The Treatment of Eruptive Syringomas in an African American Patient with a Combination of Trichloroacetic Acid and CO2 Laser Destruction

BACKGROUND: Eruptive syringomas are uncommon benign adnexal neoplasms. They are numerous and disseminated and often have a predilection for the neck, face, chest, and axillary fossae. Because they are persistent, usually numerous, and often on exposed sites, the lesions may be disfiguring and often pose significant cosmetic concerns for patients. Many treatment modalities such as dermabrasion, electrodesiccation with curettage, and scissors excision have been tried with some success, but more recently lasers have provided good to excellent results. OBJECTIVE: To describe an approach to the treatment of eruptive syringomas in an African American patient with a combination of trichloroacetic acid (TCA) and CO2 laser resurfacing, providing acceptable cosmetic results without significant side effects. METHODS: We describe an African American patient with eruptive syringomas of the face treated with a combination of TCA and CO2 laser resurfacing with good results. RESULTS: While the syringomas were not completely ablated, the combination of TCA and CO2 laser resurfacing provided acceptable cosmetic results without significant side effects. CONCLUSION: The TCA pretreatment probably removed some of the bulk of the surface of the lesions, thereby reducing the number of laser passes required to flatten the remainder of the lesions and thus lessening the potential for thermal damage at the treated sites and of surrounding normal skin.     

Anchor residues in protein-protein interactions

We show that the mechanism for molecular recognition requires one of the interacting proteins, usually the smaller of the two, to anchor a specific side chain in a structurally constrained binding groove of the other protein, providing a steric constraint that helps to stabilize a native-like bound intermediate. We identify the anchor residues in 39 protein-protein complexes and verify that, even in the absence of their interacting partners, the anchor side chains are found in conformations similar to those observed in the bound complex. These ready-made recognition motifs correspond to surface side chains that bury the largest solvent-accessible surface area after forming the complex (> or =100 A2). The existence of such anchors implies that binding pathways can avoid kinetically costly structural rearrangements at the core of the binding interface, allowing for a relatively smooth recognition process. Once anchors are docked, an induced fit process further contributes to forming the final high-affinity complex. This later stage involves flexible (solvent-exposed) side chains that latch to the encounter complex in the periphery of the binding pocket. Our results suggest that the evolutionary conservation of anchor side chains applies to the actual structure that these residues assume before the encounter complex and not just to their loci. Implications for protein docking are also discussed.     

A prospective study on the efficacy of oral estrogen in female patients with acromegaly

Pituitary - To evaluate the efficacy and safety of oral estrogen therapy in female patients of childbearing age with uncontrolled acromegaly and to verify the significance of the presence of...     

Hodgkin and Reed-Sternberg cells harbor alterations in the major tumor suppressor pathways and cell-cycle checkpoints: analyses using tissue microarrays

Tumoral cells in Hodgkin lymphoma (HL) display an increased growth fraction and diminished apoptosis, implying a profound disturbance of the cell cycle and apoptosis regulation. However, limitations of molecular techniques have prevented the analysis of the tumor suppressor pathways and cell-cycle checkpoints. Tissue microarray (TMA) is a powerful tool for analyzing a large number of molecular variables in a large series of tumors, although the feasibility of this technique has not yet been demonstrated in heterogeneous tumors. The expression of 29 genes regulating the cell cycle and apoptosis were analyzed by immunohistochemistry and in situ hybridization in 288 HL biopsies using TMA. The sensitivity of the technique was validated by comparing the results with those obtained in standard tissue sections. The results revealed multiple alterations in different pathways and checkpoints, including G1/S and G2/M transition and apoptosis. Striking findings were the overexpression of cyclin E, CDK2, CDK6, STAT3, Hdm2, Bcl2, Bcl-X(L), survivin, and NF-kappaB proteins. A multiparametric analysis identified proteins associated with increased growth fraction (Hdm2, p53, p21, Rb, cyclins A, B1, D3, and E, CDK2, CDK6, SKP2, Bcl-X(L), survivin, STAT1, and STAT3), and proteins associated with apoptosis (NF-kappaB, STAT1, and RB). The analysis also demonstrated that Epstein-Barr virus (EBV)-positive cases displayed a characteristic profile, confirming the pathogenic role of EBV in HL. Survival probability depends on multiple biologic factors, including overexpression of Bcl2, p53, Bax, Bcl-X(L), MIB1, and apoptotic index. In conclusion, Hodgkin and Reed-Sternberg cells harbor concurrent and overlapping alterations in the major tumor suppressor pathways and cell-cycle checkpoints. This appears to determine the viability of the tumoral cells and the clinical outcome.