Surface Antifouling Modification on Polyethylene Filtration Membranes by Plasma Polymerization.

Surface modification on microporous polyethylene (PE) membranes was facilitated by plasma polymerizing with two hydrophilic precursors: ethylene oxide vinyl ether (EO1V) and diethylene oxide vinyl ether (EO2V) to effectively improve the fouling against mammalian cells (Chinese hamster ovary, CHO cells) and proteins (bovine serum albumin, BSA). The plasma polymerization procedure incorporated uniform and pin-hole free ethylene oxide-containing moieties on the filtration membrane in a dry single-step process. The successful deposition of the plasma polymers was verified by Fourier-transform infrared (FTIR), scanning electron microscopy (SEM), and X-ray photoelectron spectroscopy (XPS) analyses. Water contact angle measurements and permeation experiments using cell and protein solutions were conducted to evaluate the change in hydrophilicity and fouling resistance for filtrating biomolecules. The EO1V and EO2V plasma deposited PE membranes showed about 1.45 fold higher filtration performance than the pristine membrane. Moreover, the flux recovery reached 80% and 90% by using deionized (DI) water and sodium hydroxide (NaOH) solution, indicating the efficacy of the modification and the good reusability of the modified PE membranes.

Mirror-image pain is mediated by nerve growth factor produced from tumor necrosis factor alpha-activated satellite glia after peripheral nerve injury.

Mirror-image pain is characterized by mechanical hypersensitivity on the uninjured mirror-image side. Recent reports favor central mechanisms, but whether peripheral mechanisms are involved remains unclear. We used unilateral spinal nerve ligation (SNL) to induce mirror-image pain in rats. On the mirror-image (contralateral) side, we found that satellite glia in the dorsal root ganglion (DRG) were activated, whereas macrophages/Schwann cells in the DRG and astrocytes/oligodendrocytes/microglia in the dorsal spinal cord were not. Subsequently, an increase in nerve growth factor (NGF) was detected in the contralateral DRG, and NGF immunoreactivity was concentrated in activated satellite glia. These phenomena were abolished if fluorocitrate (a glial inhibitor) was intrathecally injected before SNL. Electrophysiological recordings in cultured small DRG neurons showed that exogenous NGF enhanced nociceptor excitability. Intrathecal injection of NGF into naive rats induced long-lasting mechanical hypersensitivity, similar to SNL-evoked mirror-image pain. Anti-NGF effectively relieved SNL-evoked mirror-image pain. In the contralateral DRG, the SNL-evoked tumor necrosis factor alpha (TNF-α) increase, which started later than in the ipsilateral DRG and cerebrospinal fluid, occurred earlier than satellite glial activation and the NGF increase. Intrathecal injection of TNF-α into naive rats not only activated satellite glia to produce extra NGF in the DRG but also evoked mechanical hypersensitivity, which could be attenuated by anti-NGF injection. These results suggest that after SNL, satellite glia in the contralateral DRG are activated by TNF-α that diffuses from the injured side via cerebrospinal fluid, which then activates satellite glia to produce extra NGF to enhance nociceptor excitability, which induces mirror-image pain.