Postoperative mechanical small bowel obstruction induced by V-Loc barbed absorbable suture after laparoscopic distal gastrectomy.

When performing laparoscopic gastrectomy, suturing the intestinal anastomosis presents one of the greatest challenges. The V-Loc unidirectional barbed suture has been introduced to eliminate the need to tie knots during closure. This device offers a fast, secure, and effective alternative to conventional suture repair during laparoscopic surgery. However, there have been reported cases of surgical complications associated with the use of barbed suture devices. We describe here a case of small bowel obstruction resulting from improper use of barbed suture during total laparoscopic distal gastrectomy performed for gastric cancer. Following diagnosis of small bowel obstruction, the patient underwent immediate laparoscopic repair that identified the cause and relieved the small bowel obstruction. This case highlights the need for surgeons to carefully perform proper suturing technique in order to prevent complications. Surgeons should maintain a high index of suspicion for diagnosing and treating potentially severe complications when using barbed sutures.

Hypoxia antagonizes glucose deprivation on interleukin 6 expression in an Akt dependent, but HIF-1/2α independent manner.

Although both glucose deprivation and hypoxia have been reported to promote cascades of biological alterations that lead to induction of inflammatory mediators, we hypothesized that glucose deprivation and hypoxia might show neutral, synergistic or antagonistic effects to each other on gene expression of inflammatory mediators depending on the regulatory components in their promoters. Gene expression of interleukin 6 (IL-6) was analyzed by real-time PCR, ELISA, or Western blot. Effects of glucose deprivation and/or hypoxia on activation of signaling pathways were analyzed by time-dependent phosphorylation patterns of signaling molecules. We demonstrate that hypoxia antagonized the effects of glucose deprivation on induction of IL-6 gene expression in microglia, macrophages, and monocytes. Hypoxia also antagonized thapsigargin-induced IL-6 gene expression. Hypoxia enhanced phosphorylation of Akt, and inhibition of Akt was able to reverse the effects of hypoxia on IL-6 gene expression. However, inhibition of HIF-1/2α did not reverse the effects of hypoxia on IL-6 gene expression. In addition, phosphorylation of p38, but not JNK, was responsible for the effects of glucose deprivation on IL-6 gene expression.