Giant malignant triton tumor of the scalp

Malignant triton tumor is a malignant schwannoma with rhabdomyoblastic differentiation. This tumor is very rare. Case reports and small series have been reported in medical literature. Malignant triton tumor occurs predominantly in the trunk, head, neck, and lower extremities. There is an important relationship with Von Recklinghausen disease. Patients with this tumor have a very poor prognosis, with a rapid and fatal course. We present a clinical case with a giant malignant triton tumor of the scalp.Level of Evidence: Level V, diagnostic study.     

The Medical Management of Pediatric Arrhythmias

OPINION STATEMENT: Arrhythmias are an important cause of morbidity and mortality in children. Despite recent technological advances in treatment, pharmacologic therapy remains the most common treatment modality for pediatric arrhythmias. The choice of antiarrhythmic agent, the duration of therapy, and the dosing schedule depend on multiple factors including the recurrence risk and the arrhythmia burden (the latter being determined by the hemodynamic effect of the arrhythmia), and the frequency and duration of episodes. As with all pediatric medications, consideration must be given to the drug formulation, palatability, adverse effects and adherence issues. There are very few randomized trials available to guide the choice of therapy for pediatric arrhythmias, and thus treatment options often reflect physician or institutional preferences. Although various classification schemes exist, we classify antiarrhythmic agents based on their primary site of action: atrial muscle/accessory pathway (class IA, IC, and III agents); the atrioventricular node (beta-blockers, calcium channel blockers, digoxin, and class III agents); or ventricular muscle (class I and III agents). This type of categorization assists in the approach to treatment required for each type of arrhythmia encountered.     

First characterization of fluoroquinolone resistance in Streptococcus suis

We have identified and sequenced the genes encoding the quinolone-resistance determining region (QRDR) of ParC and GyrA in fluoroquinolone-susceptible and -resistant Streptococcus suis clinical isolates. Resistance is the consequence of single point mutations in the QRDRs of ParC and GyrA and is not due to clonal spread of resistant strains or horizontal gene transfer with other bacteria.     

Dehydro-β-proline Containing α4β1 Integrin Antagonists: Stereochemical Recognition in Ligand–Receptor Interplay

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Early lesions of follicular lymphoma: a genetic perspective

The pathogenesis of follicular lymphoma is a multi-hit process progressing over many years through the accumulation of numerous genetic alterations. Besides the hallmark t(14;18), it is still unclear which other oncogenic hits contribute to the early steps of transformation and in which precursor stages these occur. To address this issue, we performed high-resolution comparative genomic hybridization microarrays on laser-capture micro-dissected cases of follicular lymphoma in situ (n=4), partial involvement by follicular lymphoma (n=4), and duodenal follicular lymphoma (n=4), assumed to represent, potentially, the earliest stages in the evolution of follicular lymphoma. Cases of reactive follicular hyperplasia (n=2), uninvolved areas from follicular lymphoma in situ lymph nodes, follicular lymphoma grade 1–2 (n=5) and follicular lymphoma grade 3A (n=5) were used as controls. Surprisingly, alterations involving several relevant (onco)genes were found in all entities, but at significantly lower proportions than in overt follicular lymphoma. While the number of alterations clearly assigns all these entities as precursors, the pattern of partial involvement by follicular lymphoma alterations was quantitatively and qualitatively closer to that of follicular lymphoma, indicating significant selective pressure in line with its faster rate of progression. Among the most notable alterations, we observed and validated deletions of 1p36 and gains of the 7p and 12q chromosomes and related oncogenes, which include some of the most recurrent oncogenic alterations in overt follicular lymphoma (TNFRSF14, EZH2, MLL2). By further delineating distinctive and hierarchical molecular and genetic features of early follicular lymphoma entities, our analysis underlines the importance of applying appropriate criteria for the differential diagnosis. It also provides a first set of candidates likely to be involved in the cascade of hits that pave the path of the various progression phases to follicular lymphoma development.