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# A Graph Model for the Evolution of Specificity in Humoral Immunity

## 1 Introduction

The immune system is one of the body’s major regulatory systems. One of its main known functions is to fight agents that are potentially harmful to the body, including foreign agents and body cells whose behavior is abnormal or dangerous, as in the case of cancerous or virus-infected cells. These and other immune functions arise from complex interactions involving numerous molecules and cells, as well as some of the body’s organs. The immunity an individual is born with is the *innate immunity*. It is highly nonspecific, in the sense that the mechanisms associated with it are not the result of adaptation during previous encounters with extraneous agents, but is nonetheless capable of destroying several types of pathogens. The individual’s *acquired immunity*, on the other hand, is the result of the continual exposition of the body to the action of extraneous substances, called *antigens*, and tends to become more specific at each new encounter with the same antigen.

Of the several players involved in acquired immunity, the molecules known as *cytokines* and *antibodies*, and the cells known as *B cells*, *helper T cells*, and *cytotoxic T cells*, suffice for a description of the basic mechanism at a very high level of abstraction.111We provide very little detail on the functioning of the immune system in this paper. The reader is referred to one of the several textbooks available, as for example Abbas (2003). When a B cell recognizes an antigen with which its receptors have high affinity, the cell becomes stimulated and eventually displays on its surface portions of the antigen. This is one of the necessary signals for helper T cells to become activated and liberate cytokines that, in turn, signal the previously stimulated B cells to proliferate in a process that leads to the production of antibodies that can bind to the antigen and lead to its destruction. Such a mechanism is the essence of the so-called *humoral immunity*, the one that takes place in the body’s fluids (or humors) and is mediated by antibodies. The other type of acquired immunity, known as *cellular immunity*, is also triggered by the cytokines that the activated helper T cells liberate, and culminates in the destruction of the cells displaying antigen portions on their surfaces by the cytotoxic T cells.

This basic mechanism of antigen detection and destruction lies at the core of acquired immunity, but several higher functions of the immune system are known to take place that need to be accounted for on more solid theoretical underpinnings. Two notorious such functions are the immune memory and the ability of the system to discriminate between self and nonself entities. The leading theoretical framework to explain these and other phenomena is the *clonal selection theory* (Burnet, 1957, 1959; Forsdyke, 1995): groups of B cells with similar recognition capabilities, or *clones*, are selected for proliferation. According to this theory, some of the B cells that result from the proliferation elicited by the antigen become memory cells,222The question of memory-cell persistence in the absence of the stimulating antigen remained open for quite some time, but seems to have been settled recently (Maruyama et al., 2000). which in turn fight that same antigen more effectively when it is next encountered. As for the proper discrimination between self and nonself entities, the current best candidate explanations seem to come from the “danger theory” discussed by Bennett et al. (1998), Ridge et al. (1998), and Schoenberger et al. (1998), which postulates the need for more specific signals for T-cell activation.

The clonal selection theory is philosophically reductionist, meaning that the explanations for more and more phenomena are expected to come from discovering more and more details on how the several molecules and cells involved in acquired immunity interact. This inherent bias may have caused several important properties of the immune system to be discovered belatedly, as for example the involvement of the immune system in several phenomena related to morphogenesis (Golub, 1992). Together with the theory’s having so far failed to account for various other immune-related phenomena, particularly those that bear on autoimmunity, this bias has resulted in considerable criticism (although, arguably, some of it appears misdirected (Silverstein, 2002)).

Another major theoretical framework in modern immunology is the *functional* (or *idiotypic*) *network theory* (Jerne, 1974). This theory arose in an attempt to address several questions that the clonal selection theory, being centered on the antigen, seemed unable to answer. For example, how is the B-cell repertoire regulated before antigens are ever encountered? Departing from experimental evidence that B cells and T cells interact with one another in much the same way as they interact with antigens, the functional network theory postulates that such interactions lead to a self-organized system out of which immune functions like the immune memory and the self-nonself discrimination ability emerge naturally.

The functional network theory was met with enthusiasm originally, but interest in it has waned considerably of late. The reasons for this include the difficulty of verifying the theory’s usefulness in practice and also the fact that it too, like the clonal selection theory, remained centered on the antigen, thereby weakening the interest in it as an opposing theory. But the functional network theory continues to attract the interest of those who recognize the aesthetic appeal of its elegant systemic approach and that of other similar autonomous systems (Segel and Cohen, 2001; de Castro and Timmis, 2002). Also, it seems that, of the two theoretical frameworks, this is the most promising one in terms of where insight into autoimmunity is expected to come from. Coupled with recent studies on the appearance of immunity in organisms that never had contact with antigens, these observations are helping restore the functional network theory to a place of great relevance in theoretical immunology (Coutinho, 1995).

At various levels of abstraction, and incorporating the postulates of both clonal selection and the functional network, several proposals have been put forward of how to model the functioning of the immune system mathematically (Perelson and Oster, 1979; De Boer, 1988; De Boer et al., 1992; Bernardes and dos Santos, 1997; Perelson and Weisbuch, 1997; Harada and Ikegami, 2000; Kleinstein and Seiden, 2000). In this paper, we introduce a new model of the functional network. In our model, the network is represented by a weighted directed graph whose weights correspond to the degrees of affinity involved in humoral immunity, especially those related to B cells and antigens. Our model is built on the B model of De Boer (1988) and De Boer et al. (1992), and contributes a new concept in immune-network modeling, namely the evolution of specificity by the dynamic updating of the graph’s weights. What we have found through several different computational experiments on this model is that it is capable of reproducing, in qualitative terms, several of the main immune-system attributes, including the response to antigens, the immune memory, and some degree of self-nonself differentiation.333An earlier version of the study in this paper is found in Flores and Barbosa (2002).

The remainder of the paper is organized into five additional sections. We start in Section 2 with a brief review of the most relevant aspects of the functional network theory, then proceed to Section 3 for the relevant aspects of the B model. Our model is introduced in Section 4, and in Section 5 we report on our computational experiments. We conclude with closing remarks in Section 6.

## 2 The functional network

B-cell receptors are known as *paratopes*.444T cells have paratopes, too. However, since in our model (as in its precursor, the B model) T cells are not taken into account explicitly, we henceforth omit them from our discussion whenever possible. The B cells that result from B-cell proliferation have paratopes that are not exact copies of those of the original cell, but rather are the result of the high mutation rates of the process known as *hypermutation* (Kleinstein and Seiden, 2000). The antigen regions that can be recognized by the immune system are called *epitopes*. Ultimately, the immune response is the result of cell activation due to the affinity, as given by the complementarity of several types of properties, between paratopes and epitopes.

The immune system’s repertoire of paratopes is limited, so in order for its recognition capabilities to be suitably wide-ranging, it has been argued that some conditions need to be satisfied (Stewart, 1992; Perelson and Weisbuch, 1997). These are that each paratope must recognize a small group of slightly different epitopes, that the repertoire of paratopes must be in the order of at least $`10^6`$, and that paratopes must be randomly distributed along the possible range of different paratopes (itself limited to a maximum of $`10^{15}`$ (Abbas, 2003)).

The key observation at the core of the functional network theory comes from a closer look at the structure of paratopes. There are light and heavy chains, and in each chain constant and variable regions. The variable regions can bind to antigens and are known to contain sub-regions that can be recognized by other paratopes. That is, B cells also have epitopes. The group of epitopes of a B cell is called an *idiotype*, while each idiotypic epitope is known as an *idiotope*.

It follows from this observation that B cells can recognize one another. A group of B cells having similar paratopes (a clone, as in the clonal selection theory) is characterized by this set of similar paratopes and also by the corresponding collective idiotype. These paratope-idiotype pairs, denoted generically by $`p_k`$-$`i_k`$, are illustrated in Figure 1. In this figure, an arrow is drawn from a clone’s idiotype to another clone’s set of paratopes to indicate that the former clone stimulates (is recognized by) the latter. Equivalently, one may think of the arrow as indicating that the latter clone inhibits (recognizes and seeks to eliminate) the former.

Using Figure 1 as an example, the functioning of the network can be intuitively grasped as follows. Before an antigen comes into the body, the network remains in population equilibrium. Clone $`p_1`$-$`i_1`$ stimulates clone $`p_3`$-$`i_3`$, which in turn inhibits clone $`p_1`$-$`i_1`$. Meanwhile, clone $`p_2`$-$`i_2`$ stimulates $`p_1`$-$`i_1`$ and $`p_1`$-$`i_1`$ inhibits $`p_2`$-$`i_2`$. This stimulation-inhibition interplay maintains the clonal population’s balance in the network.

When antigens are introduced in the system and interfere with clone $`p_1`$-$`i_1`$, they cause its population to increase, thus taking the network out of balance. Both the stimulatory action of $`p_1`$-$`i_1`$ over $`p_3`$-$`i_3`$ and the inhibitory action of $`p_1`$-$`i_1`$ over $`p_2`$-$`i_2`$ increase, which leads the population of $`p_3`$-$`i_3`$ to increase and that of $`p_2`$-$`i_2`$ to decrease. As a result, $`p_3`$-$`i_3`$ inhibits $`p_1`$-$`i_1`$ more intensely, while $`p_2`$-$`i_2`$ stimulates $`p_1`$-$`i_1`$ less intensely. These two forces then concur toward making the population of $`p_1`$-$`i_1`$ decrease, and eventually let it stabilize once again.

## 3 The B model

As we indicated earlier, the affinity between paratopes and idiotypes is due to the complementarity that exists between molecules in terms of geometric or physicochemical characteristics. If $`c`$ is the number of relevant characteristics, then a $`c`$-dimensional vector space, known as the *shape space* (Perelson and Oster, 1979), can be used to formalize the notion of affinity. A point $`(z_1,\mathrm{},z_c)`$ in the shape space can be taken to represent some multimolecular structure as far as the $`c`$ characteristics are concerned. One possibility to indicate the affinity between this structure and another is to start by identifying the point in the shape space that corresponds to the structure that has the greatest affinity with it. If we use symmetry with respect to $`(0,\mathrm{},0)`$, for example, then this point is $`(z_1,\mathrm{},z_c)`$.

Beyond this characterization of maximum affinity, several other possibilities exist for the treatment of features of interest when studying the immune system. For example, suppose we identify a certain clone $`C`$ with a point $`z`$ in the shape space. In order to represent the property that $`C`$ can be stimulated by various other clones,555This is the property known as *cross link* (Perelson and Weisbuch, 1997). not only by the clone $`C^{}`$ of maximum affinity to $`C`$, a sphere of small radius can be used to represent a set of clones with idiotypes similar to those of $`C^{}`$. This sphere is centered on the point $`z^{}`$ of the shape space that is identified with $`C^{}`$. Every point inside the sphere corresponds to a clone that can stimulate clone $`C`$ with some significant degree of affinity, but this degree is ever smaller as the point is located farther from $`z^{}`$ (De Boer et al., 1992).

One prominent model that employs the shape-space formalism is the B model. This model has appeared as numerous variations of the same basic idea (De Boer, 1988; De Boer et al., 1992; Perelson and Weisbuch, 1997; Harada and Ikegami, 2000), but we limit ourselves to describing only the key elements on which we build in Section 4.

The B model is one of the simplest mathematical representations of the immune system: it only seeks to describe the dynamics of B-cell populations, and takes into account the roles of T cells and antibodies only implicitly. For a system with $`n`$ clones, the B-model equation for clone $`i`$, with $`1in`$, is

$$\frac{dx_i(t)}{dt}=b+\left[pg\left(h_i(t)\right)d\right]x_i(t),$$
(1)
where $`x_i(t)`$ is the population of clone $`i`$ at time $`t`$, $`b`$ is the rate at which new clones are inserted in the system by the bone marrow, $`p`$ is the rate of clone proliferation, $`d`$ is the rate of clone death, $`g`$ is an activation function, and $`h_i(t)`$ is the so-called field of clone $`i`$ at time $`t`$.

The field of clone $`i`$ depends on the affinity between clone $`i`$ and the other clones. It is given by

$$h_i(t)=\underset{j=1}{\overset{n}{}}w_{ij}x_j(t),$$
(2)
where $`w_{ii}=0`$ and $`w_{ij}=w_{ji}`$ represents the symmetric affinity between clones $`i`$ and $`j`$. This affinity can be determined from neighborhoods in the shape space, for example, as we indicated earlier.

The activation function $`g`$ is intended to model the three possible activation states of a clone: the virgin state, in which the clone is not yet stimulated; the immune state, in which the clone proliferates; and the inhibited state, in which proliferation stops. Modeling the inhibited state, in special, is important because it provides an indirect means of precluding clonal proliferation due to the overabundance of stimulation, as in the case of self-antigens, and thereby a means of accounting for the elimination of self-recognizing paratopes that is known to occur in the immune system.

One possibility for $`g`$ is to use the window function

$$g(h)=\{\begin{array}{cc}1,\hfill & \text{if }\mathrm{}hu\text{;}\hfill \\ 0,\hfill & \text{otherwise,}\hfill \end{array}$$
(3)
where $`\mathrm{}`$ and $`u`$ delimit the possible values of a clone’s field if it is to remain in the immune state. By (3), the clone remains virgin if the field is less than $`\mathrm{}`$, it enters the immune state if the field is between $`\mathrm{}`$ and $`u`$, or it is in the inhibited state if the field is greater than $`u`$.

Some assumptions are implicit in the B model that must be brought to the fore clearly. One of them concerns the insertion of new clones in the system by the bone marrow. By adopting the constant rate $`b`$ for all clones, it has been assumed that the bone marrow generates B-cell paratopes uniformly randomly across the entire range of possibilities, independently of what may be taking place in the immune system (the preferential generation of B cells with certain paratopes that is known to take place when a specific antigen is being fought—cf. Abbas (2003)—is thus ignored). It has been assumed, furthermore, that this range of possibilities is restricted to the paratopes of the $`n`$ different clones. Another assumption is that the parameter $`p`$ suffices to summarize the role of helper T cells in the proliferation of stimulated B cells for all clones, and similarly for the parameter $`d`$ with respect to the destruction of B cells.

## 4 Modeling the dynamics of specificity

Like the B model, our model of humoral immunity concentrates on the dynamics of B-cell populations and only considers explicitly one of the other major participants, the bone marrow. It also inherits from the B model the assumptions discussed in Section 3 regarding the use of the parameters $`b`$ and $`p`$ to model the functioning of the bone marrow and the proliferation of clones, respectively.

Notwithstanding these similarities with the B model, the model we introduce in this section contributes four major innovations to the modeling of the functional network. The first innovation is the use of clusters of clones, as opposed to clones, as the basic modeling unit. Each cluster is to be thought of as a small sphere in the shape space containing clones that, to some degree, have paratopes (and hence idiotypes) with similar geometric and physicochemical properties. The adoption of clusters makes the implicit assumption represented by the $`b`$ parameter less stringent, since now new paratopes generated by the bone marrow are assumed to fall within one of the existing clusters, not clones. We denote by $`N`$ the total number of clusters.

The second innovation is the explicit use of a directed graph on $`N`$ nodes (one for each cluster) to represent the interactions among clusters. A similar graph has been implicit since Section 2, for example in Figure 1 and also in the underlying connections among clones—via the $`w_{ij}`$’s—in the B model. The explicit adoption of the directed graph allows any connection pattern on the $`N`$ nodes to be explored, and indirectly a multitude of possible complementarity criteria among the clones of different clusters.

We denote our directed graph by $`D`$. In $`D`$, an edge exists directed from cluster $`i`$ to cluster $`j`$ with $`ij`$ to indicate that the clones in cluster $`i`$ have the capability of stimulating (being recognized by) those in cluster $`j`$. Associated with this edge is a positive weight, $`w_{ij}^+`$, indicating the average affinity with which this stimulation occurs. The same edge can, of course, be examined from a dual perspective: clones in cluster $`j`$ have the capability of inhibiting (recognizing and seeking to eliminate) those in cluster $`i`$. This alternative view leads to another edge weight, $`w_{ji}^{}`$, indicating the average affinity with which the inhibition occurs. Of course, stimulation and inhibition between the two clusters occur with the same degree of affinity, so we have $`w_{ij}^+=w_{ji}^{}`$.666Note that this is not the same symmetry that is assumed in the B model. Using the terminology of this section, that symmetry reads $`w_{ij}^+=w_{ji}^+`$ or, equivalently, $`w_{ij}^{}=w_{ji}^{}`$. We do not make this assumption.

The third innovation that our model contributes is a more detailed treatment of B-cell removal from the system. While in the B model this is accounted for exclusively by the $`d`$ parameter, we make a distinction between B-cell removal by inhibition by other clones777These are the anti-idiotypic clones of Jerne (1974). and removal by other causes (e.g., by apoptosis). The former will be accounted for by a new term introduced in our model’s equations, while the latter will continue to be modeled by the $`d`$ parameter.

The last innovation we wish to highlight has also been the major motivation in this study, and has to do with modeling the evolution of the functional network’s specificity. The idea to be captured by the model is the following. When cluster $`i`$ stimulates cluster $`j`$, those clones in cluster $`j`$ having greater affinity with the stimulus tend to proliferate more than the others. As a result, the distribution of clones in the population of cluster $`j`$ is altered and the cluster becomes more specific in terms of its ability to respond to that stimulus. When the stimulus is withdrawn, the preferential proliferation in cluster $`j`$ ceases and the random insertion of new clones by the bone marrow tends to homogenize the clone population in that cluster once again. In this case, cluster $`j`$ becomes less specific with respect to the stimulus.

The notion of stimulus here is intended to capture a quantity that is proportional to both the idiotypic population in cluster $`i`$ and the stimulatory weight of cluster $`i`$ upon cluster $`j`$, $`w_{ij}^+`$. In our model, the specificity of a cluster, say $`j`$, is associated with the collective stimulatory weights of all the edges that in $`D`$ are directed toward $`j`$, that is, $`w_{ij}^+`$ for every cluster $`i`$ such that an edge directed from $`i`$ to $`j`$ exists in $`D`$. We allow for the evolution of specificity by letting such weights be dynamic (and, thus, their inhibitory counterparts as well).888Another study of the evolution of specificity on a variation of the B model is the one of Harada and Ikegami (2000), but its authors’ approach is altogether different. In particular, they employ an unchanging matrix of stimulation weights. This is done in such a way that the instantaneous change incurred by weight $`w_{ij}^+`$ is proportional to how close the stimulus provided by cluster $`i`$ is to being the greatest individual stimulus received by cluster $`j`$ at that instant. This is, clearly, a Hebbian-style rule for the dynamics of specificity. We provide more details shortly.

Our model’s equations are given in terms of a discrete-time parameter $`t0`$. The equation that describes the evolution of the population of clones in cluster $`i`$, for $`1iN`$, is the extension of (1) given by

$$x_i(t+1)=x_i(t)+b+\left[pg_n\left(h_i^+(t)\right)d\right]x_i(t)qh_i^{}(t).$$
(4)
In (4), $`x_i(t)`$ is the population of cluster $`i`$ at time $`t`$ and $`q`$ is the rate of clone removal by inhibition. The field of cluster $`i`$ at time $`t`$ is no longer given as the field of a clone in the B model, but rather is split into a stimulatory field, $`h_i^+(t)`$, and an inhibitory field, $`h_i^{}(t)`$. The activation function is no longer the $`g`$ of (3), but rather a “nodal” $`g_n`$—also a zero-one function—to be discussed in more detail shortly. The remaining entities in (4) are all the same as in the B model.

While most of what is intended with (4) is self-explanatory, we feel the fundamental difference between the addition of new clones by stimulation and the removal of clones by inhibition requires a little further elaboration. While, understandably, new clones are inserted in proportion to how many there are already, the term that accounts for the removal of clones by inhibition is in (4) independent of $`x_i(t)`$. There are two reasons for this. The first stems from the fact that the inhibitory potential of a cluster upon cluster $`i`$ at time $`t`$ is the same regardless of the particular magnitude that the population of cluster $`i`$ has at that time, since it ultimately depends on the populations of other clusters. Considering that the removal of clones from cluster $`i`$ by inhibition occurs through the binding of clones in those other clusters to clones in cluster $`i`$, we see that the number of clones that get removed by inhibition from time $`t`$ to time $`t+1`$ is nearly independent of the population of cluster $`i`$ at time $`t`$. An exception, of course, is the case of a very low population at time $`t`$, in which case, to become completely rigorous, (4) should be rewritten to prevent $`x_i(t+1)`$ from falling below zero. But we refrain from doing so explicitly for the sake of clarity.

The second reason is a little more subtle. Consider some hypothetical scenario in which a sudden populational growth occurs in cluster $`i`$.999For example, while attempting to obtain, in the model, effects similar to those of passive immunization. In this scenario, a dependence of the inhibitory term upon $`x_i(t)`$ would lead to a sudden increase in the number of clones removed as well, which in turn could only be explained if a sudden growth were to take place also in the populations of the clusters exerting the inhibition. This, however, would only be plausible if we were considering antibody, instead of B-cell, populations.

Thus, the several rates appearing in (4) are to be regarded as being dimensionally distinct. While $`b`$ is expressed as a number of clones, $`p`$ and $`d`$ are given as nondimensional quantities. The rate $`q`$, in turn, is a number of clones per unit of the inhibitory field.

Before we describe the stimulatory and inhibitory fields of a cluster, we need additional notation. We let $`a_i(t)`$ denote the amount of antigen present in cluster $`i`$ at time $`t`$, i.e., antigens with epitopes similar to the idiotypes of cluster $`i`$. We also let $`s_{ij}(t)`$ denote one of the aforementioned stimuli, specifically the stimulus exerted by cluster $`i`$ upon cluster $`j`$ at time $`t`$. Clearly, $`a_i(t)`$ participates in the stimulus of cluster $`i`$ on cluster $`j`$ on equal footing with $`x_i(t)`$, so we have

$$s_{ij}(t)=w_{ij}^+(t)\left[x_i(t)+a_i(t)\right].$$
(5)
One should notice, in (5), that the time-dependency of the weights is now accounted for explicitly; this is how weights will be denoted henceforth. Also, for notational convenience we assume $`w_{ij}^+(t)=0`$ whenever $`i`$ and $`j`$ are such that no directed edge exists from $`i`$ to $`j`$, including the case of $`i=j`$.

The stimulatory and inhibitory fields of cluster $`i`$ are given, respectively, by

$`h_i^+(t)`$ $`=`$ $`{\displaystyle \underset{j=1}{\overset{N}{}}}s_{ji}(t)g_e\left(s_{ji}(t)\right)`$ (6)
$`=`$ $`{\displaystyle \underset{j=1}{\overset{N}{}}}w_{ji}^+(t)\left[x_j(t)+a_j(t)\right]g_e\left(s_{ji}(t)\right)`$
and

$`h_i^{}(t)`$ $`=`$ $`{\displaystyle \underset{j=1}{\overset{N}{}}}w_{ji}^{}(t)x_j(t)g_e\left(s_{ij}(t)\right)`$ (7)
$`=`$ $`{\displaystyle \underset{j=1}{\overset{N}{}}}w_{ij}^+(t)x_j(t)g_e\left(s_{ij}(t)\right).`$
The $`g_e`$ that appears in (6) and (7) is yet another zero-one activation function, this one related to the edges of $`D`$.

The node- and edge-related activation functions, respectively $`g_n`$ and $`g_e`$, are such that

$$g_n(h)=\{\begin{array}{cc}1,\hfill & \text{if }h>0\text{;}\hfill \\ 0,\hfill & \text{otherwise}\hfill \end{array}$$
(8)
and

$$g_e(s)=\{\begin{array}{cc}1,\hfill & \text{if }\mathrm{}su\text{;}\hfill \\ 0,\hfill & \text{otherwise.}\hfill \end{array}$$
(9)
The $`g_n`$ in (8) is a step function at $`h=0`$, while the $`g_e`$ in (9) is the same window function of the B model (cf. (3)) with suitably adapted parameter values. Together with (6) and (7), they are meant to elicit the following behavior from (4). The stimulatory field of cluster $`i`$ is given by the sum of every stimulus on that cluster that is neither too weak (below $`\mathrm{}`$) nor too strong (above $`u`$); if nonzero, this stimulatory field causes the clones in cluster $`i`$ to proliferate. Similarly, only clusters that cluster $`i`$ stimulates inside the $`[\mathrm{},u]`$ window contribute to the inhibitory field of cluster $`i`$ and thereby to the removal by inhibition of clones from cluster $`i`$.

This use of the function $`g_e`$ can be thought of as a distribution of the role played by the function $`g`$ in the B model through the edges that in $`D`$ are incoming to cluster $`i`$. When the windowing mechanism is thus distributed, each individual stimulus on $`i`$ must lie within the desired bounds to be effective, not simply the combined stimuli. This is a more reasonable approach when the graph’s nodes stand for clusters of clones, not simply for clones, and therefore represent a much greater variety of paratopes and idiotypes. The removal of clones by inhibition is now also more selective, as we already remarked, and also the removal of antigens, which for cluster $`i`$ we model by

$$a_i(t+1)=a_i(t)rh_i^{}(t),$$
(10)
where we have refrained from explicitly indicating that $`a_i(t+1)`$ must be prevented from falling below zero.

In (10), $`r`$ is the rate of antigen removal, the same for all clusters, and is expressed in antigen units per unit of the inhibitory field. Note that the process described in (10) is entirely analogous to the process of clone removal by inhibition modeled by the last term of (4). In particular, by the definition of the inhibitory field in (7), antigen removal only happens at cluster $`i`$ if at least one other cluster is stimulated by cluster $`i`$ within the corresponding edge’s window. As a by-product, we see that parameter values can be chosen so that any antigen appearing in overwhelming quantities, like self-antigens, stimulates no cluster and consequently undergoes no attempts at removal.

We finalize the section by returning to the dynamics of specificity. For $`ij`$, our criterion for the update of the stimulatory weight of cluster $`i`$ on cluster $`j`$ from time $`t`$ to time $`t+1`$ is based on the set $`S_j(t)`$, which we define to be the set of clusters whose stimuli on cluster $`j`$ at time $`t`$ are, individually, within the $`[\mathrm{},u]`$ window. Notice that we have placed no restrictions on $`i`$ or $`j`$ beyond their being distinct from each other, which means that even pairs of clusters not currently connected in a certain direction in the graph are considered for weight update in that direction.

If $`iS_j(t)`$, then

$$w_{ij}^+(t+1)=w_{ij}^+(t)+\rho ,$$
(11)
where $`\rho `$ is a random variable uniformly distributed in the interval $`[\mathrm{R}/2,\mathrm{R}/2]`$ intended to capture the effect of hypermutation on inter-cluster affinity. This form of weight update happens, in particular, if $`s_{ij}(t)`$ is too large due to the presence of a massive amount of antigen in cluster $`i`$, so self-antigens cause no weight changes beyond what is effected randomly.

On the other hand, if $`iS_j(t)`$, then

$$w_{ij}^+(t+1)=\left(\frac{\delta s_{ij}(t)}{\underset{kS_j(t)}{\mathrm{max}}s_{kj}(t)}+1\frac{\delta }{2}\right)w_{ij}^+(t)+\rho .$$
(12)
According to (12), the value of $`w_{ij}^+(t)`$ for $`iS_j(t)`$ is either expanded or contracted before it is added to $`\rho `$ to yield $`w_{ij}^+(t+1)`$. The factor determining this expansion or contraction has the Hebbian nature we discussed earlier: within the set $`S_j(t)`$, the weight associated with the largest stimulus on cluster $`j`$ undergoes the greatest expansion (it is multiplied by $`1+\delta /2`$); all other weights undergo proportionally smaller expansions or may even get contracted (in the worst case, by a factor of $`1\delta (0.5\gamma )`$, where $`\gamma =\mathrm{}/\mathrm{max}_{kS_j(t)}s_{kj}(t)`$). What dictates whether a weight is expanded or contracted is whether the corresponding stimulus is above or below half the largest stimulus, respectively.101010An alternative to this half is to use $`\alpha `$ such that $`0<\alpha <1`$, so the expansion/contraction factor in (12) becomes $`\delta s_{ij}(t)/\mathrm{max}_{kS_j(t)}s_{kj}(t)+1\alpha \delta `$. In this case, the threshold between expansion and contraction occurs as the stimulus $`s_{ij}(t)`$ becomes less than $`\alpha \mathrm{max}_{kS_j(t)}s_{kj}(t)`$. We use $`\alpha =0.5`$ throughout, though. The parameter $`\delta `$ can be chosen in the interval $`[0,2]`$ to regulate the range of possible weight expansion or contraction.111111The upper limit in this interval can, in principle, be determined more precisely by finding the value of $`\delta `$ that solves $`\delta (0.5\gamma )=1`$. But $`\gamma `$ has a different value for each cluster and is also time-varying. The upper limit of $`2`$ comes from setting $`\mathrm{}`$, and hence $`\gamma `$, to $`0`$.

While (11) and (12) express the essential principle of our weight-update mechanism, a few observations are in order regarding some crucial details. First of all, once again complete mathematical rigor requires both (11) and (12) to be rewritten to prevent $`w_{ij}^+(t+1)`$ from becoming negative. In addition, no weight is ever allowed to grow without bounds, being subjected to an upper bound $`W`$ representing a conceptual maximum that the affinity between the clones of any two clusters can attain. A more precise formulation of our criterion for updating weights is then the following. Let $`w(i,j,t)`$ be such that

$$w(i,j,t)=w_{ij}^+(t)+\rho ,$$
(13)
if $`iS_j(t)`$, or such that

$$w(i,j,t)=\left(\frac{\delta s_{ij}(t)}{\underset{kS_j(t)}{\mathrm{max}}s_{kj}(t)}+1\frac{\delta }{2}\right)w_{ij}^+(t)+\rho ,$$
(14)
if $`iS_j(t)`$. Then

$$w_{ij}^+(t+1)=\{\begin{array}{cc}0,\hfill & \text{if }w(i,j,t)<0\text{;}\hfill \\ w(i,j,t),\hfill & \text{if }0w(i,j,t)W\text{;}\hfill \\ W,\hfill & \text{if }w(i,j,t)>W\text{.}\hfill \end{array}$$
(15)
By (15), it is possible for $`w_{ij}^+(t+1)`$ to become zero. By the definition of the directed graph $`D`$, we take this to be synonymous with the disappearance from $`D`$ of the edge from $`i`$ to $`j`$ between times $`t`$ and $`t+1`$. Similarly, $`w_{ij}^+(t+1)`$ may also become positive by the addition of the $`\rho `$ term in (11), meaning that the edge from $`i`$ to $`j`$ may reappear in $`D`$ (or appear for the first time, if it never existed) from time $`t`$ to time $`t+1`$. In the sequel, whenever needed we refer to $`D`$ more precisely as $`D(t)`$ to indicate the dynamic character of its edge set.

## 5 Computational experiments

We have conducted extensive computational experimentation in order to discover the properties that emerge out of the model introduced in Section 4. Naturally, the different possibilities for combined parameter values are overwhelmingly too many, so we have settled for a fixed combination that was found to elicit qualitatively interesting behavior. The parameter values we have employed in all the experiments we report henceforth are the ones given in Table 1.

The initial conditions for each experiment were generated randomly by sampling $`x_i(0)`$ uniformly from the interval $`[0,1]`$ for all $`i\{1,\mathrm{},100\}`$ and $`w_{ij}^+(0)`$ from $`[0,2]`$ for all $`i,j\{1,\mathrm{},100\}`$ with $`ij`$. Notice that the corresponding $`100`$-node graph $`D(0)`$ is completely connected (an edge exists directed from every node to every other node) with probability $`1`$, and is therefore structurally meaningless. Even though, for $`t>0`$, $`D(t)`$ may evolve into a structurally more interesting graph (we discuss this later in this section), we often analyze an experiment’s outcomes by looking exclusively at edges whose weights are above a certain minimum. So, in essence, the graphs we deal with can be regarded as being sparsely connected to the degree that those threshold weights allow.

For $`t0`$, such sparser graphs are all spanning subgraphs of $`D(t)`$, i.e., they have the same set of nodes as $`D(t)`$. We consider subgraphs of two types. The first type of subgraph is obtained from $`D(t)`$ by removing every edge whose stimulatory weight is not locally significant, in the sense that it is of small magnitude when compared to the stimulatory weights of the other edges arriving at the same node. For $`f`$ such that $`0<f<1`$, a subgraph of this type is denoted by $`D_f^+(t)`$. In $`D_f^+(t)`$, an edge exists directed from $`i`$ to $`j`$ if and only if $`w_{ij}^+(t)fW_j^+(t)>0`$, where

$$W_j^+(t)=\underset{1kN}{\mathrm{max}}w_{kj}^+(t).$$
(16)
The second type of spanning subgraph of $`D(t)`$ that we consider comes from $`D(t)`$ by removing those edges whose inhibitory weights are not locally significant, that is, they are of small magnitude when compared to the inhibitory weights of the other edges leaving the same node. For $`f`$ given as before, we denote a subgraph of this type by $`D_f^{}(t)`$. In $`D_f^{}(t)`$, an edge exists directed from $`i`$ to $`j`$ if and only if $`w_{ji}^{}fW_i^{}(t)>0`$, where

$`W_i^{}(t)`$ $`=`$ $`\underset{1kN}{\mathrm{max}}w_{ki}^{}(t)`$ (17)
$`=`$ $`\underset{1kN}{\mathrm{max}}w_{ik}^+(t).`$
We start our presentation of computational results with the data shown in Figure 2(a), where the evolution of the clone populations of three clusters is depicted. We found the overall behavior shown in the figure to be typical across all $`100`$ clusters, so we selected the three clusters by first randomly selecting one cluster (the target cluster) and then finding the target cluster’s main stimulator and main inhibitor. The latter clusters are, respectively, the $`k`$ that yields the maximum in (16) when $`j`$ is the target cluster, and the $`k`$ that yields the maximum in (17) when $`i`$ is the target cluster.121212Adopting the denominations of main stimulator and main inhibitor on the basis of the weights alone may seem confusing, as stimuli depend not only on weights but also on clone populations. The same holds for an “inhibition” that we could define as each of the terms that make up a cluster’s inhibitory field (cf. (7)). We are justified, however, because our weight-update rule already accounts for adapting weights as a function of the most significant stimuli. The two denominations are then to be understood as they relate to the stimulatory and inhibitory weights, respectively. The typical behavior that is illustrated in Figure 2(a) is that populations undergo a transient phase of a few thousand time steps, and then accommodate into a steady regime in which the oscillations that we expect from Holmberg et al. (1989) and other studies are nonetheless present. A zoom of Figure 2(a) on two thousand steps of this steady-regime phase is shown in Figure 2(b).

Figures 2(c) and (d), the latter a zoom of the former on the same two thousand steps as before, were generated from the same initial conditions that yielded the data shown in Figures 2(a) and (b), including the seed for the random-number generator in order to ensure the same evolution. In fact, this is what happens up until $`t=5000`$, where we started a series of four antigen injections at the target cluster. This series consisted of setting $`a_i(5000)`$, $`a_i(5150)`$, $`a_i(5300)`$, and $`a_i(6000)`$ to $`150`$ for $`i`$ the target cluster. As shown in Figure 2(c), significant populational disturbances occur in all three clusters, with a brief attempt at returning to stability shortly before $`t=6000`$ and then a return to stability after roughly $`t=8000`$. Examining the zoom in Figure 2(d) reveals additional details. Specifically, each antigen injection elicits a boost in the population of the target’s main inhibitor, probably due to the activation of proliferation in that cluster. The target’s population, in turn, becomes severely depleted, reflecting a significant increase in its inhibitory field as the antigen is fought. At the target’s main stimulator the population is seen to increase significantly as a consequence, since inhibition from the target nearly disappears as its population sinks.

What happens to the antigens at the target cluster in the meantime is shown in Figure 3, which is essentially a reproduction of Figure 2(d) with the evolution of the antigen amount in the foreground. Notice that the antigen is always successfully removed. The first three antigen injections, occurring relatively in close succession to each other, reveal unequivocally the presence of the immune memory that the increase in specificity is expected to entail. The fourth injection, occurring relatively farther in the future, finds the system with the specificity to that antigen restored to its old situation, and removal is once again only as fast as when the first injection was performed.

Our remaining computational results refer to the structure of the graphs $`D(t)`$, $`D_f^+(t)`$, and $`D_f^{}(t)`$, for suitable $`f`$ and $`t`$. We analyze the structure of these graphs by concentrating on their nodes’ degrees. The degree of a node in a graph is the number of nodes to which it is directly connected. In the case of a directed graph, we split a node’s degree into its in-degree (number of nodes from which a directed edge arrives) and out-degree (number of nodes to which a directed edge departs).

We start in Figure 4 by showing the average in- and out-degree distributions of $`D(t)`$ as obtained from $`10^3`$ independent runs. Clearly, as we anticipated earlier in this section, $`D(0)`$ is in fact completely connected. In addition, the passage of time tends to widen the distributions considerably due to the appearance of zero weights (i.e., the disappearance of edges), but the distribution continues to be centered around very high means. $`D(t)`$ is then very densely connected throughout.

Let us then investigate what happens with the sparser subgraphs of $`D(t)`$, starting with their average degrees. Although a node’s in- and out-degree may differ from each other, summing up the in-degrees of all nodes or the out-degree of all nodes must yield the total number of directed edges in the graph. Consequently, the graph’s average in- and out-degree are the same, so we may refer to it simply as an average degree.

We show in Figure 5(a) the evolution of the average degree of $`D_{0.2}^+(t)`$ (labeled “Edges from greatest stimulus”) and of $`D_{0.2}^{}(t)`$ (labeled “Edges from greatest inhibition”) in the absence of antigens. Our choice of $`f=0.2`$ seeks to privilege edges whose weights at time $`t`$ are within a large factor (of $`1f`$) of the weights that are locally most significant. The main effect of this choice is, as we will see shortly, that it yields two subgraphs of $`D(t)`$ that differ from each other significantly. Higher values of $`f`$ tend to, expectedly, lead to two subgraphs that resemble each other very closely, in addition to having in- and out-degree more concentrated near one for practically all nodes if $`t`$ is large (i.e., way inside the system’s steady-regime zone). What we see in Figure 5(a), of which a zoom is given in Figure 5(b), is that the average degrees of both graphs stabilize relatively early in the evolution. Also, in $`D_{0.2}^+(t)`$ nodes tend to have in-degree (our out-degree) slightly above one on average, while in $`D_{0.2}^{}(t)`$ a higher figure is obtained with small oscillations around a center value.

Repeating the experiment from the exact same initial conditions (including the seed for random-number generation) yields what is shown in Figures 5(c) and (d) (the latter a zoom on the former) for an antigen injection of $`a_i(5000)=150`$, $`i`$ the target cluster. Clearly, such a disturbance affects the graphs’ average degrees, briefly in the case of $`D_{0.2}^+(t)`$, but in a more lasting fashion for $`D_{0.2}^{}(t)`$.

Additional insight into the structure of $`D_{0.2}^+(t)`$ and $`D_{0.2}^{}(t)`$ can be gained by looking at how the graphs’ degrees are distributed for each value of $`t`$. Now, of course, it is once again necessary to separate in- and out-degrees. Our results are shown in Figure 6 as the average outcomes of $`10^3`$ independent runs. We show the resulting in-degree distributions of $`D_{0.2}^+(t)`$ and $`D_{0.2}^{}(t)`$ (parts (a) and (c), respectively), and the resulting out-degree distributions of $`D_{0.2}^+(t)`$ and $`D_{0.2}^{}(t)`$ (parts (b) and (d), respectively). All distributions start off nearly symmetrically shaped around the value of $`80`$ (given by $`(1f)N`$, as expected), but very quickly migrate to the relatively tight concentration around relatively small values we have come to expect from Figure 5.

But Figure 6 also evidences important differences between the degree distributions of $`D_{0.2}^+(t)`$ and those of $`D_{0.2}^{}(t)`$. While the two distributions of $`D_{0.2}^+(t)`$ become tightly concentrated around their means as $`t`$ grows, in the case of $`D_{0.2}^{}(t)`$ this only seems to hold for the in-degree distribution, although much more spread than the distributions of $`D_{0.2}^+(t)`$. The out-degree distribution of $`D_{0.2}^{}(t)`$ for large $`t`$ has the same narrow peak around a very low value, and also a wider but less pronounced peak at the higher end of the degree range. This wider peak indicates the occasional occurrence in $`D_{0.2}^{}(t)`$ of nodes with high out-degrees.

These results can be taken back to our original context of modeling the evolution of specificity and re-interpreted there. When we consider the average affinities with which the stimulation of clusters upon one another occurs, and only take into account those affinities that are sufficiently strong with respect to some thresholding criterion that is local to the stimulated cluster, then we have seen that in the long run clusters tend to be chiefly stimulated by very few other clusters, very likely by only one. Conversely, and likewise, a cluster tends to be the most significant stimulator of very few other clusters, again most likely only one. This is, of course, consistent with our underlying approach of increasing stimulatory weights to reflect increases in specificity.

The system can also be examined from a dual perspective, namely the one that considers the average affinities with which clusters are inhibited by one another. Such affinities are, of course, the same as the average affinities with which stimulation occurs. But looking at them from this perspective makes it possible to filter out, once again by a thresholding mechanism that now is local to the inhibited cluster, every average affinity that represents an insignificant inhibition. When we do this, we have seen that in the long run a cluster can be among the chief inhibitors of a significant number of other clusters. Conversely, most clusters have one single principal inhibitor, although there may exist a few clusters for which a very high number of such inhibitors exist.

## 6 Closing remarks

We have in this paper introduced a new model of the idiotypic network. Our model has roots in the B model but departs significantly from it by the introduction of four major innovations: the use of clusters of clones, as opposed to clones, as the basic modeling unit; the explicit use of a directed graph to describe affinities and complementarity criteria with great flexibility; a treatment of B-cell removal that separates removal by inhibition from removal by other causes; and, most significantly, a framework for modeling the evolution of the network’s specificity by the evolution of edge weights.

Our numerous computational experiments, of which we showed representative examples, indicate a great ability of the model to capture, in qualitative terms, some of the major functions of humoral immunity. We find our model to be quite flexible, and believe it may grow by the incorporation of several modifications targeted at modeling different specificity-evolution rules, for example, or the incorporation of more detailed modeling elements aimed at reflecting current biological knowledge.

But even at its current level of abstraction the model is still challenging in a number of interesting ways. For example, we would like to detect signs, if they exist, that our model gives rise to critically self-organized behavior (cf., e.g., Jensen (1998) and Bak (1999)). One of the telltale signs of this type of behavior in other network models has been the finding that degrees are distributed according to a power law (Bollobás and Riordan, 2003), that is, that the probability that a degree equals $`k0`$ is proportional to $`k^\alpha `$ for some $`\alpha >0`$. Our results in Section 5, particularly the ones shown in Figure 6, are generally not supportive of the existence of such a distribution.

One possible exception to this conclusion may be the degree distributions of $`D_{0.2}^+(t)`$ for $`t=10^4`$ (that is, well into the system’s steady regime). These two distributions are re-plotted from Figures 6(a) and (b) in Figure 7(a), where we can see a glimmer of the straight-line behavior that characterizes power laws when plotted against doubly-logarithmic scales. Confirmation that such a behavior is really present depends on investigating substantially larger systems and also different values of $`f`$ to see what trends exist. One example already appears in Figure 7(b) for the same system size as we have been investigating but with $`f=0.8`$, that is, for a graph significantly sparser than $`D_{0.2}^+(t)`$. Seemingly, the presence of power-law distributions is less likely for such a value of $`f`$.

### Acknowledgments

The authors acknowledge partial support from CNPq, CAPES, the PRONEX initiative of Brazil’s MCT under contract 41.96.0857.00, and a FAPERJ BBP grant. They also thank Denise Carvalho and Alberto Nóbrega for their many insightful comments.


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# Superluminal Solutions to the Klein-Gordon Equation and a Causality Problem

## Abstract

We present a new axially symmetric monochromatic free-space solution to the Klein-Gordon equation propagating with a superluminal group velocity and show that it gives rise to an imaginary part of the causal propagator outside the light cone. We address the question about causality of the spacelike paths and argue that the signal with a well-defined wavefront formed by the superluminal modes would propagate in vacuum with the light speed.

A long-standing question of objects or waves traveling faster than the light speed in vacuum $`c`$ has received a renewed interest in the past decade. In particular, it was shown experimentally that light pulses can propagate with abnormally large group velocities greater than $`c`$ although an interpretation of the observations still remains a matter for debate and controversies (recent highlights on the problem as well as all important references on this subject can be found in a special issue of the IEEE Journal of Selected Topics in Quantum Electronics review ). In this context, it is necessary to emphasize that superliminal group velocities at any case do not contradict the causality principle in the special theory of relativity because, in contrast to a widespread opinion, group velocity, like phase velocity, is not synonymous with a signal speed (see, for instance, overviews of the problem by Vainshtein Vainshtein  and recently by Chiao and Milonni Chiao  and Büttiker and Washburn Buttiker ). A real signal should start from zero at some instant and hence should have a well-defined wavefront. Its arrival at a given point can occur only when the point is reached by the front. Because it is associated with infinite frequencies, the asymptotic behavior of a group velocity defines the front spreading. It means that group velocity at finite frequencies is no longer a meaningful concept and there are no restrictions on its value which can be even infinite Chiao1 ; Chiao2 . What is important is only the high-frequency asymptote that, of course, cannot propagate faster than $`c`$, an upper bound to the signal velocity.

Below we are concerned to cylindrically symmetrical free-space solutions of the Klein-Gordon (KG) equation with sub- and superluminal group velocities $`v`$. The former ones belong to a class of localized diffraction-free modes that have been found for a homogeneous wave equation Durnin  and studied in a number of papers (see Ref. Lunardi,  and references therein). The discussion of the latter solutions as well as their relation to the causal Green function, up to our knowledge, has not been done yet.

The KG equation follows from the well-known relation between energy $`E`$, momentum $`p`$, and particle rest mass $`m`$

$$E^2=c^2(p^2+m^2c^2)$$
(1)
through the operator transformation $`Ei\mathrm{}/t`$ and $`𝐩𝐢\mathrm{}`$. The particle velocity is defined as a first derivative $`𝐯=𝐄/𝐩`$. Comparing with the basic formula of the relativistic mechanics $`E=mc^2/\sqrt{1v^2/c^2}`$, Eq. (1) contains well-known additional solutions for negative-energy states that were understood as antimatter (within the classical theory it should be interpreted as a negative rest mass). What we want to emphasize here is that this equation is also valid for a relativistic particle with $`v>c`$. This statement, of course, cannot be regarded as a proof of the existence of tachyons, the faster-than-light objects, but only as a hint that the corresponding wave equation may contain modes with a superluminal $`v`$. Another hint comes from the physics of a free relativistic particle. A causal propagator for the KG equation is known to be manifestly nonvanishing outside the light cone Feynman  and, as it was stated in Ref. Redmount, , the path-integral formulation of relativistic quantum mechanics does include the contribution of spacelike trajectories. What we do not agree with the authors of the paper Redmount  is that this behavior is acausal, i.e., backward in time in some Lorentz frames. Below we shall find a dispersion law for superluminal solutions and show that in any case a signal velocity formed by the modes and defined as that of a wavefront cannot exceed the light speed in vacuum. Moreover, we shall demonstrate that an expression for a causal propagator outside the light cone does follow directly from the dispersion law with superluminal velocities.

Let us look for superluminal modes within a class of axially ($`\phi `$ invariant) symmetric monochromatic solutions of the KG equation propagating in the $`z`$ direction $`\psi (𝐫,𝐭)=\varphi (\rho )\mathrm{exp}(\mathrm{𝐢𝐤}_𝐳𝐳𝐢\omega 𝐭)`$, where $`\rho =\sqrt{x^2+y^2}`$, $`\omega `$ is the angular frequency, and $`k_z`$ is the axial wavenumber. For $`\varphi (\rho )`$ we obtain the following equation

$$[\mathrm{\Delta }_\rho +((\omega /c)^2k_z^2(mc/\mathrm{})^2)]\varphi (\rho )=0$$
(2)
with a two-dimensional Laplace operator $`\mathrm{\Delta }_\rho =^2/x^2+^2/y^2`$ in the plane perpendicular to the $`z`$-axis. The usually used solutions of Eq. (2) are plane waves proportional to $`\mathrm{exp}(ik_xx+ik_yy)`$, another ones are Bessel functions whose form depends on the sign of the expression in brackets. If it is positive, i.e.,

$$(\omega /c)^2k_z^2(mc/\mathrm{})^2=Q^2>0,$$
(3)
then $`J_0(Q\rho )`$, the Bessel function of the first kind and zero order, is a solution of Eq. (2), and

$$\psi (\rho ,z,t)=J_0(Q\rho )\mathrm{exp}(ik_zzi\omega t).$$
(4)
This axially symmetric mode for a wave equation ($`m=0`$) was found and realized experimentally by Durnin et al. Durnin  and is known now as a Bessel beam Lunardi . Its group velocity $`v_z=\omega /k_z`$ is always less than $`c`$ but the relating wave packet would propagate with the light speed in vacuum (as it was shown by detailed calculations in Ref. Lunardi,  and follows from the asymptotic behavior of $`v_z`$).

Another possibility, i.e.,

$$(\omega /c)^2k_z^2(mc/\mathrm{})^2=q^2<0,$$
(5)
has not been discussed yet. The corresponding solution of Eq. (2) is a familiar modified Bessel function of the first kind and zero order $`K_0(q\rho )`$ and the whole solution to the KG equation looks as

$$\psi (\rho ,z,t)=K_0(q\rho )\mathrm{exp}(ik_zzi\omega t).$$
(6)
Together with the relation $`k_z(\omega )=\pm \sqrt{(\omega /c)^2+q^2(mc/\mathrm{})^2}`$, Eq. (6) is the main result of the Letter. It is evident that the relating group velocity $`v_z`$ exceeds the value of $`c`$ for all available $`k_z`$. But for great $`\omega `$ it asymptotically goes to $`c`$ and it means that the signal formed by these modes will propagate with the light speed in vacuum never destroying the causality principle.

Following the paper BK , we can now construct fundamental solutions of the KG equation (Green functions) for timelike and spacelike paths in the Minkowski 4D space. Eq. (4) with the dispersion law (3) yields BK  a real part of the causal Feynman propagator $`\mathrm{\Delta }^c`$ Feynman  valid inside the light cone

$`{\displaystyle \frac{c}{2\pi }}{\displaystyle _0^{\mathrm{}}}Q𝑑QJ_0(Q\rho ){\displaystyle 𝑑k_z\frac{\mathrm{sin}\omega (k_z)|t|}{\omega (k_z)}\mathrm{exp}(ik_zz)}`$
$`={\displaystyle \frac{1}{2\pi }}{\displaystyle _0^{\mathrm{}}}Q𝑑QJ_0(Q\rho )J_0(\tau \sqrt{Q^2+(mc/\mathrm{})^2})=\mathrm{Re}\mathrm{\Delta }^c(\lambda ),`$
where $`\tau =\sqrt{c^2t^2z^2}`$ is the 2D timelike interval and $`\lambda =\sqrt{c^2t^2r^2}`$ is the 4D timelike interval. From the solution (6) with the dispersion relation (5) we obtain (see Ref. BK,  for details) the Green function outside the light cone

$`{\displaystyle \frac{1}{2\pi c}}{\displaystyle _{mc/\mathrm{}}^{\mathrm{}}}q𝑑qK_0(q\rho ){\displaystyle 𝑑\omega \frac{\mathrm{sin}k_z(\omega )|z|}{k_z(\omega )}\mathrm{exp}(i\omega t)}`$
$`={\displaystyle \frac{1}{2\pi }}{\displaystyle _{mc/\mathrm{}}^{\mathrm{}}}q𝑑qK_0(q\rho )J_0(\stackrel{~}{\tau }\sqrt{q^2(mc/\mathrm{})^2})={\displaystyle \frac{mc}{2\pi \mathrm{}\stackrel{~}{\lambda }}}K_1(mc\stackrel{~}{\lambda }/\mathrm{}),`$
where $`\stackrel{~}{\tau }=\sqrt{z^2c^2t^2}`$ is the 2D spacelike interval, $`\stackrel{~}{\lambda }=\sqrt{r^2c^2t^2}`$ is the 4D spacelike interval, $`K_1`$ is the modified Bessel function of the first order. The latter result is just an imaginary part of the causal Feynman propagator $`\mathrm{\Delta }^c`$ Feynman  for spacelike paths. In the limit $`\mathrm{}0`$ it vanishes for all classically forbidden trajectories.

Resuming, we worked out a novel solution to the free-space Klein- Gordon equation propagating with a superluminal group velocity outside the light cone. We have rejected any conclusions Redmount  about acausality of the spacelike paths and argued that a signal carried by a wave packet belonging to this class of modes propagates with the light speed in vacuum $`c`$. In our opinion, there are no objections to possible realizations of such solutions in nature. If they do exist, their thermodynamical properties would be very exotic due to the unusual spectrum (5).


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# The Infrared Supernova Rate

## 1 The problem

Supernovae (SNe) exploding inside dusty regions could dominate, even by a large amount, the number of core-collapse events in the universe, as most of the star-forming activity is hidden by dust. Nevertheless, centuries of optical searches have discovered only very few SNe in dusty regions and no very obscured event.

This is clearly a selection effect, and infrared or radio observations are needed to reveal highly obscured SNe. Events detected at these long wavelengths can be used to study the properties of the SNe in dusty galaxies, to obtain a complete estimate of the total SN rate in the local universe, important to calibrate the SN rate at high redshift now under study. In principle the number of events could also be used to derive information on the main energy source (starburst vs. AGN) of the galaxies when they are dominated by a hidden central source, as for the Luminous Infrared Galaxies (LIRGS).

## 2 Optical vs. near-infrared

The observed rates of the core-collapse SNe, when derived from optical observations and normalized to the B luminosity of the galaxy, don’t show any significant dependence on the galaxy type. Normal galaxies between Sa and Sm cap99 , starburst galaxies ric98 , galaxies with an active nuclei cap99 , and interacting galaxies nav01 , all show the same SN rate of about 1 in SN units SNu (number of SNe per century per $`10^{10}`$ solar luminosities in the B band).

This is a puzzling result, as when a new episode of star formation starts in an old galaxy, both the B luminosity and the SN rate increase (if the obscuration by the dust is neglected) but the SN rate expressed in SNu is not expected to remain constant. The SN rate, barely contaminated by the underlying old population, is expected to show a sharper increase and evolve on different time scales. As a result the constancy of the SN rate cannot be explained by dust-free models of galaxy evolution.

Large amount of dust are always present in starburst galaxies, effecting both the B luminosity and the SN rate. Extinctions of $`A_V10`$ are often found, preventing the detection of SNe by optical observations. It is therefore crucial to use radio or infrared observation to derived a more complete view of the SN events. Already in the near-infrared, at 2 $`\mu `$m of wavelength, dust extinction is much reduced, being about 1/10 of that in V.

When dealing with dusty active galaxies, the normalization based on the B luminosity has no clear meaning as this band is produced by both the old and new populations and is absorbed by the dust. In this case we prefer to use the “far infrared SN unit” SNuIR, define as the number of SNe per century per $`10^{10}`$ solar luminosities in the Far InfraRed (FIR). This normalization is more meaningful as the FIR luminosity is proportional to the current Star-Formation Rate (SFR). It is actually possible to predict the number of expect SN from the FIR luminosity man03 ; mat01 . This prediction depends on several factors, as the radio properties of the SN (used to estimate the intrinsic SN rate in nearby galaxies), the relation between SFR and FIR luminosity, the Initial Mass function (IMF), the presence of an AGN. The number of detected SN can also be used to constrain these parameters.

## 3 The ground-based observations

Several groups have completed or started near-IR SN searches van94 ; gro99 ; swirt ; mat01 , but these works produced only two detections and no spectroscopic follow-up. The reason of these negative results are probably due to a combination of low spatial resolution, limited field-of-view, low sensitivity and small number of expected events.

Our campaign started in 1999. Observations up to 2001 are described in man03 , while in this contribution we present the updated results up to summer 2003. The galaxies were selected to have large FIR luminosities, between $`2\times 10^{11}L_{}`$ and $`2\times 10^{12}L_{}`$, corresponding to about 0.3$``$3 expected SNe per year per galaxy. Such high expected rates were chosen to assure significant statistical results even in a short period of time. The distances are below 200 Mpc, assuring enough sensitivity and resolution to detect point sources over the bright galaxy background. We monitored 47 starburst galaxies in the K band (2.2$`\mu `$m) mainly by using 4m class telescope in sites of good seeing, the TNG in La Palma and the NTT at La Silla. Some observations were also obtained by the UoA 61” telescope. In 2002 and 2003 we obtained 50 new images, mainly with the NTT. The total number of observations is now 304, with an average number of 6.5 observations per galaxy. A sample of less distant, less luminous galaxies were also monitored with the TIRGO 1.5m telescope. The results will be discussed in a different paper (Cresci et al., in preparation).

The various images of the same galaxy were carefully aligned, scaled to the same flux, reduced to the same PSF and subtracted. Typical limiting magnitude were K$``$17 on the nucleus and K$``$19 at distances larger that about 1 arcsec.

These observations produced the detection of 4 events, the first significant sample of events detected in the near-infrared. For one event, SN2001db mai01 , we also obtain a spectroscopic follow-up: this event is a type II SN discovered after maximum light. The extinction, measured by the H$`\beta `$/H$`\alpha `$ and Br$`\alpha `$/H$`\alpha `$ line ratios mai02  is $`A_V5.6`$. As expect, this one was the SN with the highest extinction know at that time.

Obtaining an infrared SN rate from the data is not straightforward and is subject to large uncertainties: this is due to the small number of detected events, to the variability of the properties of core-collapse SNe in the near-IR and to the dependence of the detection limit on the distance from the galaxy nucleus. Using the same hypothesis of man03  we derive an expected number of 55 SNe if they are all out of the nucleus and 16 if they are in the central arcsec. Reducing these numbers to the observed 4 events imply extinctions of $`A_V=33`$ and $`A_V=10`$, respectively. The measured SN rate SN$`{}_{}{}^{NIR}{}_{r}{}^{}`$, assuming that 80% of the SNe explode in the nucleus (see man03 ), is 0.40 SNuIR.

These limits are already quite high and are based on 4 years of (sparse) observations. To do better it is necessary to use instruments with higher sensitivity to point sources, as the HST.

## 4 Archive HST observations

The NICMOS camera on the HST is an ideal instrument to look for SNe in the near-infrared. Its resolution is a few times higher than from the ground under average seeing, and the PSF is much more stable allowing for a better subtraction even near the bright galactic nucleus.

Most nearby starburst galaxies were already observed with this camera. Unfortunately, the HST target selection policy does not usually allow for duplicate observations of the same object with the same instrument setting. As a consequence, only very few archive data can be used to look for variability.

In a pilot study, we have searched the NICMOS archive for repeated observations of starburst galaxies with a long time span. We found 4 objects: NGC34, NGC5256, Arp200 and NGC6240. For NGC34 and Arp220 a narrow-band filter image was acquired a few months after the corresponding broad-band one. In this case each pixel of the broad-band image can be ”scaled” to the other bandpass by interpolation over the observed broad-band colors. NGC5356 was observed twice with the same F160W filter but with a different camera. NGC6240 was observed twice in the same broad-band filter and camera, probably because of problems with the PSF of the first observation. All the images have short exposure times, up to 4 minutes: nevertheless the resulting limit magnitudes are between H=18.8 and 21.0. The nuclear region where the residuals of the subtraction are large is confined in the central 0.3 arcsec, but we expect to reduce it when the same instrument setting is used.

Despite the small sample of only 4 objects, the small number of observations and the far than ideal instrument settings, the galaxies should produce about 5 observable SNe given their FIR luminosities, the time span of the observations and limit magnitudes. Despite of these expectations, no SN was detected. Also in this case we attribute this lack of detection to the presence of high extinctions, but the limits are less stringent.

## 5 Incoming HST and VLA observations

In order to obtain more useful data, recently an HST proposal by our group was approved for cycle 12. The aim of the proposal is to obtain second epoch images of a sample of 37 nearby starburst galaxies already observed by NICMOS in the F160W filter. This “snapshot” program is already active and at the moment of writing the first galaxy was already observed (see the figure). If all the galaxies will be observed, we expect to detect up to 50 SNe, value corresponding to no extinction. Even if all SNe suffer an extinction of $`A_V=30`$ we would still expect to detect 8 SNe. Therefore we are looking forward these observations.

All the detected objects will be observed spectroscopically. Any event detected in galaxies within 100 Mpc will be observed by VLA: in these starburst galaxies we expect to find SNe with peculiar radio properties, as the emission of the core-collapse SN at these wavelength is dominated by the interaction of the ejecta with the circumstellar medium. The radio properties of these SNe can be used to derive the density and the structure of the circumstellar medium and the details of the late stages of the presupernova stellar evolution. Comparison with the existing radio SN models will also test their validity in a wider range of physical conditions than previously available.

## Index


text:
# Calogero-Sutherland Model and Bulk-Boundary Correlations in Conformal Field Theory

## The O$`(n)`$ model.

The most immediate example of such a bulk field is in the non-unitary, non-minimal CFT that is supposed to represent the scaling limit of the O$`(n)`$ model with $`n[2,2]`$. This may be realised as a gas of non-intersecting closed loops and open curves, in which open curves ending on the boundary are known to be described by $`\varphi _{2,1}`$ fields. The above result for $`x_N^\mathrm{f}`$ then agrees with the known value for the bulk $`N`$-leg field. That is, the correlation function (1) is proportional to the probability that $`N`$ non-intersecting curves connect the origin to the points $`e^{i\theta _j}`$ on the boundary.

For $`N=1`$ and $`P0`$ we find a weight $`x_\mathrm{\Phi }=x_1^\mathrm{f}+(\kappa /2)P^2`$ with $`P`$ an integer. The physical interpretation of these new primary fields is in terms of winding number states: each curve linking the origin and the boundary with winding number $`\chi `$ is weighted by $`e^{iP\chi }`$.

For $`N=2`$, in addition to the winding states with $`P0`$, there are new spinless primary fields corresponding to $`k_2=k_1=\beta /4+p`$, with weights $`x_\mathrm{\Phi }=x_2^\mathrm{f}+\frac{1}{2}\kappa p^2+2p`$, where $`p`$ is a positive integer: these correspond in the O$`(n)`$ model to excited modes of the pair of curves, confined by their mutual repulsion. In the case of a finite cylinder, or annulus, their weights give the exponents of correction terms in the correlation function. There are further $`N=2`$ primary fields corresponding to purely bosonic boundary conditions, with $`\gamma =1\beta /2`$. These correspond to $`\mathrm{\Lambda }_2=(1\beta /2)^2E_2^{\mathrm{ff}}`$, which gives $`x_2^\mathrm{b}=0`$ for all $`\kappa `$. This is consistent with the OPE (10): the two boundary fields are fusing to the identity on the boundary, which then couples to the identity field in the bulk. However, once again there are excited states in this sector, which correspond to possible new bulk primary fields with weights $`x_\mathrm{\Phi }=\frac{1}{2}\kappa p(p+1)2p`$. These two types of boundary condition may be understood within the O$`(n)`$ model as follows: each boundary field $`\varphi _{2,1}`$ and its attached curve carry an O$`(n)`$ vector index. If the two labels are different, the curves cannot join, and the fusion is into a $`\varphi _{3,1}`$ field transforming according to a tensor representation of O$`(n)`$. However, if the labels are the same, the curves can join up before reaching the origin. The fusion in this case is into the identity field, and the fact that the leading coupling is now to a bulk primary field with $`x_\mathrm{\Phi }=0`$ means that the probability of the curves joining, and not therefore passing thorugh the origin, is unity. The weights corresponding to the excited states, with $`p1`$, then give the exponents of correction terms to this for an annulus. $`p=1`$ corresponds to the bulk energy density field of the O$`(n)`$ model.

However, still for $`N=2`$, there are other possible ‘mixed’ boundary conditions which are fermionic as $`\theta _2\theta _10+`$, and bosonic as $`\theta _2\theta _12\pi `$. The ground state in this sector has energy $`\mathrm{\Lambda }_2=\frac{1}{16}`$, which gives $`x_\mathrm{\Phi }=(3\kappa 8)(8\kappa )/32\kappa `$. This is the exponent determining the relative probability that a curve, whose ends are attached at nearby points on the boundary, should enclose the origin or not. For $`\kappa =6`$, this is the ‘one-arm’ exponent of percolation (related to the probability that the origin lies in a cluster which touches the boundary), as computed by LSW. Once again, there are excited states in this sector whose energies give corrections to scaling.

## Minimal models.

These correspond to rational $`\kappa =4k/k^{}`$, and the allowed values of the weights of scalar bulk primary fields are given by the Kac formula $`x_{r,s}=((4r\kappa s)^2(4\kappa )^2)/8\kappa `$ with $`1rk1`$ and $`1sk^{}1`$. For these to agree with (4) imposes a severe constraint. If it cannot be satisfied, it implies that the correlation function (1) must vanish. For example, the weight of the $`1`$-leg field corresponds formally to $`x_{1/2,0}`$, but for this to appear in the table of allowed values it is necessary that $`k`$ is odd, with $`r=(k1)/2`$, and $`k^{}`$ even, with $`s=k^{}/2`$. This is of course consistent with the fusion rules of boundary conformal field theory. For $`N=2`$, with fermionic boundary conditions, no solution for $`(r,s)`$ in the allowed range is possible, indicating that, in a minimal model, two $`\varphi _{2,1}`$ fields on the boundary can couple to the bulk only through fusion into the identity. In that case, coupling is allowed, as long as $`p[k/2]1`$, because the corresponding allowed weight is $`x_\mathrm{\Phi }=x_{1,2p+1}`$.

## Comparison with multiple SLEs.

Although the above CFT arguments are self-contained, it is instructive to compare them with those of Ref. . There, a multi-particle generalisation of SLE was proposed in which the $`N`$ curves connecting the boundary with the origin are ‘grown’ dynamically, starting from the boundary at time $`t=0`$ and reaching the origin as $`t\mathrm{}`$. This process is described in terms of the evolution of the conformal mapping $`g_t(z)`$ which sends the simply connected region not yet excluded by the curves into the whole unit disc. This turns out to satisfy $`dg_t=_jb_j\alpha _j(g_t)`$, with $`\alpha _j`$ having the same form as in (5). In this picture, however, the $`\theta _j`$ become functions of $`t`$, evolving, if we take $`b_j=dt`$ for all $`j`$, according to Dyson’s brownian motion:

$$d\theta _j=\underset{kj}{}\mathrm{cot}((\theta _j\theta _k)/2)dt+dB_j(t)$$
(12)
The terms on the right hand side correspond to a mutual repulsion and a stochastic noise. For $`N=1`$ it is known that this process (radial SLE) gives the correct measure on the continuum limit of a single curve. The corresponding Fokker-Planck equation for the joint probability distribution $`P(\{\theta _j\};t)`$ has the form $`dP/dt=P`$, and it was argued in Ref.  that the asymptotic equilibrium solution of this equation, satisfying $`P_{\mathrm{eq}}=0`$, should give the distribution of the points on the boundary in an equilibrium 2$`d`$ critical system such as the O$`(n)`$ model. This gives the result $`|\mathrm{\Psi }_N|^{4/\kappa }`$, in contradiction with the CFT prediction $`|\mathrm{\Psi }_N|^{2/\kappa }`$.

This discrepancy may be traced to the form of

$$^{}=\frac{\kappa }{2}\underset{j}{}\frac{^2}{\theta _j^2}+\underset{j}{}\underset{kj}{}\mathrm{cot}\frac{\theta _k\theta _j}{2}\frac{}{\theta _k}$$
(13)
The first term comes from averaging over the white noise $`dB_j`$, and the second from the repulsion. Comparing this with the expression (7) for the conformal generator $`G`$, we see that the last term, proportional to $`h_{2,1}`$, is absent. This arises, in the CFT calculation, from the transformation of $`\varphi (e^{i\theta _k})`$ under the local scale transformation induced by the conformal mapping $`\alpha _j`$, but it is missing in the multiple SLE approach. Indeed, there is no obvious way of modifying (12) so as to incorporate such a term.

However, the argument in Ref.  that the joint distribution of the boundary points $`\{\theta _j\}`$ in a critical system should be given by the equilibrium distribution of the process (12) was also based on the assumption that the measure on the $`N`$ curves was strictly conformally invariant under $`g_t`$. For the case of a single curve with each end on the boundary of a simple connected region, this is known not to be the case in general – rather, it is conformally covariant. The covariance factor is just the product of the local scale transformations at each end, raised to the power $`h_{2,1}`$. When the arguments of Ref.  are modified to take into account these factors, the result agrees precisely with that of the CFT argument given earlier. The fact that SLEκ is now associated with $`H_N(\beta )`$ with $`\beta =8/\kappa `$ is much more satisfactory. For example, it suggests that the duality of SLE under $`\kappa 16/\kappa `$ is related to the known duality of the C-S hamiltonian under $`\beta 4/\beta `$.

To summarise, we have shown that the quantum Calogero-Sutherland model arises in a very simple way in bulk-boundary conformal field theory. The full spectrum is realised in the non-unitary CFT of the O$`(n)`$ model, and it predicts the scaling dimensions of new primary fields in that theory. In minimal models, it places severe restrictions on which bulk fields can couple to the boundary. In general, because of the Galilean invariance of the C-S hamiltonian, any scalar primary bulk operator is associated with a tower of other primaries of spin $`s`$, with the differences in conformal weights proportional to $`s^2`$. Thus, although the spectrum of Virasoro descendants in a CFT is relativistic, the spectrum of these primaries has a non-relativistic form.

Although we have considered only the case of $`\varphi _{2,1}`$ fields on the boundary, our arguments can be generalised to include other boundary fields corresponding to degenerate Virasoro representations. These will lead to higher-order differential operators. Similar generalisations to WZWN models are also possible.

Recently Bauer and Bernard have extended their analysis of CFT as a probe of SLE to the radial case. Some of their results overlap with ours.

The author acknowledges both helpful and critical conversations with D. Bernard, G. Lawler and W. Werner. This work was supported in part by the EPSRC under Grant GR/J78327.


text:
# CHARM PHYSICS AT CDF II

## 1 Introduction

The CDF II detector is a major upgrade of the original CDF detector which last took data in 1996. In Run I of the Tevatron, CDF made important contributions to $`B`$ physics, providing some of the best measurements of masses, lifetimes, mixing and branching ratios.

For charm physics results, the most important part of the upgrade are the new integrated tracking system and the new trigger system. The integrated tracking system consists of three silicon systems (L00 , SVXII , ISL ) and a low-material, large-radius drift chamber (COT) . The detector has a brand new three-level trigger system. The new features of the trigger include triggering on muons with lower transverse momenta, and triggering on displaced tracks and vertices .

## 2 $`𝐉/\psi `$ Production Cross Section

The mechanisms of $`J/\psi `$ production in $`p\overline{p}`$ collisions are not well understood. Production cross sections from the assumed two major sources, $`bJ/\psi X`$ and direct prompt decays, were measured to be higher than the initial theoretical predictions . Recent theoretical advances in the extraction of the non-perturbative fragmentation functions of the $`B`$ mesons from LEP data in a way that is consistent with the NLO QCD calculations of the $`b`$ hadroproduction cross-sections have improved agreement between theoretical predictions and CDF Run I $`bJ/\psi X`$ cross section measurements to better than 50 %.

The CDF II detector has an improved dimuon trigger with a lower $`p_T`$ threshold ($`p_T>1.4\mathrm{GeV}/c`$). This has extended the low transverse momentum range of triggered $`J/\psi \mu ^+\mu ^{}`$ down to $`p_T(\mu ^+\mu ^{})0\mathrm{GeV}/c`$. In $`39.7\mathrm{pb}`$ of the initial Run-II data, 300 000 $`J/\psi \mu ^+\mu ^{}`$ decays have been reconstructed. As shown in Figure 1, the transverse momentum of the reconstructed $`J/\psi `$ extends to 0 $`\mathrm{GeV}/c`$ . After correcting for acceptance, trigger and reconstruction efficiencies, an integrated production cross section of $`240\pm 1(stat)_{28}^{+35}(syst)\mathrm{nb}`$ has been measured for $`J/\psi `$ mesons with $`p_T(J/\psi )>0\mathrm{GeV}/c`$ and $`|\eta (J/\psi )|<0.6`$.

## 3 $`𝐃_𝐬^+𝐃^+`$ Mass Difference

One of the first measurements done with the new sample of charmed meson decays was the measurement of the mass difference $`m(D_s^+)m(D^+)`$. In a sample corresponding to 11.6 $`\mathrm{pb}^1`$, 2 400 $`D_s\varphi \pi `$ and $`1400`$ $`D^+`$ decays were reconstructed. The detector invariant mass resolution for these decays is about 8 $`\mathrm{MeV}/c^2`$ . The momentum scale of the detector was calibrated using 50 000 $`J/\psi \mu ^+\mu ^{}`$ decays. An outline of the procedure is depicted in Figure 2. The invariant mass of the $`J/\psi `$ decays shows a dependance on the transverse momentum of the reconstructed $`J/\psi `$ because the energy loss in the tracking system is not accounted for. After accounting for energy loss according to the GEANT material map, a residual $`p_T`$ dependence can still be seen. Conversion scans of the tracking volume confirm that there is material missing in the GEANT description so material is added by hand to remove the $`p_T`$ dependence of the $`J/\psi `$ mass. The magnetic field is scaled so that the $`J/\psi `$ mass agrees with the world average . The results of the calibration (the amount of missing material and the magnetic field) are cross-checked by reconstructing other charmed and bottom meson decays ($`D^+,D^0,\mathrm{{\rm Y}}`$), and the reconstructed masses are in good agreement with the corresponding world averages. This calibration was then applied to the $`D_s^+,D^+\varphi \pi `$ decays and the mass difference was found to be $`m(D_s^+)m(D^+)=99.41\pm 0.38(stat)\pm 0.21(syst)\mathrm{MeV}/c^2`$. The result is in good agreement with previous measurements , . The systematic error is dominated by signal and background modeling.

## 4 Charmed Meson Production Cross Sections

In Run I, the B cross section for the $`B^+J/\psi K^+`$ mode for transverse momentum $`p_T(B^+)>6\mathrm{GeV}/c`$ and rapidity $`|y(B^+)|<1`$ was measured to be $`3.6\pm 0.6\mu \mathrm{b}`$ . A preliminary measurement of the cross section for $`D^0`$, $`D^+`$, $`D^+`$ and $`D_s^+`$ mesons was done with 5.7 $`\mathrm{pb}^1`$ of Run II data. The production cross sections were found to be larger than the corresponding bottom meson cross sections: $`4.3\pm 0.1(stat)\pm 0.7(syst)\mu \mathrm{b}`$ for $`D^+`$, $`9.3\pm 0.1(stat)\pm 1.1(syst)\mu \mathrm{b}`$ for $`D^0`$ and $`5.2\pm 0.1(stat)\pm 0.8(syst)\mu \mathrm{b}`$ for $`D^+`$ mesons. In the case of the $`D_s^+`$ mesons, the integrated production cross section was measured for $`p_T(D_s^+)>8\mathrm{GeV}/c,|y(D_s^+)|<1`$ and found to be $`0.75\pm 0.05(stat)\pm 0.22(syst)\mu \mathrm{b}`$. The differential production cross sections ($`d\sigma /dp_T`$) for all the mesons are depicted in Figure 3. Theoretical predictions (FONLL ) are overlaid in the plots. The error band from the theory curve corresponds to the maximum variation from changing the renormalization scale and the factorization scales between $`0.5`$ and $`2.0\times \sqrt{p_T^2+m^2}`$.

## 5 Branching Ratios and $`CP`$ Asymmetry

The study of the precise structure of the CKM matrix has been guided by measurements of mixing and $`CP`$ violation in the neutral $`K`$ and $`B`$ meson sectors. The Standard Model predictions for the rate of mixing and $`CP`$ violation in the charm sector are small, with the predictions in both cases ranging from 0.1% to 1% . Observation of $`CP`$ violation above the $`1\%`$ level would be strong evidence for physics outside the Standard Model. The SU(3) flavor symmetry predicts $`\mathrm{\Gamma }(D^0K^+K^{})/\mathrm{\Gamma }(D^0\pi ^+\pi ^{})=1`$ , while the world average value is $`2.88\pm 0.15`$ . This deviation is most likely caused by large final state interactions (FSI). In the initial $`65\pm 4\mathrm{pb}^1`$ of Run II data, 93 000 $`D^0K^{}\pi ^+`$, 8 300 $`D^0K^+K^{}`$ and 3 700 $`D^0\pi ^+\pi ^{}`$ decays were reconstructed, as shown in Figure 4. Good signal to background was obtained by requiring that the $`D^0`$ always originates from a $`D^+`$ decay: $`D^+D^0\pi ^+`$. Using these samples of $`D^0`$ decays, the following measurements of the ratios of branching ratios were obtained by correcting the raw number of reconstructed candidates by the relative trigger and reconstruction efficiencies::

$$\frac{\mathrm{\Gamma }(D^0K^+K^{})}{\mathrm{\Gamma }(D^0K\pi )}=9.38\pm 0.18(stat)\pm 0.10(syst)\%$$
(1)
$$\frac{\mathrm{\Gamma }(D^0\pi ^+\pi ^{})}{\mathrm{\Gamma }(D^0K\pi )}=3.686\pm 0.076(stat)\pm 0.036(syst)\%$$
(2)
The direct $`CP`$ asymmetries for $`D^0`$ decays were found to be $`2.0\pm 1.7(stat)\pm 0.6(syst)\%`$ for $`D^0K^+K^{}`$ decays and $`3.0\pm 1.9(stat)\pm 0.6(syst)\%`$ for $`D^0\pi ^+\pi ^{}`$ decays.

## 6 Rare Charm Decays

For the flavor changing neutral current decay $`D^0\mu ^+\mu ^{}`$, the Standard Model predicts a branching ratio of $`Br(D^0\mu ^+\mu ^{})10^{13}`$. The present experimental limit is $`Br(D^0\mu ^+\mu ^{})4.1\times 10^6`$ from BEATRICE  ($`4.2\times 10^6`$ from E771 ), 7 orders of magnitude from the prediction.

New physics can substantially enhance this mode. In charm meson decays we are constraining couplings to up-type quarks not necessarily constrained by $`B`$ decays. This makes $`D^0\mu ^+\mu ^{}`$ an unexplored region to search for new physics.

Using $`69\mathrm{pb}^1`$ of Run II data, a search for $`D\mu ^+\mu ^{}`$ decays was performed. As in the $`CP`$ asymmetry analysis, the $`D^0`$ decays were reconstructed in a clean final state by requiring that they originate from $`D^+D^0\pi ^+`$ decays. The kinematically similar $`D^0\pi ^+\pi ^{}`$ decay was used as a normalization mode. The sources of background for this decay are $`D^0\pi ^+\pi ^{}`$ events in which both pions are misidentified as muons and combinatorial background. Both the pion misidentification rate and the level of the combinatorial background were measured from a kinematically similar but statistically independant set of events. The estimated number of background events in the search window was $`1.7\pm 0.7`$. No events were found in the search window, as seen in Figure 5, and a limit was set on the branching ratio: $`Br(D^0\mu ^+\mu ^{})<2.4\times 10^6`$ at 90% C.L. This is currently the worlds best limit on the $`D^0\mu ^+\mu ^{}`$ branching ratio.

## 7 Summary

The upgraded CDF II detector is back in operation and has gathered around 65 $`\mathrm{pb}^1`$ of data which can be used for charm analyses. Due to its ability to trigger on displaced tracks and vertices, the spectrum of charm results has extended from $`J/\psi \mu ^+\mu ^{}`$ decays to include hadronic decays of $`D^0,D^+,D^+,`$ and $`D_s^+`$. With the modest amount of data gathered so far, world class results have already been obtained.