Addition and update of compounds for the 2025 Wayne state university compound descriptor database for use with the solvation parameter model.

Colorectal cancer (CRC) with peritoneal dissemination remains a major therapeutic challenge because of poor prognosis and limited treatment options. Experimental models that accurately recapitulate tumor-mesothelial interactions are scarce. Here, we report the establishment of a novel autologous paired model comprising a CRC cell line (OMUCR-1) and matched cancer-associated mesothelial cells (CAmeso), both simultaneously derived from the malignant ascites of the same patient. Lineage marker analysis using qPCR demonstrated that OMUCR-1 selectively expressed epithelial markers (EPCAM, KRT20), whereas CAmeso strongly expressed mesothelial-mesenchymal markers (ACTA2, MSLN) and lacked epithelial marker expression. These mutually exclusive expression patterns confirm that the two cell populations are phenotypically distinct and rule out cross-contamination. OMUCR-1 displayed strong tumorigenic capacity across multiple transplantation models. CAmeso enhanced CRC cell migration and invasion invitro, and co-transplantation with OMUCR-1 resulted in larger tumors enriched with αSMA-positive stromal components. RNA sequencing of co-injected xenografts revealed increased expression of murine stromal Fgfr3. Treatment with the FGFR inhibitor BGJ398 reduced tumor growth and decreased stromal FGFR3-positive components, suggesting that stromal FGFR3 may represent a potential microenvironmental vulnerability in CRC with peritoneal dissemination. This autologous CRC-mesothelial system provides a physiologically relevant platform for dissecting tumor-stroma interactions in peritoneal metastasis and may advance stromal-targeted therapeutic strategies.

Complex role of mTOR signaling pathway in glioblastoma and its stem cells.

Prenatally elevated glucocorticoid disrupts social behavior via GR-Id3/E47-dependent astroglial dysfunction in LPS-induced autism-like rats.

This study aimed to evaluate clinical signs, visceral changes, and weight development in intermediate hosts infected with oocysts of a Cystoisospora ohioensis-like coccidian from naturally infected dogs. Using 135 albino mice divided into three groups-INFECTED (inoculated with oocysts), PAIR-FED (given the same food as infected mice), and CONTROL (fed ad libitum)-researchers monitored weight and pathological changes over 35 days. Mice were euthanized at various intervals post-inoculation (1-35 days), with organs from some INFECTED mice fed to dogs on day 60 for a biological assay. The INFECTED group showed higher body weight and weight gain than the CONTROL group, though organ weights were greater, leading to lower carcass yield. Tissue cysts with hypnozoites were found in the intestines (1st day), Peyer's patches (up to 5th day), and lymph nodes/spleen (up to 35th day). Dogs inoculated with hypnozoites (from infected mice) had a shorter prepatent period, longer patent period, and higher oocyst shedding compared to those given sporulated oocysts. The findings indicate that the C. ohioensis-like coccidian affect mouse weight, persist in visceral tissues for up to 60 days, and exhibit biological differences in infectivity between sporozoites and hypnozoites in dogs.

This study aimed to investigate whether spontaneous hyperphagic behavior can be induced in mule ducks through a protocol combining feed restriction followed by 1-h concentrated meals and to assess the resulting hepatic metabolic responses. To achieve this, two protocols were tested. The first protocol initially demonstrated that a 5-day acclimation phase, consisting of alternating 23-h fasting periods and 1-h refeeding periods, was necessary to induce hyperphagia in ducks. Then, an increase in liver weight and glycogen content was measured up to 12 h after the substantial meal, before returning to baseline after 24 h, whereas total lipid levels remained unchanged. Based on these observations, a second protocol was designed to assess whether an additional meal provided 12 h after the last substantial meal could promote lipid storage in the liver. A significant increase in liver weight and glycogen content was measured after each 1-h meal, whereas total hepatic lipid content increased significantly after the last meal provided 12 h after the previous one. This was associated with an upregulation of genes involved in lipogenesis (FASN, SCD1, and ELOVL6) and carbohydrate oxidation (HK1), and a downregulation of a gene involved in lipid oxidation (ACSL1). Together, these results demonstrate for the first time that voluntary feeding alone can induce measurable hepatic lipid accumulation in mule ducks. This new protocol represents a valuable experimental model for the study of hepatic lipid metabolism in ducks and could contribute to the development of alternative strategies for liver fattening.NEW & NOTEWORTHY This study provides new insights into the physiological effects of a substantial voluntary meal on hepatic energy metabolism in the mule duck, a species for which information on this topic remains limited. Our findings show for the first time that hepatic lipid deposition can be induced through voluntary feeding, without the need for force-feeding. In the longer term, these results may support the development of alternative practices to force-feeding for foie gras production.

Advancing Peripheral Nerve Regeneration (Nerve SPACE 2025).

Pathogenesis of NGPV and DuCV CO-infection pathogenicity analysis of co-infection with novel goose parvovirus and duck circovirus in Cherry Valley meat ducks.

Essential oils (EOs) are plant-derived bioactive compounds, primarily made up of terpenoids, which possess various biological and pharmacological effects. Lavender essential oil (LEO) is one of the most extensively studied options. LEO contains terpenes, ketones, alcohols, polyphenols, and flavonoids. Aromatherapy, a practice dating back to ancient civilizations such as the Egyptians, Romans, and Chinese, involved the use of incense, baths, and embalming rituals. Anxiety disorders have gained significant attention in understanding both physical and mental health. Many people are turning to complementary and alternative therapies for the management of anxiety due to the side effects of pharmacological treatments. Several preclinical studies suggest that LEO may alleviate anxiety-like behaviors in experimental models. This review examines the chemical composition, pharmacological properties, and mechanisms of LEO that contribute to its role in managing anxiety in humans. The literature indicates that LEO-based aromatherapy may effectively reduce anxiety in various groups, such as nursing students, patients undergoing surgery, and those involved in clinical procedures. While the exact mechanisms behind LEO's anxiolytic effects remaining unclear, active compounds in EOs may influence the production and release of neurotransmitters through pathways involving γ-aminobutyric acid, dopamine, and serotonin. More extensive preclinical and clinical studies with diverse subject groups are needed to better understand the molecular mechanisms of LEO's anxiolytic properties, which could ultimately help in developing optimized treatments for managing anxiety disorders.

Airway diseases such as asthma, COPD, pulmonary fibrosis, and other inflammatory airway conditions remain a significant threat to global health. Traditional medicine (TM) has been extensively used over centuries to prevent and treat respiratory disorders due to its multi-component, multi-target therapeutic approach, and holistic nature. Increasing experimental evidence suggests that TM formulations have beneficial effects by modulating key pathological mechanisms, including oxidative stress, immune dysregulation, mucus hypersecretion, airway inflammation and hyperresponsiveness, and airway remodelling. However, the inherent complexity of TM, characterized by an abundance of bioactive constituents and synergistic effects, present significant challenges for mechanistic characterisation, standardization, and clinical authentication. Recent development in network pharmacology, artificial intelligence, and drug delivery systems based on nano formulations have presented potent tools to improve therapeutic efficacy, increase pulmonary targeting, and obtain a deeper understanding of TM mechanisms. Despite significant developments, the absence of large-scale, well-designed randomized controlled trials and consistent quality control persist as a major barrier to widespread clinical acceptance. This review summarizes current evidence on the role of traditional medicine in respiratory disease management, highlights key mechanism involved in and diseases incidents in experimental models and discusses future perspectives for integrating traditional medicine with modern scientific and clinical frameworks to support its evidence-based application in respiratory healthcare.

Marijuana smoking during pregnancy alters placenta morphology in BALB/c mice.

Integrating STING activation with programmed death-ligand 1 inhibition: Novel approaches for cancer treatment.

This review examines how bacterial pathogens disrupt vascular barrier integrity and manipulate coagulation with a focus on endothelial signaling pathways, bacterial effectors, and contextual determinants of host-pathogen interactions. Particular attention is given to a contact activation system member, factor XII (FXII), that operates in infection not merely via coagulation but also through immune modulation and direct antimicrobial activity. Emerging work reveals that loss of endothelial barrier integrity arises from both inflammatory cues and pathogen-directed manipulation of junctional complexes, the glycocalyx, and cell death programs such as pyroptosis. These mechanisms are influenced by pathogen diversity, tissue-specific environments, and heterogeneity across experimental models. Studies demonstrate that FXII function is context-dependent, supporting pathogen containment through fibrin deposition in some infections, yet promoting inflammation and dissemination in others. Additionally, pathogens such as Acinetobacter baumannii directly inhibit FXII, thereby impairing immune defense and coagulation-driven containment. Therapeutic efforts now increasingly target endothelial stabilization and coagulation-immune crosstalk, yet outcomes depend on timing, infectious context, and host state. While approaches such as glycocalyx restoration, inflammasome inhibition, and FXII-based biomimetics show promise, successful intervention will likely require combination strategies that preserve host defense while limiting vascular damage. Given the diversity of host-pathogen interactions, no single therapy is expected to be universally effective.

Cold exposure impairs the muscle growth-promoting effect of nighttime-restricted feeding by desynchronizing mitochondrial energy supply rhythm in rabbits.

Matrix-integrated microfluidic tumor models for evaluating drug delivery systems and pre-clinical testing.

Polycyclic Aromatic Hydrocarbons (PAHs) are persistent and toxic organic pollutants to which humans are exposed via inhalation, dermal absorption, and ingestion, increasing cancer risk, particularly among smokers and occupationally exposed individuals. This research aims to expand current knowledge by identifying the oral mucosae as an additional gateway for PAHs, owing to their high lipophilicity and the greater permeability of oral mucosae to xenobiotics, a finding that is particularly relevant given the established correlation between tobacco-derived PAHs and oral, head, and neck cancers. Here, ex vivo permeation studies were carefully designed using vertical Franz diffusion cells and porcine buccal and sublingual mucosae, a widely used ex vivo model for permeability studies. Five PAHs congeners were selected as representative of those highlighted from the US EPA as priority control pollutants: fluorene, acenaphthene, phenanthrene, pyrene and benzo(a)pyrene. The studied PAHs were found to permeate the oral mucosae, likely via passive diffusion (permeation∝logP), suggesting a potential relevant contribution to the overall systemic PAHs burden and thus toxicity, especially for individuals with pronounced oromucosal exposure, such as smokers. Additionally, all PAHs exhibited significant retention in the mucosal tissues, suggesting possible loco-regional toxicity. Specifically, the observed BaP accumulation in the buccal and sublingual mucosae (1781.27±397.64 and 1338.78±269.47ng/cm2, respectively) may support its correlation with oral cancers. Despite the experimental model not fully mimic the complexity of living system (e.g., enzymatic activity, active transport processes, blood perfusion, real-life exposure scenario), these findings address a major gap in the literature by identifying the oral mucosae as a previously unrecognized entry route for PAHs, a key point since the oral cavity is part of both the gastrointestinal and respiratory systems, already recognized PAHs exposure routes. The evidence reported here provides both a foundation for further multidisciplinary investigations as well as a rationale for developing cosmetic/medical devices aimed at detoxifying the oral cavity from PAHs. ENVIRONMENTAL IMPLICATION: This study aims to expand knowledge on PAHs permeation and accumulation through oral mucosal tissues. Demonstrating PAHs permeation and accumulation through this route would have major clinical and toxicological implications, including identifying a new exposure route, refining toxicokinetic, elucidating mechanisms linking tobacco-derived PAHs to head and neck carcinogenesis, and guiding preventive interventions to limit oral exposure (e.g., development of PAHs-sequestering cosmetics or medical devices).

Animal-based experimental models in dry eye research: Current approaches and limitations.

Aripiprazole is a drug that modulates both the dopaminergic and serotonergic systems. It is currently widely used in the treatment of schizophrenia and mental disorders due to its stabilizing effect on the dopaminergic system. Studies on psychotropic drugs have demonstrated negative effects on hormonal regulation and sexual behavior as a consequence of their mechanism of action; however, the potential genotoxic effects of aripiprazole have not yet been fully clarified. Given the limited number of studies on the changes that this drug can cause in the reproductive system, the present study aimed to evaluate the impacts of aripiprazole on fertility and female sexual behavior, focusing on metabolic and endocrine-reproductive responses through biochemical and toxicological parameters related to reproduction. For this purpose, adult rats were divided into four experimental groups and subjected to different doses of aripiprazole (0, 0.3, 3.0, and 6.0 mg/kg), diluted in the vehicle (DMSO and saline) by gavage for 21 days. Estrous cyclicity was monitored, and reproductive and biochemical parameters were evaluated at the end of treatment. The results showed that there was no increase in body weight and that the data, in general, did not follow the monotonic dose-response curve. Biochemical changes in creatinine, albumin, and triglycerides were observed, in addition to adverse effects on cyclicity and sexual behavior. Thus, aripiprazole at doses of 0.3 and 6.0 mg/kg in this experimental model may cause toxic effects on the endocrine-reproductive system of fertile rats.

Molecular characterization and pathogenicity of a porcine Teschovirus 5 isolate in Shandong Province in China.

Modulating glymphatic clearance in Alzheimer's disease: Molecular mechanisms, imaging biomarkers, and emerging interventions.