Reconstruction of Large Facial Malignant Tumor Defects Using Local Angular Perforator Flap.

OBJECTIVE: To investigate the 1-stage repair for postoperative wound of large facial malignant tumors. MATERIALS AND METHODS: The angular perforator flap of the face and neck was used for 1-stage rotary advancement repair of the large skin wound following tumor resection. RESULTS: After using the angular perforator flap for 1-stage wound repair, the flap was completely preserved, and the donor incision site healed well. The suture was removed after some 7 to 9 days, and the flap color was similar to that of the surrounding skin. After 12 months follow-up, there was no obvious scar growth observed. CONCLUSION: The design of the neck and face angular perforator flap was flexible with a good blood supply, and thus can be used for 1-stage repair of the large defect wound after facial malignant tumor resection. Also, the observed prognosis was good.

Effect of BTXA on Inhibiting Hypertrophic Scar Formation in a Rabbit Ear Model.

BACKGROUND: Hypertrophic scar (HS) is a refractory skin disease caused by major physical damage or other inflammation. Some reports found that botulinum toxin type A (BTXA) could be an alternative treatment of the HS. Therefore, the authors studied the effects of BTXA on the treatment of HS and the dose response of BTXA. METHODS: Hypertrophic scars were harvested from the ears of 18 young adult New Zealand big-eared rabbits and treated with BTXA or triamcinolone acetonide (TAC) in vivo experiment. The hypertrophic index (HI) was measured by histological examination. Collagen fibrils were checked by sirius red straining, and the cell nucleuses of fibroblasts were checked by Ki67. RESULTS: The HI of hypertrophic scars with BTXA treatment was lower than that with phosphate-buffered saline treatment (P < 0.05). Compared with the TAC treatment group, the efficacy of treatment with the middle dose of BTXA (1.0, 1.5 IU) had no significant difference, as shown by sirius red staining and immunohistochemistry Ki67. CONCLUSION: These results demonstrated that BTXA effectively improved the appearance of hypertrophic scars and inhibited the formation of collagen fibrils and fibroblasts in vivo. Treatment with the middle dose of BTXA achieved similar efficacy as TAC treatment, indicating that BTXA might be useful for inhibiting hypertrophic scars and worth investigating further. NO LEVEL ASSIGNED: This journal requires that authors assign a level of evidence to each submission to which Evidence-Based Medicine rankings are applicable. This excludes Review Articles, Book Reviews, and manuscripts that concern Basic Science, Animal Studies, Cadaver Studies, and Experimental Studies. 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 .

Decreased plasma neuroactive amino acids and increased nitric oxide levels in melancholic major depressive disorder.

BACKGROUND: Amino acid neurotransmitters and nitric oxide (NO) are involved in the pathogenesis of major depressive disorder (MDD). Here we want to establish whether changes in their plasma levels may serve as biomarker for the melancholic subtype of this disorder. METHODS: Plasma levels of glutamic acid (Glu), aspartic acid (Asp), glycine (Gly), gamma-aminobutyric acid (GABA), and NO were determined in 27 medicine-naïve melancholic MDD patients and 30 matched controls. Seven of the MDD patients participated also in a follow-up study after 2 months' antidepressant treatment. The relationship between plasma and cerebral-spinal fluid (CSF) levels of these compounds was analyzed in an additional group of 10 non-depressed subjects. RESULTS: The plasma levels of Asp, Gly and GABA were significantly lower whereas the NO levels were significantly higher in melancholic MDD patients, also after 2 months of fluoxetine treatment. In the additional 10 non-depressed subjects, no significant correlation was observed between plasma and CSF levels of these compounds. CONCLUSION: These data give the first indication that decreased plasma levels of Asp, Gly and GABA and increased NO levels may serve as a clinical trait-marker for melancholic MDD. The specificity and selectivity of this putative trait-marker has to be investigated in follow-up studies.

TSG-6 Inhibits the Growth of Keloid Fibroblasts Via Mediating the TGF-ß1/Smad Signaling Pathway.

BACKGROUND: The cytokine TNF-α-stimulated gene-6 (TSG-6) had been verified to have a certain inhibitory effect on the inflammation. During wound healing, fibroblasts increasingly proliferated and deposited collagen fibers, leading to the formation of pathological scars. We sought to elucidate the mechanism by which the TGF-ß1/Smad pathway was mediated by TSG-6 in human keloid fibroblasts. MATERIALS AND METHODS: Human keloid fibroblast cells were isolated from keloid tissue by enzyme digestion and identified by immunocytochemistry. Lentiviral vectors pLVX-puro-TSG-6 and pLVX-shRNA1-TSG-6 were constructed which were then transfected into human keloid fibroblasts. The mRNA and protein levels of TSG-6 were detected respectively by RT-PCR and western blot assay. The intracellular localization of TGF-ß1-induced proteins and phosphorylated (p)-Smad2/3 in keloid fibroblasts were investigated using an immunofluorescence assay. Plasminogen activator inhibitor-1 (PAI-1) transcriptional activity was detected by RT-PCR. RESULTS: TSG-6 could effectively interfere the TGF-ß1/Smad signal transduction pathway in keloid fibroblasts rather than in normal fibroblasts. The phosphorylation levels of Smad2/3 were notably reduced by TSG-6 treatment. TSG-6 blocked the complex formation of Smad2/3/4, and their nuclear translocation. However, it upregulated Smad7 expression, presenting dose dependence. PAI-1 was also suppressed by TSG-6 treatment. CONCLUSIONS: TSG-6 inhibits proliferation by inducing apoptosis in keloid fibroblasts, which may be associated with TGF-ß1/Smad pathway.