Lipid rafts, specialised microdomains within cell membranes, play a central role in orchestrating various aspects of neurodevelopment, ranging from neural differentiation to the formation of functional neuronal networks. This review focuses on the multifaceted involvement of lipid rafts in key neurodevelopmental processes, including neural differentiation, synaptogenesis and myelination. Through the spatial organisation of signalling components, lipid rafts facilitate precise signalling events that determine neural fate during embryonic development and in adulthood. The evolutionary conservation of lipid rafts underscores their fundamental importance for the structural and functional complexity of the nervous system in all species. Furthermore, there is increasing evidence that environmental factors can modulate the composition and function of lipid rafts and influence neurodevelopmental processes. Understanding the intricate interplay between lipid rafts and neurodevelopment not only sheds light on the fundamental mechanisms governing brain development but also has implications for therapeutic strategies aimed at cultivating neuronal networks and addressing neurodevelopmental disorders.

Uterine physiology encompasses the intricate processes governing the structure, function, and regulation of the uterus, a pivotal organ within the female reproductive system. The escalating prevalence of obesity has emerged as a significant global health issue, profoundly impacting various facets of well-being, including female reproductive health. These effects extend to uterine structure and function, influencing reproductive health outcomes in women. They encompass alterations in uterine morphology, disruptions in hormonal signaling, and inflammatory processes. Insulin and leptin, pivotal hormones regulating metabolism, energy balance, and reproductive function, play crucial roles in this context. Insulin chiefly governs glucose metabolism and storage, while leptin regulates appetite and energy expenditure. However, in obesity, resistance to both insulin and leptin can develop, impacting uterine function. Inflammation and oxidative stress further exacerbate the development of uterine dysfunction in obesity. Chronic low-grade inflammation and heightened oxidative stress, characteristic of obesity, contribute to metabolic disruptions and tissue damage, including within the uterus. Obesity significantly disrupts menstrual cycles, fertility, and pregnancy outcomes in women. The accumulation of excess adipose tissue disrupts hormonal equilibrium, disturbs ovarian function, and fosters metabolic irregularities, all of which detrimentally impact reproductive health.

Teachers must enhance their teaching skills in accordance with institutional policies at higher education institutions. This research aims to determine effective professional development techniques for biology teachers in higher education. The modified OZON form (cro. obrazac za opažanje nastave, teaching observation form) facilitated self-reflection and assessed the impact of reflection-based actions on the learning environment. Teachers participated in workshops, experiencing both student and curriculum-designer roles. Proficiency in creating an engaging learning environment and using technology was well developed. However, teachers should improve their understanding of curricular aspects, constructive alignment, outcome-driven selection of activities and formative and summative evaluation. Our research suggests modifying professional learning strategies to align with biology teachers' needs in higher education. Combining extended learning time, implementation in teaching practice, ongoing expert support, and action research fosters positive changes in a constructively aligned classroom. The results indicate that biology teachers in higher education need the continuous support of experts in the didactic design of the lesson plan to improve the creation of a learning environment through positive alignment. This approach promotes active professional development management in a concise format.

The purpose of this review is to succinctly examine the methodologies used in lipid raft research in the brain and to highlight the drawbacks of some investigative approaches. Lipid rafts are biochemically and biophysically different from the bulk membrane. A specific lipid environment within membrane domains provides a harbor for distinct raftophilic proteins, all of which in concert create a specialized platform orchestrating various cellular processes. Studying lipid rafts has proved to be arduous due to their elusive nature, mobility, and constant dynamic reorganization to meet the cellular needs. Studying neuronal lipid rafts is particularly cumbersome due to the immensely complex regional molecular architecture of the central nervous system. Biochemical fractionation, performed with or without detergents, is still the most widely used method to isolate lipid rafts. However, the differences in solubilization when various detergents are used has exposed a dire need to find more reliable methods to study particular rafts. Biochemical methods need to be complemented with other approaches such as live-cell microscopy, imaging mass spectrometry, and the development of specific non-invasive fluorescent probes to obtain a more complete image of raft dynamics and to study the spatio-temporal expression of rafts in live cells.

Background/Objectives: The ketogenic diet (KD) induces profound metabolic shifts, yet the sex-specific long-term effects on skeletal muscle metabolism and sterol homeostasis across tissues remain insufficiently characterized. This study tested the hypothesis that a prolonged KD would elicit distinct, sex-dependent metabolic and sterol adaptations in mice. Methods: We examined how a 12-week KD, compared with a standard diet, affected body mass, the skeletal muscle metabolome, hepatic lipid and collagen content, and sterol profiles in the skeletal muscle, liver, spleen, and serum in male and female C57BL/6J mice. Three-month-old mice of both sexes were randomized to a KD or standard diet and evaluated using the histological quantification of hepatic steatosis and collagen deposition, matrix-assisted laser desorption/ionization time-of-flight imaging mass spectrometry (MALDI-TOF IMS) of skeletal muscle, and LC-MS/MS-based sterol profiling. Results: The KD induced rapid body mass gain in males and delayed weight gain in females, promoted hepatic steatosis in both sexes, and generated clearly segregated, sex- and diet-specific skeletal muscle metabolomic signatures. These signatures included reduced tricarboxylic acid cycle precursors and a marked decrease in S-adenosylmethionine in KD-fed females. Across tissues, the KD consistently suppressed precursor sterols, including 7-dehydrocholesterol and desmosterol in the skeletal muscle, liver, and spleen, while elevating serum cholesterol and desmosterol (male-biased), with changes generally more pronounced in males. Conclusions: Collectively, these findings demonstrate that a long-term KD drives sex- and organ-specific metabolic remodeling, with evidence of greater metabolic flexibility but a shared risk of hepatic steatosis in females. These results underscore the importance of personalized, sex-stratified approaches when considering long-term ketogenic interventions.

The ketogenic diet (KD), a high-fat, low-carbohydrate diet, causes profound metabolic adaptations that go beyond energy production and affect endocrine function and thyroid hormone regulation. By shifting the body’s primary fuel source from glucose to fatty acids and ketones, the KD alters insulin signaling, inflammation levels and deiodinase activity, which together affect thyroid hormone metabolism. While this metabolic shift offers potential benefits such as improved insulin sensitivity and reduced systemic inflammation, it also raises concerns about reduced triiodothyronine (T3) levels and altered hypothalamic–pituitary–thyroid (HPT) axis dynamics. This review explores the mechanisms by which the KD affects thyroid function, highlighting both the potential therapeutic benefits and associated risks. Special attention is given to how genetic predispositions, gut microbiota composition and sex-based hormonal differences influence thyroid adaptation to a KD. In addition, there are indications that the influence of the KD on cell metabolism could have therapeutic potential in conditions such as autoimmune thyroid diseases and thyroid cancer. Understanding the delicate balance between the benefits and risks of KD for thyroid health is essential for optimizing its clinical applications and defining individual nutritional strategies.