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Methionine, as an essential amino acid, play roles in antioxidant defense and the regulation of immune responses. This study was designed to determine the effects and mechanisms of increased consumption of methionine by sows and piglets on the capacity of the progeny to counteract lipopolysaccharide (LPS) challenge-induced injury in the liver and spleen of piglets. Primiparous sows (n = 10/diet) and their progeny were fed a diet that was adequate in sulfur amino acids (CON) or CON + 25% total sulfur amino acids as methionine from gestation day 85 to postnatal day 35. A total of ten male piglets were selected from each treatment and divided into 2 groups (n = 5/treatment) for a 2 × 2 factorial design [diets (CON, Methionine) and challenge (saline or LPS)] at 35 d old. After 24 h challenge, the piglets were euthanized to collect the liver and spleen for the histopathology, redox status, and gene expression analysis. The histopathological results showed that LPS challenge induced liver and spleen injury, while dietary methionine supplementation alleviated these damages that were induced by the LPS challenge. Furthermore, the LPS challenge also decreased the activities of GPX, SOD, and CAT and upregulated the mRNA and(or) protein expression of TLR4, MyD88, TRAF6, NOD1, NOD2, NF-kB, TNF-α, IL-8, p53, BCL2, and COX2 in the liver and (or) spleen. The alterations of GPX and SOD activities and the former nine genes were prevented or alleviated by the methionine supplementation. In conclusion, the maternal and neonatal dietary supplementation of methionine improved the ability of piglets to resist LPS challenge-induced liver and spleen injury, potentially through the increased antioxidant capacity and inhibition of TLR4 and NOD signaling pathway.

The objective of this study was to explore the mechanism of Hedyotis diffusa (HD) in mediating the detoxification of aflatoxin B1 (AFB1)-induced hepatic injury in chicks. A total of 144 one-day-old male broilers (Cobb 500) were randomly assigned to four treatment groups (n = 6 cages/diet, 6 chicks/cage). After three days of acclimation, the broilers were fed either a control diet (Control), Control plus 0.5 mg/kg of AFB1, or Control plus 0.5 mg/kg AFB1 with 500 or 1000 mg/kg HD for two weeks. Both serum and liver were collected at the end of the feeding trial for biochemistry, histology, and NF-E2-related nuclear factor 2 (NRF2)/antioxidant response element (ARE) signaling analysis. Compared with Control, the AFB1 treatment caused liver injury and decreased (p < 0.05) body weight gain, feed intake, feed conversion ratio, and serum albumin and total protein by 6.2–20.7%. AFB1 also induced swelling, necrosis, and severe vacuolar degeneration in chicks’ livers. Notably, HD supplementation at 500 and 1000 mg/kg mitigated (p < 0.05) the alterations induced by AFB1. HD supplementation alleviated (p < 0.05) AFB1-induced impairment in hepatic glutathione peroxidase activity, protein carbonyl, and exo-AFB1-8,9-epoxide (AFBO)–DNA concentrations by 57.7–100% and increased (p < 0.05) the activities of superoxide dismutase and catalase by 23.1–40.9% more than those of AFB1 treatment alone. Furthermore, HD supplementation at the two doses upregulated (p < 0.05) NRF2, NAD(P)H: quinone oxidoreductase-1, heme oxygenase-1, glutathione cysteine ligase catalytic subunit, and glutathione-S transferase A2 and A3 in livers relative to the AFB1 group by 0.99–3.4-fold. Overall, dietary supplementation of HD at a high dose displayed better protection effects against aflatoxicosis. In conclusion, a dietary HD supplementation at 500 and 1000 mg/kg protected broilers from AFB1-induced hepatotoxicity, potentially due to the activation of NRF2/ARE signaling in the chicks.

Staphylococcus aureus is the most common cause of bacterial arthritis in broiler breeder chickens. In this study, we established a model of broiler breeder chicken arthritis inoculated with Staph. aureus isolated from a spontaneously occurring bacterial arthritis in chickens. We evaluated the model by bacteriology, serology, pathology, and immunology. The results showed that 2.5 × 109 cfu Staph. aureus injected into the right joint cavity can successfully induce a chicken arthritis model. The majority of the infected chickens suffered lameness and joint swelling at 3 days post-inoculation (DPI). The death peak time was on 7 DPI and the mortality rate was 51.1%. Staph. aureus can be continuously isolated from the blood and left joint synovial fluid of the infected chickens. Lesions found on the infected chickens consisted of swollen joints full of caseous exudates, cartilage injury, and synovial membrane thickening with infiltration of inflammatory cells. The center of the lesion contained many round bacterial cocci. With joint injury aggravation, intra-articular hyaluronic acid gradually decreased, and serum interleukin-6 became significantly higher compared with the control (P

In this work, robust approach for a highly sensitive point-of-care virus detection was established based on immunomagnetic nanobeads and fluorescent quantum dots (QDs). Taking advantage of immunomagnetic nanobeads functionalized with the monoclonal antibody (mAb) to the surface protein hemagglutinin (HA) of avian influenza virus (AIV) H9N2 subtype, H9N2 viruses were efficiently captured through antibody affinity binding, without pretreatment of samples. The capture kinetics could be fitted well with a first-order bimolecular reaction with a high capturing rate constant kf of 4.25 x 109 (mol/L)-1 s-1, which suggested that the viruses could be quickly captured by the well-dispersed and comparable-size immunomagnetic nanobeads. In order to improve the sensitivity, high-luminance QDs conjugated with streptavidin (QDs-SA) were introduced to this assay through the high affinity biotin-streptavidin system by using the biotinylated mAb in an immuno sandwich mode. We ensured the selective binding of QDs-SA to the available biotin-sites on biotinylated mAb and optimized the conditions to reduce the nonspecific adsorption of QDs-SA to get a limit of detection low up to 60 copies of viruses in 200 μL. This approach is robust for application at the point-of-care due to its very good specificity, precision, and reproducibility with an intra-assay variability of 1.35% and an interassay variability of 3.0%, as well as its high selectivity also demonstrated by analysis of synthetic biological samples with mashed tissues and feces. Moreover, this method has been validated through a double-blind trial with 30 throat swab samples with a coincidence of 96.7% with the expected results. [ABSTRACT FROM AUTHOR]

The article presents the study of Chang-qing Xie and colleagues regarding the impact of chlorine on the expression of aquaporin-4 in the organs of KunMing mouse using immunohistochemical method.

The emergence of variant pseudorabies virus caused great economic losses in domestic farms in the recent past. The mice were infected with Halv strain PRV via intragastric administration, intranasal and subcutaneous into the cervical skin to study the Pseudorabies in mouse model. The gross lesions, microscopic lesions and the distribution of PRV in mice were investigated. All the mice in each group showed exciting and roughening of the fur and frequent scratching. Microscopic lesions included mild-to-severe interstitial pneumonia, hemorrhage and nonsuppurative encephalitis in brain. The distribution of PRV in three groups was different. In intragastric administration group, PRV antigens were distributed in brain hippocampus, medulla oblongata, gray substance spinal cord and intestinal submucosa. In intranasal group, PRV antigens were detected in gray substance spinal cord, pons, myocardial cells, pulmonary epithelial cells and lymphocytes in red pulp of the spleen. In subcutaneous group, the PRV antigens were located in the sensory and motor cortex, prefrontal cortex, gray matter in spinal cord, purkinje cells in the cerebellum and lymphocytes in the splenic red pulp. These findings provided evidence that the distribution of PRV was depended on injected-routes. [ABSTRACT FROM AUTHOR]

Porcine circovirus type 2 (PCV2) is often associated with subclinical infections and swine post weaning multisystemic wasting syndrome (PMWS). In the present study, 28-day-old piglets were inoculated with PCV2, porcine reproductive and respiratory syndrome virus (PRRSV), as well as PCV2+PRRSV. Macroscopic lesions, histologic lesions, virus distribution in tissues were systematically examined. Histologic lesions were found in both single PCV2 and dual PCV2+PRRSV- inoculated piglets, including lymphoid depletion and intracytoplasmic inclusion bodies within histiocytes, as well as bronchointerstitial pneumonia and granulomatous inflammation in the lungs. The lesions were more severe in piglets inoculated with PCV2+PRRSV than in those with PCV2. PRRSV-inoculated piglets showed lymphoid depletion and moderate interstitial pneumonia, but no inclusion body or granulomatous inflammation. PCV2 antigen intensity in many tissues was higher in the coinfection group than in the single PCV2, but PRRSV antigen intensity had no difference between the PRRSV and PCV2+PRRSV groups. Therefore, PCV2, not PRRSV, induced the inclusion bodies and granulomatous inflammation that characterizes PMWS. PRRSV+PCV2 coinfection also promoted the replication of PCV2, but not of PRRSV. [ABSTRACT FROM AUTHOR]

A 14-year-old female Mongrel dog presented with multiple, cherry-sized, wellcircumscribed papillary masses on the right upper hard palate and gingival area. Histologically, the masses contained biphasic components composed of hyperplastic squamous epithelium forming papillary fronds, and underlying tortuous dilated ducts and cysts. Immunohistochemistry demonstrated that both squamous and ducts epithelium were pan-Cytokeratin (pCK) positive, but they were negative of Alpha smooth muscle (α-SMA), Vimentin and Protein 53 (P53). Duct epithelial cells were strong positive of Cytokeratin 8 & 18 (CK8&18), Ki-67, and weakly positive of S-100, whereas squamous component were strong positive of Cytokeratin 5&6 (CK5&6). Sialadenoma papilliferum (SP) was diagnosed based on clinical sign, gross and histopathological findings, and biochemistry. [ABSTRACT FROM AUTHOR]