OBJECTIVETo study whether combined detection of the methylation status of vimentin, sFRP1, and HPP1 gene can increase the positive methylation rate in colorectal cancer.

METHODSTissue samples were collected from 90 patients with colorectal cancer, 60 patients with adenomatous polyp, and 20 healthy controls. DNA was extracted and the methylation status of vimentin, sFRP1, and HPP1 gene was detected by Methylation-specific PCR (MSP). The relationship between clinicopathologic features of colorectal cancer and gene methylation was analyzed.

RESULTSThe methylation rates of vimentin, sFRP1, and HPP1 were 66.7%, 68.9%, and 72.2% in colorectal cancer, 53.3%, 55.0%, and 50.0% in colorectal adenomas, and 0, 0, and 5.0% in healthy controls, respectively. The methylation of each of the three genes in colorectal cancer tissues was higher than colorectal adenomas and healthy controls(P<0.05). The diagnostic sensitivity by combining three methylation markers was 93.3% in colorectal cancer, 76.7% in colorectal adenomas, which was higher than the sensitivity using single gene testing(P<0.05). No significant associations existed between the methylation status of the three genes and clinical characteristics including sex, age, tumor location, lymph node metastases, distant metastasis, and TNM stage(P>0.05).

CONCLUSIONSDNA methylation levels of vimentin, sFRP1 and HPP1 are significantly higher in colorectal cancer tissue. Combined detection significantly improves the positive rate of methylation, and may be used as early diagnosis method for colorectal cancer.

Adult ; Aged ; Aged, 80 and over ; Ataxia Telangiectasia Mutated Proteins ; genetics ; Case-Control Studies ; Colorectal Neoplasms ; diagnosis ; genetics ; DNA Methylation ; Female ; Humans ; Male ; Membrane Proteins ; genetics ; Middle Aged ; Neoplasm Proteins ; genetics ; Promoter Regions, Genetic ; genetics ; Vimentin ; genetics

OBJECTIVETo investigate the changes of blood lipid in patients with colorectal cancer complicated by coronary heart disease (CHD) and the effect of lipid-lowering therapy with statins in these patients.

METHODSIn 32 pathologically confirmed colorectal cancer patients with CHD, the concentrations of total cholesterol (TC), triglyceride (TG), high-density lipoprotein-cholesterol (HDL-C), low-density lipoprotein-cholesterol (LDL-C) and lipoprotein (a) (Lp(a)) were detected at the baseline, before and after the operation, and at 6 months of postoperative atorvastatin treatment. Thirty patients with TC over 5.70 mmol/L and established coronary artery disease served as the control group.

RESULTSTC, TG and LDL-C in the 30 control patients were significantly decreased after 6 months of 20 mg atorvastatin treatment, and even further decreased till 12 months (P<0.01), but no significant changes occurred in HDL-C and Lp(a). The baseline level of TC, TG, LDL-C and HDL-C were significantly decreased (P<0.01), while Lp(a) increased (P<0.05) in the 32 cancer patients with CHD. Continuing atorvastatin treatment further decreased TC, TG and LDL-C (P<0.05) and increased HDL-C (P<0.05) without affecting Lp(a). The cancer patients had significantly lower TC and LDL-C levels than the control group (P<0.05), but had significantly increased Lp(a) (P<0.05). Six months of atorvastatin treatment further decreased LDL-C and HDL-C in the cancer patients (P<0.05), while TC and Lp(a) had no significant changes.

CONCLUSIONSIncreased Lp(a) in colorectal cancer patients can be associated with its anti-tumor effect. Alterations in the blood lipid profile raises a new issue concerning the safety of lipid-lowering therapy in colorectal cancer patients complicated by CHD.

Aged ; Anticholesteremic Agents ; therapeutic use ; Atorvastatin Calcium ; Cholesterol, HDL ; blood ; Cholesterol, LDL ; blood ; Colorectal Neoplasms ; blood ; complications ; drug therapy ; Coronary Disease ; blood ; complications ; drug therapy ; Female ; Heptanoic Acids ; therapeutic use ; Humans ; Lipoprotein(a) ; blood ; Male ; Middle Aged ; Pyrroles ; therapeutic use ; Treatment Outcome ; Triglycerides ; blood

OBJECTIVETo compare the diagnostic performance of prospective electrocardiogram (ECG)-triggered computed tomography coronary angiography (CTCA) versus retrospective ECG-gated CTCA.

METHODSPatients with suspected coronary artery disease divided into two groups which underwent 64-slice CTCA with prospective ECG-triggered or retrospective ECG-gated scanning (n = 100 each, HR < or = 65 bpm). Multi-planar reconstruction (MPR), curved-planar reconstruction (CPR), maximum intensity projection (MIP) and volume rendering (VR) were made to demonstrate the coronary arteries. The image quality was defined as excellent, good and poor by motion and stair-step artifacts. Individual radiation exposure dose was estimated from the dose-length product.

RESULTSThe mean effective radiation dose of prospective ECG-triggered CTCA [(2.81 +/- 0.48) mSv] was significantly lower than that of retrospective ECG-gated CTCA [(10.16 +/- 1.09) mSv, P < 0.01]. Segments of diagnostic image quality (95.2%, 1165/1224) and non-diagnostic coronary segments (4.8%, 59/1224) in prospective ECG-triggered group were similar as those of retrospective ECG-gated group (94.1%, 1186/1261 and 5.9%, 75/1261, all P > 0.05).

CONCLUSIONThough the radiation exposure dose required is significantly lower, the diagnostic performance of prospective ECG-triggered 64 slice CTCA is comparable with that of retrospective ECG-gated 64 slice CTCA on patients with stable heart rates up to 65 bpm.

Adult ; Aged ; Aged, 80 and over ; Coronary Angiography ; methods ; Electrocardiography ; methods ; Female ; Humans ; Male ; Middle Aged ; Prospective Studies ; Retrospective Studies ; Tomography, X-Ray Computed ; methods

BACKGROUNDKetanserin (KT), a selective serotonin (5-HT) 2-receptor antagonist, reduces peripheral blood pressure by blocking the activation of peripheral 5-HT receptors. In this study electrophysiological method was used to investigate the effect of KT and potassium ion on Kv1.3 potassium channels and explore the role of blocker KT in the alteration of channel kinetics contributing to the potassium ion imbalances.

METHODSKv1.3 channels were expressed in xenopus oocytes, and currents were measured using the two-microelectrode voltage-clamp technique.

RESULTSKCl made a left shift of activation and an inactivation curve of Kv1.3 current and accelerated the activation and inactivation time constant. High extracellular [K(+)] attenuated the blockade effect of KT on Kv1.3 channels. In the presence of KT and KCl the activation and inactivation time constants were not influenced significantly no matter what was administered first. KT did not significantly inhibit Kv1.3 current induced by tetraethylammonium (TEA).

CONCLUSIONSKT is a weak blocker of Kv1.3 channels at different concentrations of extracellular potassium and binds to the intracellular side of the channel pore. The inhibitor KT of ion channels is not fully effective in clinical use because of high [K(+)](o) and other electrolyte disorders.

Animals ; Electrophysiology ; Female ; Ketanserin ; pharmacology ; Kv1.3 Potassium Channel ; drug effects ; metabolism ; Oocytes ; Patch-Clamp Techniques ; Potassium ; pharmacology ; Serotonin Antagonists ; pharmacology ; Xenopus laevis

Objective: To observe the effect of modified Chaihu Shugantang on the expression of miRNA-204 in hippocampus of epileptic mice, and to explore its mechanism of neuroprotection. Method: The sixty mice were randomly divided into 6 groups:normal group, model group (pilocarpine 180 mg·kg^-1), and modified Chaihu Shugantang group (7 g·kg^-1·d^-1), modified Chaihu Shugantang+miRNA-204 mimic group (7 g·kg^-1·d^-1+ 2 μL), modified Chaihu Shugantang+miRNA-204 inhibitor group (7 g·kg^-1·d^-1+2 μL), carbamazepine group (30 mg·kg^-1·d^-1),each was given intragastric administration for 2 weeks,using pilocarpine to cause epilepsy in mice, respectively, add flavor to Bupleurum after intragastric administration, inhibition and overexpression of miRNA-204, the mice were sacrificed and their hippocampus tissues were harvested.The indicators of each group were observed, Real-time quantitative PCR detecting system (Real-time PCR) was used to detect mouse hippocampal miRNA-204 expression, Western blot analysis of autophagy-related protein microtubule-associated protein light chain 3 (LC3), autophagy-associated marker protein 7 (ATG7) expression, hematoxylin pathological condition of hippocampus in each group was observed by hematoxylin-eosin(HE)staining.The autophagy of hippocampus in each group was observed by transmission electron microscopy. Result: Compared with normal group, the expression of miRNA-204 was significantly decreased in model group (P<0.01), the pathological changes in the hippocampal C1 area were the most obvious, the expression of ATG7, LC3Ⅱ/LC3Ⅰ was increased (P<0.01), and the autophagy was small. Compared with model group, the expression of miRNA-204 in the hippocampus of the modified Chaihu Shugantang group was increased (P<0.05), the pathological changes in the hippocampal C1 area were alleviated, the expression of ATG7, LC3Ⅱ/LC3Ⅰ was decreased (P<0.05), and the autophagy was small. The number of body decreased,the expression of miRNA-204 in hippocampus of modified Chaihu Shugantang+miRNA-204 mimic group was significantly increased (P<0.01), the pathological changes in hippocampal C1 area were the lightest, and the expression of ATG7, LC3Ⅱ/LC3I was decreased (P<0.01), the number of autophagosomes was the least.Compared with modified Chaihu Shugantang group, the above-mentioned indicators of modified Chaihu Shugantang+miRNA-204 inhibitor group had the same change trend and the change range decreased (P<0.05). Conclusion: Modified Chaihu Shugantang can improve the pathological changes of hippocampus in mice with epilepsy and play a neuroprotective role. The mechanism may be to increase the expression of miRNA-204 in hippocampus of mice with epilepsy, inhibit excessive autophagy of neurons and reduce apoptosis.