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A recently developed biopesticide made of safflower and cottonseed oils has excellent ovicidal activity against the hard-to-control spider mite Tetranychus urticae Koch (Acari: Tetranychidae). It has attracted attention as a sustainable treatment for controlling T. urticae because it has low potential for promoting resistance and little effect on the predatory mite Neoseiulus californicus (McGregor) (Acari: Phytoseiidae), which is an important natural enemy of spider mites. Here, we investigated the mechanism of its ovicidal activity against T. urticae . The oil droplets in the oil-in-water emulsion of the biopesticide strongly adhered to T. urticae eggs, seeped through the chorion being cut during hatching, and inhibited the embryonic rotational movement necessary for cutting and hatching. No adverse effect was observed on N. californicus eggs even in undiluted biopesticide. We conclude that this biopesticide and N. californicus can be used simultaneously in the integrated management of T. urticae in oily biopesticide-tolerant plant species., Competing Interests: This study was funded by OAT Agrio Co., Ltd., which employs Shimpei Noyama and Shigekazu Wakisaka., (© 2020 The Authors. Engineering in Life Sciences published by Wiley‐VCH GmbH.)

Introduction: Dual-hemostat techniques for port closure have previously been reported, but their safety and efficacy have not been evaluated. Here, we describe the dual-hemostat port closure technique employed at our institution, which uses a customized surgical suture for safe and certain port closure, and we assess the incidence rate of trocar-site hernia (TSH) after laparoscopic cholecystectomy., Methods: From March 1999 to March 2017 at our institution, 316 patients underwent elective laparoscopic cholecystectomy performed by a single experienced surgeon. We routinely used a dual-hemostat technique with a customized surgical suture to achieve safe and certain port closure. We assessed the incidence rate of TSH after laparoscopic cholecystectomy (defined as a reoperation for a TSH or clinical hernia at the port site) based on follow-up data from patient questionnaires and clinical examinations., Results: After 67 patients were excluded because of death, unknown address, or conversion to open cholecystectomy, 249 eligible patients received questionnaires, of which 173 were returned (response rate, 69.5%). From these responses, TSH was suspected in three patients, but only one underwent reoperation for TSH after laparoscopic cholecystectomy. Thus, the incidence rate of TSH after laparoscopic cholecystectomy was 0.6% (1/173)., Conclusions: Our single-center experience demonstrated that our port closure technique using a dual-hemostat technique with customized surgical suture provides an appropriate option for laparoscopic cholecystectomy, especially given its ease and low incidence of TSH., (© 2019 Japan Society for Endoscopic Surgery, Asia Endosurgery Task Force and John Wiley & Sons Australia, Ltd.)

The binding of p120-catenin and β-catenin to the cytoplasmic domain of E-cadherin establishes epithelial cell-cell adhesion. Reduction and loss of catenin expression degrades E-cadherin-mediated carcinoma cell-cell adhesion and causes carcinomas to progress into aggressive states. Since both catenins are differentially regulated and play distinct roles when they dissociate from E-cadherin, evaluation of their expression, subcellular localization and the correlation with E-cadherin expression are important subjects. However, the same analyses are not readily performed on squamous cell carcinomas in which E-cadherin expression determines the disease progression. In the present study, we examined expression and subcellular localization of p120-catenin and β-catenin in oral carcinomas (n = 67) and its implications in the carcinoma progression and E-cadherin expression using immunohitochemistry. At the invasive front, catenin-membrane-positive carcinoma cells were decreased in the dedifferentiated (p120-catenin, P < 0.05; β-catenin, P < 0.05) and invasive carcinomas (p120-catenin, P < 0.01; β-catenin, P < 0.05) and with the E-cadherin staining (p120-catenin, P < 0.01; β-catenin, P < 0.01). Carcinoma cells with β-catenin cytoplasmic and/or nuclear staining were increased at the invasive front compared to the center of tumors (P < 0.01). Although the p120-catenin isoform shift from three to one associates with carcinoma progression, it was not observed after TGF-β, EGF or TNF-α treatments. The total amount of p120-catenin expression was decreased upon co-treatment of TGF-β with EGF or TNF-α. The above data indicate that catenin membrane staining is a primary determinant for E-cadherin-mediated cell-cell adhesion and progression of oral carcinomas. Furthermore, it suggests that loss of p120-catenin expression and cytoplasmic localization of β-catenin fine-tune the carcinoma progression.

A 63-year-old male with an esophageal cancer invading the bronchus was treated with radiation therapy (70 Gy) from November 1995, resulting in the disappearance of the lesion. He was later readmitted due to dysphagia from the recurrence of the esophageal cancer. We diagnosed, by endoscopic and chest CT scan findings, that the esophageal cancer was invading the right bronchus. We inserted an expandable metallic stent endoscopically, and the patient could eat well. We performed two courses of FLEP chemotherapy (consisting of 5-FU, leucovorin, etoposide and cisplatin) from November 12, 1997. He then suffered from an esophagobronchial fistula, but was cured by a covered expandable metallic stent replacement. No esophageal stenoses or recurrences were seen endoscopically and he could eat well on December 7, 1998. The standard modality of treatment for patients with advanced esophageal cancer invading adjacent structures is not yet established, and the prognosis for such patients remains quite poor. We performed combination therapy with an expandable metallic stent replacement and FLEP chemotherapy, and improved the patient's quality of life. This form of therapy was thus proved useful for patients with esophageal cancer invading adjacent structures.