Depression is a psychological illness defined by persistent sadness, loss of interest or pleasure in daily activities (anhedonia), hopelessness, and a range of cognitive and physical symptoms. Untreated depression can have serious implications, such as a deteriorating mental and physical state and an increased risk of suicidal behaviour. Early diagnosis and treatment can help to prevent these adverse outcomes. Traditional diagnostic approaches primarily rely on self-reported symptoms, clinical evaluations, and questionnaire-based assessments, which, although significant, may vary and depend on perspective, necessitating the exploration of biological markers. This narrative review is based on the existing literature regarding the role of Brain-Derived Neurotrophic Factor (BDNF) in the neurobiological function and evaluates its potential as a biomarker for the diagnosis, treatment, and monitoring of disease progression. The Brain-Derived Neurotrophic Factor (BDNF) is the most common neurotrophin abundantly present in the central nervous system and peripheral tissues, and it is found in both serum and plasma. In the context of depression, BDNF has a fundamental function in the serotonergic, noradrenergic, and dopaminergic pathways, which are linked to the progression of clinical depression and are implicated in mood regulation. An extensive quantity of research on BDNF supports the neurotrophic theory of depression. According to this theory, low BDNF levels cause neuroplastic alterations such as neuronal atrophy, impaired hippocampus neurogenesis, and synaptic plasticity, contributing to its inception and progression. Several clinical findings consistently established that people with depression show lower levels of BDNF, with these levels generally increasing after successful antidepressant therapy, further supporting this hypothesis. This article provides an overview of BDNF's effect on the aetiology of depression, highlighting its significance as a possible marker.

Background The rapid evolution of health monitoring technologies has transformed the landscape of chronic and preventive healthcare, with applications spanning diabetes, cardiovascular, and general health management. Continuous glucose monitoring systems, wearable electrocardiography (ECG), and mobile health applications provide real-time, accessible data to support early diagnosis, personalized treatment, and proactive patient engagement. This review aims to systematically examine current health monitoring technologies, their diagnostic accuracy, patient outcomes, and implementation challenges. Methods A systematic literature search of 55 peer-reviewed articles was conducted, focusing on diabetes and cardiovascular monitoring devices, general health trackers, and methodological approaches in health monitoring. Results Findings indicate that diabetes monitoring technologies, such as continuous glucose monitors, significantly improve glycemic control and reduce emergency hospitalizations. Cardiovascular health monitoring technologies, including wearable ECG and blood pressure devices, demonstrate potential in early detection and continuous risk assessment. General health monitoring tools, particularly fitness and wellness applications, show effectiveness in promoting preventive behaviors, though long-term efficacy remains uncertain. Common challenges identified include data security, integration into healthcare systems, and reliability across diverse populations. Conclusion This review underscores the strengths and limitations of these technologies and highlights the need for robust data management strategies and evidence-based integration into clinical practices. Future research should focus on enhancing interoperability, addressing privacy concerns, and evaluating outcomes across diverse populations to fully harness the potential of health monitoring technologies in clinical and community health settings.

Lipoprotein Lipase (LPL) is an essential lipid metabolism enzyme affecting both the brain and peripheral tissues. Its impact on neuronal lipid homeostasis, synaptic function, and plasticity is increasingly recognized. This review explores the various functions of LPL in the brain and how it may affect neurological health, especially in Alzheimer's disease. We explore how LPL regulates lipid uptake and utilization in the brain, its influence on synaptic function, neurogenesis, and myelination, and its role in the pathophysiology of AD. Genetic and environmental factors modulating LPL activity are also discussed. The review provides insights into LPL's role in neurodegenerative diseases, acknowledges current limitations and challenges in research, and highlights the therapeutic potential of targeting LPL for AD treatment. Ultimately, this review underscores the importance of LPL in maintaining brain health and its promising potential as a therapeutic target for AD.

Aim Despite advances in diagnosis and treatment, cardiometabolic diseases remain a major worldwide health problem. A new direction in identifying biomarkers that increase diagnostics predictive potential is the study of the WNT and JAK/STAT signaling pathways. Experimental and clinical studies have provided mixed evidence that determined the purpose of the study. This study aimed to examine the characteristics of the production of certain JAK/STAT and WNT signaling proteins in cardiometabolic pathology patients. Materials and Methods The research involved patients with myocardial infarction and cardiometabolic syndrome, as well as healthy individuals. Measurement of proteins STAT-1, STAT-3, STAT-6, β-catenin, sclerostin, WIF-1, GSK-3 α, and β, DVL-1 serum concentrations was carried out by ELISA. Results We established a wide range of JAK/STAT and WNT signaling protein values in the patient’s blood serum. In cardiometabolic syndrome, there was an increase in the concentrations of β-catenin, DVL-1, GSK-3α, and GSK-3β and a decrease in STAT-1, 3, compared with healthy individuals. During myocardial infarction, an increase in β-catenin, WIF-1, and DVL-1 and a decrease in sclerostin, GSK-3α, STAT-1, STAT-3, and STAT-6 were recorded compared with healthy individuals. The most significant intergroup differences were found for β-catenin, WIF -1, DVL-1, GSK-3α and STAT-6. Statistically significant correlations between the levels of a number of JAK/STAT and WNT signaling proteins and lipid profile parameters were revealed. Conclusion The data received about changes in the production of proteins of the WNT and JAK/STAT signaling pathways expand the molecular mechanisms of cardiometabolic diseases' immunopathogenesis understanding.

Background and Aim Although α-fetoprotein (AFP) is the main marker used for the diagnosis of hepatocellular carcinoma(HCC), its sensitivity and specificity as a screening tool have been questionable. Red blood cell distribution width (RDW) has been involved as a prognostic tool for many diseases and cancers including liver diseases. Still, its role in the diagnosis of HCC needs to be identified. This study aimed to evaluate the clinical importance of RDW as a novel marker in the diagnosis of HCC in Egyptian cirrhotic patients. Patients and Methods This cross-sectional study was carried out on 162 cirrhotic patients who attended Tropical medicine department clinics and inpatient wards at the Faculty of Medicine, Tanta University. Then they were divided into 2 groups of 81 patients each depending on their diagnosis with or without HCC (group I and group II respectively). Complete blood picture (CBC) that included red cell distribution width- coefficient of variation (RDW-CV) and AFP were obtained from all patients. Results There was a statistically significant elevation in RDW-CV in the HCC group as its mean± SD was 15.2.± 1.86 in HCC group versus 13.8 ± 1.99 in non HCC group (P<0.001). In addition, AFP was significantly elevated in group I than in group II (P<0.001). RDW-CV at a cut–off >14% had a 66.76%sensitivity and 61.73%specificity while AFP at a cut-off value>20 ng/ml had a 60.49%sensitivity and 79.01%specificity in the diagnosis of HCC. The combination of RDW-CV and AFP increased the sensitivity and specificity for the diagnosis of HCC(72.84% and 87.65% respectively) than each marker alone. Conclusions RDW may be considered a novel and cheap biomarker for the diagnosis of HCC either alone or in combination with AFP as it is readily available in CBC and does not need sophisticated techniques.

Approximately 20% of invasive Breast Cancers (BCs) are characterized by Human Epidermal growth factor Receptor 2 (HER2) protein overexpression or HER2 gene amplification. HER2 represents a standard diagnostic test and a predictive biomarker for the use of HER2-directed treatments in patients with BC. At present, the HER2 Immunohistochemistry (IHC) assay is applied for screening purposes, and the In Situ Hybridization (ISH) test serves as a confirmation, when HER2 IHC results are equivocal. However, an accurate assessment and interpretation of the HER2 status can be complicated in many women with BC. These difficulties can be attributed to various factors such as HER2 Intratumoral Heterogeneity (ITH) and changes of HER2 in the process of BC metastatic progression or post neoadjuvant Chemotherapy (CHT). In particular, the status of biomarkers (e.g., HER2 and co-expressed Hormone Receptor (HR)) can be altered in patients with metastatic BC and such receptor changes influence the therapeutic responses and clinical outcomes. The goal of this article is to present challenges in the assessment of HER2 expression and to underscore a need for the biomarker status reevaluation in patients with metastatic BC. This mini-review also provides some insights into the interpretation of equivocal HER2 status in women with metastatic BC and discusses the impact of HER2 and HR biomarker conversions on therapeutic decision-making and the patient prognosis in metastatic BC. It is crucial to correctly interpret the HER2 biomarker status and to assess conversions of HER2 and HR in the BC metastatic lesions since timely detection of such alterations is critical to management modifications of individual patients with metastatic BC.

Background: We aimed to assess the level of DNA damage and susceptibility to exogenous mutagens in peripheral blood cells of Chronic Obstructive Pulmonary Disease (COPD) patients and healthy individuals by comet assay. Oxidative stress was also evaluated by means of thiobarbituric acid reactive species (TBARS) in blood plasma. Methods: Case-control study enrolling 51 COPD patients and 51 controls. Peripheral blood was used to perform the alkaline (pH>13) and neutral (pH=8.5) comet assay. For the assessment of susceptibility to exogenous DNA damage, the cells were treated with methylmethane sulfonate (MMS) for 1-hour or 3-hour at 37° C. The percentage of residual DNA damage after 3-h MMS treatment was calculated using the value of 1-h MMS treatment for each subject as 100%. Lipid peroxidation was evaluated by measuring TBARS in blood plasma. Results: DNA damage in patients was significantly higher than in controls as measured by the neutral and alkaline comet assay. Residual DNA damage detected after MMS treatment increased in patients, in contrast to controls, indicating higher susceptibility to alkylation damage and/or repair inhibition. High susceptibility to exogenous DNA damage in COPD patients correlates with high amount of TBARS and low forced vital capacity and expiratory volume. Conclusion: The positive correlation between increased susceptibility to exogenous DNA damage and TBARS levels in COPD patients suggests the possible involvement of oxidative stress in damage induction and/or repair inhibition.

We evaluated the association of plasma uric acid alone and in combination with b-type natriuretic peptide (BNP) for emergency department (ED) diagnosis and 30-day prognosis in patients evaluated for acute heart failure (AHF). We prospectively enrolled 322 adult ED patients with suspected AHF. Wilcoxon rank sum test, multivariable logistic regression and likelihood ratio (LR) tests were used for statistical analyses. Uric acid's diagnostic utility was poor and failed to show significant associations with 30-day clinical outcomes. Uric acid also did not add significantly to BNP results. Among ED patients with suspected AHF, uric acid has poor diagnostic and prognostic utility.

The detection of circulating breast cancer cells in blood could be of special interest as an indicator of diagnosis and prognosis, and for the selection of treatment. In a previous report, our research group determined gene expression profiles in samples of breast cancer tissue, identifying over-expression of the BIK/NBK mRNA gene in 90% of the analyzed samples. In this paper, we analyze the BIK/NBK gene expression as a possible biomarker of circulating breast cancer cells in blood. We demonstrate that the BIK/NBK gene expression is not a significant biomarker in the detection of circulating breast cancer cells in the blood of women with breast cancer. Several studies have evaluated the regulation of apoptosis by estrogens in breast cancer cells, demonstrating the importance of BIK/NBK protein, in estrogen-regulated breast cancer cell apoptosis, which suggests that the regulation of its expression may be an important therapeutic target or strategy in the management of cancer, and, although we did not find statistically significant differences among the patient groups to demonstrate that BIK/NBK gene expression is a biomarker of circulating breast cancer cells in blood, we consider it necessary to continue the study of this gene in breast cancer tissue and its role in the development and progression of breast cancer, its prognostic value, and its potential use as therapeutic target.