The Round Identification and Location System (RILS) is a standalone Doppler radar scoring system. The heart of RILS is the Non-Contact Hit Sensor (NCHS) that provides location and identification of projectile types along with velocity and angle of approach in realtime. Hit data from the NCHS is uploaded to the laptop ground station through a WLAN.
Data gathered by the ground station is displayed in a Windows-based application that includes utilities for report generation. If desired, the RILS can generate a preprogrammed hit pulse to knock down the associated target. The NCHS is adaptable to all target lifters, moving and stationary, and may also be used for hard targets.


In this special Campfire, Comedy Store pianist Jeff Scott joins us to discuss the haunted history of The Comedy Store (once Ciro's)…many comedians and customers have experienced more than laughs…Jeff tells how comedians like the late Sam Kinison have actually had ashtrays thrown at them by the specters of yesterday! Tune in for the spooky stories.
If you want to attend The Comedy Store's upcoming Haunted Midnights show you can go to TheComedyStore.com be sure to use the discount code Jeff tells us about in the show.
For more info you can check out the Ciro's page on Facebook and the Comedy Store Haunted Midnights page on Facebook.


text:
COUNTY NEWS: Warning issued after cigarette sparks house blaze
The county's fire service has issued a warning to smokers following a house blaze last night
SMOKERS are being urged to ensure their cigarettes are put out properly after a blaze wrecked a Sussex home.
Firefighters were called to a terraced house at the Quadrant in Maybridge, Worthing, just after 10pm last night (Tuesday, June 2).
It was after neighbours saw smoke and flames billowing out of a first floor window and raised the alarm.
Two West Sussex Fire and Rescue Service crews from Worthing were both on the scene within seven minutes of the 999 call and on arrival faced a well-developed fire on the first floor of the property.
Additional crews were then requested from Worthing and Lancing.
Firefighters wearing breathing apparatus carried out an immediate search of the house and established that nobody was inside.
Despite difficult conditions, crews managed to bring the blaze under control quickly using hose reels.
Once the fire was extinguished a positive pressure ventilation fan was used to ventilate.
The fire, which has left the house seriously damaged by fire and smoke, is believed to have started by the careless disposal of a cigarette on the bedroom sofa, the fire service said.
Incident commander from Worthing Fire Station, Adam Condell said afterwards: "In this case we believe the occupier had gone out without checking that his cigarette was properly extinguished.
"Fires caused by smoking materials result in more deaths than any other type of fire but they are preventable.
"It's absolutely vital people put their cigarettes out fully when they have finished smoking.
"If they don't, they risk causing a fire that could destroy not just their home, but their life."
West Sussex Fire and Rescue has offered the following simple safety advice to smokers:
Stub out cigarettes properly and dispose of them carefully.
Use a proper ashtray - never a wastepaper basket.
Make sure your ashtray can't tip over and is made of material that won't burn.
Take extra care when you are tired, have been drinking alcohol or taking medication.
Keep all matches and lighters well out of the reach of children.
Never leave lit cigarettes, cigars or pipes unattended.

redpajama_set_name: RedPajamaCommonCrawl


Lymphocytes are responsible for the astonishing specificity of adaptive immune responses. They occur in large numbers in the blood and lymph (the colorless fluid in the lymphatic vessels that connect the lymph nodes in the body to each other and to the bloodstream) and in lymphoid organs, such as the thymus, lymph nodes, spleen, and appendix (Figure 24-3).
In this section, we discuss the general properties of lymphocytes that apply to both B cells and T cells. We shall see that each lymphocyte is committed to respond to a specific antigen and that its response during its first encounter with an antigen ensures that a more rapid and effective response occurs on subsequent encounters with the same antigen. We consider how lymphocytes avoid responding to self antigens and how they continuously recirculate between the blood and lymphoid organs, ensuring that a lymphocyte will find its specific foreign antigen no matter where the anitgen enters the body.
There are about 2 × 1012 lymphocytes in the human body, making the immune system comparable in cell mass to the liver or brain. Despite their abundance, their central role in adaptive immunity was not demonstrated until the late 1950s. The crucial experiments were performed in mice and rats that were heavily irradiated to kill most of their white blood cells, including lymphocytes. This treatment makes the animals unable to mount adaptive immune responses. Then, by transferring various types of cells into the animals it was possible to determine which cells reversed the deficiency. Only lymphocytes restored the adaptive immune responses of irradiated animals, indicating that lymphocytes are required for these responses (Figure 24-4).
As mentioned earlier, lymphocytes usually respond to foreign antigens only if the innate immune system is first activated. As discussed in Chapter 25, the innate immune responses to an infection are rapid. They depend on pattern recognition receptors that recognize patterns of pathogen-associated molecules (immunostimulants) that are not present in the host organism, including microbial DNA, lipids, and polysaccharides, and proteins that form bacterial flagella. Some of these receptors are present on the surface of professional phagocytic cells such as macrophages and neutrophils, where they mediate the uptake of pathogens, which are then delivered to lysosomes for destruction. Others are secreted and bind to the surface of pathogens, marking them for destruction by either phagocytes or the complement system. Still others are present on the surface of various types of host cells and activate intracellular signaling pathways in response to the binding of pathogen-associated immunostimulants; this leads to the production of extracellular signal molecules that promote inflammation and help activate adaptive immune responses.
Some cells of the innate immune system directly present microbial antigens to T cells to initiate an adaptive immune response. The cells that do this most efficiently are called dendritic cells, which are present in most vertebrate tissues. They recognize and phagocytose invading microbes or their products at a site of infection and then migrate with their prey to a nearby peripheral lymphoid organ. There they act as antigen-presenting cells, which directly activate T cells to respond to the microbial antigens. Once activated, some of the T cells then migrate to the site of infection, where they help other phagocytic cells, mainly macrophages, destroy the microbes (Figure 24-5). Other activated T cells remain in the lymphoid organ and help B cells respond to the microbial antigens. The activated B cells secrete antibodies that circulate in the body and coat the microbes, targeting them for efficient phagocytosis.
Thus, innate immune responses are activated mainly at sites of infection, whereas adaptive immune responses are activated in peripheral lymphoid organs. The two types of responses work together to eliminate invading pathogens.
T cells and B cells derive their names from the organs in which they develop. T cells develop in the thymus, and B cells, in mammals, develop in the bone marrow in adults or the liver in fetuses.
Despite their different origins, both T and B cells develop from the same pluripotent hemopoietic stem cells, which give rise to all of the blood cells, including red blood cells, white blood cells, and platelets. These stem cells (discussed in Chapter 22) are located primarily in hemopoietic tissues—mainly the liver in fetuses and the bone marrow in adults. T cells develop in the thymus from precursor cells that migrate there from the hemopoietic tissues via the blood. In most mammals, including humans and mice, B cells develop from stem cells in the hemopoietic tissues themselves (Figure 24-6). Because they are sites where lymphocytes develop from precursor cells, the thymus and hemopoietic tissues are referred to as central (primary) lymphoid organs (see Figure 24-3).
The development and activation of T and B cells. The central lymphoid organs, where lymphocytes develop from precursor cells, are labeled in yellow boxes. Lymphocytes respond to antigen in peripheral lymphoid organs, such as lymph nodes or spleen.
As we discuss later, most lymphocytes die in the central lymphoid organ soon after they develop, without ever functioning. Others, however, mature and migrate via the blood to the peripheral (secondary) lymphoid organs—mainly, the lymph nodes, spleen, and epithelium-associated lymphoid tissues in the gastrointestinal tract, respiratory tract, and skin (see Figure 24-3). As mentioned earlier, it is in the peripheral lymphoid organs that T cells and B cells react with foreign antigens (see Figure 24-6).
T and B cells become morphologically distinguishable from each other only after they have been activated by antigen. Nonactivated T and B cells look very similar, even in an electron microscope. Both are small, only marginally bigger than red blood cells, and contain little cytoplasm (Figure 24-7A). Both are activated by antigen to proliferate and mature into effector cells. Effector B cells secrete antibodies. In their most mature form, called plasma cells, they are filled with an extensive rough endoplasmic reticulum (Figure 24-7B). In contrast, effector T cells (Figure 24-7C) contain very little endoplasmic reticulum and do not secrete antibodies.
There are two main classes of T cells—cytotoxic T cells and helper T cells. Cytotoxic T cells kill infected cells, whereas helper T cells help activate macrophages, B cells, and cytotoxic T cells. Effector helper T cells secrete a variety of signal proteins called cytokines, which act as local mediators. They also display a variety of costimulatory proteins on their surface. By means of these cytokines and membrane-bound costimulatory proteins, they can influence the behavior of the various cell types they help. Effector cytotoxic T cells kill infected target cells also by means of proteins that they either secrete or display on their surface. Thus, whereas B cells can act over long distances by secreting antibodies that are distributed by the bloodstream, T cells can migrate to distant sites, but there they act only locally on neighboring cells.
The most remarkable feature of the adaptive immune system is that it can respond to millions of different foreign antigens in a highly specific way. B cells, for example, make antibodies that react specifically with the antigen that induced their production. How do B cells produce such a diversity of specific antibodies? The answer began to emerge in the 1950s with the formulation of the clonal selection theory. According to this theory, an animal first randomly generates a vast diversity of lymphocytes, and then those lymphocytes that can react against the foreign antigens that the animal actually encounters are specifically selected for action. As each lymphocyte develops in a central lymphoid organ, it becomes committed to react with a particular antigen before ever being exposed to the antigen. It expresses this commitment in the form of cell-surface receptor proteins that specifically fit the antigen. When a lymphocyte encounters its antigen in a peripheral lymphoid organ, the binding of the antigen to the receptors activates the lymphocyte, causing it both to proliferate and to differentiate into an effector cell. An antigen therefore selectively stimulates those cells that express complementary antigen-specific receptors and are thus already committed to respond to it. This arrangement is what makes adaptive immune responses antigen-specific.
The term "clonal" in clonal selection theory derives from the postulate that the adaptive immune system is composed of millions of different families, or clones, of lymphocytes, each consisting of T or B cells descended from a common ancestor. Each ancestral cell was already committed to make one particular antigen-specific receptor protein, and so all cells in a clone have the same antigen specificity (Figure 24-8). According to the clonal selection theory, then, the immune system functions on the "ready-made" principle rather than the "made-to-order" one.
There is compelling evidence to support the main tenets of the clonal selection theory. For example, when lymphocytes from an animal that has not been immunized are incubated in a test tube with a number of radioactively labeled antigens, only a very small proportion (less than 0.01%) bind each antigen, suggesting that only a few cells are committed to respond to these antigens. Moreover, when one antigen is made so highly radioactive that it kills any cell that it binds to, the remaining lymphocytes can no longer produce an immune response to that particular antigen, even though they can still respond normally to other antigens. Thus, the committed lymphocytes must have receptors on their surface that specifically bind that antigen. Although most experiments of this kind have involved B cells and antibody responses, other experiments indicate that T cells, like B cells, operate by clonal selection.
How can the adaptive immune system produce lymphocytes that collectively display such an enormous diversity of receptors, including ones that recognize synthetic molecules that never occur in nature? We shall see later that the antigen-specific receptors on both T and B cells are encoded by genes that are assembled from a series of gene segments by a unique form of genetic recombination that occurs early in a lymphocyte's development, before it has encountered antigen. This assembly process generates the enormous diversity of receptors and lymphocytes, thereby enabling the immune system to respond to an almost unlimited diversity of antigens.
Most large molecules, including virtually all proteins and many polysaccharides, can serve as antigens. Those parts of an antigen that combine with the antigen-binding site on either an antibody molecule or a lymphocyte receptor are called antigenic determinants (or epitopes). Most antigens have a variety of antigenic determinants that can stimulate the production of antibodies, specific T cell responses, or both. Some determinants of an antigen produce a greater response than others, so that the reaction to them may dominate the overall response. Such determinants are said to be immunodominant.
The diversity of lymphocytes is such that even a single antigenic determinant is likely to activate many clones, each of which produces an antigen-binding site with its own characteristic affinity for the determinant. Even a relatively simple structure, like the dinitrophenyl (DNP) group in Figure 24-9, can be "looked at" in many ways. When it is coupled to a protein, as shown in the figure, it usually stimulates the production of hundreds of species of anti-DNP antibodies, each made by a different B cell clone. Such responses are said to be polyclonal. When only a few clones are activated, the response is said to be oligoclonal; and when the response involves only a single B or T cell clone, it is said to be monoclonal. Monoclonal antibodies are widely used as tools in biology and medicine, but they have to be produced in a special way (see Figure 8-6), as the responses to most antigens are polyclonal.
The adaptive immune system, like the nervous system, can remember prior experiences. This is why we develop lifelong immunity to many common infectious diseases after our initial exposure to the pathogen, and it is why vaccination works. The same phenomenon can be demonstrated in experimental animals. If an animal is immunized once with antigen A, an immune response (either antibody or cell-mediated) appears after several days, rises rapidly and exponentially, and then, more gradually, declines. This is the characteristic course of a primary immune response, occurring on an animal's first exposure to an antigen. If, after some weeks, months, or even years have elapsed, the animal is reinjected with antigen A, it will usually produce a secondary immune response that is very different from the primary response: the lag period is shorter, and the response is greater. These differences indicate that the animal has "remembered" its first exposure to antigen A. If the animal is given a different antigen (for example, antigen B) instead of a second injection of antigen A, the response is typical of a primary, and not a secondary, immune response. The secondary response must therefore reflect antigen-specific immunological memory for antigen A (Figure 24-10).
The clonal selection theory provides a useful conceptual framework for understanding the cellular basis of immunological memory. In an adult animal, the peripheral lymphoid organs contain a mixture of cells in at least three stages of maturation: naïve cells, effector cells and memory cells. When naïve cells encounter antigen for the first time, some of them are stimulated to proliferate and differentiate into effector cells, which are actively engaged in making a response (effector B cells secrete antibody, while effector T cells kill infected cells or help other cells fight the infection). Instead of becoming effector cells, some naïve cells are stimulated to multiply and differentiate into memory cells—cells that are not themselves engaged in a response but are more easily and more quickly induced to become effector cells by a later encounter with the same antigen. Memory cells, like naïve cells, give rise to either effector cells or more memory cells (Figure 24-11).
Thus, immunological memory is generated during the primary response in part because the proliferation of antigen-stimulated naïve cells creates many memory cells—a process known as clonal expansion—and in part because memory cells are able to respond more sensitively and rapidly to the same antigen than do naïve cells. And, unlike most effector cells, which die within days or weeks, memory cells can live for the lifetime of the animal, thereby providing lifelong immunological memory.
As discussed in Chapter 25, cells of the innate immune system recognize molecules on the surface of pathogens that are not found in the host. The adaptive immune system has a far more difficult recognition task: it must be able to respond specifically to an almost unlimited number of foreign macromolecules, while avoiding responding to the large number of molecules made by the host organism itself. How does it do it? For one thing, self molecules do not induce the innate immune reactions that are required to activate adaptive immune responses. But even when an infection triggers innate reactions, self molecules still do not normally induce adaptive immune responses. Why not?
One answer is that the adaptive immune system "learns" not to respond to self antigens. Transplantation experiments provide one line of evidence for this learning process. When tissues are transplanted from one individual to another, as long as the two individuals are not identical twins, the immune system of the recipient usually recognizes the donor cells as foreign and destroys them. (For reasons we discuss later, the foreign antigens on the donor cells are so powerful that they can stimulate adaptive immune responses in the absence of infection or an adjuvant.) If, however, cells from one strain of mouse are introduced into a neonatal mouse of another strain, some of these cells survive for most of the recipient animal's life, and the recipient will now accept a graft from the original donor, even though it rejects "third-party" grafts. Apparently, nonself antigens can, in some circumstances, induce the immune system to become specifically unresponsive to them. This antigen-specific unresponsiveness to foreign antigens is known as acquired immunological tolerance (Figure 24-12).
The unresponsiveness of an animal's adaptive immune system to its own macromolecules (natural immunological tolerance) is acquired in the same way. Normal mice, for example, cannot make an immune response against one of their own protein components of the complement system called C5 (discussed in Chapter 25). Mutant mice, however, that lack the gene encoding C5 (but are otherwise genetically identical to the normal mice) can make a strong immune response to this blood protein when immunized with it. Natural immunological tolerance for a particular self molecule persists only for as long as the molecule remains present in the body. If a self molecule such as C5 is removed, an animal gains the ability to respond to it after a few weeks or months. Thus, the immune system is genetically capable of responding to self molecules but learns not to do so.
The learning process that leads to self-tolerance can involve killing the self-reactive lymphocytes (clonal deletion), functionally inactivating them (clonal anergy or inactivation), stimulating the cells to produce modified receptors that no longer recognize the self antigen (receptor editing), or the suppression of self-reactive lymphocytes by a special type of regulatory T cell. The process begins in the central lymphoid organs when newly formed self-reactive lymphocytes first encounter their self antigen. Instead of being activated by binding antigen, the immature lymphocytes are induced to either alter their receptors or die by apoptosis. Lymphocytes that could potentially respond to self antigens that are not present in the central lymphoid organs often die or are either inactivated or suppressed after they have matured and migrated to peripheral lymphoid organs.
Why does the binding of self antigen lead to tolerance rather than activation? As we discuss later, for a lymphocyte to be activated in a peripheral lymphoid organ, it must not only bind its antigen but must also receive a costimulatory signal. The latter signal is provided by a helper T cell in the case of a B lymphocyte and by an antigen-presenting cell in the case of a T lymphocyte. The production of costimulatory signals usually depends on exposure to pathogens, and so a self-reactive lymphocyte normally encounters its antigen in the absence of such signals. Without a costimulatory signal, an antigen tends to kill or inactivate a lymphocyte rather than activate it (Figure 24-13).
Tolerance to self antigens sometimes breaks down, causing T or B cells (or both) to react against the organism's own tissue antigens. Myasthenia gravis is an example of such an autoimmune disease. Affected individuals make antibodies against the acetylcholine receptors on their own skeletal muscle cells. These antibodies interfere with the normal functioning of the receptors so that the patients become weak and may die because they cannot breathe. The mechanisms responsible for the breakdown of tolerance to self antigens in autoimmune diseases are unknown. It is thought, however, that activation of the innate immune system by infection may help trigger certain anti-self responses in genetically susceptible individuals.
Pathogens generally enter the body through an epithelial surface, usually through the skin, gut, or respiratory tract. How do the microbial antigens travel from these entry points to a peripheral lymphoid organ, such as a lymph node or the spleen, where lymphocytes are activated (see Figure 24-6)? The route and destination depend on the site of entry. Antigens that enter through the skin or respiratory tract are carried via the lymph to local lymph nodes; those that enter through the gut end up in gut-associated peripheral lymphoid organs such as Peyer's patches; and those that enter the blood are filtered out in the spleen. In most cases, dendritic cells carry the antigen from the site of infection to the peripheral lymphoid organ, where they become antigen-presenting cells (see Figure 24-5), specialized for activating T cells (as we discuss later).
But the lymphocytes that can recognize a particular microbial antigen in a peripheral lymph organ are only a tiny fraction of the total lymphocyte population. How do these rare cells find an antigen-presenting cell displaying their antigen? The answer is that they continuously circulate between the lymph and blood until they encounter their antigen. In a lymph node, for example, lymphocytes continually leave the bloodstream by squeezing out between specialized endothelial cells lining small veins called postcapillary venules. After percolating through the node, they accumulate in small lymphatic vessels that leave the node and connect with other lymphatic vessels that pass through other lymph nodes downstream (see Figure 24-3). Passing into larger and larger vessels, the lymphocytes eventually enter the main lymphatic vessel (the thoracic duct), which carries them back into the blood (Figure 24-14). This continuous recirculation between the blood and lymph ends only if a lymphocyte encounters its specific antigen (and a costimulatory signal) on the surface of an antigen-presenting cell in a peripheral lymphoid organ. Now the lymphocyte is retained in the peripheral lymphoid organ, where it proliferates and differentiates into effector cells. Some of the effector T cells then leave the organ via the lymph and migrate through the blood to the site of infection (see Figure 24-5).
Lymphocyte recirculation depends on specific interactions between the lymphocyte cell surface and the surface of the specialized endothelial cells lining the postcapillary venules in the peripheral lymphoid organs. Many cell types in the blood come into contact with these endothelial cells, but only lymphocytes adhere and then migrate out of the bloodstream. The lymphocytes initially adhere to the endothelial cells via homing receptors that bind to specific ligands (often called counterreceptors) on the endothelial cell surface. Lymphocyte migration into lymph nodes, for example, depends on a homing receptor protein called L-selectin, a member of the selectin family of cell-surface lectins discussed in Chapter 19. This protein binds to specific sugar groups on a counterreceptor that is expressed exclusively on the surface of the specialized endothelial cells in lymph nodes, causing the lymphocytes to adhere weakly to the endothelial cells and to roll slowly along their surface. The rolling continues until another, much stronger adhesion system is called into play by chemo-attractant proteins (called chemokines; see below) secreted by endothelial cells. This strong adhesion is mediated by members of the integrin family of cell adhesion molecules (discussed in Chapter 19), which become activated on the lymphocyte surface. Now the lymphocytes stop rolling and crawl out of the blood vessel into the lymph node (Figure 24-15).
Chemokines are small, secreted, positively charged proteins that have a central role in guiding the migrations of various types of white blood cells. They are all structurally related and bind to the surface of endothelial cells, and to negatively charged proteoglycans of the extracellular matrix in organs. By binding to G-protein-linked receptors (discussed in Chapter 15) on the surface of specific blood cells, chemokines attract these cells from the bloodstream into an organ, guide them to specific locations within the organ, and then help stop migration. (The AIDS virus (HIV) also binds to chemokine receptors, which allows the virus to infect white blood cells.) T and B cells initially enter the same region of a lymph node but are then attracted by different chemokines to separate regions of the node—T cells to the paracortex and B cells to lymphoid follicles (Figure 24-16). Unless they encounter their antigen, both types of cells soon leave the lymph node via lymphatic vessels. If they encounter their antigen, however, they remain in the node, proliferate, and differentiate into either effector cells or memory cells. Most of the effector cells leave the node, expressing different chemokine receptors that help guide them to their new destinations—T cells to sites of infection and B cells to the bone marrow.
Innate immune responses are triggered at sites of infection by microbe-specific molecules associated with invading pathogens. In addition to fighting infection directly, these responses help activate adaptive immune responses in peripheral lymphoid organs. Unlike innate immune responses, adaptive responses provide specific and long-lasting protection against the particular pathogen that induced them.
The adaptive immune system is composed of millions of lymphocyte clones, with the cells in each clone sharing a unique cell-surface receptor that enables them to bind a particular antigen. The binding of antigen to these receptors, however, is usually not sufficient to stimulate a lymphocyte to proliferate and differentiate into an effector cell that can help eliminate the pathogen. Costimulatory signals provided by another specialized cell in a peripheral lymphoid organ are also required. Helper T cells provide such signals for B cells, while antigen-presenting dendritic cells usually provide them for T cells. Effector B cells secrete antibodies, which can act over long distances to help eliminate extracellular pathogens and their toxins. Effector T cells, by contrast, act locally at sites of infection to either kill infected host cells or help other cells to eliminate pathogens. As part of the adaptive immune response, some lymphocytes proliferate and differentiate into memory cells, which are able to respond faster and more efficiently the next time the same pathogen invades. Lymphocytes that would react against self molecules are either induced to alter their receptors, induced to kill themselves, inactivated, or suppressed, so that the adaptive immune system normally reacts only against foreign antigens. Both B and T cells circulate continuously between the blood and lymph. Only if they encounter their specific foreign antigen in a peripheral lymphoid organ do they stop migrating, proliferate, and differentiate into effector cells or memory cells.
Alberts B, Johnson A, Lewis J, et al. Molecular Biology of the Cell. 4th edition. New York: Garland Science; 2002. Lymphocytes and the Cellular Basis of Adaptive Immunity.


text:
Q: how does the recursive template deduction works I read some complex template class design, it looks like recirsive template deduction with template parameter refers to the template itself.
I simplified the codes as follow, does anybody can help explain how the template deduction works for the follow codes.
also I want to know more knowledge about the programming technique used in this demo and can you share me any c++ standard material about this topic.
#include <iostream>

template<typename X = char, class T = int>
class ABC;

template<class X, class T>
class ABC <X, ABC<X, T>>{
public:
    T t;
};

template<class T, class M>
class ABC : public ABC<T, ABC<T,M>> {};

int main() {
    ABC<int, char> abc;
    abc.t = 1;
    ABC<> abcd;
    abcd.t = 3;
    std::cout << abc.t << " " << abcd.t << std::endl;
}

as shown above, I tried simplified the code and write a little demo.
my compiler is gcc 9.4.0 released with ubuntu20, with compile args -std=c++17.
What I concerned most is how abc or abcd is deduced as ABC<T, M> is inherited from ABC<T, ABC<T, M>>, and ABC<T, M> seems is a self-referencing template class?
And also how the template deduction terminated as it seems there is only a template class declaration template<typename X = char, class T = int> class ABC; and seems no implemention of it.
abc.t is print as unvisable char succeeding with a whitespace and then a charater 3, as below.
 3

redpajama_set_name: RedPajamaStackExchange


text:
Secular. Jewish. Social Justice.
info@winchevskycentre.org
Contact Us: 416.789.5502
Morris Winchevsky School
Camp Naivelt
United Jewish People's Order
United Jewish People's Order
Welcome to UJPO
The United Jewish People's Order (UJPO) is a non-partisan, independent, socialist-oriented, secular cultural and educational organization with branches in Toronto, Winnipeg and Vancouver, and members in Montreal and other Canadian centres.
Our organization supports racial, economic and environmental justice. We encourage people of all ages, backgrounds, and sexual and gender identities who support our aims and purposes to join us and participate in our activities. We continue to support the continuity and strengthening of Canada's social safety net, universal health care and education, affordable child care and adequate housing. The UJPO supports a strong, democratic federal government with recognition of Quebec's national aspirations and self-rule for Indigenous peoples.
As a national organization we are affiliated to: Canadian Peace Alliance, Congress of Secular Jewish Organizations, International Federation of Secular and Humanistic Judaism, and the International Institute for Secular Humanistic Judaism.
Mindful of the deteriorating health of the environment at local, national, and global levels, we support efforts to reverse climate change and to prevent further regression. Our organization views "globalization" of the economy as a threat to employment, labour standards, national autonomy, and the quality of life in Canada and throughout the world. We support universal human rights – the right to food, housing and secure employment.
We support a negotiated agreement between the Israelis and Palestinians, which would mutually determine the sharing of the land and in which both peoples would live peacefully, securely and prosperously.
© 2018 by the United Jewish People's Order
585 Cranbrooke Avenue, Toronto, Ontario M6A 2X9


text:
info@dic-asset.de
Structure & Strategy
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News Detail - DIC Assets
Letter to the Shareholders: Commercial Portfolio Value of DIC Asset AG increases by over 10% Like-for-like after Strong Operative Performance in 2018
DGAP-News: DIC Asset AG / Key word(s): Preliminary Results
Frankfurt am Main, 22 January 2019.
Value of the Commercial Portfolio rises by around 10% like-for-like
Vacancy in proprietary portfolio reduced by 24% to 7.2%
FFO increased to EUR 68 million, up 13% year-on-year
Dear Shareholders,
Today, with the new year just getting under way, we would like to brief you on the first preliminary figures for the operating activities in 2018, which have just become available.
DIC Asset AG is looking back at a highly successful financial year. In an increasingly demanding real estate market, our long-term expertise and regional market know-how paid off. We scored major operating achievements during the year now ended, meeting or indeed exceeding all of our annual targets:
The intense efforts of our asset management and property management in managing the Commercial Portfolio achieved a noticeable reduction of the EPRA vacancy rate by 24% down to 7.2% (previous year: 9.5%) and a rise in weighted average lease term (WALT) to 5.8 years (previous year: 5.1 years). The resulting like-for-like market value increase amounted to c. EUR 160 million or 10.4%.With transactions taken into account, the market value climbed to EUR 1.7 billion by the end of the year (previous year: EUR 1.6 billion).
At the same time, we continued to expand our platform in the fund business, and significantly increased our revenues from this business line by EUR 12.7 million to EUR 31.6 million by launching two additional institutional funds, and by selling share certificates and properties.
As far as acquisitions and sales went, our transaction team generated the impressive volume of over EUR 1 billion across segments in 2018, demonstrating a high-powered performance here as elsewhere.
All things considered, the real estate assets under management (AuM) rose to a record level of EUR 5.6 billion as of 31 December 2018.
The sound operative performance in all three segments resulted in a substantial increase in Funds from Operations (FFO) by 13% to a total of EUR 68.0 million.
On 08 February 2019, we will publish the full-length annual report for 2018 with a detailed outlook for the company's prospective performance in the current year.
At this time, we would like to thank you for the faith in our company that you have shown in recent years, specifically during the 2018 financial year concluded. True to our belief "dynamics create growth", we will do everything we can to continue our successful approach in the years to come and to deepen your faith in the high productivity of our company.
Sonja Wärntges, Dirk Hasselbring, Johannes von Mutius
(Members of the Management Board of DIC Asset AG)
For more details on DIC Asset AG, go to the internet at www.dic-asset.de.
Nina Wittkopf
Phone +49 69 9454858-1462
Mobile +49 151 2990-5223
ir@dic-asset.de
About DIC Asset AG:
DIC Asset AG is one of Germany's leading listed property companies, and specialises in commercial real estate. With around 20 years of experience on the German real estate market, the company maintains a regional footprint on all major German markets through six branch offices, and has 181 assets with a combined market value of
c. EUR 5.1 billion under management. DIC uses a hybrid business model to manage its business divisions Commercial Portfolio, Funds and Other Investments. Taking an active asset management approach, DIC employs its proprietary, integrated real estate management platform to raise capital appreciation potential in its business divisions and to boost its revenues.
In its Commercial Portfolio division (EUR 1.6 billion in assets under management), DIC acts as proprietor and property asset holder, and thus generates revenues both from the management of the assets and through the value optimisation of its own real estate portfolio. The Funds division (EUR 1.9 billion in assets under management) generates its revenues by acting as issuer and manager of special real estate funds for institutional investors. Gathered in the business unit Other Investments (EUR 1.6 billion in assets under management) are strategic financial investments, the management of properties in which the company holds no equity stakes, equity investments in property developments and joint venture investments. DIC Asset AG has been included in the SDAX(R) segment of the Frankfurt Stock Exchange since June 2006. The Company's shares are also included in the EPRA index, which tracks the performance of the most important European real estate companies.
(as of: 30/09/2018)
Company: DIC Asset AG
Neue Mainzer Straße 20 * MainTor
Phone: +49 69 9454858-1462
Fax: +49 69 9454858-9399
E-mail: ir@dic-asset.de
Internet: www.dic-asset.de
ISIN: DE000A1X3XX4, DE000A1TNJ22, DE000A12T648
WKN: A1X3XX, A1TNJ2, A12T64
Indices: S-DAX
Listed: Regulated Market in Frankfurt (Prime Standard); Regulated Unofficial Market in Berlin, Dusseldorf, Hamburg, Hanover, Munich, Stuttgart, Tradegate Exchange; Luxembourg Stock Exchange
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Analysts' Assessment
Shareholders' meeting 2020
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CDC - Seasonal Influenza (Flu) - Influenza A (H3N2) Variant Virus
Influenza A (H3N2) Variant Virus
Influenza viruses that normally circulate in pigs are called "variant" viruses when they are found in people. Influenza A H3N2 variant viruses (also known as "H3N2v" viruses) with the matrix (M) gene from the 2009 H1N1 pandemic virus were first detected in people in July 2011. The viruses were first identified in U.S. pigs in 2010. In 2011, 12 cases of H3N2v infection were detected in the United States (Indiana, Iowa, Maine, Pennsylvania, and West Virginia). In 2012, 309 cases of H3N2v infection across 12 states were detected. Reports of H3N2v infections in 2013 began in June with the state of Indiana . These infections have mostly been associated with prolonged exposure to pigs at agricultural fairs. Limited human-to-human spread of this virus has been detected in the past as well (Iowa, West Virginia) but no sustained or community spread of H3N2v has been identified at this time. It's possible that sporadic infections and even localized outbreaks among people with this virus will continue to occur. The Centers for Disease Control and Prevention (CDC) continues to monitor this situation closely and will report cases of H3N2v and other variant influenza viruses weekly in FluView and on the case count tables on this website. CDC has developed guidance for the public to protect against H3N2v, and guidance for public health and health care workers.
See Past Updates »
CDC Assessment
What is H3N2v, Who has Been Impacted, Prevention, Treatment…
Protect Yourself, Take Action to Prevent the Spread, Fact Sheets…
Drugs to Treat H3N2v, Stay Home When Sick, Caring for Someone Who is Sick…
H3N2v Developments, Updates, Feature Stories, Spotlights…
CDC Health Advisory, Prevention Strategies, Diagnostic Testing…
Guidance for Public Health
Surveillance Guidance, Laboratory Testing Guidance…
Interim Guidance for Fair Organizers and School Administrators…
Materials & Resources
Printable materials including Flyers and Posters, Webinars…
Outbreak Characterization
Localized outbreaks
Swine-to-human transmission; rare, limited human-to-human
No sustained or community transmission
Case Count Table »
Info for Specific Audiences
People Who Raise Pigs
Fair Managers and Exhibitors
Fair Goers
What's New & Updated
FluView - Weekly Influenza Surveillance Reportviernes, 02 de agosto de 2013 12:15:00
Updated Print Material: American Indian & Alaska Natives, Protect the Circle of Life Poster and Factsheet PDFsjueves, 01 de agosto de 2013 15:06:00
NEW: Un Amor Perdido (A Lost Love)jueves, 01 de agosto de 2013 9:19:00
Preventive Actions
CDC Recommendations For People At High Risk:
If you are at high risk of serious flu complications and are going to a fair where pigs will be present, avoid pigs and swine barns at the fair. This includes children younger than 5 years, people 65 years and older, pregnant women, and people with certain long-term health conditions (like asthma, diabetes, heart disease, weakened immune systems, and neurological or neurodevelopmental conditions).
If you are not at high risk, take these precautions:
Don't take food or drink into pig areas; don't eat, drink or put anything in your mouth in pig areas.
Don't take toys, pacifiers, cups, baby bottles, strollers, or similar items into pig areas.
Wash your hands often with soap and running water before and after exposure to pigs. If soap and water are not available, use an alcohol-based hand rub.
Avoid close contact with pigs that look or act ill.
Take protective measures if you must come in contact with pigs that are known or suspected to be sick. This includes wearing personal protective equipment like protective clothing, gloves and masks that cover your mouth and nose when contact is required.
To further reduce the risk of infection, minimize contact with pigs in the pig barn and arenas.


Original Tractor Cab Hard Top Cab Enclosure Fits John Deere 1023E 1025R 1026R. This cab is NOT COMPATIBLE with the newly designed ROPS on the 1-Series Tractors. (These new ROPS lean forward into the operators station), therefor, the cab and ROPS are not compatible.
New hard top cab enclosure that will fit the 1023E & 1026R Compact Utility tractors. Installation time will take roughly three to four hours. There will be no holes to drill, the cab mounts use existing holes. Fully enclosed cab with an ABS plastic hard top. Clear shatter resistant Lexan plastic is used in the rear curtain, side doors and the windshield for maximum visibility. Forward inclination of the windshield minimizes glare and contact with falling snow and rain. Doors are hinged with latches so getting in and out of the cab is easy and quick. This hard top cab enclosure is not a genuine Deere item. It is manufactured by one of the leading aftermarket cab, canopy and sunshade manufacturers.
It is made in the USA. Optional Accessories Include the Following and are available Separately. The item "Original Tractor Cab Hard Top Cab Enclosure Fits John Deere 1023E 1025R 1026R" is in sale since Friday, July 21, 2017.
This item is in the category "Home & Garden\Yard, Garden & Outdoor Living\Lawn Mowers\Lawn Mower Parts & Accessories". The seller is "originaltractorcab" and is located in Arlington, Indiana. This item can be shipped to United States, Canada, United Kingdom, Denmark, Romania, Slovakia, Bulgaria, Czech republic, Finland, Hungary, Latvia, Lithuania, Malta, Estonia, Australia, Greece, Portugal, Cyprus, Slovenia, Japan, China, Sweden, South Korea, Indonesia, Taiwan, South africa, Thailand, Belgium, France, Hong Kong, Ireland, Netherlands, Poland, Spain, Italy, Germany, Austria, Israel, Mexico, New Zealand, Singapore, Switzerland, Norway, Saudi arabia, Ukraine, United arab emirates, Qatar, Kuwait, Bahrain, Croatia, Malaysia, Brazil, Chile, Colombia, Costa rica, Panama, Trinidad and tobago, Guatemala, Honduras, Jamaica, Barbados, Bangladesh, Bermuda, Brunei darussalam, Bolivia, Ecuador, Egypt, French guiana, Guernsey, Gibraltar, Guadeloupe, Iceland, Jersey, Jordan, Cambodia, Cayman islands, Liechtenstein, Sri lanka, Luxembourg, Monaco, Macao, Martinique, Maldives, Nicaragua, Oman, Peru, Pakistan, Paraguay, Reunion.


Text Editor - Which One Should You Choose?
First of all, this is the point where you leave your "There is no free lunch" mentality and be thankful for this great software provided to you for FREE by those who have chosen to do so. You can still choose to support the product in one way or another but you do not need to pay a dime to start rolling out great web applications.
I will not dictate the kind of editor you should use. So, to be fair, I will list a few other editors that I can remember and that might help you decide on what you want to use.
Thank you for visiting and I hope this post either helped you decide on which text editor you want or gave you the necessary information that will guide you as you look for one!
You can download Aptana Studio 3 by visiting Aptana Studio or simply search for Sublime Text on your favorite search engine!
Good luck, thank you and remember to subscribe!
Exactly. I just find the dark background so cool! It is like one of those things you just can't explain why. Thanks for stopping by Sean and I hope to see you around and we can learn from each other!


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CS Santosh Out of Dakar Rally 2021 After Suffering a Huge Crash in Stage 4
Home News TVS to scale up its production plans in West Bengal
TVS to scale up its production plans in West Bengal
In a recent Bengal Leads ceremony in Kolkata, the boss man at TVS Motors announced his plans to increase their production capacities. TVS is the third largest two wheeler manufacturer in India and they are planning to bring out more bikes on the road. As claimed by Mr. Venu Srinivasan, Chairman & MD, TVS Motors, the Ulberia plant will soon be used to produce a considerable chunk of TVS motorcycles.
Mr.Srinivasan said that the plant in Ulberia will mostly produce units for the eastern region of the country. He hopes to start with 20,000 vehicles a year and then, as the market grows, hopes to take it up to a couple of lakhs. In his words, "We are going to increase production of motorcycles at the Uluberia plant from 1600 units per year to 2.4 lakh units per year over a period of three years."
The company is looking at an investment of close to 400 crores which will be invested over a period of next three years. The Chennai based company had announced that it planned to resume the Mahabharat Motors assembly unit in Ulberia. Currently they are waiting for permission from the High Court in Calcutta.
All in all, we wish them all the best for putting out more pocket rockets (Apache) and girly toys (Scooty pep) on the road.
Posted on behalf of car & bike aficionado Tapan Jadhav, Pune


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Strong visitor growth continues in the Pacific region
The South Pacific Tourism Organisation says tourist arrivals to the region have grown strongly.
Fiji continues to be the top destination in the region.
Arrivals to the organisation's member countries provisionally reached over 460,000 in the March quarter of 2018.
The latest quarterly review reports visitors to the Asia and Pacific region were up 8.2 percent from 7.3 percent in the December quarter.
The latest figures outperformed last March's quarter by about 6 percent.
CEO Chris Cocker said Fiji continues to be the top destination with 36.7 percent of visitors followed by French Polynesia at 9.7 percent, Palau on 7.3 and PNG 7.2.
Samoa, the Cook Islands, Timor Leste, New Caledonia and Vanuatu rounded out the top nine destinations in the Asia Pacific.
Most tourists came from Australia which had a market share of nearly 27 percent, followed by New Zealand at 16 percent and the USA at just over 11 percent.


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DS » Action Adventure » Open-World
All Review Articles
Cheat Happens 03/24/09 8 out of 10 80.00%
AusGamers 03/18/09 9.5 out of 10 95.00%
gamrReview 05/01/09 9.3 out of 10 93.00%
GameCritics 08/12/09 8 out of 10 80.00%
Gamer Limit 07/29/09 9.6 out of 10 96.00%
GameDaily *	 07/13/09 10 out of 10 100.00%
Gaming Nexus 07/08/09 A- 90.00%
Video Game Talk 07/01/09 4 out of 5 80.00%
Cubed3 05/26/09 8 out of 10 80.00%
ZTGD 05/07/09 9 out of 10 90.00%
Zentendo 04/27/09 9 out of 10 90.00%
ImpulseGamer 04/27/09 9.1 out of 10 91.00%
Fragland 04/24/09 93 out of 100 93.00%
Hooked Gamers 04/22/09 9 out of 10 90.00%
gamesTM 05/01/09 8 out of 10 80.00%
GamesMaster UK 05/01/09 95 out of 100 95.00%
NintendoWorldReport 04/18/09 9 out of 10 90.00%
UltraNinjas 04/16/09 10 out of 10 100.00%
Worthplaying 04/14/09 9 out of 10 90.00%
Nintendo Life 04/10/09 9 out of 10 90.00%
Gaming Target 04/10/09 9.5 out of 10 95.00%
Nintendo Power 05/01/09 9 out of 10 90.00%
Games Xtreme 04/09/09 9 out of 10 90.00%
Modojo 04/09/09 4 out of 5 80.00%
GameFocus 04/08/09 9.5 out of 10 95.00%
Lawrence 04/08/09 9.2 out of 10 92.00%
Edge Magazine UK 05/01/09 9 out of 10 90.00%
Nintendo Gamer 05/01/09 94 out of 100 94.00%
GameShark 04/06/09 A 95.00%
Gamervision 04/06/09 9.5 out of 10 95.00%
Nintendojo 04/06/09 9.5 out of 10 95.00%
Gamestyle 04/06/09 10 out of 10 100.00%
AceGamez 04/05/09 10 out of 10 100.00%
AtomicGamer 04/03/09 93 out of 100 93.00%
Gaming Age 04/01/09 A- 90.00%
Game Vortex 04/01/09 100 out of 100 100.00%
Kombo 04/01/09 9 out of 10 90.00%
The Gamers Temple 04/01/09 96 out of 100 96.00%
GamingTrend 03/31/09 96 out of 100 96.00%
HonestGamers 03/31/09 9 out of 10 90.00%
VideoGamer 03/30/09 9 out of 10 90.00%
Extreme Gamer 03/30/09 9.2 out of 10 92.00%
Digital Chumps 03/30/09 9.4 out of 10 94.00%
DarkZero 03/30/09 10 out of 10 100.00%
Game Revolution 03/28/09 A- 90.00%
Kikizo 03/27/09 10 out of 10 100.00%
Game Chronicles 03/26/09 9.4 out of 10 94.00%
GameTrailers 03/25/09 9 out of 10 90.00%
WonderwallWeb 03/25/09 9.5 out of 10 95.00%
PGNx Media *	 03/25/09 10 out of 10 100.00%
Gamers Daily News 03/21/09 9 out of 10 90.00%
Gamer 2.0 03/24/09 9.3 out of 10 93.00%
GameZone 03/23/09 9.3 out of 10 93.00%
Giant Bomb 03/23/09 5 out of 5 100.00%
NZGamer 03/23/09 9.3 out of 10 93.00%
Nintendo-x2 03/23/09 9.6 out of 10 96.00%
Gameplanet 03/23/09 10 out of 10 100.00%
play.tm 03/23/09 93 out of 100 93.00%
GamePlasma 03/22/09 9.8 out of 10 98.00%
PALGN 03/20/09 9 out of 10 90.00%
Thunderbolt 03/19/09 9 out of 10 90.00%
Official Nintendo Magazine UK 03/19/09 94 out of 100 94.00%
Cheat Code Central 03/18/09 4.6 out of 5 92.00%
G4TV 03/18/09 5 out of 5 100.00%
Pocket Gamer UK 03/17/09 10 out of 10 100.00%
GameSpot 03/17/09 9.5 out of 10 95.00%
UGO 03/16/09 A 95.00%
Game Informer 05/01/09 9.25 out of 10 92.50%
GameSpy 03/16/09 4.5 out of 5 90.00%
Total Video Games 03/16/09 9 out of 10 90.00%
Gameplayer 03/16/09 9.5 out of 10 95.00%
IGN 03/16/09 9.5 out of 10 95.00%
Computer & Video Games UK 03/16/09 9.2 out of 10 92.00%
Eurogamer 03/16/09 10 out of 10 100.00%
1UP 03/16/09 A- 90.00%
GamePro 03/16/09 5 out of 5 100.00%
Reviews with an asterisk (*) do not count toward the average ratio for a game.
More Grand Theft Auto: Chinatown Wars
FAQs, Reviews, Cheats, Saves, Images, Boards and more
MetaScore: 93 (85 Reviews)
GTA 5 Parent Company "Excited" About Nintendo Switch
GTA: Chinatown Wars Hits Android Today
GTA 5 unaffected by GameSpy shutdown; some Rockstar games not so lucky
GTA is America "viewed only through movies and advertising"


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Georgia Department Of Transportation Project Officials Vague On Who Initiated Request For Oconee County To Approve Three Road Projects
Called Group Effort
Georgia Department of Transportation Engineer Brandon Kirby said that the decision to send three project framework agreements to Oconee County for approval was the result of a "group effort."
But he would not say who was in the group that decided it was time to move forward with the widening and reconstruction of Jimmy Daniell Road, the widening of Daniells Bridge Road, and the construction of an extension of Daniells Bridge Road with a flyover of SR Loop 10.
Those three projects will be reviewed by the Madison Athens-Clarke Oconee Regional Transportation Study (MACORTS) in a public hearing it will hold from 5 to 7 p.m. tomorrow night in the Community Center at Veterans Park on Hog Mountain Road.
The three projects also are likely to be discussed by the Oconee County Citizen Advisory Committee for Land Use and Transportation Planning, which will follow MACORTS and hold its usual monthly meeting tomorrow evening, also in Veterans Park.
The discussions will take place without an explanation of why the county is being asked at this time by GDOT to agree on a project time line and on sources of funding.
Davis And Daniell
At the Aug. 26 Board of Commissioners meeting, Commissioner John Daniell posed just that question to Commission Chairman Melvin Davis, who brought the requests from GDOT to the Board for action.
Davis told Daniell that the answer to that question would have to come from GDOT, as the brief video clip below shows.
I posed the question to three people at GDOT last week but didn't get a clear answer.
Two of the people said that the projects almost certainly were sent to the county after discussions with county officials.
Davis received three letters, two dated July 3 and one dated July 9, from Kim R. Coley, district planning and programming engineer in GDOT's Gainesville office.
I talked with Coley by telephone on Thursday of last week.
Coley told me that she did not initiate but only signed the project framework agreements, which were given to her by the project manager, Dylan Curtis. She suggested I talk to Curtis.
Coley did say that the project manager typically would have given the project framework agreements to her for distribution to the local government if money had become available or after "simple discussions between the project manager and local officials that the local officials are ready to start this process."
The New Project Manager
I talked with Curtis on Friday, who said my question about the timing of the project framework agreements was "a really good" one.
Curtis told me that she was named project manager only while Coley was preparing the project framework agreements and that she knew relatively little about them.
"I believe it is something that the locals discussed," she said. She said he also believed that the members of the state Transportation Board were involved.
Jamie Boswell, who owns the Boswell Group, a local commercial real estate firm with listings along the three roadways, is the local representative to the state Transportation Board.
Curtis stressed that Kirby would know more than she does about the timing of the project framework agreements.
The Old Project Manager
I talked with Kirby on Friday as well.
He told me that the three projects were on the MACORTS list of future projects, but he said that the decision to move them from long range projects to ones with shorter schedules was not made by MACORTS.
Rather, he said, the Department of Transportation simply had decided it was time to take action on them.
"I'm not giving you names," he said. "I'm not sure what your angle is. If you are trying to single out an individual person that has done something right or wrong, I'm not going to assist you with that."
"It is a group effort," Kirby said. "Not just one person works on that."
BOC Passes
At that meeting on Aug. 26, the Board of Commissioners decided it didn't want to take action on the GDOT project framework agreements until the three projects had been reviewed by the Land Use and Transportation Planning Committee.
That is how the Land Use and Transportation Planning Committee got the assignment it is likely to take up tomorrow night.
The MACORTS public hearing is wide-ranging, dealing with a longer list of road projects in the county and the region. The hearing is on its 2040 Long Range Transportation Plan.
The time lines and the project scopes and costs for the Jimmy Daniell Road and Daniells Bridge Road projects are different in the MACORTS documents than in the project framework agreements.
Posted by Lee Becker at 9:37 PM
THAT, young man, is some good reporting. The stink of Melvin Davis' relationship with Jamie Boswell is starting to get putrid.
Joshua Sharp said...
Brandon Kirby just flat-out refused to name the people who made the decision? Isn't that illegal? Good reporting!
Beanne said...
Yes, great job. Mr. Boswell sure inserted himself into the right board. It is a terrible stench!
Georgia Department Of Transportation Project Offic...


According to the Facebook page Sacramento Kings Kingdom, fans are organizing a final tailgate party in Lot J.
"Sleep Train Arena, or Arco, is such a special place for our fans and our community, that we simply want to give it the moment it deserves – legends, highlights, special guests and a few surprises," Chris Granger, the team's president and chief operating officer, told The Bee earlier this week.
Inside the arena, celebrations will include on-court photo opportunities, a commemorate ticket, a complimentary limited T-shirt and postgame program.
In fall, the team will play in the new $519 million Golden 1 Center downtown. It will feature ultra-fast Wi-Fi and the NBA's largest video scoreboard.