Single-Incision Laparoscopic-Assisted Right Colon Resection for Cancer

The authors suggest that laparoscopic right colectomy utilizing a single port may be performed with excellent cosmetic results

Single incision laparoscopic cholecystectomy: A single center experience

AbstractIntroductionSingle Incision Laparoscopic Surgery (SILS) is a variation in which trocar scars are hidden in the umbilicus. We sought to determine whether SILS cholecystectomy is a safe alternative to a conventional laparoscopic cholecystectomy.MethodsWe retrospectively reviewed our series of 205 SIL cholecystectomies (SILC) performed between May 2008–June 2010. The first 50 cases were done by initially insufflating the abdomen with a veress needle through the umbilicus and then placing 3, 5 mm ports in the umbilicus. The remaining cases were performed using a cut down approach at the umbilicus, followed by placement of a three-trocar SILS port under direct vision.ResultsTwo hundred and five patients (M:F = 48:157) underwent SILC during the study period. Median age was 45 (range = 21–62). Mean BMI range was 35 (range = 21–44). Mean operative time was 60 min (range = 40–120 min) and a follow up period that ranges from 1 to 21 months. Patient pathologies included: Chronic cholecystitis (74%), Acute cholecystitis (17%), Choledocholithiasis (6.8%), Gallstone pancreatitis (2%) and gallbladder polyp (0.5%). An additional port was placed in the umbilicus in 3% of cases. No cases were converted to open. Complications occurred in 4% of cases including: 3 patients with retained stones, 2 patients with post-op wound infection, 2 patients with incisional hernias in the umbilical region and 1patient with a veress injury.ConclusionSIL cholecystectomy can be done safely. It offers a better cosmetic result, which may lead to greater patient satisfaction

Adipocyte-Specific IKKβ Signaling Suppresses Adipose Tissue Inflammation through an IL-13-Dependent Paracrine Feedback Pathway

Summary: Adipose tissue inflammation is one pathway shown to mediate insulin resistance in obese humans and rodents. Obesity induces dynamic cellular changes in adipose tissue to increase proinflammatory cytokines and diminish anti-inflammatory cytokines. However, we have found that anti-inflammatory interleukin-13 (IL-13) is unexpectedly induced in adipose tissue of obese humans and high-fat diet (HFD)-fed mice, and the source of IL-13 is primarily the adipocyte. Moreover, HFD-induced proinflammatory cytokines such as tumor necrosis factor alpha (TNF-α) and IL-1β mediate IL-13 production in adipocytes in an IKKβ-dependent manner. In contrast, adipocyte-specific IKKβ-deficient mice show diminished IL-13 expression and enhanced inflammation after HFD feeding, resulting in a worsening of the insulin-resistant state. Together these data demonstrate that although IKKβ activates the expression of proinflammatory mediators, in adipocytes, IKKβ signaling also induces the expression of the anti-inflammatory cytokine IL-13, which plays a unique protective role by limiting adipose tissue inflammation and insulin resistance. : IKKβ is known to be a proinflammatory mediator. However, IKKβ in adipocytes also mediates IL-13 expression to suppress high-fat-diet-induced inflammation in adipose tissue. This feedback mechanism may be the molecular basis of diet-induced chronic low-grade inflammation, resulting in systemic insulin resistance