RESUMO
In this article, the authors describe the 1-stage surgical technique that has been used by the senior author since 1990 for all his primary grade 2 and grade 3 augmentation-mastopexies. The article provides a safe, simple, and reproducible approach to a challenging procedure, one that tends to be the most litigious in aesthetic breast surgery. The key points of this technique are simple preoperative markings; the augmentation is performed with a true submuscular placement of smooth implants; and the mastopexy is performed with an inferior pedicle technique with unlimited skin flap undermining and no limitation of nipple elevation. Seventy-eight consecutive cases of augmentation mastopexy performed since 1999 by a single surgeon (V.S.) using the same technique were reviewed. The age range was 26-62 years old; the range of implant volume was 150-375 cc; and the follow-up time period was from 1 year to 22 years. After an extensive patient case review, the authors enforce true extended submuscular augmentation (TESMA) as a reliable augmentation technique that can be used as the first procedure in any grades 2 and 3 ptosis, 1-stage augmentation-mastopexies including bariatric cases. The authors believe that the split inferior pedicle for the mastopexy in combination with the TESMA is a breakthrough approach that eliminates the second stage for any augmentation mastopexy procedure. No major complications such as nipple necrosis, implant bottoming, malpositioning, or extrusions were observed. It is a safe, simple, and reproducible procedure.
RESUMO
The CD36/FAT scavenger receptor/fatty acids transporter regulates cellular lipid accumulation important for inflammation, atherosclerosis, lipotoxicity, and initiation of cellular senescence. Here we compared the regulatory effects of the vitamin E analogs alpha-tocopherol (αT), alpha-tocopheryl phosphate (αTP), and αTP/ßCD (a nanocarrier complex between αTP and ß-cyclodextrin [ßCD]) and investigated their regulatory effects on lipid accumulation, phagocytosis, and senescence in THP-1 monocytes and macrophages. Both, αTP and αTP/ßCD inhibited CD36 surface exposition stronger than αT leading to more pronounced CD36-mediated events such as inhibition of DiI-labeled oxLDL uptake, phagocytosis of fluorescent Staphylococcus aureus bioparticles, and cell proliferation. When compared to ßCD, the complex of αTP/ßCD extracted cholesterol from cellular membranes with higher efficiency and was associated with the delivery of αTP to the cells. Interestingly, both, αTP and more so αTP/ßCD inhibited lysosomal senescence-associated beta-galactosidase (SA-ß-gal) activity and increased lysosomal pH, suggesting CD36-mediated uptake into the endo-lysosomal phagocytic compartment. Accordingly, the observed pH increase was more pronounced with αTP/ßCD in macrophages whereas no significant increase occurred with αT, alpha-tocopheryl acetate (αTA) or ßCD. In contrast to αT and αTA, the αTP molecule is di-anionic at neutral pH, but upon moving into the acidic endo-lysosomal compartment becomes protonated and thus is acting as a base. Moreover, it is expected to be retained in lysosomes since it still carries one negative charge, similar to lysosomotropic drugs. Thus, treatment with αTP or αTP/ßCD and/or inhibition of conversion of αTP to αT as it occurs in aged cells may counteract CD36-mediated overlapping inflammatory, senescent, and atherosclerotic events.
