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Dive into the research topics where Khalil M. Bitar is active.

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Featured researches published by Khalil M. Bitar.


Nuclear Physics | 1989

The QCD finite temperature transition and hybrid Monte Carlo

Khalil M. Bitar; A.D. Kennedy; Roger Horsley; Steffen Meyer; Pietro Rossi

Using the hybrid Monte Carlo method we consider lattice quantum chromodynamics with Kogut-Susskind staggered fermions on 43 × 4, 63 × 4, 83 × 4 lattices with m = 0.1. Applying finite size scaling methods for a first-order phase transition we find some evidence for a two-phase state.


Physics Letters B | 1987

On solving four-dimensional SU (2) gauge theory by numerically finding its partition function

Gyan Bhanot; Khalil M. Bitar; Román Salvador

Abstract We demonstrate a method to directly simulate the partition function of non-abelian lattice theories. We determine the partition function of the SU(2) lattice gauge theory in four dimensions both for the full SU(2) group and the 120 element icosahedral subgroup on a variety of lattice actions for lattices of size up to 4 4 . All the phenomena (transitions, crossovers, etc.) of these theories are readily observed in our simulation. In addition, even from small lattice simulations, we can distinguish potential critical behavior from rapid changes in order parameters. With the Wilson and adjoint actions we also see a clear line of zeros pointing to the zero temperature ( g 0 2 = 0) fixed point of this theory. We discuss how a finite size scaling analysis of the position of such zeros would yield the beta function of the theory.


Physics Letters B | 1987

The partition function of Z(2) and Z(8) lattice gauge theory in four dimensions, a novel approach to simulations of lattice systems☆

Gyan Bhanot; Khalil M. Bitar; Steve Black; Paul Carter; Román Salvador

Abstract A new method to simulate lattice systems is described. We demonstrate our method by computing the complete partition functions of Z(2) and Z(8) gauge theories in four dimensions on lattices of size up to 64. Our method yields a clear signal for the first order transition(s) in these models without hysteresis or critical slowing down effects. We show how finite size scaling of the zeros of the partition function provides an unambiguous identification of the order of the transition.


Nuclear Physics | 1991

φ4 on F4: Numerical results

Gyan Bhanot; Khalil M. Bitar; Urs M. Heller; Herbert Neuberger

Abstract In this paper we present results from numerically simulating the scalar sector of the minimal standard model on an F 4 lattice. This lattice obeys Lorentz invariance to a higher degree than hypercubic lattices previously used in this context. The major result of our study is that if one is willing to tolerate cutoff effects up to about 3% in the W L -W L scattering cross section, the upper bound on the mass of the Higgs boson in the simplest F 4 model is 590 GeV with an error of about 60 GeV.


Nuclear Physics | 1990

φ4 on F4: analytical results

Gyan Bhanot; Khalil M. Bitar; Urs M. Heller; Herbert Neuberger

Abstract The need to preserve Lorentz invariance including the leading order corrections in the inverse cutoff leads one to pursue the investigation of the Higgs mass bound on an F 4 lattice. In this paper we discuss lattice scattering, scaling violations and finite size effects on F 4 lattices. This allows us to compare the F 4 cutoff to the hypercubic one in the perturbative regime and provides several for formulae that will be needed for analyzing Monte Carlo results in the future.


Physics Letters B | 1994

The heavy quark potential in QCD with 2 flavors of dynamical quarks

Urs M. Heller; Khalil M. Bitar; Robert G. Edwards; A.D. Kennedy

Abstract We compute the heavy quark potential on configurations generated by the HEMCGC Collaboration with dynamical staggered fermions at 6/g2=5.6 and with dynamical Wilson fermions at 6/g2= 5.3. The computations are done on 163 × 32 lattices, corresponding to physical sizes of about 1.6 and 2.3 fm, respectively. Up to the distances probed no sign of string breaking is detectable. We also compute the recently proposed scale r0 defined by r02F(r0) = 1.65.


Comparative Biochemistry and Physiology Part A: Physiology | 1997

Binding of 125I-Insulin on Capillary Endothelial and Myofiber Cell Membranes in Normal and Streptozotocin-Induced Diabetic Perfused Rat Hearts

Raja E. Haddad; Abdu R. Jurjus; Mohamad Z.M. Ibrahim; Zaher A. Nahle; Muna M. El-Kasti; Khalil M. Bitar; Sawsan Ibrahim Kreydiyyeh; Faysal A. Saadeh; Anwar B. Bikhazi

A heart-perfusion technique was employed to measure 125I-insulin binding on capillary endothelial and myocyte cell membranes in Sprague-Dawley rats. Animals were anesthetized, and the anterior chest wall excised to expose the mediastinal contents. The right and left superior and inferior venae cavae were dissected and tied, and another tie was passed around the aorta. A polyethylene catheter was introduced into the aortic lumen from cephalad to caudad to sit with its tip above the aortic valve. Another catheter was introduced into the cavity of the right atrium and both were anchored by sutures. Oxygenated Ringer-Lock buffer containing 20 mM/L K+ and 125I-insulin was perfused at a rate of 1 mL/min via the aortic catheter. Concomitantly, the distal ascending aorta and venae cavae were ligated. The effluent was collected from the right atrial catheter at the same infusion rate. Animals were divided into two groups, the normal group and streptozotocin-induced diabetic group. Heart perfusion was done on both groups either without or after treatment with detergent (CHAPS) to remove the capillary endothelial lining. A physical model for 125I-insulin sequestration as a ligand to its receptors on endothelial and/or myocyte plasma membranes was proposed. The model described a reversible binding of ligand on cellular surface receptor concentration to fit a conservation equation and a first order Bessel function. The binding constants (kn), reversal constants (k-n), dissociation constants kd = k-n/kn, and residency time constants tau = 1/k-n of 125I-insulin in normal untreated, normal CHAPS-treated, diabetic untreated, and diabetic CHAPS-treated hearts were estimated using a theoretically generated curve-fit to the data. Since insulin receptor binding on the capillary endothelial cell surfaces may serve to transport insulin from the intravascular to the subendothelial space, and since streptozotocin-induced diabetes was shown to diminish receptor autophosphorylation and kinase activity and hence internalization of insulin, then one can conclude the following from the data. In the normal heart, removal of the capillary endothelial lining with CHAPS did not alter kn, k-n, kd, and tau of insulin binding as compared to the normal untreated, whereas in the diabetic untreated heart these constants were altered, compared to the diabetic treated. Furthermore, the kn and k-n values in the diabetic CHAPS-treated hearts were the same as for the normals untreated and CHAPS-treated, respectively. In conclusion, the dissociation constants and residency time constants of all groups indicated the possible existence of two types of insulin receptors: the capillary endothelial cell surface insulin receptors with lower residency time (low affinity receptor or combination of insulin and IGF-1 receptors) and the myocyte plasma membrane insulin receptors with higher residency times (high affinity).


Journal of Hypertension | 2005

Effect of insulin and angiotensin II receptor subtype-1 antagonist on myocardial remodelling in rats with insulin-dependent diabetes mellitus

Wael A. Al Jaroudi; Nuha Nuwayri-Salti; Julnar Usta; Darine S. Zwainy; Chehade N. Karam; Khalil M. Bitar; Anwar B. Bikhazi

Objectives To assess the role of insulin or an angiotensin II receptor antagonist (losartan), or both, in preventing cardiomyocyte damage in rats suffering from insulin-dependent diabetes mellitus (IDDM), and to correlate it with insulin receptor modulation at the cardiomyocyte, coronary endothelium and skeletal muscle cell level. Design Animals were divided into groups of normal rats, diabetic rats, and diabetic rats given insulin, each subdivided into a control group and an experimental group treated with losartan. Methods The animals were killed 1 month after enrollment to the study. Perfusion of the heart with iodine-125-labelled insulin was carried out for all the groups and the binding kinetics of insulin to its receptors on the coronary endothelial cells and the cardiomyocytes were determined using a physical/mathematical model. In addition, tissue samples from the heart and intercostal skeletal muscle were snap frozen and used for histological, indirect immunofluorescence and western blot analysis. Results Cardiac muscle from diabetic animals exhibited diffuse cardiomyopathic changes consisting of widespread vacuolation, loss of striation and cellular hypertrophy, which were reduced and even prevented by treatment with insulin and losartan. In addition, losartan seemed to mediate the upregulation of insulin receptor density on cardiomyocytes and skeletal muscle, and increase insulin receptor affinity at the coronary endothelial site. Finally, treatment with losartan induced a significant decrease in glucose concentrations in the diabetic group compared with the appropriate controls. Conclusions Addition of losartan to the standard insulin treatment in non-hypertensive animals with IDDM offers new benefits concerning cardiac protection and prevention of damage. This may be attributed, in part, to insulin receptor density and sensitization.


Annals of Physics | 1991

Path integrals and Voronin's theorem on the universality of the Riemann zeta function☆

Khalil M. Bitar; N.N. Khuri; H.C. Ren

Abstract We present a new approach to the path integral in latticized quantum theories. Our method is based on Voronins theorems on the universality of the Riemann zeta function. We obtain a formula for the partition function as a discrete sum over “paths” with each path labeled by an integer and given by a zeta function evaluated at a fixed set of points in the critical strip. These points are the image of the space-time lattice resulting from a simple linear mapping. A new measure appears in our sum, and its properties are extensively discussed and a method to calculate it is given. We carried out extensive checks of the method for Euclidean quantum mechanics, and compared the results with those obtained from well-established methods as well as exact results. The comparison confirms the validity of the zeta-function method and our calculation of the measure.


Comparative Biochemistry and Physiology C-toxicology & Pharmacology | 2001

Kinetics of lipopolysaccharide clearance by Kupffer and parenchyma cells in perfused rat liver.

Anwar B. Bikhazi; Abdo Jurjus; Maud Kamal; Ali Alhousseini; Rola N Saab; Wael A. Al Jaroudi; Khalil M. Bitar

We studied the kinetics of [3H]lipopolysaccharide ([3H]LPS) (endotoxin) binding to Kupffer cells and hepatocytes at the level of the microtubular system after treatment with gadolinium chloride (GdCl(3)) and colchicine. Liver perfusion in Sprague-Dawley rats involves both portal vein and thoracic inferior vena cava cannulations as inlet and outlet, respectively. The subhepatic inferior vena cava is ligated to prevent perfusate leakage. Buffer containing 2% serum and [3H]LPS is administered at 1 ml/min and collected for 50 min. Rate constants for hepatocellular clearance of [3H]LPS in controls, colchicine-treated rats, GdCl(3)-treated rats, and colchicine plus GdCl(3)-treated rats are assessed using a simplified mathematical model. Forward-binding, reversal-binding, residency time, and influx rate constants are estimated. Results show that in GdCl(3)-treated rats, the hepatocytes effectively clear endotoxin from the circulation, and its ultimate binding affinity at the hepatocyte site is somewhat reduced compared to the Kupffer cells. In colchicine-treated rats, the disruption of the microtubule network altered [3H]LPS binding with Kupffer cells, suggesting that the microfilament-microtubular network also affects Kupffer cell function. Simultaneous treatments with colchicine and GdCl(3) increased the influx rate constant, suggesting that the compiled morphological alterations up-regulated endotoxin clearance by the liver, as indicated by a drastic increase in cellular vacuolation. In conclusion, the kinetics of the trafficking process of [3H]LPS clearance are regulated by apical-sinusoidal endocytotic and canalicular routes.

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Urs M. Heller

Florida State University

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A.D. Kennedy

Florida State University

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Robert G. Edwards

Thomas Jefferson National Accelerator Facility

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Michael C. Ogilvie

Washington University in St. Louis

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Anwar B. Bikhazi

American University of Beirut

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Pietro Rossi

University of California

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D.K. Sinclair

Argonne National Laboratory

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Steven Gottlieb

Indiana University Bloomington

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R. L. Sugar

University of California

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