlying mechanisms and lasting effects. Integrating sleep management into obesity prevention and treatment could offer a valuable strategy to address the global obesity epidemic.