ABSTRACT.A previous study has revealed that miR-29c functions as a tumor suppressor in hepatocellular carcinoma (HCC), but the clinical significance and prognostic value of miR-29c in HCC have not been investigated. Paired human HCC tissues and adjacent noncancerous tissues were obtained from 91 patients, between 2008 to 2014. Quantitative real-time PCR (qRT-PCR) was used to analyze miR-29c expression. Kaplan-Meier survival plots and log-rank tests were used to assess differences in the overall survival of different subgroups of HCC patients. It was observed that miR-29c expression was remarkably decreased in HCC tissues relative to that in normal hepatic tissues (P < 0.001). The low miR-29c level was significantly associated with histologic grade (P = 0.001), microvascular invasion (P = 0.005), and tumor stage (P < 0.001). Kaplan-Meier analysis showed that decreased miR-29c expression correlated with shorter overall survival (P = 0.002). Multivariate Cox regression analysis showed that decreased miR-29c 2 C.W. Dong et al. Genetics and Molecular Research 15 (3): gmr.15037316 expression (hazard ratio = 2.19, 95%CI = 1.361-6.779, P = 0.025) was independently associated with poor survival in HCC. Our findings demonstrate that miR-29c expression is significantly downregulated in HCC patients and that miR-29c can act as an independent predictor of unfavorable clinical outcome.
Gastrointestinal: Segmental portal hypertension caused by pancreatic mucinous cystadenomaA 30-year-old woman was admitted to our hospital for abdominal pain of two years duration. She had no history of upper gastrointestinal bleeding and her laboratory tests yielded normal results. Contrast-enhanced computerized tomography (CT) demonstrated a multilobular cystic tumor at the pancreatic tail, and massive splenomegaly with grossly dilated and tortuous veins ( Fig. 1a). CT angiogram demonstrated the isolated occlusion of splenic vein, which caused the dilation of the right and left gastro-omental veins, and a venous arch was developed between them, forming a congested vascular bridge between the splenic and portal veins (Fig. 1b). The diagnosis of pancreatic segmental portal hypertension caused by pancreatic tumor was rendered.During operation, massive dilation of right and left gastroomental veins was detected (Fig. 1c). Distal pancreatectomy and splenectomy were performed successfully and pathologic exami-nation confirmed the diagnosis of pancreatic mucinous cystadenoma. The patient was followed up to 3 years without evidence of recurrence. Segmental portal hypertension because of isolated splenic vein obstruction is a rare, but important entity as it is the only curable cause of portal hypertension by splenectomy. It is more often caused by pancreatic disease and constitutes 5-10% of all patients with portal hypertension. The diagnosis should be suspected in patients with gastroesophageal varices, but without signs of a liver disease, especially if isolated gastric varices are found. a b c Figure 1 (a) Contrast-enhanced computed tomography (CT) demonstrated a multilobular cystic tumor at the pancreatic tail, and massive splenomegaly with grossly dilated and tortuous veins; (b) CT angiogram demonstrated the isolated occlusion of splenic vein, and a venous arch was developed between the dilated right and left gastro-omental veins, forming a congested vascular bridge between the splenic and portal veins; (c) massive dilation of right and left gastro-omental veins was detected during operation.
Boerhaave's syndrome (spontaneous esophageal perforation) involving a complete and transmural laceration caused by a rapid rise in intraluminal pressure in the distal esophagus is a rare but serious condition with a mortality rate of 20~40%. Late diagnosis or misdiagnosis occurs in more than 50% patients owing to the rarity of classic Mackler's triad of stretching vomiting, low thoracic pain and subcutaneous emphysema. Herein, we reported a case of Boerhaave's syndrome in a 71-year-old man presenting chest pain, dyspnea on exertion and orthopnea for 1 day after stretching vomiting. Chest X-ray and computed tomographic scan showed subcutaneous emphysema of neck, pneumomediastinum and lobulated pleural effusion suggestive of esophageal perforation. Immediate left thoracotomy with primary repair for a 2 cm esophageal perforation over left anterolateral side above the esophagogastric junction was performed. The culture of pleural effusion yielded Klebsiella pneumoniae, Citrobacter koseri and Pseudomonas fluorecens. He was discharged on the twenty-sixth day.
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