Although obesity is a multifactorial disorder caused by various behavioural, genetic and environmental influences, early life factors affecting certain critical periods during childhood (prenatal period, adiposity rebound period at 3-5 years and around 5-7 years, as well as puberty) are important in promoting obesity in adulthood. The objective was to determine the association between the birth weight, birth length, breastfeeding and time of introduction of complementary food with obesity among 302 healthy Caucasian children 6-7 years old. Binary logistic regression analysis was used to assess the impact of a number of perinatal and socioeconomic confounding factors on the likelihood for overweight and obesity among children. The level of significance was set at p <0.05. Our findings indicate that duration of breastfeeding for at least 3 months, with introduction of complementary food after the age of 6 months have an important role in preventing obesity. This findings are crucial for planning preventive strategies to prevent further increases in the prevalence of overweight and obesity.

Human endogenous retroviruses (HERVs) are genomic fragments integrated into human DNA from germline infections by exogenous retroviruses that threatened primates early in their evolution and are inherited vertically in the germline. So far, HERVs have been studied in the context of extensive immunopathogenic, neuropathogenic and even oncogenic effects within their host. In particular, in our paper, we elaborate on the aspects related to the possible correlation of transposable HERV elements’ activation and SARS-CoV-2 spike protein’s presence in cells of COVID-19 patients or upon COVID-19 vaccination with implications for natural and adaptive immunity. In particular, the release of cytokines TNF-α, IL-1β and IL-6 occurs in such cases and plays a notable role in sustaining chronic inflammation. Moreover, well-known interindividual variations of HERVs might partially account for the interpersonal variability of COVID-19 symptoms or unwanted events post-vaccination. Accordingly, further studies are required to clarify the SARS-CoV-2 spike protein’s role in triggering HERVs.

Introduction and importance: Extrapelvic endometriosis, confined exclusively to the body of the rectus abdominis muscle, is a rare form of abdominal wall endometriosis. While its etiopathology remains unclear, it is often diagnosed in healthy women who present with atypical symptoms and localization unrelated to any incision site, or in the absence of a history of endometriosis or previous surgery. Presentation of the case: Here, we describe a unique case of intramuscular endometriosis of the rectus abdominis muscle in a healthy 39-year-old Caucasian woman. The condition was located away from any prior incisional scars and presented without typical symptoms or concurrent pelvic disease, making diagnostic imaging unclear. After partial surgical resection of the endometriotic foci, the diagnosis was confirmed histologically. Progestogen-based supportive medication was initiated to prevent the need for additional surgeries and to reduce the risk of recurrence. After 6 years of follow-up and continued progestogen treatment, the patient remains symptom-free and has shown no recurrence of the disease. Clinical discussion: Endometriosis of the rectus abdominis muscle exhibits specific characteristics in terms of localization, etiopathology, symptomatology, and diagnostic imaging, suggesting that it should be considered a distinct clinical entity. Conclusions: Although rare, primary endometriosis of the rectus abdominis muscle should be included in the differential diagnosis for women of childbearing age. Early diagnosis is essential to avoid delayed recognition, tissue damage, and to minimize the risk of recurrence or malignant transformation. Given the increasing frequency of gynecologic and laparoscopic surgeries worldwide, it is crucial to establish standardized reporting protocols, follow-up timelines, and imaging assessments during specific phases of the menstrual cycle. Standardization will help raise awareness of this disease, and further our understanding of its pathogenesis, risk factors, recurrence patterns, and potential for malignant transformation—factors that are still not fully understood.

Brain-derived neurotrophic factor (BDNF) is a key regulator of neuronal survival, synaptic plasticity, and neurogenesis and has emerged as a potential biomarker and therapeutic target in neurodegenerative diseases. This narrative review critically summarizes current evidence on BDNF dysregulation in Alzheimer’s disease, Parkinson’s disease, Huntington’s disease, and amyotrophic lateral sclerosis, with emphasis on biomarker potential, therapeutic modulation, and translational challenges. Relevant literature was identified through targeted PubMed searches and reference-list screening, prioritizing original experimental and clinical studies, meta-analyses, and recent reviews. Altered BDNF expression and impaired signaling through tropomyosin receptor kinase B (TrkB) and the p75 neurotrophin receptor (p75NTR) are implicated in synaptic dysfunction, disrupted axonal transport, abnormal protein-related pathology, and neuronal vulnerability. Peripheral and central BDNF alterations have been associated with disease severity, but methodological heterogeneity and inconsistent findings for variants such as Val66Met limit biomarker application. TrkB-targeting approaches, gene delivery, pharmacological modulation of BDNF-related pathways, and physical activity show neuroprotective potential, predominantly in experimental studies. BDNF therefore represents a promising translational link between neurodegenerative mechanisms, biomarker development, and therapeutic innovation, but clinical translation requires standardized assessment, improved delivery strategies, biomarker-guided patient selection, and selective modulation of disease- and receptor-specific signaling.

Renal cell carcinoma (RCC) is acknowledged as a heterogeneous malignancy underlined by complex genetic, metabolic, and immune dysregulation. In particular, molecular studies have revealed distinct oncogenic mechanisms that have been exploited and studied as therapeutic intervention targets. These include hypoxia-driven signaling, chromosomal translocations, and gene fusion events that affect tumor progression. This review provides a comprehensive overview of these targets and rethinks RCC management. Therapeutic concepts include the targeting of genomic fusion biology with emerging cell-based immunotherapies or targeted molecular inhibition, and orthomolecular therapeutic strategies are presented. Two clinical and pathological features are highlighted—namely, the TFE3 fusion proteins in translocation RCC and the growing role of hypoxia-inducible factor-2α (HIF-2α) inhibitors in clear-cell RCC. We also present recent data on novel immunotherapeutic approaches, including autologous hematopoietic stem and progenitor cell-based interferon-α gene therapy, as well as chimeric antigen receptor T-cell therapy. These therapies are discussed in light of their mechanistic rationale, translational potential, and existing clinical challenges due to unwanted side effects. At last, orthomolecular and natural product-based therapies are reviewed for their potential as adjunctive therapies that might be used for oxidative stress management, the targeting of tumor metabolism and immune effects, and to increase standard treatment tolerance. This review points to a multidimensional framework that might support further research and studies in precision-guided RCC management, as integrative approaches may enhance therapeutic efficacy, reduce toxicity, and support the development of personalized interventions for advanced or treatment-resistant RCC.