A trade-off between antifouling and the electrochemical stabilities of PEDOTs.

Strong nonspecific protein/cell adhesion on conducting polymer (CP)-based bioelectronic devices can cause an increase in the impedance or the malfunction of the devices. Incorporating oligo(ethylene glycol) or zwitterionic functionalities with CPs has demonstrated superior performance in the reduction of nonspecific adhesion. However, there is no report on the evaluation of the antifouling stability of oligo(ethylene glycol) and zwitterion-functionalized CPs under electrical stimulation as a simulation of the real situation of device operation. Moreover, there is a lack of understanding of the correlation between the molecular structure of antifouling CPs and the antifouling and electrochemical stabilities of the CP-based electrodes. To address the aforementioned issue, we fabricated a platform with antifouling poly(3,4-ethylenedioxythiophene) (PEDOT) featuring tri(ethylene glycol), tetra(ethylene glycol), sulfobetaine, or phosphorylcholine (PEDOT-PC) to evaluate the stability of the antifouling/electrochemical properties of antifouling PEDOTs before and after electrical stimulation. The results reveal that the PEDOT-PC electrode not only exhibits good electrochemical stability, low impedance, and small voltage excursion, but also shows excellent resistance toward proteins and HAPI microglial cells, as a cell model of inflammation, after the electrical stimulation. The stable antifouling/electrochemical properties of zwitterionic PEDOT-PC may aid its diverse applications in bioelectronic devices in the future.

C1qTNF-related protein-6 protects against doxorubicin-induced cardiac injury.

The clinical use of doxorubicin (DOX) is limited by its toxic effect. However, there is no specific drug that can prevent DOX-related cardiac injury. C1qTNF-related protein-6 (CTRP6) is a newly identified adiponectin paralog with many protective functions on metabolism and cardiovascular diseases. However, little is known about the effect of CTRP6 on DOX-induced cardiac injury. The present study aimed to investigate whether CTRP6 could protect against DOX-related cardiotoxicity. To induce acute cardiotoxicity, the mice were intraperitoneally injected with a single dose of DOX (15 mg/kg). Cardiomyocyte-specific CTRP6 overexpression was achieved using an adenoassociated virus system at 4 weeks before DOX injection. The data in our study demonstrated that CTRP6 messenger RNA and protein expression were decreased in DOX-treated hearts. CTRP6 attenuated cardiac atrophy induced by DOX injection and inhibited cardiac apoptosis and improved cardiac function in vivo. CTRP6 also promoted the activation of protein kinase B (AKT/PKB) signaling pathway in DOX-treated mice. CTRP6 prevented cardiomyocytes from DOX-induced apoptosis and activated the AKT pathway in vitro. CTRP6 lost its protection against DOX-induced cardiac injury in mice with AKT inhibition. In conclusion, CTRP6 protected the heart from DOX-cardiotoxicity and improves cardiac function via activation of the AKT signaling pathway.

Association between matrix metalloproteinase 9 C-1562T polymorphism and the risk of coronary artery disease: an update systematic review and meta-analysis.

Polymorphism (rs3918242) in the MMP9 gene has been reported to be associated with coronary artery disease (CAD). This study aims to investigate a more accurate estimation of the relationship between CAD and rs3918242 polymorphism by a meta-analysis method. We systematically searched studies on the association of rs3918242 polymorphism and CAD in PubMed, Web of Science, the Cochrane Library, Wanfang Data and CNKI. We used Stata 12.0 and RevMan 5.3 software to perform the meta-analyses. A total of 37 case-control studies involving 13,035 CAD patients and 11,372 non-CAD controls were included. A statistically significant association between rs3918242 polymorphism and CAD was observed in allelic model (Odds ratio (OR) 1.34; 95% confidence interval (CI) 1.20-1.50; p < 0.00001), recessive model (OR 1.43; 95% CI 1.17-1.75; p = 0.0004), and in dominant model ( OR 1.36; 95% CI 1.20-1.53; p < 0.00001). Moreover, we also found that there is a statistically significant association between rs3918242 polymorphism and myocardial infarction (MI) in Asians with allelic model (OR 1.66; 95% CI 1.29-2.14; p < 0.0001), recessive model (OR 2.29; 95% CI 1.44-3.63; p = 0.004), and dominant (OR 1.74; 95% CI 1.29-2.35; p = 0.0003) model. A similar result in Caucasians with allelic model (OR 1.14; 95% CI 1.02-1.27; p = 0.02), and in dominant (OR 1.17; 95% CI 1.04-1.32; p = 0.01) model. Our meta-analysis suggested that the MMP9 T allele is a risk factor for CAD and MI.

Combined value of red blood cell distribution width and global registry of acute coronary events risk score on predicting long-term major adverse cardiac events in STEMI patients undergoing primary PCI.

The combined value of RDW and GRACE risk score for cardiovascular prognosis in ST-segment elevation myocardial infarction (STEMI) undergoing primary percutaneous coronary intervention (PCI) has not been fully investigated. This study was designed to explore the combined value of RDW and GRACE risk score on predicting long-term major adverse cardiac event (Mace) in STEMI patients undergoing primary PCI. This study included 390 STEMI patients. The primary endpoint at the (33.5 ± 7.1) months follow-up was composed of cardiac death and nonfatal myocardial infarction. The relationship between clinical parameters and clinical outcomes was evaluated using Cox regression model and receiver operating characteristic (ROC) analysis. Mace occurred in 126 (32.3%) patients including 54 (13.8%) cardiac deaths and 72 (18.5%) nonfatal myocardial infarctions. Patients in Mace group had significantly higher RDW and GRACE score than the patients in non-Mace group. According to the Cox model, RDW and GRACE score were the most important independent predictors of Mace and cardiac death. The best cut-off value for RDW to predict the occurrence of primary events was 13.25% (AUC = 0.694, 95% CI:0.639-0.750, P < 0.001) and that for GRACE score was 119.5 (AUC = 0.721, 95% CI:0.666-0.777, P < 0.001). The combination of RDW and GRACE score were more valuable (AUC = 0.775, 95% CI: 0.727-0.824, P < 0.001). Kaplan-Meier analysis provided significant prognostic information with the highest risk for cardiac death (Log-Rank χ2 = 24.684, P < 0.001) in group with both high RDW (> 13.25%) and high GRACE score (> 119.5). The combination of RDW level and GRACE score may be valuable and simple independent predictors of Mace and cardiac death in STEMI patients undergoing primary PCI. They may be useful tools for risk stratification and may indicate long-term clinical outcomes.

Prenatal exposure to lipopolysaccharide combined with pre- and postnatal high-fat diet result in lowered blood pressure and insulin resistance in offspring rats.

BACKGROUND: Adult metabolic syndrome may in part have origins in fetal or early life. This study was designed to explore the effect of prenatal exposure to lipopolysaccharide and high-fat diet on metabolic syndrome in offspring rats. METHODS: 32 pregnant rats were randomly divided into four groups, including Control group; LPS group (pregnant rats were injected with LPS 0.4 mg/kg intraperitoneally on the 8(th), 10(th) and 12(th) day of pregnancy); High-fat group (maternal rats had high-fat diet during pregnancy and lactation period, and their pups also had high-fat diet up to the third month of life); LPS + High-fat group (rats were exposed to the identical experimental scheme with LPS group and High-fat group). RESULTS: Blood pressure elevated in LPS group and High-fat group, reduced in LPS+High-fat group, accompanied by the increase of serum leptin level in LPS and High-fat group and increase of serum IL-6, TNF-a in High-fat group; both serum insulin and cholesterol increased in High-fat and LPS+High-fat group, as well as insulin in LPS group. HOMA-IR value increased in LPS, High-fat and LPS+High-fat group, and QUICKI decreased in these groups; H-E staining showed morphologically pathological changes in thoracic aorta and liver tissue in the three groups. Increased serum alanine and aspartate aminotransferase suggest impaired liver function in LPS+High-fat group. CONCLUSION/SIGNIFICANCE: Prenatal exposure to lipopolysaccharide combined with pre- and postnatal high-fat diet result in lowered blood pressure, insulin resistance and impaired liver function in three-month old offspring rats. The lowered blood pressure might benefit from the predictive adaptive response to prenatal inflammation.

Imidapril provides a protective effect on pulmonary hypertension induced by low ambient temperature in broiler chickens.

OBJECTIVE: The objective of this article is to explore the role of imidapril on pulmonary hypertension induced by low ambient temperature in broiler chickens. MATERIALS AND METHODS: Ninety chickens were randomly divided into three groups (n = 30): a control group, a low-temperature group and an imidapril group. Chickens in the low-temperature group and imidapril group were exposed to low ambient temperature from 14 days of age until 45 days of age; chickens in the imidapril group were gavaged with imidapril 3 mg/kg once daily for 30 days. The pulmonary arterial pressure, main pulmonary arterial diameter and pulmonary arterial wall thickness were measured, and lung tissue ACE, ACE2 mRNA expression, proliferating cell nuclear antigen (PCNA)-positive cells and Ang II, Ang (1-7) concentration were evaluated. RESULTS: The pulmonary arterial pressure was higher, the main pulmonary arterial diameter was wider and the pulmonary arterial wall was thicker in the low-temperature group than those in the control group and the imidapril group. ACE mRNA and PCNA-positive cells increased significantly in the low-temperature group compared with the control group and imidapril group; lung tissue Ang II concentration in the low-temperature group was higher, but Ang (1-7) content was lower than that in the control group and imidapril group. CONCLUSION: Imidapril provides a protective effect on pulmonary hypertension induced by low ambient temperature in broiler chickens.

Imidapril inhibits right ventricular remodeling induced by low ambient temperature in broiler chickens.

This study explored the effect of imidapril on the right ventricular remodeling induced by low ambient temperature in broiler chickens. Twenty-four broiler chickens were randomly divided into 3 groups (n = 8), including the control group, low temperature group, and imidapril group. Chickens in the control group were raised at normal temperature, whereas chickens in the low temperature group and imidapril group were exposed to low ambient temperature (12 to 18°C) from 14 d of age until 45 d of age. At the same time, chickens in the imidapril group were gavaged with imidapril at 3 mg/kg once daily for 30 d. The thickness of the right ventricular wall was observed with echocardiography. The BW and wet lung weight as well as weight of right and left ventricles and ventricular septum were measured. Both wet lung weight index and right ventricular hypertrophy index were calculated. Pulmonary arterial systolic pressure was assessed according to echocardiography. The expression of ACE and ACE2 mRNA in the right ventricular myocardial tissue was quantified by real-time PCR. Proliferating cell nuclear antigen-positive cells were detected by immunohistostaining. The concentration of angiotensin (Ang) II and Ang (1-7) in the right ventricular myocardial tissue was measured with ELISA. The results showed that right ventricular hypertrophy index, wet lung weight index, pulmonary arterial systolic pressure, expression of ACE mRNA in the right ventricular tissue, Ang II concentration, and the thickness of the right ventricular wall in the low temperature group increased significantly compared with those in the control group and imidapril group. The ACE2 mRNA expression increased 36%, whereas Ang (1-7) concentration decreased significantly in the low temperature group compared with that in the control group and imidapril group. In conclusion, imidapril inhibits right ventricular remodeling induced by low ambient temperature in broiler chickens.

Alteration of embryonic AT(2)-R and inflammatory cytokines gene expression induced by prenatal exposure to lipopolysaccharide affects renal development.

UNLABELLED: Prenatal exposure to LPS(lipopolysaccharide) results in renal damage in offspring rats, but the mechanism is unknown. The present study was to explore the role of angiotensin II and inflammation in the development of renal damage induced by prenatal exposure to LPS. The pregnant rats were randomly divided into two groups, i.e., control group, LPS group. The rats in the two groups were administered intraperitoneally with vehicle or 0.79 mg/kg LPS on 8th, 10th and 12th day during gestation. The mRNA expression of angiotensinogen, renin, AT(1)-R, AT(2)-R, TNF-α and IL-6 in embryos were assessed. Renal Ang II-positive cells, monocytes/macrophages, lymphocytes, collagen I and TUNEL-positive cells were identified by immunohistochemical staining in newborn and 7-week-old offspring rats. The number of glomeruli and creatinine clearance rate were determined in offspring at 7 weeks of age. The results showed that prenatal LPS decreased AT(2)-R mRNA expression but increased TNF-α and IL-6 mRNA expression in embryos. Prenatal LPS decreased renal angiotensin II-positive cells in newborn offspring rats, while these increased in 7-week-old offspring rats. Prenatal LPS decreased glomerular number and creatinine clearance rate but increased renal infiltrating monocytes/macrophages and lymphocytes at 7 weeks of age. Prenatal LPS also increased TUNEL-positive cells and collagen I expressions in newborn rats and 7-week-old offspring rats. CONCLUSION: Alteration of embryonic AT(2)-R and inflammatory cytokines gene expression induced by prenatal exposure to lipopolysaccharide affects renal development.

Effects of IFN-γ on IL-18 Expression in Pregnant Rats and Pregnancy Outcomes.

The present study focused on establishing the effects of interferon-gamma (IFN-γ) on interleukin-18 (IL-18) expression patterns and pregnancy outcomes in pregnant rats. Pregnant rats at the post-implantation stage were randomized into control, low IFN-γ (L-IFN-γ) and high IFN-γ groups (H-IFN-γ) that received normal saline, 100 IU/g of IFN-γ and 500 IU/g of IFN-γ vaginal muscular injection, respectively. The effects of IFN-γ on IL-18 expression and pregnancy outcomes were assessed systematically using several methods, including immunohistochemistry streptavidin-perosidase (SP), image pattern analysis, enzyme-linked immune-sorbent assay (ELISA), whole blood count (WBC) count, microscopy and visual observation. IL-18 was detected in the uteri of all pregnant rats, and mainly distributed in the endometrium, decidual cells, vascular endothelium and myometrium. Immunohistochemistry and image pattern analyses revealed significantly lower IL-18 expression in the H-IFN-γ group compared to the L-IFN-γ and control groups (p<0.01), indicating that high doses of IFN-γ induce downregulation of IL-18 in the uterus of pregnant rats. ELISA results disclosed that IL-18 expression in peripheral blood of the H-IFN-γ group was lower than that of the L-IFN-γ group (p<0.05), and significantly reduced compared to the control group (p<0.01). Moreover, the number of peripheral leukocytes in the H-IFN-γ group was significantly higher than those in the control and L-IFN-γ groups (p<0.01). Morphology analysis showed no evident differences between the L-IFN-γ and control groups. However, for the H-IFN-γ group, uterine mucosa bleeding, necrosis and excoriation were observed using microscopy. Visual observation revealed marroon, swelling, crassitude and no embryo in the uterus, which are obvious indicators of abortion. These results indicate that IFN-γ plays a regulatory role in IL-18 expression in the uterus and peripheral blood of pregnant rats at the post-implantation stage. Moreover, high levels (500 IU/g) of IFN-γ influence normal pregnancy at the early stages in rats by downregulating IL-18 expression in the uterus and peripheral blood and increasing the number of peripheral leukocytes, consequently triggering termination of pregnancy.

Clinical analysis of transcatheter closure of perimembranous ventricular septal defects with occluders made in China.

BACKGROUND: Results of perimembranous ventricular septal defects (pmVSD) transcatheter closure have been reported in the literature mostly using a Amplatzer VSD device. However, the data of percutaneous closure of pmVSD with VSD occluder (VSD-O) made in China are still limited. We sought to analyze safety, efficacy, and follow-up results of percutaneous closure of pmVSD with VSD-O made in China. METHODS: Between February 2005 and June 2009, 78 patients underwent percutaneous closure of pmVSD at our institution. A VSD device made in China was used for all subjects. The safety and the efficacy of the VSD-O were investigated. RESULTS: The average age at closure was 11 years (range 2.5 to 44 years). The attempt to place device was successful in 74 patients (94.9%). The average device size used was 8 mm (range 5 to 16 mm). No deaths occurred. Total occlusion rate was 62.8% at completion of the procedure, rising up to 87.2% at discharge and 99.0% during follow-up. A total of eight early complications occurred (10.3%), but in all subjects these were transient. The average follow-up period was 40.5 months. The most significant complication was complete atrioventricular block (cAVB) in the early phase (five subjects, 6.4%) and during the follow-up (1 subject, 1.3%), which saw no need for pacemaker implantation in six subjects. Cox proportional hazards regression analysis showed that the age was only the variable significantly associated with the occurrence of this complication during the procedure (P = 0.025; relative risk 0.22). The subjects who experienced this complication were less than five years old. CONCLUSIONS: Percutaneous pmVSD closure used VSD-O made in China is associated with excellent success and closure rates, no mortality, and low morbidity. Longer follow-up data and improvements in device characteristics are needed to reduce the risk of cAVB.

Congenital long QT syndrome caused by the F275S KCNQ1 mutation: mechanism of impaired channel function.

Congenital long QT syndrome is characterized by a prolongation of ventricular repolarization and recurrent episodes of life-threatening ventricular tachyarrhythmias, often leading to sudden death. We previously identified a missense mutation F275S located within the S5 transmembrane domain of the KCNQ1 ion channel in a Chinese family with long QT syndrome. We used oocyte expression of the KCNQ1 polypeptide to study the effects of the F275S mutation on channel properties. Expression of the F275 mutant, or co-expression with the wild-type S275 polypeptide, significantly decreased channel current amplitudes. Moreover, the F275S substitution decreased the rates of channel activation and deactivation. In transfected HEK293 cells fluorescence microscopy revealed that the F275S mutation perturbed the subcelluar localization of the ion channel. These results indicate that the F275S KCNQ1 mutation leads to impaired polypeptide trafficking that in turn leads to reduction of channel ion currents and altered gating kinetics.

[Factors related to the use of reperfusion strategies in elderly patients with acute myocardial infarction].

OBJECTIVE: To examine the use of reperfusion strategies in elderly patients with acute myocardial infarction (AMI) and investigate the factors affecting its use. METHODS: This survey population consisted of 338 consecutive elderly patients with AMI (> or = 65 years) who were admitted to the department of cardiology of Beijing Military General Hospital between December 2003 and November 2007. The patients were divided into two groups based on the receiving of reperfusion strategies: a reperfusion group (n = 252) and a non-reperfusion therapeutic group(n = 86). Qualitative data were compared between the two groups using Chi-square tests and multiple binary logistic regression was used to determine the relationship between various patient-related factors with the probability of choosing reperfusion therapies or not. RESULTS: About 74.6% of the elderly patients with AMI received reperfusion strategies [62.2% percutaneous coronary intervention (PCI) and 12.4% thrombolysis]. Stepwise logistic regression analysis revealed that age > or = 75 years (OR = 0.255, P = 0.000), history of angina(OR = 0.570, P = 0.016) and high Killip classification (OR = 0.671, P = 0.012) were confirmed factors for receiving less reperfusion therapy. Meanwhile, inferior wall myocardial infarction (MI) with complicating right ventricular MI(OR = 4.585, P = 0.002), sweating (OR = 1.970, P = 0.016), unbearable symptoms (OR = 1.836, P = 0.038) and medical insurance (OR = 1.968, P = 0.029) were independent predictors for receiving reperfusion therapy. Intracranial hemorrhage (2.8% vs 7.1%, P = 0.000), left ventricular ejection time < 45% (12% vs 31%, P = 0.016) and mortality rate within 1 year (2.3% vs 4.7%, P = 0.039) were obviously decreased in the PCI group as compared with the thrombolysis group. CONCLUSIONS: Aging, medical history of angina, high Killip classification, inferior MI with complicating right ventricular MI, sweating, unbearable symptoms and medical insurance were independent predictors for receiving reperfusion strategies.

[Effects of socioeconomic status on the distribution of cardiovascular risk factors and clinical treatments of patients with acute myocardial infarction in Beijing].

OBJECTIVE: To evaluate the effects of socioeconomic status on the distribution of cardiovascular risk factors and clinical treatments of patients with acute myocardial infarction in Beijing. METHODS: In Beijing, a prospective, multi-center, registration study was carried out which including 800 patients who were consecutively hospitalized for ST-segment elevation acute myocardial infarction within 24 hours after event attack in 19 different hospitals in Beijing between November, 2005 and December, 2006. Indicators of socioeconomic status included self-reported personal income (< 500, 500-2000, > 2000 RMB/ month), educational attainment (< or = 12 and > 12 years) and status of medical insurance (yes/no). According to categories of education, patients were categorized into two groups of lower socioeconomic status and higher socioeconomic status. Differences of cardiovascular risk factors and clinical treatments were compared across the two groups respectively. RESULTS: Proportion of diabetes and hyperlipidemia in patients with higher socioeconomic status was much higher than that of patients with lower socioeconomic status (P < 0.05, P < 0.01 respectively). Patients with lower socioeconomic status were more likely to be smokers (P < 0.05). The rates of receiving coronary angiography and PTCA were much lower in patients with lower socioeconomic status. Medical insurance and income were the most important two socioeconomic factors determining the use of PTCA. CONCLUSION: Compared to patients with lower socioeconomic status, patients with higher socioeconomic status had higher rates of hyperlipidemia and diabetes but lower smoking rate among cardiovascular risk factors. The rates of receiving interventional therapies were much lower in patients with lower socioeconomic status.

Current management of patients with ST elevation myocardial infarction in Metropolitan Beijing, China.

PURPOSE: To assess clinical practices and in-hospital outcomes of patients with ST elevation myocardial infarction (STEMI) in Beijing, China. METHODS: This study was a prospective multicentre registry study in Metropolitan Beijing, China. Demographics, delay time, management strategy and in-hospital outcome data were collected from patients with STEMI enrolled in 19 hospitals. RESULTS: A total of 803 patients (mean age 61+/-13 yr ,22% women and 42.1% >or= 65 yr) with STEMI were enrolled. More than half had a history of hypertension (50.4%) and current smoking (55.2%). Six hundred and fifty patients (80.9%) received reperfusion therapy: 124 (15.4% ) treated with thrombolysis and 526 (65.5% ) with primary percutaneous coronary intervention (PCI). The median door-to-needle time for thrombolysis was 83 min and door-to-balloon time for primary PCI was 132 min. Only 7% of patients treated with thrombolysis met the guidelines goal of the door-to-needle time

[Associations between the plasma inflammatory markers and plaque morphologies of coronary artery lesions].

OBJECTIVE: To evaluate the vulnerability of coronary artery plaque with coronary angiography (CAG), intravascular ultrasound (IVUS) and the levels of plasma inflammatory markers. METHODS: 58 consecutive patients with lesion of a single blood vessel demonstrated successfully by CAG were randomly divided into 3 groups based on the angiographic morphology of the the lesions: type I lesion group (n = 16), type II lesion group (n = 25), type III lesion group (n = 17). Meantime, a control group of stable angina (n = 17) was established. A subgroup of 28 patients (including 18 acute coronary syndrome (ACS) patients and 10 stable angina control patients) who underwent IVUS study were analyzed. Then the plasma levels of high sensitivity CRP (hs-CRP), matrix metalloproteinase (MMP, including MMP-2 and MMP-9), CD(40) ligand (CD(40)L) and pregnancy associated plasma protein-A (PAPP-A) were measured with ELISA. Analyses were performed by statistical package SPSS 11.0. RESULTS: The plasma levels of MMP-2, MMP-9 and PAPP-A in type II lesion group were significantly higher than the other groups (P < 0.05, 0.05, 0.001, respectively). In type II lesion group, linear correlation analysis manifested significantly positive correlation between levels of hs-CRP and MMP-2 (r = 0.508); MMP-2 and MMP-9, CD(40)L, PAPP-A (r = 0.647, 0.704, 0.751, respectively); MMP-9 and CD(40)L, PAPP-A (r = 0.491, 0.639, respectively); CD(40)L and PAPP-A (r = 0.896). IVUS subgroup analysis showed that the area of plaques and plaques burden in culprit lesion, the incidence of high-risk plaques, remodeling index (RI) and positive remodeling percentage in ACS patients were significantly greater than those in the control group (P = 0.000, 0.037, 0.028, 0.015, 0.040, respectively). Compared with the control group, the plasma levels of hs-CRP, MMP-2, MMP-9 and PAPP-A were markedly elevated (P = 0.033, 0.000, 0.000, 0.027, respectively). CONCLUSIONS: CAG and IVUS combined with the study on plasma levels of inflammation mediators were helpful in judging the vulnerability of coronary artery plaques.

Plasma B-type natriuretic peptide for early diagnosis of allograft rejection after renal transplantation.

B-type natriuretic peptides are predominantly synthesized in the ventricular myocytes. This is the response to volume overload or increased stress to the ventricular wall. Plasma B-type natriuretic peptide levels are elevated in patients with chronic renal failure due to reduced glomerular filtration and/or increased myocardial biosynthesis. Allograft renal transplantation significantly reduces plasma B-type natriuretic peptide. Our previous clinical observations have demonstrated that acute allograft renal rejection is associated with a sudden increase in plasma B-type natriuretic peptides. We hypothesized that plasma B-type natriuretic peptide may be used as a sensitive and specific biomarker for clinical diagnosis of acute allograft renal rejection.

Public knowledge of heart attack symptoms in Beijing residents.

BACKGROUND: Definitive treatment for heart attack is early reperfusion with either angioplasty or thrombolytic therapy, and the benefit is strictly time-dependent. Patient outcomes are improved with either therapy when initiated as soon as possible. Recognition of heart attack symptoms is logically tied to taking action to receive prompt emergency care. Inadequate knowledge of heart attack symptoms may prolong delay. The purpose of this study was to document knowledge about heart attack symptoms in Beijing residents and to identify the characteristics associated with increased knowledge of heart attack. METHODS: A structured survey was conducted in 18 communities in Beijing from March 1 through June 10 in 2006. Addresses and participants were selected randomly following a stratification. The survey was designed to collect knowledge of heart attack symptoms from sampled adults in each community. RESULTS: A total of 4627 respondents completed the questionnaires correctly, and 50.29% of them were female. Totally 64.15% of the respondents reported chest pain or discomfort (common symptoms) as a symptom of heart attack; 75.38% reported at least one of the following eight symptoms as a symptom of heart attack: back pain, shortness of breath, arm pain or numbness, nausea or vomiting, neck, jaw or shoulder pain, epigastric pain, sweating, weakness (less common symptoms); 20.36% correctly reported four or more heart attack symptoms, only 7.4% knew all the correct heart attack symptoms, and 28.94% knew about reperfusion therapy for heart attack; 31.7% reported to call 120 or 999 while having a heart attack themselves; however 89.6% reported to call 120 or 999 when someone else is suffering from a heart attack. Very old persons and those with health insurance coverage, high education level, high household income, longer living in Beijing and previous experience with heart disease had greater knowledge of heart attack symptoms. CONCLUSIONS: Public knowledge of common heart attack symptoms as well as less common heart attack symptoms is deficient in Beijing residents. But their knowledge of calling emergency medical services when someone is having a heart attack is relatively adequate. Public health efforts are needed to increase the recognition of the major heart attack symptoms in both the general public and groups at high risk for an acute cardiac event, especially in socioeconomically disadvantaged subgroups, including persons with low education level, low household income, and no health insurance coverage.

[Relationship between congenital long QT syndrome and Brugada syndrome gene mutation].

OBJECTIVE: To investigate the molecular pathology in families with long QT syndrome (LQTS) including Jervell-Longe-Nielsen syndrome (JLNS) and Romano-ward syndrome (RWS) and Brugada syndrome (BS) in Chinese population. METHODS: Polymerase chain reaction and DNA sequencing were used to screen for KCNQ1, KCNH2, KCNE1, and SCN5A mutation. RESULTS: We identified a novel mutation N1774S in the SCN5A gene of the BS family, a novel mutation G314S in a RWS family which had also been found in Europe, North America, and Japan, and a single nucleotide polymorphisms (SNPs) G643S in the KCNQ1 of the JLNS family. In this JLNS family, another heterozygous novel mutation in exon 2a was found in KCNQ1 of the patients. CONCLUSION: New mutations were found in our experiment, which expand the spectrum of KCNQ1 and SCN5A mutations that cause LQTS and BS.

[Mutation analysis of a Chinese family with inherited long QT syndrome].

OBJECTIVE: To identify the mutation of a Chinese family with inherited long QT syndrome(LQTS). METHODS: The disease-causing gene was tentatively determined in light of the clinical manifestations and electrophysiological properties, and then polymerase chain reaction and DNA sequencing were used for screening and identifying mutation. RESULTS: A missense mutation G940A(G314S) in the KCNQ1 gene was identified, which was the 'hot spot' of long QT syndrome mutation. CONCLUSION: The mutation that is involved with long QT syndrome in Chinese patients is the same as that in the European, American and Japanese patients.