Diagnosis of Metastatic Breast Cancer to an Intraabdominal Lymph Node by Endoscopic Ultrasound

Breast cancer can present with metastatic disease initially or as a systemic relapse despite seemingly adequate initial treatment. We report a case of suspected metastatic breast cancer to an intraabdominal lymph node based on imaging, which was subsequently confirmed by tissue sampling at the time of endoscopic ultrasound (EUS). While previous studies have shown the utility of EUS in the diagnosis of metastatic breast cancer, this is the first case to our knowledge that describes the use of EUS in diagnosing recurrent breast cancer to an intraabdominal lymph node

On the Semi-centre of a Poisson Algebra

If g is a Lie algebra then the semi-centre of the Poisson algebra S(g) is the subalgebra generated by ad(g) -eigenvectors. In this paper we abstract this definition to the context of integral Poisson algebras. We identify necessary and sufficient conditions for the Poisson semi-centre Asc to be a Poisson algebra graded by its weight spaces. In that situation we show the Poisson semi-centre exhibits many nice properties: the rational Casimirs are quotients of Poisson normal elements and the Poisson Dixmier–Mœglin equivalence holds for Asc

Generalization of the Bound State Model

In the bound state approach the heavy baryons are constructed by binding, with any orbital angular momentum, the heavy meson multiplet to the nucleon considered as a soliton in an effective meson theory. We point out that this picture misses an entire family of states, labeled by a different angular momentum quantum number, which are expected to exist according to the geometry of the three-body constituent quark model (for N_C=3). To solve this problem we propose that the bound state model be generalized to include orbitally excited heavy mesons bound to the nucleon. In this approach the missing angular momentum is ``locked-up'' in the excited heavy mesons. In the simplest dynamical realization of the picture we give conditions on a set of coupling constants for the binding of the missing heavy baryons of arbitrary spin. The simplifications made include working in the large M limit, neglecting nucleon recoil corrections, neglecting mass differences among different heavy spin multiplets and also neglecting the effects of light vector mesons.Comment: 35 pages (ReVTeX), 2 PostScript Figure

Full-length genomic analysis of korean porcine sapelovirus strains.

Porcine sapelovirus (PSV), a species of the genus Sapelovirus within the family Picornaviridae, is associated with diarrhea, pneumonia, severe neurological disorders, and reproductive failure in pigs. However, the structural features of the complete PSV genome remain largely unknown. To analyze the structural features of PSV genomes, the full-length nucleotide sequences of three Korean PSV strains were determined and analyzed using bioinformatic techniques in comparison with other known PSV strains. The Korean PSV genomes ranged from 7,542 to 7,566 nucleotides excluding the 3' poly(A) tail, and showed the typical picornavirus genome organization; 5'untranslated region (UTR)-L-VP4-VP2-VP3-VP1-2A-2B-2C-3A-3B-3C-3D-3'UTR. Three distinct cis-active RNA elements, the internal ribosome entry site (IRES) in the 5'UTR, a cis-replication element (CRE) in the 2C coding region and 3'UTR were identified and their structures were predicted. Interestingly, the structural features of the CRE and 3'UTR were different between PSV strains. The availability of these first complete genome sequences for PSV strains will facilitate future investigations of the molecular pathogenesis and evolutionary characteristics of PSV

An Allosteric Inhibitor of KRas Identified Using a Barcoded Rapid Assay Microchip Platform

Protein catalyzed capture agents (PCCs) are synthetic antibody surrogates that can target a wide variety of biologically relevant proteins. As a step toward developing a high-throughput PCC pipeline, we report on the preparation of a barcoded rapid assay platform for the analysis of hits from PCC library screens. The platform is constructed by first surface patterning a micrometer scale barcode composed of orthogonal ssDNA strands onto a glass slide. The slide is then partitioned into microwells, each of which contains multiple copies of the full barcode. Biotinylated candidate PCCs from a click screen are assembled onto the barcode stripes using a complementary ssDNA-encoded cysteine-modified streptavidin library. This platform was employed to evaluate candidate PCC ligands identified from an epitope targeted in situ click screen against the two conserved allosteric switch regions of the Kirsten rat sarcoma (KRas) protein. A single microchip was utilized for the simultaneous evaluation of 15 PCC candidate fractions under more than a dozen different assay conditions. The platform also permitted more than a 10-fold savings in time and a more than 100-fold reduction in biological and chemical reagents relative to traditional multiwell plate assays. The best ligand was shown to exhibit an in vitro inhibition constant (IC_(50)) of ∼24 μM

Large-density field theory, viscosity, and "2kF2k_F" singularities from string duals

We analyze systems where an effective large-N expansion arises naturally in gauge theories without a large number of colors: a sufficiently large charge density alone can produce a perturbative string ('tHooft) expansion. One example is simply the well-known NS5/F1 system dual to $AdS_3\times T^4\times S^3$, here viewed as a 5+1 dimensional theory at finite density. This model is completely stable, and we find that the existing string-theoretic solution of this model yields two interesting results. First, it indicates that the shear viscosity is not corrected by $\alpha'$ effects in this system. For flow perpendicular to the F1 strings the viscosity to entropy ratio take the usual value $1/4\pi$, but for flow parallel to the F1's it vanishes as $T^2$ at low temperature. Secondly, it encodes singularities in correlation functions coming from low-frequency modes at a finite value of the momentum along the $T^4$ directions. This may provide a strong coupling analogue of finite density condensed matter systems for which fermionic constituents of larger operators contribute so-called "$2k_F$" singularities. In the NS5/F1 example, stretched strings on the gravity side play the role of these composite operators. We explore the analogue for our system of the Luttinger relation between charge density and the volume bounded by these singular surfaces. This model provides a clean example where the string-theoretic UV completion of the gravity dual to a finite density field theory plays a significant and calculable role.Comment: 28 pages. v2: added reference

Mechanical unloading activates FoxO3 to trigger Bnip3‐dependent cardiomyocyte atrophy

BACKGROUND: Mechanical assist device therapy has emerged recently as an important and rapidly expanding therapy in advanced heart failure, triggering in some patients a beneficial reverse remodeling response. However, mechanisms underlying this benefit are unclear. METHODS AND RESULTS: In a model of mechanical unloading of the left ventricle, we observed progressive myocyte atrophy, autophagy, and robust activation of the transcription factor FoxO3, an established regulator of catabolic processes in other cell types. Evidence for FoxO3 activation was similarly detected in unloaded failing human myocardium. To determine the role of FoxO3 activation in cardiac muscle in vivo, we engineered transgenic mice harboring a cardiomyocyte‐specific constitutively active FoxO3 mutant (caFoxO3(flox);αMHC‐Mer‐Cre‐Mer). Expression of caFoxO3 triggered dramatic and progressive loss of cardiac mass, robust increases in cardiomyocyte autophagy, declines in mitochondrial biomass and function, and early mortality. Whereas increases in cardiomyocyte apoptosis were not apparent, we detected robust increases in Bnip3 (Bcl2/adenovirus E1B 19‐kDa interacting protein 3), an established downstream target of FoxO3. To test the role of Bnip3, we crossed the caFoxO3(flox);αMHC‐Mer‐Cre‐Mer mice with Bnip3‐null animals. Remarkably, the atrophy and autophagy phenotypes were significantly blunted, yet the early mortality triggered by FoxO3 activation persisted. Rather, declines in cardiac performance were attenuated by proteasome inhibitors. Consistent with involvement of FoxO3‐driven activation of the ubiquitin‐proteasome system, we detected time‐dependent activation of the atrogenes program and sarcomere protein breakdown. CONCLUSIONS: In aggregate, these data point to FoxO3, a protein activated by mechanical unloading, as a master regulator that governs both the autophagy‐lysosomal and ubiquitin‐proteasomal pathways to orchestrate cardiac muscle atrophy