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Ankle fracture is common in active young males. Treating ankle fractures can be straightforward or much more complicated; treatment options include nonoperative management or open anatomical reduction with rigid internal fixation. Successful treatment will allow early mobilization to avoid complications. Inadequate treatment, either nonoperative or operative management, may result in malunited ankle fractures. However, malunited ankle fractures due to the delayed presentation are very rare. An 18-year-old male presented to the clinic with a history of twisting injury to his right ankle two years ago. The patient sought medical advice once after injury, applied a back slab, and was advised for operative intervention. He refused the surgical intervention and was lost in follow-up. After two years, he presented again with ankle deformity and swelling. Assessment at initial presentation includes fibula malunion, medial malleolus malunion, and widening of the ankle mortise with talar tilt. Fogel and Morrey's performance index was used to evaluate the biomechanical result postoperatively. Delayed open anatomical reduction and rigid internal fixation of malunited ankle fractures to achieve normal ankle alignment will delay the onset of future degenerative changes and minimize the chance for early arthrodesis.

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Background: Data on the outcomes of microsurgical resection (SR) and stereotactic gamma knife radiosurgery (GKRS) in patients with trigeminal neuralgia associated with small petrous apex meningiomas are scarce. Objective: We conducted this study to evaluate the pain relief, tumor control, and procedure costs following SR and GKRS for small petroclival meningiomas (less than 3 cm in maximal diameter) using real-world data from our center in Egypt. Material and Methods: We conducted a retrospective cohort study of 47 patients with small petrous apex meningiomas presenting with intractable trigeminal nerve pain (SR: n = 22 and GKRS: n = 25). Data regarding pain relief on Barrow Neurological Institute (BNI), procedure cost, and tumor control were retrieved and analyzed using appropriate statistical tests. Results: Patients who underwent SR had lower median BNI pain intensity scores compared to those patients who underwent GKRS, and a significantly higher proportion of patients in the SR group had good BNI scores compared to those in GKRS group (P < 0.05); however, the total costs of SR were significantly less than GKRS (30,519$ vs. 92,372$, respectively). Conclusion: Both SR and GKRS provide pain relief and tumor control in patients with trigeminal neuralgia associated with petrous apex meningioma. However, in the present study, SR achieved better pain control and was more affordable than GKRS.

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Extensive evidence exists that the reaction of estrogen metabolites with DNA produces depurinating adducts that, in turn, induce mutations and cellular transformation. While it is clear that these estrogen metabolites result in a neoplastic phenotype in vitro, further evidence supporting the link between estrogen-DNA adduct formation and its role in neoplasia induction in vivo would strengthen the evidence for a genotoxic mechanism. Diethylstilbestrol (DES), an estrogen analogue known to increase the risk of breast cancer in women exposed in utero, is hypothesized to induce neoplasia through a similar genotoxic mechanism. Cultured MCF-10F human breast epithelial cells were treated with DES at varying concentrations and for various times to determine whether the addition of DES to MCF-10F cells resulted in the formation of depurinating adducts. This is the first demonstration of the formation of DES-DNA adducts in human breast cells. A dose-dependent increase in DES-DNA adducts was observed. Demonstrating that treatment of MCF-10F cells with DES, a known human carcinogen, yields depurinating adducts provides further support for the involvement of these adducts in the induction of breast neoplasia. Previous studies have demonstrated the ability of antioxidants such as resveratrol to prevent the formation of estrogen-DNA adducts, thus preventing a key carcinogenic event. In this study, when MCF-10F cells were treated with a combination of resveratrol and DES, a dose-dependent reduction in the level of DES-DNA adducts was also observed.

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Catechol estrogens, especially 4-hydroxylated metabolites of 17beta-estradiol (E(2)), are responsible for estrogen-induced carcinogenesis. 4-Hydroxyestradiol (4-OHE(2)), a major metabolite of E(2) formed preferentially by cytochrome P-450 1B1, is oxidized to E(2)-3,4-quinone, which can react with DNA to yield the depurinating adducts 4-OHE(2)-1-N3Ade and 4-OHE(2)-1-N7Gua. The apurinic sites generated by the loss of these depurinating adducts induce mutations that could lead to cancer initiation. In this study, we have evaluated the effects of N-acetylcysteine (NAcCys) on the metabolism of two cell lines, MCF-10F (a normal human breast epithelial cell line) and E6 (a normal mouse mammary epithelial cell line), treated with 4-OHE(2) or its reactive metabolite, E(2)-3,4-quinone. Extensive HPLC with electrochemical detection and UPLC-MS/MS analyses of the cell media demonstrated that the presence of NAcCys very efficiently shifted the estrogen metabolism toward protective methoxylation and conjugation pathways in multiple ways, whereas formation of depurinating DNA adducts was inhibited. Protection by NAcCys seems to be similar in both cell lines, irrespective of their origin (human or mouse) or the presence of estrogen receptor-alpha. This finding suggests that NAcCys, a common dietary supplement, could be used as a potential chemopreventive agent to block the initial step in the genotoxicity caused by catechol estrogen quinones.

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