The present invention provides methods of determining cell sensitivity to a therapeutic agent.

Plasma source assemblies comprising a housing with an RF hot electrode and a return electrode are described. The housing includes a gas inlet and a front face defining a flow path. The RF hot electrode includes a first surface oriented substantially parallel to the flow path. The return electrode includes a first surface oriented substantially parallel to the flow path and spaced from the first surface of the RF hot electrode to form a gap. Processing chambers incorporating the plasma source assemblies and methods of using the plasma source assemblies are also described.

Provided herein are methods and assays for isolating and culturing seborrheic keratosis cells ex vivo. Also provided herein are screening assays using cultured seborrheic keratosis cells and methods for treating seborrheic keratosis in a subject.

Provided is an activatable probe that undergoes intramolecular cyclization and subsequent aggregation in apoptotic tumor cells upon peptidase-initiated, and most advantageously caspase-3, activation. These caspase-sensitive nano-aggregation probes (C-SNAFs) are generally biocompatible, possess NIR spectral properties or may serve as PET or MRI imaging agents, and have a mechanism of target-mediated nanostructure self-assembly amenable to in vivo use. The probes encompass biocompatible condensation chemistry products that comprise D-cysteine and 2-cyano-6-hydroxyquinoline (CHQ) moieties linked to an amino-luciferin scaffold, and which can be activated by a two-step reaction requiring caspase-3/7-mediated cleavage of an aspartate-glutamate-valine-aspartate (L-DEVD) capping peptide and the free intracellular thiol-mediated reduction of the disulfide bond.

The present invention provides a pharmaceutical composition comprising naltrexone or an analogue thereof for use in the treatment of a subject having a tumour/cancer; wherein the naltrexone or the analogue thereof is to be administered to the subject in a first treatment phase, followed by a recovery phase; wherein, following the recovery phase, a small molecule signalling inhibitor selected from the group consisting of PI3-kinase inhibitors, AKT inhibitors, taxanes, antimetabolites, alkylating agents and cell cycle inhibitors is to be administered to the subject in a second treatment phase; the recovery phase being characterised by the absence of administration of the naltrexone or the analogue thereof and the small molecule signalling inhibitor. Also envisaged are a diagnostic test to assess the response of a subject to the first treatment phase, an in vitro method of testing the efficacy of a small molecule signalling inhibitor when for use in combination with naltrexone, and the use of naltrexone in such a method when in vivo.

The present invention provides methods and compositions for selective modulation of certain protein kinases, and especially mTor complexes. The methods and compositions are particularly useful in inhibiting mTor selectively for therapeutic applications.

This application provides devices for modeling ischemic stroke conditions. The devices can be used to culture neurons and to subject a first population of the neurons to low-oxygen conditions and a second population of neurons to normoxic conditions. The neurons are cultured on a porous barrier, and on the other side of the barrier run one or more fluid-filled channels. By flowing fluid with different oxygen levels through the channels, one can deliver desired oxygen concentrations to the cells nearest those channels.

A cell composition composed of spermatogonial stem cells, Sertoli cells, Leydig cells and optionally peritubular cells, is provided, as is a culture composition, artificial testicular construct, hydrogel composition, and device containing the same. A method for using the device as a physiologically relevant in vitro model of human testicular function to screen compounds for pharmacological or toxicological activity is also provided.

Provided herein are methods and compositions related to a retinoid receptor-selective pathway. As described herein, this pathway can be targeted to manipulate a tumor microenvironment. For example, the methods and compositions described herein can be used to induce apoptosis in a cancer cell. Further, the compositions described herein, including Sulindac and analogs thereof, can be used to target this pathway for the treatment or prevention of cancer in human patients.

A composition comprising a TRAIL-R2 receptor or fragment thereof bound to a ligand in crystalline form is presently provided along with novel binding sites and binding agents of a TRAIL receptor. Also provided are methods of designing a compound, protein or peptide and identifying a binding agent that interacts with a TRAIL receptor. The present invention further provides methods of modulating binding of a TRAIL receptor to a ligand, the methods comprising contacting the TRAIL receptor with a binding agent, ligand, or an agonist or antagonist thereof, that interacts with a novel binding site described herein.