Preoperative prognostic nutritional index as an independent prognostic factor for resected ampulla of Vater cancer.

INTRODUCTION: Prognostic nutritional index (PNI) reflects the nutritional and immunologic status of the patients. The clinical application of PNI is already well-known in various kinds of solid tumors. However, there is no study investigating the relationship between PNI and oncological outcome of the resected ampulla of Vater (AoV) cancer. MATERIALS AND METHODS: From January 2005 to December 2012, the medical records of patients who underwent pancreaticoduodenectomy for pathologically confirmed AoV cancer were retrospectively reviewed. Long-term oncological outcomes were compared according to the preoperative PNI value. RESULT: A total of 118 patients were enrolled in this study. The preoperative PNI was 46.13±6.63, while the mean disease-free survival was 43.88 months and the mean disease-specific survival was 55.3 months. In the multivariate Cox analysis, initial CA19-9 (p = 0.0399), lymphovascular invasion (p = 0.0031), AJCC 8th N-stage (p = 0.0018), and preoperative PNI (p = 0.0081) were identified as significant prognostic factors for resected AoV cancer. The disease-specific survival was better in the high preoperative PNI group (≤48.85: 40.77 months vs. >48.85: 68.05 months, p = 0.0015). A highly accurate nomogram was developed based on four clinical components to predict the 1, 3, and 5-year disease-specific survival probability (C-index 0.8169, 0.8426, and 0.8233, respectively). CONCLUSION: In resected AoV cancer, preoperative PNI can play a significant role as an independent prognostic factor for predicting disease-specific survival.

Toxic effects of Microcystis cell extracts on the reproductive system of male mice.

In this paper, the reproductive toxicity of male mice treated with Microcystis aeruginosa cell extracts containing microcystins was examined. In contrast to the control group, male mice exposed intraperitoneally to 3.33 or 6.67 microg microcystins/kg body weight for 14 days had decreased mean body weight, and the mean absolute weight of the testes and epididymides was decreased. However, the mean relative weight of the testes increased compared to the controls. In addition, histological examination of microcystin-treated mice indicated that the testes were damaged and the space between the seminiferous tubules was more pronounced compared to control mice. The quality of mature sperm in the seminiferous tubules was also decreased in treated mice compared with the control group. Further studies showed that motility and viability of the sperm from microcystin-treated mice were reduced, but no significant difference was found in the concentration and abnormality of the sperm from treated mice compared to the control. This study indicated that microcystins had numerous toxic effects on the reproductive system of male mice.

Microcystins cause embryonic toxicity in mice.

Microcystins produced by freshwater cyanobacteria are potent hepatotoxins and can cause animal intoxications and human illnesses. In the present study, the effects of microcystins on the embryonic development of Kunming mice were determined using cell extracts of Microcystis aeruginosa from the Nanwan reservoir, China. Forty-eight pregnant mice were divided into four groups of 12 mice. Pregnant mice in three experimental groups were injected intraperitoneally with cell extracts at doses equivalent to 3, 6, or 12 microg microcystins/kg body weight daily from gestational days 6-15, while the mice in the control group were injected on the same schedule with sterilized saline. Mice were killed on the 18th day of gestation and embryonic and fetal developmental indexes checked. The fetal mice were also examined for anomalies of external, skeletal, and internal organs. The results demonstrated a significant decrease in body weight gain of pregnant mice in the 12 microg/kg dose group when compared to the control group (p<0.05). Differences in mean body weight, body length, and tail length of the fetuses were also found in these two groups (p<0.05). However, no significant difference in these characteristics was detected in the 6 or 3 microg/kg dose groups when compared to the control group (p>0.05). Four fetuses in the 6 microg/kg body dose group were found to have a curving tail. Additionally, petechial hemorrhage and hydropic degeneration were observed in the livers of fetuses in the 6 and 12 microg/kg experimental groups. These results suggested that microcystins had both maternal and embryonic toxicity in mice.

Oral exposure to Microcystis increases activity-augmented antioxidant enzymes in the liver of loach (Misgurnus mizolepis) and has no effect on lipid peroxidation.

Recently, eutrophication has induced severe cyanobacterial blooms in the Naktong River, the second largest river of Korea. In the present study, lipid peroxidation and the antioxidant enzymes superoxide dismutase, catalase, and glutathione peroxidase, were evaluated in the liver of loach (Misgurnus mizolepis) that were orally exposed to a low dose of Microcystis through dietary supplementation with bloom scum. Loach received 75 mg of dry cells/kg body weight mass (equal to 10 microg microcystin-RR/kg body mass), for 28 days under controlled conditions. Antioxidant enzymatic activity and lipid peroxidation were measured after termination of exposure. The activities of antioxidant enzyme were significantly increased in the livers of toxin-exposed loach after 28 days of exposure, as compared to control fish. However, lipid peroxidation remained stable in both groups. These results suggest that antioxidant enzymes were able to eliminate oxidative stress induced by low concentrations of microcystins and to prevent increased lipid peroxidation in the liver of loach.

Subchronic oral toxicity of microcystin in common carp (Cyprinus carpio L.) exposed to Microcystis under laboratory conditions.

The subchronic oral toxicity of microcystin in common carp (Cyprinus carpio L.) was investigated in this study. The fish (mean body weight of 322+/-36 g, n=10) were orally exposed to Microcystis by feeding with bloom scum at a dose of 50 microg microcystins/kg body weight under laboratory conditions for 28 days. Growth assay results showed that microcystin could completely inhibit the growth of carp, but failed to change the fish hepatosomatic index. Ultrastructural examination by electron microscope revealed severe damage in hepatocytes derived from the treated fish. Serum biochemical assays with commercial kits indicated that alanine aminotransferase and aspartate aminotransferase activities were significantly increased as compared to control levels, but gamma-glutamyl transferase, alkaline phosphatase and lactate dehydrogenase activities remained unchanged. Protein phosphatase inhibition assay revealed that the microcystin concentrations were 261.0+/-108.3 ng microcystin-LR equivalent/g fresh weight in hepatopancreas and 38.3+/-12.3 ng microcystin-LR equivalent/g fresh weight in muscle. The latter is above the limit recommended by the World Health Organization for human consumption. Therefore, we recommend that a warning system be instituted for announcing the occurrence of microcystin-producing water bloom and the possible risk of human intoxication.