Adsorption of thallium(I) on rutile nano-titanium dioxide and environmental implications

Rutile nano-titanium dioxide (RNTD) characterized by loose particles with diameter in 20–50 nm has a very large surface area for adsorption of Tl, a typical trace metal that has severe toxicity. The increasing application of RNTD and widespread discharge of Tl-bearing effluents from various industrial activities would increase the risk of their co-exposure in aquatic environments. The adsorption behavior of Tl(I) (a prevalent form of Tl in nature) on RNTD was studied as a function of solution pH, temperature, and ion strength. Adsorption isotherms, kinetics, and thermodynamics for Tl(I) were also investigated. The adsorption of Tl(I) on RNTD started at very low pH values and increased abruptly, then maintained at high level with increasing pH >9. Uptake of Tl(I) was very fast on RNTD in the first 15 min then slowed down. The adsorption of Tl(I) on RNTD was an exothermic process; and the adsorption isotherm of Tl(I) followed the Langmuir model, with the maximum adsorption amount of 51.2 mg/g at room temperature. The kinetics of Tl adsorption can be described by a pseudo-second-order equation. FT-IR spectroscopy revealed that -OH and -TiOO-H play an important role in the adsorption. All these results indicate that RNTD has a fast adsorption rate and excellent adsorption amount for Tl(I), which can thus alter the transport, bioavailability and fate of Tl(I) in aqueous environment

Cornuside ameliorated experimental autoimmune encephalomyelitis by limiting the recruitment of CD4+ T lymphocytes in the spinal cord

We conducted this study to determine whether cornuside could improve the neurological deficit symptoms of experimental autoimmune encephalomyelitis (EAE) rats, as well as determine the potential involvement of CD4+ T lymphocytes, vascular cell adhesion molecule-1 (VCAM-1), intercellular adhesion molecule-1 (ICAM-1), and tumor necrosis factor-α (TNF-α). Altogether, 32 Lewis rats were randomly divided into control, EAE, EAE/prednisolone, and EAE/cornuside, wherein their neurological function was assessed every day. CD4+ T lymphocyte recruitment into the spinal cord (SC) was evaluated using immunohistochemistry. The VCAM-1, ICAM-1 and TNF-α mRNA expressions in the SC were determined by real-time quantitative PCR, and the VCAM-1 and ICAM-1 proteins were determined by western blotting. Compared to the control group, the EAE group rats with neurological deficits had enhanced CD4+ T lymphocyte infiltration and higher expression levels of VCAM-1, ICAM-1, and TNF-α in the SC. Meanwhile, compared with the EAE group, the EAE/cornuside and EAE/prednisolone groups had lower neurological scores, less CD4+ T lymphocyte infiltrations, and lower expression levels of VCAM-1, ICAM-1, and TNF-α in the SC. Thus, cornuside ameliorated EAE, which could be owed to the inhibition of CD4+ T lymphocyte recruitment and VCAM-1, ICAM-1, and TNF-α expressions in the SC

Low-Copy Number Polymorphism in DEFA1/DEFA3 Is Associated with Susceptibility to Hospital-Acquired Infections in Critically Ill Patients

DEFA1/DEFA3, genes encoding human neutrophil peptides (HNP) 1–3, display wide-ranging copy number variations (CNVs) and is functionally associated with innate immunity and infections. To identify potential associations between DEFA1/DEFA3 CNV and hospital-acquired infections (HAIs), we enrolled 106 patients with HAIs and 109 controls in the intensive care unit (ICU) and examined their DEFA1/DEFA3 CNVs. DEFA1/DEFA3 copy number ranged from 2 to 16 per diploid genome in all 215 critically ill patients, with a median of 7 copies. In HAIs, DEFA1/DEFA3 CNV varied from 2 to 12 with a median of 6, which was significantly lower than that in controls (2 to 16 with a median of 8, p=0.017). Patients with lower DEFA1/DEFA3 copy number (CNV < 7) were far more common in HAIs than in controls (52.8% in HAIs versus 35.8% in controls; p=0.014; OR, 2.010; 95% CI, 1.164–3.472). The area under the receiver operating characteristic (AUROC) of DEFA1/DEFA3 CNV combined with clinical characteristics to predict the incidence of HAIs was 0.763 (95% CI 0.700–0.827), showing strong predictive ability. Therefore, lower DEFA1/DEFA3 copy number contributes to higher susceptibility to HAIs in critically ill patients, and DEFA1/DEFA3 CNV is a significant hereditary factor for predicting HAIs