Interparticle interaction and structure of deposits for competitive model in (2+1)- dimensions

A competitive (2+1)-dimensional model of deposit formation, based on the combination of random sequential absorption deposition (RSAD), ballistic deposition (BD) and random deposition (RD) models, is proposed. This model was named as RSAD$_{1-s}$(RD$_f$BD$_{1-f}$)$_s$. It allows to consider different cases of interparticle interactions from complete repulsion between near-neighbors in the RSAD model ($s=0$) to sticking interactions in the BD model ($s=1, f=0$) or absence of interactions in the RD model ($s=1$, $f=0$). The ideal checkerboard ordered structure was observed for the pure RSAD model ($s=0$) in the limit of $h \to \infty$. Defects in the ordered structure were observed at small $h$. The density of deposit $p$ versus system size $L$ dependencies were investigated and the scaling parameters and values of $p_\infty=p(L=\infty)$ were determined. Dependencies of $p$ versus parameters of the competitive model $s$ and $f$ were studied. We observed the anomalous behaviour of the eposit density $p_\infty$ with change of the inter-particle repulsion, which goes through minimum on change of the parameter $s$. For pure RSAD model, the concentration of defects decreases with $h$ increase in accordance with the critical law $\rho\propto h^{-\chi_{RSAD}}$, where $\chi_{RSAD} \approx 0.119 \pm 0.04$.Comment: 10 pages,4 figures, Latex, uses iopart.cl

Percolation in deposits for competitive models in (1+1)-dimensions

The percolation behaviour during the deposit formation, when the spanning cluster was formed in the substrate plane, was studied. Two competitive or mixed models of surface layer formation were considered in (1+1)-dimensional geometry. These models are based on the combination of ballistic deposition (BD) and random deposition (RD) models or BD and Family deposition (FD) models. Numerically we find, that for pure RD, FD or BD models the mean height of the percolation deposit $\bar h$ grows with the substrate length $L$ according to the generalized logarithmic law $\bar h\propto (\ln (L))^\gamma$, where $\gamma=1.0$ (RD), $\gamma=0.88\pm 0.020$ (FD) and $\gamma=1.52\pm 0.020$ (BD). For BD model, the scaling law between deposit density $p$ and its mean height $\bar h$ at the point of percolation of type $p-p_\infty \propto \bar h^{-1/\nu_h}$ are observed, where $\nu_h =1.74\pm0.02$ is a scaling coefficient. For competitive models the crossover, %in $h$ versus $L$ corresponding to the RD or FD -like behaviour at small $L$ and the BD-like behaviour at large $L$ are observed.Comment: 8 pages,4 figures, Latex, uses iopart.cl

Expression of Xenobiotic Metabolizing Enzymes in Different Lung Compartments of Smokers and Nonsmokers

BACKGROUND: Cytochrome P450 monooxygenases (CYP) play an important role in the defense against inhaled toxicants, and expression of CYP enzymes may differ among various lung cells and tissue compartments. METHODS: We studied the effects of tobacco smoke in volunteers and investigated gene expression of 19 CYPs and 3 flavin-containing monooxygenases, as well as isoforms of gluthathione S-transferases (GST) and uridine diphosphate glucuronosyltransferases (UGT) and the microsomal epoxide hydrolase (EPHX1) in bronchoalveolar lavage cells and bronchial biopsies derived from smokers (n = 8) and nonsmokers (n = 10). We also investigated gene expression of nuclear transcription factors known to be involved in the regulation of xenobiotic metabolism enzymes. RESULTS: Gene expression of CYP1A1, CYP1B1, CYP2S1, GSTP1, and EPHX1 was induced in bronchoalveolar lavage cells of smokers, whereas expression of CYP2B6/7, CYP3A5, and UGT2A1 was repressed. In bronchial biopsies of smokers, CYP1A1, CYP1B1, CYP2C9, GSTP1, and GSTA2 were induced, but CYP2J2 and EPHX1 were repressed. Induction of CYP1A1 and CYP1B1 transcript abundance resulted in increased activity of the coded enzyme. Finally, expression of the liver X receptor and the glucocorticoid receptor was significantly up-regulated in bronchoalveolar lavage cells of smokers. CONCLUSIONS: We found gene expression of pulmonary xenobiotic metabolizing enzymes and certain key transcription factors to be regulated in bronchoalveolar lavage cells and bronchial biopsies of smokers. The observed changes demonstrate tissue specificity in xenobiotic metabolism, with likely implications for the metabolic activation of procarcinogens to ultimate carcinogens of tobacco smoke

Crossover effects in a discrete deposition model with Kardar-Parisi-Zhang scaling

We simulated a growth model in 1+1 dimensions in which particles are aggregated according to the rules of ballistic deposition with probability p or according to the rules of random deposition with surface relaxation (Family model) with probability 1-p. For any p>0, this system is in the Kardar-Parisi-Zhang (KPZ) universality class, but it presents a slow crossover from the Edwards-Wilkinson class (EW) for small p. From the scaling of the growth velocity, the parameter p is connected to the coefficient of the nonlinear term of the KPZ equation, lambda, giving lambda ~ p^gamma, with gamma = 2.1 +- 0.2. Our numerical results confirm the interface width scaling in the growth regime as W ~ lambda^beta t^beta, and the scaling of the saturation time as tau ~ lambda^(-1) L^z, with the expected exponents beta =1/3 and z=3/2 and strong corrections to scaling for small lambda. This picture is consistent with a crossover time from EW to KPZ growth in the form t_c ~ lambda^(-4) ~ p^(-8), in agreement with scaling theories and renormalization group analysis. Some consequences of the slow crossover in this problem are discussed and may help investigations of more complex models.Comment: 16 pages, 7 figures; to appear in Phys. Rev.

Percolation in Models of Thin Film Depositions

We have studied the percolation behaviour of deposits for different (2+1)-dimensional models of surface layer formation. The mixed model of deposition was used, where particles were deposited selectively according to the random (RD) and ballistic (BD) deposition rules. In the mixed one-component models with deposition of only conducting particles, the mean height of the percolation layer (measured in monolayers) grows continuously from 0.89832 for the pure RD model to 2.605 for the pure RD model, but the percolation transition belong to the same universality class, as in the 2- dimensional random percolation problem. In two- component models with deposition of conducting and isolating particles, the percolation layer height approaches infinity as concentration of the isolating particles becomes higher than some critical value. The crossover from 2d to 3d percolation was observed with increase of the percolation layer height.Comment: 4 pages, 5 figure

Range expansion with mutation and selection: dynamical phase transition in a two-species Eden model

The colonization of unoccupied territory by invading species, known as range expansion, is a spatially heterogeneous non-equilibrium growth process. We introduce a two-species Eden growth model to analyze the interplay between uni-directional (irreversible) mutations and selection at the expanding front. While the evolutionary dynamics leads to coalescence of both wild-type and mutant clusters, the non-homogeneous advance of the colony results in a rough front. We show that roughening and domain dynamics are strongly coupled, resulting in qualitatively altered bulk and front properties. For beneficial mutations the front is quickly taken over by mutants and growth proceeds Eden-like. In contrast, if mutants grow slower than wild-types, there is an antagonism between selection pressure against mutants and growth by the merging of mutant domains with an ensuing absorbing state phase transition to an all-mutant front. We find that surface roughening has a marked effect on the critical properties of the absorbing state phase transition. While reference models, which keep the expanding front flat, exhibit directed percolation critical behavior, the exponents of the two-species Eden model strongly deviate from it. In turn, the mutation-selection process induces an increased surface roughness with exponents distinct from that of the classical Eden model

Dysregulation of Chemokine/Chemokine Receptor Axes and NK Cell Tissue Localization during Diseases.

Chemokines are small chemotactic molecules that play key roles in physiological and pathological conditions. Upon signaling via their specific receptors, chemokines regulate tissue mobilization and trafficking of a wide array of immune cells, including natural killer (NK) cells. Current research is focused on analyzing changes in chemokine/chemokine receptor expression during various diseases to interfere with pathological trafficking of cells or to recruit selected cell types to specific tissues. NK cells are a heterogeneous lymphocyte population comprising several subsets endowed with distinct functional properties and mainly representing distinct stages of a linear development process. Because of their different functional potential, the type of subset that accumulates in a tissue drives the final outcome of NK cell-regulated immune response, leading to either protection or pathology. Correspondingly, chemokine receptors, including CXCR4, CXCR3, and CX3CR1, are differentially expressed by NK cell subsets, and their expression levels can be modulated during NK cell activation. At first, this review will summarize the current knowledge on the contribution of chemokines to the localization and generation of NK cell subsets in homeostasis. How an inappropriate chemotactic response can lead to pathology and how chemokine targeting can therapeutically affect tissue recruitment/localization of distinct NK cell subsets will also be discussed

From dynamical scaling to local scale-invariance: a tutorial

Dynamical scaling arises naturally in various many-body systems far from equilibrium. After a short historical overview, the elements of possible extensions of dynamical scaling to a local scale-invariance will be introduced. Schr\"odinger-invariance, the most simple example of local scale-invariance, will be introduced as a dynamical symmetry in the Edwards-Wilkinson universality class of interface growth. The Lie algebra construction, its representations and the Bargman superselection rules will be combined with non-equilibrium Janssen-de Dominicis field-theory to produce explicit predictions for responses and correlators, which can be compared to the results of explicit model studies. At the next level, the study of non-stationary states requires to go over, from Schr\"odinger-invariance, to ageing-invariance. The ageing algebra admits new representations, which acts as dynamical symmetries on more general equations, and imply that each non-equilibrium scaling operator is characterised by two distinct, independent scaling dimensions. Tests of ageing-invariance are described, in the Glauber-Ising and spherical models of a phase-ordering ferromagnet and the Arcetri model of interface growth.Comment: 1+ 23 pages, 2 figures, final for

Epidemiology of injuries presenting to the national hospital in Kampala, Uganda: implications for research and policy

BackgroundDespite the growing burden of injuries in LMICs, there are still limited primary epidemiologic data to guide health policy and health system development. Understanding the epidemiology of injury in developing countries can help identify risk factors for injury and target interventions for prevention and treatment to decrease disability and mortality.AimTo estimate the epidemiology of the injury seen in patients presenting to the government hospital in Kampala, the capital city of Uganda.MethodsA secondary analysis of a prospectively collected database collected by the Injury Control Centre-Uganda at the Mulago National Referral Hospital, Kampala, Uganda, 2004-2005.ResultsFrom 1 August 2004 to 12 August 2005, a total of 3,750 injury-related visits were recorded; a final sample of 3,481 records were analyzed. The majority of patients (62%) were treated in the casualty department and then discharged; 38% were admitted. Road traffic injuries (RTIs) were the most common causes of injury for all age groups in this sample, except for those under 5 years old, and accounted for 49% of total injuries. RTIs were also the most common cause of mortality in trauma patients. Within traffic injuries, more passengers (44%) and pedestrians (30%) were injured than drivers (27%). Other causes of trauma included blunt/penetrating injuries (25% of injuries) and falls (10%). Less than 5% of all patients arriving to the emergency department for injuries arrived by ambulance.ConclusionsRoad traffic injuries are by far the largest cause of both morbidity and mortality in Kampala. They are the most common cause of injury for all ages, except those younger than 5, and school-aged children comprise a large proportion of victims from these incidents. The integration of injury control programs with ongoing health initiatives is an urgent priority for health and development