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A 54-year-old man with end-stage renal disease presented with chest pain. Five months before presentation the patient had a right-foot cellulitis that was treated with amoxicillin clavulanate. Two weeks later, the patient suffered an inferior wall ST-elevation myocardial infarction that required immediate percutaneous coronary intervention with paclitaxel-eluting stents (Taxus, Boston Scientific, Natick, Mass) in the proximal and mid-right coronary artery (RCA). Over the next 4 months, the patient had recurrent fevers and grew Staphylococcus aureus on repeat blood cultures. The source of infection was attributed to recurrent infected dialysis catheters. The patient had 3 catheter replacements and was treated with intravenous vancomycin and oral rifampin. On examination, the patient had a continuous murmur along the right sternal border and an elevated troponin I level of 2.45 ng/mL (normal range: 0.00 to 0.09 ng/mL).Coronary angiography revealed an occluded proximal RCA stent (asterisks in Figure 1, and Movie I, online-only Data Supplement), a large pseudoaneurysm off the stent (arrowhead in Figure 1), and a fistula into the right atrium (RA) (arrow in Figure 1). A 64-slice multidetector computed tomographic angiogram (GE Healthcare, Chalfont St. Giles, United Kingdom) confirmed both the pseudoaneurysm (arrowhead in Figures 2 and 3) and fistula into the RA (arrow in Figures 2 and 3). Transesophageal echocardiogram (Siemens, Malvern, Pa) identified serpiginous echodensities (arrowhead in Figure 4A, and Movie II, online-only Data Supplement) along the RA wall consistent with vegetation and a fistula inflow from the RCA (arrow in Figure 4B, and Movie III, online-only Data Supplement).The patient underwent a resection of the RCA stents and pseudoaneurysm, evacuation of the RA vegetation, and coronary bypass to the distal RCA with a saphenous vein graft. Microscopic specimen from the RA revealed tissue necrosis with a predominance of neutrophils consistent with an abscess ( Figure 5). The patient received intravenous nafcillin and oral rifampin for an additional 6 weeks after surgery. The patient is doing well 6 months after the operation.To date, there have been only 4 other reported cases of drug-eluting coronary stent infections. [1][2][3][4] In all cases S. aureus bacteremia was responsible for causing mycotic stent complications. Although mycotic aneurysms, pseudoaneurysms, and abscesses have been previously reported in both bare-metal and drug-eluting stent infections, this is the first reported case of an infected coronary stent that developed an intracardiac fistula. The mechanism of drug-eluting stent infection is not well understood. Potential causes for drugeluting stent infections include impairment of local immunosuppression and endothelialization caused by the paclitaxel or sirolimus released from the stent and/or bacteremia at the time of catheterization. [1][2][3][4] In fact, Ramsdale et al reported that up to 17.7% of patients who underwent complex percutaneous coronary interventions had detectable b...

Background Although MYCN (aka N-myc) amplification is reported in ∼20% of neuroblastomas, MYC (aka C-myc) amplification appears to be a rare event in this disease. As of today, only 2 MYC-amplified neuroblastomas have been briefly mentioned in the literature. Methods We studied here the clinicopathological features of 3 MYC-amplified neuroblastomas. Results All 3 patients (2 females and 1 male) had stage 4 disease. One female is currently alive and well 52 months after the diagnosis, while the other female and male patients died of disease 24 and 20 months after the diagnosis, respectively. Further analysis on 2 tumors revealed unfavorable histology with MYC protein overexpression but with neither MYCN amplification nor MYCN protein overexpression. Both of these tumors exhibited "large cell neuroblastoma" histology with enlarged, uniquely open nuclei and nucleolar hypertrophy, along with "aberrant" desmin expression. Conclusions MYC-amplified neuroblastomas are extremely rare and seem to present with distinct clinicopathological features.

This study examined whether melatonin-induced inhibition of testicular weight and body weight in vivo could be antagonized by luzindole, a competitive melatonin receptor antagonist, or methysergide, a competitive serotonin receptor antagonist. Adult male Siberian hamsters were exposed to a long photoperiod (16L:8D) and given daily injections of drugs 3 h before lights off for 7 weeks. Hamsters treated with melatonin (0.375 mg/kg) exhibited testicular regression and loss of body weight. These effects were also marked in hamsters treated concomitantly with melatonin (0.375 mg/kg) and luzindole (10 mg/kg). In other studies, chronic injections of luzindole (30 mg/kg) to juvenile hamster failed to antagonize testicular regression induced by either melatonin injections or exposure to a short day photoperiod (12L: 12D). In contrast, concommitant injections of methysergide (6.25 mg/kg) and melatonin attenuated testicular regression and loss of body weight. When administered alone, neither luzindole nor methysergide affected testicular weight or body weight, whereas chronic injections of 5-methyoxyluzindole (10 mg/kg) mimicked the inhibitory effects of melatonin. 5-Methoxyluzindole inhibits 2-[125I]-iodomelatonin binding to median eminence/pars tuberalis membranes with an affinity similar to that of melatonin. Luzindole shows lower affinity for the inhibition of 2-[125I]-iodomelatonin binding than melatonin, which may explain why luzindole is not an effective melatonin receptor antagonist when administered in vivo. Methysergide, which has a very low affinity for inhibition of 2-[125I]-iodomelatonin binding, probably inhibits the effects of melatonin by blocking serotonergic neurotransmission.