Functional Gastrointestinal Disorders (FGIDs), also recently referred to as disorders of gut-brain interaction, are common in the pediatric population and vary according to age groups, i.e., neonatal/toddler and child/adolescent FGIDs. Pediatric FGIDs tend to evolve and persist into adulthood, contributing to financial burdens and psychological problems. Despite several decades of progress and advancements in molecular biology and medical sciences, the exact pathophysiology remains unknown, although genetic, psychosocial, gut dysbiosis, visceral hypersensitivity, and neuroimmune causes have been implicated. The ROME IV criteria facilitate easier and earlier diagnosis of FGIDs, excluding organic causes while minimizing unnecessary investigations. Dietary, psychosocial, neuro-stimulatory, and pharmacological management methods exist, although fewer trials have focused on pediatric drug-based management. Early identification and appropriate treatment hold the potential for cure and improvement in quality of life.

Medication non-adherence among youth with chronic health conditions is a healthcare crisis in the United States. Nearly 20% of youth experience a chronic illness, yet most do not comply with their treatment regimen. Various challenges to adherence arise, such as not understanding the purpose of treatment, painful or difficult administration, forgetfulness, and mood disorders such as anxiety. Cognitive behavioral therapy (CBT) is an empirically supported approach to increasing treatment adherence. Modular CBT incorporates psychoeducation, cognitive restructuring, and behavioral experiments to promote better disease management. This article focuses on the application of CBT to four medical conditions characterized by elevated levels of non-adherence: pill-swallowing difficulties, asthma, type 1 diabetes, and inflammatory bowel disease in youth. The review integrates findings on contextual issues (e.g., ethnocultural variations, the impact of the COVID-19 pandemic), research on non-adherence, and CBT outcome studies. Additionally, limitations of the existing literature and training recommendations are provided.

Essential oils, known for their pleasant aromas, not only calm the mind and elevate the mood but also captivate the interest of researchers aiming to unveil their vast potential. Various methodologies are employed to explore the diverse capabilities of essential oils, often yielding promising and significant outcomes. This review aims to elucidate the molecular mechanisms of essential oils at the cellular level. It identifies multiple mechanisms through which essential oils exhibit their therapeutic effects across various systems. However, a comprehensive understanding of their fundamental mechanisms still necessitates extensive research. In this review, we discuss the mechanisms underlying the biological activities of essential oils, specifically their antioxidant, antimicrobial, anticarcinogenic, anti-diabetic, and anti-inflammatory properties.

Obesity has become a global epidemic affecting diverse populations and leading to metabolic syndrome across different sexes and age groups. A significant aspect of obesity is the development of leptin resistance, primarily due to the inefficient transport of leptin across the blood-brain barrier and other mechanisms such as protein folding and dysregulation of leptin signaling in brain areas related to energy and adipose tissue metabolism. This hindrance in leptin delivery poses a challenge to using this adipokine as a potential therapy for obesity. Current research focuses on understanding the complex molecular pathways that link diet-induced obesity, characterized by increased levels of leptin, to the onset of metabolic syndrome. This syndrome encompasses various health issues, including type 2 diabetes mellitus, and involves intricate mechanisms primarily affecting pancreatic β-cells. This bioinformatics-assisted review describes key biological elements of known pathways, such as the forkhead box protein O1/leptin receptor and Janus kinase/signal transducer and activator of transcription 3, and discusses future directions that might contribute to understanding the relationship between obesity, leptin resistance, and metabolic complications (e.g., Rac1/cell division control protein 42 homolog), paving the way for future research on targeted therapeutic interventions.

This review discussed experimental mouse models used in the pre-clinical study of liver fibrosis regression, a pivotal process in preventing the progression of metabolic dysfunction-associated steatohepatitis to irreversible liver cirrhosis. These models provide a valuable resource for understanding the cellular and molecular processes underlying fibrosis regression in different contexts. The primary focus of this review is on the most commonly used models with diet- or hepatotoxin-induced fibrosis, but it also touches upon genetic models and mouse models with biliary atresia or parasite-induced fibrosis. In addition to emphasizing in vivo models, we briefly summarized current in vitro approaches designed for studying fibrosis regression and provided an outlook on evolving methodologies that aim to refine and reduce the number of experimental animals needed for these studies. Together, these models contribute significantly to unraveling the underlying mechanisms of liver fibrosis regression and offer insights into potential therapeutic interventions. By presenting a comprehensive overview of these models and highlighting their respective advantages and limitations, this review serves as a roadmap for future research.

Metabolic dysfunction-associated steatotic liver disease (MASLD) is currently a pressing public health issue associated with adverse outcomes such as cirrhosis, malignancy, transplantation, and mortality. Lifestyle modifications constitute the most effective and fundamental management approach, but they often pose challenges in sustaining long-term clinical benefits. Hence, there is a critical need to enhance our understanding through pharmacological management, which unfortunately remains limited. Glucagon-like peptide-1 receptor agonists (GLP-1RAs) have emerged as a leading treatment in the fields of diabetes and obesity, with recent preclinical and clinical studies indicating significant benefits in the management and treatment of MASLD. Our article begins by reviewing the beneficial therapeutic components of GLP-1RAs in MASLD. Subsequently, from a clinical research perspective, we concluded with the liver outcomes of current primary GLP-1RAs and co-agonists. Finally, we presented our insights on clinical concerns such as appropriate trial endpoints, management of comorbidities, and future developments. In conclusion, the benefits of GLP-1RAs in MASLD are promising, and background therapy involving metabolic modulation may represent one of the future therapeutic paradigms.

Information on the survival of urothelial cancer (UCa) patients with brain metastases (BM) is largely unreliable due to the rarity of such cases. Previous studies that have attempted to capture the prevalence and survival of these patients are limited to case series and retrospective studies with small cohort sizes. This study aimed to explore patient characteristics and treatment outcomes based on treatment modalities from a large sample of patients with UCa and BM.

In this retrospective study, we utilized the TriNetX Research Network, a real-world and in-house database with longitudinal electronic medical records from 92 institutions. The database was queried for patients with UCa who also had BM. Kaplan–Meier plots were used to assess overall survival (OS). Log-rank tests were applied for stratified outcomes. The Cox proportional hazards model was used for continuous data.

We identified 357 patients with UCa and BM, representing 4.7% of the 7,521 patients diagnosed with primary UCa. The mean age at diagnosis was 65.6 years, with a predominance of male patients (67%). The median OS from BM diagnosis was 18.6 months. For patients treated solely with stereotactic radiosurgery (SRS), the median OS was 20.8 months. For those treated with both SRS and surgical resection, the median OS was 18.6 months. There was no significant difference in survival between patients treated with SRS alone and those treated with both SRS and surgical resection (p = 0.875). For patients treated only with gemcitabine chemotherapy, the median OS was 15.4 months.

This study represents the largest known retrospective analysis of UCa patients with BM. Survival trends for patients treated with surgical resection, SRS, and systemic therapies are described in detail.

Autoimmune hepatitis (AIH) is a chronic, progressive inflammatory liver disease caused by autoimmune reactions, with an unknown etiology. If left untreated, it can progress to cirrhosis, liver failure, or even death. While most patients respond well to first-line treatments, a significant number experience poor responses or intolerance, requiring the use of second- or third-line therapies. Ongoing research into the pathogenesis of AIH is leading to the development of novel therapeutic approaches. This review summarized recent advancements in the treatment of AIH both domestically and internationally.