Objective To explore the expression of heme oxygenase-1 (HO-1) in gastric mucosa of patient with portal hypertensive gastropathy (PHG),and its role in the pathogenesis of PHG.Methods The specimens were obtained from the gastric mucosa of 22 healthy subjects,20 portal hypertension (PHT) without PHG,and 22 PHG patients.Histological changes of the gastric mucosa were detected,and portal venous flow (PVF) was measured.The expression of HO-1 protein in gastric mucosal specimens was assessed by immunohistochemistry and Western blot analysis,respectively.The relationship between HO-1 expression and PHG severity score,HO-1 expression and PVF,PHG severity score and clinical parameters were investigated.Results HO-1 protein expression in gastric mucosa of PHG and PHT was significantly higher than that of the control (P ＜ 0.05),while there was no significant difference in this variable between PHG and PHT (P ＞ 0.05).The positive correlation was detected between HO-1 expression and PHG severity score in PHG patients (r =0.459,P ＜0.05),however,PHG severity score was irrelevant to severity of esophageal varice (r =0.059,P ＞ 0.05) or to Child-Pugh classification (r =-0.001,P ＞ 0.05).Of all the patients with PHT and PHG,no significant correlation was found between HO-1 expression and PVF (r =0.071,P ＞ 0.05).Conclusion HO-1 protein is up-regulated in gastric mucosa of PHG patients,which may contribute to gastric circulation disorder of PHG.

Objective To explore the frequencies of MPL exon 10 mutations in JAK2 V617F-negative myeloproliferative neoplasms patients. Methods MPLW515K/L was processed through allele-specific PGR combined with direct sequence analysis. The mutations of others MPL exon 10 were detected by single strand conformation polymorphism PGR (PCR-SSCP) combined with direct sequencing. Results Of the 103 patients with JAK2 V617F-negtive myeloproliferative neoplasms patients, 1 carried MPLW515K mutation (TGG→AAG)in PMF; 1 was found to have new mutation (CTGGTGATCGCT insert) in ET and have homozygous mutation. Conclusion JAK2 V617F-negtive myeloproliferative neoplasms patients carried additional mutations in addition to W515K/L mutations in MPL exon 10, but its frequency of mutation is low.

【Objective】 To make bioinformatics analysis of inflammatory cardiomyopathy so as to screen out hub genes related to etiology and therapeutic targets. 【Methods】 Differential expression analysis of inflammatory cardiomyopathy gene chip data from Gene Expression Omnibus （GEO） Database was carried out via GEO2R tool. Protein-protein interaction（PPI）network and hub genes identification were realized by String database and CytoHubba. GO and KEGG enrichment analysis for functional annotation and pathway analysis of hub genes were conducted by R language. Web-based enrichment analysis platform Enrichr and Drug Signatures database were applied to screen out candidate drugs targeting hub genes for inflammatory cardiomyopathy. 【Results】 The 149 DEGs were statistically significant， among which 44 were upregulated and 105 were downregulated. To identify hub genes， PPI network consisting of 37 nodes and 116 edges was constructed， and 16 hub genes were NDUFB7， POLR2L， NDUFS7， UQCR11， NDUFA13， NDUFA2， PHPT1， NDUFB10， UBA52， ATP5D， NDUFA3， COX6B1， POLR2J， COX4I2， AURKAIP1 and MRPL41. Hub genes were enriched to 113 different GO terms， and the most significant terms were mitochondrial ATP synthesis coupled electron transport， respiratory electron transport chain， oxidative phosphorylation， respiratory chain， mitochondrial inner membrane， NADH dehydrogenase activity and oxidoreductase activity. DEGs were enriched to 13 different signal pathways， including oxidative phosphorylation， non-alcoholic fatty liver disease， diabetic cardiomyopathy， and cardiac muscle contraction. We screened out candidate drugs targeting hub genes， namely， metformin hydrochloride， clindamycin， and hydralazine. 【Conclusion】 Hub genes screened out by decoding the expression profiles are convolved in the etiology and mechanism of inflammatory cardiomyopathy， which might serve as latent therapeutic targets and benefit patients with inflammatory cardiomyopathy.