The mechanism underlying the bioinertness of the self-assembled monolayers of oligo(ethylene glycol)-terminated alkanethiol (OEG-SAM) was investigated with protein adsorption experiments, platelet adhesion tests, and surface force measurements with an atomic force microscope (AFM). In this work, we performed systematic analysis with SAMs having various terminal groups (-OEG, -OH, -COOH, -NH(2), and -CH(3)). The results of the protein adsorption experiment by the quartz crystal microbalance (QCM) method suggested that having one EG unit and the neutrality of total charges of the terminal groups are essential for protein-resistance. In particular, QCM with energy dissipation analyses indicated that proteins absorb onto the OEG-SAM via a very weak interaction compared with other SAMs. Contrary to the protein resistance, at least three EG units as well as the charge neutrality of the SAM are found to be required for anti-platelet adhesion. When the identical SAMs were formed on both AFM probe and substrate, our force measurements revealed that only the OEG-SAMs possessing more than two EG units showed strong repulsion in the range of 4 to 6 nm. In addition, we found that the SAMs with other terminal groups did not exhibit such repulsion. The repulsion between OEG-SAMs was always observed independent of solution conditions [NaCl concentration (between 0 and 1 M) and pH (between 3 and 11)] and was not observed in solution mixed with ethanol, which disrupts the three-dimensional network of the water molecules. We therefore concluded that the repulsion originated from structured interfacial water molecules. Considering the correlation between the above results, we propose that the layer of the structured interfacial water with a thickness of 2 to 3 nm (half of the range of the repulsion observed in the surface force measurements) plays an important role in deterring proteins and platelets from adsorption or adhesion.

Background This study aimed to demonstrate the feasibility of endoscopic hand-suturing (EHS) and attainability of sustained closure after colorectal endoscopic submucosal dissection (ESD). Methods EHS was defined as uninterrupted endoscopic suturing of the mucosal defect after colorectal ESD using an absorbable barbed suture and a through-the-scope needle holder. Following individual EHS training using an ex vivo porcine colonic model, two experienced endoscopists performed EHS. Repeat colonoscopy was performed on the third or fourth day after ESD to examine the EHS site. The primary end point was the complete EHS closure rate, and secondary end points were sustained closure and post-ESD bleeding rates. Results 11 lesions were included. Median size of the mucosal defect was 38 mm (range 25 – 55 mm) and the lesion characteristics were as follows: lower rectum/upper rectum/ascending colon/cecum = 3/3/2/3, and 0-IIa/0-Is + IIa/others = 5/4/2. EHS was not attempted in two patients owing to difficulty in colonoscope reinsertion after ESD and intraoperative perforation, respectively. EHS was performed for nine lesions, and the complete EHS closure rate was 73 %. Median procedure time for suturing was 56 minutes (range 30 – 120 minutes) and median number of stitches was 8 (range 6 – 12). Sustained closure and post-ESD bleeding rates were 64 % and 9 %, respectively. Conclusions EHS achieved complete and sustained closure in the colorectum. However, EHS is not currently clinically applicable given the long procedure time. Further modifications of the technique and devices are desirable.

Objectives: A phase II study was performed to investigate the safety and efficacy of concurrent chemoradiotherapy (CCRT) combined with an orally active fluoropyrimidine, S-1, plus cisplatin for locally advanced esophageal cancer (LAEC). Methods: CCRT comprised 2 courses, a 30-Gy radiotherapy over 3 weeks plus daily oral S-1 (80 mg/m²/day) for 2 weeks and a 24-hour cisplatin infusion (70 mg/m²) on day 8, and an identical course administered after a 2-week break. Results: One hundred and sixteen patients, 12 with stage II, 71 with stage III, and 33 with stage IVa LAEC participated, and 106 of them (91.4%) completed the CCRT course. The most serious toxicity was myelosuppression: grade 3 and 4 neutropenia occurred in 28.4 and 9.5% of patients, respectively. Nonhematologic toxicity was moderate. Complete response rates in patients with stage II, III, and IVa LAEC were 91.7, 67.6, and 36.4%, respectively. The overall median survival time was 2.3 years and that of patients with stage II, III, and IVa cancer was 7.0, 2.6, and 1.3 years, respectively. Conclusions: CCRT combined with S-1 plus cisplatin showed promising safety and efficacy. Potentially, this combination therapy could become a baseline medication for patients with LAEC.

Overexpression of MICA/B, a component of DAMPs induced by NACRT, may play an important role in acquiring a favorable immune response for pancreatic cancer which contributes to longer survival, suggesting the potential of immunotherapy of this recalcitrant disease, especially for patients with overexpression of DAMPs.

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