RESUMO
Here we describe a template of DIEP flap inset that prioritises projection, lateral flow and natural ptosis; key elements of an aesthetically successful delayed breast reconstruction. By not excising the full length of the mastectomy scar, and preserving the scar laterally, we increase the 3-dimensional aesthetic of the breast, moving the final reconstructed breast aesthetic further away from an unintentional 2-dimensional resurfacing. Through controlling the initial take-off around the whole circumference of the breast footprint, a favourable and durable breast conus is consistently achieved. This technique employs designated segments of comparatively more rigid irradiated mastectomy skin flaps, to positively influence reconstructed breast aesthetics at the time of flap inset. Conceptually, this reminds the authors of how the green sepals of a rose shape the bud of petals.
Assuntos
Estética , Mamoplastia , Mastectomia , Humanos , Mamoplastia/métodos , Feminino , Mastectomia/métodos , Retalho Perfurante/irrigação sanguínea , Neoplasias da Mama/cirurgia , Artérias Epigástricas/transplante , Retalhos Cirúrgicos/irrigação sanguínea , Cicatriz/prevenção & controle , Cicatriz/etiologia , Pessoa de Meia-IdadeRESUMO
We describe a visual algorithm to help prevent severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) contagion as well as manage COVID-19 disease according to categories of clinical severity. The algorithm is timely, with multiple countries worldwide declaring repeat surges in SARS-CoV-2 infections following the easing of lockdown measures. Its flowchart assimilates key effective interventions in a visual manner that will assist healthcare workers to manage COVID-19 disease algorithmically, and policymakers to suppress further SARS-CoV-2 waves. Importantly, we include the innovative use of topical p-menthane-3,8-diol spray by the British Army for COVID-19 Support Force personnel, which in light of its coronavirucidal properties, deserves wider dissemination. This algorithm has the potential to be updated as numerous studies are concluded globally.
RESUMO
Recipient vessels for microsurgical breast reconstructions include the internal mammary and thoracodorsal systems. This review will focus on the advantages of the thoracodorsal artery and vein.
Assuntos
Mama/irrigação sanguínea , Retalhos de Tecido Biológico/irrigação sanguínea , Mamoplastia/métodos , Microcirurgia/métodos , Anastomose Cirúrgica , Artérias/cirurgia , Mama/cirurgia , Feminino , Humanos , Artéria Torácica Interna/cirurgia , Veias/cirurgiaRESUMO
BACKGROUND: Interrupting recruitment of allergen-specific T(H)2 cells to the airway is an attractive potential therapeutic strategy for allergic disease. CC chemokine receptor 4 (CCR4) is preferentially expressed on T(H)2 cells, and CCR4-expressing cells have been described at sites of allergic inflammation. However, whether selective recruitment of allergen-specific T(H)2 cells to the airways occurs through CCR4 or other chemokine receptors remains controversial. OBJECTIVE: We investigated the expression of the T(H)2-associated chemokine receptors (CCR3, CCR4, and CCR8) by primary antigen-specific human airway T(H)2 cells. METHODS: Children undergoing elective adenoidectomy were recruited, and their atopic status was determined. Adenoid cells were cultured with allergen or recall antigen. Flow cytometric analyses permitted identification of T(H) cells proliferating in response to antigen and characterization of chemokine receptor and cytokine expression. RESULTS: An increased proportion of airway CD4(+) T cells proliferated to allergen in atopic children (n = 6, of which 4 were given diagnoses of asthma or rhinitis) compared with nonatopic children (P =.0004). These cells were 44.7% (32.6% to 50.0%) IL-4(+) and only 2.5% (0.6% to 3.3%) IFN-(gamma) and showed a greater than 5-fold upregulation of CCR4 expression to 54.0% (40.7% to 67.8%) after culture, whereas CCR3 was expressed on 9.7% (7.4% to 18.9%) of allergen-reactive cells and CCR8 on less than 1%. Interestingly, increased expansion of recall antigen-specific cells was also seen in atopic children, and these cells were also predominantly of a T(H)2 CCR4(+) phenotype. CONCLUSION: We conclude that airway allergen-specific T(H)2 cells are CCR4(+), but in the atopic child CCR4 does not distinguish between recall antigen and allergen specificity.
Assuntos
Tonsila Faríngea/imunologia , Alérgenos/imunologia , Antígenos/imunologia , Receptores de Quimiocinas/metabolismo , Células Th2/imunologia , Tonsila Faríngea/citologia , Antígenos de Dermatophagoides/imunologia , Proteínas de Artrópodes , Complexo CD3/metabolismo , Linfócitos T CD4-Positivos/imunologia , Candida albicans/imunologia , Criança , Pré-Escolar , Cisteína Endopeptidases , Feminino , Humanos , Hipersensibilidade Imediata/imunologia , Ativação Linfocitária , Masculino , Phleum/imunologia , Receptores CCR4 , Células Th2/metabolismoRESUMO
Eotaxin-3 (CCL26) is a CC chemokine that signals exclusively via the CCR3 receptor and has eosinophil-selective chemoattractant activity. Comparison of Eotaxin-1 (CCL11) and Eotaxin-2 (CCL24), demonstrates differences in their expression profiles, cell specificity and effector kinetics, implying distinct biological actions. But little data in this regard have been reported for Eotaxin-3. We aimed to analyse the effect of Th2 cytokines and glucocorticoids on Eotaxin-3 mRNA expression in human lung epithelial cells and dermal fibroblasts; cells implicated in the pathogenesis of allergic asthma and allergic dermatitis respectively. Eotaxin-3 mRNA levels in primary dermal fibroblasts and NCI-H727 lung epithelial cells were determined by Northern hybridization. In contrast to Eotaxin-1, Eotaxin-3 mRNA expression was not detected in unstimulated cells. The Th2 cytokines IL-4 and IL-13 induced Eotaxin-3 expression in a time and dose dependent manner, with IL-4 demonstrating a 100-fold greater potency. Unlike Eotaxin-1, Eotaxin-3 mRNA expression was not induced by either tumour necrosis factor (TNF)-alpha or interleukin (IL)-1 beta alone. Both IL-4 and IL-13 acted synergistically with TNF-alpha in superinducing Eotaxin-3 mRNA expression. Dexamethasone pre-treatment diminished induction of Eotaxin-3 mRNA expression. We conclude that modulation of Eotaxin-3 mRNA expression by Th(2) cytokines is different from that of Eotaxin-1 and Eotaxin-2, further supporting a distinct biological role for Eotaxin-3.