With the development of straw baling mechanization technology, straw is stored in the form of square baling or round baling. At present, hammer mill or the guilt-cutting and rubbing combined mill is widely used to crush square bales of straw. These two kinds of crushing equipment have disadvantages such as low productivity, large power consumption, and poor crushing effect. This paper aims to study and analyze the crushing characteristics of square baled straw after unbaling, and lay a theoretical foundation for the later research and development of a special square baled straw crusher with high productivity, low power consumption, good crushing effect, and the simulation of the square baled corn straw crushing process. For this purpose, this study carried out a corn bale crushing experiment on the Instron 8801 fatigue test machine, and studied the effects of blade angle, water content and loading speed on corn bale crushing force through the response surface method. Test results showed that the crushing process includes the compression stage and shearing stage; in terms of single factor effect, with the increase in water content and blade angle, the crushing force of the corn bale increased, but the loading speed had no significant effect on the crushing force of the corn bale. In terms of interaction effect, there was interaction effect between moisture content and blade inclination angle, when moisture content was 10%, with the increase in blade inclination angle, the incremental speed of the crushing force also increased gradually. When the blade inclination angle was 10°, with the increase in moisture content, the incremental speed of the crushing force also increased, and the interaction effect of them jointly acted on the crushing force of the corn bales.

Tylosin is a commonly used macrolide antibiotic, which is commonly utilized in livestock; its release through animal excrement can have detrimental environmental effects. Biodegradation of tylosin (TYL) is an effective bioremediation method. In this study, we identified a novel and efficient TYL-degrading bacterial strain, Kurthia gibsonii TYL-A1, capable of degrading 75 mg/L of TYL within 5 days at 30°C, pH 7, with 3% inoculum and yeast extract as the nitrogen source. The bacterium degraded 99% of 75 mg/L TYL in 5 days. Both intracellular and extracellular enzymes collaborated to degrade TYL. Metabolites were analyzed by liquid chromatography-mass spectrometry (LC-MS), revealing that strain TYL-A1 could remove mycophenolic sugar, cleave the ester bond, and further degrade TYL into smaller molecules. The toxicity of the degradation products was lower than that of the parent compound and its natural degradation products. Whole-genome sequencing results indicated that genes encoding glycoside hydrolases and glycosyltransferases, along with metabolism-related genes, were involved in TYL degradation. This study elucidated the degradation mechanism of TYL and highlighted the potential of strain TYL-A1 to remove TYL from the environment. IMPORTANCE: Tylosin (TYL) contamination has become a hot issue, and microbial removal systems have been widely considered as an economical and environmentally friendly alternative. Our study proposed a new TYL degradation pathway through the biological metabolic pathway of LC-MS metabolite analysis. Whole-genome sequencing further provided the genetic mechanism involved in the degradation process and explained the degradation effect of strain TYL-A1 on TYL. The application of TYL-A1 to actual wastewater highlights the practical relevance of TYL pollution in the environment. This application highlights the importance of microbial germplasm resources in the bioremediation of TYL-contaminated ecosystems. All in all, our study provides a theoretical basis for reducing the pollution of antibiotics in the environment and promoting the sustainable development of the ecological environment.

Introduction: Fine particulate matter (PM_2.5) is an important factor in the induction of a variety of respiratory diseases and associated cellular damage. The composition of PM_2.5 in the animal farm environments is complex, which poses a significant threat to the respiratory health of both workers and livestock, but the causative mechanisms are unclear.Methods: In order to investigate targeted treatment options, this study focused on the role of microbial components in cowshed PM_2.5-induced respiratory damage. Utilizing the common pathogenic bacteria (Pasteurella multocida) in cowshed PM_2.5 as a perspective, the intrinsic connection and interaction mechanism between PM_2.5 particles and bacterial components were explored through in vivo and in vitro experiments. Bacterial components can interact with PM_2.5 and are important factors in the respiratory toxicity of PM_2.5 in farm animal environments by scanning electron microscopy (SEM), Fourier infrared spectroscopy (FTIR) and Zeta potential measurements.Results: We demonstrate that Bacteria adhered to PM_2.5 particles and modified the original surface functional groups characteristics, significantly enhanced toxic effects of PM_2.5 on cells (including oxidative stress levels, release of inflammatory factors, etc.). Furthermore, PM_2.5 particles significantly enhanced bacterial intracellular invasion, initiated the guanylate-binding protein 2 (GBP2)-mediated intracellular bacterial defense mechanism, further triggered the non-canonical NLRP3 pathway, and ultimately induced a cascade of inflammatory responses and pyroptosis. To explore therapeutic strategies, siRNA silencing of GBP2 and inhibition of NLRP3 were done; GBP2 silencing initially delayed cytotoxicity, but eventually increased the inflammatory response. However, inhibition of NLRP3 expression maintained cell viability and delayed pyroptosis, with potential as an effective solution for treatment of PM_2.5-induced lung injury in farm-animal environments.Conclusion: In conclusion, the results of this study demonstrated the interaction between particulate matter and bacteria during cowshed PM_2.5-induced respiratory injury and clarified the signaling mechanisms among intracellular bacteria, GBP2, NLRP3, and pyroptosis. These findings provide a theoretical basis for developing therapeutic strategies against PM_2.5-related respiratory diseases in farm-animal environments.

Fine particulate matter (PM2.5)-induced ovarian damage has attracted widespread attention, but differences in cytotoxicity and underlying mechanisms of water-soluble (WS-PM2.5) and water-insoluble (WIS-PM2.5) fractions are unclear. To investigate potential effects of PM2.5 from livestock farming environments on animal ovaries, PM2.5 samples were collected from large-scale cattle barns. There were significant differences between fractions regarding elemental composition, proportion of water-soluble ions, polycyclic aromatic hydrocarbon content, and endotoxin concentrations. Based on transcriptome sequencing results, in a cowshed PM2.5 exposure model (rats), differentially expressed ovarian mRNAs were significantly enriched in signaling pathways such as cytokine interaction and the Hippo pathway, with the expression of thioredoxin-interacting protein (Txnip) significantly increased. In vitro (primary rat ovarian granulosa cells), short-term exposure to WS-PM2.5 (12 h) significantly induced inflammatory factor release, acute oxidative stress, mitochondrial dysfunction, and intracellular Ca²⁺ overload, with characteristics of rapid acute injury. However, extended (24 h) WIS-PM2.5 exposure had greater disruptive effects on estrogen homeostasis, intracellular enzyme release (LDH), and mitochondrial structure (subacute characteristics). Furthermore, downregulating Txnip expression via inhibitors effectively mitigated cowshed PM2.5-induced ovarian granulosa cell toxicity, oxidative stress, and mitochondrial and hormonal dysfunction. In summary, solubility of cowshed PM2.5 components affected cytotoxic characteristics, and Txnip was a key factor linking oxidative stress to granulosa cell damage. The study provided a mechanistic basis and potential targets for preventing and controlling PM2.5-induced ovarian damage in livestock environments.

With the increasing prevalence of antibiotic–heavy metal co-contamination in agricultural wastewater, elucidating the antibiotic removal capacity of degrading bacteria under heavy metal stress, as well as their adaptive mechanisms, is of considerable theoretical significance and practical value. In this study, the highly efficient TYL-degrading strain TYL-A1 was selected as a model organism, and the effects of Pb²⁺ exposure on its TYL removal performance, oxidative stress response, cell surface characteristics, and transcriptional regulation were systematically investigated. The results showed that TYL removal remained above 85% after 72 h under a nominal Pb²⁺ concentration of 100 mg/L in the phosphate-containing MSM system. The phosphate may have reduced Pb²⁺ bioavailability. Nominal Pb²⁺ exposure increased the activities of superoxide dismutase (SOD) and catalase (CAT), accompanied by elevated levels of reactive oxygen species (ROS) and malondialdehyde (MDA), as well as a decrease in adenosine triphosphate (ATP) content. This indicates that the strain experienced pronounced oxidative stress and altered energy metabolism. Meanwhile, cell membrane permeability increased. Scanning electron microscopy (SEM) and Fourier-transform infrared spectroscopy (FTIR) analyses showed that the overall cellular morphology remained intact, whereas the membrane surface structure and related cellular components underwent adaptive changes. According to a transcriptomic analysis, the differentially expressed genes were mainly enriched in pathways associated with primary metabolism, transmembrane transport, ABC transporters, and two-component systems. In summary, strain TYL-A1 maintained high TYL removal performance under the tested nominal Pb²⁺ concentrations in the present phosphate-containing culture system, suggesting its potential applicability in the bioremediation of water bodies co-contaminated with antibiotics and heavy metals.

Fine particulate matter (PM_2.5) can directly impact pulmonary epithelial cells, resulting in lung injury. While it is known that PM_2.5 can alter the expression profile of microRNAs in the lung, its specific role in damaging pulmonary epithelial cells remains unclear. This study, therefore, employed RT-qPCR, Western blotting, and dual luciferase reporter assays to investigate the regulatory role of microRNAs in PM_2.5-induced cellular damage. PM_2.5 exposure induces oxidative stress, autophagy, and ferroptosis in rat lung alveolar epithelial cells (RLE-6TN). Further functional rescue experiments confirm that the ferroptosis-specific inhibitor Fer-1 can block PM_2.5-induced ferroptosis. Bioinformatics analysis and validation indicate that miR-212-5p plays a crucial role by negatively regulating RASSF1 through targeted inhibition. Overexpression of miR-212-5p activates the PI3K/AKT signaling pathway, thereby promoting autophagy and ferroptosis. However, when the expression of both miR-212-5p and RASSF1 is suppressed, PM_2.5-induced autophagy and ferroptosis are significantly alleviated by inhibiting the PI3K/AKT/mTOR signaling pathway. Rescue validation experiments demonstrated that, under PM_2.5 exposure combined with RASSF1 overexpression, miR-212-5p exacerbates the aforementioned cellular damage process. This study reveals that miR-212-5p regulates autophagy and ferroptosis by targeting RASSF1. These findings provide a multi-target intervention strategy for PM_2.5-related lung diseases.