Lymphangiogenesis was significantly associated with lymph node metastasis, high TNM, and poor outcome in breast carcinoma. LVD may serve as a predictor of lymph node metastasis and a prognostic factor in breast carcinoma. VEGF-C and VEGF-D play an important role in lymphangiogenesis making the carcinoma more aggressive and leading to a poor prognosis.

Background: The aim of this study was to systematically analyze the randomized trials comparing fibrin glue mesh fixation with suture mesh fixation in open inguinal hernia repair. Methods: Information was collected from a literature search using PubMed, Springer, Cochrane Library database and reference lists. The methodological quality of included publications was evaluated. Statistical analysis was performed using Review Manager Version 5.2.5 software. Results: Nine articles were identified for inclusion: four randomized controlled trials (RCTs) and five prospective observational clinical studies. All the trials were considered to be of fair quality. The results showed that there was a lower incidence of chronic pain (RR 0.42, 95% CI 0.22-0.79, I² 11%; p < 0.01), and hematoma/seroma (RR 0.43, 95% CI 0.21-0.87, I² 0%; p < 0.05) in the fibrin glue mesh fixation group. However, the results of meta-analysis revealed that the incidence of recurrence or urinary problems between the two procedures were similar. Conclusions: During the 6-15 months follow-up, fibrin glue mesh fixation is a feasible alternative for mesh fixation with sutures in open inguinal hernia repair. However, the poor quality of the included trials limits the evidence; rigorously designed trials are warranted to confirm this conclusion.

Resina Draconis (RD) is a type of dragon's blood resin obtained from Dracaena cochinchinensis (Lour.) S.C. Chen (Yunnan, China). It has been used as a medicine since ancient times by many cultures. The ethanolic extract of Resina Draconis (RDEE) was evaluated for its wound-healing activity using excision and incision wound models in rats. Group I, the control group, was treated with ointment base. Group II, which served as a reference standard, was treated with moist exposed burn ointment (MEBO). Group III was treated with RDEE. The parameters observed were percentage of wound contraction, epithelialization period, tensile strength, histopathological studies, microvessel density (MVD), and the expression of vascular endothelial growth factor (VEGF) and transforming growth factor-β1 (TGF-β1). The group treated with RDEE showed significantly better wound contraction and better skin-breaking strength as compared with the control group. The results of histopathological examination, MVD, and the expression levels of growth factors supported the outcome of the wound models as well. The present study provided a scientific rationale for the traditional use of RD in the management of wounds.

Colorectal cancer is the second leading cause of cancer-related deaths. Drug resistance and/or off-target toxicity against normal cells limit the effectiveness of current chemotherapies for the treatment of colorectal cancer. In the current study, we studied the potential cytotoxic effects of short-chain and cell-permeable C6 ceramide in cultured colorectal cancer HT-29 cells and focused on the underlying mechanisms. We observed that C6 ceramide-induced HT-29 cell death and growth inhibition in a dose- and time-dependent manner. However, no significant apoptosis was observed in C6 ceramide-treated HT-29 cells. Our data support that autophagy contributed to C6 ceramide-induced cytotoxic effects, as autophagy inhibitors, 3-methyladenine (3-MA) and hydroxychloroquine, inhibited C6 ceramide's effect; however, autophagy activators, everolimus (RAD001) and temsirolimus, mimicked C6 ceramide effects and induced HT-29 cell death. Further, we indentified that AMP-activated protein kinase (AMPK)/Ulk1 signaling was required for autophagy induction by C6 ceramide, and AMPK silencing by a specific short hairpin RNA suppressed C6 ceramide-induced autophagy and cytotoxic effects. Reversely, forced activation of AMPK by its activator AICAR or by genetic manipulation caused autophagic death in HT-29 cells, which was inhibited by 3-MA. Our results suggest that autophagy, but not apoptosis, is a major contributor for C6 ceramide-induced cytotoxic effects in HT-29 cells, and activation of AMPK/Ulk1 is required for the process.