Controlled release of heparin from polypyrrole-poly(vinyl alcohol) assembly by electrical stimulation

A surface modification technique was developed for the covalent immobilization of poly(vinyl alcohol) (PVA)-heparin hydrogel onto electrically conductive polypyrrole (PPY) film with the objective of achieving controlled release of heparin. First, aldehyde groups were introduced onto PPY film through poly(ethylene glycol) monomethacrylate graft copolymerization and subsequent oxidation in acetic anhydride and dimethyl sulfoxide mixture. Then, the prepared PVA-heparin hydrogel was cast onto the PPY film and covalently immobilized to the film through the reaction between the aldehyde groups on the PPY film and the hydroxyl groups of PVA. X-ray photoelectron spectroscopy was used to characterize the surface-modified film after each stage. The strong attachment of the PVA-heparin layer on the PPY film was confirmed by peel test and scanning electron microscopy. The release behavior of heparin from the substrate with and without electrical stimulation was studied and the experimental results showed that the heparin release rate from the prepared substrate using an electric current of 3.5 mA is twofold higher than that without current.     

Imaging of metastatic orbital leiomyosarcoma

A 74-year-old man with a previous history of lower leg soft tissues leiomyosarcoma and multiple metastasis presented with a progressive painless proptosis of the left eye. Orbital ultrasound, CT, and MRI revealed a large mass in the left medial orbit. The mass was surgically removed and pathologic examination confirmed the diagnosis of a metastatic orbital leiomyosarcoma. The imaging characteristics of this rare tumor are comprehensively detailed, using complementary ultrasound, CT, and MRI, the combination of which allowed planning of total excision of the lesion.     

Induction of apoptosis by the ginsenoside Rh2 by internalization of lipid rafts and caveolae and inactivation of Akt

Background and purpose:

Lipid rafts and caveolae are membrane microdomains with important roles in cell survival signalling involving the Akt pathway. Cholesterol is important for the structure and function of these microdomains. The ginsenoside Rh2 exhibits anti-tumour activity. Because Rh2 is structurally similar to cholesterol, we investigated the possibility that Rh2 exerted its anti-tumour effect by modulating rafts and caveolae.

Experimental approach:

A431 cells (human epidermoid carcinoma cell line) were treated with Rh2 and the effects on cell apoptosis, raft localization and Akt activation measured. We also examined the effects of over-expression of Akt and active-Akt on Rh2-induced cell death.

Key results:

Rh2 induced apoptosis concentration- and time-dependently. Rh2 reduced the levels of rafts and caveolae in the plasma membrane and increased their internalization. Furthermore, Akt activity was decreased and consequently, Akt-dependent phosphorylation of Bad, a pro-survival protein, was decreased whereas the pro-apoptotic proteins, Bim and Bax, were increased upon Rh2 treatment. Unlike microdomain internalization induce by cholesterol depletion, Rh2-mediated internalization of rafts and caveolae was not reversed by cholesterol addition. Also, cholesterol addition did not restore Akt activation or rescue cells from Rh2-induced cell death. Rh2-induced cell death was attenuated in MDA-MB-231 cells over-expressing either wild-type or dominant-active Akt.

Conclusions and implications:

Rh2 induced internalization of rafts and caveolae, leading to Akt inactivation, and ultimately apoptosis. Because elevated levels of membrane rafts and caveolae, and Akt activation have been correlated with cancer development, internalization of these microdomains by Rh2 could potentially be used as an anti-cancer therapy.