[Relationship between c-kit mRNA expression and prognosis in patients with rectal carcinoma].

Objective: To investigate the correlation between c-kit mRNA expression and prognosis in patients with rectal carcinoma. Methods: The expression of c-kit mRNA in rectal carcinoma tissues(n=66) was detected by multiplex branched-DNA liquid chip method. According to the expression level, the patients were classified into the c-kit mRNA high expression group and the low group. We analyzed the relationship between the c-kit mRNA expression and the clinicopathological characteristics of patients, as well as the factors affecting patients'prognosis. Results: Of the 66 rectal carcinoma patients, 18(27.3%)cases were c-kit mRNA high expression. No significant correlation was found between the c-kit mRNA expression and gender, age, preoperative carcinoembryonic antigen, preoperative hemoglobin, distance to verge, lymph node metastasis, tumor thrombus, T stage, TNM stage and tumor differentiation (P>0.05). In follow-up, 34 patients died, 32 patients and 36 patients were recurrence or metastasis. The 1-, 3-, 5-year overall survival(OS) of c-kit mRNA high expression group were 100.0%, 77.8%, 77.8%, respectively, while those of the low one were 93.8%, 56.3%, 45.8%, respectively. The difference was statistically significant(P=0.025). Lymph node metastasis, T stage and TNM stage were also significant associated with OS(P<0.05). The 1-, 3-, 5-year disease free rate (DFS)of the c-kit mRNA high expression group were 100.0%, 77.8% and 77.8%, respectively, while those of the low one were 77.1%、43.8% and 41.7%, respectively, and the difference between the two groups was significant (P=0.044). As a reslut, c-kit mRNA expression (P=0.038) and TNM stage (P=0.039) were the independent prognostic factors affecting the OS in rectal cancer patients. Conclusions: Low expression of c-kit was associated with poor prognosis of rectal carcinoma. And the mechanism underlying this phenomenon deserves further exploration.

Cytochrome c oxidase subunit VIIb as a potential target in familial hypercholesterolemia by bioinformatical analysis.

OBJECTIVE: The aim of the study is to explore the potential familial hypercholesterolemia markers by comparing with healthy controls. MATERIAL AND METHODS: We downloaded the gene expression profile GSE13985 from Gene Expression Omnibus database including five patients diagnosed with familial hypercholesterolemia (FH) and five age, sex, status matched controls. We applied t-test, Wilcox test and Fisher test in Multtest package of R language to identify the differentially expressed genes (DEGs) with p < 0.05 and |logFC| > 1, and constructed the interaction network of the top 3 up- and down-regulated genes using STRING. Besides, the modules of network were analyzed with Cytoscape and screened out with Mcode plugin, and the functional annotation of the genes involved in the modules was analyzed with BiNGO (Biological Networks Gene Ontology). RESULTS: Firstly, totally 101 differentially expressed genes were identified in FH samples compared with control samples, the genes ranked in top 3 up- and down-regulated genes were selected. Then, basing on the interaction network of these selected genes, ribosomal L24 domain containing 1 (RSL24D1) and cytochrome c oxidase subunit VIIb (COX7B) showed a central position in the interaction network, and also exited in the modules of the network. The functional annotation of the genes in modules showed that COX7B was associated with oxidative phosphorylation. CONCLUSIONS: COX7B might play vital roles in FH via oxidative phosphorylation system, and might be potential target in the treatment of FH.

Fabp3 inhibits proliferation and promotes apoptosis of embryonic myocardial cells.

Fatty acid binding protein 3 (FABP3) is a member of a family of binding proteins. The protein is mainly expressed in cardiac and skeletal muscle cells, and it has been linked to fatty acid metabolism, trafficking, and signaling. Using suppression subtractive hybridization, we previously found that FABP3 is highly regulated in ventricular septal defect (VSD) patients and may play a significant role in the development of human VSD. We therefore aimed to identify the biological characteristics of the FABP3 gene in embryonic myocardial cells. On the basis of RT-PCR and western blotting analyses, we demonstrated that the expression levels of FABP3 mRNA and protein were up-regulated initially and then gradually decreased with P19 cell differentiation. MTT assays and cell cycle analysis showed that FABP3 inhibits P19 cell proliferation, and data from annexin V-FITC assays revealed that FABP3 can promote apoptosis of P19 cells. Further data from quantitative real-time RT-PCR revealed lower expression levels of cardiac muscle-specific molecular markers (cTnT, alpha-MHC, GATA4, and MEF2c) in FABP3-overexpressing cell lines than in the control cells during differentiation. Our results demonstrate that FABP3 may be involved in the differentiation of cardiac myocytes.

Cardiac lymphatic obstruction impairs left ventricular function and increases plasma endothelin-1 and angiotensin II in rabbits.

The treatment of end-stage heart failure can include heart transplantation. During this procedure, cardiac lymphatics are disrupted, which has been demonstrated in animal models to alter left ventricular function, and this compromise itself can cause an increase in endothelin-1 and angiotensin II. We undertook a study in rabbits to assess the effect of cardiac lymphatic obstruction on left ventricular function and plasma levels of endothelin-1 and angiotensin II. Sixty-three New Zealand white rabbits were divided into study (n = 41) and control (n = 22) groups. Plasma levels of endothelin and angiotensin II were measured before, and at 3, 7, 14, 30, 90 and 180 days following the obstruction of cardiac lymphatic vessels. Left ventricular function was assessed by echocardiography. Six months following the surgery, 18 study and 6 control animals survived. In the study group, a significant decrease was seen in left ventricular ejection fraction within the first three months following the lymphatic obstruction (0.76 +/- 0.04 vs 0.72 +/- 0.01, p < 0.01). Levels of plasma endothelin-1 and angiotensin II were elevated following ligation of cardiac lymphatic vessels with a peak between 3-7 days following lymphatic obstruction (all p < 0.05). Plasma endothelin-1 and angiotensin II began to decline 14 days after lymphatic obstruction and returned to almost baseline levels in 6 months. The left ventricular ejection fraction, plasma endothelin-1 and angiotensin in the control group remained unchanged (all p > 0.05). We conclude that cardiac lymphatic obstruction reduces left ventricular function in the first three months following obstruction. Cardiac lymphatic obstruction also increases plasma levels of endothelin-1 and angiotensin II. The clinical significance of these transitory changes requires further investigation.