Wilson loops stability in the gauge/string correspondence

We study the stability of some classical string worldsheet solutions employed for computing the potential energy between two static fundamental quarks in confining and non-confining gravity duals. We discuss the fixing of the diffeomorphism invariance of the string action, its relation with the fluctuation orientation and the interpretation of the quark mass substraction worldsheet needed for computing the potential energy in smooth (confining) gravity background. We consider various dual gravity backgrounds and show by a numerical analysis the existence of instabilities under linear fluctuations for classical string embedding solutions having positive length function derivative $L'(r_0)>0$. Finally we make a brief discussion of 't Hooft loops in non-conformal backgrounds.Comment: 34 pages, 36 figures. Reference added. Final version JHEP accepte

Thermodynamics and Instabilities of a Strongly Coupled Anisotropic Plasma

We extend our analysis of a IIB supergravity solution dual to a spatially anisotropic finite-temperature N=4 super Yang-Mills plasma. The solution is static, possesses an anisotropic horizon, and is completely regular. The full geometry can be viewed as a renormalization group flow from an AdS geometry in the ultraviolet to a Lifshitz-like geometry in the infrared. The anisotropy can be equivalently understood as resulting from a position-dependent theta-term or from a non-zero number density of dissolved D7-branes. The holographic stress tensor is conserved and anisotropic. The presence of a conformal anomaly plays an important role in the thermodynamics. The phase diagram exhibits homogeneous and inhomogeneous (i.e. mixed) phases. In some regions the homogeneous phase displays instabilities reminiscent of those of weakly coupled plasmas. We comment on similarities with QCD at finite baryon density and with the phenomenon of cavitation.Comment: 62 pages, 13 figures; v2: typos fixed, added reference

The role of mast cells in the pathogenesis of pain in chronic pancreatitis

BACKGROUND: The biological basis of pain in chronic pancreatitis is poorly understood. Mast cells have been implicated in the pathogenesis of pain in other conditions. We hypothesized that mast cells play a role in the pain of chronic pancreatitis. We examined the association of pain with mast cells in autopsy specimens of patients with painful chronic pancreatitis. We explored our hypothesis further using an experimental model of trinitrobenzene sulfonic acid (TNBS) -induced chronic pancreatitis in both wild type (WT) and mast cell deficient mice (MCDM). METHODS: Archival tissues with histological diagnoses of chronic pancreatitis were identified and clinical records reviewed for presence or absence of reported pain in humans. Mast cells were counted. The presence of pain was assessed using von Frey Filaments (VFF) to measure abdominal withdrawal responses in both WT and MCDM mice with and without chronic pancreatitis. RESULTS: Humans with painful chronic pancreatitis demonstrated a 3.5-fold increase in pancreatic mast cells as compared with those with painless chronic pancreatitis. WT mice with chronic pancreatitis were significantly more sensitive as assessed by VFF pain testing of the abdomen when compared with MCDM. CONCLUSION: Humans with painful chronic pancreatitis have an increased number of pancreatic mast cells as compared with those with painless chronic pancreatitis. MCDM are less sensitive to mechanical stimulation of the abdomen after induction of chronic pancreatitis as compared with WT. Mast cells may play an important role in the pathogenesis of pain in chronic pancreatitis

Transforming growth factor-β and breast cancer: Tumor promoting effects of transforming growth factor-β

The transforming growth factor (TGF)-βs are potent growth inhibitors of normal epithelial cells. In established tumor cell systems, however, the preponderant experimental evidence suggests that TGF-βs can foster tumor-host interactions that indirectly support the viability and/or progression of cancer cells. The timing of this 'TGF-β switch' during the progressive transformation of epithelial cells is not clear. More recent evidence also suggests that autocrine TGF-β signaling is operative in some tumor cells, and can also contribute to tumor invasiveness and metastases independent of an effect on nontumor cells. The dissociation of antiproliferative and matrix associated effects of autocrine TGF-β signaling at a transcriptional level provides for a mechanism(s) by which cancer cells can selectively use this signaling pathway for tumor progression. Data in support of the cellular and molecular mechanisms by which TGF-β signaling can accelerate the natural history of tumors will be reviewed in this section

Peroxovanadate inhibits Ca2+ release from mitochondria

Mitochondria contain a specific Ca2+ release pathway which operates when oxidized mitochondrial pyridine nucleotides are hydrolyzed. NAD+ hydrolysis and therefore Ca2+ release is possible when some vicinal thiols are cross-linked. Here we report that the thiol oxidant peroxovanadate inhibits the specific Ca2+ release pathway. In mitochondria, peroxovanadate causes a complete loss of reduced glutathione, which is not accompanied by formation of glutathione disulfide, and a partial loss of protein thiols. In model reactions, peroxovanadate oxidizes reduced glutathione predominantly to the sulfonate derivative, but does not react with glutathione disulfide. When the vicinal thiols relevant for Ca2+ release are cross-linked, Ca2+ release is no longer inhibited by peroxovanadate. Conversely, pretreatment of mitochondria with peroxovanadate makes them insensitive to compounds promoting the disulfide state. These results suggest that peroxovanadate inhibits the prooxidant-induced Ca2+ release from mitochondria by (i) depleting mitochondria of reduced glutathione and (ii) oxidizing the vicinal thiols relevant for Ca2+ release to a state higher than disulfide, presumably the sulfonate state. The findings provide further insight into the regulation of Ca2+ release from intact mitochondria, and may be relevant for a better understanding of the action of peroxovanadate in cells, where the compound can be insulin mimetic

Oncological Applications of Positron Emission Tomography with Fluorine-18 Fluorodeoxyglucose

Positron emission tomography (PET) is now primarily used in oncological indication owing to the successful application of fluorine-18 fluorodeoxyglucose (FDG) in an increasing number of clinical indications at different stages of diagnosis, and for staging and follow-up. This review first considers the biological characteristics of FDG and then discusses methodological considerations regarding its use. Clinical indications are considered, and the results achieved in respect of various organs and tumour types are reviewed in depth. The review concludes with a brief consideration of the ways in which clinical PET might be improved