[A Case of Early Detection of Hepatocellular Carcinoma using Abdominal Ultrasonography after Endoscopic Submucosal Dissection for Early Gastric Cancer].

We treated an 82-year-old man with early gastric cancer using endoscopic submucosal resection.Ultrasonography, which was performed to screen for metastasis, revealed hepatocellular carcinoma, and the tumor was curatively resected.Ultrasonography can be considered a useful examination tool to detect double cancer, even in cases of early cancer.

[A Case of Primary Squamous Cell Carcinoma of the Jejunum in the Ultra-Elderly].

We treated a 91-year-old man with squamous cell carcinoma that originated from his jejunum, which is very rare; only 8 cases have been reported previously.Surgery was performed because of the small bowel obstruction caused by the large cancerous mass, but he died 23 days later.Early detection and early treatment are important, especially for the ultra-elderly from a standpoint of tolerating surgery.

25 mg versus 50†mg dose of rectal diclofenac for prevention of post-ERCP pancreatitis in Japanese patients: a retrospective study.

OBJECTIVES: The aim of the present study was to assess the appropriate administration dose of non-steroidal anti-inflammation drugs to prevent pancreatitis after endoscopic retrograde cholangiopancreatography (ERCP). Importantly, the 100 mg dose of diclofenac recommended in Western countries has not been permitted in Japan. DESIGN: A retrospective study. SETTINGS: A single centre in Japan. PARTICIPANTS: This study enrolled patients who underwent ERCP at the Department of Gastroenterology, Osaka Saiseikai Senri Hospital, from April 2011 through June 2013, and who received either a 25 or a 50 mg dose of rectal diclofenac after ERCP. PRIMARY OUTCOME MEASURE: The occurrence of post-ERCP pancreatitis (PEP). A multivariate regression model was used to assess the effect of the 50 mg dose (the 50 mg group) of rectal diclofenac and to compare it to the occurrence of PEP referring to the 25 mg group. RESULTS: A total of 155 eligible patients received either 25 mg (84 patients) or 50 mg (71 patients) doses of rectal diclofenac after ERCP to prevent PEP. The proportion of PEP was significantly lower in the 50 mg group than in the 25 mg group (15.5% (11/71) vs 33.3% (28/84), p=0.018). In a multivariate analysis, the occurrence of PEP was significantly lower in the 50 mg group than in the 25 mg group even after adjusting potential confounding factors (adjusted OR=0.27, 95% CI 0.11 to 0.70). CONCLUSIONS: From this observation, the occurrence of PEP was significantly lower among ERCP patients with the 50 mg dose of rectal diclofenac than among those with the 25 mg dose.

The endoplasmic reticulum-resident chaperone heat shock protein 47 protects the Golgi apparatus from the effects of O-glycosylation inhibition.

The Golgi apparatus is important for the transport of secretory cargo. Glycosylation is a major post-translational event. Recognition of O-glycans on proteins is necessary for glycoprotein trafficking. In this study, specific inhibition of O-glycosylation (Golgi stress) induced the expression of endoplasmic reticulum (ER)-resident heat shock protein (HSP) 47 in NIH3T3 cells, although cell death was not induced by Golgi stress alone. When HSP47 expression was downregulated by siRNA, inhibition of O-glycosylation caused cell death. Three days after the induction of Golgi stress, the Golgi apparatus was disassembled, many vacuoles appeared near the Golgi apparatus and extended into the cytoplasm, the nuclei had split, and cell death assay-positive cells appeared. Six hours after the induction of Golgi stress, HSP47-knockdown cells exhibited increased cleavage of Golgi-resident caspase-2. Furthermore, activation of mitochondrial caspase-9 and ER-resident unfolded protein response (UPR)-related molecules and efflux of cytochrome c from the mitochondria to the cytoplasm was observed in HSP47-knockdown cells 24 h after the induction of Golgi stress. These findings indicate that (i) the ER-resident chaperon HSP47 protected cells from Golgi stress, and (ii) Golgi stress-induced cell death caused by the inhibition of HSP47 expression resulted from caspase-2 activation in the Golgi apparatus, extending to the ER and mitochondria.

[A case of hepatocellular carcinoma treated with specific substance of Maruyama resulting in a partial response].

We treated a 41-year-old man with hepatocellular carcinoma and chronic liver disease. He experienced leg edema. Following additional examinations, we diagnosed the patient with hepatocellular carcinoma and ascites with liver cirrhosis. Due to renal dysfunction, he could not undergo treatment with transcatheter arterial chemoembolization(TACE)or transcatheter arterial infusion(TAI). Therefore, he was treated with specific substance of maruyama(SSM), and survived.

[A case in which good quality of life was maintained by stent therapy for duodenal stenosis caused by gallbladder cancer invasion].

We treated an 80-year-old woman with gallbladder cancer. Because of her advanced age, chemotherapy was performed, but obstructive jaundice and duodenal stenosis were caused by invasion of the tumor. We inserted a metallic stent into the common bile duct and duodenum 3 times. As a result, she could eat and live at home with good quality of life.

[A case of partial response achieved by chemotherapy for a duodenal cancer].

We treated a 73-year-old woman with adenocarcinoma of the duodenum. She complained of poor appetite and weight loss. Upon close inspection, we diagnosed duodenal cancer with obstructive jaundice. Curative resection could not be performed because of swelling of the para-aortic lymph nodes. Chemotherapy using mFOLFOX6 was performed, and she survived.

[A clinical case of the esophagogastric malignancy palliated with covered metallic stent with anti-reflux mechanism].

Esohophageal stents are often used in treating malignant stricture. But, when stents are placed across the esophagogastric junction, they may lead to esophagogastric reflux. We report a case of successfully treated esophagogastric strictures using the new stent with anti-reflux mechanism (long cover type Niti-S™ esophageal stent). A 78-year-old man presenting with severe strictures from the lower esophagus to cardiac part of stomach was histopathologically diagnosed as adenocarcinoma. CT scan images showed multiple liver metastatic tumors. However, he refused chemotherapy. Palliation using long cover type Niti-S™ esophageal stent was performed. No adverse effect was occurred. He started solid meals on the 7th postoperative day. He was thereafter able to ingest solid meals without the symptom of esophgogastric reflux and stenosis until he died of the primary disease two month later.

[An operated case of retroperitoneal venous hemangioma complicated with Kasabach-Merritt syndrome which was well controlled by danaparoid sodium].

A 32-year-old woman was admitted with intermittent rectal bleeding with disseminated intravascular coagulation (DIC)-like coagulopathy. CT and MRI revealed a retroperitoneal tumor, and we diagnosed giant retroperitoneal hemangioma complicated with Kasabach-Merritt syndrome, following blood pool scintigraphy. Corticosteroid and interferon-alpha were not effective, and gabexate mesilate was also ineffective for coagulopathy. Immediately after receiving danaparoid sodium, she recovered from DIC. We performed tumor resection successfully, and she had no symptoms of coagulopathy thereafter.

Chimaerins act downstream from neurotrophins in overcoming the inhibition of neurite outgrowth produced by myelin-associated glycoprotein.

Several myelin-derived proteins are inhibitory cues that contribute to the lack of regeneration of the CNS and inhibit neurite outgrowth from some neurons in vitro. This inhibition is blocked if neurons are exposed to neurotrophins before encountering the inhibitors. Here, we demonstrate that chimaerin, one of the Rho GTPase activating proteins, is transcriptionally up-regulated after exposure to neurotrophins in post-natal cerebellar neurons. The expression of alpha chimaerin in the cerebellum is developmentally correlated with the abolishment of the inhibitory effect of myelin-associated glycoprotein (MAG). Ectopic expression of alpha chimaerin in cerebellar neurons results in resistance to MAG in regard to neurite outgrowth. These results suggest that up-regulated expression of chimaerin counteracts the activation of RhoA, which is a key molecule in transducing inhibitory signals in neurons.