Architecting neonicotinoid-scavenging nanocomposite hydrogels for environmental remediation

The ubiquitous presence of neonicotinoid insecticides in the environment poses potential health concerns across all biomes, aquatic systems, and food chains. This global environmental challenge requires robust, advanced materials to efficiently scavenge and remove these harmful neonicotinoids. In this work, we engineered nanocomposite hydrogels based on sustainable cellulose acetate for water treatment. The nanocomposite hydrogels were incorporated with small quantities of polymers of intrinsic microporosity (PIM-1) and graphene oxide (GO). We prepared the hydrogels using green solvents such as Cyrene and MeTHF via simple dropwise phase inversion. High adsorption capacity and fast kinetic behavior toward acetamiprid, clothianidin, dinotefuran, imidacloprid, and thiamethoxam were observed. We also developed a rapid and sustainable ultrasound-assisted regeneration method for the hydrogels. Molecular dynamics of the complex quaternary system revealed the synergistic effects of the components, and the presence of PIM-1 was found to increase the GO surface area available for neonicotinoid scavenging. We demonstrated the robustness and practicality of the nanocomposites in continuous environmental remediation by using the hydrogels to treat contaminated groundwater from the Adyar river in India. The presented methodology is adaptable to other contaminants in both aqueous environments and organic media

IFNβ Protects Neurons from Damage in a Murine Model of HIV-1 Associated Brain Injury.

Infection with human immunodeficiency virus-1 (HIV-1) causes brain injury. Type I interferons (IFNα/β) are critical mediators of any anti-viral immune response and IFNβ has been implicated in the temporary control of lentiviral infection in the brain. Here we show that transgenic mice expressing HIV-1 envelope glycoprotein 120 in their central nervous system (HIVgp120tg) mount a transient IFNβ response and provide evidence that IFNβ confers neuronal protection against HIVgp120 toxicity. In cerebrocortical cell cultures, neuroprotection by IFNβ against gp120 toxicity is dependent on IFNα receptor 1 (IFNAR1) and the β-chemokine CCL4, as IFNAR1 deficiency and neutralizing antibodies against CCL4, respectively, abolish the neuroprotective effects. We find in vivo that IFNβ mRNA is significantly increased in HIVgp120tg brains at 1.5, but not 3 or 6 months of age. However, a four-week intranasal IFNβ treatment of HIVgp120tg mice starting at 3.5 months of age increases expression of CCL4 and concomitantly protects neuronal dendrites and pre-synaptic terminals in cortex and hippocampus from gp120-induced damage. Moreover, in vivo and in vitro data suggests astrocytes are a major source of IFNβ-induced CCL4. Altogether, our results suggest exogenous IFNβ as a neuroprotective factor that has potential to ameliorate in vivo HIVgp120-induced brain injury

Investigation of the hydrodynamic behaviour of particles and aggregates by particle image velocimetry (PIV)

The IWA International Conference on Particle Separation (PS2007), Toulouse, France, 9-12 July 2007