Microcalcifications are an important diagnostic marker for breast cancer on mammograms, yet the mechanism of their formation is poorly understood. Indeed, there is presently no short-latency, high-yield, syngeneic rodent model of the process. Bone morphogenetic protein 2 (BMP-2) is a key mediator of physiologic bone formation and pathologic vasculature calcification, but its role in breast cancer microcalcification is unknown. In this study, R3230 rat breast tumors were adapted to cell culture, transduced with adenoviral BMP-2, and inoculated into a syngeneic host. Tumor growth and calcium salt deposition were quantified in living animals over time using micro-computed tomography and probed chemically using near-infrared fluorescence. Plasma BMP-2 levels were quantified over time by enzyme-linked immunosorbent assay. Within 3 weeks, 100% of the breast tumors developed microcalcifications, which were absent from all normal tissues. Importantly, when two tumors were initiated in a single host, the ipsilateral tumor expressing BMP-2 was able to induce microcalcification in the contralateral tumor that was not expressing BMP-2, suggesting that BMP-2 can act humorally. Taken together, we describe the first reproducible rodent model of breast cancer microcalcification, prove that BMP-2 expression is sufficient for initiating the process, and lay the foundation for a new generation of targeted diagnostic agents.

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In both models, thermal dosimetry required to achieve coagulation was not constant, but current and distance dependent. Hence, other formulas for thermal dose equivalence may be needed to predict conditions for thermal ablation.

For a standardized RF dose, the combination of high dose XRT and RF increased ablation size compared to RF and liposomal doxorubicin or RF alone. Increased ablation size is more closely associated with decreased temperature threshold necessary to induce coagulation, rather than the total thermal dose.

Large zones of coagulation of 5-7 cm can be created with optimized RF algorithms that help reduce number of tine extensions compared with manufacturer's recommendations. Such algorithms are likely to facilitate the utility of these devices for RF ablation of focal tumors in clinical practice.

Our study demonstrates that the thermal dosimetry of ablation is not based solely on a fixed end temperature at the margin of the coagulation zone. Thermal dosimetry is not constant, but dependent on the type and amount of energy applied and distance suggesting the need to take into account the rate of heat transfer for ablation dosimetry.

A 67 -year -old man received a dual -chamber pacemaker 26 years earlier owing to pharmacologically induced bradycardia (β -blockers used for treatment of long QT syndrome). The patient was scheduled for transvenous lead extraction (TLE) and dual-chamber implantable cardioverter--defibrillator (ICD -DR) implantation at the time of elective pacemaker replacement. A routine transthoracic echocardiogram (TTE) showed a vegetation or clot in the right atrium at lead crossing (FIGURE 1A), which was confirmed by transesophageal echocardiogram (TEE). The patient had no local or systemic clinical signs of infection and inflammatory markers were negative. TLE was delayed for a few weeks. A low -molecular -weight heparin and wide -spectrum antibiotics were administered. After the treatment, inflammatory markers remained negative and echocardiography showed unaltered images.The TLE procedure of DDD removal and ICD implantation was successful although it was long and technically difficult owing to venous occlusion and firm lead adhesions to the vessels and cardiac walls. Eight days after the procedure, the patient was admitted to the hospital because of severe dyspnea and chest pain. Telemetric control showed ineffective ventricular pacing with sensing and impedance changes characteristic of cardiac wall perforation, which was further confirmed in TTE, chest X -ray, and CT. CT additionally showed small mediastinal edema and air presence in the pericardial sac with the ICD lead penetrating to the lung (FIGURE 1B). D -dimer levels were 5-fold higher, while the levels of other inflammatory markers were normal. A TLE of the perforating ICD lead with constant TEE monitoring was performed (FIGURE 1C). A cardiac surgeon was present during the whole procedure in case of massive hemorrhage to the mediastinum or lung tissue after lead removal. Owing to large pus outflow after the opening of the pocket, a decision was made to remove the whole system. The procedure and hospitalization were uneventful. Subsequent contralateral ICD implantation was delayed (FIGURE 1D).Our case shows an unusual presentation of pacemaker -related infection and a life -threatening complication of electrotherapy. Festering of the ICD pocket might be related to the first TLE procedure, which was long and complex. However, it might also be explained by pocket contact with the lead, which previously touched vegetation or the clot -like structure. It is an example of severe infection of the stimulation system without typical symptoms of inflammation and negative inflammatory markers. The available literature reports a different picture of the infection process-with fever and elevated inflammatory markers. 1 In our case, we observed vegetation or clot in the heart, venous obstruction on infected leads, and late ventricular perforation of the ICD lead. Owing to the presence of an additional structure in the heart, we scheduled diagnostic procedures and treatment; however, they did not resolve the problem.There were no indications to diagnose lead--dependent infectiv...