Alzheimer's disease is the most common form of dementia, a complex and progressive neurodegenerative disorder that slowly decreases memory, thinking skills and the ability to perform the simplest tasks. It is characterised by the formation of extracellular amyloid-beta (Aβ) plaques and intracellular neurofibrillary tangles (NFTs). In the human body, amino acids are a source of metabolites and neurotransmitters. Various studies have also proven their association with Alzheimer's disease. Therefore, the research was conducted to review the effects of amino acids and their mechanisms on Alzheimer's disease. This descriptive study is a narrative review of articles on in vivo and in vitro amino acid-induced Alzheimer's disease in the PubMed and ScienceDirect databases. The selected papers were in English, topic-relevant and published from 2011 to 2021 in journals of Q1, Q2 or Q3 category according to the Scimago Journal & Country Rank. The search yielded 27 relevant articles, but only 22 with 12 types of amino acids were included. Amino acids with positive effects were glutamine, d-serine, selenomethionine, s-adenosylmethionine, d-ribose-l-cysteine, s-allyl-cysteine, N-acetylcysteine, Se-methyl-selenocysteine and l-theanine, whereas some negative results come from homocysteine and N-methylamino-L-alanine. While taurine generally has a positive effect, there is a mechanism that negatively influences Alzheimer's disease. These amino acids are involved in all parts of the pathophysiology mechanism of Alzheimer's disease differently. The mechanisms include preventing (positive impact) or inducing (negative impact) mitochondrial dysfunction, inflammation, oxidative stress, formation of oligomers/plaque Aβ, tau hyperphosphorylation and neuronal/synaptic damage. Thus, not all amino acids have the activity of preventing/treating Alzheimer's disease.

Endocrine-disrupting chemicals (EDCs) and environmental pollutants are ubiquitous and increasingly linked to the aetiology of cancer. This review synthesises existing evidence on the carcinogenic potential of EDCs, including bisphenols, phthalates, pesticides, heavy metals and persistent organic pollutants, with a focus on genetic and epigenetic pathways. The molecular mechanisms by which these chemicals induce carcinogenesis, including DNA damage, chromosomal aberrations, dysregulation of oncogenes and tumour suppressor genes and alterations in DNA repair was critically accessed. Epidemiological research emphasises epigenetic changes, including aberrant DNA methylation, histone modifications and deregulated non-coding RNA expression, which mediate long-term and potentially transgenerational effects of exposure. The interplay among endocrine signalling, oxidative stress, inflammation and epigenetic reprogramming is discussed in relation to hormone-dependent and hormone-independent cancers. Epidemiological, in vivo and in vitro experimental evidence, together with high-throughput omics data, were integrated to strengthen mechanistic plausibility. This review identified important research gaps, including low-dose and mixture effects, timing of exposure and population-wide vulnerability and provides future directions for risk assessment and regulatory policy. Greater insight into the genetic and epigenetic effects of EDCs is needed to advance cancer prevention and inform evidence-based community health interventions.

Pharmacotherapy in high-risk pregnancies necessitates customised, evidence-based strategies to provide optimal results for women and their infants. A keen awareness that physiological changes during pregnancy can affect medication pharmacokinetics necessitates careful consideration of dose and therapeutic selection to reduce teratogenic risk without compromising treatment efficacy. Likewise, non-obstetric problems such as hypertension in pregnancy, gestational diabetes, auto-immune disorders and infections necessitate immediate medical intervention according to safety classifications and evolving labelling systems. Multidisciplinary care involving obstetricians, pharmacists, subspecialists and mental health professionals is crucial for managing the intricate relationships between maternal comorbidities and foetal development. Moreover, emerging domains including pharmacogenomics, placental-drug-delivery and diversity in clinical trials are further transforming the future of perinatal pharmacotherapy. This article aimed to examine the role of pharmacotherapy in high-risk pregnancies, emphasising the contemporary paradigm of safe drug use, collaboration within a multidisciplinary framework and prospective advancements to optimise maternal and foetal health outcomes. The personalised, evidence-based pharmacotherapeutic approach that improves high-risk pregnancy outcomes is based on body modifications, safe medication use, multidisciplinary approaches and advances in pharmacogenomics and placenta-targeted therapies.

Extensive work over the past 6 decades in the field of cardiovascular medicine has revealed that haemodynamic, hormonal, metabolic, cellular and molecular mechanisms of heart failure are not only complex but are also dependent upon the type and stage of heart disease. Although various agents such as b-adrenoreceptor blockers, angiotensin converting enzyme inhibitors, angiotensin II receptor antagonists and vasodilators are available for the treatment of heart failure, these interventions delay the progression of heart failure without reducing mortality and morbidity. In this article, literature on the pathophysiology of heart failure due to myocardial infarction and haemodynamic overload to identify molecular targets for future drug development is reviewed. Particularly, objective was to focus on the mechanisms of heart failure involving pathways for the generation of oxidative stress, myocardial inflammation and Ca2+-handling abnormalities. It is evident that elevated levels of plasma vasoactive hormones and growth factors as well as increased preload and afterload play critical roles in stimulating various signal transduction pathways for the occurrence of increased ventricular wall stress, cardiac remodelling and subsequent cardiac dysfunction. These alterations are associated with development of oxidative stress, myocardial inflammation, endothelial dysfunction, metabolic defects, intracellular Ca2+-handling abnormalities, apoptosis, fibrosis and changes in the extracellular matrix. In view of such pathogenic abnormalities in failing hearts, it is suggested these parameters may serve as excellent targets for drug development for the therapy of heart failure. In addition, there occurs activation of proteases and phospholipases as well as depression in cardiac gene expression for the induction of subcellular remodelling in failing hearts and thus interventions affecting these parameters may also be considered to exert beneficial effects in heart failure. There is also an urgent need to develop some existing and newer agents such as metabolic inhibitors, antioxidants and sodium-glucose cotransporter-2 inhibitors as well as gene and RNA based therapies for the treatment of heart failure.

The gut microbiome plays a crucial role in perioperative care. Surgical stress and anaesthesia disrupt the balance of intestinal flora, known as dysbiosis, which can affect gut health and metabolism. Pain relievers like morphine and certain anaesthetics contribute to this imbalance. Dysbiosis may also lead to memory loss and cognitive issues post-surgery. Future studies aim to use probiotics and beneficial substances to improve health and prevent cognitive decline.

Background/Aim: Photoageing causes collagen degradation, leading to sagging skin, increased wrinkles and rough surfaces as signs of skin ageing. UV-B radiation increases reactive oxygen species (ROS) production, affecting the mitogen-activated protein kinase (MAPK) pathways, resulting in the expression of the MMP1 gene, which can induce collagen fibre degradation. This study aimed to compare the MMP1 gene expression and collagen percentage in response to polydioxanone (PDO), poly-L-lactic acid (PLLA) and polycaprolactone (PCL) thread implantation in ageing rat skin. Methods: The study involved female Wistar rats, divided into six groups: young rats without UV-B exposure, old rats without UV-B exposure, ageing model rats exposed to UV-B and ageing model rats implanted with PDO, PLLA and PCL threads. UV-B exposure was given 3 times per week for 4 weeks with a total dose of 840 mJ/cm<sup>2</sup>. Parameters assessed included MMP1 gene expression and skin collagen percentage. Results: Data analysis showed that the ageing model skin organ had higher MMP1 gene expression (p < 0.05) and lower collagen percentage (p < 0.05) compared to young rats without UV-B exposure. MMP1 gene expression in the three thread implantation groups was equivalent to other groups (p > 0.05). Collagen percentage was equivalent in the three thread treatment groups (p > 0.05), higher (p < 0.05) than an ageing model, but did not differ (p > 0.05) from young rats without UV-B exposure. Conclusions: The study concludes that the implantation of the three types of threads, PDO, PLLA and PCL, does not reduce MMP1 gene expression but has an equivalent ability to increase collagen percentage in ageing rat models.

Interventional pain management is crucial as a minimally invasive procedure because it offers targeted therapy, reduces opioid dependence, provides rapid and long-lasting relief, is less risky, has fewer side effects, enhances function and healing and is supported by clinical evidence and guidelines. A bibliometric study in interventional pain management aimed to provide a comprehensive overview of the research landscape, highlighting trends, key topics and gaps in knowledge that can inform future studies and clinical practices. The use of bibliometric tools in pain management studies has evolved to include more advanced methodologies, increase global participation and a focus on specific pain types. The integration of software visualisation tools and the use of various bibliometric indicators have enhanced the ability to analyse and understand the utilisation of interventional pain management research landscape. The compilation of data were retrieved from Scopus database from 2014-2024. A total of 13,606 publications (100 % in English) with topic interventional pain management as minimally invasive procedure from 2014-2024 were retrieved covering 3,313 sources with total authors 63,460. The number of publications showed a noticeable increase starting in the early 2016 with the peak at 2022. The most relevant sources for documents include BMJ Open (954 documents), followed by Archives of Physical Medicine and Rehabilitation (353 documents), PM and R (264 documents) and Pain Physician (237 documents). Recent trends in interventional pain management, particularly focusing on minimally invasive techniques are characterised by a significant increase in publication frequency, emphasis on targeted and non-destructive treatments and improved clinical outcomes. These factors collectively highlight the importance and growing recognition of these methods in modern pain management practices.

Cardiovascular health is influenced not only by the quality of diet but also by the timing of meals. Circadian rhythms, the body's internal biological clock, regulate physiological processes, including metabolism, hormone secretion and cardiovascular function. Disruptions in these rhythms, such as irregular meal timing, have been linked to an increased risk of cardiovascular diseases (CVD). There is a strong association between delayed meal timing, particularly late-night eating and breakfast skipping and heightened cardiovascular and cerebrovascular risks. A large-scale European study has suggested that prolonged overnight fasting may lower the risk of CVD and stroke. Emerging dietary approaches, such as time-restricted eating (TRE) and chrono-nutrition, have gained attention for their potential in mitigating metabolic disorders and promoting cardiovascular health. This review explores the intricate relationship between circadian-regulated meal timing and cardiovascular outcomes, analysing molecular mechanisms, clinical evidence and possible dietary interventions. By understanding the role of chrono-nutrition, this review aimed to provide insights into optimising meal schedules to enhance cardiovascular well-being and reduce disease risk. In addition to melatonin's endogenous regulation, dietary sources of melatonin and chronobiotic nutrients (eg, walnuts, tart cherries, oats) may help support circadian alignment. Strategic intake of these foods, especially during evening hours, could enhance melatonin levels and improve cardiovascular outcomes. Moreover, the timing of other compounds like caffeine has emerged as a modifiable factor, with studies showing that morning coffee consumption may reduce cardiovascular and cancer mortality. While intermittent fasting and caloric restriction both reduce caloric intake, these operate through distinct mechanisms. Caloric restriction focuses on reducing total energy consumption, whereas meal timing strategies emphasise aligning food intake with circadian rhythms without necessarily altering caloric quantity. This distinction is critical, as it supports the view on circadian physiology in metabolic regulation.

The article discusses evolving pharmacological strategies for addressing the neuroinflammation in depression, highlighting its role in major depressive disorder. Neuroinflammation is linked to neurotransmitter imbalances, hypothalamic-pituitary-adrenal axis dysregulation and impaired neurogenesis. Key treatments explored include anti-inflammatory agents such as N-acetylcysteine, toll-like receptor (TLR) inhibitors and cytokine blockers like anti-interleukin-6 and tumour necrosis factor Alpha (TNF-a) agents. Glutamate modulation, antioxidants and omega-3 fatty acids are also examined for their therapeutic efficacy. The article emphasises the need for combination therapies and novel approaches like ketamine and microbiome-targeted treatments to combat inflammation-related depression. Despite significant progress, further research is needed to fully understand the mechanisms and optimise therapeutic strategies.

The majority of nonsteroidal anti-inflammatory drugs (NSAIDs) are categorised as Biopharmaceutics Classification System (BCS) class II or IV drugs, indicating their limited solubility and permeability. The nanostructured lipid carriers (NLCs) can be utilised in drug delivery of NSAIDs to decrease adverse effects and create controlled-release oral formulations. The utilisation of NLCs in transdermal and topical formulations of NSAIDs has demonstrated better efficacy in alleviating inflammation and pain, both at the site of application and throughout the body. This review offers concise insights into the characteristics and mode of action of NSAIDs in the inflammatory cascade. The current review provides a complete overview of the advanced functions of NLCs in delivering NSAIDs through various routes of administrations, including buccal, cutaneous, transdermal, ocular, oral controlled, parenteral and pulmonary routes. To accomplish this objective, an extensive literature search was conducted utilising the ScienceDirect, PubMed and Google Scholar databases. A systematic review was undertaken using scholarly publications published in peer-reviewed journals from 2000 to 2024. Research has established that NLCs possess considerable potential in offering diverse benefits in the delivery of NSAIDs. These benefits include improved skin penetration and precise targeting when applied topically, enhanced drug retention on the corneal surface and effective transport across ocular barriers when administered to the eyes, extended drug residence period in the lungs and increased diffusion mobility when administered through the pulmonary route, as well as prolonged and sustained duration of action when administered buccally, parenterally, or orally. This analysis emphasises the considerable capacity of NLCs to efficiently transport NSAIDs while reducing their negative impacts in the management of inflammatory diseases.