Gastrointestinal discomfort and hypotension in a patient with Reutealis trisperma seeds intoxication: A case report.

RATIONALE: Reutealis trisperma is a plant belonging to the Euphorbiaceae family and Reutealis genus and is often mistaken for a plant of the genus Aleurites. Accidental ingestion of R trisperma seeds is relatively rare in Taiwan than that of Vernicia fordii. Mostly, the clinical course of R trisperma seed poisoning is similar to that of V fordii poisoning. Recent studies have shown that the median lethal dose 50 of R trisperma seeds in mice is approximately 4954 mg/kg. R trisperma seed extract has a significant effect on the autonomic nervous system by causing ptosis and disrupting breathing, and affects the central nervous system by reducing motor activity. PATIENT CONCERNS: A 51-year-old man with underlying gout and hepatitis B picked several seeds of R trisperma, which he misidentified at chestnuts, at an elementary school. He prepared soup by boiling 3 to 4 seeds and consumed it. He experienced abdominal pain, vomiting, and watery diarrhea with hypotension. DIAGNOSIS: R trisperma seeds intoxication. INTERVENTIONS: The patient was given a soft diet, input and output were recorded, and intravenous fluid supplements were administered. OUTCOMES: The patient was discharged after 3 days of hospitalization, once a relatively stable condition was achieved. LESSONS: Human poisoning by accidental consumption of R trisperma seeds is relatively rare in Taiwan. It may cause gastrointestinal symptoms and even hypotension. Patients can recover within 2 to 3 days of receiving proper treatment and intravenous fluid infusion.

Ten-eleven translocation 1 dysfunction reduces 5-hydroxymethylcytosine expression levels in gastric cancer cells.

A sixth base, 5-hydroxymethylcytosine (5hmC), is formed by the oxidation of 5-methylcytosine (5mC) via the catalysis of the ten-eleven translocation (TET) protein family in cells. Expression levels of 5hmC are frequently depleted during carcinogenesis. However, the detailed mechanisms underlying the depletion of 5hmC expression in gastric cancer cells remains unclear, and further research is required. The present study examined the expression levels of 5mC and 5hmC and the expression levels of TET1 and TET2 in gastric cancer tissues using immunohistochemistry. The results revealed that 5hmC expression levels were markedly lower in gastric cancer tissues compared with corresponding adjacent normal tissues. Furthermore, a decrease in 5hmC expression levels was associated with a decrease in TET1 protein expression levels in gastric cancer tissues. The ectopic expression level of TET1 may increase the 5hmC expression level in gastric cancer cells. In addition, the results revealed that TET1 protein expression was markedly different in regards to subcellular localization, and mislocalization was significantly associated with the depletion of 5hmC expression levels in gastric cancer. Together, the results of the present study indicated that TET1 dysfunction reduces 5hmC expression levels, and this phenomenon may serve a crucial role in gastric cancer progression.

Analysis of gallstone disease after gastric cancer surgery.

BACKGROUND: The incidence rate of newly developed gallstone disease after gastrectomy for gastric cancer is thought to be higher than that in the general population. However, the presentation and management of these gallstones remain under debate, and the role of prophylactic cholecystectomy remains questionable. METHODS: Data on adult patients who were diagnosed with gastric cancer and received gastrectomy between 2000 and 2011 were extracted from the Taiwan National Health Insurance Research Database. A patient was excluded if he or she had gallstone disease or received cholecystectomy before the index date. The incidence of newly developed gallstone disease and its subsequent management were recorded. Data were analyzed to evaluate the factors associated with gallstone development and treatment options. RESULTS: A total of 17,325 gastric cancer patients who underwent gastrectomy were eligible for analysis. During the follow-up period (mean 4.1 years; median, 2.9 years), 1280 (7.4%) patients developed gallstone disease and 560 (3.2%) patients subsequently underwent cholecystectomy. The in-hospital mortality for cholecystectomy was 1.8% (10/560). Development of gallstone disease was associated with older age, total gastrectomy, duodenal exclusion, diabetes, cirrhosis, and more comorbidities. Factors associated with the use of cholecystectomy to treat gallstone disease included younger age, fewer comorbidities, medical center admission, and presentation as cholecystitis. CONCLUSIONS: Although few patients required further gallbladder removal after gastrectomy for gastric malignancy, the increased mortality rate for subsequent cholecystectomy was worth noting. The decision to undergo prophylactic cholecystectomy might be individualized based upon patient characteristics and the surgeon's discretion.

Isocitrate Dehydrogenase 2 Dysfunction Contributes to 5-hydroxymethylcytosine Depletion in Gastric Cancer Cells.

The isocitrate dehydrogenase (IDH) family of enzymes comprises of the key functional metabolic enzymes in the Krebs cycle that catalyze the conversion of isocitrate to α-ketoglutarate (α-KG). α-KG acts as a cofactor in the conversion of 5-methylcytosine (5mC) to 5-hydroxymethylcytosine (5hmC). However, the relationship between 5hmC and IDH in gastric cancer remains unclear. Our study revealed that the 5hmC level was substantially lower and 5mC level was slightly higher in gastric cancer tissues; however, 5-formylcytosine (5fC) and 5-carboxylcytosine (5caC) levels did not change significantly in these tissues. We further examined the expression levels of IDH1 and IDH2 in gastric cancer tissues and observed that IDH2 levels were significantly lower in gastric cancer tissues than in the adjacent normal tissues. The ectopic expression of IDH2 can increase 5hmC levels in gastric cancer cells. In conclusion, our results suggested that IDH2 dysfunction is involved in 5hmC depletion during gastric cancer progression.

Effect of methoxychlor on Ca²âº homeostasis and apoptosis in HA59T human hepatoma cells.

Methoxychlor, an organochlorine pesticide, is thought to be an endocrine disrupter that affects Ca²âº homeostasis and cell viability in different cell models. This study explored the action of methoxychlor on cytosolic free Ca²âº concentrations ([Ca²âº]i) and apoptosis in HA59T human hepatoma cells. Fura-2, a Ca²âº-sensitive fluorescent dye, was applied to measure [Ca²âº]i. Methoxychlor at concentrations of 0.1-1 µM caused a [Ca²âº]i rise in a concentration-dependent manner. Removal of external Ca²âº abolished methoxychlor's effect. Methoxychlor-induced Ca²âº influx was confirmed by Mn²âº-induced quench of fura-2 fluorescence. Methoxychlor-induced Ca²âº entry was inhibited by nifedipine, econazole, SK&F96365, and protein kinase C modulators. Methoxychlor killed cells at concentrations of 10-130 µM in a concentration-dependent fashion. Chelation of cytosolic Ca²âº with 1,2-bis(2-aminophenoxy) ethane-N,N,N',N'-tetraacetic acid/AM (BAPTA/AM) did not prevent methoxychlor's cytotoxicity. Methoxychlor (10 and 50 µM) induced apoptosis concentration-dependently as determined by using Annexin V/propidium iodide staining. Together, in HA59T cells, methoxychlor induced a [Ca²âº]i rise by inducing Ca²âº entry via protein kinase C-sensitive Ca²âº-permeable channels, without causing Ca²âº release from stores. Methoxychlor also induced apoptosis that was independent of [Ca²âº]i rises.

Balloon-occluded retrograde transvenous obliteration for intractable gastric variceal bleeding.

Balloon-occluded retrograde transvenous obliteration (BRTO) is an interventional radiologic technique that obliterates gastric varices (GV) from draining veins under balloon occlusion. A 54-year-old man presented with Stage IV hepatocellular carcinoma and tumor thrombi in main portal vein. Intractable GV bleeding had no response to repeated endoscopic sclerotherapy and pharmacotherapy well. Additionally, his medical condition could not allow transjugular intrahepatic portosystemic shunt or surgical portal decompression. Due to spontaneous gastrorenal shunt proved with abdominal computed tomography, we conducted BRTO to prevent further bleeding. The immediate postprocedural venogram showed total occlusion of the gastrorenal shunt and no visualization of the GV. Follow-up endoscopy was performed at 1 month, 2 months, and 4 months after BRTO. It revealed shrinkage of gastric varices and no worsening of esophageal varices after 4 months of BRTO. The patient was free from repeated GV bleeding for 4 months. Our experience proved BRTO could be the other effective treatment for intractable GV bleeding.

Number of involved lymph nodes is important in the prediction of prognosis for primary duodenal adenocarcinoma.

BACKGROUND: The significance of lymph node involvement regarding the prognosis of primary duodenal adenocarcinoma remains controversial. This study aims to evaluate the prognostic accuracy of nodal metastasis using the seventh edition American Joint Committee on Cancer staging system in patients with primary duodenal adenocarcinoma. METHODS: Between 1993 and 2010, 36 patients who had undergone surgical resection for primary duodenal adenocarcinoma at the Kaohsiung Veterans General Hospital were retrospectively reviewed. RESULTS: The median disease-free survival for all patients was 19 months and the median overall survival was 21 months. Lymph node metastases were found in 26 (72%) of the patients, and 14 patients (39%) patients had in excess of three positive lymph nodes (N2). Patients with N2 disease had significantly reduced overall survival, as compared to patients with three or fewer positive lymph nodes (N1; p = 0.036). In univariate analysis, factors including age >75 years, body weight loss, tumor size ≤ 4 cm, N2 disease and lymph node ratio >0.4 predicted shorter overall survival. Multivariate analysis demonstrated that N2 and lymph node ratio >0.4 are significant risk factors associated with overall survival (p = 0.026 and p = 0.042 respectively). N2 is also the only independent predictive factor for disease-free survival (p = 0.023). CONCLUSION: Subdivision of metastatic lymph nodes into N1 and N2 improves predictive ability. The seventh edition American Joint Committee on Cancer staging system is applicable in the present study with regard to the prediction of the prognosis for primary duodenal adenocarcinoma.

Desipramine-induced Ca-independent apoptosis in Mg63 human osteosarcoma cells: dependence on P38 mitogen-activated protein kinase-regulated activation of caspase 3.

1. It has been shown that the antidepressant desipramine is able to induce increases in [Ca(2+)](i) and cell death in MG63 human osteosacroma cells, but whether apoptosis is involved is unclear. In the present study, the effect of desipramine on apoptosis and the underlying mechanisms were explored. It was demonstrated that desipramine induced cell death in a concentration- and time-dependent manner. 2. Cells treated with 100-800 mmol/L desipramine showed typical apoptotic features, including an increase in sub-diploid nuclei and activation of caspase 3, indicating that these cells underwent apoptosis. Immunoblotting revealed that 100 mmol/L desipramine activated extracellular signal-regulated kinase (ERK), c-Jun N-terminal kinase (JNK) and p38 mitogen-activated protein kinase (MAPK). Although pretreatment of cells with 20 mmol/L PD98059 (an ERK inhibitor) or 20 mmol/L SP600125 (an inhibitor of JNK) did not inhibit cell death, the addition of 20 mmol/L SB203580 (a p38 MAPK inhibitor) partially rescued cells from apoptosis. Desipramine-induced caspase 3 activation required p38 MAPK activation. 3. Pretreatment of cells with BAPTA/AM (20 mmol/L) to prevent desipramine-induced increases in [Ca(2+)](i) did not protect cells from death. 4. The results of the present study suggest that, in MG63 human osteosarcoma cells, desipramine causes Ca(2+)-independent apoptosis by inducing p38 MAPK-associated activation of caspase 3.

Econazole-evoked [Ca2+]i rise and non-Ca2+-triggered cell death in rabbit corneal epithelial cells (SIRC).

The effects of econazole, an antifungal drug applied for treatment of keratitis and mycotic corneal ulcer, on cytosolic-free Ca(2+) concentrations ([Ca(2+)](i)) and viability of corneal cells was examined by using SIRC rabbit corneal epithelial cells as model. [Ca(2+)](i) and cell viability were measured by using the fluorescent dyes fura-2 and WST-1, respectively. Econazole at concentrations > or = 1 microM increased [Ca(2+)](i) in a concentration-dependent manner. The Ca(2+) signal was reduced partly by removing extracellular Ca(2+). The econazole-induced Ca(2+) influx was insensitive to L-type Ca(2+) channel blockers and protein kinase C modulators. In Ca(2+)-free medium, after pretreatment with 20 microM econazole, [Ca(2+)](i) rises induced by 1 microM thapsigargin (an endoplasmic reticulum Ca(2+) pump inhibitor) were abolished. Conversely, thapsigargin pretreatment also abolished econazole-induced [Ca(2+)](i) rises. Inhibition of phospholipase C with 2 microM U73122 did not change econazole-induced [Ca(2+)](i) rises. At concentrations between 10 and 80 microM, econazole killed cells in a concentration-dependent manner. The cytotoxic effect of 20 microM econazole was not reversed by prechelating cytosolic Ca(2+) with BAPTA. This shows that in SIRC cells econazole induces [Ca(2+)](i) rises by causing Ca(2+) release from the endoplasmic reticulum and Ca(2+) influx from unknown pathways. Econazole-caused cytotoxicity was independent from a preceding [Ca(2+)](i) rise.

Thimerosal-induced apoptosis in human SCM1 gastric cancer cells: activation of p38 MAP kinase and caspase-3 pathways without involvement of [Ca2+]i elevation.

Thimerosal is a mercury-containing preservative in some vaccines. The effect of thimerosal on human gastric cancer cells is unknown. This study shows that in cultured human gastric cancer cells (SCM1), thimerosal reduced cell viability in a concentration- and time-dependent manner. Thimerosal caused apoptosis as assessed by propidium iodide-stained cells and caspase-3 activation. Although immunoblotting data revealed that thimerosal could activate the phosphorylation of extracellular signal-regulated kinase, c-Jun NH2-terminal protein kinase, and p38 mitogen-activated protein kinase (p38 MAPK), only SB203580 (a p38 MAPK inhibitor) partially prevented cells from apoptosis. Thimerosal also induced [Ca2+](i) increases via Ca2+ influx from the extracellular space. However, pretreatment with (bis(o-aminophenoxy)ethane-N,N,N',N'-tetraacetate)/AM, a Ca2+ chelator, to prevent thimerosal-induced [Ca2+](i) increases did not protect cells from death. The results suggest that in SCM1 cells, thimerosal caused Ca2+-independent apoptosis via phosphorylating p38 MAPK resulting in caspase-3 activation.