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Abdominal spacers are useful for maintaining the distance between the target tumors and surrounding tissues, such as the gastrointestinal tract, in patients treated with carbon ion radiotherapy. Surgical intervention to remove the spacers is sometimes necessary because of abdominal infections triggered by long-term spacer placement or intestinal perforation. Therefore, spacers that do not require surgical removal and provide effective drainage against abdominal infections are urgently needed. This study aimed to develop a spacer that could be removed non-surgically and one that provides the therapeutic effect of drainage in patients who receive carbon ion radiotherapy for abdominal tumors. A novel fan-shaped spacer was constructed from a film drain that was folded along the trigger line. Simple withdrawal of the trigger line caused the film drain to fold and the holding lines to become free. We performed laparoscopy-assisted insertion with pneumoperitoneum and blind removal of the spacer fourteen times using a porcine model. Saline in the abdominal cavity was effectively aspirated using the spacer. Our novel fan-shaped spacer could be removed safely without surgery and was able to drain fluid effectively from the abdominal cavity., Competing Interests: The authors have declared that no competing interests exist.

While screening genes encoding G protein-coupled receptors (GPCRs) in the human genome, we and other groups have identified a GPCR named hGPCR48 as a high affinity receptor for 5-oxo-6,8,11,14-eicosatetraenoic acid (5-oxo-ETE), which is arachidonic acid metabolite and an endogenous chemoattractant for granulocytes. Using Chinese hamster ovary (CHO) cells stably expressing hGPCR48, we show here that activation of the receptor causes the chemotaxis of the cells toward 5-oxo-ETE. We also show that the chemotaxis of human granulocytes toward 5-oxo-ETE is inhibited by pretreatment with anti-hGPCR48 antibodies, indicating that hGPCR48 is an endogenous receptor responsible for chemotaxis of granulocytes toward 5-oxo-ETE. In addition, we show that the chemotaxis of CHO cells expressing hGPCR48 is suppressed by pretreatment with pertussis toxin, and enhanced by overexpression of the carboxy terminal peptides of Galpha (12/13) subunits or a regulator of the G protein signaling domain of p115RhoGEF, both of which are known to suppress G(12/13)-dependent signaling pathways. These results indicate that hGPCR48 couples with G(i/o) and G(12/13) proteins, which then initiate or attenuate the chemotaxis of the cells toward 5-oxo-ETE, respectively.