Our strategy for suspected T2 gallbladder GBC is safe and useful, avoids unnecessary procedures, and is associated with similar oncologic outcomes as the open method.

In patients with bullous pemphigoid (BP), early lesions appear as exudative erythematous patches. Histologically, the inflammatory infiltrate is composed mainly of mononuclear cells (MNCs) in the erythematous lesion, although eosinophils and neutrophils are also present. The MNCs are predominantly helper/inducer T cells even in the bullous lesions. Some of the MNCs infiltrated were stained in cytoplasm by antihuman gamma-interferon (IFN-γ) monoclonal antibody (MoAb) immunohistologically. These infiltrates are considered to produce IFN-γ. In the bullous fluids of early BP lesions, high levels of IFN-γ are detected by radioimmunoassay using antihuman IFN-γ MoAb. The results suggest that infiltrating lymphocytes are stimulated immunologically in BP bullous lesions. Cell-mediated immune reaction as well as autoantibody to the basement membrane zone may also play an important role in blister formation in BP.

Neural vascular barrier is essential for the life of multicellular organisms, and its impairment by tissue hypoxia is known to be a central of pathophysiology accelerating the progression of various intractable neural diseases. Therefore, the molecules involved in hypoxia-induced impairment of vascular barrier can be the targets to establish new therapies for intractable diseases. Here, we demonstrate that a disintegrin and metalloproteinases (ADAMs) 12 and 17 expressed in endothelial cells are the molecules responsible for the impairment of neural vascular barrier by hypoxia. Brain microvascular endothelial cells in vitro lost their barrier properties immediately after hypoxic stimulation through diminished localization of claudin-5, a tight junction molecule, on cell membranes. Hypoxic disappearance of claudin-5 from cell membranes and the consequent loss of barrier properties were completely suppressed by inhibition of the metalloproteinase activity which was found to be attributed to ADAM12 and ADAM17. Inhibition of either ADAM12 or ADAM17 was sufficient to rescue the in vivo neural vasculature under hypoxia from the loss of barrier function. This is the first report to specify the molecules which are responsible for hypoxia-induced impairment of neural vascular barrier and furthermore can be the targets of new therapeutic strategies for intractable neural diseases.

Aim The appropriate extent of lymphadenectomy for pancreatic cancer of the body/tail has not been standardized worldwide. The present study evaluated the optimal extent of harvesting lymph nodes. Methods Patients who underwent distal pancreatectomy for invasive ductal carcinoma of the pancreas between 2007 and 2018 were retrospectively reviewed. Patients were subclassified into three groups depending on the tumor location: pancreatic body (Pb), proximal pancreatic tail (Ptp), and distal pancreatic tail (Ptd). The pancreatic tail was further divided into even sections of Ptp and Ptd. Patterns of lymph node metastasis and the impact of lymph node metastasis on the prognosis were examined. Results A total of 120 patients were evaluated. Fifty‐eight patients had a tumor in the Pb, 38 in the Ptp, and 24 in the Ptd. No patients with a Ptd tumor had metastasis beyond the peripancreatic and splenic hilar lymph nodes (LN‐PSH). All patients with metastasis to the lymph nodes along the common hepatic artery (LN‐CHA) or along the left lateral superior mesenteric artery (LN‐SMA) also had metastasis to the LN‐PSH. Recurrence after surgery occurred significantly earlier in this population. In a multivariate analysis, metastasis to the LN‐CHA or LN‐SMA (hazard ratio [HR] 3.3; P = .04) was an independent risk factor for overall survival. Furthermore, high levels of preoperative serum CA19‐9 (HR 10.9; P = .013) were a predictive factor for metastasis to the LN‐CHA or LN‐SMA. Conclusions Metastasis to the LN‐CHA or LN‐SMA was rare but a significant prognostic factor in patients with pancreatic body/tail cancer.

Aim Sorafenib inhibits multiple kinase signaling pathways, including the rat sarcoma virus (Ras)/rapidly accelerated fibrosarcoma (Raf)/mitogen‐activated protein kinase kinase (MEK)/extracellular signal‐regulated kinase (ERK) pathway, and is a promising therapy for hepatocellular carcinoma (HCC). However, the role of ERK activation in HCC remains unclear. This study was designed to investigate the potential link between ERK activation and aggressive HCC phenotypes. Methods We evaluated nuclear ERK expression by immunohistochemistry in 154 resected HCC nodules from 136 patients. We then investigated the associations of ERK expression with the clinicopathological characteristics of HCC, c‐MET expression, and the molecular subclass biomarkers Ki‐67, keratin 19 (KRT19, CK19, or K19), and sal‐like protein 4. Multivariate Cox regression analysis was carried out to determine independent prognostic factors for overall survival and recurrence‐free survival. The effects of ERK activation by hepatocyte growth factor (HGF) on eight HCC cell lines were further examined. Results High‐level nuclear expression of ERK was observed in 20 (13%) of 154 nodules and was significantly associated with higher serum alpha‐fetoprotein levels (P = 0.034), poorer differentiation (P = 0.003), a higher Ki‐67 index (P < 0.001), high‐level expression of c‐MET (P = 0.008), KRT19 (P = 0.002), or sal‐like protein 4 (P < 0.001), and shorter overall survival (multivariate hazard ratio 3.448; P = 0.028) and recurrence‐free survival (multivariate hazard ratio 2.755; P = 0.004). HCC cells treated with hepatocyte growth factor showed enhanced cell proliferation together with ERK activation and upregulated KRT19 expression, both of which were inhibited by sorafenib. Conclusions High‐level ERK activation is associated with a KRT19‐positive highly proliferative subtype of HCC with a dismal prognosis. These findings support the key role of the hepatocyte growth factor/c‐MET/ERK axis in HCC progression.

An Augmented Reality (AR) system on mobile phones has recently attracted attention because smartphones have increasingly been popular. For an AR system, we have to know a camera pose of a smartphone. A sensor-based method is one of the most popular ways to estimate the camera pose, but it cannot estimate an accurate pose. A vision-based method is another way to estimate the camera pose, but it is not suitable to a scene with few interest points such as a sports field. In this paper, we propose a novel method of a camera pose estimation for a scene without interest points by combining a sensor-based and a vision-based approach. In our proposed method, we use an acceleration and a magnetic sensor to roughly estimate a camera pose, then search the accurate pose by matching a captured image with a set of reference images. Our experiments show that our proposed method is accurate and fast enough to apply a real-time AR system.

BackgroundBloodstream infection (BSI) is a life‐threatening complication after living donor liver transplantation (LDLT). We aimed to explore the incidence and predisposing factors of BSI at our institution.MethodsWe conducted a retrospective cohort analysis on all consecutive adults with BSI within 6 months after LDLT performed between 2005 and 2016. For antimicrobial prophylaxis, ampicillin/sulbactam, cefotaxime, and micafungin were administered. From 2011, methicillin‐resistant Staphylococcus aureus (MRSA) carriers were decolonized using mupirocin ointment and chlorhexidine gluconate soap. Risk factors for BSI were identified by uni‐ and multivariate logistic regression.ResultsOf a total of 106 LDLTs, 42 recipients (40%) suffered BSI. The BSI group demonstrated significantly higher in‐hospital mortality rates compared with the non‐BSI group (24% vs. 7%, P = .01). We identified MRSA carrier (odds ratio [OR], 19.1; P < .001), ABO incompatibility (OR, 2.9; P = .03), and estimated glomerular filtration rate <30 mL/min/1.73m2 (OR, 15.8; P = .02) as independent risk factors for BSI. Decolonization treatment for MRSA carriers did not reduce the incidence of all‐cause BSI but reduced the frequency of BSI caused by MRSA.ConclusionTo our knowledge, for the first time, MRSA carriers were revealed to be highly vulnerable to BSI after LDLT.

Background: Although surgery is the definitive curative treatment for biliary tract cancer (BTC), outcomes after surgery alone have not been satisfactory. Adjuvant therapy with S-1 may improve survival in patients with BTC. This study examined the safety and efficacy of 1 year adjuvant S-1 therapy for BTC in a multi-institutional trial. Methods: The inclusion criteria were as follows: histologically proven BTC, Eastern Cooperative Oncology Group (ECOG) performance status 0 or 1, R0 or R1 surgery performed, cancer classified as Stage IB to III. Within 10 weeks post-surgery, a 42-day cycle of treatment with S-1 (80 mg/m 2 /day orally twice daily on days 1-28 of each cycle) was initiated and continued up to 1 year post surgery. The primary endpoint was adjuvant therapy completion rate. The secondary endpoints were toxicities, disease-free survival (DFS), and overall survival (OS). Results: Forty-six patients met the inclusion criteria of whom 19 had extrahepatic cholangiocarcinoma, 10 had gallbladder carcinoma, 9 had ampullary carcinoma, and 8 had intrahepatic cholangiocarcinoma. Overall, 25 patients completed adjuvant chemotherapy, with a 54.3% completion rate while the completion rate without recurrence during the 1 year administration was 62.5%. Seven patients (15%) experienced adverse events (grade 3/4). The median number of courses administered was 7.5. Thirteen patients needed dose reduction or temporary therapy withdrawal. OS and DFS rates at 1/2 years were 91.2/80.0% and 84.3/77.2%, respectively. Among patients who were administered more than 3 courses of S-1, only one patient discontinued because of adverse events.