A Note on Pretzelosity TMD Parton Distribution

We show that the transverse-momentum-dependent parton distribution, called as Pretzelosity function, is zero at any order in perturbation theory of QCD for a single massless quark state. This implies that Pretzelosity function is not factorized with the collinear transversity parton distribution at twist-2, when the struck quark has a large transverse momentum. Pretzelosity function is in fact related to collinear parton distributions defined with twist-4 operators. In reality, Pretzelosity function of a hadron as a bound state of quarks and gluons is not zero. Through an explicit calculation of Pretzelosity function of a quark combined with a gluon nonzero result is found.Comment: improved explanation, published version in Phys. Lett.

Myths of the High Medical Cost of Old Age and Dying

The rising costs of medical care in the United States are often erroneously linked to the growing population of older adults. Despite public perception, health care costs associated with aging are limited. Part of the ILC-USA's project on Ageism In America with generous support from the Open Society Institute, this report identifies and dispels seven myths about caring for older people at the end of life

Numerical Simulation of Electroosmotic Flow with Step Change in Zeta Potential

Electroosmotic flow is a convenient mechanism for transporting polar fluid in a microfluidic device. The flow is generated through the application of an external electric field that acts on the free charges that exists in a thin Debye layer at the channel walls. The charge on the wall is due to the chemistry of the solid-fluid interface, and it can vary along the channel, e.g. due to modification of the wall. This investigation focuses on the simulation of the electroosmotic flow (EOF) profile in a cylindrical microchannel with step change in zeta potential. The modified Navier-Stoke equation governing the velocity field and a non-linear two-dimensional Poisson-Boltzmann equation governing the electrical double-layer (EDL) field distribution are solved numerically using finite control-volume method. Continuities of flow rate and electric current are enforced resulting in a non-uniform electrical field and pressure gradient distribution along the channel. The resulting parabolic velocity distribution at the junction of the step change in zeta potential, which is more typical of a pressure-driven velocity flow profile, is obtained.Singapore-MIT Alliance (SMA

The effects of escitalopram on myocardial apoptosis and the expression of Bax and Bcl-2 during myocardial ischemia/reperfusion in a model of rats with depression

BackgroundMajor depressive disorder (MDD) is an independent risk factor for coronary heart disease (CHD), and influences the occurrence and prognosis of cardiovascular events. Although there is evidence that antidepressants may be cardioprotective after acute myocardial infarction (AMI) comorbid with MDD, the operative pathophysiological mechanisms remain unclear. Our aim was therefore to explore the molecular mechanisms of escitalopram on myocardial apoptosis and the expression of Bax and Bcl-2 in a rat model of depression during myocardial ischemia/reperfusion (I/R).MethodsRats were divided randomly into 3 groups (n = 8): D group (depression), DI/R group (depression with myocardial I/R) and escitalopram + DI/R group. The rats in all three groups underwent the same chronic mild stress and separation for 21 days, at the same time, in the escitalopram + DI/R group, rats were administered escitalopram by gavage (10 mg/kg/day). Ligation of the rat¿s left anterior descending branch was done in the myocardial I/R model. Following which behavioral tests were done. The size of the myocardial infarction was detected using 1.5% TTC dye. The Tunel method was used to detect apoptotic myocardial cells, and both the Rt-PCR method and immunohistochemical techniques were used to detect the expression of Bcl¿2 and Bax.ResultsCompared with the D and DI/R groups, rats in Escitalopram + DI/R group showed significantly increased movements and sucrose consumption (P < .01). Compared with the DI/R group, the myocardial infarct size in the escitalopram + DI/R group was significantly decreased (P < .01). Compared with the D group, there were significantly increased apoptotic myocardial cells in the DI/R and escitalopram + DI/R groups (P < .01); however compared with the DI/R group, apoptotic myocardial cell numbers in the escitalopram + DI/R group were significantly decreased (P < .01). Compared with the DI/R group, there was a down-regulated Bax:Bcl-2 ratio in the escitalopram + DI/R group (P < .01).ConclusionsThese results suggest that in patients with AMI comorbid with MDD, there is an increase in pro-apoptotic pathways that is reversed by escitalopram. This suggests that clinically escitalopram may have a direct cardioprotective after acute myocardial infarction

The Transverse Particle Migration of Highly Filled Polymer Fluid Flow in a Pipe

Shear-induced particle migration was investigated by using a continuum diffusive -flux model for the creep flow of nickel powder filled polymers, which are viscous with shear-thinning characteristic. The model, together with flow equations, was employed for solving the non-Newtonian flow patterns and non-uniform particle concentration distribution of mono-modal suspensions in a pressure-driven tube flow. Particle volume fraction and velocity fields for the non-homogenous shear flow field were predicted for 40% particle volume fraction. The model captures the trends found in experimental investigations.Singapore-MIT Alliance (SMA

The epidermal growth factor receptor (EGFR) is proteolytically modified by the Matriptase–Prostasin serine protease cascade in cultured epithelial cells

AbstractProstasin is expressed at the apical surface of normal epithelial cells and suppresses in vitro invasion of cancer cells. Prostasin re-expression in the PC-3 prostate carcinoma cells down-regulated the epidermal growth factor receptor (EGFR) protein expression and EGF-induced phosphorylation of the extracellular signal-regulated kinases (Erk1/2). We report here that prostasin and its activating enzyme matriptase are capable of inducing proteolytic cleavages in the EGFR extracellular domain (ECD) when co-expressed in the FT-293 cells, generating two amino-terminally truncated fragments EGFR135 and EGFR110, at 135 and 110 kDa. Prostasin's role in EGFR cleavage is dependent on the serine active-site but not the GPI-anchor. The modifications of EGFR were confirmed to be on the primary structure by deglycosylation. EGFR135 and EGFR110 are not responsive to EGF stimulation, indicating loss of the ligand-binding domains. EGFR110 is constitutively phosphorylated and in its presence Erk1/2 phosphorylation is increased in the absence of EGF. The protease-induced EGFR cleavages are not dependent on EGFR phosphorylation. The EGFR ECD proteolytic modification by matriptase–prostasin is also observed in the BEAS-2B normal lung epithelial cells, the BPH-1 benign prostate hyperplasia and the MDA-MB-231 breast cancer cell lines; and represents a novel mechanism for epithelial cells to modulate EGF-EGFR signaling

Some integral inequalities on time scales

In this paper, some new integral inequalities on time scales are presented by using elementarily analytic methods in calculus of time scales.Comment: 8 page

C-terminal truncated hepatitis B virus X protein promotes hepatocellular carcinogenesis through induction of cancer and stem cell-like properties

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Activation of NRG1-ERBB4 signaling potentiates mesenchymal stem cell-mediated myocardial repairs following myocardial infarction

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