ObjectiveTo assess the surgical results and implications of clinicopathologic features on the prognosis of patients with hepatic matastases from gastric adenocarcinoma. MethodsNinety one of 834 patients with primary gastric cancer were diagnosed with synchronous ( n =79) or metachronous ( n =12)hepatic metastases. Twenty-one cases underwent hepatectomy for the metastasis. Results The actuarial 1-year, 3-year survival rates after hepatic resection were respectively 69% and 30%. Solitary and metachronous metastases were significant determinants for a favorable prognosis after hepatic resection. Pathologically, tumor pseudomembrane was found in 13 out of 21 patients which was associated with a favorable prognosis. ConclusionsSolitary and metachronous hepatic metastases from gastric cancer should be treated by a surgical approach which confers a good prognosis. The formation of pseudomembrane of the metastatic tumor predicts a favourable postoperative survival.

Objective To evaluate the complication rate of secondary surgery in patients with benign thyroid disease. Methods From June 1992 to June 2003, 65 patients underwent reoperation. Operative procedures. pathology and complications were reviewed. Results The first surgery was unilateral in 27 cases (41.5%), bilateral in 38 (58.5%). Reoperation identified carcinoma in 8 cases with complications developed in 8 cases and left over permanent in 1 case (1.5%). Conclusion The complication rate of second operation is higher than that of first thyroid surgery, but still acceptable.

Background The key enzymes of serine synthesis pathway (SSP) play an important role in tumor growth, proliferation, and invasion, but their roles in arsenic carcinogenesis are unclear. Objective To observe the effects of NaAsO₂ treatment on the expressions of key enzymes [such as phosphoglycerate dehydrogenase (PHGDH), phosphoserine aminotransferase 1 (PSAT1), and phosphoserine phosphatase (PSPH)] of SSP and on the ability to proliferate and migrate in human immortalized skin keratinocytes (HaCaT) and NaAsO₂-induced malignantly transformed HaCaT (T-HaCaT), and to explore the roles of SSP key enzymes in arsenic carcinogenesis. Methods (1) The T-HaCaT cells constructed earlier by our research team were divided into a passage control (0 μmol·L⁻¹ NaAsO₂) group, a T-HaCaT (0.5 μmol·L⁻¹ NaAsO₂) group, a NCT503 (PHGDH inhibitor, 25 μmol·L⁻¹) group, and a NCT503 (25 μmol·L⁻¹) + T-HaCaT (0.5 μmol·L⁻¹ NaAsO₂) group. Western blotting was used to detect the protein expression levels of SSP key enzymes in the passage control group and the T-HaCaT group. CCK8 assay and cell scratch test were used to detect the proliferation and migration rates of cells in each group respectively. (2) Well-grown logarithmic-phase HaCaT cells were treated with 0, 0.625, 1.25, and 2.5 μmol·L⁻¹ NaAsO₂ for 0, 24, 48, and 72 h to detect cell proliferation rate and protein expression levels of SSP key enzymes. In the subsequent experiment, HaCaT cells were pretreated with 25 μmol·L⁻¹ NCT503 for 6 h, and then treated with 2.5 μmol·L⁻¹ NaAsO₂ for 72 h continuously. The experimental groups included a control (0 μmol·L⁻¹ NaAsO₂) group, an exposure (2.5 μmol·L⁻¹ NaAsO₂) group, a pretreatment (25 μmol·L⁻¹ NCT503) group, and a pretreatment (25 μmol·L⁻¹ NCT503) + exposure (2.5 μmol·L⁻¹ NaAsO₂) group, to detect the proliferation rate of cells in each group. Results The protein expression level of PHGDH in the T-HaCaT group were 1.60 times higher than that in the passage control group (P<0.05), and its proliferation rate (177.51%±14.69%) and migration rate (53.85%±0.94%) were also higher than the passage control group’s (100.00%±0.00% and 24.30%±2.26%) (both Ps<0.05), respectively. After the NCT503 intervention, the proliferation rate (144.97%±8.08%) and migration rate (35.80%±0.99%) of cells in the NCT503 + T-HaCaT group were lower than those in the T-HaCaT group (both P<0.05). The proliferation rate of HaCaT cells after NaAsO₂ exposure for 72 h increased with the increase of exposure concentration (r=0.862, P<0.05), and consistently, the protein levels of SSP key enzymes in HaCaT cells in each exposure group were higher than those in the control group (all P<0.05). The proliferation rate of HaCaT cells treated with 2.5 μmol·L⁻¹ NaAsO₂ increased with the extension of exposure time (r=0.775, P<0.05), which was consistent with the changes of PHGDH levels in cells. After the NCT503 intervention, the proliferation rate of the pretreatment + exposure group was significantly lower than that of the exposure group (P<0.05). Conclusion The key enzymes of SSP may play an important role in the proliferation of T-HaCaT cells induced by NaAsO₂.