A case of early-stage type 3 gastric neuroendocrine tumor in the upper body of the stomach: is endoscopic resection feasible?

Although gastric neuroendocrine tumors (NETs) are uncommon compared with gastric carcinomas, the incidence of NETs has been recently increasing. Gastric NETs are classified into three subgroups, and among these, gastrin-independent sporadic type 3 gastric NETs have a poor prognosis because of frequent lymph node or distant metastasis. We experienced a case of an early-stage type 3 gastric NET associated with lymphovascular and submucosal invasion.

[Significance of Inflammatory/Nutritional Index in Pathological Stage Ⅱ-Ⅲ Colorectal Cancer].

The aim of this study was to evaluate the inflammatory/nutritional index in patients with colorectal cancer. A total of 600 patients with pStage Ⅱ-Ⅲ colorectal cancer who underwent radical resection at our hospital between January 2008 and September 2022 were retrospectively reviewed. Onodera's prognostic nutritional index(OPNI), CRP-to-albumin ratio, modified Glasgow prognostic score, neutrophil-to-lymphocyte ratio, platelet-to-lymphocyte ratio, lymphocyte-to-monocyte ratio were measured preoperatively.

Gastric type III heterotopic pancreas presenting as adenomyoma in the antrum of the stomach: a case report.

Although heterotopic pancreas usually occurs in the stomach and rarely presents as a submucosal tumor, an accurate preoperative diagnosis is often difficult because of the variety of clinical symptoms and findings depending on the size and location of the lesion. We experienced a case of gastric type III heterotopic pancreas presenting as a gastric adenomyoma in the antrum of the stomach. A 62-year-old woman visited a local hospital for epigastric discomfort.

Gastric collision tumor composed of early-stage gastric carcinoma and gastrointestinal stromal tumor: a case report.

Collision tumors composed of adenocarcinoma and gastrointestinal stromal tumor (GIST) of the stomach are extremely uncommon, and only a few cases have been reported in the English literature. In the present case, a 67-year-old woman visited a local hospital for vomiting and hematemesis. An esophagogastroduodenoscopy study indicated an elevated lesion with ulceration.

A case of gastric ischemia caused by massive gastric dilatation due to superior mesenteric artery syndrome.

Gastric ischemia is extremely rare and its endoscopic findings appear similar to those of malignant tumors, which makes accurate diagnosis difficult. We present the case of a 41-year-old woman who was admitted to our hospital for severe abdominal pain and vomiting. Laboratory data at the time of admission indicated high serum levels of C-reactive protein, fibrin/fibrinogen degradation products and D-dimer.

The alterations in hepatic microcirculation and Kupffer cell activity after biliary drainage in jaundiced mice.

Background/purpose: The aim of this study is to examine the effects of biliary drainage on hepatic microcirculation and Kupffer cell activity in the liver with obstructive jaundice.

Methods: Common bile duct ligation and division was performed on C57BL/6 mice to induce obstructive jaundice. Seven or 14 days after surgery, some mice underwent biliary drainage.

[A case of advanced esophageal cancer with no recurrence treated biweekly with postoperative docetaxel/nedaplatin combined chemotherapy after non-curative surgery].

We report a case of non-curatively resected esophageal cancer with no recurrence biweekly treated with postoperative docetaxel/nedaplatin combined chemotherapy. A 59-year-old woman underwent non-curative resection with esophagectomy for advanced esophageal cancer with direct invasion to the descending aorta in August, 2007. Postoperatively, she was treated biweekly with docetaxel/nedaplatin combined chemotherapy 32 times.

Obstructive jaundice impedes hepatic microcirculation in mice.

Background/aims: To explore the mechanisms by which postoperative complications frequently occur in patients with obstructive jaundice, we examined the effects of obstructive jaundice on hepatic microcirculation and Kupffer cell activity in mice.

Methodology: Common bile duct ligation and division was performed on C57BL/6 mice to induce obstructive jaundice. One and 2 weeks after surgery, sinusoidal perfusion, leukocyte rolling and sticking in the postsinusoidal venules, and diameters of sinusoids containing blood flow were evaluated using intravital microscopy.

Spermidine/spermine-N1-acetyltransferase ablation protects against liver and kidney ischemia-reperfusion injury in mice.

Expression of spermine/spermidine-N1-acetyltransferase (SSAT), the rate-limiting enzyme of polyamine backconversion cascade, increases after ischemia-reperfusion injuries (IRI). We hypothesized that SSAT plays an important role in the mediation of IRI. To test our hypothesis, wild-type (SSAT-wt) and SSAT-deficient (SSAT-ko) mice were subjected to liver or kidney IRI by ligation of hepatic or renal arteries.

Hepatocyte NF-kappaB activation is hepatoprotective during ischemia-reperfusion injury and is augmented by ischemic hypothermia.

The present study examined the role of hepatocyte NF-kappaB activation during ischemia-reperfusion injury. Second, we evaluated the effects of ischemic hypothermia on NF-kappaB activation and liver injury. C57BL/6 mice underwent 90 min of partial hepatic ischemia and up to 8 h of reperfusion.

Age-dependent responses to hepatic ischemia/reperfusion injury.

The current study explored the concept that adult and pediatric populations differ in their response to major injury. Male C57BL/6 mice of a "young adult" (8-12 weeks) or "mature adult" (12-13 months) age were subjected to partial hepatic ischemia and reperfusion. Mature adult mice displayed significantly more liver injury than young adult mice as assessed histologically and by serum levels of alanine aminotransferase.

Divergent functions of CD4+ T lymphocytes in acute liver inflammation and injury after ischemia-reperfusion.

Hepatic ischemia-reperfusion results in an acute inflammatory response culminating in the recruitment of activated neutrophils that directly injure hepatocytes. Recent evidence suggests that CD4+ lymphocytes may regulate this neutrophil-dependent injury, but the mechanisms by which this occurs remain to be elucidated. In the present study, we sought to determine the type of CD4+ lymphocytes recruited to the liver after ischemia-reperfusion and the manner in which these cells regulated neutrophil recruitment and tissue injury.

Liver-specific pRB loss results in ectopic cell cycle entry and aberrant ploidy.

The liver exhibits an exquisitely controlled cell cycle, wherein hepatocytes are maintained in quiescence until stimulated to proliferate. The retinoblastoma tumor suppressor, pRB, plays a central role in proliferative control by inhibiting inappropriate cell cycle entry. In many cases, liver cancer arises due to aberrant cycles of proliferation, and correspondingly, pRB is functionally inactivated in the majority of hepatocellular carcinomas.

Distinct and sequential upregulation of genes regulating cell growth and cell cycle progression during hepatic ischemia-reperfusion injury.

Ischemia-reperfusion injury (IRI) in liver and other organs is manifested as an injury phase followed by recovery and resolution. Control of cell growth and proliferation is essential for recovery from the injury. We examined the expression of three related regulators of cell cycle progression in liver IRI: spermidine/spermine N-acetyltransferase (SSAT), p21 (a cyclin-dependent kinase inhibitor), and stathmin.

Hepatic expression of S32A/S36A IkappaBalpha does not reduce postischemic liver injury.

Background: Activation of the transcription factor, NF-kappaB, during hepatic ischemia/reperfusion injury is associated with proinflammatory mediator expression and is thought to be one of the initial triggers for the inflammatory response after reperfusion. In the current study, we sought to determine whether in vivo adenoviral transfection of a mutant inhibitor of kappaB-alpha (IkappaBalpha), which cannot be serine phosphorylated or degraded (IkappaBalphaSR), would inhibit NF-kappaB and ameliorate the hepatic inflammatory response to ischemia/reperfusion.

Materials And Methods: Male C57BL/6 mice were subjected to sham surgery or partial hepatic ischemia (90 min) and reperfusion (up to 8 h).

Peroxisome proliferator-activated receptor-alpha regulates postischemic liver injury.

Peroxisome proliferator-activated receptor-alpha (PPARalpha) is a transcription factor that in some in vitro systems has been linked with downregulation of proinflammatory mediators, thus implicating a potential role for PPARalpha in the regulation of inflammatory processes. Hepatic ischemia-reperfusion injury is characterized by an intense acute inflammatory response that is dependent on a number of proinflammatory mediators. PPARalpha is abundantly expressed in hepatic parenchymal cells but not in Kupffer cells.

Cytokine cascades and the hepatic inflammatory response to ischemia and reperfusion.

Ischemia/reperfusion injury of the liver has two distinct phases that contribute to hepatocyte damage. The acute phase is characterized by Kupffer cell production of reactive oxygen species, which results in moderate hepatocyte injury. The later phase includes an intricate cascade of inflammatory events culminating in neutrophil infiltration of the postischemic liver.

Endogenous IL-13 protects hepatocytes and vascular endothelial cells during ischemia/reperfusion injury.

Hepatic ischemia/reperfusion injury involves a complex inflammatory cascade resulting in neutrophil-mediated injury of hepatocytes. Previous studies from our laboratory have established that exogenous administration of the anti-inflammatory cytokines interleukin 10 (IL-10) and IL-13 can ameliorate the inflammatory response and significantly reduce hepatocellular injury. The purpose of the present study was to determine if IL-10 and IL-13 function as endogenous regulators of the hepatic inflammatory response to ischemia/reperfusion.

Specific role of interleukin-1 in hepatic neutrophil recruitment after ischemia/reperfusion.

Hepatic ischemia/reperfusion injury is caused primarily by the products of neutrophils recruited into the liver after reperfusion. The mediators responsible for the development of this inflammatory response are thought to be tumor necrosis factor-alpha and interleukin (IL)-1. Although there is abundant evidence to support a role for tumor necrosis factor-alpha, much less is known about the function of IL-1 in this injury.