Spring 1999 Edition

1999 ACVIM Forum in Chicago (June 10-13)

The C.G.S. Symposium - The C.G.S. will sponsor a half-day symposium at the 1999 ACVIM Forum in Chicago. An exciting program has been assembled by Colin Burrows and Society President-Elect, Dr. Allen Roussel. Symposia speakers will include Drs. Colin Burrows ("Overview of Mucosal Injury and Healing"), Dennis McCarthy ("The Role of COX1 and COX2 Inhibitors in Mucosal Injury and Healing", "Gastrointestinal Complications of Non-Steroidal Anti-Inflammatory Drugs"), and Frank Andrews ("Equine Gastric Ulcer Disease"). This Symposium promises to be a particularly informative session in light of several new COX2 inhibitors (e.g., Celebra-Searle, Vioxx-Merck/Pfizer) that have been marketed, or are scheduled for marketing this year.

The Liver Study Group - The L.S.G. will host an impressive half-day symposium on "Specialized Imaging and Diagnosis of Hepatobiliary Tract Disease" at the 1999 ACVIM Forum. Symposia speakers will include Drs. Dave Hager ("Specialized Imaging of the Liver - Parts I & II"), Dave Biller ("Clinical Utility of Ultrasonography in the Diagnosis of Hepatobiliary Disease"), and Keith Richter ("Non-Invasive Diagnosis of Hepatobiliary Disease"). Congratulations to Dr. Susan Bunch on another tremendous L.S.G. program.

Endoscopy S.I.G. - "What's Your Diagnosis"? - Dr. Mike Leib will once again organize and host the Endoscopy Special Interest Group at the ACVIM Forum. Mike is hoping to see greater Society participation at this year's Forum. Please review endoscopic case histories, and let Mike know of your interest (540-231-4621 Office; 540-231-7367 FAX; mleib@vt.edu). Mike has done a fantastic job with this Special Interest Group, and, on behalf of the Society, I extend a special "Thank You" to our Gastroenterology colleague from Virginia Tech University.

Other Gastroenterology Symposia at the ACVIM Forum - The Small and Large Animal Internal Medicine Program Sub-Committees have assembled several other gastroenterology programs for the Chicago Forum, including: 1. "What's New in Inflammatory Bowel Disease" (S.A.I.M.) - Al Jergens, Dave Williams, and Joerg Steiner 2. "Small Intestinal Bacterial Overgrowth - Point/Counter-Point" (S.A.I.M.) - Roger Batt and Kenny Simpson 3. "Equine Infectious Gastroenteric and Hepatobiliary Disease" (L.A.I.M.) - Jose Traub-Dargatz, Mark Donaldson, Michelle Barton, S. Peek4. "What's New in the Diagnosis and Management of Gastroenterologic Disease?" (S.A.I.M.) - Kenny Simpson, Mike Willard, Mike Leib, and Deb Zoran 5. "Swallowing Disorders in Dogs and Cats" (S.A.I.M.) - Mike Willard and Robert Washabau 6. "Diagnosis and Management of Difficult Liver Presentations" (S.A.I.M.) - Cyndie Webster, Dave Twedt, Denny Meyer, and Kathy Michel

***Society Luncheon Meeting - Please mark your calendars for the C.G.S. membership luncheon meeting on Saturday, June 12, from 12:30-1:45 pm. Drs. Aine McCarthy and Larry McDaniel of Ralston Purina have graciously agreed to sponsor our business meeting.***

1999 Digestive Disease Week in Orlando (May 17-19)

The AGA PhD, MD/PhD, DVM Committee will hold an AGA Research Symposium on "Current Topics in Comparative Gastroenterology on Tuesday, May 18, from 8:00 -10:30 am. The symposium focus this year will be on "Animal Models of Motilide Receptor Heterogeneity: Motility vs. Transit". Session speakers will include Sushil Sarna ("In vivo and in vitro locus of action of prokinetics"), Theo Peeters ("Neurogenic and myogenic effects of motilides"), and Charles Malbert ("Erythromycin-induced gastrokinesis in swine"). C.G.S. Members Al Merritt and Colin Burrows will be chairing this symposium. Hats off to Al and Colin for organizing an excellent symposium!

1999 North American Veterinary Conference

The C.G.S. sponsored an eight-hour symposium at the 1999 NAVC meeting in Orlando, Florida. The focus of the symposium was primary gastrointestinal tract disorders (i.e., stomach, intestine, colon) of companion animals. C.G.S. speakers included Drs. Mike Leib and Bob DeNovo. Congratulations to Drs. Leib and DeNovo on an outstanding program.

1998 Conference of Research Workers in Animal Disease

The C.G.S. Research Abstract Award was presented to Y. Hu for his work entitled "Development of an optimized PCR assay for detection of E. coli 0157.Ht in bovine feces". This work was carried out in conjunction with J.C. Meitzler and Q. Zhang at the Food Animal Health Research Program in Wooster, Ohio. Congratulations to Dr. Hu.

1998 American Motility Society Meeting in Philadelphia

Interesting Research Abstracts

White RJ, Miller DV, Paterson WJ: Impairment of the deglutition reflex by acute acid/pepsin-induced esophagitis: a contributor to the pathogenesis of gastroesophageal reflux disease? (Abstract #A3) - Esophagitis was induced by perfusing the esophagus of opossums with a 100 mM HCl/0.02 mg/ml pepsin solution. Deglutition was monitored by intraluminal esophageal manometry and mylohyoid electromyography following pharyngeal or superior laryngeal nerve stimulation. The deglutition reflex was shown to be inhibited following the induction of esophagitis, and the investigators concluded that "the study may have major implications regarding the pathogenesis of gastroesophageal reflux disease."
Editor's Comment - It is well established that normal swallowing mechanisms contribute to the anti-reflux barrier by clearing refluxed gastric contents from the esophagus, and by salivary bicarbonate neutralization of gastric acid. The investigators did not address the question raised in the title of their abstract, however. Deglutition was impaired following, but not before, the induction of esophagitis. Are animals with impaired swallowing at increased risk for gastroesophageal reflux? There is some preliminary evidence to suggest this may be the case in humans with oropharyngeal dysphagia, but this has not been substantiated in animals.

Otterson MF, Leming S, Liu X, Moulder J. The role of the NMDA receptor in radiation induced colonic motility (Abstract # A26) - Extramural strain gauges were sutured to the canine ileum and colon, and dogs were exposed to abdominal irradiation (250 cGy, 3X/week, alternate days, total dose of 1500 cGy) in the presence or absence of felbamate (16 mg/kg BID), an NMDA receptor antagonist. Felbamate decreased the frequency of radiation-induced small intestinal giant migrating contractions (GMC's) that propagate into the colon. Felbamate also decreased clinical signs of diarrhea associated with radiation injury.
Editor's Comment - Otterson et al. reported three significant findings: a) the results confirmed earlier findings that NMDA receptors are involved in the regulation of gastrointestinal motility; b) radiation-induced abnormalities in colonic motility (i.e., GMC's) and clinical signs (i.e., diarrhea) are similar to those observed in experimental colitis (Sethi and Sarna); and, c) blockade of NMDA receptors resolves GMC's and clinical signs.

Bouras EP, Burton DD, Camilleri M. Selective stimulation of proximal colonic transit by the benzofuran 5-HT4 agonist, prucalopride, in healthy humans (Abstract # A32) - Using a nuclear scintigraphic technique, investigators from the Mayo Clinic studied gastric emptying, small bowel transit time, and proximal colonic emptying in healthy humans following treatment with placebo, 0.5, 1, 2, or 4 mg of prucalopride. Prucalopride had no effect on gastric emptying or small bowel transit, but it did accelerate proximal colonic transit.
Editors Comment: Janssen Pharmaceutical investigators have previously shown similar effects in the canine and feline colon. Prucalopride stimulates canine colonic contractile patterns (Gastroenterology 1997; 112: A704), and enhances defecation frequency in conscious cats (Gastroenterology 1997; 112: A705a). Investigations of this drug should now logically focus on the utility of this drug in treating constipation in any of these animal species.

Shi X-Z, Sarna SK. Inflammation activates M2 receptor coupling to adenylate cyclase in canine ileal circular muscle cells (Abstract # A5) - Canine ileal inflammation was induced by a series of mucosal exposures to acetic acid and ethanol. This is a well-established, well-characterized model that has been developed by the Sarna laboratory. Circular and longitudinal smooth muscle cells were dispersed, and muscarinic cholinergic receptor sub-type and cAMP levels were determined. Inflammation was shown to be coupled to expression of the M2 muscarinic sub-type, adenylate cylase activation, and inhibition of contraction of circular, but not longitudinal, smooth muscle.
Editor's Comment: Sarna and his colleagues have previously shown (Gastroenterology 1998; Vol: G3406) that cholinergic and nitronergic stimulation of L-type calcium channels, phospholipase C, and G proteins are all down-regulated during inflammation. These studies illustrate abnormalities, i.e., expression of the M2 receptor, more proximal in the signal transduction pathway.

Interesting Symposia - Dr. Allen Roussel of Texas A & M University attended this meeting along with Drs. Colin Burrows and Peter Rakestraw. Dr. Roussel offers the following summary from his attendance at several of the symposia:

One of the themes was differentiation and development of enteric smooth muscle cells and neurons. Dr. Ray Kaper discussed the pathogenesis of Hirshsprung Disease. There are at least six different genes involved with different degrees of penetrance and expressivity associated with aganglionosis. There is also variability in the location and length of bowel involved. I wondered if some of the ill-defined undiagnosed dysmotilities and chronic gastrointestinal diseases we see in animals is due to mild to moderate regional aganglionosis. In another presentation by Dr. Martin Graham, it was explained that in acute inflammatory disease, collagen is laid down and resorbed, facilitated by collagenases. In chronic inflammation, collagen fibers are cross-linked which prevents their resorption. Scarring, and eventually stricture, are endstages of this disease. The success of collagenase in the period after collagen deposition determines the end result. Another effect of chronic inflammation is the phenotypic modification of smooth muscle cells to more immature myocytes with primary responsibilities of repair and prevention of perforation.

In another session, Dr. Kathleen Trybus presented a video display of individual myosin contractions. Muscle biologists are now able to measure the force of contraction of single myosin molecules. This cow doctor was amazed and impressed.

I also attended the workshop on Colorectal Motility. I was struck by several things. One was the controversy over the use of specific diagnostic tests for assessing constipation. Another was the relative paucity of effective drugs for refractory cases of constipation in people. Dr. Skip Eakers lamented that physicians faced with treating patients with refractory constipation must use drugs *extra-lable* that have side effects of diarrhea. Examples are misoprostol and colchicine. Veterinarians can identify with having a scarcity of label drugs to use for a variety of conditions. Lastly, I was somewhat surprised to hear rather tepid enthusiasm for cisapride in the treatment of constipation. A tidbit that I picked up that may be of interest to some of you in small animal practice is that *Golytely* is out of favor as a laxative because the sulfate that acts as a non-absorbable electrolyte laxative in normal animals (people) is absorbed in substantial quantity in animals (people) with slow transit. Therefore, *Nulytely* is recommended for constipated patients. The final day featured a symposium on gut inflammation. As expected, cytokines were in the spotlight, with cytokine modulation being mentioned as a future therapeutic strategy for IBD. ( I saw an ad for a anti-TNF antibody this week, so I guess the time is here) The role of the enteric nervous system(ENS) was also addressed. The ENS is altered in IBD both morphologically and functionally. The ENS proliferates, and expression and release of transmitters is altered during inflammation. Capsaicin exacerbates and lidocaine attenuates IBD end experimental colitis. You may want to read Dr. Claudio Fiocchi's review "Inflammatory Bowel Disease-Etiology and Pathogenesis", Gastroenterology, 115(1): 182-205, 1998.

In a presentation on "Emerging Techniques in the Evaluation of Gastric Motility", Dr. Henry Parkman had some interesting comments on gastric scintigraphy. To reduce costs, most medical centers are using percent remaining at 2 hours rather than T50 to assess gastric emptying scintigraphically. Dr. Parkman suggests 4 hours as the optimal time to image patients instead of 2 hours. Nevertheless, the fact that two images instead of 10 or so, can provide useful clinical information, would substantially reduce the cost of diagnostic scintigraphy. Dr. Parkman also described dynamic antral scintigraphy in which contraction amplitude can be assessed non-invasively. He also described regional gastric scintigraphy and showed how more accurate information might be gained by defining areas of interest over the proximal and distal stomach separately, rather than simply looking at the entire stomach.

Abstracts from this meeting were published in Digestive Diseases and Sciences 43(7) 1998. Of interest from the abstract sessions, a group from the University of Pittsburgh reported on the role of inflammation in post-operative ileus. Both ischemia/reperfusion and surgical manipulation induced an inflammatory response with rapid migration of leukocytes into the smooth muscle layer and release of inflammatory mediators. Inducible nitric oxide production was dramatically increased also. Respectfully submitted - Dr. Allen Roussel.

1998 American Association for the Study of Liver Disease Review - Dr. Cynthia Leveille-Webster of Tufts University attended this meeting, and she offers the following summary of interesting research findings:

619: The HBV genome and possibly infectious viral particles may persist for long periods of time in the guts of bedbugs and may be shed into the environment via their excrement. This is a questionable method of viral transmission.

326: Dodecafluoropentane emulsion (Echogen), an ultrasound contrast agent, was evaluated in the imaging of hepatic lesions. It was given as a 2% emulsion IV. The average enhancement time was only 5 minutes, but it did enhance visualization of vascular lesions in patients with primary or secondary malignancies.

358: This abstract addressed the relatively high incidence of complications and mortality in patients with obstructive jaundice that go to surgery. Many patients get systemic inflammatory syndrome after surgery. It has been postulated that this inflammatory reaction is due to endotoxemia. This study looked at the effect of molsidomine, a nitric oxide donor pro drug, on endotoxin induced damage in rats that had undergone a bile duct ligation. Molsidomine enhanced survival in BDL rats treated with endotoxin and this protection was associated with decreased levels of TNF-alpha.

363: It is known that endotoxin down regulates the production of the bile salt transporter on hepatocyte and that this is likely involved in the cholestasis of sepsis. This abstract suggested that macrophages secrete a factor which is responsible for this down regulation. They exposed a rat hepatocyte cell line to conditioned media derived from activated macrophage cell lines and demonstrated decreased uptake of bile salts in the hepatocytes. This decreased uptake of bile salts was associated with decreased expression of the RNA message for the bile salt transporter.

378: This study looked at 7 patients receiving long term hetastarch therapy. They had histologic deposition of HES in their liver. The clinical significance of this was not addressed.

587: Cytochrome C, a critical component of mitochondrial oxidative phosphorylation, is known to initiate a degradative proteolytic cascade that culminates in apoptosis. Cytochrome C released from the mitochondria interacts with Apaf-1 and caspase 9 to form the so called apoptosome. This complex activates procaspase 3 which then drives apoptosis. The regulation of formation of this apoptosome complex is the subject of intense investigation since it may hold the key to modulating cell death. Glutathione is the major antioxidant in the liver. It is present in both the hepatocyte cytosol and is also within the mitochondria. This study looked to see if the mitochondrial glutathione might be pivotal in regulating the release of cytochrome C. They depleted cultured hepatocytes of mitochondrial glutathione with 3-hydroxy-4-pentane or by chronic ethano feeding and looked at the sensitivity of the cells to TNF-alpha. Compared to control cells, the cells depleted of mitochondria glutathione showed enhanced generation of reactive oxygen species and increased loss of viability (apoptosis). This preliminary result suggests that therapeutic agents which increase hepatocyte glutathione levels (s-adenosylmethionine, N-acetylcystiene) or increase the overall level of protection from reactive oxygen species (vitamin E, vitamin C) might be beneficial in slowing the progression of hepatopathies associated with enhanced apoptosis.

648: This study looked at the effect of fasting in a rat model of fatty liver. Rats were fed a choline deficient diet for 10 days to induce fatty liver. It is already known that fatty livers transplant poorly and that this may be due to an imbalance of oxidants/antioxidants in these livers. Rats were divided into 3 groups; 1. Control fasted for 18 hrs, 2. fatty liver fasted for 18 hours and 3. fatty liver fasted for 18 hours with glucose infusion. In the FL rats there were increases in serum ALT and in parameters of oxidative stress and decreases in glutathione levels and ATP levels as well as EM evidence of mitochondrial damage. Even the control animals that were fasted had increased evidence of oxidant stress and decreased glutathione levels compared to normal rats. Infusion of glucose to the rats with FL during fasting ameliorated the changes seen.

666. This study looked at the effect of ursodeoxycholate on bilirubin induced damage to astrocytes. The underlying mechanism responsible for damage to the astrocyte from bilirubin is unknown. They cultured astrocytes and exposed them to unconjugated bilirubin (concentrations from 5 to 85 uM!!!). They saw concentration dependent cell toxicity with UCB and this appeared to be due to apoptosis as assessed by morphologic means. Pretreatment with UDCA protected the astrocyes against damage from UCB.

894. This group looked at the effect of ursodeoxycholate on nonalcoholic steatohepatitis. Patients were maintained on a low fat diet +/- UDCA (10 mg/jg/day). Liver enzymes normalized by three months in 10/16 on LFD + URSO and 2/15 on only LFD. At the end of 6 months 14/16 had normal LE in the URSO group and only 1/15 in the LFD. No histology was reported.

895. This was another study which showed decreased leptin levels in patients with chronic liver disease. These patients had hepatitis due to chronic alcohol abuse. Leptin is a hormone produced in adipocytes which controls appetite. The theory behind this study and others which had demonstrated leptin deficiency in patients with liver disease is that the leptin deficiency might contribute to chronic anorexia which accompanies many hepatopathies. It makes on wonder what the role of leptin might be in idiopathic hepatic lipidosis in cats.

1073. This study in hepatocyte cultures showed an additive effect of s-adenosylmethionine (SAM) and URSO on cholestsis induced by the toxic bile salt, lithocholate. SAM seemed to act as a sulfate precursor enhancing elimination of LC as its sulfate conjugate.

1127. This study looked at cultures of bile obtained from patients with primary sclerosing cholangitis (PSC), cholilithiasis (CL), bile duct cancer (BDC) and some patients with other forms of cholestasis. Positive cultures were as follows: PSC 9/22 with a-hemolytic Staph sps being the most common; CL 64% positive with 75% being enteric pathogens and the rest gram positives, BDC 56% positive, other forms of cholestsis only 25% positive. They obtained most of the cultures during endoscopic retrograde cholecystoduodenostomy.

1169. This study looked at the characteristics and outcome in patients with acute portal thrombosis. They excluded patients with cancer or portal hypertension. The causes were septic emboli (Bacteroides sp) or the presence of a prothrombotic state (oral contraceptive use, protein C deficiency, antiphospholipied syndrome, ATIII deficiency, protein S deficiency or a myeloproliferative disorder). Complete recanalization of the portal vein was obtained in 17/27 patients and partial in 8/27. All patients underwent anti-coagulation. No patients had further thrombotic events.

1162. This study looked at the frequency of anti-phospholipid antibodies in patients with liver disease and portal vein thrombosis. They found that plasminogen, protein C, protein S and ATIII levels were decreased in liver disease and seem to correlate with clinical stage of disease. None of these factors, however, were associated with the development of PVT. High levels of antiphospholipid antibodies were related to the development of PVT.

1324. A study out of England looked at 1000 patients with acute liver failure. About 40% had evidence of bacterial infection and 18% fungal infection.

1490. This study sought to answer the question what does alkaline phosphatase do. We know it hydrolyzes ATP and others have shown that it may actually neutralize endotoxin. This group showed data that it decreases the activity of the Cl-/HCO- exchanger on the cholangiocyte membrane and by doing so inhibits secretion into the bile ducts.

1348. This group used rat hepatocytes in culture to show that restoration of glutathione levels with N-acetylcystiene decreases the amount of apoptosis after exposure to ethanol.

1349. This group looked at a rat model of ethanol intoxication and showed that SAM levels are decreased and that this is associated with decreased DNA methylation. But the enzymes catalyzing the conversion of methionine SAM, MAT 1 and MAT 2 were actually upregulated following ethanol exposure.

1392 This study evaluated the use of losartan, an angiotensin II receptor antagonist, to treat portal hypertension. They had 30 patients with biopsy proven cirrhosis by most of them were Child Pugh score of A (15) with only 2 patients with a grade C. All had increased hepatic venous pressure gradient. They received an oral dose of 25 mg daily for seven days. They observed a quite impressive decrease in the HVPG in all of the patients without a significant drop in systemic blood pressure. Renal function as assessed by BUN and creatinine was normal. They did not examine urinary sodium excretion or creatinine clearance. Only one patient had an adverse reaction and the was attributed to a first dose effect. This patient went on to complete the study. None of the patients had ascites at the time of diagnosis, but some were on diuretics. The audience was concerned that in patients with ascites who were heavily dependent on the renin angiotensin system to maintain systemic BP would have more problems with systemic hypotension than noted in this select group.

1519 and 1520. This group showed that bile acids in vitro activate eosinophils. The results should be interpreted with caution since used high concentrations of bile acids that likely would not be obtainable clinically. They then looked at the effect of URSO on eosinophil infiltration and circulating EOS counts in patients with primary biliary cirrhosis and noted a decrease in both after two years of treatment.

1536. This abstract looked at the effect of silymarin (the active ingredient in milk thistle), 50 mg/kg orally for 6 weeks, on the development of fibrosis in bile duct ligated rats. They saw a decrease in mRNA for collagen type 1 and for the tissue inhibitor of metalloproteinases TIMP-1 in rats receiving silymarin. TIMP-1 inhibits MMP which is the major collagen 1 degrading proteinase.

1574. This abstract looked at plasma zinc levels in patients with liver disease. They found low plasma levels of zinc which correlated with the severity of the liver disease. They found no evidence that this deficiency was linked to the development of subclinical hepatic encephalopathy.

Hopefully by now everyone has read the recent review article published in the New England Journal of Medicine concerning the molecular pathogenesis of cholestasis (Trauner M. et al NEJM 1998; 339: 1217). This article summarizes the impressive advancements that have been made in the last 10 years to identify the transporters involved in bile secretion. The cloning and characterization of these transporters has enabled scientists to unravel the molecular basis of several familial cholestatic disorders. Benign recurrent intrahepatic cholestasis and the three types of progressive familial intrahepatic cholestasis (PFIC) are due to defects in the transporters for bile acids or phospholipids. One abstract at the meeting presented the data (which has already been published in the PNAS) showing that type 3 PFIC is due to a mutation in mdr 3. Mdr 3 is a gene which encodes the phospholipid transporter on the hepatocyte canalicular membrane. The presence of phospholipids in the bile are very important to protect the biliary epithelial cells from the detergent actions of bile salts which are normally present in mM concentrations. When mdr 3 is absence there are no phospholipids in the bile. The result is that there is nothing to "buffer" the high concentrations of bile acids in the bile and the result is biliary cell damage and cholestsis.

The other important information that has been generated in the study of these transporters is the role they play in the pathogenesis of all cholestatic disorders. The expression of these transporters is regulated after hepatocyte injury. The basolateral bile salt transporter is down-regulated in patients with biliary disease and following exposure to endotoxin. This may be an adaptive advantage to prevent the build up of potentially toxic bile salts within hepatocytes. Conversely, the expression of the bilirubin transporter on the basolateral membrane is upregulated in some patients with chronic liver disease. The canalicular transporters for bile acids and organic anions are downregulated in experimental models of cholestasis. The promoter and regulatory elements may be able to administer therapeutic agents to modulate the expression of these transporters. Just think of it as a "pill" to make the icterus go away.

Society Grant Applications - The 1999 grant applications have been collated by the Society's Immediate Past President, Dr. David Williams. Applications are now under review; and the grant awardee will be announced at the Society business luncheon on Saturday May 12 (12:30-1:45 pm).

Society Elections - Congratulations to the new Officers of the Society. Dr. Kenny Simpson has been elected President-Elect of the Society, Dr. Susan Bunch has been elected At-Large Director, and Dr. Deborah Davenport has been re-elected as Society Secretary-Treasurer. Congratulations also to our new President, Dr. Allen Roussel. I will be retired from the Presidency at the Society's business meeting in Chicago, and Allen will step into this responsibility. I take this opportunity to thank Allen for his help as President-Elect, and I wish him the very best in his new role.

Society System Alias - As many of you know, a system alias ( cgs-membership@vet.upenn.edu) has been created for the Society. The system alias has been used to call attention to interesting cases, grant announcements, meetings, and ongoing and new research projects. Please let me know if you foresee other uses. I have been threatening to organize a Society-led effort to standardize endoscopy protocols for companion animal studies. A number of you have expressed interest in such an endeavor. Please sustain your interest - I'm hoping to begin this effort after leaving the Presidency and becoming Immediate Past President (June 1999-2001).

Society Newsletter - Great news. Dr. Noah Cohen of Texas A & M University has graciously volunteered to become the new Society Newsletter Editor. Noah will assume this responsibility on June 12. Noah's appointment should create additional synergies since our incoming President is also located at the Texas A & M University. Thanks, Noah!

Planning for the CGS Symposium at the 2000 ACVIM Forum - What topics would you like to be considered for the CGS symposium at the 2000 ACVIM Forum? Please forward your ideas to Dr. Allen Roussel (ARoussel@cvm.tamu.edu) before the CGS business meeting. Ideas will be discussed at the business meeting. There were a number of interesting ideas that were discussed at the 1998 business meeting. Perhaps some of those can be resurrected.

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