Greetings, and welcome to the Navidea Biopharmaceuticals Quarter Three Earnings Call and Business Update. At this time, all participants are in a listen-only mode. A brief question- and- answer session will follow the formal presentation. If anyone should require operator assistance during the conference, please press star zero on your telephone keypad. As a reminder, this conference call is being recorded. It is now my pleasure to introduce Dr. Michael Rosol, Chief Medical Officer. Thank you, Michael. You may begin. Thank you, and welcome to everybody. Thank you for joining us here today on our earnings call. This call is being webcast live on our website, ir.navidea.com, and a replay will be made available. Following prepared remarks, we will be conducting a live Q&A session. Navidea's Chair of its Board of Directors, Mr. Alex Cappello, its Vice Chair, Mr. Kim Scott, its Vice President of Finance and Administration, Erika Eves, and me are joining you on the call here today. During the course of this conference call, we will be making forward-looking statements regarding future events and the future performance of the company. These events relate to our business plans to develop Navidea's molecular diagnostics and immunotherapeutics, which include clinical and regulatory developments and timing of clinical data readouts, along with capital resources and strategic matters. All of these statements are based on the beliefs and expectations of management as of today. These statements involve certain assumptions, risks, and uncertainties and could cause actual results to differ materially. We assume no obligation to revise or update forward-looking statements, whether as a result of new information, future events, or otherwise. Investors should read carefully the risks and uncertainties described within the Safe Harbor section of our website, as well as the risk factors included in the company's most recent quarterly and annual filing with the SEC. As we begin our update, I thought it would be helpful to detail a few of our key areas of focus in our 2023 planning. One, we'll continue the RA phase III trial success to full enrollment, NDA submission, and FDA approval. Two, we'll fully fund the phase III trial. Company management and the Board of Directors are engaged with multiple potential capital providers in support of our mission to identify this full RA trial funding. Our goal is to be fully funded in 2023. Three, we'll attract and retain top biopharmaceutical talent. As our RA development program success grows, so does the need to grow our team to help support key milestone achievements, support key strategic relationships, and initiate new PR, IR efforts as a way to share our trial and milestone success. As we look at Q3 specifically, the company successfully received an additional $1 million in capacity bridge using the same bridge loan facility currently in place from the company's Vice Chair of its Board of Directors, Mr. Scott. The company also successfully raised $6.2 million in proceeds from its most recent rights offering with the investment banking arm of Maxim Group. If exercised, additional proceeds of up to $11.6 million may be received through the exercise of warrants at same rights offering. We also received an accelerated reimbursement payment of $800,000 for certain research and development expenses from a strategic partner. We have advanced our clinical trials in rheumatoid arthritis as well as our pipeline in other diagnostic indications and in therapeutics. We continue to make solid progress on our phase II-B trial in rheumatoid arthritis or RA, comparing imaging to biopsy, and we this week presented at this international conference our very promising preliminary results supporting tilmanocept's ability to distinguish the fibroid pathotype from the non-fibroid in the first participants evaluated by the time of the presentation finalization. More on that in a moment. These strong early results do support our hypotheses and provide excellent data in support of tilmanocept imaging as a biomarker of CD206 expression in joints of patients with RA. We also continue to enroll into the phase III and open up an additional sites in August and early September, bringing our total open to 12. We also continue to advance our therapeutics and imaging applications through key existing collaborations with well-known institutions and investigators across the globe as we work to grow and advance the company's intellectual property. We are very proud of the progress we have made and the planning we are putting in place to benefit our associates and our shareholders here at Navidea. Regarding the CRG and Dr. Goldberg litigation matters, the company has had two rulings that essentially bracket its exposure in both. The company will continue to minimize exposure. Now, I would like to provide a brief update specific to our clinical results. I'll begin with the progress in our rheumatoid arthritis program. We continue to enroll into our phase III trial, as I just mentioned in RA, as we've recently announced that we have opened up those nine additional sites. The initial indications we're pursuing for FDA approval are, one, early prediction of treatment response to a new or first time anti-TNF alpha therapy, and two, to identify RA patients with low levels of localization who are less likely to respond to anti-TNF alpha therapy. As we have discussed previously, there is a large unmet need for a reliable early predictor of whether a therapy is working in a patient with RA. Because if a drug is not working, the patient's disease is not being treated, and this can lead to long-term health consequences, along with unnecessary high drug costs for ineffective therapies that bring with them possible side effects. Our phase III trial will establish the ability of tilmanocept imaging to serve as an early predictor of treatment response in RA patients switching to an anti-TNF alpha therapy, addressing that unmet medical need. NAV3-32, our comparison study of tilmanocept imaging to joint biopsy remains in active recruitment. As we've announced and discussed previously, the preliminary results of this trial are promising. Our aim is to recruit patients with each of the three pathotypes of RA to obtain comparative imaging and pathology results, and the trial is designed so that we enroll a minimum of four subjects in each of the three subtypes of RA, fibroid, diffuse myeloid, and lympho-myeloid. Overall, trial size has been expected to range between 12 and 24 participants. To date, we have enrolled 14 participants and achieved the minimum of more or more in two out of three of those pathotype buckets, with patients having had both their imaging and joint biopsies completed. The primary objective of this study is to assess the relationship between joint-specific tilmanocept uptake values and the pathobiology of RA-involved joint tissue. Knowledge of an individual RA patient's pathotype may be clinically important because it may predict to which RA therapy a patient is likely to respond. There's a growing body of literature suggesting that those patients with the fibroid type of RA are much less responsive to the anti-TNF alpha drugs. A means of determining whether or not a patient has this particular pathotype is seen as extremely important to a number of key opinion leaders in rheumatology. As of this time, there is no reliable way of assessing a patient's pathotype of RA other than by doing an invasive biopsy. We have hypothesized that tilmanocept could provide this information by providing a way to do a virtual biopsy of a patient's RA. We just finished showing updated preliminary results on the first 13 patients at this week's American College of Rheumatology meeting. This is the largest rheumatology conference in the world. These results indicated that tilmanocept uptake in RA-inflamed joints is able to discretely differentiate patients with the fibroid pathotype, i.e. those with low macrophage involvement, from those having either the diffuse myeloid or lympho-myeloid pathotypes of RA, i.e. those with higher macrophage involvement. As of this time today, we've been able to clearly classify patients as either fibroid or non-fibroid based on our imaging results taken before biopsy in all 15 participants. These data also provide support for one of our indications in the phase III trial. That ability to predict from a baseline scan alone whether a patient is likely to receive a meaningful clinical benefit from an anti-TNF alpha therapy. Since, as I mentioned, there is increasing evidence that if a patient has the fibroid type of RA, they're less likely to receive significant benefit from anti-TNF alpha. You might recall that in our previously completed phase II-B study, NAV3-31, where we looked at the efficacy of tilmanocept imaging at early prediction of treatment response. Those patients in that trial who exhibited a low level of tilmanocept uptake in their joints on their baseline scan alone had an almost 90% non-response rate to anti-TNF alpha therapy using the clinical gold standard assessment. Importantly, these promising early results have opened up conversations with pharmaceutical companies developing therapeutics for RA, with the possibility of tilmanocept imaging being used as a biomarker in drug development pipeline. The key differentiator between now and prior discussions we have had is that we have these additional promising data in hand. As we move forward to trial completion, if these current results hold, we'll be in an even better position for discussions with companies with which to work. We continue to make very good progress in automating the image quantification as well, which will have significant benefit for the commercial product. We have the letter of intent and continue to work closely with MIM Software on the full agreement for them to be our commercial partner for image quantification of tilmanocept imaging in RA. Once again, MIM is a leading medical imaging software company with a large footprint in the nuclear medicine space. They completed a pilot study using data from our earlier trials, demonstrating that they can develop a fully automated application that can robustly reproduce our quantitative imaging readouts using our proprietary algorithm. This will be important for rollout of a commercial product. The ability to perform quantitative reads of our images rapidly and reproducibly and at large- scale through automated means is critical to widespread use and adoption of tilmanocept for RA. Keep in mind that all of this, the image analysis methodology, as well as the data upon which it is built, including the normative database we discussed before, is not only critical to deriving the most accurate and sensitive read of our RA images, but it also serves as a significant barrier to entry to possible competitors in this space. We will continue to work with MIM to finalize terms of our partnership and will make an announcement when completed. In other areas of our diagnostics pipeline development, in cardiovascular disease, the group at the Massachusetts General Hospital in Boston published the results of the investigator-initiated atherosclerotic plaque imaging study that we helped to support. The data are promising in terms of localization of tilmanocept to sites of atherosclerotic plaque, and were in line with what was reported in the pilot study we co-published with them previously. We press-released this publication, the most recent publication, and you can find reference to it in that release. Preclinical studies on Gallium 68 tilmanocept for PET imaging and related next-generation Manocept imaging agents have progressed significantly through internal work here at Navidea and through extramural collaborations with researchers at the University of Alabama at Birmingham, or UAB. We have completed work on our NIH-funded preclinical studies for evaluating Gallium 68 tilmanocept and various new imaging agents similar to tilmanocept in a mouse model of atherosclerosis. Work with UAB on another important set of preclinical imaging studies was completed and presented at the Society of Nuclear Medicine and Molecular Imaging meeting last summer. A manuscript is currently in the second round of peer review. This work looked at a method to increase the localization of our imaging agent to target tissues, while additional technology was designed to block off-target imaging agent localization to the liver, which is a major site of localization when tilmanocept is administered by intravenous injection. These studies were highly successful, showing that we can dramatically increase localization of a new tilmanocept-like imaging agent to tumors while simultaneously and significantly blocking off-target localization to the liver. This has important implications for our therapeutics as well. On the therapeutic asset front, we are advancing our candidates in the oncology and anti-inflammatory spaces in preclinical studies, with the goal of filing investigational new drug applications, or INDs, to advance to human studies in 2024. These filings will be significant inflection points and opportunities for licensing and partnering deals. Work on new drug delivery constructs and new targeted payloads has progressed. These new constructs carry new drug payloads that may be more effective than doxorubicin for beneficially altering the immune status of tumor macrophages, for example. Results in mice have demonstrated that when administered alone or in combination with another cancer drug, these therapeutic constructs significantly reduce the rate of tumor growth by an average of 76%. Some of our results covering new bisphosphonate payload constructs were recently presented at the Tumor Myeloid-Directed Therapies Summit meeting. More recently, on November 10 in fact, the full spectrum of results for both our paclitaxel and novel bisphosphonate constructs were presented at the annual meeting of the Society for Immunotherapy of Cancer, or SITC, held in Boston, Massachusetts. This work is about advancing to a lead candidate for macrophage phenotype-altering drugs for oncology indications. I can tell you the work presented at SITC was well-received, and we had a steady stream of attention. In vitro studies examining the ability of our dexamethasone constructs for inflammatory indications have shown positive results as well, demonstrating macrophage phenotype change. These constructs will soon be tested in preclinical models. Preclinical studies are also ongoing in leishmaniasis. Leishmaniasis is a vector-borne chronic disease caused by a protozoan parasite that replicates in CD206-positive macrophages. It is transmitted to humans through the bite of infected sandflies found in parts of the tropics, subtropics, and Southern Europe. It's rare in the U.S., but in more tropical countries where the sandfly vectors are found, it is a common, serious, and potentially life-threatening disease. The FDA has designated leishmaniasis as a neglected tropical disease, making new therapeutics potentially eligible for a priority review voucher that, in our case, we could sell potentially for more than enough to back-cover costs of development, as well as accelerate a number of other pipeline candidates. We have earlier work we published in 2017 showing that high CD206-expressing macrophages play a role in the dominant form of the disease. We recently renewed preclinical studies with one of the world leaders in leishmaniasis at the NIH, and we now have promising results from several preclinical studies. The last of these studies was just recently replicated, demonstrating that one of the company's therapeutic constructs could dramatically reduce the growth of leishmanial parasites in a mouse model of the disease. These exciting results indicate a new mechanism of action for our therapeutic constructs and set the stage for further in vivo preclinical studies with these collaborators at NIH. If these continue to hold, we will perform preclinical safety and toxicity studies and advance towards IND status application as well. Our therapeutic pipeline is robust and moving forward. That brings me to our overall intellectual property front. We received notification of issuance of patent from the USPTO, as well as the State of Israel, for our patent application covering the Manocept-based therapeutic for leishmaniasis. We continue to submit new provisional applications and work on pending ones. We have filed a new provisional patent application describing a novel degradable linker for the therapeutic payloads dexamethasone and paclitaxel containing Manocept therapeutic constructs. This linker was used in some of the studies I just mentioned a few moments ago. These constructs are being evaluated preclinically for effects on macrophages and in animal models of oncology and inflammatory indications. All told, we have filed five new provisional patents since the end of last year. In partnership with our excellent patent attorneys, we have an active IP protection strategy for the company that will provide needed protections and rights to both our current diagnostic and therapeutic agents, as well as to our next generation molecules and disease indications. Regarding Lymphoseek Europe and the rest of the world, our strategy has been and remains to find the right partners for marketing and distribution for Lymphoseek and other company pipeline candidates in Europe and beyond. The reason for this is we are focusing on a long-term strategy of partnering for marketing and distribution. On that drug manufacturing and supply front, for both Lymphoseek and the RA product, we have been and continue to work with a new active pharmaceutical ingredient or API supplier, as well as a final drug product supplier. Progress continues, and as of this time we are advancing towards completion of these and readiness for clinical and commercial supply. This work has implications for Lymphoseek in China and Lymphoaim in India, as we need to be able to supply a steady and reliable stream of product to our partners in these countries. You might have seen our press release announcing publication of a manuscript by an Australian investigator using tilmanocept. This was the first such study coming out of Australia, and this investigator and his colleagues are enthusiastic about using Lymphoseek in Australia going forward. These are just some of the highlights of the last quarter that I wanted to touch on for this update. We remain largely focused on the RA pipeline, specifically the phase II imaging to biopsy trial as well as the phase III, while we continue to support and push for progress on our other diagnostic and therapeutic indications. As always, I want to thank the team here for their tireless efforts to keep things moving, our network of clinical trial sites and academic research collaborators for all of their hard work. Our strategy remains to advance our pipeline products to key inflection points and seek appropriate partnerships for commercialization and marketing. With that, I'll now turn it over to Erika for financial updates. Erika? Thank you, Mike. Consistent with peers focused on the successful completion of phase III trials, our revenues for Q3 were minimal. Total revenues for the third quarter of 2022 were approximately $8,000 compared to $96,000 for the same period in 2021. Total revenues for the first nine months of 2022 were $65,000 compared to $481,000 for the same period in 2021. The decrease was primarily due to the 2021 partial recovery of debts that were previously written off in 2015, the 2021 receipt of reimbursement from Cardinal Health of certain R&D costs, decreased grant revenue related to small business innovation research grants from the National Institutes of Health supporting Manocept development, and decreased license revenue from transitional sales of tilmanocept in Europe. Research and development expenses for the third quarter of 2022 were $1.2 million, compared to $1 million for the same period of 2021. R&D expenses for the first nine months of 2022 were $4.1 million, compared to $3.8 million for the same period in 2021. Selling, general and administrative expenses for the third quarter of 2022 were $3.6 million, compared to $1.5 million for the same period in 2021. SG&A expenses for the first nine months of 2022 were $6.7 million, compared to $5.1 million for the same period in 2021. Following the ruling by the Texas Court in August 2022, the company recorded $2.6 million in legal fees pursuant to the CRG judgment, and that was recorded in SG&A. Navidea's net loss attributable to common stockholders for the third quarter of 2022 was $7.7 million or $0.25 per share, compared to $2.4 million or $0.08 per share for the same period in 2021. Our net loss attributable to common stockholders for the first nine months of 2022 was $13.7 million or $0.45 per share, compared to $8.1 million or $0.28 per share for the same period in 2021. Finally, Navidea ended the third quarter of 2022 with $4.6 million in cash and cash equivalents. Back to Mike. Thank you, Erika. Now I'll turn the call over to any questions that might be out there. We'd be happy to address. Once again, joining me on the call is our Chair of the Board, Alex Cappello, as well as Mr. Kim Scott, our Vice Chair, and Erika Eves. I think we should be able to handle any questions that come our way. Thank you. We will now be conducting a question- and- answer session. If you would like to ask a question, please press star one on your telephone keypad. A confirmation tone will indicate that your line is in the question queue. You may press star two if you would like to remove your question from the queue. For participants using speaker equipment, it may be necessary to pick up your handset before pressing the star keys. We ask that you please limit yourself to one question and one follow-up, and if you have more, please reenter the queue. Thank you. One moment please, while we poll for any question. Our first question comes from the line of Michael Okunewitch with Maxim Group. Please proceed with your question. Hey, guys. Thank you for taking the question, and congrats on the progress this quarter. Thanks, Michael. I guess I just wanted to first touch on for those nine additional sites, were any of those used in prior studies for Tc-til? How has the above average rate of recruitment held up as you've added in these new sites? Yeah, great question. Yes, we took advantage of the kind of conglomeration of research centers in certain geographic areas as well as the imaging centers that we've worked with before. There is an imaging center, for example, that we worked with in prior trials that is fed into by several different rheumatology practices. We took advantage of that and so that is happening. It's an imaging center we've used before. As well, we have a couple of rheumatology sites we've used previously that we've opened up into the study. We try to take advantage of prior experience with sites that have been excellent recruiters to bring them in. There are several other sites that are in the queue to come into the phase III that we worked with in prior studies, and they're actually to come in. We just need the accelerant of increased capital into the company so we can go full bore on that front. Yes, right now we're a bove the average recruitment rate for RA trials phase II and phase III in North America historically. We continue to maintain that. We're doing that even with the fact that, you know, we just opened nine of these sites in, as I mentioned, end of August, early September. Very frequently, it'll take a month or two or more for sites to really get rolling, and some of the sites are in that boat, to be frank. Other sites just started enrolling rapidly right away. There are different reasons for that. Overall, we're maintaining above the average recruitment rate significantly. Things are looking very good. All right. Thank you for that. Just one follow-up from me. I wanted to see if you could give an update on either, you know, how many or the proportion of responders versus non-responders which have enrolled in the study so far since this could impact the overall trial size? Great question. Yeah, we are tracking that, and what we're doing is, without unblinding the study, we're able to see the clinical response rates at three and six months. Right now, we have a good number of patients at the three-month milestone, and so we can look at their clinical responses. Without going into the details, without releasing too much information here, we're trending more towards the lower end of the trial size possibilities, which would be great. As you know, maybe not others on the phone here, the phase III trial size could range from about 200- 672, and we're trending more towards the mid to lower end of that based on the response rate. Things are looking really good there. All right. Thank you very much. Again, thanks for taking my questions. You're welcome. Thank you. Thank you, and our next question comes from the line of Mike Rocchielli, a private investor. Please proceed with your question. Yes, Dr. Rosol, appreciate the concise strategic outlook you presented at the beginning. That was very useful. My first question is, are you able to share how many people have been enrolled in the phase, the 3-33 so far? Thanks, Mike. Good question. Yeah, I'm not going to share that today. What we'll do is we're tracking that, and when we hit certain milestones, we'll make announcements as appropriate when those are hit. Stay tuned is what I'd say, but enrollment is going well. Okay. Follow-up on 3-32, you said you've had 15 patients enrolled now. Are you still running at a 100% match? Yeah, we're at 100% match. Can't do better than that, right? Mike, I know you can 14. Yeah, yeah, it's 14. 14? Okay. Now on that 100% match, that's excellent. How important is it to now differentiate between the fibroid and the non-fibroid? I know you're still trying to differentiate between the diffuse and the lympho. Is that really that critical? Yeah, great question. What we're hearing from the rheumatologists out there, and I was just at the American College of Rheumatology meeting over the weekend, and I met with a number of key opinion leaders in rheumatology and really the big players in rheumatology in the world, not just in the U.S. That's not me bragging, that's me giving them compliments. The word from those folks is primarily the... They're really excited about the fibroid and non-fibroid differentiation because there's a nice body of literature already suggesting that being able to distinguish between those two types can really give you significant information for helping guide patients to a more appropriate therapy or guide them away from a therapy that is less appropriate for their type of disease. That I think is a primary importance. Distinguishing between the diffuse myeloid and lympho-myeloid is important as well, and it depends on who you ask. There are certain scenarios where its importance may rise, particularly for example, in the development of therapeutics that may target one of these specific subtypes or two out of three of the subtypes of RAs. You can imagine scenarios where its importance is elevated, and we've heard that from key opinion leaders as well as pharmaceutical companies directly. There's a growing body of literature suggesting that some agents work better on one of those two types than the other as well, but that's more of an evolving field currently. Really the fibroid/non-fibroid is seen kind of across the board as extremely important and very exciting because right now you can't do it any other way other than by doing an invasive biopsy. Our virtual biopsy is a way to do it non-invasively and quickly. There's growing emergence of the idea of looking, distinguishing between the other two types. Would you still be considered the gold standard if you could only do the fibroid versus the non-fibroid, would you still be t he gold standard? That is absolutely tremendous value, because again, you can't do it any other way than doing the biopsies. The biopsies, depending on who does them, have a 15% ±, you know, 5% or so margin of error. They're difficult to do. Patients don't like to do them. That's why these trials are hard to recruit for, these biopsy trials. With our scan being able to distinguish fibroid from non-fibroid, the word I heard on the street is that would be tremendous value to the field of rheumatology. Excellent. Well, you know, your science is so robust. I'll go back into the queue and come back in. Thank you. Oh, actually, I think you're back in the queue. Yeah. You're back. You're number one, Mike. Or get back in. Is he gone already? No, no, number one. Okay. Okay. All right. Thank you. There are no further questions at this time, and I would like to turn the floor back over to Michael for any closing comments. Oh, that's all right. Mike Rocchielli has one more question. We'll let him ask now. Oh, I'm sorry. I do see that he just re-queued. Thank you. Yep. Mike, you are last. All right. Well, thank you. Thanks very much. On the science, you mentioned that being at these conferences and that you did have a lot of feedback, particularly at the Cancer Immunotherapy conference. Can you give us some generalization of the type of questions they were probing you with? Sure. One of the interesting things of our constructs is what we're doing is we're attaching these known therapeutics like paclitaxel, doxorubicin, and now bisphosphonates, which in general are known drugs, although importantly, we've created a novel bisphosphonate, so that's also very exciting. Those drugs have known mechanisms of action. When they are attached to our molecule, our Manocept platform, and delivered through the CD206 pathway, they actually have different mechanisms of action than the free drugs themselves. What they're doing is they are actually changing the phenotype of the macrophage. Rather than doing what they do as pure cancer drugs, for example, the paclitaxel and doxorubicin, they're not achieving their effect in that same way where they go in and stop cell division or, you know, cause cell death. They're actually going into the macrophage and changing the phenotype in this case more, or in these cases, more towards the pro-inflammatory type, which rallies and stimulates the body's immune response in our animal models against the tumors. This is very exciting. We had a number of questions related to that mechanism of action, and that led to a lot of excitement. Then the results themselves, and I'll post the poster onto our website in the coming days. We're posting the American College of Rheumatology posters on the website later today or tomorrow as well. You can look at the poster. In our data, what we've done is not only are we driving the phenotype more towards the pro-inflammatory state, but we're also having other effects like we're reducing the SIRP alpha signal, which relates to the macrophage, I'm sorry, the tumor cell "don't eat me" signal. What we're doing is we're suppressing SIRP alpha, which would then work in a roundabout way to get over the hurdle that the tumor cells present, where they stop the macrophages from eating them, basically, keeping things simple. We have a surprising and really cool unexpected additional mechanism of action that's really on the cutting edge of immunotherapies in cancer. Not only can we drive the phenotype a certain way. In so doing, we're actually stimulating the phenotype in a way that is at the leading edge of what's going on in the immuno-oncology space. We had a large number of people who were very excited by that and the encouraging thing for this small company from Columbus, Ohio or Dublin, Ohio, specifically, is we're at the forefront. Our data are right there at the forefront of this kind of medicine. You know, our need is to get the accelerant, as I said earlier, to drive these things more rapidly into the clinic. The technology is there, the science is there, and we're doing all we can to advance it as rapidly as possible. It's really very exciting. Would that forefront kinda like be driving CD163 lower, as an example? Yeah. There's all sorts of things going on here. Some of the macrophage markers that represent macrophages that are more anti-inflammatory or wound healing, those are going down in these cells and with our immuno-oncology agents. The ones that are recognized as the pro-inflammatory markers, those are going up. As part of those, some markers are going up that interact with T cells to tell the T cells to attack the tumor cells, and those are going up as well. Then these other things that are involved in what's called checkpoint inhibition are going down. We have this concert of different things going on when we introduce our constructs that all work together to rally the body's immune response, the macrophages and the T cells against the tumors, and we're seeing all of that in our studies. Yeah. That's it. It's just really exciting. Thank you. There are no further questions at this time, and I would like to turn the floor back over to Michael for any closing comments. Thank you. I'd like to thank you all for joining us today and for your support of the company and the people here. We will close the call now and see you, I believe, at the annual meeting. It will be the next milestone on the calendar. Thank you very much. This concludes today's teleconference. You may now disconnect your lines at this time. Thank you for your participation.