A discrete gas-cavity model that considers the frictional effects of unsteady pipe flow

Abstract not availableAnton Bergant, Uroš Karadžić, John Vitovský, Igor Vušanović, Angus R. Simpso

Closure to “Systematic Evaluation of One-Dimensional Unsteady Friction Models in Simple Pipelines”

J. P. Vítkovský, A. Bergant, A. R. Simpson and M. F. Lamber

A boundary layer growth model for one-dimensional turbulent unsteady pipe friction

Unsteady flow in pipe networks is efficiently modelled using a one-dimensional flow approximation. It is general practice in engineering to assume a quasi-steady state approximation of the friction for unsteady pipe flows. The result of this approximation is an under-estimation of the damping during fast transient events. To remedy this shortcoming, an unsteady friction model is often employed. Unsteady friction models for laminar flow can be theoretically determined and have been successfully used for many years. However, the same cannot be said for unsteady friction in turbulent flows. A number of empirical unsteady friction models have been formulated, but only perform well for certain unsteady transient event types. This paper presents a new unsteady friction model for turbulent flows based on the growth and destruction of the boundary layer during a transient event.MF Lambert, JP Vítkovský, AR Simpson & A Bergan

Numerical error in weighting function-based unsteady friction models for pipe transients

The accurate simulation of pressure transients in pipelines and pipe networks is becoming increasingly important in water engineering. Applications such as inverse transient analysis for condition assessment, leak detection, and pipe roughness calibration require accurate modeling of transients for longer simulation periods that, in many situations, requires improved modeling of unsteady frictional behavior. In addition, the numerical algorithm used for unsteady friction should be highly efficient, as inverse analysis requires the transient model to be run many times. A popular model of unsteady friction that is applicable to a short-duration transient event type is the weighting function-based type, as first derived by Zielke in 1968. Approximation of the weighting function with a sum of exponential terms allows for a considerable increase in computation speed using recursive algorithms. A neglected topic in the application of such models is evaluation of numerical error. This paper presents a discussion and quantification of the numerical errors that occur when using weighting function-based models for the simulation of unsteady friction in pipe transients. Comparisons of numerical error arising from approximations are made in the Fourier domain where exact solutions can be determined. Additionally, the relative importance of error in unsteady friction modeling and unsteady friction itself in the context of general simulation is discussed.John Vítkovský, Mark Stephens, Anton Bergant, Angus Simpson, and Martin Lamber

Developments in unsteady pipe flow friction modelling

This paper reviews a number of unsteady friction models for transient pipe flow. Two distinct unsteady friction models, the Zielke and the Brunone models, are investigated in detail. The Zielke model, originally developed for transient laminar flow, has been selected to verify its effectiveness for "low Reynolds number" transient turbulent flow. The Brunone model combines local inertia and wall friction unsteadiness. This model is verified using the Vardy's analytically deduced shear decay coefficient C* to predict the Brunone's friction coefficient k rather than use the traditional trial and error method for estimating k. The two unsteady friction models have been incorporated into the method of characteristics water hammer algorithm. Numerical results from the quasi-steady friction model and the Zielke and the Brunone unsteady friction models are compared with results of laboratory measurements for water hammer cases with laminar and low Reynolds number turbulent flows. Conclusions about the range of validity for the three friction models are drawn. In addition, the convergence and stability of these models are addressed.Anton Bergant, Angus Ross Simpson, John Vìtkovsk

Analysis of Blood Stem Cell Activity and Cystatin Gene Expression in a Mouse Model Presenting a Chromosomal Deletion Encompassing Csta and Stfa2l1

The cystatin protein superfamily is characterized by the presence of conserved sequences that display cysteine protease inhibitory activity (e.g., towards cathepsins). Type 1 and 2 cystatins are encoded by 25 genes of which 23 are grouped in 2 clusters localized on mouse chromosomes 16 and 2. The expression and essential roles of most of these genes in mouse development and hematopoiesis remain poorly characterized. In this study, we describe a set of quantitative real-time PCR assays and a global expression profile of cystatin genes in normal mouse tissues. Benefiting from our collection of DelES embryonic stem cell clones harboring large chromosomal deletions (to be reported elsewhere), we selected a clone in which a 95-kb region of chromosome 16 is missing (Del16qB3Δ/+). In this particular clone, 2 cystatin genes, namely Csta and Stfa2l1 are absent along with 2 other genes (Fam162a, Ccdc58) and associated intergenic regions. From this line, we established a new homozygous mutant mouse model (Del16qB3Δ/16qB3Δ) to assess the in vivo biological functions of the 2 deleted cystatins. Stfa2l1 gene expression is high in wild-type fetal liver, bone marrow, and spleen, while Csta is ubiquitously expressed. Homozygous Del16qB3Δ/16qB3Δ animals are phenotypically normal, fertile, and not overtly susceptible to spontaneous or irradiation-induced tumor formation. The hematopoietic stem and progenitor cell activity in these mutant mice are also normal. Interestingly, quantitative real-time PCR expression profiling reveals a marked increase in the expression levels of Stfa2l1/Csta phylogenetically-related genes (Stfa1, Stfa2, and Stfa3) in Del16qB3Δ/16qB3Δ hematopoietic tissues, suggesting that these candidate genes might be contributing to compensatory mechanisms. Overall, this study presents an optimized approach to globally monitor cystatin gene expression as well as a new mouse model deficient in Stfa2l1/Csta genes, expanding the available tools to dissect cystatin roles under normal and pathological conditions

Regulation of Cathepsin G Reduces the Activation of Proinsulin-Reactive T Cells from Type 1 Diabetes Patients

Autoantigenic peptides resulting from self-proteins such as proinsulin are important players in the development of type 1 diabetes mellitus (T1D). Self-proteins can be processed by cathepsins (Cats) within endocytic compartments and loaded to major histocompatibility complex (MHC) class II molecules for CD4+ T cell inspection. However, the processing and presentation of proinsulin by antigen-presenting cells (APC) in humans is only partially understood. Here we demonstrate that the processing of proinsulin by B cell or myeloid dendritic cell (mDC1)-derived lysosomal cathepsins resulted in several proinsulin-derived intermediates. These intermediates were similar to those obtained using purified CatG and, to a lesser extent, CatD, S, and V in vitro. Some of these intermediates polarized T cell activation in peripheral blood mononuclear cells (PBMC) from T1D patients indicative for naturally processed T cell epitopes. Furthermore, CatG activity was found to be elevated in PBMC from T1D patients and abrogation of CatG activity resulted in functional inhibition of proinsulin-reactive T cells. Our data suggested the notion that CatG plays a critical role in proinsulin processing and is important in the activation process of diabetogenic T cells