We used a new radiopharmaceutical agent, [131I]meta-iodobenzylguanidine ([131I]MIBG), to produce scintigraphic images of pheochromocytomas in eight patients. One day or more after injection, the only normal organ that displayed distinct concentrations of radioactivity was the urinary bladder. The [131I]MIBG was probably concentrated in adrenergic vesicles; in tissues where vesicles are numerous, such as pheochromocytomas, the radionuclide was retained for days. The spectrum of pheochromocytomas shown the scintigrams was broad: intra-adrenal and extraadrenal in location, benign and malignant in character, 0.2 to 65 g in weight, and with different hormone patterns in secretion. Tumors in four patients were not detected by computed tomography. In one patient, reoperation was undertaken only because the scintigram located the extra-adrenal tumors and thereby directed the surgeon's exploration. The method offers hope of safe and reliable localization of pheochromocytomas in their many guises.

Acute, potentially life-threateningsystemic reactions to contrast media are less frequent with lower osmolality, nonionic contrast agents, but they are not totally eliminated. Severe reactions remain a reality in all radiology departments. Typical reactions to contrast media include nausea and/or vomiting, scattered to extensive urticarla, bronchospastic reaction, hypotenslon (isolated) with compensating tachycardia, anaphylactoid reaction, vagal reaction, cardiovascular collapse, convulsion, and seizure. For each type of reaction, rapid recognition and initiation of specific corrective therapy enhance response and minimize side effects of drugs. Specific drugs for treating each reaction type are reviewed, Including recommended dose, contraindlcations, and alternative choices. An approach to the high-risk patient and prevention of acute systemic reactions is discussed and pretreatment protocols are outlined.

BACKGROUND.Honest broker services are essential for tissue‐ and data‐based research. The honest broker provides a firewall between clinical and research activities. Clinical information is stripped of Health Insurance Portability and Accountability Act‐denoted personal health identifiers. Research material may have linkage codes, precluding the identification of patients to researchers. The honest broker provides data derived from clinical and research sources. These data are for research use only, and there are rules in place that prohibit reidentification. Very rarely, the institutional review board (IRB) may allow recontact and develop a recontact plan with the honest broker. Certain databases are structured to serve a clinical and research function and incorporate ‘real‐time’ updating of information. This complex process needs resolution of a variety of issues regarding the precise role of the HB and their interaction with data. There also is an obvious need for software solutions to make the task of deidentification easier.METHODS.The University of Pittsburgh has implemented a novel, IRB‐approved mechanism to address honest broker functions to meet the specimen and data needs of researchers. The Tissue Bank stores biologic specimens. The Cancer Registry culls data and annotating information as part of state‐ and federal‐mandated functions and collects data on the clinical progression, treatment, and outcomes of cancer patients. The Cancer Registry also has additional IRB approval to collect data elements only for research purposes. The Clinical Outcomes Group is involved in patient safety and health services research. Radiation Oncology and Medical Oncology provide critical treatment related information. Pathology and Oncology Informatics have designed software tools for querying availability of specimens, extracting data, and deidentifying specimens and annotating data for clinical and translational research. These entities partnered and submitted a joint IRB proposal to create an institutional honest broker facility. The employees of this conglomerate have honest broker agreements with the University of Pittsburgh and the Medical Center. This provides a large group of honest brokers, ensuring availability for projects without any conflict of interest.RESULTS.The honest broker system has been an IRB‐approved institutional entity at the University of Pittsburgh since 2003. The honest broker system currently includes 33 certified honest brokers encompassing the multiple partners of this system. The honest broker system has handled >1600 requests over the past 4 years with a 25% increase in volume each year.CONCLUSIONS.The current results indicate that the collaborative honest broker model described herein is robust and provides a highly functional solution to the specimen and data needs for critical clinical and translational research activities. Cancer 2008. © 2008 American Cancer Society.

SUMMARY To assess the ability of ibuprofen to influence the extent of platelet aggregation and leukocyte infiltration during acute myocardial infarction, autologous indium-111 ("IIn)-labeled platelets or leukocytes were injected before 60 minutes of left circumflex coronary artery (LCx) occlusion, followed by 24 hours of reperfusion in the canine heart. Myocardial infarct size, as a percent of the area at risk, was reduced in the ibuprofen-treated group (12.5 mg/kg i.v. every 4 hours beginning 30 minutes before LCx occlusion) by 40%, from 48 4% in control animals to 29 4% in ibuprofen-treated dogs (p = 0.005).Quantification of the platelet-associated "l'In radioactivity in irreversibly injured myocardium indicated that ibuprofen did not alter the accumulation of platelets in infarcted myocardium. In contrast, leukocyte accumulation in infarcted tissue was reduced significantly. In tissue samples with 0.414.60 gram infarct, the in'farcted/normal ratio of leukocyte radioactivity was 12 ± 2 in control dogs and 4 + 1 in ibuprofentreated dogs, which represents a 67% reduction in leukocyte accumulation in ibuprofen-treated compared with control dogs. Similar reductions were found in other gram-infarct-weight categories. Although both platelets and leukocytes accumulate in infarcted canine myocardium, ibuprofen may exert its beneficial effect on ischemic myocardium by suppressing the inflammatory response associated with myocardial ischemia and infarction.THE GOAL of much cardiovascular research has been to develop pharmacologic means of managing patients before or soon after an acute ischemic insult to minimize the extent of irreversible myocardial injury and subsequent loss of ventricular function. Several agents are effective in reducing the extent of myocardial infarction resulting from experimentally induced acute myocardial ischemia in a variety of animal models.1 One such agent, ibuprofen, is a nonsteroidal antiinflammatory compound that has been reported to exert cardioprotective effects by significantly reducing the extent of irreversible myocardial injury to experimental ischemia in the dog,2'3 the cat,4 and the rat.5 Ibuprofen renders its cardioprotective effects administered orally,3 intravenously2 or intramuscularly.5Several independent investigators have demonstrated protective effects in a variety of experimental models of myocardial ischemia and infarction, but little is known about ibuprofen's mechanism of action. Apparently, the beneficial effects of ibuprofen do not derive from alteration of the balance of myocardial oxygen supply and demand in a favorable manner. Intravenous ibuprofen reportedly has negligible hemodynamic effects2' 6 and almost no effect on the calculated ratepressure product, an accepted approximation of myocardial oxygen consumption,7 during myocardial ischemia in the dog.6 Moreover, in the nonischemic, isolated, blood-perfused cat heart, an animal model that permits careful control of hemodynamic variables, ibuprofen did not alter myocardial oxygen consumption as measured by art...

These results indicate that In-111 labeling of hepatocytes is useful for the short-term noninvasive analysis of the biodistribution of transplanted hepatocytes.