Abstract:We tested trifluralin against Trypanosoma cruzi in a model of chronic Chagas disease in mice. CF1 mice (nΩ 148) were intraperitoneally infected with 10 5 trypomastigotes of T. cruzi, H510C8C3 clone. One hundred mice were partially treated with benznidazole. Mortality was 100% at day 41 in the control group (nΩ48). At day 90 of the chronic disease (74% survival) mice were divided into three groups and treated orally with trifluralin (50 mg/kg/day, nΩ26), benznidazole (50 mg/kg/day, nΩ25) and vehicle (peanut oil; control group, nΩ23) for 60 days. Electrocardiography (under pentobarbital anaesthesia, 30 mg/kg/dose), serologic immunofluorescence and microstrout were performed at the beginning and at the end of the treatment. Mice were sacrificed at day 10 after treatment; cardiac tissue was studied histopathologically and polymerase chain reaction (PCR) was performed. Spontaneous mortality was 30.43%, 3.85% and 4% in the control, trifluralin and benznidazole groups, respectively (significant survival, PΩ0.03). Microstrouts were negative in all three groups. Negative immunofluorescence titers were 0%, 16% (PΩ0.05) and 29% (PϽ0.02) in the control, trifluralin and benznidazole groups, respectively. The prevailing electrocardiographic disorder was prolongation of the PR interval in the control group, which was not significantly altered in trifluralin-and benznidazole-treated mice, suggesting that trifluralin and benznidazole improve or even stop the damage caused by the disease on the conduction system. Trifluralinand benznidazole-treated animals showed similar histologic patterns of myocarditis. PCR results were negative for benznidazole and trifluralin (100% and 70.8%, respectively). These results show the therapeutic potential of trifluralin in the treatment of chronic Chagas disease.

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Large congenital arteriovenous malformations (AVM) may result in heart failure and death. We are reporting such combination with the AVM localized to the right thoracobrachial region. Remarkable postmortem findings included right renal and adrenal hemihyperplasia; the right adrenal fetal cortex presenting cytomegaly, endocrine pancreas hyperplasia, and heterotopic adrenal cortex with cytomegaly in the left lateral ventricle choroids plexus. The combination appears to be unique. The only previously reported example of adrenal cortex in the choroid plexus presented several features strongly suggestive of Beckwith-Wiedemann syndrome. Therefore, we postulate that additional uncommon findings in Beckwith-Wiedemann syndrome may include arteriovenous malformations and heterotopic adrenal tissue in choroids plexus.

This article deals with the presence of nontumoral striated muscle fibers in the lungs of 3 neonates. These cells were diffusely distributed in one lung (case 1) or in both (case 2), or focally localized to the lung parenchyma adjacent to the liver in a case with a large right diaphragmatic hernia (case 3). The striated muscle fibers were located in the walls of small bronchi and bronchioli or in the alveolar interstitium. Other major lung malformations found simultaneously were absence of lobation, hypoplastic lungs, and hypoplastic pulmonary vessels. The origin of striated muscle fibers in the neonatal lung has been attributed to anomalous differentiation of mesoblastic cells (as in cases 1 and 2). The presence of striated muscle cells in the lower margin of a hypoplastic lung associated with a right diaphragmatic hernia (case 3) suggests that intrapulmonary inclusion of diaphragmatic muscle fibers might be a source as well. Striated muscle fibers in the lung are commonly associated with major malformations involving heart and lungs, suggesting a much wider morphogenetic error.