CORE and the Haldane Conjecture

The Contractor Renormalization group formalism (CORE) is a real-space renormalization group method which is the Hamiltonian analogue of the Wilson exact renormalization group equations. In an earlier paper\cite{QGAF} I showed that the Contractor Renormalization group (CORE) method could be used to map a theory of free quarks, and quarks interacting with gluons, into a generalized frustrated Heisenberg antiferromagnet (HAF) and proposed using CORE methods to study these theories. Since generalizations of HAF's exhibit all sorts of subtle behavior which, from a continuum point of view, are related to topological properties of the theory, it is important to know that CORE can be used to extract this physics. In this paper I show that despite the folklore which asserts that all real-space renormalization group schemes are necessarily inaccurate, simple Contractor Renormalization group (CORE) computations can give highly accurate results even if one only keeps a small number of states per block and a few terms in the cluster expansion. In addition I argue that even very simple CORE computations give a much better qualitative understanding of the physics than naive renormalization group methods. In particular I show that the simplest CORE computation yields a first principles understanding of how the famous Haldane conjecture works for the case of the spin-1/2 and spin-1 HAF.Comment: 36 pages, 4 figures, 5 tables, latex; extensive additions to conten

The novel histone deacetylase inhibitor, AR-42, inhibits gp130/Stat3 pathway and induces apoptosis and cell cycle arrest in multiple myeloma cells

Multiple myeloma (MM) remains incurable with current therapy, indicating the need for continued development of novel therapeutic agents. We evaluated the activity of a novel phenylbutyrate-derived histone deacetylase inhibitor, AR-42, in primary human myeloma cells and cell lines. AR-42 was cytotoxic to MM cells at a mean LC(50) of 0.18 ± 0.06 μmol/l at 48 hr and induced apoptosis with cleavage of caspases 8, 9 and 3, with cell death largely prevented by caspase inhibition. AR-42 downregulated the expression of gp130 and inhibited activation of STAT3, with minimal effects on the PI3K/Akt and MAPK pathways, indicating a predominant effect on the gp130/STAT-3 pathway. AR-42 also inhibited interleukin (IL)-6-induced STAT3 activation, which could not be overcome by exogenous IL-6. AR-42 also downregulated the expression of STAT3-regulated targets, including Bcl-xL and cyclin D1. Overexpression of Bcl-xL by a lentivirus construct partly protected against cell death induced by AR-42. The cyclin dependent kinase inhibitors, p16 and p21, were also significantly induced by AR-42, which together with a decrease in cyclin D1, resulted in G(1) and G(2) cell cycle arrest. In conclusion, AR-42 has potent cytotoxicity against MM cells mainly through gp130/STAT-3 pathway. The results provide rationale for clinical investigation of AR-42 in MM

IQGAP1 and IQGAP2 are Reciprocally Altered in Hepatocellular Carcinoma

<p>Abstract</p> <p>Background</p> <p>IQGAP1 and IQGAP2 are homologous members of the IQGAP family of scaffold proteins. Accumulating evidence implicates IQGAPs in tumorigenesis. We recently reported that IQGAP2 deficiency leads to the development of hepatocellular carcinoma (HCC) in mice. In the current study we extend these findings, and investigate IQGAP1 and IQGAP2 expression in human HCC.</p> <p>Methods</p> <p>IQGAP1 and IQGAP2 protein expression was assessed by Western blotting and immunohistochemistry. IQGAP mRNA was measured by quantitative RT-PCR. The methylation status of the <it>Iqgap2 </it>promoter was determined by pyrosequencing of bisulfite-treated genomic DNA.</p> <p>Results</p> <p>IQGAP1 and IQGAP2 expression was reciprocally altered in 6/6 liver cancer cell lines. Similarly, immunohistochemical staining of 82 HCC samples showed that IQGAP2 protein expression was reduced in 64/82 (78.0%), while IQGAP1 was present in 69/82 (84.1%). No IQGAP1 staining was detected in 23/28 (82.1%) normal livers, 4/4 (100.0%) hepatic adenomas and 23/23 (100.0%) cirrhosis cases, while IQGAP2 was increased in 22/28 (78.6%), 4/4 (100.0%) and 23/23 (100.0%), respectively. Although the <it>Iqgap2 </it>promoter was not hypermethylated in HCC at any of the 25 CpG sites studied (N = 17), IQGAP2 mRNA levels were significantly lower in HCC specimens (N = 23) than normal livers (N = 6).</p> <p>Conclusions</p> <p>We conclude that increased IQGAP1 and/or decreased IQGAP2 contribute to the pathogenesis of human HCC. Furthermore, downregulation of IQGAP2 in HCC occurs independently of hypermethylation of the <it>Iqgap2 </it>promoter. Immunostaining of IQGAP1 and IQGAP2 may aid in the diagnosis of HCC, and their pharmacologic modulation may represent a novel therapeutic strategy for the treatment of liver cancer.</p

Effects of antiplatelet therapy after stroke due to intracerebral haemorrhage (RESTART): a randomised, open-label trial

Antiplatelet therapy reduces the risk of major vascular events for people with occlusive vascular disease, although it might increase the risk of intracranial haemorrhage. Patients surviving the commonest subtype of intracranial haemorrhage, intracerebral haemorrhage, are at risk of both haemorrhagic and occlusive vascular events, but whether antiplatelet therapy can be used safely is unclear. We aimed to estimate the relative and absolute effects of antiplatelet therapy on recurrent intracerebral haemorrhage and whether this risk might exceed any reduction of occlusive vascular events

Cosmological Constraints from the ROSAT Deep Cluster Survey

The ROSAT Deep Cluster Survey (RDCS) has provided a new large deep sample of X-ray selected galaxy clusters. Observables such as the flux number counts n(S), the redshift distribution n(z) and the X-ray luminosity function (XLF) over a large redshift baseline (z\lesssim 0.8) are used here in order to constrain cosmological models. Our analysis is based on the Press-Schechter approach, whose reliability is tested against N-body simulations. Following a phenomenological approach, no assumption is made a priori on the relation between cluster masses and observed X-ray luminosities. As a first step, we use the local XLF from RDCS, along with the high-luminosity extension provided by the XLF from the BCS, in order to constrain the amplitude of the power spectrum, \sigma_8, and the shape of the local luminosity-temperature relation. We obtain \sigma_8=0.58 +/- 0.06 for Omega_0=1 for open models at 90% confidence level, almost independent of the L-T shape. The density parameter \Omega_0 and the evolution of the L-T relation are constrained by the RDCS XLF at z>0 and the EMSS XLF at z=0.33, and by the RDCS n(S) and n(z) distributions. By modelling the evolution for the amplitude of the L-T relation as (1+z)^A, an \Omega_0=1 model can be accommodated for the evolution of the XLF with 1<A<3 at 90% confidence level, while \Omega_0=0.4^{+0.3}_{-0.2} and \Omega_0<0.6 are implied by a non--evolving L-T for open and flat models, respectively.Comment: 12 pages, 9 colour figures, LateX, uses apj.sty, ApJ, in press, May 20 issu