Zwitterionic chitosan, a chitosan derivative with a unique pH-dependent charge profile, was employed to create a stealth coating on the cationic surface of drug carriers. Zwitterionic chitosans were synthesized by amidation of chitosan with succinic anhydride. The succinic anhydride-conjugated chitosan had an isoelectric point, which could be easily tuned from pH 4.9 to 7.1, and showed opposite charges below and above the isoelectric point. The succinic anhydride-conjugated chitosan was able to inhibit the protein adsorption to the cationic surface at physiological pH, compatible with blood components, and well tolerated upon intraperitoneal injection. The succinic anhydride-conjugated chitosan has the potential to serve as a coating material to prevent protein adsorption to cationic surfaces, which can be removed in a pH-responsive manner.

A study was conducted to evaluate the effects of 3 different plant extracts on growth performance and immune responses of weaned pigs experimentally infected with porcine reproductive and respiratory syndrome virus (PRRSV). A total of 64 weaned pigs (7.8 ± 0.3 kg BW), free of PRRSV, were randomly allotted to 1 of 8 treatments in a 2 × 4 factorial arrangement with a randomized complete block design. Pigs were blocked by initial BW. Sex and ancestry were equalized across treatments. The first factor was with or without PRRSV challenge (intranasal dose; 10(5) 50% tissue culture infective dose). The second factor was represented by 4 diets: a nursery basal diet (CON), 10 mg/kg capsicum oleoresin (CAP), garlic botanical (GAR), or turmeric oleoresin (TUR). Pigs were housed in disease containment chambers for 28 d [14 d before and after the inoculation (d 0)]. Blood was collected on d 0, 7, and 14 to measure the total and differential white blood cells (WBC), and serum was collected to measure viral load by quantitative PCR, PRRSV antibody titer, tumor necrosis factor-α (TNF-α), IL-1β, C-reactive protein (CRP), and haptoglobin (Hp) by ELISA. In the unchallenged group, all piglets were PRRSV negative during the overall period postinoculation. All data were analyzed using PROC MIXED of SAS. The PRRSV challenge decreased (P < 0.01) ADG, ADFI, and G:F from d 0 to 14. Feeding TUR improved G:F of the PRRSV-infected pigs from d 0 to 14. The numbers of WBC and neutrophils were decreased (P < 0.05) by PRRSV on d 7 but increased (P < 0.05) by PRRSV on d 14, indicating the PRRSV-infected pigs undergo a stage of weak immune responses. Feeding GAR increased (P < 0.05) B cells and CD8+ T cells of PRRSV-infected pigs compared with the CON. Furthermore, the PRRSV challenge increased (P < 0.05) serum viral load, TNF-α, and IL-1β on d 7 and serum viral load, CRP, and Hp on d 14, but feeding plant extracts to PRRSV-infected pigs reversed (P < 0.05) this increase. Infection with PRRSV increased (P < 0.05) rectal temperature of pigs on d 7, 9, and 11, but PRRSV-infected pigs fed plant extracts had lower rectal temperature (P < 0.05) than pigs fed the CON, indicating feeding plant extracts delayed the fever caused by PRRSV infection. In conclusion, results indicate that supplementation with plant extracts reduces the adverse effects of PRRSV by improving the immune responses of pigs, and the 3 plant extracts tested here show different effects. Supplementation with TUR improved feed efficiency of pigs challenged with PRRSV.

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Bone loss associated with menopause leads to an increase in skeletal fragility and fracture risk. Relevant animal models can be useful for evaluating the impact of ovarian failure on bone loss. A chemically induced model of menopause in which mice gradually undergo ovarian failure yet retain residual ovarian tissue has been developed using the chemical 4-vinylcyclohexene diepoxide (VCD). This study was designed to compare skeletal effects of VCD-induced ovarian failure to those associated with ovariectomy (OVX). Young (28 day) C57Bl/6Hsd female mice were dosed daily with vehicle or VCD (160 mg/kg/d, IP) for 15 days (n = 6–7/group) and monitored by vaginal cytology for ovarian failure. At the mean age of VCD-induced ovarian failure (∼6 wk after onset of dosing), a different group of mice was ovariectomized (OVX, n = 8). Spine BMD (SpBMD) was measured by DXA for 3 mo after ovarian failure and OVX. Mice were killed ∼5 mo after ovarian failure or OVX, and bone architecture was evaluated by μCT ex vivo. In OVX mice, SpBMD was lower than controls 1 mo after OVX, whereas in VCD-treated mice, SpBMD was not lower than controls until 2.9 mo after ovarian failure (p < 0.05). Both VCD-induced ovarian failure and OVX led to pronounced deterioration of trabecular bone architecture, with slightly greater effects in OVX mice. At the femoral diaphysis, cortical bone area and thickness did not differ between VCD mice and controls but were decreased in OVX compared with both groups (p < 0.05). Circulating androstenedione levels were preserved in VCD-treated mice but reduced in OVX mice relative to controls (p < 0.001). These findings support that (1) VCD-induced ovarian failure leads to trabecular bone deterioration, (2) bone loss is attenuated by residual ovarian tissue, particularly in diaphyseal cortical bone, and (3) the VCD mouse model can be a relevant model for natural menopause in the study of associated bone disorders.