The High-Superior-Tension Technique: Evolution of Lipoabdominoplasty

Because abdominoplasty is associated with complications such as seroma and necrosis as well as epigastric bulging and a suprapubic scar located too high, the demand for this procedure is not as high as it otherwise might be. However, although these negative effects were common many years ago, their incidence has decreased dramatically with modern abdominoplastic techniques. One approach using a combination of abdominoplasty and liposuction or lipoabdominoplasty has resolved many of the problems faced with earlier techniques, offering aesthetically pleasing results and excellent reliability. The keys to successful lipoabdominoplasty, first developed as the high-superior-tension technique, are extensive liposuction, preservation of lymphatic trunks, preaponeurotic epigastric dissection, major muscle fascia plication, two high-tension paraumbilical sutures, hypogastric tension sutures, and closure of the dead spaces. The most recent updates to this technique are described in this article

Peroxiredoxin 6 mediates Gαi protein-coupled receptor inactivation by cJun kinase

Inactivation of opioid receptors limits the therapeutic efficacy of morphine-like analgesics and mediates the long duration of kappa opioid antidepressants by an uncharacterized, arrestin-independent mechanism. Here we use an iterative, discovery-based proteomic approach to show that following opioid administration, peroxiredoxin 6 (PRDX6) is recruited to the opioid receptor complex by c-Jun N-terminal kinase (JNK) phosphorylation. PRDX6 activation generates reactive oxygen species via NADPH oxidase, reducing the palmitoylation of receptor-associated Gαi in a JNK-dependent manner. Selective inhibition of PRDX6 blocks Gαi depalmitoylation, prevents the enhanced receptor G-protein association and blocks acute analgesic tolerance to morphine and kappa opioid receptor inactivation in vivo. Opioid stimulation of JNK also inactivates dopamine D2 receptors in a PRDX6-dependent manner. We show that the loss of this lipid modification distorts the receptor G-protein association, thereby preventing agonist-induced guanine nucleotide exchange. These findings establish JNK-dependent PRDX6 recruitment and oxidation-induced Gαi depalmitoylation as an additional mechanism of Gαi-G-protein-coupled receptor inactivation.Opioid receptors are important modulators of nociceptive pain. Here the authors show that opioid receptor activation recruits peroxiredoxin 6 (PRDX6) to the receptor-Gαi complex by c-Jun N-terminal kinase, resulting in Gαi depalmitoylation and enhanced receptor-Gαi association