Repair of lower abdominal incisional hernia is always a surgical challenge. TAPE technique has been described for the repair of supra-pubic midline incisional hernia with satisfactory outcome. Its indication can be extended for treatment of non-midline lower abdominal hernia. Peritoneal incision is created just below the hernia defect with pre-peritoneal dissection to expose supra-pubic preperitoneal space with Cooper's ligament exposed. Non-adhesive mesh then placed over preperitoneal space and partially intra-peritoneally, and cover the whole extra-peritoneal space prepared to ensure enough overlapping. Mesh is fixed by tackers for intra-peritoneal part, most inferior fixation points were at peritoneal incision line. Extra-peritoneal part of meshes is fixed at the safety zone and covered up by the peritoneal flap to avoid mesh migration. Fixation of the meshes at the lateral aspects were facilitated by the peritoneal flap and subsequent fibrosis and adhesion to the extra-peritoneal structures in cases of lateral lower abdominal hernia. Repair of midline and lateral lower abdominal incisional hernia with this novel modified technique with prosthetic mesh is safe and effective. A larger case series and longer follow-up is required for validation of this technique.
Fibrosis ; Follow-Up Studies ; Hernia ; Hernia, Abdominal ; Hernia, Ventral* ; Incisional Hernia ; Ligaments

Epstein-Barr virus (EBV) infection is closely associated with undifferentiated nasopharyngeal carcinoma (NPC), strongly implicating a role for EBV in NPC pathogenesis; conversely, EBV infection is rarely detected in normal nasopharyngeal epithelial tissues. In general, EBV does not show a strong tropism for infecting human epithelial cells, and EBV infection in oropharyngeal epithelial cells is believed to be lytic in nature. To establish life-long infection in humans, EBV has evolved efficient strategies to infect B cells and hijack their cellular machinery for latent infection. Lytic EBV infection in oropharyngeal epithelial cells, though an infrequent event, is believed to be a major source of infectious EBV particles for salivary transmission. The biological events associated with nasopharyngeal epithelial cells are only beginning to be understood with the advancement of EBV infection methods and the availability of nasopharyngeal epithelial cell models for EBV infection studies. EBV infection in human epithelial cells is a highly inefficient process compared to that in B cells, which express the complement receptor type 2 (CR2) to mediate EBV infection. Although receptor(s) on the epithelial cell surface for EBV infection remain(s) to be identified, EBV infection in epithelial cells could be achieved via the interaction of glycoproteins on the viral envelope with surface integrins on epithelial cells, which might trigger membrane fusion to internalize EBV in cells. Normal nasopharyngeal epithelial cells are not permissive for latent EBV infection, and EBV infection in normal nasopharyngeal epithelial cells usually results in growth arrest. However, genetic alterations in premalignant nasopharyngeal epithelial cells, including p16 deletion and cyclin D1 overexpression, could override the growth inhibitory effect of EBV infection to support stable and latent EBV infection in nasopharyngeal epithelial cells. The EBV episome in NPC is clonal in nature, suggesting that NPC develops from a single EBV-infected nasopharyngeal epithelial cell, and the establishment of persistent and latent EBV infection in premalignant nasopharyngeal epithelium may represent an early and critical event for NPC development.
Carcinoma ; Cell Transformation, Neoplastic ; Cells, Cultured ; Epithelial Cells ; Epstein-Barr Virus Infections ; Herpesvirus 4, Human ; Humans ; Nasopharyngeal Neoplasms ; Nasopharynx ; Precancerous Conditions

Mitochondria as a signaling platform play crucial roles in deciding cell fate. Many classic anticancer agents are known to trigger cell death through induction of mitochondrial damage. Mitophagy, one selective autophagy, is the key mitochondrial quality control that effectively removes damaged mitochondria. However, the precise roles of mitophagy in tumorigenesis and anticancer agent treatment remain largely unclear. Here, we examined the functional implication of mitophagy in the anticancer properties of magnolol, a natural product isolated from herbal