Oozing-type rupture caused by right ventricular intramural hematoma after right ventricular infarction.

An 81-year-old man was admitted to the hospital because of decreased level of consciousness. He had bradycardia (27 beats/min). Electrocardiography showed ST-segment elevation in leads II, III, and aVF and ST-segment depression in leads aVL, V1. Transthoracic echocardiography (TTE) visualized reduced motion of the left ventricular (LV) inferior wall and right ventricular (RV) free wall. Coronary angiography revealed occlusion of the right coronary artery. A primary percutaneous coronary intervention was successfully performed with temporary pacemaker backup. On the third day, the sinus rhythm recovered, and the temporary pacemaker was removed. On the fifth day, a sudden cardiac arrest occurred. Extracorporeal cardiopulmonary resuscitation was performed. TTE showed a high-echoic effusion around the right ventricle, indicating a hematoma. The drainage was ineffective. He died on the eighth day. An autopsy showed the infarcted lesion and an intramural hematoma in the RV. However, no definite perforation of the myocardium was detected. The hematoma extended to the epicardium surface, indicative of oozing-type RV rupture induced by RV infarction. The oozing-type rupture induced by RV infarction might develop asymptomatically without influence on the vital signs of the patient. Frequent echocardiographic evaluation is essential in cases of RV infarction taking care of silent oozing-type rupture. Learning objective: Inferior left ventricular infarction sometimes complicates right ventricular (RV) infarction. The typical manifestations of RV infarction include low blood pressure, low cardiac output, and elevated right atrium pressure. Although the frequency is low, fatal complications of oozing-type RV rupture might progress asymptomatically. Frequent echocardiographic screening is necessary to detect them.

Case of pneumatosis cystoides intestinalis with intra-abdominal free air developed during treatment with voglibose.

Contrast-enhanced computed tomography (CT) scan (portal phase) at the onset. Emphysema is detected in the ileal wall (b, c: Arrows) and free air is detected in the abdominal cavity (a: Arrowhead). CT scan imaging settings: (a-c) window level (WL) 60 and window width (WW) 300. (d-f) WL 0 and WW 433. By changing the imaging settings, intestinal emphysema and free air can be more easily identified.

Mesenteric phlebosclerosis associated with the oral intake of Japanese traditional (Kampo) medicines containing Gardeniae Fructus.

We report a case of mesenteric phlebosclerosis (MP) in a woman in her 50s who had been taking Kamishoyosan for 13 years. Colonoscopic findings 13 years after the start of oral administration were nonspecific, with decreased vascular permeability and redness of the mucosa. The extent of the lesion was initially from the cecum to the ascending colon but expanded over time to the transverse colon. In colon biopsies, there was a remarkable deposition of collagen fibers around the small vessels in the lamina propria of the cecum or the ascending colon over time, and the specific lesions expanded to the transverse colon. The deposition of collagen fibers around the vessels in the lamina propria was already present when the total oral dose of the Sanshishi component was low. In this valuable case of MP, changes after the start of oral administration of Kamishoyosan could be followed over time via endoscopy and biopsy.

A mucinous cystic neoplasm of the pancreas containing an undifferentiated carcinoma component and harboring the NRAS driver mutation.

A woman in her 20s visited our hospital with a chief complaint of abdominal distension and back pain. She was diagnosed with a cystic tumor (diameter 16 cm) in the tail of the pancreas and underwent a combined distal pancreatectomy, splenectomy, and left adrenalectomy. Histopathologically, the tumor presented as a mucinous cystic neoplasm with an undifferentiated carcinoma component of the pancreas. In addition, the cells demonstrated a partial rhabdoid-like morphology. These findings were considered relatively typical for a mucinous cystic neoplasm in the tail of the pancreas in a young woman. However, NRAS mutation, which is rare in pancreatic tumors, was detected.

Adenocarcinoma with intraductal papillary mucinous neoplasm arising in a duodenal heterotopic pancreas: a case report.

A woman in her 70 s was diagnosed with a tumor in her duodenal wall during a routine visit for diabetes. She subsequently underwent subtotal stomach-preserving pancreatoduodenectomy. Histologically, the tumor was present mainly in the duodenal wall, and atypical cystic ducts were seen in the muscularis propria and subserosa. Invasive well-differentiated adenocarcinoma was seen in the duodenal submucosal and mucosal layers. Heterotopic pancreatic tissue was seen within the tumor, and atypical epithelium had proliferated and replaced the cystic ductal epithelium of the heterotopic pancreas. Therefore, adenocarcinoma with intraductal papillary mucinous neoplasm arising in duodenal heterotopic pancreas was the final histopathological diagnosis, which is considered rare.

An autopsy case of primary jejunal pouch cancer which protruded from the abdominal wall 14 years after total gastrectomy for gastric cancer.

Adenocarcinoma which develops in the jejunal pouch has rarely been reported, but most of such cases tend to be a recurrence of primary cancer due to the presence of residual or disseminated cancer cells. Primary jejunal pouch cancer is extremely rare. We experienced an autopsy case of primary jejunal pouch cancer which occurred 14 years after proximal gastrectomy for gastric cancer. A female in her late 60s was admitted because of hypoglycemia with liver dysfunction. She underwent total gastrectomy for fundic cancer and had been reconstructed by jejunal pouch interposition 14 years prior to this presentation. Hypoglycemia recovered by nutritional support. Computed tomography demonstrated severe fatty liver and liver biopsy proved non-alcoholic steatohepatitis, which was supposed to have been induced by malnutrition. Screening esophagogastroduodenoscopy (EGD) revealed no tumorous lesions in the jejunal pouch at this time. However, her anorexia gradually progressed and the symptom of bowel obstruction appeared. EGD performed 5 months after the previous EGD revealed adenocarcinoma which extended from the anastomosis of the interposed jejunum. Then liver metastasis developed and jejunal pouch cancer invaded the abdominal wall and protruded with ulcer formation. Finally, the patient died of malnutrition. An autopsy revealed adenocarcinoma which had developed in the interposed jejunal pouch and protruded through the abdominal wall accompanied with lung and liver metastasis. We herein describe this rare case of primary interposed jejunal pouch cancer and discuss our findings including a review of the pertinent literature.

Adenosquamous Carcinoma of the Choledochus.

The patient was an 86-year-old man who was admitted with obstructive jaundice. Computed tomography revealed a tumor in the hilar choledochus with peripheral hepatic duct dilatation. Endoscopic cholangiography (ERC) demonstrated the defect in the choledochus. Brushing cytology during ERC showed Orange-G-philic keratinized atypical cells, which led to a diagnosis of squamous cell carcinoma. Chemotherapy with tegafur-gimeracil-oteracil potassium was ineffective and was discontinued due to adverse effects. The patient died 5 months after the diagnosis and autopsy revealed tubular adenocarcinoma of the hilar bile duct with squamous cell carcinoma component. Progression of the disease might influence the distribution of adenosquamous carcinoma. The clinicopathological sequence of adenosquamous carcinoma of the choledochus was documented.

Inhibitory effect of fucoidan on Huh7 hepatoma cells through downregulation of CXCL12.

The aim of this study is to assess whether fucoidan modulates the expression of chemokine ligand 12 (CXCL12)/chemokine receptor 4 (CXCR4) and exerts antitumor activity toward Huh7 hepatoma cells. According to 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assays, fucoidan inhibited the growth of Huh7 cells and HepG2 cells in a dose-dependent manner, with a 50% inhibition of cell growth (IC50) of 2.0 and 4.0 mg/ml, respectively. alpha-fetoprotein levels in medium collected from fucoidan-treated cells were significantly decreased in Huh7 cells but not in HepG2 cells. Western blotting revealed that the amount of alpha-fetoprotein was decreased by 1.0 mg/ml of fucoidan in Huh7 cells, whereas it was unchanged in HepG2 cells. In Huh7 cells, CXCL12 mRNA expression was significantly downregulated by 1.0 mg/ml of fucoidan, whereas CXCR4 mRNA expression was unchanged by fucoidan. CXCL12 and CXCR4 mRNA were barely expressed in HepG2 cells. In addition, 1.0 mg/ml of fucoidan mildly arrested the cell cycle and induced apoptosis in Huh7 cells. The findings suggest that fucoidan exhibits antitumor activity toward Huh7 cells through the downregulation of CXCL12 expression.

Regulation of calcium-permeable TRPV2 channel by insulin in pancreatic beta-cells.

OBJECTIVE: Calcium-permeable cation channel TRPV2 is expressed in pancreatic beta-cells. We investigated regulation and function of TRPV2 in beta-cells. RESEARCH DESIGN AND METHODS: Translocation of TRPV2 was assessed in MIN6 cells and cultured mouse beta-cells by transfecting TRPV2 fused to green fluorescent protein or TRPV2 containing c-Myc tag in the extracellular domain. Calcium entry was assessed by monitoring fura-2 fluorescence. RESULTS: In MIN6 cells, TRPV2 was observed mainly in cytoplasm in an unstimulated condition. Addition of exogenous insulin induced translocation and insertion of TRPV2 to the plasma membrane. Consistent with these observations, insulin increased calcium entry, which was inhibited by tranilast, an inhibitor of TRPV2, or by knockdown of TRPV2 using shRNA. A high concentration of glucose also induced translocation of TRPV2, which was blocked by nefedipine, diazoxide, and somatostatin, agents blocking glucose-induced insulin secretion. Knockdown of the insulin receptor attenuated insulin-induced translocation of TRPV2. Similarly, the effect of insulin on TRPV2 translocation was not observed in a beta-cell line derived from islets obtained from a beta-cell-specific insulin receptor knockout mouse. Knockdown of TRPV2 or addition of tranilast significantly inhibited insulin secretion induced by a high concentration of glucose. Likewise, cell growth induced by serum and glucose was inhibited by tranilast or by knockdown of TRPV2. Finally, insulin-induced translocation of TRPV2 was observed in cultured mouse beta-cells, and knockdown of TRPV2 reduced insulin secretion induced by glucose. CONCLUSIONS: TRPV2 is regulated by insulin and is involved in the autocrine action of this hormone on beta-cells.

A simple method to induce differentiation of murine bone marrow mesenchymal cells to insulin-producing cells using conophylline and betacellulin-delta4.

The present study was conducted to establish a method to induce differentiation of bone marrow (MB)-derived mesenchymal cells into insulin-producing cells. When mouse BM-derived mesenchymal cells were cultured for 60 days in medium containing 10% fetal calf serum and 25 mM glucose, they expressed insulin. Addition of activin A and betacellulin (BTC) accelerated differentiation, and immunoreactive insulin was detected 14 days after the treatment. Insulin-containing secretory granules were observed in differentiated cells by electron microscopy. Treatment of BM-derived mesenchymal cells with conophylline (CnP) and BTC-delta4 further accelerated differentiation, and mRNA for insulin was detected 5 to 7 days after the treatment. Mesencymal cells treated with CnP and BTC-delta4 responded to a high concentration of glucose and secreted mature insulin. When these cells were transplanted into streptozotocin-treated mice, they markedly reduced the plasma glucose concentration, and the effect continued for at least 4 weeks. These results indicate an efficacy of the combination of CnP and BTC-delta4 in inducing differentiation of BM-derived mesenchymal cells into insulin-producing cells.