Identification of reproductive and molecular biomarkers associated with clinical metritis in dromedary camels (Camelus dromedarius)

Nucleotide sequence variations, gene expression profiles, and host biomarkers associated with ovine mange caused by Sarcoptes and Psoroptes mites: implications for diagnosis and disease control

Introduction Ovine mange is a highly contagious skin disease that causes substantial economic losses. This study assessed the prevalence, SNPs, gene expression, serum APPs, and immune and antioxidant markers to elucidate the immunological and oxidative mechanisms of mange in Barki sheep. Methods A total of 320 adult Barki ewes were enrolled in the study, comprising 80 clinically affected animals and 240 apparently healthy controls. Blood samples were collected from all animals for the determination of acute-phase proteins, immunological and antioxidant biomarkers, and gene expression analyses of CARD9, CLEC7A, TNFAIP3, IL33, SESN2, ATF4, HSPA1A, and SLC7A11. Only clinically affected sheep underwent parasitological confirmation by microscopic examination of deep skin scrapings collected from active skin lesions to identify mange mites. Results Microscopic examination confirmed mange in 25% (80/320) of the ewes, with Sarcoptes spp. accounting for 75% and Psoroptes spp. for 25% of the cases. Infected sheep showed upregulation of CARD9, CLEC7A, IL33, SESN2, ATF4, and HSPA1A, and downregulation of TNFAIP3 and SLC7A11 (p < 0.05), with 14 SNPs differing significantly between the healthy and infected groups. Infected animals showed elevated APPs, pro-inflammatory cytokines, and oxidative stress, with reduced IL-10 levels. Conclusion Ovine mange is associated with distinct molecular, immunological, and oxidative stress responses that reflect the host’s reaction to mite infestation. To our knowledge, this is the first study to integrate transcriptional profiling with SNP characterization of CARD9, CLEC7A, TNFAIP3, IL33, SESN2, ATF4, HSPA1A, and SLC7A11 in naturally occurring ovine mange. The identified sequence variants, together with gene expression signatures, provide novel candidate molecular biomarkers for disease susceptibility and may support future genetic selection and precision disease management strategies. Additional studies involving larger and independent sheep populations are needed to validate these findings and determine their potential value in disease susceptibility assessment and genetic improvement programs.

Identification and Validation of Genes Involved in Immune and Ferroptosis in Polycystic Ovarian Syndrome Using Bioinformatics and Experimental Approach.

BACKGROUND Polycystic ovary syndrome (PCOS) is a highly prevalent endocrine and metabolic disease. This study aimed to investigate the synergistic role of immune dysregulation and ferroptosis during the pathogenesis of PCOS. METHODS Through integrating multiple Gene Expression Omnibus (GEO) datasets, differentially expressed genes (DEGs) were screened and subjected to functional enrichment analysis; weighted gene co‑expression network analysis combined with LASSO, RandomForest, and support vector machine‑recursive feature elimination algorithms were employed to identify key candidate genes; in vitro, human ovarian granulosa cells (KGN) were treated with dihydrotestosterone (DHT), NNMT expression was regulated via lentiviral vectors together with ferroptosis inhibitor intervention, and cell viability, cytotoxicity, and ferroptosis‑related indicators were examined; in vivo, a PCOS mouse model was established using dehydroepiandrosterone, and ovarian pathology, hormone levels, as well as molecular expression of the ferroptosis pathway were analyzed. RESULTS DEGs in PCOS were significantly enriched in immune response and ferroptosis pathways. Twelve candidate genes were identified through screening multiple GEO datasets and demonstrated diagnostic potential. DHT induced ferroptosis in KGN cells by upregulating NNMT, manifesting as reduced cell viability, increased LDH release, accompanied by Fe²⁺ accumulation, enhanced lipid peroxidation, downregulation of SLC7A11/GPX4, and upregulation of ACSL4. This process could be partially reversed by ferroptosis inhibitors. Knockdown of NNMT effectively alleviated the DHT‑induced ferroptosis phenotype. Ovaries from PCOS mice exhibited typical pathological alterations, concurrent with elevated NNMT expression and abnormal activation of the ferroptosis pathway. CONCLUSION This study has uncovered novel mechanisms underlying the development and progression of PCOS, offering potential targets for its diagnosis and treatment.

Unraveling the Molecular Landscape of Follicular Fluid: A Comparative Proteomic Study Between Bali and Brahman Cattle

Background Protein biomarkers are increasingly recognized as indicators of metabolic status, immune response, and reproductive performance in cattle. However, comparative data among different breeds commonly raised in Indonesia remain limited. Objectives This study aimed to compare the specific proteins in follicular fluid (FF) of Bali and Brahman cows. Methods Samples from FF (n = 20 pairs of ovarium) were analyzed for identification of specific proteins using LC–HRMS analysis. Results Proteomic analysis revealed distinct breed‐specific FF profiles, with 16 proteins uniquely identified in Bali cattle and 23 proteins in Brahman. Bali FF was enriched with proteins associated with protease inhibition, coagulation regulation, extracellular matrix remodeling, and cytoskeletal dynamics, including CORO1C, ZER1, YARS1, and L3MBTL3. In contrast, Brahman FF showed enrichment of proteins involved in lipid oxidation, one‐carbon metabolism, and peroxisomal activity, notably ACOX2, BHMT, and KIAA0586. Conclusion Here, we present the proteomic characterization of FF from Bali and Brahman cattle, where several bioactive proteins are candidate proteins potentially associated with reproductive processes. These findings highlight the potential of protein biomarkers in guiding cattle breeding and management strategies in tropical regions.

Exploring the Association of TMPRSS6 rs1421312 Variant with Hepcidin, sTfR1, and Iron Deficiency Anemia in Reproductive-Age Women

It is concluded that no detectable association was found between the TMPRSS6 rs1421312 SNP and IDA, and no detectable associations were found with Hepcidin levels, sTfR1, or the sTfR1-Ferritin Index.

Evaluation of gastrointestinal biomarkers in jaguars (Panthera onca) housed in zoologic institutions from 1992 to 2025

A previous study showed that the feline trypsin-immunoreactivity assay (fTLI) does not crossimmunoreact with cheetahs, and cobalamin and folate concentrations were well below the reference interval limits for domestic cats, but this has not been evaluated in jaguars.4 The objective of this study was to obtain gastrointestinal (GI) biomarker measurements in jaguars under managed care, compare the values to the domestic cat reference range, and determine their validity for future medical protocols. Serum samples from participating institutions were submitted to the GI Lab at Texas A&M University to measure serum concentrations of cobalamin, folate, fTLI, and feline pancreatic lipase immunoassay. Any documented GI medical conditions were also recorded. Results (n = 104) were analyzed from 72 jaguars (28 males and 44 females; 1.25–23 yr old) and compared with reference intervals established in domestic cats.14–16 The majority of results for pancreatic-like immunoassay (n = 68) were within reference intervals for domestic cats (median 0.4 µg/L, range 0.3–4.3), but many samples tested for cobalamin (n = 63; mean 199 ng/L; range 149–290), fTLI (n = 62; median 7.4 µg/L; range 0.1–11.7) and folate concentrations (n = 54; median 5.5 µg/L; range 1.04–34.2) were below them. All jaguars with abnormal fTLI concentrations lacked clinical signs associated with exocrine pancreatic insufficiency, such as poor hair coat, weight loss, or malodorous feces. This study demonstrated that domestic cat reference intervals for GI biomarkers such as cobalamin and fTLI are most likely not valid for jaguars as well.

[Study of a patient with azoospermia due to variant of MOV10L1 gene].