BackgroundThe large defects resulting from head and neck tumour surgeries present a reconstructive challenge to surgeons. Although numerous methods can be used, they all have their own limitations. In this paper, we present our experience with cervicofacial and cervicothoracic rotation flaps to help expand the awareness and application of this useful system of flaps.MethodsTwenty-one consecutive patients who underwent repair of a variety of defects of the head and neck with cervicofacial or cervicothoracic flaps in our hospital from 2006 to 2009 were retrospectively analysed. Statistics pertaining to the patients' clinical factors were gathered.ResultsCheek neoplasms are the most common indication for cervicofacial and cervicothoracic rotation flaps, followed by parotid tumours. Among the 12 patients with medical comorbidities, the most common was hypertension. Defects ranging from 1.5 cm × 1.5 cm to 7 cm × 6 cm were reconstructed by cervicofacial flap, and defects from 3 cm × 2 cm to 16 cm × 7 cm were reconstructed by cervicothoracic flap. The two flaps also exhibited versatility in these reconstructions. When combined with the pectoralis major myocutaneous flap, the cervicothoracic flap could repair through-and-through cheek defects, and in combination with a temporalis myofacial flap, the cervicofacial flap was able to cover orbital defects. Additionally, 95% patients were satisfied with their resulting contour results.ConclusionsCervicofacial and cervicothoracic flaps provide a technically simple, reliable, safe, efficient and cosmetic means to reconstruct defects of the head and neck.

Existing methods for tensor completion (TC) have limited ability for characterizing low-rank structures. To depict the complex hierarchical knowledge with implicit sparsity attributes hidden in a tensor, we propose a new multi-layer sparsity-based tensor decomposition (MLSTD) for low-rank tensor completion (LRTC). The method encodes structured sparsity of a tensor by multiple layer representation. Specifically, we use the CANDECOMP/PARAFAC (CP) model to decompose a tensor into an ensemble of sum of rank-1 tensors, and the number of rank-1 component is easily interpreted as a first layer sparsity measure. Presumably, the factor matrices are smooth since local piece-wise property exists in within-mode correlation. In subspace, the local smoothness can be regarded as the second layer sparsity. To describe the refined structures of factor/subspace sparsity, we introduce a new sparsity insight of subspace smoothness: a self-adaptive low-rank matrix factorization scheme, called the third layer sparsity. By progressive description of sparsity structure, we formulate a MLSTD model and embed it into the LRTC problem. Then an effective ADMM algorithm is designed for the MLSTD minimization problem. Various experiments in RGB images, hyperspectral images and videos substantiate the proposed LRTC method is superior to state-of-the-art methods.

Objective: Cancer stem cells (CSCs) are responsible for the drug resistance of breast cancers. Vitamin D deficiency promotes tumor resistance. The present study examined the effect of vitamin D and vitamin D receptor (VDR) expression on the tamoxifen resistance of CSCs. Methods: MCF-7 cells were treated with 1,25(OH)2D3 and their levels of VDR expression, viability, and apoptosis were detected. CD133+ MCF-7 stem cells were identified and transfected with a VDR-overexpression plasmid. The tamoxifen concentration that reduced MCF-7 cell viability by 50% (IC50) was determined. The activation of Wnt/β-catenin signaling was also investigated. Results: Vitamin D reduced the viability of MCF-7 cells and promoted their apoptosis. Vitamin D enhanced VDR expression and induced DNA damage. When CD133+ stem cells were separated from MCF-7 cells, the IC50 of tamoxifen for stem cells was significantly higher than that of parental MCF-7 cells, suggesting a higher tamoxifen resistance in MCF-7 stem cells. Levels of VDR expression and Wnt/β-catenin signaling in CD133+ cells were markedly lower and higher than those in CD133− cells, respectively. Stem cells transfected with VDR overexpression plasmids showed decreased tamoxifen IC50 values, viability, spheroid formation, and expression of Wnt and β-catenin proteins when compared with control cells. Cell apoptosis was increased by transfection with a VDR overexpression plasmid. Finally, the inhibitory effects induced by VDR overexpression could be reversed by the VDR inhibitor, calcifediol. Conclusion: Stem cells contributed to the tamoxifen resistance of MCF-7 cells. Vitamin D-induced VDR expression increased the sensitivity of MCF-7 stem cells to tamoxifen by inhibiting Wnt/β-catenin signaling.