Pathway from childhood trauma to nonsuicidal self-injury in adolescents with major depressive disorder: the chain-mediated role of psychological resilience and depressive severity.

This study aimed to explore the pathway from childhood trauma to nonsuicidal self-injury (NSSI) in adolescents with major depressive disorder (MDD) and to examine the chain-mediating role of psychological resilience and depressive symptoms in this pathway. A total of 391 adolescents with MDD were recruited in the present study. The Chinese version of the Childhood Trauma Questionnaire-Short Form (CTQ-SF), the Chinese version of the Symptoms Check List-90 (SCL-90), the Chinese version of the Conner-Davidson Resilience Scale (CD-RISC), and the Ottawa Self-Injury Inventory Chinese Revised Edition (OSIC) were used to evaluate childhood trauma, depressive symptoms, psychological resilience and NSSI, respectively. Our results showed that 60.87% of adolescents with MDD had NSSI in the past month. Childhood trauma frequency was negatively correlated with psychological resilience but positively correlated with depressive symptoms and NSSI severity in adolescents with MDD. The stepwise logistic regression analysis identified that age, childhood trauma and depressive symptoms could independently predict the occurrence of NSSI, and the three-step hierarchical regression showed that childhood trauma, psychological resilience and depressive symptoms were all significantly associated with NSSI frequency in adolescents with MDD. Furthermore, the chain-mediation analysis revealed that psychological resilience and depression serially mediated the relationship between childhood trauma and NSSI in adolescents with MDD. Interventions targeted at improving resilience and depression may mitigate the impact of childhood trauma severity on NSSI risk in adolescents with MDD.

Calcitonin gene-related peptide alleviates hypertrophic scar formation by inhibiting the inflammation.

The present study aims to explore the roles of calcitonin gene-related peptide (CGRP) in the hypertrophic scar and its underlying mechanism. The levels of CGRP were determined in human hypertrophic scar and mouse cutaneous scar using ELISA and Western blot. In in vivo studies, A cutaneous excision mouse model was established and treated with exogenous CGRP or CGRP antagonist. In in vitro studies, bone marrow-derived macrophages (BMDMs) were isolated and treated with exogenous CGRP in the presence of lipopolysaccharide (LPS). qRT-PCR and Western blot were applied to determine the mRNA and protein levels of scar formation and inflammation-related genes, respectively. Flow cytometry was operated to determine the populations of macrophages in the scar. Elevated levels of CGRP were observed in the hypertrophic scar. In the cutaneous excision mouse model, treatment of exogenous CGRP or CGRP antagonist-affected scar formation-related genes including Col1, Tgfb1, and α-SMA, inflammation-related genes including Il1b, Il6, Tnfa, and Ccl2, and CD45+F4/80+ macrophage. In LPS-induced BMDMs, treatment of exogenous CGRP also altered inflammation-related genes by regulating NF-κB and ERK signaling pathways. The ameliorated effects of CGRP on inflammation in hypertrophic scar formation are associated with its regulative effects on NF-κB and ERK signaling pathways.

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.

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.

Experience of 56 patients using a retrograde sural neurovascular flap to repair lower limb tissue defects.

This study was made to investigate the clinical effects of repairing lower limb defects with an improved retrograde sural nerve flap. From November 1996 to September 2010, a total of 56 patients with soft-tissue defects of the lower limb received improved retrograde sural neurocutaneous flap repair. There were 21 women and 35 men ranging in age from 12-73 years (average age 45.9). Eight patients had dorsal foot defects, five patients had foot bottom defects, four patients had heel defects, six patients had defects around the ankle, and 15 patients had defects below the lower third of the leg. Of these, 10 patients had exposed wounds and six cases had exposed tendons. The size of the surgical repair was between ∼6 cm × 5 cm and ∼25 cm × 9 cm. Four patients retained the donor's sural neurovascular flap and normal sural nerve function, and 10 patients retained the retrograde sural neurovascular flap with a thin layer of muscle. All grafted flaps survived in all 56 patients. Patient follow-up lasted between 3 months and 3 years. The shape and function of their lower limbs were satisfactory. Two-point discrimination detection in the donor area and nerve-control area revealed that the sensory function recovered well in the four patients with retained nerves. The partial necrosis of the distal flap in two patients healed successfully after dressing, and no other adverse reactions or complications were observed. Through clinical treatment of the 56 patients, good experience was accumulated. The operation methods made the flap blood supply more abundant, improved the survival rate, and retained the sensory function of the donor site of the lower limb flap. This reduced the damage to the donor site and made the operation safer.