Endometriosis is traditionally conceptualized as a pelvic lesion-centered disease; however, mounting evidence indicates it is a chronic, systemic, and multifactorial inflammatory disorder. This review examines the molecular dialog between ectopic endometrial tissue, the immune system, and peripheral organs, highlighting mechanisms that underlie disease chronicity, symptom variability, and therapeutic resistance. Ectopic endometrium exhibits distinct transcriptomic and epigenetic signatures, disrupted hormonal signaling, and a pro-inflammatory microenvironment characterized by inflammatory mediators, prostaglandins, and matrix metalloproteinases. Immune-endometrial crosstalk fosters immune evasion through altered cytokine profiles, extracellular vesicles, immune checkpoint molecules, and immunomodulatory microRNAs, enabling lesion persistence. Beyond the pelvis, systemic low-grade inflammation, circulating cytokines, and microRNAs reflect a molecular spillover that contributes to chronic pain, fatigue, hypothalamic-pituitary-adrenal axis dysregulation, and emerging gut-endometrium interactions. Furthermore, circulating biomarkers-including microRNAs, lncRNAs, extracellular vesicles, and proteomic signatures-offer potential for early diagnosis, patient stratification, and monitoring of therapeutic responses. Conventional hormonal therapies demonstrate limited efficacy, whereas novel molecular targets and delivery systems, including angiogenesis inhibitors, immune modulators, epigenetic regulators, and nanotherapeutics, show promise for precision intervention. A systems medicine framework, integrating multi-omics analyses and network-based approaches, supports reconceptualizing endometriosis as a systemic inflammatory condition with gynecologic manifestations. This perspective emphasizes the need for interdisciplinary collaboration to advance diagnostics, therapeutics, and individualized patient care, ultimately moving beyond a lesion-centered paradigm toward a molecularly informed, holistic understanding of endometriosis.
Forests are an important component of nature-based solutions for climate mitigation as trees both regulate local microclimate and store carbon. Forest restoration provides a critical link between the biodiversity and climate crises. This is especially important in the tropics where shifting agriculture is one of the biggest drivers of deforestation. However, an important knowledge gap remains how quickly ecological succession stabilizes understory microclimate and restores the buffering capacity of forests to reduce climatic extremes. In the Ecuadorian Choco, we examined natural ecological succession after previous agricultural land use for pasture and cacao along a 40-year chronosequence, comparing the effects of increasing vegetation cover on microclimate to understory conditions in old-growth stands. In this wet lowland rainforest ecosystem, trees regulated hot and dry extremes during the day, whereas nighttime conditions did not vary with land use. In open agricultural areas, maximum temperatures (Tmax) decreased -4.6 degrees C during the first 1-2 decades of succession, at a rate of -0.7 degrees C per 10% increase in canopy cover. Tmax was also -1.2 degrees C cooler in cacao plots relative to pasture, as small Theobroma trees helped to stabilize the understory microclimate. In later successional stages, Tmax decreased another -2.1 degrees C until full recovery at 30-40 years for cacao compared to estimated recovery of 50-80 years for pasture. Plant transpiration stabilized daytime relative humidity (RHmin) and vapor pressure deficit (VPDmax) at least a decade before Tmax, which was sensitive to high solar radiation and reduced cloud cover. In this system, cloud cover increased at higher elevation maintaining cool ridgetop microclimates important for threatened endemics. Although natural regeneration stabilized microclimate in the forest understory, our results indicate that if the cloud bank changes, agricultural conversion may increase the long-term vulnerability of tropical rainforests to climatic extremes.
IntroductionInclusive education (IE) in Higher Education (HE) has become a global priority, driven by the mandate of the United Nations Convention on the Rights of Persons with Disabilities (CRPD). However, the implementation remains uneven, characterized by fragmented institutional responses and conceptual ambiguities. This article presents an international, critical narrative review of the advances and persistent challenges concerning IE for Students with Special Educational Needs (SEN) and Students with Disabilities (SWDs).MethodologyA narrative review was conducted on international peer-reviewed literature and policy documents published mainly between 2015 and 2025. The analysis is critically structured around six dimensions: (1) conceptualizations of SEN and disability; (2) characteristics and academic trajectories of SWDs; (3) institutional and pedagogical models; (4) the use of digital and assistive technologies; (5) legislative and policy frameworks; and (6) the economic and financial costs associated with inclusion.Key findingsThe review confirms a necessary paradigm shift from the reactive Medical Model to the proactive, Rights-Based Model. Universal Design for Learning (UDL) and innovative, student-centered pedagogies are crucial tools for systemic change, supported by the transformative potential of emerging technologies like AI and Virtual Reality for personalization. Despite these advances, a critical gap persists between policy and practice. Major challenges include the persistent lack of faculty readiness to implement UDL effectively, fragmented policy management, and inadequate financial models that treat inclusion as a cost rather than an investment.Conclusion and implicationsAchieving genuine equity in HE requires moving beyond minimal legal compliance toward an integrated, systemic commitment. Future research must focus on longitudinal studies measuring the impact of UDL on retention, efficacy of faculty training, and developing robust, bifurcated financial models. The ultimate success hinges on redesigning the educational environment—pedagogically, technologically, and financially—to establish diversity as the institutional norm.
Natural products have emerged as promising multi-target agents for addressing the complex biology of gastric cancer, a malignancy characterized by marked molecular heterogeneity, late clinical presentation, and frequent resistance to systemic therapies. This narrative synthesis integrates primarily preclinical evidence, with emerging clinical data, on how naturally derived compounds modulate three central molecular processes that drive gastric tumor progression and therapeutic failure: evasion of programmed cell death, persistent tumor-promoting inflammation, and chemoresistance. Compounds such as curcumin, resveratrol, berberine, ginsenosides, quercetin, and epigallocatechin gallate restore apoptotic competence by shifting the balance between pro-survival and pro-death proteins, destabilizing mitochondrial membranes, promoting cytochrome c release, and activating caspase-dependent pathways. These agents also exert potent anti-inflammatory effects by inhibiting nuclear factor kappa B and signal transducer and activator of transcription signaling, suppressing pro-inflammatory cytokine production, reducing cyclooxygenase activity, and modulating the tumor microenvironment through changes in immune cell behavior. In parallel, multiple natural compounds function as chemo-sensitizers by inhibiting drug efflux transporters, reversing epithelial-mesenchymal transition, attenuating cancer stem cell-associated traits, and suppressing pro-survival signaling pathways that sustain resistance. Collectively, these mechanistic actions highlight the capacity of natural products to simultaneously target interconnected hallmarks of gastric cancer biology. Ongoing advances in formulation strategies may help overcome pharmacokinetic limitations; however, rigorous biomarker-guided studies and well-designed clinical trials remain essential to define the translational relevance of these compounds.
The UN Decade on Ecosystem Restoration aims to stop biodiversity losses1. Approximately 60% of tropical forests have already been lost or severely degraded2, making restoration essential to achieve conservation goals. Recovery trajectories of trees have been studied intensively3,4, but a comprehensive understanding of biodiversity recovery is lacking. Here we analyse recovery trajectories across trophic levels including 16 taxonomic groups from three kingdoms in a lowland tropical forest by investigating resistance to perturbation, recovery times and return rates to old-growth forest conditions. Abundance and diversity regained more than 90% and composition approximately 75% similarity to old-growth forests within 30 years, but full recovery takes several decades. Mobile animal communities acting as seed dispersers or pollinators had high resistance levels and recovered faster than trees or tree seedlings. Return rates contributed 1-2.5 times more than resistance to the recovery times of species composition. Taxon-specific recovery times could not be explained by simple mechanisms (life-history strategies, trophic level or mobility). We show the enormous potential of protecting naturally recovering secondary forests to stop and reverse biodiversity losses.
