Myopericytoma of low grade malignancy in the oral cavity

Myopericytoma (MPC) of the oral cavity is extremely rare. Herein reported is a case of MPC of low grade malignancy in the oral cavity. A 61-year-old man noticed a tumor of the cheek mucosa, and admitted to our hospital. Oral examination revealed a reddish elevated tumor of the cheek mucosa. Tumorectomy with wide margins was performed. The clinical diagnosis was pyogenic granuloma. Grossly, the tumor was reddish, and measured 1×1×1 cm. Microscopically, oval to spindle tumor cells with hyperchromatic vesicular nuclei and many vasculatures were seen. The tumor cells were contiguous and mixed with endothelial cells in many blood vessels, thus resembling pericytes. Mitotic figures were scattered. The surgical margins were negative for tumor cells. Immunohistochemically, the tumor cells were positive for vimentin, α-smooth muscle actin and p53. The Ki67 labeling was 40%. The tumor cells were negative for cytokeratins (AE1/3 and CAM5.2), CD31, CD34, S100 protein, HMB45, CD10, vimentin, desmin, and factor VIII-related antigen. The endothelium of the vessels were positive for vimentin, CD31, CD34 and factor VIII-related antigen, but negative for α-smooth muscle actin, p53, cytokeratins (AE1/3 and CAM5.2), S100 protein, HMB45, CD10, vimentin, and desmin. The Ki67 labeling was 5%. Because the pericytoid tumor cells showed α-smooth muscle actin and negative for endothelial markers, MPC was diagnosed. In addition, because there was some atypia and mitotic figures were scatters and also because the tumor cells were positive for p53 and Ki67 labeling was high, a pathological diagnosis of MPC with low grade malignancy was made. No recurrence was observed, and the patient is now free from tumor 6 months after the operation

Strain Sensor’s Network for Low-Velocity Impact Location Estimation on Carbon Reinforced Fiber Plastic Structures: Part-I

In this work, we have investigated the strain response (angular/spatial) from fiber Bragg grating (FBG) sensor & resistance strain gauge (RSG) sensors bonded to the composite structure due to the projectile low velocity impact (LVI). The number of sensor & its orientating has been optimized based on such experimental data and designed an optimum sensor network for faithful LVI detection. In order to study the efficacy of the sensor network, an impact localization algorithm based on peak strain amplitude from the sensor bonded to the structure was used in this study. Further the detection efficiency of the algorithm has been improved using weighted average value around the peak amplitude of strain experienced by the sensor. We found that for the high energy (~35 J) LVI the maximum distance error (Euclidian distance) was 50 mm for 80% of total trail case. Furthermore, we have developed and compared the relative performance of the algorithm cited in the literature, will be presented in PART-II of the same Journal

Trim17, novel E3 ubiquitin-ligase, initiates neuronal apoptosis

Accumulating data indicate that the ubiquitin-proteasome system controls apoptosis by regulating the level and the function of key regulatory proteins. In this study, we identified Trim17, a member of the TRIM/RBCC protein family, as one of the critical E3 ubiquitin ligases involved in the control of neuronal apoptosis upstream of mitochondria. We show that expression of Trim17 is increased both at the mRNA and protein level in several in vitro models of transcription-dependent neuronal apoptosis. Expression of Trim17 is controlled by the PI3K/Akt/GSK3 pathway in cerebellar granule neurons (CGN). Moreover, the Trim17 protein is expressed in vivo, in apoptotic neurons that naturally die during post-natal cerebellar development. Overexpression of active Trim17 in primary CGN was sufficient to induce the intrinsic pathway of apoptosis in survival conditions. This pro-apoptotic effect was abolished in Bax(-/-) neurons and depended on the E3 activity of Trim17 conferred by its RING domain. Furthermore, knock-down of endogenous Trim17 and overexpression of dominant-negative mutants of Trim17 blocked trophic factor withdrawal-induced apoptosis both in CGN and in sympathetic neurons. Collectively, our data are the first to assign a cellular function to Trim17 by showing that its E3 activity is both necessary and sufficient for the initiation of neuronal apoptosis. Cell Death and Differentiation (2010) 17, 1928-1941; doi: 10.1038/cdd.2010.73; published online 18 June 201

Glueball masses in the large N limit

The lowest-lying glueball masses are computed in SU($N$) gauge theory on a spacetime lattice for constant value of the lattice spacing $a$ and for $N$ ranging from 3 to 8. The lattice spacing is fixed using the deconfinement temperature at temporal extension of the lattice $N_T = 6$. The calculation is conducted employing in each channel a variational ansatz performed on a large basis of operators that includes also torelon and (for the lightest states) scattering trial functions. This basis is constructed using an automatic algorithm that allows us to build operators of any size and shape in any irreducible representation of the cubic group. A good signal is extracted for the ground state and the first excitation in several symmetry channels. It is shown that all the observed states are well described by their large $N$ values, with modest ${\cal O}(1/N^2)$ corrections. In addition spurious states are identified that couple to torelon and scattering operators. As a byproduct of our calculation, the critical couplings for the deconfinement phase transition for N=5 and N=7 and temporal extension of the lattice $N_T=6$ are determined.Comment: 1+36 pages, 22 tables, 21 figures. Typos corrected, conclusions unchanged, matches the published versio

D-meson decay constants and a check of factorization in non-leptonic B-decays

We compute the vector meson decay constants fD*, fDs* from the simulation of twisted mass QCD on the lattice with Nf = 2 dynamical quarks. When combining their values with the pseudoscalar D(s)-meson decay constants, we were able (i) to show that the heavy quark spin symmetry breaking effects with the charm quark are large, fDs*/fDs = 1.26(3), and (ii) to check the factorization approximation in a few specific B-meson non-leptonic decay modes. Besides our main results, fD* = 278 \pm 13 \pm 10 MeV, and fDs* = 311 \pm 9 MeV, other phenomenologically interesting results of this paper are: fDs*/fD* = 1.16 \pm 0.02 \pm 0.06, fDs*/fD = 1.46 \pm 0.05 \pm 0.06, and fDs/fD* = 0.89 \pm 0.02 \pm 0.03. Finally, we correct the value for B(B0 \rightarrow D+ pi-) quoted by PDG, and find B(B0 \rightarrow D+ pi-) = (7.8 \pm 1.4) \times 10-7. Alternatively, by using the ratios discussed in this paper, we obtain B(B0 \rightarrow D+ pi-) = (8.3 \pm 1.0 \pm 0.8)\times10-7.Comment: 16 pages, 4 eps figure

CTLA-4 Activation of Phosphatidylinositol 3-Kinase (PI 3-K) and Protein Kinase B (PKB/AKT) Sustains T-Cell Anergy without Cell Death

The balance of T-cell proliferation, anergy and apoptosis is central to immune function. In this regard, co-receptor CTLA-4 is needed for the induction of anergy and tolerance. One central question concerns the mechanism by which CTLA-4 can induce T-cell non-responsiveness without a concurrent induction of antigen induced cell death (AICD). In this study, we show that CTLA-4 activation of the phosphatidylinositol 3-kinase (PI 3-K) and protein kinase B (PKB/AKT) sustains T-cell anergy without cell death. CTLA-4 ligation induced PI 3K activation as evidenced by the phosphorylation of PKB/AKT that in turn inactivated GSK-3. The level of activation was similar to that observed with CD28. CTLA-4 induced PI 3K and AKT activation also led to phosphorylation of the pro-apoptotic factor BAD as well as the up-regulation of BcL-XL. In keeping with this, CD3/CTLA-4 co-ligation prevented apoptosis under the same conditions where T-cell non-responsiveness was induced. This effect was PI 3K and PKB/AKT dependent since inhibition of these enzymes under conditions of anti-CD3/CTLA-4 co-ligation resulted in cell death. Our findings therefore define a mechanism by which CTLA-4 can induce anergy (and possibly peripheral tolerance) by preventing the induction of cell death

A frequentist framework of inductive reasoning

Reacting against the limitation of statistics to decision procedures, R. A. Fisher proposed for inductive reasoning the use of the fiducial distribution, a parameter-space distribution of epistemological probability transferred directly from limiting relative frequencies rather than computed according to the Bayes update rule. The proposal is developed as follows using the confidence measure of a scalar parameter of interest. (With the restriction to one-dimensional parameter space, a confidence measure is essentially a fiducial probability distribution free of complications involving ancillary statistics.) A betting game establishes a sense in which confidence measures are the only reliable inferential probability distributions. The equality between the probabilities encoded in a confidence measure and the coverage rates of the corresponding confidence intervals ensures that the measure's rule for assigning confidence levels to hypotheses is uniquely minimax in the game. Although a confidence measure can be computed without any prior distribution, previous knowledge can be incorporated into confidence-based reasoning. To adjust a p-value or confidence interval for prior information, the confidence measure from the observed data can be combined with one or more independent confidence measures representing previous agent opinion. (The former confidence measure may correspond to a posterior distribution with frequentist matching of coverage probabilities.) The representation of subjective knowledge in terms of confidence measures rather than prior probability distributions preserves approximate frequentist validity.Comment: major revisio

Bcl-2 protein family: Implications in vascular apoptosis and atherosclerosis

Apoptosis has been recognized as a central component in the pathogenesis of atherosclerosis, in addition to the other human pathologies such as cancer and diabetes. The pathophysiology of atherosclerosis is complex, involving both apoptosis and proliferation at different phases of its progression. Oxidative modification of lipids and inflammation differentially regulate the apoptotic and proliferative responses of vascular cells during progression of the atherosclerotic lesion. Bcl-2 proteins act as the major regulators of extrinsic and intrinsic apoptosis signalling pathways and more recently it has become evident that they mediate the apoptotic response of vascular cells in response to oxidation and inflammation either in a provocative or an inhibitory mode of action. Here we address Bcl-2 proteins as major therapeutic targets for the treatment of atherosclerosis and underscore the need for the novel preventive and therapeutic interventions against atherosclerosis, which should be designed in the light of molecular mechanisms regulating apoptosis of vascular cells in atherosclerotic lesions

The Minimal Scale Invariant Extension of the Standard Model

We perform a systematic analysis of an extension of the Standard Model that includes a complex singlet scalar field and is scale invariant at the tree level. We call such a model the Minimal Scale Invariant extension of the Standard Model (MSISM). The tree-level scale invariance of the model is explicitly broken by quantum corrections, which can trigger electroweak symmetry breaking and potentially provide a mechanism for solving the gauge hierarchy problem. Even though the scale invariant Standard Model is not a realistic scenario, the addition of a complex singlet scalar field may result in a perturbative and phenomenologically viable theory. We present a complete classification of the flat directions which may occur in the classical scalar potential of the MSISM. After calculating the one-loop effective potential of the MSISM, we investigate a number of representative scenarios and determine their scalar boson mass spectra, as well as their perturbatively allowed parameter space compatible with electroweak precision data. We discuss the phenomenological implications of these scenarios, in particular, whether they realize explicit or spontaneous CP violation, neutrino masses or provide dark matter candidates. In particular, we find a new minimal scale-invariant model of maximal spontaneous CP violation which can stay perturbative up to Planck-mass energy scales, without introducing an unnaturally large hierarchy in the scalar-potential couplings.Comment: 71 pages, 34 eps figures, numerical error corrected, clarifying comments adde

Retroviral expression of a kinase-defective IGF-I receptor suppresses growth and causes apoptosis of CHO and U87 cells in-vivo

BACKGROUND: Phosphatidylinositol-3,4,5-triphosphate (PtdInsP3) signaling is elevated in many tumors due to loss of the tumor suppressor PTEN, and leads to constitutive activation of Akt, a kinase involved in cell survival. Reintroduction of PTEN in cells suppresses transformation and tumorigenicity. While this approach works in-vitro, it may prove difficult to achieve in-vivo. In this study, we investigated whether inhibition of growth factor signaling would have the same effect as re-expression of PTEN. METHODS: Dominant negative IGF-I receptors were expressed in CHO and U87 cells by retroviral infection. Cell proliferation, transformation and tumor formation in athymic nude mice were assessed. RESULTS: Inhibition of IGF-IR signaling in a CHO cell model system by expression of a kinase-defective IGF-IR impairs proliferation, transformation and tumor growth. Reduction in tumor growth is associated with an increase in apoptosis in-vivo. The dominant-negative IGF-IRs also prevented growth of U87 PTEN-negative glioblastoma cells when injected into nude mice. Injection of an IGF-IR blocking antibody αIR3 into mice harboring parental U87 tumors inhibits tumor growth and increases apoptosis. CONCLUSION: Inhibition of an upstream growth factor signal prevents tumor growth of the U87 PTEN-deficient glioma to the same extent as re-introduction of PTEN. This result suggests that growth factor receptor inhibition may be an effective alternative therapy for PTEN-deficient tumors