Astroviruses are non-enveloped, positive-sense single-stranded RNA viruses known to infect various mammals and birds, including humans, often causing gastrointestinal disorders. In recent years, astroviruses have also been linked to neurological and respiratory diseases across several species, including ruminants, mink, deer, and other mammals. Notably, astrovirus infections in goats have been documented in countries such as Switzerland and China, where novel genotypes have been identified in fecal samples. However, their role in the context of disease remains unclear, and reports focusing solely on goat astrovirus in the United States have not been published. A necropsy case of a Boer goat kid with a history of diarrhea was submitted for investigation following death in January 2025. Fresh tissues were received and used for histopathology and enteric pathogen testing, including parasitic, bacterial, and viral workups. Metagenomic-based next-generation sequencing (mNGS) was also applied for this case. Histological examination revealed severe necrotizing enterocolitis. The small intestine exhibited epithelial ulcerations, villus atrophy, hyperplastic and dilated crypts with necrotic debris, few intraenterocytic coccidian parasites, and increased inflammatory cells in the lamina propria. The large intestine showed similar findings with pleomorphic crypt enterocytes. Standard enteric pathogen tests were negative except for aerobic culture that identified Escherichia.coli and Enterococcus hirae. mNGS and bioinformatic analysis identified a novel astrovirus in the intestinal content that showed the highest nucleotide identity (86%) to the sheep strain Mamastrovirus 13 sheep/HA3 from China based on BLAST analysis. Phylogenetic analysis indicated that the newly identified caprine astrovirus IL90175 clustered with astrovirus strains from small ruminants in Asia and Europe. This research reports the discovery, histopathologic features, and genetic characteristics of a gastrointestinal disease-causing astrovirus in a goat kid, which had not been previously described in the United States.

Background: Advanced glycation end-products (AGEs) are formed and deposited in tissues, contributing to various disorders, including diabetes, other metabolic diseases, and aging. A new epitope, AGE10, was identified in human and animal tissues using a monoclonal antibody raised against synthetic melibiose-derived glycation end-products (MAGE), which were synthesized under anhydrous conditions with bovine serum albumin or myoglobin. The biology of the AGE10 epitope, particularly its role in diseases and in cancer tissues, is not well understood. Methods: The study was aimed at investigating the immunohistochemical recognition of AGE10 with the MoAb-anti-MAGE antibody. Results: Data obtained show that AGE10 is recognized in striated muscles but not in tumors of muscular origin. AGE10 is also stained in both normal and cancerous salivary glands and in adenomas of the large intestine. The staining is cytoplasmic. Discussion: Our approach may provide a methodology for cell biology research; AGE10 may be related to an advanced lipoxidation end-product; further investigation of MAGE may clarify disease mechanisms, support the development of novel therapeutic strategies. Conclusions: The key finding is that antibodies recognize mainly the epitope in epithelial and some mesenchymal tissues. Thus, the potential for AGE10 as a diagnostic marker is limited. The implications concern the biology of this epitope, the unique tissue distribution, and a role in cellular metabolism.

Obtaining pharmacokinetic curves is crucial for drug dosage selection, and for assessment of efficacy and adverse effects in clinical practice. The aim of this study was to utilize a minimal physiologically-based pharmacokinetic model to predict concentration-time profiles of cinacalcet hydrochloride, a poorly soluble drug, under fasting and fed conditions, and further to establish correlations between in vivo and in vitro dissolution profiles of cinacalcet hydrochloride. The mPBPK model consisted of six tissue compartments, and an additional compartmental absorption and transit model, incorporating the stomach, seven small intestinal compartments, and the large intestine along with Johnson's equation, was integrated to enable precise calculations of in vivo dissolution. External validations for three dosages showed that the average fold error and the absolute average fold error were all within a two-fold error range, indicating the accuracy and reliability of the established model. Subsequently, the model was used to calculate the in vivo dissolution profile and to establish a correlation with the in vitro dissolution profile (R2=0.991 in fasting conditions and R2=0.991 in fed conditions, both in water medium). Notably, under fasting conditions, this correlation exhibited superior performance compared to convolution, deconvolution, and Wagner-Nelson methods. However, under fed conditions, all four methods demonstrated satisfactory correlations. The mPBPK model can accurately predict the plasma concentration-time curves under both fasted and fed conditions, and provides a new perspective for establishing in vivo-in vitro correlations of drug products such as incomplete in vivo release, sustained/controlled release, and poor absorption.

The administration of the investigated metabiotic feed additive to calves demonstrated a positive impact on growth performance. The inclusion of this additive into the diet, which comprised culture fluids with metabolites from Bacillus pumilus B-13250 and Kluyveromyces lactis in a 50:50 ratio, resulted in a statistically significant increase in the live weight of the experimental group compared to the control group. By the end of the first month, the experimental calves were heavier by 4.5 kg (7.2 %, p < 0.05). This difference increased to 7.6 kg (9.3 %, p < 0.05) at the end of the second month and reached 15.2 kg (14.7 %, p < 0.001) by three months of age. The average daily gain (ADG) during the initial application period (0–1 month) was significantly higher in the experimental group by 123.8 g (20.3 %, p < 0.01). From the first to the second month, the ADG remained significantly elevated by 100.0 g (16.2 %, p < 0.01), and between the second and third months, the ADG in the experimental group was 995.2 g, which exceeded the control by 257.1 g (34.8 %, p < 0.001). Furthermore, the calf survival rate was 100 % in the experimental group, compared to 90 % in the control group. The specific metabolite ratio from B. pumilus and K. lactis also positively modulated the gut microbiota in the large intestine, leading to a 6.7 % increase in mesophilic aerobic and facultative anaerobic microorganisms, a 93.5 % rise in lactic acid bacteria, alongside a 52.2 % reduction in coliform bacteria and a 16.7 % decrease in microscopic fungi.

Nonsteroidal anti-inflammatory drugs (NSAIDs), particularly Ibuprofen, are widely used for their analgesic and anti-inflammatory properties. However, irrational or prolonged use may lead to gastrointestinal injury, including NSAID-induced colitis, due to the inhibition of protective prostaglandins in the mucosa. Syzygium polyanthum (bay leaf) extract contains flavonoids, tannins, saponins, and essential oils with antioxidant and anti-inflammatory properties, making it a potential agent for improving mucosal damage in the colon. Objective to determine the effect of bay leaf (Syzygium polyanthum) extract on the histopathological features of the colon in Sprague Dawley rats induced with Ibuprofen. This study was an experimental laboratory research using a posttest-only control group design. Thirty male Sprague Histopathological assessment of the colon was performed across five fields of view using the scoring system. Data were analyzed using the Kruskal–Wallis test followed by the Mann–Whitney test. The positive control group exhibited severe mucosal damage with extensive epithelial erosion and inflammatory infiltration. The P1 group (50 mg/kgBW) showed moderate improvements, while the P2 group (150 mg/kgBW) demonstrated reduced inflammation and ulceration. The highest dose group, P3 (250 mg/kgBW), showed the most prominent mucosal recovery, with significantly milder lesions compared to other groups. Bay leaf extract significantly improves the histopathological condition of the colon in Ibuprofen-induced rats. Higher doses of the extract result in better mucosal healing and reduced tissue damage.

Diabetes mellitus (DM) is associated with gastrointestinal complications, including structural and functional changes in both small and large intestine. CDC42, a Rho GTPase, plays a critical role in maintaining epithelial integrity through regulation of tight junctions and cytoskeletal organization. Moreover, CDC42 expression has been reported in inflammatory bowel disease (IBD). However, its expression patterns and regulatory mechanisms in the diabetic gut remain poorly defined, particularly in the context of DM - IBD comorbidity. Our study aimed to evaluate histological changes and CDC42 gene and protein expression in the small intestine (ileum) and large intestine (colon) of streptozotocin-induced female and male Sprague-Dawley rats. Rats were divided in control (n = 10) and diabetic (n = 12) group. Histological analysis was based on hematoxylin-eosin staining sections. CDC42 gene and protein expression were quantified using RT-qPCR, western blotting, and immunofluorescence. Correlation analyses were performed to examine the relationship between CDC42 gene expression and clinical parameters, including blood glucose levels and weight gain, stratified by gender. Histological examination revealed marked inflammatory cell infiltration in both intestinal segments (ileum and colon). CDC42 gene expression was significantly increased in the small and large intestine of diabetic rats, particularly in females (for small intestine p < 0.001; for large intestine p < 0.01), suggesting a gender-specific response potentially mediated by hormonal regulation. Reduced expression of CDC42 was detected at protein level in the colon (p < 0.001). These findings highlight a differential expression of CDC42 in the small and large intestine under diabetic conditions. Since CDC42 expression in our study has been found to be related to the intestinal changes under diabetic conditions, future research should be directed towards CDC42 modulation to reduce the pathological changes in the intestine. Getting better insight in CDC42 molecular pattern related to IBD and DM, and development of strategies for its modulation, could be beneficial in clinical setting to control both IBD and DM disease progression.

Diabetes mellitus and inflammatory bowel disease are chronic inflammatory disorders characterized by immune dysregulation and rising global prevalence. Epidemiological studies increasingly suggest a bidirectional association between the two conditions, linked through shared mechanisms of intestinal barrier dysfunction, microbial dysbiosis, and sustained innate immune activation. Activated macrophages play a central role in driving mucosal inflammation through polarization toward a pro-inflammatory M1 phenotype, accompanied by increased production of inflammatory cytokines. These mediators disrupt tight junctions, induce epithelial apoptosis, and perpetuate cycles of immune activation and tissue injury. This macrophage-cytokine axis not only amplifies local inflammation but also sustains chronic barrier dysfunction, creating a pathogenic overlap between diabetes mellitus-associated intestinal injury and intestinal bowel disease. In this study, we used a low dose streptozotocin and high-fat diet-induced diabetic Sprague-Dawley rat model in both sexes to investigate the effects of chronic hyperglycemia on intestinal inflammation, with particular emphasis on macrophage activation and pro-inflammatory cytokine responses. We found inflammation in both small and large intestines with mucosal injury and barrier disruption, and immune activation involving macrophages and enhanced expression of CD68, iNOS, TNF-α, and IL-6. Female rats were more susceptible to gut-related inflammatory changes due to diabetes. These findings suggest a complex interplay between epithelial stress, immune signaling, and microbial factors supporting the role of intestinal inflammation in the immune-metabolic interaction in diabetes-associated intestinal changes, which may contribute to the pathogenesis of inflammatory bowel disease.

Escherichia coli is a Gam-negative, short rod-shaped, non-spore-forming bacterium that normally inhabits the human intestine. However, when its population exceeds the normal limit or when it relocates from its natural habitat (the large intestine) to other parts of the body, it can pose a serious health risk. Numerous reports have indicated increasing antibiotic resistance in E. coli, which has encouraged the use of natural products for disease prevention and treatment. Honey and red ginger (Zingiber officinale var. rubrum) are among the natural ingredients known to contain antibacterial compounds such as polyphenols, flavonoids, glycosides, and phenolic derivatives including gingerol and shogaol. This study aimed to determine the inhibitory activity of Amfoang honey enriched with red ginger extract (Zingiber officinale var. rubrum) against the growth of Escherichia coli. Red ginger extracts at concentrations of 25%, 50%, 75%, and 100% were mixed with wild honey in a 1:1 ratio. Antibacterial testing was conducted using the disc diffusion method. Amoxicillin 30 µg served as the positive control, while a blank disc soaked in sterile distilled water was used as the negative control. After 24 hours of incubation, inhibition zone diameters were recorded as 24.1 mm, 25.0 mm, 24.0 mm, and 15.8 mm for concentrations of 25%, 50%, 75%, and 100%, respectively. These results indicate that the 50% concentration produced the geatest antibacterial activity, with an inhibition zone of 25.0 mm.

Bovine coronavirus (BCoV) causes neonatal calf diarrhea, winter dysentery, and respiratory disease worldwide. However, its primary replication site remains uncertain, and systemic studies on tissue tropism are limited. We, therefore, intranasally inoculated colostrum-fed Holstein calves (6-13-day-old) with a BCoV isolate derived from diarrheic calf, and monitored clinical signs, gross and histopathological lesions, antigen distribution, and viral replication in multiple tissues. All calves were seropositive before challenge. Infected animals developed diarrhea without respiratory manifestations. Viral RNA appeared first in nasal swabs and subsequently in feces, yet viral load in nasal secretions was not associated with clinical signs. Apart from enlargement of the mesenteric lymph nodes, no characteristic gross lesions were observed. Digital RT-PCR and immunohistochemistry detected BCoV in tonsil, trachea, lung, liver, kidney, abomasum, and both small and large intestines, indicating epithelial tropism at each site. Although the inoculum originated from a diarrheic calf, histopathology revealed enteritis, mild interstitial pneumonia, tonsillitis, and hepatitis. These data indicate that BCoV initiates replication in respiratory epithelia and subsequently disseminates to the digestive tract, with no correlation between gross pathology and viral detection. We conclude that BCoV exhibits broad tissue tropism and may contribute to disorders beyond classical respiratory and enteric disease, thereby refining the current understanding of BCoV pathogenesis.

P0100Role of Ethyl Pyruvate on Large Intestinal Inflammatory and Oxidative Markers in TNBS-Induced Colitis

A first comprehensive quantification of microplastic contamination in the gastrointestinal tract of endangered caspian seals (Pusa caspica) from the Caspian Sea.

Targeted deletion of Cyp24a1 in the intestine reduces mucosal injury and preserves epithelial proliferation after 5-fluorouracil treatment.

Sigmoid colon and rectum represent the distal segments of the large intestine. Their associated anatomical variants usually identified incidentally during radiological or surgical interventions. The present report details right-sided mega sigmoid colon associated with elongated rectum (abdominal-pelvic rectum) observed in a 51-year-old formalin embalmed male cadaver. This existence highlights attention during planning and implementation of radiological and surgical procedures involving the lower abdomen and pelvic visceral.

Hemorrhoidal disease is ranked first amongst diseases of the rectum and large intestine, of which more than 4 are symptomatic.

Microbiological study of wounds and large intestine of sturgeons using β‑cyclodextrin complex with levofloxacin

Short-chain fatty acids are organic acids manufactured by the gut microbiota. The type and amount of microflora in the colon, the source of substrate and the transition period through the intestine affect the rate and amount of Short-chain fatty acids production. Ferrostatin-1, a synthetic compound and a potent inhibitor of ferroptosis, is an antioxidant capable of inhibiting ferroptosis. Paclitaxel is a type of chemotherapy called taxane and causes peripheral neuropathy as a side effect of cancer treatment. In this study, we researched the effect of paclitaxel and ferrostatin-1 administration on fecal Short- chain fatty acids. For this purpose, rats were divided into four groups as control (n = 6), paclitaxel (n = 8), ferrostatin (n = 9) and paclitaxel + ferrostatin (n = 9). Paclitaxel (10 mg/kg) and ferrostatin-1 (5 mg/kg) were administered intraperitoneally once a week for 4 weeks. At the end of the experiment, the amounts of Short-chain fatty acids (acetate, propionate and butyrate) and branched-chain fatty acids (iso-butyrate and iso-valerate) in the feces were determined by gas chromatography. According to the results obtained, acetate level increased significantly (P &lt; 0.05) in Ferrostatin-1 treated group compared to control group and total Short-chain fatty acids level increased significantly (P &lt; 0.05) in Ferrostatin-1group compared to Ferrostatin-1 + Paclitaxel group. Although statistically insignificant, it was observed that ferrostatin-1 increased all the Short-chain fatty acids except butyrate, while paclitaxel decreased all the Short-chain fatty acids. The findings of this study suggest that ferrostatin-1 and paclitaxel may affect the functions of microorganisms in the large intestine and thus the amount of microbial Short-chain fatty acids. In addition, it is clear that therapeutic targeting of these specific bacteria, and thus the produced Short-chain fatty acids, will be important for successful treatment regimens and improved quality of life, especially in cancer patients, and may improve treatment outcomes.

Pelvic Floor Disorders (PFDs) are a common problem affecting women of various ages. Pelvic floor defects are one of the entities that belong to pelvic floor disorders. Each pelvic floor defect is caused by specific damage to the anatomical and functional integrity of the pelvic floor. Understanding the underlying pathological anatomy is crucial for the proper therapeutic approach in treating this condition. Pelvic organ prolapse refers to the descent of pelvic organs into or through the vaginal canal. This includes the bladder, uterus, vaginal vault, small intestine, and large intestine. There are three groups of prolapse: anterior, posterior, and apical. Prolapses occur due to damage to the fibromuscular support system known as the endopelvic fascia, which maintains the pelvic organs in their normal position. To understand the normal statics of pelvic organs, the concept of DeLancey’s levels of support—comprising three levels—is essential. The first level of support consists of the cardinal and uterosacral ligaments. The second level of support consists of the pubocervical and rectovaginal fascia. The third level of support consists of the connection of the vagina to surrounding structures. Each prolapse occurs due to damage to individual levels of support. Thus, defects of the endopelvic fascia have been recognized as key in the pathophysiology of pelvic organ prolapse. Pelvic floor defects often impair the normal mechanisms of maintaining continence, resulting in urinary incontinence as a common symptom of this condition. Only by repairing such damage and restoring the original anatomical relationships can success in surgical therapy be achieved. The aim of this paper is to describe in detail the anatomy of each defect with the purpose of creating a foundation for diagnostic and therapeutic approaches.

Aeromonas caviae, Gram-negative bacteria ubiquitous in the environment, are an emerging human pathogen associated with various infectious diseases, particularly gastroenteritis. Despite recent studies demonstrating A. caviae is the most predominant Aeromonas species underlying human infection, A. caviae remains understudied, and no A. caviae-specific virulence factors associated with human disease have been identified. To identify A. caviae-specific putative virulence factors, we conducted comparative genomic analyses among clinical Aeromonas isolates (n = 431), which identified a variant of flgB, predicted to encode a polar flagellum machinery protein, as over-represented in A. caviae isolates. To examine the role of flgB in virulence and host-pathogen interactions, we generated an A. caviae flgB deletion mutant and genetic complementation constructs. Swimming motility and polar flagella assembly were abolished in the mutant and functionally rescued with genetic complementation. As it remains unknown where A. caviae infects the human gastrointestinal tract, we assessed host-pathogen interactions in HT-29 and Caco2 human intestinal cell lines, representative of the large and small intestine, respectively. Deletion of flgB significantly decreased bacterial adherence in only HT-29 cells and also decreased production of proinflammatory cytokines, IL-8, IL-13, IL-1β, and IL-6, by both cell types. Given the lack of relevant mammalian models for studying most enteric pathogens in vivo, we characterized in vivo virulence in a Galleria mellonella larval survival model, where the flgB deletion modestly attenuated virulence. Deletion of flgB altered aspects of virulence and host-pathogen interactions, and this study provides a framework for identification and characterization of A. caviae-specific putative virulence factors.IMPORTANCEAeromonas caviae is an emerging human bacterial pathogen associated with gastroenteritis, wound infections, and numerous other infectious diseases. Recent studies demonstrate that A. caviae accounts for the greatest burden of human Aeromonas infections. Despite this, A. caviae is understudied as a human pathogen. To address this gap in knowledge, this study characterizes A. caviae-specific virulence genes. We examined 431 clinical Aeromonas isolates using comparative genomics and identified and functionally characterized a putative A. caviae-specific virulence factor, flgB. Genetic deletion of flgB in A. caviae resulted in deficiencies in bacterial motility, adherence, host-cell proinflammatory cytokine production, and in vivo virulence in an invertebrate model. This work establishes the foundation for further study of additional A. caviae-specific virulence factors.

Stiffening of the extracellular matrix underlying the epithelial cells of the large intestine is associated with aging as well as many diseases. Yet the impact of the stiffened matrix on epithelial physiology remains poorly understood. A 2D and 3D microphysiological model of the large intestine was developed using a collagen scaffold with a physiologic or excessive stiffness (Young's moduli of 2.84 ± 0.85 kPa and 15.9 ± 0.73 kPa) by altering the collagen concentration within the substrate. Diffusion of a 10 and 40 kDa fluorescent dextran was significantly different between the physiologic and stiff scaffold (97.8 vs 79.8µm2s-1[10 kDa] and 68.2 vs 56.8µm2s-1[40 kDa], respectively). When primary human epithelial cells of the large intestine were grown as a 2D monolayer, cultures on the physiologic scaffold grew to a significantly higher density with more proliferative and fewer differentiated cells than cultures on the stiffened scaffold. Three-dimensional crypt arrays were also fabricated with the physiologic and stiff substrates, populated with cells, and a growth factor gradient applied. The cell density, proliferation, and height-to-width ratio was significantly greater for cells on the physiologic scaffold relative to that of cells on the stiffened scaffolds. Placement of a layer of intestinal fibroblasts below the epithelium on the crypt arrays did not mitigate the impact of the stiffened substrate. Bulk-RNA sequencing revealed 378 genes that were significantly upregulated and 385 genes significantly downregulated in the stiffened vs physiologic scaffolds. This work demonstrates that a molded collagen hydrogel can be used to mimic the biophysical characteristics of a stiffened intestinal stroma, recapitulating physiology observedin vivo. Thisin vitromodel of polarized crypts with a tunable underlying substrate will enable an improved understanding of intestinal epithelial cell morphology, stem cell maintenance and lineage allocation within a stiffened environment.

Lymphoma is a common neoplasm in cats, in which alimentary lymphoma is a common subtype, and it is usually diagnosed in elderly, feline leukemia virus (FeLV)-negative cats. This study aimed to describe the pathological features of lymphoma with involvement of the alimentary tract in FeLV-antigen-positive cats. In a 12-year retrospective study, 32 necropsied and FeLV-infected cats with lymphoma affecting the alimentary tract were identified. Twenty-one cases were multicentric lymphomas with secondary involvement of the alimentary tract, and the remaining 11 cats were considered to have primary alimentary lymphoma. The small intestine was the most common anatomic location (23/32; 72%), followed by the large intestine (19/32; 59%) and stomach (18/32; 56%). In 22/32 cases (69%), multiple organs within the alimentary tract were concomitantly affected. Thickening of the intestinal and gastric walls was the most common gross lesion (23/32; 72%), while mural nodules were observed in 16/32 cats (50%). The mesenteric lymph nodes were frequently affected (22/32; 69%). Most lymphomas were composed of large (17/32; 53%) and intermediate cells (14/32; 44%). B-cell lymphomas were more frequent (24/32; 75%), and diffuse large B-cell lymphoma was the most common diagnosis (15/32; 47%). In 31/32 (97%) cases, FeLV gp70 antigen was detected in neoplastic lymphocytes by immunohistochemistry. Lymphomas affecting the alimentary tract may be observed in FeLV-infected, young adult cats, in which large to intermediate cell and B-cell lymphomas are more frequently observed, and small cell T-cell intestinal lymphoma is unlikely to be diagnosed.