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|Publication number
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|Jul 28, 1998
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|Jun 2, 1995
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|Jun 2, 1994
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|Grzegorz Ocieczek, Mika Tiusanen
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|Abb Atom Ab
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|Patent Citations (5), Non-Patent Citations (2), Referenced by (32), Classifications (13), Legal Events (5)
|External Links: USPTO, USPTO Assignment, Espacenet
The present invention relates to a method for supervision of a neutron flux detector in the reactor core of a nuclear reactor comprising a plurality of neutron flux detectors.
A core in a nuclear reactor comprises a plurality of fuel assemblies. These are arranged vertically in the core in spaced relationship to each other. A fuel assembly comprises a plurality of vertical fuel rods, each of which contains a stack of circular-cylindrical pellets of a nuclear fuel, arranged in a cladding tube. The core is immersed into water which serves both as coolant and as neutron moderator. The reactor core also comprises a plurality of control rods which, by being inserted into and withdrawn from the core, control the reactivity of the core and hence its output power.
A boiling-water nuclear reactor (BWR) comprises a large number of neutron-sensitive detectors, so-called LPRM (Linear Power Range Monitor) detectors. The core comprises, regularly spaced from each other, a plurality of detector tubes, each one comprising four LPRM detectors placed at four different levels in the vertical direction. The detectors, which form a regular lattice in the core, measure the neutron flux which is directly proportional to the power. The output signals from the detectors are used as a basis for supervising the core and calculating the margins of the reactor and are connected to different safety functions. It is, therefore, important that any faults in the detectors be discovered and that the faulty detector be identified as soon as possible.
The LPRM detectors comprise a fissile material for detection of the neutron flux. When the detector is subjected to neutron irradiation, the fissile material is consumed, which means that the detector deflection is changed with time. The reduction of fissile material in the detectors is different for different detectors and depends on the amount of radiation to which the detector has been exposed. To compensate for this, the detectors are calibrated at regular intervals, approximately once every month. For this purpose, a movable neutron-sensitive detector, a so-called TIP detector (Traveling Incore Probe) is used, which is inserted through all the detector tubes in the core. The TIP detector measures the neutron flux at the same locations in the tube at which the LPRM detectors are placed. These TIP measured values are used as reference values and all the LPRM detectors are adjusted so as to coincide with the TIP measured values.
The LPRM measurements contain a high degree of noise. In addition, the detectors operate under extremely difficult conditions where the risk of faults arising in the detectors is relatively high. The LPRM detectors are filled with gas, for example argon. A frequently occurring fault is that a crack in the detector causes the gas slowly to leak out, which in turn causes the detector to drift. This type of fault is difficult to discover and requires that the output signals from the detector be studied for a long period of time.
The method currently used for supervising the LPRM detectors compares the output signals from the detectors with calculated values from a core simulator. This method has many uncertainties since the calculated values may be subjected to both model faults and faults in the input signals to the calculations. If the output signal from a detector differs from the calculated value, it may be difficult to determine whether there is a fault in the detector or a fault in the calculated value.
The LPRM detector may also be supervised by studying the output signal from the detector for a long period to see whether the detector is drifting or is otherwise defective. This method is not completely reliable either since it does not take into consideration whether the operating conditions have been changed during the period studied.
The invention aims to provide a method for supervision of a neutron detector in a reactor core, which method on the one hand indicates that the detector is defective and on the other hand gives an indication as to the type of fault occurring. The method is suitable for continuous supervision of the detector.
FIG. 1 is a schematic view of a reactor core with a detector tube in a cross section.
FIG. 2 shows part of the core in FIG. 1 in a horizontal section through level D.
FIG. 3 shows an enlarged view of part of the reactor core in FIG. 2.
FIG. 4 shows an example of a process element.
FIG. 5 shows a sigmoid function.
FIG. 6 shows an example of a neural network with three levels.
FIGS. 7a-7e show different trends of the output signal from an LPRM detector.
FIG. 8 shows a neural network for identifying trends in the output signal from an LPRM detector according to one embodiment of the invention; and
FIG. 9 shows a table of how different types of fault can be determined based on the state signals of the supervised detector and a number of reference values.
FIGS. 1, 2 and 3 show an example of a reactor core with neutron detectors to which the invention is applicable.
FIG. 1 shows a reactor vessel 1, associated with a boiling-water reactor, in cross section. The reactor core 2 contains fuel in the form of fuel assemblies between and through which cooling water is pumped. A plurality of vertical neutron detector tubes are arranged evenly distributed over the core. The figure shows a cross section of a neutron detector tube 3. The neutron detector tube includes four equidistantly distributed, fixedly mounted neutron flux detectors 4A, 4B, 4C, 4D, so-called LPRM detectors. All the LPRM detectors in the core are distributed at four levels, 80%, 60%, 40% and 20% of the height of the core. The levels are designated A, B, C, D in FIG. 1. The core comprises about 80-150 LPRM detectors, depending on the reactor type. The LPRM detectors form a rectangular lattice in the core. A movable neutron flux detector 5, a so-called TIP detector, may be run up and down in the neutron detector tube.
FIG. 2 shows part of the core in FIG. 1 in a horizontal section through level D. Fuel assemblies 6 with a substantially square cross section are arranged vertically in the core at a certain distance from each other. This forms a check pattern of vertically extending gaps between the fuel assemblies. The section includes 36 fuel assemblies. The total number of fuel assemblies in a whole cross section amounts to several hundred. The reactor core comprises a plurality of control rods 7, placed parallel to the fuel assemblies in the vertically extending gaps. In the vertically extending gaps, LPRM detectors 4D1 -4D9 are arranged. The control rods in the core are divided into control rod groups. When the control rods are to be moved, this is done in groups. An individual detector is normally never moved alone, but only together with the other control rods included in the same control rod group.
FIG. 3 shows an enlarged view of part of the reactor core in FIG. 2. The fuel assemblies 6 are enclosed in fuel channels 8, which are provided with a hollow support member 9 of cruciform cross section. The fuel channel with the support member is divided into four vertical channel-formed parts 10, so-called sub-assemblies, with at least substantially square cross section. Each sub-assembly contains a plurality of fuel rods 11. The rods are arranged in a lattice in which each rod is included in two rows perpendicular to each other. The rods are kept in their positions by so-called spacers (not shown), placed between top tie and bottom tie plates (also not shown) on the fuel assembly. The spaces between the fuel rods 11 within each sub-assembly 10 are traversed by water as is the cruciform channel 12 formed by the support member 9. The gaps between the fuel assemblies are also traversed by water.
The control rods 7 have a cruciform cross section with four blades 13 which are perpendicular to each other and which extend from a central part. The gaps into which the control rods can be inserted, the so-called control rod gaps 14b, are in this embodiment wider than the gaps where no control rods can be inserted, the so-called narrow gaps 14a. Centered between four control rods, that is, at the intersectional point between two narrow gaps 14a, a neutron detector tube 3 is arranged. The neutron detector tube comprises an LPRM detector 4D5.
The output signal from a defective detector may occur in different ways depending on the fault of the detector. If the detector does not react at all, the output signal remains constant at the same level no matter what happens around it. If the detector drives upwards or downwards, it behaves as normal, but its output signal is somewhat higher/lower than earlier. For different reasons, a detector may suddenly break and then exhibits a jump upwards or downwards in the output signal. FIGS. 7a-7e show five different trends of the output signal which may indicate that the detector is defective.
FIG. 7a shows an example of a constant output signal. The output signal consists only of noise on an otherwise constant signal. FIG. 7b shows an example of a weakly decreasing signal. FIG. 7c shows an example of a suddenly decreasing signal. FIG. 7d shows an example of a weakly increasing signal. FIG. 7e shows an example of a suddenly increasing signal.
The output signal from a detector often consists of a great deal of noise and it may, therefore, be difficult to discover faults, such as a drifting or a non-reacting detector. To identify certain patterns in the output signal which may indicate a fault in the detector, a neural network is used according to the invention.
A neural network comprises a number of process elements distributed at different levels and connected to one another through one-way connections. A process element has a plurality of inputs but only one output. FIG. 4 shows an example of a process element where x0 -xn constitute input signals. The input signals are multiplied by a connection weight W0 -Wn, specific for each input signal, and are summed. ##EQU1##
The output signal from the process element consists of the sum, Y=f(I), transformed via a transfer function. FIG. 5 shows a sigmoid function which is an often used transfer function. The output signal from the process element may, in turn, constitute the input signal to a plurality of other process elements at a higher level.
FIG. 6 shows an example of how a large number of process elements 20 may be organized in different layers so as to form a neural network. The number of layers and the number of process elements in each layer depend on the intended application. The network in FIG. 6 consists of three layers. An input layer 21, having n process elements, functions as a buffer for the input signals x1 -xn. A hidden layer 22 consists of k process elements. An output layer 23 contains m process elements which buffer the output signals Y1 -Ym. How the network behaves for different input signals is determined by the connection weights Wx and these are determined in a learning phase.
Before the network can be used, it has to undergo a learning phase to learn how to respond to different input signals. For that purpose, a plurality of sets of input signals with associated known output signals and a back-propagation algorithm are required. Each set of input signals is sent through the network and the output signals obtained are compared with the known output signals, and based on the comparison a total error is calculated. The total error is minimized by modifying the connection weights. The back-propagation algorithm distributes the total error among all the process elements in the network by sending the error backwards through the network while at the same time the connection weights Wx are adjusted. The input signals are sent through the network again and the total error between the new output signals and the known output signals is calculated. If the total error exceeds a minimum allowed error, the error is sent backwards while at the same time the connection weights are adjusted again. This process is repeated until the total error is less than the minimum allowed error. By being repeatedly trained with different sets of input signals with associated known output signals in this way, the network learns how to behave.
Neural networks are known per se and more about their function is described in The Electrical Engineering Handbook, pages 420-429, editor Richard C. Dorf, 1993, by CRC Press. For using neural networks there are ready-to-use computer programs, which are provided freely. In the following embodiments, there is used an ANN back-propagation algorithm program called ASPRIN V 5.0 published by MITRE Corporation, U.S.A.
The invention is based on the fact that a neural network is taught to identify a number of different trends on the basis of a plurality of input signals. In the following a preferred embodiment is described in which the neural network identifies the following five different trends: constant, weakly decreasing, suddenly decreasing, weakly increasing, and suddenly increasing.
The input signals to the neural network consist of a time window. An LPRM detector is read at regular intervals, in this example every tenth second. A suitable time window consists of the last 50 readings from the detector. The measured values from the last 50 readings are saved and constitute input signals to the neural network which calculates new trends every tenth second.
FIG. 8 shows an example of a neural network for identifying the above-mentioned trends in the output signal from an LPRM detector. Such a neural network is hereinafter referred to as a trend network. The input layer 31 consists of 50 process elements which are supplied with input signals S(t)-S(t-49Δt) corresponding to the measured values from the last 50 readings of the detector. Δt is the time between two readings and in this example Δ=10s. The hidden layer 32 contains 25 process elements. The number may, of course, be both greater and smaller than 25. A greater number of process elements in the hidden layer gives greater accuracy while at the same time the calculations take longer. A smaller number of process elements gives faster calculations and less accuracy. The output layer 33 consists of four process elements, the output signals of which are hereinafter referred to as state signals N1-N4, of which
N1 indicates a weakly decreasing trend
N2 indicates a suddenly decreasing trend
N3 indicates a weakly increasing trend
N4 indicates a suddenly increasing trend.
If none of the state signals indicates any trend, this means that the trend is constant. The transfer function consists of a sigmoid function with a definition range 0.1!.
During a learning phase, the network learns to identify the five different trends. For teaching the trend network, data can be used either as proper data from a nuclear power plant under operation, or as data calculated during simulations. In this example, only simulated data are used. Sets of simulated input signals are stored in a data file and then constitute input data to a back-propagation algorithm program, for example ASPRIN V 5.0. At the beginning of the learning period, the input signals to the network are pure, that is, free of noise, and with a clear inclination. Gradually during the learning, the noise level is increased and the inclination reduced. A suitable number of sets of input signals may be between 2000 and 3000. The state signal is set at 0.9 when it indicates a trend, and at 0.0 when it does not indicate a trend.
To supervise the LPRM detector, the trend network is supplied with measured signals from the detector, and based on the connection weights determined during the learning phase, four state signals, N1s, N2s, N3s, N4s, are calculated for the supervised detector. During operation, the output signal of the detector rises and falls because of quite normal phenomena, for example a power increase or a power decrease. The output signal of the detector largely depends on the movements of the control rods. To be able to determine on the basis of the state signals of the detector whether the detector is defective, the state signals must be compared with state signals from other detectors in the core. In case of a power increase, a power decrease or control rod movements, a single detector is never influenced alone but a plurality of detectors exhibit the same tendencies.
Four reference detectors are selected for each supervised detector. The reference detectors should be chosen such that they behave in the same way as the investigated detector with regard to the movements of the control rods. In this embodiment, the reference detectors are chosen such that they are located at the same level in the core as the investigated detector. Two of the reference detectors are chosen such that they are located in the immediate vicinity of the investigated detector. The other two reference detectors are chosen such that they are located further away in the core, and in a position which is symmetrical in relation to a control rod which is included in the same control rod group as the investigated detector.
During the supervision, the trend network is supplied with measured signals from the reference detectors, and based on the connection weights determined during the learning phase, four state signals are calculated for each one of the reference detectors, N1ri, N2ri, N3ri, N4ri, i=1 . . . 4. To be able to determine whether the supervised detector is defective, its state signals must be compared with the state signals of the reference detectors. To facilitate the comparison, four reference values R1, R2, R3, R4 are calculated, which constitute the mean value of the corresponding state signals for the reference detectors. ##EQU2##
The state signals for the supervised detector are compared with the reference values. Based on the comparison, conclusions may be drawn as to whether the detector is defective and which type of fault has occurred in the detector. A number of types of fault, which may be read from the comparisons, are listed below. FIG. 9 shows how different types of fault may be determined based on the state signals of the detector and the reference values. If the magnitude of a reference value or a state signal is of no importance for the interpretation of a certain type of fault, it has been marked with an x in the table.
Error No. 1: The detector does not respond. All four state signals for the supervised detector are smaller than 0.1, and at least one of the reference values is greater than 0.4. This means that the supervised detector does not move in spite of the fact that the reference detectors are moving.
Error No. 2: The detector drives downwards. N1s is greater than 0.4 and R1 is smaller than 0.1. The supervised detector exhibits a decreasing trend not exhibited by the reference detectors.
Error No. 3: The detector makes a jump downwards. N2s is greater than 0.4 and R2 is smaller than 0.1. The supervised detector exhibits a suddenly decreasing trend not exhibited by the reference detectors.
Error No. 4: The detector drives upwards. N3s is greater than 0.4, and R3 is smaller than 0.1. The supervised detector exhibits an increasing trend not exhibited by the reference detectors.
Error No. 5: The detector makes a jump upwards. N4s is greater than 0.4 and R4 is smaller than 0.1. The supervised detector exhibits a suddenly increasing trend not exhibited by the reference detectors.
Error No. 6: The detector oscillates. Within one and the same time window, the output signal both rises and falls in spite of the fact that the reference signal is substantially constant.
Error No. 7: Fast oscillations or an abnormally high noise level give this type of error.
In the examples above, four reference detectors have been selected but, of course, the number may be both greater and smaller than four and their location in the core may be chosen in some other way.
With the method described above, a selected number of, or all the detectors in the core, may be supervised. A supervised detector may, while at the same time being supervised, constitute a reference detector for one or more other supervised detectors.
|Cited Patent
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|Doryokuro Kakunenryo Kaihatsu Jigyodan
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|Electric Power Research Institute, Inc.
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|Martin Marietta Energy Systems, Inc.
|Automated method for the systematic interpretation of resonance peaks in spectrum data
|The Electrical Engineering Handbook, pp. 420 429, editor Richard C. Dorf, 1993, CRC Press.
|The Electrical Engineering Handbook, pp. 420-429, editor Richard C. Dorf, 1993, CRC Press.
|Citing Patent
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|Nov 22, 2000
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|Smartsignal Corporation
|Inferential signal generator for instrumented equipment and processes
|Aug 31, 2001
|Oct 14, 2003
|Hitachi, Ltd.
|Reactor power output measurement device
|Mar 9, 2001
|Aug 10, 2004
|Smartsignal Corporation
|Generalized lensing angular similarity operator
|Mar 20, 2003
|Apr 5, 2005
|Smartsignal Corporation
|Inferential signal generator for instrumented equipment and processes
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|Oct 4, 2005
|Smartsignal Corporation
|Signal differentiation system using improved non-linear operator
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|Smartsignal Corporation
|Complex signal decomposition and modeling
|Jun 7, 2002
|Dec 13, 2005
|Smartsignal Corporation
|Residual signal alert generation for condition monitoring using approximated SPRT distribution
|Feb 27, 2001
|Jun 19, 2007
|Smartsignal Corporation
|Adaptive modeling of changed states in predictive condition monitoring
|May 11, 2005
|Aug 5, 2008
|Smartsignal Corporation
|Complex signal decomposition and modeling
|Oct 9, 2003
|May 26, 2009
|Smartsignal Corporation
|Diagnostic systems and methods for predictive condition monitoring
|Feb 16, 2001
|Jun 15, 2010
|Smartsignal Corporation
|System for extraction of representative data for training of adaptive process monitoring equipment
|Mar 26, 2008
|Aug 7, 2012
|Smartsignal Corporation
|Complex signal decomposition and modeling
|Sep 18, 2007
|Sep 25, 2012
|Smartsignal Corporation
|Kernel-based method for detecting boiler tube leaks
|Dec 14, 2007
|Nov 13, 2012
|Smartsignal Corporation
|Robust distance measures for on-line monitoring
|Jan 29, 2010
|Feb 26, 2013
|Honeywell International Inc.
|Noisy monitor detection and intermittent fault isolation
|Jun 15, 2009
|Mar 25, 2014
|International Business Machines Corporation
|Managing component coupling in an object-centric process implementation
|Feb 20, 2013
|Dec 8, 2015
|Westinghouse Electric Company Llc
|Method of validating nuclear reactor in-vessel detector output signals
|Apr 1, 2009
|Apr 26, 2016
|Ge-Hitachi Nuclear Energy Americas Llc
|Methods and apparatuses for operating nuclear reactors and for determining power levels in the nuclear reactors
|Feb 12, 2001
|May 9, 2002
|Wegerich Stephan W.
|Signal differentiation system using improved non-linear operator
|Feb 27, 2001
|Sep 19, 2002
|Wegerich Stephan W.
|Adaptive modeling of changed states in predictive condition monitoring
|Jun 7, 2002
|Mar 20, 2003
|Wegerich Stephan W.
|Residual signal alert generation for condition monitoring using approximated SPRT distribution
|Oct 22, 2002
|Jul 24, 2003
|Wegerich Stephan W.
|Diagnostic systems and methods for predictive condition monitoring
|Mar 20, 2003
|Aug 21, 2003
|Wegerich Stephen W.
|Inferential signal generator for instrumented equipment and processes
|Jul 16, 2004
|Dec 23, 2004
|Smartsignal Corporation
|Generalized lensing angular similarity operator
|Jul 12, 2004
|Dec 30, 2004
|Neuralab Limited
|Prevention and treatment of amyloidogenic disease
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|Complex signal decomposition and modeling
|Sep 30, 2008
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|Honeywell International Inc.
|Intermittent fault detection and reasoning
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|Dec 16, 2010
|International Business Machines Corporation
|Managing componenet coupling in an object-centric process implementation
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|Honeywell International Inc.
|Noisy monitor detection and intermittent fault isolation
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|Korea Hydro & Nuclear Power Co., Ltd.
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|U.S. Classification
|376/254, 706/31, 706/16, 706/915, 376/215, 706/25
|International Classification
|Cooperative Classification
|European Classification
|Feb 27, 1997
Owner name: ABB ATOM AB, SWEDEN
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It is widely accepted that the development of carcinomas, the most common type of human cancer, is due to accumulation of somatic mutations in epithelial cells. The behavior of carcinomas is also influenced by the tumour microenvironment that includes extracellular matrix, blood vasculature, inflammatory cells and fibroblasts. Recent studies reveal that fibroblasts have a more profound influence on the development and progression of carcinomas than previously appreciated. These new findings also have therapeutic implications.
Work over the past two decades have delineated the genetic lesions that occur in epithelial cells leading to the initiation and progression of carcinomas, the most common form of human cancer1. The discoveries of genetic changes in somatic cancer cells have not only advanced our basic understanding of tumour formation but also significantly influenced the treatment of cancer with the use of new therapies targeted to specific pathways affected by genetic lesions (see Overview).
Carcinoma cells, like normal epithelial cells, live in a complex microenvironment that includes the extracellular matrix (ECM), diffusible growth factors and cytokines, and a variety of non-epithelial cell types, including those comprising the vasculature (endothelial cells, pericytes, smooth muscle cells), those that can respond to infection and injury (lymphocytes, macrophages, mast cells), and fibroblasts. It has long been recognized that carcinomas induce a modified stroma through expression of growth factors that promotes angiogenesis, altered ECM expression, accelerated fibroblast proliferation, and increased inflammatory cell recruitment2,3 (Figure 1).
Blood vessels are a critical component of the tumour microenvironment. Without formation of new blood vessels, carcinomas cannot grow beyond a very small size or metastasize and reform in distant organs4. Tumour angiogenesis is due in part to secretion of endothelial growth factors by tumours, and indeed, a targeted therapy (Avastin) that blocks the action of one of these factors (VEGF) has recently been approved (see also Overview)5.
There is also a functional relationship between inflammation and cancer9. Cancers frequently arise in areas of chronic inflammation [see also review article by Beachy]. Examples include colon carcinoma associated with inflammatory bowel disease, stomach cancer in H. pylori infection, and hepatocellular carcinomas in hepatitis C infection. Inflammatory cells are also a key component of the microenvironment of carcinomas arising independent of chronic inflammation. Mechanisms whereby inflammatory cells influence cancer initiation and promotion likely involve secretion of cytokines, growth factors and chemokines by inflammatory cells that stimulate proliferation of epithelia as well as the generation of reactive oxygen species that can cause DNA damage9. [BM: Lucy, I swapped these two paragraphs around, thus references need to be renumbered]
The three-dimensional structure supporting epithelia through the ECM is critically important, and impaired interactions of epithelial cells with ECM can result in transformation of the epithelia6,7. The specialized ECM that separates the epithelial and endothelial cells from the stromal components is termed the basement membrane. Whereas stromal ECM proteins are produced by fibroblasts, the major structural proteins of the basement membrane including collagen VI, laminin, entactin, and heparan-sulphate proteoglycans are expressed by basal epithelia, myoepithelia, and fibroblasts in a tissue specific manner8. In turn, the unique composition of the basement membrane is thought to confer tissue specificity, epithelial polarity and functionality8.
Fibroblasts also play a well-recognized role in the carcinogenic process. They are responsible for synthesis, deposition and remodeling of much of the ECM in tumour stroma (Figure 1), and they are recognized as a source of paracrine growth factors that influence the growth of carcinoma cells. However, fibroblasts have largely been assumed to play a more passive role in cancer, responding to signals from the carcinoma cells. New data promote stromal fibroblasts from the mere role of "enablers" of cancer to the potential stature of "inducers" of certain carcinomas. In this review, we will use selected examples to illustrate the influence of the stromal fibroblasts in epithelial neoplasia.
The importance of stromal (or mesenchymal) - epithelial interactions in embryonic development and tumourigenesis is well established. The concept of a link between stromal cell maturation and adjacent epithelial proliferation was introduced over twenty years ago10, a view that has been supported by others11–16. This interaction is mediated by soluble paracrine signals and secreted ECM from developing mesenchyme that induce the adjacent epithelia to rapidly proliferate. As the epithelial cells differentiate, adjacent mesenchymal cells develop into differentiated stromal cells. These differentiated stromal cells generally express lower quantities of growth factors, and differentiated epithelia express cytokines for the maintenance of stromal differentiation, suggesting that a new balance of mesechymal-epithelial crosstalk is reached during tissue maturation. However, during tumourigenesis the prevailing model suggestsa process whereby pre-cancerous epithelial cells acquire multiple genetic mutations17 and the associated stroma becomes "activated", commonly expressing myofibroblastic markers2,3. The characteristics of an activated carcinoma-associated fibroblast are not completely understood. However in our interpretation such cells express α-smooth muscle actin, ECM proteins, and growth factors that act in an autocrine and paracrine fashion to potentiate and support the survival of a tumour.
Early evidence indicating an important role for stromal cells in cancer come from tissue culture experiments where epithelium from submandibular glands transformed by polyoma virus grow only in the presence of embryonic salivary gland mesenchyme, but not when the epithelium is cultured by itself29. The differences in structure of normal stroma and tumour stroma are well known2,3 (Figure 1) 3. Apart from histologic differences, tumour fibroblasts exhibit enhanced proliferation and migratory behavior in vitro30,31. The constituents of the extracellular matrix and the vascular architecture in tumour stroma also differ from that associated with normal epithelia4. These stromal events are in part mediated through autocrine growth factor singalling involving the factors discussed above32. In vitro co-culture and in vivo tissue recombination using xenograft systems demonstrate that tumour fibroblast-derived factors contribute to the transformation of immortalized epithelia33,34. In these studies, human fibroblasts from normal or tumour prostate were grown together with epithelial cells derived from SV40-T antigen immortalized benign prostate hyperplasia. Tumour fibroblasts, but not normal prostatic fibroblasts, stimulated epithelial proliferation and malignant transformation. However, tumour fibroblasts do not stimulate the growth of normal primary epithelial cells under identical conditions. This lead to the suggestion that cancer-associated fibroblasts express ECM proteins and growth factors that influence the insipient tumours cells and promote angiogenesis that is necessary to maintain epithelial transformation.
Further evidence for a a role of fibroblast in epithelial cancers comes from experiments in which irradiation of fibroblasts to cause sub-lethal DNA damage will induced genetic changes. When non-transformed mammary epithelial cells were transplanted into cleared fat pads of irradiated mice containing such irradiated fibroblasts, an elevated incidence of breast tumours was observed compared to the same epithelial cells inserted into non-irradiated fat pads35. Recently, tissue recombination of pancreatic cancer cells with irradiated pancreatic fibroblasts resulted in a more aggressive and invasive cancer, than when normal fibroblasts were used36. Together, these reports demonstrate that changes in fibroblasts can contribute to epithelial transformation and more invasive behavior. They also suggest that the mechanism of radiation-induced cancer may not only be the result of deleterious mutations in the epithelia, but also from alterations in stromal fibroblasts.
Interestingly, both proliferating fibroblasts and senescent human fibroblasts can promote the proliferation of pre-malignant and malignant epithelial cell proliferation in culture and the formation of tumours in mice37. This is likely due to the fact that senescent fibroblasts and cancer-associated fibroblasts express similar sets of paracrine growth factors that can contribute to cancer proliferation. In support of the role of paracrine growth factors in the senescent fibroblast mediated effects, Krtolica et al.37 found the proliferative effects on epithelial cells were observed even when senescent fibroblasts were only 10% of the fibroblast population. However, unlike the ability of cancer-associated fibroblasts to induce epithelial oncogenesis33, senescent fibroblasts are not able to convert non-transformed epithelia into carcinomas37.
In a recent study of gene expression profiles of each of the cell types present in normal breast tissue and breast carcinomas, changes in gene expression were found to occur in all cell types38. Of particular interest was the overexpression of the chemokines, CXCL14 and CXCL12, by myoepithelial cells and myofibroblasts, respectively. These two chemokines were then shown to bind to receptors on the epithelial cells enhancing their proliferation and invasion. This study provides an elegant example of paracrine effects of factors derived from stromal cells on carcinoma cells.
Multiple families of growth factors implicated as autocrine and paracrine mediators of stromal-epithelial interactions are involved in carcinoma initiation and progression. These include the fibroblast growth factor (FGF) family, the IGF family, the EGF family, hepatocyte growth factor (HGF), and the TGF-β family (Table 1). Most of these factors are predominantly stimulators of proliferation and can play a role in promoting the carcinogenic process. The TGF-β family is different. With initial demonstrations that TGF-β could act as a growth inhibitor of most epithelial cells18,19, it was speculated that this growth factor has a role in tumour suppression. Subsequent studies have indeed supported this hypothesis. For example, transgenic mouse studies demonstrated that increased TGF-β signalling can suppress tumour formation while loss or attenuation of the pathway enhances carcinogenesis20–23. In addition, inactivating mutations have been found in genes encoding components of the TGF-β signaling pathway in human tumours (see ref. 24 for a recent review). However, a loss of TGF-β sensitivity in carcinoma cells is frequently accompanied by increased expression of TGF-β by carcinoma cells. Other sources of TGF-β in the microenvironment include the inflammatory cells and stromal fibroblasts25. Furthermore, elevated levels of plasma TGF-β1 can be detected in patients with cancer and predicts early metastasis26–28. The presence of TGF-β in the tumour microenvironment has been suggested to promote tumour growth by enhancing stromal support and angiogenesis and by impairment of immune surveillance. In addition, while mutations in the TGF-β signaling pathway downstream of receptors may impair TGF-β-mediated growth inhibition, other pathway components may be retained, permitting TGF-β-mediated loss of adherens junctions, and increased motility, changes that would favour invasion and metastasis24. Thus TGF-β can exert both tumour suppressive and promoting functions.
Recent studies provide evidence for a major role for TGF-β singalling in fibroblasts in the initiation of carcinomas. In one report, mice were generated in which the the TGF-β type II receptor gene (Tgfbr2) was inactivated specifically in stromal fibroblasts using Cre-lox technology (Tgfbr2fspko mice)42. 100% of the mice exhibited prostatic intraepithelial neoplasia, a presumed forerunner of prostatic carcinoma, as well as invasive squamous cell carcinomas of the forestomach by six weeks of age42. Tgfbr2fspko fibroblasts overexpress HGF, and increases in the activating phosphorylation of the cognate HGF receptor, c-Met, were found in forestomach carcinoma cells. This suggests activation of paracrine hepatocyte growth factor (HGF) signalling as one possible mechanism for stimulation of epithelial proliferation. The Tgfbr2fspKO mouse model demonstrates that the TGF-beta signalling pathway known to suppress cell-cycle progression and tumour formation when acting on epithelial cells can also indirectly inhibit epithelial proliferation when acting in adjacent stromal fibroblasts in vivo. Consequently, loss of this pathway in fibroblasts results in increased epithelial proliferation and potentially may also promote invasive carcinoma in some tissues.
More recently in an orthotopic transplantation model, mammary fibroblasts engineered to ectopically express HGF or TGF-β1 alone or together induced mammary epithelia to develop ductal carcinoma in situ, adenocarcinoma, and poorly differentiated cancer, whereas transplantation of the same epithelial cell population with wild-type fibroblasts did not44. Unique to this study was the transplant of human (rather than mouse) mammary epithelia and fibroblasts into cleared mammary fat pads of immune deficient mice44. This provides another example where modification of stromal fibroblasts can influcence the malignant behavior of adjacent epithelia.
The stromally-derived paracrine factors, HGF and TGF-β, have enjoyed the limelight in recent literature on epithelial-stromal crosstalk. Most cell types have the capacity to both express and respond to TGF-β25. in contrast, HGF is primarily expressed by fibroblasts, while the cognate receptor, c-Met, is primarily expressed by epithelia45. There are multiple reports to support the transforming ability of HGF46. As also discussed above, the role of TGF-beta is more complex and involves both tumour-suppressive and promoting roles.
The above mentioned report on tissue recombination of irradiated pancreatic fibroblasts with pancreatic cancer cells describe an elevated metastatic potential of the developing tumours36. This phenomenon was associated with increased c-Met activation in the carcinoma cells and TGF-β1 expression by the irradiated pancreatic fibroblasts. The fact that the authors did not observe a concomitant increase in HGF secretion by the fibroblasts suggests the possibility that the expression of an HGF-related ligand may be involved, such as MSP (macrophage stimulating protein) which can activate a heterodimeric receptor consisting of c-Met and the c-Met related molecule RON. Alternatively, the overexpression of c-Met, a common finding in many cancers, can be associated with ligand independent activation48 or increased sensitivity to physiological levels of HGF (note new reference 48A).
Apparent contradictions in our current understanding of the role of TGF-β in epithelial-stromal interactions have also emerged. How can overexpression of TGF-β with enhanced signalling and loss of TGF-β signalling through knockout of Tgfbr2 both result in enhanced tumourigenesis? The overexpression of TGF-β by fibroblasts in mammary and pancreas transplantation models of cancer formation35,36,44 can affect both epithelial cells and stromal fibroblasts. In contrast, the loss of TGF-β signalling in the Tgfbr2fspKO model affects TGF-β signalling only in fibroblasts. However, the enhanced HGF signalling in the two models developing mammary tumours is likely the result of epithelial responses to paracrine factors (since c-Met receptors are primarily found in epithelial cells48). It is of interest that conditional deletion of Tgfbr2 in the epithelia of the mammary gland and prostate have no detectable phenotypic alterations (unpublished observations).
The Tgfbr2fspko mouse model42 poses other important questions. If TGF-β is stimulatory of an activated stromal environment, how does the loss of TGF-β signalling in stromal fibroblasts still allow for an otherwise activated stromal phenotype? The fact that tumours in the Tgfbr2fspko mice are associated with an activated stroma suggests important roles for factors other than TGF-β in the development of an activated tumour microenvironment. As already discussed, a dual role for TGF-β as a tumour suppressor and promoter when acting on epithelial cells has emerged. However, in light of the above data42,44, the paradigm of the early and late roles of TGF-β singalling on tumourigenesis needs to be adapted to include the influences of both fibroblasts and epithelia in tumour susceptible tissues. In particular, both the direct effects of TGF-β on epithelia (direct via TGF-β receptors) and secondary effects (through the regulation of other growth factors) need to be considered.
While the role of TGF-β in epithelia from various tissues has long been accepted as growth inhibitory and morphogenic through multiple downstream singalling proteins39, the proliferative role of TGF-β in fibroblasts has been less clear as a result of the heterogeneity of fibroblasts (Box 1). Notably NIH3T3 and dermal fibroblasts in culture are growth stimulated when treated with TGF-β59. However, in the Tgfbr2fspko mice, the loss of TGF-β signalling in fibroblasts of the entire mouse 42, for the most part, had little effect on fibroblast abundance in most tissues examined (i.e. no evidence of stromal hyperplasia in the skin, lung, kidney, mammary gland, esophagus, liver, small intestine, or colon). This might indicate a tissue-selective role for TGF-β singalling in maintaining fibroblast homeostasis or the presence of redundant growth inhibitory signals from other factors that do not require the TGF-β type II receptor. There was however significant stromal hyperplasia in the prostate and forestomach of Tgfbr2fspko mice, the same organs that undergo epithelial transformation42. It is therefore important to keep in mind that multiple changes in several growth factor pathways as well as tissue-specific responses will ultimately determine the outcome of the complex epithelial-fibroblast interactions in tumours compared to that in the non-disease state (Box 1). In addition, our current knowledge on the role of many growth factors is primarily derived from studies of epithelial cells in culture. Undoubtedly, the ability to conditionally knock out growth factor signaling specifically in fibroblasts or epithelial cells will continue to advance our understanding of these networks of paracrine and autocrine signalling on epithelial proliferation and transformation that operate in vivo.
The figure illustrates stromal-epithelial interactions in normal and tumour tissues. Panel a illustrates wild-type stomach fibroblasts interacting with both the squamous epithelia (SE) of the forestomach and columnar glandular epithelia (GE) of the stomach body (below, green line indicates the area of epithelial transition). Panels b and c depicts the progression of squamous cell carcinoma (SC) in the forestomach as it infiltrates the glandular stomach epithelia (GE). The progression of the carcinoma is likely maintained through reciprocal signals to and from the fibroblasts (asterisk, panel b). Fibroblasts have the capacity to proliferate and/or take on an activated form that can be supportive and even initiate epithelial hyperplasia and eventual tumourigenesis. In turn, carcinoma-derived paracrine proliferative factors signal to the stroma. The cartoon in panel d depicts the non-carcinogenic balance epithelia and fibroblast maintain through dynamic interactions between the two compartments. A curious aspect of the Tgfbr2fspko model42 is that, apart from the prostate and forestomach, the other tissues in the mouse had no apparent signs of carcinogenic transformation. Functional differences between fibroblast from different organs my explain this.
In a reductionist approach to understanding epithelial-stromal interactions in normal tissues and in cancer, the fibroblast component is often generalized and obscure differences in fibroblasts from different tissues or differences within the same tissue. However, it is becoming clear that different fibroblast can have distinct functions. For example, during lung development, epithelial induction capacities are known to differ based on whether the mesenchyme is derived from the trachea or the tips of the growing lungs69. The origin of the mesenchymal fibroblasts apparently determines their sensitivity to sonic hedgehog (Shh) derived from the developing lung epithelia. Shh signals through the patched receptor homologue (Ptc) found in the adjacent mesenchyme to stimulate proliferation70. In turn, the specific mesenchyme supports the normal development and branching morphogenesis of the lung epithelia.
In mice, the fibroblasts associated with the squamous epithelium of the forestomach and esophagus appear phenotypically similar to the fibroblasts associated with the adjacent glandular epithelia of the stomach body. Although a similar proportion of fibroblasts in the esophagus, forestomach, and glandular stomach compartments were deficient for TGF-β singalling in Tgfbr2fspko mice, only the squamous epithelia of the forestomach responded to the oncogenic paracrine signals. It is possible that the loss of TGF-β signalling in stromal fibroblasts results in proliferative autocrine and paracrine signals to which the fibroblasts and squamous epithelia of the forestomach, uniquely responded with the formation of invasive carcinoma, but not other other epithelia of e.g. the esophagus which showed no hyperplastic or neoplastic response in the Tgfbr2fspko mice. Thus in this model, the paracrine signals required for malignancy of the glandular epithelia likely differ from that of the adjacent squamous epithelia.
The mechanisms involved in the microenvironmental effects on carcinoma progression are an intense area of investigation (Table 1) and have yielded important insights in addition to the roles of TGF-β and HGF. Both the extracellular matrix and the matrix degrading enzyme family of matrix metalloproteinases (MMP) can promote epithelial transformation49. MMP levels and activities are often elevated in tumours. The activities of the large and diverse family of MMPs include pro-angiogenic and metastatic actions. They can also generate growth-regulating signals through the activation of growth factors, such as IGF (mediated through the cleavage of IGF binding proteins), FGFs (through cleavage of perlecan), TGF-β and TGF-α49,50. MMP-1 and MMP-7 are of fibroblastic origin and can induce increased susceptibility to mammary cancer when overexpressed in transgenic mice50. Additionally, MMP-2 and MMP-9 knockout mice have a reduced susceptibility for lung metastases following intravenous injection of carcinoma cells50,51.
In a more complex process, PDGF expressed by immortalized skin keratinocytes induces the expression of FGF7 (KGF) by fibroblasts52. FGF7 in turn has been shown to produce further epithelial proliferation and promote carcinogenesis. In the prostate, FGF7 and FGF10 are produced by fibroblasts and stimulate the proliferation of adjacent epithelia53,54. This is countered by the paracrine growth factor FGF9, expressed by prostate epithelia, and received by fibroblasts55. This is a clear example of alterations in paracrine growth factor pathways accompanying the carcinogenesis process; the precise role for these factors in this process is still being elucidated
In a recent study, expression of PDGF by melanoma cells was shown to increase pericyte (special vascular cells) recruitment and proliferation in a B16 tumour model56. The associated growth of the tumour was, however, not attributed to the increase in vasculature, but rather to pericyte-derived factors acting on the melanoma.
Another paracrine factor, Wnt1 (a known mammary epithelial oncogene), when expressed by fibroblasts initiates a morphologic transformation of neighboring C57MG mammary epithelial cells in co-culture experiments while no transformation of the Wnt1-expressing fibroblasts themselves was observed57. More recently, Derksen et al58 provided supporting data on the paracrine role of WNT family proteins enhancing the survival and growth of multiple myeloma cells in humans. The paracrine dynamics in all of these experiments is modulated by the presence or absence of contravening influences that are unevenly distributed in tissues.
One of the more provocative implications of the recent publications by Bhowmick et al.42 and Kuperwasser et al.44 is that selected epithelial cells without apparent mutations can be induced to form carcinomas by association with genetically altered fibroblasts. In previous studies, the epithelial cells that were induced to be more carcinogenic by association with irradiated fibroblasts were already fully transformed into carcinomas36 or had p53 gene mutations35. In the studies involving recombination of human mammary epithelial cells with human fibroblasts modified to express HGF and/or TGF-β1 in cleared mammary fat pads of immune deficient mice44, it is possible of course that pre-existing mutations were present in the human mammary epithelial cells that formed carcinomas. This uncertainty is supported by the observation that only selected epithelial preparations gave carcinomas when recombined with HGF and/or TGF-β expressing fibroblasts. However, the pre-neoplastic and neoplastic lesions observed in Tgfbr2fspko mouse model42 suggest that premalignant and malignant epithelial tumours can develop due to mutations in fibroblasts preceding any subsequent tumourigenic changes in the epithelial cells. One possible explanation for this is that the rapid proliferation induced in epithelial cells by HGF (and likely other epithelial cell growth factors) secreted by the TβRII null fibroblasts leads to formation of genetic lesions (Figure 2). Another possible explanation which is not mutually exclusive with the previous one is the generation of oxygen free radicals or other endogenous mutagens, a process that could be accelerated by recruitment of inflammatory cells to involved sites60. The selective presence and timing of putative genetic alterations in some epithelial cells in the Tgfbr2fspKO model remains to be determined. The fact that only two tissue compartments evolved carcinomas in this model suggests that pre-existing mutations in epithelia may not be likely.
Earlier studies have demonstrated mutations in stromal fibroblasts that accompany carcinomas. Loss of heterozygosity (LOH) has been found with high frequency in stromal cells associated with human breast cancer61. This was determined by utilizing polymerase chain reaction (PCR) to examine microdissected tissues with 12 polymorphic DNA markers on chromosomes 2p, 3p, 11q, 16q and 17q known for a high frequency of LOH in human breast cancer. Further, mutations in two tumour suppressor genes, p53 and PTEN, were demonstrated in both mammary carcinoma cells and associated stromal fibroblasts62. However, the possibility that the stromal compartment contains fibroblasts derived from carcinoma cells that have undergone an epithelial to mesenchymal transition cannot be excluded63.
Additional evidence for a role of mutations in stromal cells in the development of epithelial hyperplasias; derives from studies of heritable juvenile polyposis syndrome, one of the hamartomatous polyposis syndromes that are characterized by an overgrowth of tissue native to the area in which they normally occur. In this condition, the loss of normal genetic function occurs predominantly in interstitial fibroblasts among colonic polyps64,65. It is of interest that the genes targeted in this syndrome encode bone morphogenetic protein (BMP) receptor 1A (BMPR1A), a member of the TGF-beta family of receptors, or SMAD4which plays a central role in signaling from both the BMP and TGF-beta receptors66.
These data along with those reported by Bhowmick et al.42 strongly support the hypothesis that TGF-β superfamily signaling in stromal fibroblasts frequently exerts a tumour-suppressive function on adjacent epithelia. This is of particular interest because TGF-β singalling pathways within epithelial cells are also tumour suppressive24. These findings suggest that normal cells in vivo restrict the malignant phenotype of neighboring cells, and that initiation and progression of carcinomas likely involves the overcoming of constraints from normal interstitial tissue through a combination of potential genetic, epigenetic, and stromal changes.
Because of the positive role TGF-β signalling in carcinomas such as an excess fibrosis, tumour progression and metastasis, the pharmaceutical industry has been developing inhibitors of TGF-β singalling pathways. Indeed, studies involving systemic inhibition of TGF-β singalling in adult animals has demonstrated no adverse effects and has decreased metastases from mammary carcinomas67. However, the more recent studes described above raise the question whether such inhibitors might potentially also promote carcinomas through the inhibition of TGF-β singalling in normal stroma, and therefore warrant caution in pursuing this approach
Another therapeutic target suggested by the data discussed in this review is HGF. As pointed out by Ohuchida et al,36 irradiation of stromal cells can cause activation of c-Met on carcinoma cells. This group further reported that specific antagonists of HGF could block the enhanced invasiveness of pancreatic carcinoma caused by irradiated fibroblasts. Overexpression and activation of c-Met is a common event in human cancer68, and a recent publication reported the development of a soluble c-Met receptor (decoy Met) that interferes with HGF binding to c-Met and c-Met homodimerization48. Local and systemic delivery of decoy Met significantly inhibited proliferation and metastasis in human tumour xenografts.
The studies discussed in this review suggest a more important role for stromal fibroblasts in carcinogenesis than was previously appreciated. Fibroblasts influence epithelial transformation by production of paracrine factors that impact both normal epithelia as well as carcinoma cells. In addition, there is now considerable evidence that mutations arising in stromal fibroblasts can precede carcinoma development. The tissue specificity of stromal-epithelial interactions likely accounts for a tissue and cell type specific role of the microenvironement in carcinoma development. Importantly, some of the data point to potential targets for therapy, specifically inhibition of the HGF-c-Met axis. This review has focused on the effect of various stroma-derived paracrine factors on epithelial cells. It is likely that these same factors also have significant effects on stromal cells, including fibroblasts, endothelial cells and inflammatory cells.
Valuable insights concerning the tissue microenvironment have been derived from co-culture and tissue recombination xenograph experiments, but such information may not be applicable to the in vivo situation because not all important environmental factors and cells are considered. The ability to overexpress specific factors or conditionally knockout specific genes in vivo in tissue fibroblasts and other cells of the normal stroma and tumour microenvironment will add greatly to our knowledge of the complex interactions involved in tissue homeostasis as well as those changes involved in the initiation and progression of cancer.
This work was supported by a DOD USAMRMC grant (to NAB), NIH grants (to HLM), and the Vanderbilt-Ingram Cancer Center Support Grant. We thank Jennifer Pietenpol and Simon Hayward for critical review of the manuscript and helpful advice.
PubMed Central Canada is a service of the Canadian Institutes of Health Research (CIHR) working in partnership with the National Research Council's national science library in cooperation with the National Center for Biotechnology Information at the U.S. National Library of Medicine(NCBI/NLM). It includes content provided to the PubMed Central International archive by participating publishers.


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How explained to Agency LETA Chairman of the trade Union Inga Vanaga, in the legal office she addressed last week in the framework of free legal aid. On Friday an email with a link to the conclusion of Sorainen was sent to the Prime Minister Marisa Kuchinskisa, factions of the Saeima, the Ministry of education and science , higher education Council, rectors ' Council.
The Union insists that the process of elimination RPIVA does not meet the regulations, but the Ministry of education and science to the opinion of the trade Union did not listen, therefore, prepared the establishment of lawyers.
Lpro requests to suspend the liquidation of the University and to see the conclusion of Sorainen.
The Ministry decided to join RPIVA to the University of Latvia with the purpose of "concentration of resources and more effective use of budgetary funds". The rector of the Academy Dinah Voight finds this argument unfounded, as about one million will only need to pay compensation to employees for unused vacation, severance pay and unemployment benefits.
Also about 20 thousand euros will be required to pay as a penalty for termination of the lease of the premises in Bauska. In addition, there will be administrative costs when changing details, student identity, etc. a Few thousand euros will have to pay to employees of local governments, Academy, Latvian University (LU), Ministry of education and science (MES) for the provision of those changes.
In the course of the reorganization will also need about 40 thousand euros to acquire databases that use students RPIVA.


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By residents, for residents. RFS Resources was developed as a collection of resources to help radiology and radiation oncology residents understand what the American College of Radiology is and what the College does. As part of the Resources we also provide materials on RFS projects and handouts with information on the unique benefits and programs that you can take advantage of as a member of the ACR-RFS.
The presentations and easy-to-print materials within the RFS Resources can also be used to educate other residents on these important topics. Residents attending the Annual Meeting and Chapter Leadership Conference may wish to preview these presentations and documents, and many use them to give presentations to their residency programs after the conference. The presentations are designed to help residents educate each other on the issues facing the field of radiology and the important role the ACR plays in advocating for the profession.
The RFS executive committee encourages you to download these presentations and materials and use them, in whole or in part, to educate those around you about the business of the College. Every resident or attending radiologist we reach makes our specialty stronger, and in the current political climate we must be strong in our ability to advocate for our specialty.
PowerPoint Presentations:
2014 RFS AMCLC Wrap-Up and Overview
2013 RFS AMCLC Wrap-Up and Overview
ACR-RFS General Overview
ACR Fellowships and Travel Grant
RFS Benefits Overview
MRI Teaching File:
General Instructions for Submission
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Guar Gum is derived from the ground endosperm of Cyamopsis Tetragonolobus, a plant of the Leguminosae family. The plant grows to about 1-2 metres high with vertical stalks. The seed pods, about 15 cm long, grow on these stalks and hold 6-9 seeds which are about 2-3 mm in diameter. Roughly, 14-16% of the seed is the hull, 38-45% is the endosperm and 40-46% germ.
The crop is sown after the first rains in June/July and is harvested after 3-4 months. It is a hardy, drought resistant crop that requires moderate rainfall at regular intervals.
Guar Gum is offered in both food and industrial grade with particle size ranging from 40 mesh to 300 mesh and viscosity ranging from ultra low (50 cps) to ultra high (7000 cps).
The Guar Seed is broken to get 2 halves referred to as Guar splits. Dehusking of the splits is achieved through heating, grinding, polishing and sieving. The endosperm is separated from the germ through sieving and is then hydrated, pulverised and dried to make a powder according to physical, chemical and microbiological specifications.
Guar Gum is a polysaccharide with a straight chain of D-mannopyranose units joined by B (1-4) linkages with a side branching unit of a single D-galactopyronase joined to every other mannose unit by L (1-6) linkages. It is a white to yellowish-white powder, practically odourless and has a bland taste.
It will disperse and swell almost completely in hot or cold water and is insoluble in organic solvents. The viscosity depends on temperature, time, pH, agitation rate and particle size of the powder.
It is useful to stabilize ice creams especially in short time, high temperature processes preventing any variation in viscosity. It gives a dry feel and slows melt down in ice creams, sorbets and popsicles.
Adding it to the dough increases yield, gives better/softer texture, improves handling and increases shelf life.
Its ability to act as a thickener proves useful as a process aid during pet food production.
In meat products, it acts as a lubricant and also prevents loss of weight during storage by binding moisture.
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It aids in the ore concentration process by depressing gangue material during froth flotation. As a settling agent it improves the settling rate of suspended solids in slimes. It lumps together small particles in slimes resulting in better filtration.
It thickens creams and lotions.
It is added to explosive mixes as its ability to swell and seal out water helps retains the properties of the mix even in wet conditions.
It acts as a stabilizer and is used to control water flow and the flow of drilling mud.


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Sorry for the delay! Now that I'm all unpacked in my new apartment, I can show off my swap goods in all of their crafty glory!
First up are some knitted (or crocheted, I'm not sure which) 'scrubbies'.
I keep some in the medicine cabinet to wash my face with...
...and a few by the sink that I use for washing dishes. They work wonderfully for both!
My amazing swap partner took an old t-shirt and some bleach and made it into this awesome creation. It now resides above the dining room table.
She also painted me this, which I hung in my kitchen.
I loved what I got in the swap! Thanks so much!


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Azumi 2 - Death Or Love (Import DVD)
Starring Aya Ueto et al
List Price R 240
eB2 090
Discovery Miles 2 090
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Gershon Ebenezer, Cresta. 26 March 2007
Not as good as the first one. For those of you that don't have Azumi, you should get it before this one! This is good cos it completes the story. The action scenes are good but not as great as the original movie. I think that if they did get the original director, the movie would've been better. This completes the story so if you've got the first one, get this one. There is only the Making of and Trailer in the extra features but the Making of is great. Anyway, the movie has a climatic action scene at the end that you must feel, tries to rival the first movie where Azumi takes on 200 men. This one doesn't come close to matching it but is good nonetheless. All in all, a good action movie.


text: Hi. Help!! I just took my first shot at smoking a boston butt. I couldnt seem to get the smoker hot enough... The charcoal pan was full of glowing embers and smoke billowing from the wood. However, the temp stayed around 160 degrees - obviously not hot enough to cook. I dont know what I am doing wrong. Any thoughts or tips to burning a hot fire. I have a vertical smoker for home use - not a large unit. Thanks, Todd


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Schumpeter's Circular Flow, Learning by Doing and Cyclical Growth
A two-sector growth model with endogenous technical change is presented. Concerning technical change, we assume that it is reflected by increases in the stock of human capital which are acquired through learning by doing. As a result, it turns out that transitory or, using the Hopf bifurcation theorem, persistent oscillations of the economic variables may be the outcome. Thus, we are able to show that learning mechanisms alone may be sufficient to destroy the circular flow as described by Schumpeter.
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Volume (Year): 4 (1994)
Issue (Month): 3 (September)
Pages: 261-271
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|Web: http://www.springer.com/economics/journal/191/PS2
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Race to Win2016
Race to Win
After losing her father, a young women must find the strength to face her fears and compete in the race of her life or her family will lose everything. While fulfilling her community service hours at a horse rescue ranch, Emma forms an unlikely bond with an abused show horse who won't let anyone ride him. Gaining new skills and confidence


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text:
May 01, 2012 Issue #5
Cover Story
Exclusive Research: The Contract Market
Hindered by the recession, the contract segment of the outdoor furniture industry is beginning to turn the corner, according to vendors answering Casual Living's exclusive survey-The Contract Market. One respondent noted, "There is a large pent-up demand for better outdoor products and it's time for this industry to explode soon."
Weather Trends
Hot Products
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Outdoor Style
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Cover Story
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text:
drive through the lanes as you pass other cars. (this is the first version, there are only two levels and a few things need fixing)
errors –
no start menu
invisible cars on level 2
to be fixed –
the start menu, instructions are wrong. to play use arrow keys.. [arrow keys] or [up arrow] [down arrow] [left arrow] [right arrow]
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Sandy Heino
Listed by Cowan And Zellers
Beautifully maintained, this three bedroom detached Condo at The Cottages at The Windchimes shows pride of ownership throughout. The spacious living room boasts a gas fireplace, cathedral ceiling and hardwood floors while offering open concept living to the fully applianced kitchen and adjacent dining area. The living room is also open to the second floor loft and balcony. There are three bedrooms including the well appointed first floor master suite with jetted tub, separate shower and over sized walk-in closet with built-ins. The second floor also has a loft den and full bath. Other features include central air, natural gas heat, laundry room with walk-in pantry, two car garage, full basement and covered porch off the living room overlooking beautifully landscaped common area. Truly an exceptional property.
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All the information you need in one place! Each Study Brief is a summary of one specific subject; facts, figures, and explanations to help you learn faster.
List price: $15.00Publisher: Knopf Doubleday Publishing GroupPublication date: 8/18/1992Binding: PaperbackPages: 368Size: 5.25" wide x 8.75" long x 0.75" tall Weight: 0.682Language: English
Robert N. Bellah, an American sociologist, received his Ph.D. from Harvard University in 1955 and teaches at the University of California at Berkeley. He is best known for his work on community and religion. Although he has written on religions in nonwestern cultures, he has focused much of his research on the notion of civil religion in the West. To Bellah, American society confronts a moral dilemma whereby communalism competes with individualism for domination. His most important book, Habits of the Heart (1985), considers the American character and the decline of community. Bellah holds that the radical split between knowledge and commitment is untenable and can result only in a stunted personal and intellectual growth. He argues for a social science guided by communal values.
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text:
rowanrosemary replied to your post: I COULD wait for someone to inbox me a number, but my dash is slow so fuck it I'm answering this shit
True colors? You went to true colors?
yes ^_^ this year was my first year since the past years I didn't go to my school's GSA enough to know about it till like the day before


text:
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An excerpt from www.HouseOfNames.com archives copyright © 2000 - 2017
Shropshire. The surname Kinnaston belongs to the category of habitation names, which are derived from pre-existing names for towns, villages, parishes, or farmsteads.
Kinnaston Early Origins
Shropshire, where they held a family seat as Lords of the Manor of Kinnerly, some say before the Norman Conquest of England by Duke William of Normandy in 1066. Conjecturally they are descended from the Princes of Powys in Wales, through Griffith, son of Joerweth Goch, Lord of Mochnan, younger son of Meredith, Prince of Powis who took refuge in Shropshire. King Henry III of England gave him lands in that county. He married Matilda, the heiress of Ralph le Strange by whom he acquired the Manor of Kinnerly. Griffith' son, Griffith Vychan settled at Tre-gynvarth, which, when anglicized, is Kynvarth's Town, which, when spoken, became slurred into Kynastown, or Kynaston.
Kinnaston Spelling Variations
Kinnaston Spelling Variations
Welsh surnames are relatively few in number, but they have an inordinately large number of spelling variations. There are many factors that explain the preponderance of Welsh variants, but the earliest is found during the Middle Ages when Welsh surnames came into use. Therefore, scribes and church officials recorded names as they sounded, which often resulted in a single person's name being inconsistently recorded over his lifetime. The transliteration of Welsh names into English also accounts for many of the spelling variations: the unique Brythonic Celtic language of the Welsh had many sounds the English language was incapable of accurately reproducing. It was also common for members of a same surname to change their names slightly, in order to signify a branch loyalty within the family, a religious adherence, or even patriotic affiliations. For all of these reasons, the many spelling variations of particular Welsh names are very important. The surname Kinnaston has occasionally been spelled Kynaston, Kynerston, Kinnaston, Kinaston, Keniston, Kennison, Kenison and many more.
Kinnaston Early History
Kinnaston Early History
This web page shows only a small excerpt of our Kinnaston research. Another 403 words (29 lines of text) covering the years 1433, 1495, 1459, 1534, 1491, 1564, 1516, 1590, 1554, 1587, 1642, 1621, 1622, 1640 and 1712 are included under the topic Early Kinnaston History in all our PDF Extended History products and printed products wherever possible.
Kinnaston Early Notables (pre 1700)
Kinnaston Early Notables (pre 1700)
Prominent amongst the family during the late Middle Ages was Francis Kynaston (1516-1590), an English politician, Member of the Parliament for Shropshire in April 1554; Sir Francis Kynaston or Kinaston (1587-1642), an English lawyer, courtier, poet and politician who sat in the House of Commons from 1621 to 1622...
Another 49 words (4 lines of text) are included under the topic Early Kinnaston Notables in all our PDF Extended History products and printed products wherever possible.
The Great Migration
The Great Migration
In the 1800s and 1900s, many Welsh families left for North America, in search of land, work, and freedom. Those who made the trip successfully helped contribute to the growth of industry, commerce, and the cultural heritage of both Canada and the United States. In the immigration and passenger lists were a number of people bearing the name Kinnaston Allen Keniston, who sailed to Virginia in 1624; Richard Keniston to Virginia in 1655; and Mary Kynaston, who landed in America in 1769.
Contemporary Notables of the name Kinnaston (post 1700)
Contemporary Notables of the name Kinnaston (post 1700)
Kinnaston Family Crest Products
Kinnaston Family Crest Products
See Also
See Also
Other References
The Kinnaston Family Crest was acquired from the Houseofnames.com archives. The Kinnaston Family Crest was drawn according to heraldic standards based on published blazons. We generally include the oldest published family crest once associated with each surname.
This page was last modified on 10 February 2016 at 12:34.
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text:
"My Aunt was a patient in the ITU ..."
About: St Bartholomew's Hospital St Bartholomew's Hospital London EC1A 7BE
Posted via NHS Choices (as ),
What I liked
My Aunt was a patient in the ITU in June and I would like to say how wonderful the whole team were in caring for her. They treated her with feeling, kindness and dignity and most of all as if she were as important as their own family members. As a family we were treated with respect and utmost kindness and kept informed throughout her stay. We have the utmost respect for the team, they are a wonderfully dedicated team who deserve to be recognised for their commitment.
What could be improved
I can't think of anything, unless it could be to improve the working conditions for these wonderful people - they deserve more respect and thought.


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The University of Illinois at Urbana-Champaign decided today that Kenneth Howell will be allowed to teach Catholicism courses again.
According to the Alliance Defense Fund, which has been representing Howell in the matter, "the University of Illinois Office of University Counsel admits no wrongdoing on the part of the university but states, 'The School of Literatures, Cultures and Linguistics will be contacting Dr. Howell to offer him the opportunity to teach Religion 127, Introduction to Catholicism, on a visiting instructional appointment at the University of Illinois, for the fall 2010 semester. Dr. Howell will be appointed and paid by the university for this adjunct teaching assignment.'"
The News-Gazette is reporting the rehiring and that the university has cut ties with the St. John's Catholic Newman Center on campus.
The Chicago Tribune also covered this breaking news.
See our coverage of Howell's firing for teaching the truth here.
the New-Gazette said that UI offered a $10,000 salary for teaching 3 courses per semester… that seems very low .... perhaps something o nthe order of $30,000 a year if he teaches in the summer also… our public school teachers with a BA get better than that here in Texas. IT sounds like a financial invitation to find another job
Please read here why this is no victory: http://cosmos-liturgy-sex.com/2010/07/29/ken-howell-the-u-of-is-response-a-poison-pill/


text: How much is my movie site worth ($2,400/month revenue?) My site has the following stats 4 months old 30,000 UV's/Month 70,000 Page Views/month I earn around $2,400/month from content locking (it is a movie site) So what could I get for it? Is it worth keeping or selling? Thanks! It just started bringing in $2400/month. I am thinking about selling it... But depends on the price.


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Fabrication Noun Synonyms
falsehood, lie, fib, prevarication, story, tale, untruth, fiction, yarn, fable, falsification, forgery, fake, sham, cock-and-bull story, fairy story, fairy tale
His war record is a complete fabrication.
Fabrication Verb Synonyms
construction, assembly, assemblage, making, fashioning, production, manufacture, putting together, building, erection, formation, formulation, structuring, constructing, organization, forming, framing, architecture
The fabrication of thousands of parts took only a month.
invention, creation, origination, make-up, manufacture, hatching, concoction, contrivance, design
Only Vanessa could have been responsible for the fabrication of such a diabolical plot.
Science / Periodic Table of Elements / Fluorine (F): Atomic number: 9, Atomic mass: 18.998403 g.mol -1, Electronegativity: 4, Density: 1.8*10-3 g.cm-3 at 20°C, Melting point: -219.6 °C, Boiling point: -188 °C, Vanderwaals radius: 0.135 nm, Ionic radi MORE


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James Downey: Fine Gael, with or without Labour -- that's the choice
ANY remaining doubts about voting intentions in the general election on Friday must surely be dispelled by the findings of the Irish Independent/Millward Brown Lansdowne opinion poll published here today.
It not only tells us a great deal about the likely -- one might well say certain -- voting patterns. It also tells us a great deal about the public mood, about how the voters have made their decisions and even about when they made them.
For its most striking feature is that it differs only insignificantly from the last poll in the series, published a week ago.


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WELSH international Marcus Browning dismissed Sam Hammam's suggestion the play-offs are not fair after Bournemouth's Third Division final triumph.
Browning's man-of-the -match display inspired the stylish Cherries to a comprehensive victory over Lincoln and a return to Division Two after only a one-year absence.
And having missed out to Wrexham on the last automatic spot, Browning said he was more than happy to enter the end-of-season lottery criticised by Cardiff City's controversial owner.
"I don't agree with what Sam's been saying and I think we've shown it can work out fair," said Browning, who won four caps during the Bobby Gould era.
"We've been doing well all season, so it was disappointing not to go straight up.
"There's a 50-50 chance when it comes to the play-offs, but we knew that if we played as well as we could we would get the result."
Bournemouth took the last place in Division Two in emphatic fashion with goals from Steve Fletcher, Stephen Purches, Gareth O'Connor and a brace from skipper Carl Fletcher, breaking the Millennium Stadium record for the number of goals scored by one team in a match.
And Lincoln's replies from Ben Futcher and Mark Bailey made it the highest scoring game seen at the ground.
But it was the commanding midfield display of Browning which caught the eye, leaving the former Huddersfield and Bristol Rovers man hoping Wales manager Mark Hughes was watching on television in California ahead of today's friendly with the United States.
"I've not played here since it became the Millennium Stadium, so it was fantastic," said Bristol-born Browning.
"It's a great stadium with a great atmosphere and I'd love to be back here again.
"I'm getting on a bit, but there's always hope. We're in the Second Division now and Mark has given boys at that level the chance before.
"I'm pleased with the way I played, but I've got to do that week in week out if I am to get any chance. I've just got to keep plugging away and keep doing what I can."
It took 29 minutes for the game to open up, a snap shot on the edge of the area from Steve Fletcher beating Alan Marriott in the Lincoln net.
Futcher clawed one back for the Imps with a towering header from a corner but Bournemouth reclaimed their advantage thanks to a deft header from Carl Fletcher.
Sean O'Driscoll's side asserted their authority and goals from Purches (53) with O'Connor (60).
Bailey gave Lincoln some hope, but that was extinguished when Carl Fletcher nodded home his second.