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Background: One advantage of endoscopic ultrasound‐guided hepaticogastrostomy (EUS‐HGS) is that it is difficult for reflux cholangitis, caused by duodenal pressure increasing due to duodenal obstruction, to occur. In addition, since stent deployment is performed away from the malignant stricture site, longer stent patency than with endoscopic retrograde cholangiopancreatography (ERCP) may be obtained. However, no study has previously compared EUS‐HGS and ERCP for patients without duodenal obstruction or surgically altered anatomy. The aim of the present study was to compare clinical outcomes between EUS‐HGS and ERCP in normal anatomy patients without duodenal obstruction. Method: In the ERCP group, patients who initially underwent biliary drainage were included. In the EUS‐HGS group, patients who underwent EUS‐HGS due to failed biliary cannulation were included. Patients with an inaccessible papilla, such as with surgically altered anatomy or duodenal obstruction, were excluded. Results: A total of 314 patients who underwent ERCP and EUS‐HGS were enrolled in this study. Of the 314 patients, 289 underwent biliary stenting under ERCP guidance, and 25 patients underwent biliary stenting under EUS‐HGS. After propensity score‐matching analysis, the adverse event rate tended to be lower in the EUS‐HGS group than in the ERCP group. Although overall survival was not significantly different between the EUS‐HGS and ERCP groups (p =.228), stent patency was significantly longer in the EUS‐HGS group (median 366.0 days) than in the ERCP group (median 76.5 days). Conclusions: EUS‐HGS had a lower adverse event rate, shorter procedure time, and longer stent patency than ERCP in cases of normal anatomy without duodenal obstruction. [ABSTRACT FROM AUTHOR]

We succeeded in developing an IGZO process with extremely high tolerance to hot carrier degradation. We verified the tolerance to hot carrier degradation by device evaluation using extremely severe DC stress. And we actually fabricated displays and confirmed that they can be displayed successfully. This high tolerance to hot carrier deterioration not only makes it possible to meet the needs for higher resolution and higher speed driving of liquid crystal displays, but also allows for higher speed rewriting of e‐Papers. [ABSTRACT FROM AUTHOR]

We are developing transflective LCD displays for signage that have good outdoor visibility and super‐low power consumption. This panel adopts a design that incorporates our technologies such as TFT, twisted‐VA technology, and MRS structure that can be driven at super‐low frequencies using IGZO technology. We would like to report that we have developed a 54.5‐inch transflective LCD. [ABSTRACT FROM AUTHOR]

Cranial neural crest cells (NCCs) are critical for craniofacial development. The administration of valproic acid (VPA) to pregnant females causes craniofacial malformations in offspring. However, the in vivo influence of VPA on mammalian cranial NCCs remains unclear. In this study, we aimed to elucidate the developmental stage‐specific effect of VPA on cranial NCCs through the administration of a single dose of VPA to pregnant rat females immediately prior to the formation of the cranial neural crest (NC). We performed whole‐mount immunohistochemistry or in situ hybridization to examine localization changes of gene transcripts associated with the epithelial–mesenchymal transition of the cranial NC (i.e., cranial NCC formation) and cranial NCC migration. The results showed that Hoxa2 mRNA was abnormally detected and Sox9 mRNA expression was decreased in the midbrain–rhombomere (R) 1/2 NC, which forms cranial NCCs that migrate to the frontonasal mass (FNM) and branchial arch (BA) 1, through VPA administration, thus reducing the formation of SNAI2‐positive NCCs. Hoxa2‐positive NCCs were detected normally in BA2 and abnormally in FNM and BA1, which are normally Hox‐free, implying VPA‐induced abnormal cranial NCC migration. In vitro verification experiments using the whole embryo culture system revealed that midbrain–R4 NCC migration was abnormal. These results indicate that VPA reduces the formation/delamination of the midbrain–R1/2 NCCs in a developmental stage‐specific manner and subsequently causes the abnormal migration of R4 NCCs, which suggests that the abnormal formation and migration of cranial NCCs contribute to the inhibition of axonal elongation in the trigeminal nerve and a reduction in head size. [ABSTRACT FROM AUTHOR]

To link to full-text access for this article, visit this link: http://dx.doi.org/10.1016/j.ydbio.2008.11.022 Byline: Kazushi Aoto (a), Yayoi Shikata (a), Hajime Imai (a)(b), Daisuke Matsumaru (c), Tomoyuki Tokunaga (d), Seiji Shioda (b), Gen Yamada (c), Jun Motoyama (a) Keywords: Holoprosencephaly; Prechordal plate; Prechordal mesoderm; Ventral cranial mesoderm; Cell fate mapping; Apoptosis; Sonic hedgehog (Shh); Gli3 Abstract: In humans, holoprosencephaly (HPE) is a common birth defect characterized by the absence of midline cells from brain, facial, and oral structures. To understand the pathoetiology of HPE, we investigated the involvement of mammalian prechordal plate (PrCP) cells in HPE pathogenesis and the requirement of the secreted protein sonic hedgehog (Shh) in PrCP development. We show using rat PrCP lesion experiments and DiI labeling that PrCP cells are essential for midline development of the forebrain, foregut endoderm, and ventral cranial mesoderm in mammals. We demonstrate that PrCP cells do not develop into ventral cranial mesoderm in Shh.sup.-/- embryos. Using Shh.sup.-/- and chimeric embryos we show that Shh signal is required for the maintenance of PrCP cells in a non-cell autonomous manner. In addition, the hedgehog (HH)-responding cells that normally appear during PrCP development to contribute to midline tissues, do not develop in the absence of Shh signaling. This suggests that Shh protein secreted from PrCP cells induces the differentiation of HH-responding cells into midline cells. In the present study, we show that the maintenance of a viable population of PrCP cells by Shh signal is an essential process in development of the midline of the brain and craniofacial structures. These findings provide new insight into the mechanism underlying HPE pathoetiology during dynamic brain and craniofacial morphogenesis. Author Affiliation: (a) Molecular Neuropathology Group, Brain Science Institute, RIKEN, 2-1 Hirosawa, Wako, Saitama 351-0198, Japan (b) Department of Anatomy, Showa University School of Medicine, Shinagawa-ku, Tokyo 142-8555, Japan (c) Center for Animal Resources and Development (CARD), Graduate School of Medical and Pharmaceutical Sciences, Kumamoto University, Kumamoto 860-0811, Japan (d) Laboratory of Development and Differentiation, National Institute of Agrobiological Sciences, Tsukuba 305-0901, Japan Article History: Received 3 April 2008; Revised 1 November 2008; Accepted 26 November 2008