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The study aimed to investigate the nutritional value of ramie (Boehmeria nivea) silage, and its consequences for chewing activity, rumen fermentation, and enteric methane (CH4) emissions in goats, by comparing it with corn stover (CS) silage. An in vitro ruminal experiment was firstly performed to investigate the substrate degradation and fermentation of CS and ramie silage. The ramie silage diet was formulated by replacing 60% of CS silage with ramie silage (dry matter (DM) basis). Eight female Xiangdong Black goats (a local breed in Southern China, 1 to 1.2 years of age) with BW of 21.0 ± 1.05 kg were used for this experiment and were randomly assigned to either one of the two dietary treatments in a cross-over design. The ramie silage had higher crude protein (CP) and ash content and lower hemicellulose content, together with decreased (p < 0.05) nutrient degradation and methane production and increased (p < 0.05) acetate molar percentage and acetate to propionate ratio through in vitro ruminal fermentation. Feeding the ramie silage diet did not alter feed intake (p > 0.05), decreased (p < 0.05) nutrient digestibility, and increased (p < 0.05) chewing activity and rumination activity, with reductions (p < 0.05) in eating activity and idle activity. Although feeding the ramie silage diet caused a greater (p < 0.05) molar percentage of acetate and lower molar percentage of propionate, it decreased the rumen-dissolved CH4 concentration and enteric CH4 emissions (p < 0.05). Feeding the ramie silage diet did not alter (p > 0.05) the population of bacteria, protozoa, and fungi; it increased the 16S rRNA gene copies of Ruminococcus flavefaciens (p < 0.05). Further 16SrRNA gene amplicon analysis indicated a distinct bacterial composition between the two treatments (p < 0.05). Feeding the ramie silage diet led to a lower abundance of genera Lawsonibacter, Sedimentibacter, Saccharofermentans, Sediminibacterium, and Bifidobacterium (p < 0.05). Ramie can be an alternative forage resource to stimulate chewing activity and reduce CH4 emissions in ruminants.

Background: Colorectal cancer (CRC) is a heterogeneous disease with many somatic mutations defining its genomic instability. Alternative Splicing (AS) events, are essential for maintaining genomic instability. However, the role of genomic instability-related AS events in CRC has not been investigated.Methods: From The Cancer Genome Atlas (TCGA) program, we obtained the splicing profiles, the single nucleotide polymorphism, transcriptomics, and clinical information of CRC. Combining somatic mutation and AS events data, a genomic instability-related AS signature was constructed for CRC. Mutations analyses, clinical stratification analyses, and multivariate Cox regression analyses evaluated this signature in training set. Subsequently, we validated the sensitivity and specificity of this prognostic signature using a test set and the entire TCGA dataset. We constructed a nomogram for the prognosis prediction of CRC patients. Differentially infiltrating immune cells were screened by using CIBERSORT. Inmmunophenoscore (IPS) analysis was used to evaluate the response of immunotherapy. The AS events-related splicing factors (SF) were analyzed by Pearson’s correlation. The effects of SF regulating the prognostic AS events in proliferation and migration were validated in Caco2 cells.Results: A prognostic signature consisting of seven AS events (PDHA1-88633-ES, KIAA1522-1632-AP, TATDN1-85088-ES, PRMT1-51042-ES, VEZT-23786-ES, AIG1-77972-AT, and PHF11-25891-AP) was constructed. Patients in the high-risk score group showed a higher somatic mutation. The genomic instability risk score was an independent variable associated with overall survival (OS), with a hazard ratio of a risk score of 1.537. The area under the curve of receiver operator characteristic curve of the genomic instability risk score in predicting the OS of CRC patients was 0.733. Furthermore, a nomogram was established and could be used clinically to stratify patients to predict prognosis. Patients defined as high-risk by this signature showed a lower proportion of eosinophils than the low-risk group. Patients with low risk were more sensitive to anti-CTLA4 immunotherapy. Additionally, HSPA1A and FAM50B were two SF regulating the OS-related AS. Downregulation of HSPA1A and FAM50B inhibited the proliferation and migration of Caco2 cells.Conclusion: We constructed an ideal prognostic signature reflecting the genomic instability and OS of CRC patients. HSPA1A and FAM50B were verified as two important SF regulating the OS-related AS.