Screening masses in quenched (2+1)d Yang-Mills theory: universality from dynamics?

We compute the spectrum of gluonic screening-masses in the $0^{++}$ channel of quenched 3d Yang-Mills theory near the phase-transition. Our finite-temperature lattice simulations are performed at scaling region, using state-of-art techniques for thermalization and spectroscopy, which allows for thorough data extrapolations to thermodynamic limit. Ratios among mass-excitations with the same quantum numbers on the gauge theory, 2d Ising and $\lambda\phi^{4}$ models are compared, resulting in a nice agreement with predictions from universality. In addition, a gauge-to-scalar mapping, previously employed to fit QCD Green's functions at deep IR, is verified to dynamically describe these universal spectroscopic patternsComment: 15 pages, 4 eps figures. Revised version, to appear in Nucl. Phys.

Front cover & preliminary pages (Journal of Irish Urban Studies, Vol.1 (No. 2), 2003

Front cover & preliminary pages, Journal of Irish Urban Studies, Vol.1 (Issue 2), 200

Using fluorescence lifetime imaging microscopy to monitor theranostic nanoparticle uptake and intracellular doxorubicin release

We describe the synthesis of iron oxide nanoparticles (IONPs) with excellent colloidal stability in both water and serum, imparted by carefully designed grafted polymer shells. The polymer shells were built with attached aldehyde functionality to enable the reversible attachment of doxorubicin (DOX) via imine bonds, providing a controlled release mechanism for DOX in acidic environments. The IONPs were shown to be readily taken up by cell lines (MCF-7 breast cancer cells and H1299 lung cancer cells), and intracellular release of DOX was proven using in vitro fluorescence lifetime imaging microscopy (FLIM) measurements. Using the fluorescence lifetime difference exhibited by native DOX (similar to 1 ns) compared to conjugated DOX (similar to 4.6 ns), the intracellular release of conjugated DOX was in situ monitored in H1299 and was estimated using phasor plot representation, showing a clear increase of native DOX with time. The results obtained from FLIM were corroborated using confocal microscopy, clearly showing DOX accumulation in the nuclei. The IONPs were also assessed as MRI negative contrast agents. We observed a significant change in the transverse relaxivity properties of the IONPs, going from 220 to 390 mM(-1) s(-1) in the presence or absence of conjugated DOX. This dependence of MRI signal on IONP-DOX/water interactions may be exploited in future theranostic applications. The in vitro studies were then extended to monitor cell uptake of the DOX loaded IONPs (IONP@P(HBA)-b-P(OEGA) + DOX) into two 3D multicellular tumor spheroids (MCS) grown from two independent cell lines (MCF-7 and H1299) using multiphoton excitation microscopy

Heparan sulfate side chains have a critical role in the inhibitory effects of perlecan on vascular smooth muscle cell response to arterial injury

Perlecan is a proteoglycan composed of a 470-kDa core protein linked to three heparan sulfate (HS) glycosaminoglycan chains. The intact proteoglycan inhibits the smooth muscle cell (SMC) response to vascular injury. Hspg2(Delta 3/Delta 3) (M Delta 3/Delta 3) mice produce a mutant perlecan lacking the HS side chains. The objective of this study was to determine differences between these two types of perlecan in modifying SMC activities to the arterial injury response, in order to define the specific role of the HS side chains. In vitro proliferative and migratory activities were compared in SMC isolated from M Delta 3/Delta 3 and wild-type mice. Proliferation of M Delta 3/Delta 3 SMC was 1.5x greater than in wild type (P < 0.001), increased by addition of growth factors, and showed a 42% greater migratory response than wild-type cells to PDGF-BB (P < 0.001). In M Delta 3/Delta 3 SMC adhesion to fibronectin, and collagen types I and IV was significantly greater than wild type. Addition of DRL-12582, an inducer of perlecan expression, decreased proliferation and migratory response to PDGF-BB stimulation in wild-type SMC compared with M Delta 3/Delta 3. In an in vivo carotid artery wire injury model, the medial thickness, medial area/lumen ratio, and macrophage infiltration were significantly increased in the M Delta 3/Delta 3 mice, indicating a prominent role of the HS side chain in limiting vascular injury response. Mutant perlecan that lacks HS side chains had a marked reduction in the inhibition of in vitro SMC function and the in vivo arterial response to injury, indicating the critical role of HS side chains in perlecan function in the vessel wall

Valproic acid as a therapeutic agent for head and neck squamous cell carcinomas

Here we investigate if valproic acid (VA) can enhance the efficacy of commonly used therapies for head and neck squamous cell carcinomas (HNSCC) and the molecular mechanisms that may be related to its anticancer effects. Proliferation and viability of distinct cell types subjected to VA treatment alone or in combination regimens were measured through BrdU incorporation and LDH release, respectively. Molecular markers compatible with histone deacetylase inhibitory activity of VA were assessed through western blots assays in lysates obtained from cultured cells and tumour biopsies. Treatment of all cell types with VA resulted in a dose-dependent increase in histone H3 acetylation and p21 expression, as well as dose-dependent cytostasis. In contrast, the cytotoxic response to VA was variable and did not correlate with cytostasis, histone acetylation or p21 induction. The variability in response to VA was also observed in tumour biopsy samples collected from patients prior to and following a 1 week oral course of VA. In addition, we found that a combination of a clinically achievable concentration of VA plus cisplatin caused a threefold to sevenfold increase in cisplatin cytotoxicity in vitro. VA acts as a histone deacetylase inhibitor (HDI) in SCC cells and normal human keratinocytes (HKs), potentiates the cytotoxic effect of cisplatin in SCC cell lines and decreases the viability of SCC cells as opposed to HKs. Taken together, the results provide initial evidence that VA might be a valuable drug in the development of better therapeutic regimens for HNSCC