Bleeding From a Ruptured, Extraluminally Growing Gastric Gastrointestinal Stromal Tumor Treated by Transcatheter Arterial Embolization: A Case Report.

A 49-year-old man with abdominal pain was referred to our hospital. Abdominal computed tomography showed an extraluminal tumor near the gastric anterior wall and intra-abdominal fluid collection. A ruptured intra-abdominal tumor was suspected, and emergency abdominal angiography was performed. Hemorrhage into the abdominal cavity was seen, and transcatheter arterial embolization (TAE) was performed, which stopped the bleeding. The tumor was surgically resected, and a diagnosis of an extraluminally growing gastric gastrointestinal stromal tumor was made. TAE should be considered for rare cases of extraluminally growing tumors with intra-abdominal hemorrhage.

A giant liposarcoma originating from peripancreatic fat tissue with identification using 3D-CT angiography: a case report.

BACKGROUND: Liposarcoma originating from peripancreatic fat tissue is extremely rare. This case report presents a surgical case of a giant liposarcoma originating from peripancreatic fat tissue with origin identification using 3-Dimensional Computed Tomography Angiography (3D-CTA). CASE PRESENTATION: A 59-year-old female was referred to our hospital with a giant abdominal tumor. Computed tomography revealed a 34 cm tumor composed of fatty tissue, exerting pressure on the posterior aspect of the pancreas. Suspecting liposarcoma, we planned for surgery. At first, the tumor appeared to be intra-abdominal tumor, based on the identification of the tumor's feeding artery as a branch of the dorsal pancreatic artery using 3D-CTA, we concluded that the liposarcoma originated from the peripancreatic fat tissue and situated in the retroperitoneum. During surgery, we observed a well-capsulated, elastic, yellowish mass without infiltration into surrounding tissues. We carefully dissected the tumor from the greater omentum and transverse mesocolon while preserving the tumor capsule. We ligated the feeding artery at the border with the pancreatic parenchyma and successfully completed the excision of the tumor. The resected specimen weighted 2620 g and was pathologically diagnosed as a well-differentiated liposarcoma. There was no injury to the tumor's capsule, and the surgical margins were negative. CONCLUSIONS: In this report, we present an extremely rare case of a liposarcoma originating in the peripancreatic fat tissue. The use of 3D-CTA was instrumental in identifying the primary site of this giant tumor, enabling us to guide the surgery and achieve complete resection successfully.

Novel anti-inflammatory agent 3-[(dodecylthiocarbonyl)-methyl]-glutarimide ameliorates murine models of inflammatory bowel disease.

OBJECTIVE AND DESIGN: To examine the effect of 3-[(dodecylthiocarbonyl)-methyl]-glutarimide (DTCM-G), a novel anti-inflammatory agent that inhibits lipopolysaccharide (LPS) activation of RAW264.7 macrophages, on murine models of colitis and RAW264.7 cells. MATERIALS AND METHODS: Colitis was induced by rectally infusing trinitrobenzenesulfonic acid (TNBS) (1.5 mg in 50% ethanol) in BALB/c mice or orally administering 3% dextran sulfate sodium (DSS) for 5 days in C57BL/6 mice. The severity of colitis was assessed after intraperitoneally injecting DTCM-G (40 mg/kg). The anti-inflammatory properties of DTCM-G and its mechanisms were investigated in LPS-stimulated RAW264.7 cells. RESULTS: DTCM-G significantly ameliorated TNBS-induced colitis, according to the body weight loss, disease activity index, colonic obstruction, macroscopic colonic inflammation score, mucosal myeloperoxidase activity, and histopathology. Immunohistochemistry and isolated lamina propria mononuclear cells showed significantly reduced colonic F4/80(+) and CD11b(+) macrophage infiltration. DTCM-G significantly suppressed tumor necrosis factor (TNF)-α and interleukin (IL)-6 messenger RNA expression in the colon and attenuated DSS-induced colitis, according to the disease activity index and histopathology. In RAW264.7 cells, DTCM-G suppressed LPS-induced TNF-α/IL-6 production and enhanced glycogen synthase kinase-3ß phosphorylation. CONCLUSIONS: DTCM-G attenuated murine experimental colitis by inhibiting macrophage infiltration and inflammatory cytokine expression. Thus, DTCM-G may be a promising treatment for inflammatory bowel disease.

Efficacy of DHMEQ, a NF-κB inhibitor, in islet transplantation: I. HMGB1 suppression by DHMEQ prevents early islet graft damage.

BACKGROUND: Pancreatic islet transplantation (PITx) is an attractive treatment option for restoring appropriate glucose homeostasis in type 1 diabetes patients. Although islet grafts can successfully engraft after PITx, large numbers of islet grafts are required mainly because immune reactions, including inflammation, destroy islet grafts. In these processes, nuclear factor (NF)-κB plays a central role. We hypothesized that the inhibition of NF-κB activation would ameliorate inflammatory responses after PITx and aid successful engraftment. METHODS: To test this hypothesis, a newly developed NF-κB inhibitor, dehydroxymethylepoxyquinomicin (DHMEQ), was used on a syngeneic mouse PITx model. One hundred seventy-five islets from C57BL/6 (B6) mice were transplanted into streptozotocin-induced diabetic B6 mice. The recipient mice were administered DHMEQ for 1, 2, or 3 days after PITx. The underlying mechanisms of DHMEQ on islet graft protection were investigated in an in vitro coculture model of pancreatic islets and macrophages. RESULTS: With a vehicle treatment, only 11.1% of the islet-recipients achieved normoglycemia after PITx. In sharp contrast, DHMEQ treatment markedly improved the normoglycemic rate, which was associated with the suppression of serum high mobility group complex-1 (HMGB1) and proinflammatory cytokines, including tumor necrosis factor-α, monocyte chemoattractant protein-1, macrophage inflammatory protein-1ß, interleukin-1ß, and interleukin-6, after PITx. In a murine macrophage-like cell line, DHMEQ inhibited HMGB1-driven activation and proinflammatory cytokine secretion and further prevented death isolated islets after coculture with these activated macrophages. CONCLUSIONS: Inhibition of NF-κB activation by DHMEQ after PITx reduces the HMGB1-triggered proinflammatory responses and results in engraftment of transplanted islets even with fewer islet grafts.