Ulcerative colitis with inflammatory polyposis in a teenage boy: a case report.

Ulcerative colitis in addition to inflammatory polyposis is common. The benign sequel of ulcerative colitis can sometimes mimic colorectal carcinoma. This report describes a rare case of inflammatory polyposis with hundreds of inflammatory polyps in ulcerative colitis which was not easy to distinguish from other polyposis syndromes. A 16-year-old Chinese male suffering from ulcerative colitis for 6 mo underwent colonoscopy, and hundreds of polyps were observed in the sigmoid, causing colonic stenosis. The polyps were restricted to the sigmoid. Although rectal inflammation was detected, no polyps were found in the rectum. A diagnosis of inflammatory polyposis and ulcerative colitis was made. The patient underwent total colectomy and ileal pouch anal anastomosis. The patient recovered well and was discharged on postoperative day 8. Endoscopic surveillance after surgery is crucial as ulcerative colitis with polyposis is a risk factor for colorectal cancer. Recognition of polyposis requires clinical, endoscopic and histopathologic correlation, and helps with chemoprophylaxis of colorectal cancer, as the drugs used postoperatively for colorectal cancer, ulcerative colitis and polyposis are different.

Inhibition of Pim-1 attenuates the proliferation and migration in nasopharyngeal carcinoma cells.

OBJECTIVE: To explore the role of proto-oncogene Pim-1 in the proliferation and migration of nasopharyngeal carcinoma (NPC) cells. METHODS: Pim-1 expressions in NPC cell lines CNE1, CNE1-GL, CNE-2Z and C666-1 were examined by RT-PCR, western blotting and immunoflucesence, respectively. After CNE1, CNE1-GL and C666-1 cells were treated with different concentrations of Pim-1 special inhibitor, quercetagetin, the cell viability, colony formation rate and migration ability were analyzed. RESULTS: Pim-1 expression was negative in well-differentiated CNE1 cells, whereas expressed weakly positive in poor-differentiated CNE-2Z cells and strongly positive in undifferentiated C666-1 cells. Interestingly, CNE1-GL cells that derived from CNE1 transfected with an Epstein Barr virus latent membrane protein-1 over-expression plasmid displayed stronger expression of Pim-1. Treatment of CNE1-GL and C666-1 cells with quercetagetin significantly decreased the cell viability, colony formation rate and migration ability but not the CNE1 cells. CONCLUSIONS: These findings suggest that Pim-1 overexpression contributes to NPC proliferation and migration, and targeting Pim-1 may be a potential treatment for anti-Pim-1-expressed NPCs.

[Pathology of myocardial fatty infiltration: an autopsy report from 117 cases].

OBJECTIVE: To explore the risk factors related to the formation of myocardial fatty infiltration and possible pathological consequences. METHODS: The macroscopic and microscopic findings in 117 autopsy cases with myocardial fatty infiltration were examined during October, 2001 to June, 2009. RESULTS: There was a significant positive correlation between the macroscopic grading of subepicardial adipose tissue and the microscopic myocardial fatty infiltrative degree(r(s) = 0.57, P < 0.01) but there was no correlations between the myocardial fatty infiltrative degree and age as well as coronary arteriosclerosis (all P > 0.05). The percent of myocardial atrophy was 39.32% (46/117), and the rate of myocardial atrophy in mild myocardial fatty infiltration group (13/63, 20.63%) was significantly lower than that in moderate myocardial fatty infiltration group (22/39, 34.92%; chi(2) = 12.14, P < 0.01) and in severe myocardial fatty infiltration group (11/15, 73.33%; chi(2) = 13.42, P < 0.01). There were 28 sudden cardiac deaths among the 117 cases including 6 deaths due to myocardial fatty infiltration. CONCLUSIONS: Myocardial fatty infiltration is often associated with myocardial atrophy, even with sudden cardiac death but is not an accompanying pathologic changes of aging and coronary arteriosclerosis.

[Pathology of accidental electrocution: an autopsy study of 16 cases].

OBJECTIVE: To study the pathologic findings seen in lethal cases due to accidental electrocution. METHODS: The macroscopic and microscopic findings in 16 autopsy cases died of electrocution encountered during the period from January, 2001 to July, 2008 were retrospectively reviewed. RESULTS: Typical electric marks were found on gross examination in 5 of the 16 cases studied. Histologically, 11 of the 16 cases showed evidence of electric burn. The morphologic features of atypical electric marks varied. Simple epidermal exfoliation and color changes were relatively common. Pathologic changes in internal viscera included disarray of myocardial fibers. Rupture of myocardial fibers was readily identified than in non-electrocution death. Sometimes, focal interstitial hemorrhage and polarization of endothelial cells were seen. CONCLUSIONS: The electric marks on the skin, as confirmed by histologic examination, remain important sequelae of electrocution. The pathologic changes seen in myocardium provide additional clues to the diagnosis.

[Histopathological characterization of drug-related death].

OBJECTIVE: To study the histopathological changes in drug-related death cases in order to provide valuable information for its diagnosis. METHODS: Thirty cases of drug-related death were collected for systemic autopsy and histopathology examination. Ante mortem history and other informations of each case were also reviewed and analyzed. RESULTS: Injection marks, emaciation, asphyxia and histopathological changes in critical organs and tissues correlated with addiction behavior. In the 30 cases, 20% died of diseases, 33.3% acute drug intoxication, 26.7% quitting drug, 10% sudden death, and 10% outside violence. CONCLUSION: Systemic autopsy and histopathology examination in drug-related death are useful for determination of the cause of death in these cases.