Feminization of Transgender Women With Thyroid Chondroplasty and Laryngoplasty.

In recent years, gender affirmation surgery has broadened significantly from its previous focus on genital conformation only to include other areas of the body as well. As society reconsiders its interpretations of masculinity, femininity, and gender definitions, transgender individuals have realized that they will only be able to truly transition if they are recognized by the public in their chosen societal role. The authors review the literature and describe their own techniques for feminizing thyroid chondroplasty and laryngoplasty.

Filling in the Details: A Review of Lipofilling of Radiated Tissues in the Head and Neck.

Adipose tissue is considered by many to be an ideal filler. Fat is the model filler in that it is biocompatible, autologous tissue which typically incorporates into the host tissue with minimal complications. Along with the increasing use of fat as a soft tissue filler has come a growing interest in the development of standardized technical protocols and indications for lipofiller use. In this review, we will examine the current literature regarding lipofilling techniques, explore the potential benefits of fat grafting in radiated tissue, and discuss recent scientific advancements to optimize fat graft survival and outcomes.

Mycobacterium Chelonae Infection of the Buttocks Secondary to Lipofilling: A Case Report and Review of the Literature.

Mycobacterium chelonae is a nontuberculous mycobacterium, classified as a Runyon type IV mycobacterium. In relation to humans, it is most commonly associated with tissue trauma or pulmonary infections. The majority of medical reports describe finding M. chelonae in the surgical setting, attributing infection to inadequate sterilization of surgical equipment. Symptoms are often nonspecific and include pain, erythema, and draining subcutaneous nodules and skin lesions. Therefore, the diagnosis of M. chelonae is often difficult to establish without prior suspicion of the disease, but can be confirmed with culture. We will describe the case of a 40-year-old female who contracted M. chelonae infection of the buttocks after abdominal liposuction and gluteal fat injection. We will describe her symptomatology, diagnosis, and successful treatment with surgical excision and antibiotics. Level of Evidence V This journal requires that authors assign a level of evidence to each article. For a full description of these Evidence-Based Medicine ratings, please refer to the Table of Contents or the online Instructions to Authors www.springer.com/00266 .

Specific HDAC6 inhibition by ACY-738 reduces SLE pathogenesis in NZB/W mice.

We sought to determine if a selective HDAC6 inhibitor (ACY-738) decreases disease in NZB/W mice. From 22 to 38weeks-of-age, mice were injected intraperitoneally with 5 or 20mg/kg of ACY-738, or vehicle control. Body weight and proteinuria were measured every 2weeks, while sera anti-dsDNA, Ig isotypes, and cytokine levels were measured every 4weeks. Kidney disease was determined by evaluation of sera, urine, immune complex deposition, and renal pathology. Flow cytometric analysis assessed thymic, splenic, bone marrow, and peripheral lymphocyte differentiation patterns. Our results showed HDAC6 inhibition decreased SLE disease by inhibiting immune complex-mediated glomerulonephritis, sera anti-dsDNA levels, and inflammatory cytokine production and increasing splenic Treg cells. Inhibition of HDAC6 increased the percentage of cells in the early-stage developmental fractions of both pro- and pre-B cells. These results suggest that specific HDAC6 inhibition may be able to decrease SLE disease by altering aberrant T and B cell differentiation.

Pediatric scalds: do cooking-related burns have a higher injury burden?

BACKGROUND: Pediatric scald burns result in frequent emergency room visits and hospitalizations. We investigated whether cooking-related burns produce greater morbidity requiring more extensive care than noncooking burns. METHODS: We performed a 6-y review at our free-standing children's hospital. Children aged <18 y admitted for accidental scald burns were included. Demographics, injury pattern, treatment, and outcome (contractures and/or limited mobility and nonhealing and/or infected wounds) data were analyzed comparing cooking versus noncooking burns. The Mann-Whitney U test, a chi-square test, and the negative binomial were used to compare continuous, categorical, and count data between groups. Bivariate analysis was performed to identify risk factors among patients with adverse outcomes. RESULTS: We identified 308 patients; 262 (85%) cooking and 46 (15%) noncooking burns. Most patients were African-American males, with public insurance, and a median age of 2 y. Cooking burns preferentially occurred over the head, neck, and upper body; noncooking burns were distributed over the lower body (P < 0.02). Median total body surface area was equal for both groups (P > 0.11). In subgroup analysis, semisolid and grease burns resulted in increased rates of wound contractures and/or limited mobility when compared with noncooking burns (P = 0.05 and P = 0.008, respectively). Patients with complications were more likely to have third degree burns and required more consults, longer hospitalization, and more surgical debridements and clinic visits. CONCLUSIONS: Most accidental scald burns occurred in young children during food preparation. Greater long-term morbidity was found in patients with semisolid and grease burns. This subset of children has a higher injury burden and requires extensive care in the acute and long-term setting.

Class I and II histone deacetylase inhibition by ITF2357 reduces SLE pathogenesis in vivo.

We sought to determine if a specific class I and II HDAC inhibitor (ITF2357) was able to decrease disease in lupus-prone NZB/W mice through regulation of T cell profiles. From 22 to 38 weeks-of-age, NZB/W and non-lupus NZW mice were treated with ITF2357 (5 mg/kg or 10 mg/kg), or vehicle control. Body weight and proteinuria were measured every 2 weeks, while sera anti-dsDNA and cytokine levels were measured every 4 weeks. Kidney disease was determined by sera IgG levels, immune complex deposition, and renal pathology. T lymphocyte profiles were assessed using flow cytometric analyses. Our results showed that NZB/W mice treated with the 10 mg/kgof ITF2357 had decreased renal disease and inflammatory cytokines in the sera. Treatment with ITF2357 decreased the Th17 phenotype while increasing the percentage of Tregs as well as Foxp3 acetylation. These results suggest that specific HDAC inhibition may decrease disease by altering T cell differentiation and acetylation.

Cellular and urinary microRNA alterations in NZB/W mice with hydroxychloroquine or prednisone treatment.

Determining alterations to disease-associated miRNAs induced by specific therapeutics may allow the use of tailored therapy in lupus. We determined miRNA alterations in female NZB/W lupus mice treated with hydroxychloroquine (HCQ) or prednisone (PRED) for 12 weeks beginning at 24 weeks-of-age. B cell, PBMC, and urinary miR-let-7a expression were decreased with HCQ or PRED treatment. HCQ or PRED treatment reduced miR-21 expression in mesangial cells, T cells, pDCs, PBMCs, and the urine. MiR-146a expression was reduced in mesangial cells with HCQ treatment and in pDCs with HCQ or PRED treatment. PRED treatment increased miR-155 expression in mesangial, B, and T cells and PBMCs yet decreased miR-155 expression in pDCs and the urine. In vitro studies confirmed that HCQ or PRED's anti-inflammatory actions are dependent on their ability to inhibit miRNA expression. Our studies indicate that lupus therapeutics may work, in part, by altering the expression of disease-associated miRNAs.

Human acellular dermis versus no acellular dermis in tissue expansion breast reconstruction.

BACKGROUND: Human acellular dermis has been adopted for routine use in tissue expander reconstruction. The purported benefits include higher intraoperative fill volume, facilitation of lower pole expansion, and enhanced definition of the lower pole of the breast. Recently, concerns have arisen about an increase in postoperative complications with its use. METHODS: A retrospective review was conducted of patients who had immediate postmastectomy breast reconstruction with a tissue expander from July of 2001 to July of 2011. All tissue expander reconstructions before 2005 were performed submuscularly only and all subsequent to 2005 with the use of AlloDerm (LifeCell, Branchburg, N.J.) acellular dermis. Patient demographics were collected, and complications were recorded. RESULTS: The study cohort included 346 patients and 511 immediate breast reconstructions; 232 patients and 346 breasts were reconstructed with and 114 patients and 165 breasts without acellular dermis. Age, body mass index, diabetes, and tobacco use were equivalent in the two groups. Seroma occurrence in the acellular dermis group was nearly twice (30.0 versus 15.1 percent) that of the no acellular dermis breasts, but the tissue expander loss was only slightly higher (11.6 versus 8.5 percent) and not statistically significant. Body mass index in patients who lost their tissue expander was 31 kg/m, statistically significantly higher than in those who did not. CONCLUSIONS: The presence of acellular dermis did not increase the incidence of tissue expander loss, despite a doubling of frequency of seroma. Prior radiation and use of acellular dermis did culminate in a prohibitively high loss rate of the tissue expander.

Heat shock protein 90 inhibition by 17-DMAG lessens disease in the MRL/lpr mouse model of systemic lupus erythematosus.

Elevated expression of heat shock protein 90 (HSP90) has been found in kidneys and serum of systemic lupus erythematosus (SLE) patients and MRL/Mp-Fas(lpr)/Fas(lpr) (MRL/lpr) autoimmune mice. We investigated if inhibition of HSP90 would reduce disease in MRL/lpr mice. In vitro, pretreatment of mesangial cells with HSP90 inhibitor Geldanamycin prior to immune-stimulation showed reduced expression of IL-6, IL-12 and NO. In vivo, we found HSP90 expression was elevated in MRL/lpr kidneys when compared to C57BL/6 mice and MRL/lpr mice treated with HSP90 inhibitor 17-DMAG. MRL/lpr mice treated with 17-DMAG showed decreased proteinuria and reduced serum anti-dsDNA antibody production. Glomerulonephritis and glomerular IgG and C3 were not significantly affected by administration of 17-DMAG in MRL/lpr. 17-DMAG increased CD8(+) T cells, reduced double-negative T cells, decreased the CD4/CD8 ratio and reduced follicular B cells. These studies suggest that HSP90 may play a role in regulating T-cell differentiation and activation and that HSP90 inhibition may reduce inflammation in lupus.