Modulating the Activity and SO2 Resistance of α-Fe2O3 Catalysts for NH3-SCR of NOx via Crystal Facet Engineering.

The development of Fe-based catalysts for the selective catalytic reduction of NOx by NH3 (NH3-SCR of NOx) has garnered significant attention due to their exceptional SO2 resistance. However, the influence of different sulfur-containing species (e.g., ferric sulfates and ammonium sulfates) on the NH3-SCR activity of Fe-based catalysts as well as its dependence on exposed crystal facets of Fe2O3 has not been revealed. This work disclosed that nanorod-like α-Fe2O3 (Fe2O3-NR) predominantly exposing (110) facet performed better than nanosheet-like α-Fe2O3 (Fe2O3-NS) predominantly exposing (001) facet in NH3-SCR reaction, due to the advantages of Fe2O3-NR in redox properties and surface acidity. Furthermore, the results of the SO2/H2O resistance test at a critical temperature of 250 °C, catalytic performance evaluations on Fe2O3-NR and Fe2O3-NS sulfated by SO2 + O2 or deposited with NH4HSO4 (ABS), and systematic characterization revealed that the reactivity of ammonium sulfates on Fe2O3 catalysts to NO(+O2) contributed to their improved catalytic performance, while ferric sulfates showed enhancing and inhibiting effects on NH3-SCR activity on Fe2O3-NR and Fe2O3-NS, respectively; despite this, Fe2O3-NR showed higher affinity for SO2 + O2. This work set a milestone in understanding the NH3-SCR reaction on Fe2O3 catalysts in the presence of SO2 from the aspect of crystal facet engineering.

Association of gallstone and polymorphisms of UGT1A1*27 and UGT1A1*28 in patients with hepatitis B virus-related liver failure.

Genetic variation in UDP-glucuronosyltransferase 1A1 gene (UGT1A1) is a lithogenic risk factor for gallstone formation. This study aimed to assess genotype and allele frequencies of common UGT1A1 variants in patients with gallstone and hepatitis B virus (HBV)-related hepatic failure. This study enrolled 113 healthy individuals (CTRL), 54 patients with HBV infection (HBV), 134 patients with gallstone-free hepatic failure and HBV infection, and 34 patients with gallstone-related hepatic failure and HBV infection (GRHF). Peripheral venous blood samples were collected for genomic DNA isolation. Polymerase chain reaction amplification was carried out for UGT1A1, followed by direct sequencing. Analysis for genotype and allele frequencies of UGT1A1 variants (UGT1A1*6, UGT1A1*27, UGT1A1*28, and UGT1A1*60) was performed. The allele distributions of the four groups did not deviate from Hardy-Weinberg equilibrium. Allele (A) and genotype (CA) frequency distributions of UGT1A1*27 were significantly different between GRHF and CTRL, or between GRHF and HBV. GRHF and CTRL exhibited significant differences in allele (A) and genotype (CA) frequency distributions of UGT1A1*28. Linkage disequilibrium analysis suggested that haplotype G-G-[TA]7-T may be associated with gallstone in HBV-related hepatic failure. Our data reveal that UGT1A1*27 and UGT1A1*28 variants are significantly observed in patients with GRHF compared to healthy individuals.

Evaluation of energy values of high-fiber dietary ingredients with different solubility fed to growing pigs using the difference and regression methods.

The objective of this study was to compare the energy values of high-fiber dietary ingredients with different solubility (sugar beet pulp [SBP] and defatted rice bran [DFRB]) in growing pigs using the difference and the regression methods. A total of 21 barrows (initial BW, 40.5 ± 1.2 kg) were assigned to 3 blocks with BW as a blocking factor, and each block was assigned to a 7 × 2 incomplete Latin square design with 7 diets and two 13-d experimental periods. The 7 experimental diets consisted of a corn-soybean meal basal diet and 6 additional diets containing 10%, 20%, or 30% SBP or DFRB in the basal diet, respectively. Each of the experimental periods lasted 12 d, with a 7 d dietary adaptation period followed by 5-d total fecal and urine collection. Results showed that the digestible energy (DE) and metabolizable energy (ME) of the SBP determined by the difference method with different inclusion levels (10%, 20%, or 30%) were 2,712 and 2,628 kcal/kg, 2,683 and 2,580 kcal/kg, and 2,643 and 2,554 kcal/kg DM basis, respectively. The DE and ME in the DFRB evaluated by the difference method with 3 different inclusion levels were 2,407 and 2,243 kcal/kg, 2,687 and 2,598 kcal/kg, and 2,630 and 2,544 kcal/kg DM basis, respectively. Different inclusion levels had no effects on the energy values of each test ingredient estimated by the difference method. The DE and ME of the SBP and the DFRB estimated by the regression method were 2,562 and 2,472 kcal/kg and 2,685 and 2,606 kcal/kg DM basis, respectively. The energy values of each ingredient determined by the regression method were similar to the values estimated by the difference method with the 20% or 30% inclusion level. However, the energy values of the SBP and DFRB estimated by the difference method with the 10% inclusion level were inconsistent with the values determined by the regression method (P < 0.05). In conclusion, the regression method was a robust indirect method to evaluate the energy values for high-fiber ingredients with different solubility in growing pigs. If the number of experimental animals was limited, the difference method with a moderate inclusion level (at least 20%) of the test high-fiber ingredient in the basal diet could be applied to substitute the regression method.

Recanalization of the occluded radial artery via distal transradial access in the anatomic snuffbox.

BACKGROUND: Radial artery occlusion is a common complication after coronary angiography and percutaneous coronary intervention via the transradial access. In recent years, coronary angiography and percutaneous coronary intervention via the distal transradial access has gradually emerged, but recanalization of the occluded radial artery through the distal transradial access has rarely been reported. CASE PRESENTATION: A 67-year-old female with arterial hypertension and diabetes mellitus was admitted to the hospital due to chest pain for three hours. She was diagnosed with acute myocardial infarction. After admission, the patient successfully underwent emergency coronary angiography and percutaneous coronary intervention through the right transradial access. Radial artery occlusion was found after the operation, and recanalization was successfully performed through the right distal transradial access before discharge. Immediately after the operation and one month later, vascular ultrasonography showed that the antegrade flow was normal. CONCLUSIONS: This report presents a case of radial artery occlusion after emergency coronary angiography and percutaneous coronary intervention in which recanalization was successfully performed through the right distal transradial access. This case demonstrates that recanalization of a radial artery occlusion via the distal transradial access is safe and feasible.

Elevated lipoprotein (a) levels are associated with the acute myocardial infarction in patients with normal low-density lipoprotein cholesterol levels.

Elevated lipoprotein (a) [Lp(a)] and coronary artery disease (CAD) risk has been renewed interested in recent years. However, the association between Lp(a) and acute myocardial infarction (AMI) risk in patients with normal low-density lipoprotein cholesterol (LDL-C) levels has yet to been established. A hospital-based observational study including 558 AMI patients and 1959 controls was conducted. Lp(a) level was significantly higher in AMI patients with normal LDL-C levels than that in non-CAD group (median: 134.5 mg/l vs 108 mg/l, P<0.001). According to Lp(a) quartiles (Q1, <51 mg/l; Q2, 51-108 mg/l; Q3, 108-215 mg/l; Q4, ≥215 mg/l), the incidence of AMI increased with the elevated Lp(a) quartiles (P<0.001 and P for trend<0.001). Logistic regression analysis suggested that patients with Q3 and Q4 of Lp(a) values had 1.666 (95%CI = 1.230-2.257, P<0.001) and 1.769 (95%CI = 1.305-2.398, P< 0.001) folds of AMI risk compared with patients with Q1, after adjusting for traditional confounders. Subgroup analyses stratified by gender and age showed that the association only existed in male and late-onset subgroups. In addition, we analyzed the association of Lp(a) with AMI risk in different cut-off values (cut-off 1 = 170 mg/l, cut-off 2 = 300 mg/l). A total of 873 (34.68%) and 432 (17.16%) participants were measured to have higher Lp(a) levels according to cut-off 1 and cut-off 2, respectively. Participants with high Lp(a) levels had 1.418- (cut-off1, 95%CI = 1.150-1.748, P<0.001) and 1.521- (cut-off 2, 95%CI = 1.179-1.963, P< 0.001) folds of AMI risk compared with patients with low Lp(a) levels. The present large-scale study revealed that elevated Lp(a) levels were associated with increased AMI risk in Chinese population with normal LDL-C levels.

Associations between PPARG polymorphisms and the risk of essential hypertension.

BACKGROUND: Peroxisome proliferator-activated receptor gamma (PPARG) plays an important role in the pathogenesis and maintenance of essential hypertension (EH). It has been suggested that polymorphisms of PPARG are associated with the risk of EH. However, findings to date remain controversial. To elucidate the associations between the PPARG Pro12Ala and C161T polymorphisms and EH risk, a meta-analysis was carried out. METHODS: A comprehensive literature search of PubMed, Embase, CNKI (Chinese National Knowledge Infrastructure), VIP and Wanfang databases was conducted. The pooled odds ratios (ORs) and 95% confidence interval (CI) were calculated to estimate the size of the effect using the random-effects model. At the same time, the pooled standardized mean difference (SMD) with 95% CI was used for the meta-analysis of the PPARG Pro12Ala polymorphism and blood pressure. RESULTS: Finally, Fifteen papers (seventeen studies) including 4,151 cases and 4,997 controls to evaluate the association of the PPARGPro12Ala polymorphism and EH risk, were included in this study. Overall, the results suggested that Ala allele was associated with the decreased EH risk (for allelic model, OR = 0.757, 95%CI: 0.624-0.918, P = 0.005; for dominant model, OR = 0.771, 95%CI: 0.627-0.946, P = 0.013). The subgroup analysis stratified by ethnicity showed that the significant association between the PPARG Pro12Ala polymorphism and EH was only detected in the Asian subgroup. There was no difference in blood pressure values between Ala carriers and non-carriers. For the C161T polymorphism, only 5 studies comprising 1,118 cases and 1,357 controls met the inclusion criteria. The overall results showed that the PPARG C161T polymorphism was not associated with the risk of EH. But in the subgroup analysis, we found that the PPARG C161T polymorphism significantly associated with the risk of EH in the Asian subgroup (for allelic model, OR = 0.719, 95% CI: 0.537-0.963, P = 0.027; for dominant model, OR = 0.653, 95% CI: 0.439-0.972, P = 0.036). CONCLUSION: Our meta-analysis suggested that the PPARG polymorphisms might be associated with the risk of EH.

Associations of Rs3744841 and Rs3744843 Polymorphisms in Endothelial Lipase Gene with Risk of Coronary Artery Disease and Lipid Levels in a Chinese Population.

OBJECTIVE: The aim of the present study was to assess the association between the 2037T/C and 2237G/A polymorphisms in the EL gene and the risk of CAD and lipid levels in a Chinese population. METHODS: A case-control study including 706 patients with CAD and 315 controls was performed. The polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) method was used to identify the genotypes. RESULTS: The EL 2037 T/C polymorphism was associated with CAD risk and HDL-C levels. No significant differences were found between the EL 2237 G/A genotypes and CAD risk and lipid levels in the whole population. However, carriers of the 2237 A allele had higher Apo A1 levels than those with the 2237 GG genotype and in the CAD subgroup (P = 0.044). The CAD cases have a significantly lower frequency of the C-G haplotypes than the controls, and the T-A haplotype was significantly more common in the CAD patients than in the controls. CONCLUSIONS: Our study concluded that the EL 2037 T/C polymorphism was associated with CAD risk and HDL-C levels, and that the C allele might be a protective factor against CAD in the Chinese Han population. In addition, the EL 2237 A allele might be associated with an increased Apo A1 level in CAD subjects.

Endothelial lipase genetic polymorphisms and the lipid-lowering response in patients with coronary artery disease on rosuvastatin.

BACKGROUND: Endothelial lipase (EL) plays an important role in the regulation of lipid metabolism by reducing the high density lipoprotein cholesterol (HDL-C) levels and inducing the macrophages to take up native low density lipoprotein cholesterol (LDL-C). Our purpose was to investigate the impact of EL genetic polymorphisms on the lipid-lowering effects of rosuvastatin in Chinese coronary artery disease (CAD) patients. METHODS: One hundred twenty-one unrelated CAD patients, who underwent the treatment with rosuvastatin (10mg/day) for four to eight weeks, were enrolled in this study. Before and after treatment, serum lipids levels were measured. Genotypes of EL 2037T/C and 2237 G/A polymorphisms were detected by polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) method. RESULTS: Patients with EL 2037C allele (CC + CT) had significantly lower LDL-C levels than those with TT genotype (CC + CT: 2.60 ± 0.74 mmol/l; TT: 2.90 ± 0.87 mmol/l; P = 0.047), before rosuvastatin treatment. No significant differences between baseline lipid levels and the EL 2237G/A genotypes were observed. After treatment with rosuvastatin, total cholesterol (TC), high triglyceride (TG) and LDL-C levels decreased from baseline, on average, by 23.09 % (4.59 ± 0.96 mmol/l to 3.47 ± 0.83 mmol/l), 6.36 % (2.01 ± 1.18 mmol/l to 1.68 ± 1.16 mmol/l), 32.48 % (2.77 ± 0.83 mmol/l to 1.79 ± 0.62 mmol/l), respectively (all P < 0.05) in all patients. While changes in HDL-C levels did not reach statistical significance. No significant effects of EL 2037T/C or 2237G/A polymorphism were observed on lipid-lowering effects of rosuvastatin. CONCLUSIONS: EL 2037T/C and 2237 G/A polymorphisms might not affect the lipid-owing effects of rosuvastatin in Chinese CAD patients.

Naturally occurring BRCA2 alternative mRNA splicing events in clinically relevant samples.

BACKGROUND: BRCA1 and BRCA2 are the two principal tumour suppressor genes associated with inherited high risk of breast and ovarian cancer. Genetic testing of BRCA1/2 will often reveal one or more sequence variants of uncertain clinical significance, some of which may affect normal splicing patterns and thereby disrupt gene function. mRNA analyses are therefore among the tests used to interpret the clinical significance of some genetic variants. However, these could be confounded by the appearance of naturally occurring alternative transcripts unrelated to germline sequence variation or defects in gene function. To understand which novel splicing events are associated with splicing mutations and which are part of the normal BRCA2 splicing repertoire, a study was undertaken by members of the Evidence-based Network for the Interpretation of Germline Mutant Alleles (ENIGMA) consortium to characterise the spectrum of naturally occurring BRCA2 mRNA alternate-splicing events. METHODS: mRNA was prepared from several blood and breast tissue-derived cells and cell lines by contributing ENIGMA laboratories. cDNA representing BRCA2 alternate splice sites was amplified and visualised using capillary or agarose gel electrophoresis, followed by sequencing. RESULTS: We demonstrate the existence of 24 different BRCA2 mRNA alternate-splicing events in lymphoblastoid cell lines and both breast cancer and non-cancerous breast cell lines. CONCLUSIONS: These naturally occurring alternate-splicing events contribute to the array of cDNA fragments that may be seen in assays for mutation-associated splicing defects. Caution must be observed in assigning alternate-splicing events to potential splicing mutations.

Dosage- and time-dependent antibacterial effect of zinc oxide nanoparticles determined by a highly uniform SERS negating undesired spectral variation.

Massive production of nanomaterials poses a high risk to environmental ecology and human health. However, comprehensive understanding of nanotoxicity is still a major challenge due to the limitations of assessment methods, especially at the molecular level. We developed a new, sensitive, and robust fingerprinting surface-enhanced Raman spectroscopy (SERS) approach to interrogate both dose- and time-dependent phenotypic bacterial responses to zinc oxide nanoparticles (ZnO NPs). SERS enhancement was provided by biocompatible Au NPs. Additionally, a novel vacuum filtration-based strategy was adopted to fabricate bacterial samples with highly uniform SERS signals, ensuring the acquisition of robust and independent spectral changes from ZnO NPs-impacted bacteria without undesirable spectral variations. Combined with multivariate analysis, clear and informative spectral alteration profiles were obtained. Much greater alterations were found in low-dose ranges than high-dose ranges, indicating a reduction in the bioavailability of ZnO NPs with doses. Time-resolved bacterial responses provided important information on toxic dynamics, i.e., rapid action of ZnO NPs within 0.5 h was identified, and ZnO NPs at low doses and long exposure time exerted similar effects to high doses, indicating the concerns associated with low-dose exposure. Further analysis of biochemical changes revealed metabolic activity decrease over both incubation time and doses. Meanwhile, a short-term protection strategy of bacteria by producing lipid-containing outer membrane vesicles to mitigate the cell of toxic NPs was suggested. Finally, Zn(2+) ions released from NPs were demonstrated to be irrelevant to bacterial responses on both dose and time scales. The new SERS methodology can potentially profile a large variety of toxic NPs and advance our understanding of nanotoxicity. Graphical Abstract A highly uniform SERS signal of bacteria negating undesired spectral variation via a novel vacuum filtration-based strategy, combined with multivariate PCA-LDA analysis, was utilized to interrogate both dose- and time-dependent antibacterial effect of zinc oxide nanoparticles, and can be extended to a variety of other toxic nanoparticles.

Surface-Enhanced Raman Spectroscopy for Identification of Heavy Metal Arsenic(V)-Mediated Enhancing Effect on Antibiotic Resistance.

Bacterial antibiotic resistance poses a threat to global public health. Restricted usage of antibiotics does not necessarily prevent its continued emergence. Rapid and sensitive screening of triggers, in addition to antibiotic, and exploring the underlying mechanism are still major challenges. Herein, by developing a homogeneous vacuum filtration-based bacterial sample fabrication enabling high surface-enhanced Raman scattering (SERS) reproducibility across multiple bacterial samples and negating interfering spectral variations from inhomogeneous sample geometry and SERS enhancement, SERS was employed to study heavy metal arsenic [As(V)]-mediated antibiotic resistance in a robust, sensitive, and rapid fashion. Independent and robust spectral changes representing phenotypic bacterial responses, combined with multivariate analysis, clearly identified that As(V) enhanced antibiotic resistance to tetracycline (Tet). Similar spectral alteration profile to As(V) and Tet indicated that cross-resistance, whereby As(V)-induced bacterial resistance simultaneously blocked Tet action, could account for the enhanced resistance. The sensitive, robust, and rich phenotypic profile provided by SERS, combined with additional advantages in imposing no need to cultivate bacteria and single-cell sensitivity, can be further exploited to evaluate resistance-intervening factors in real microbiota.

The associations between proprotein convertase subtilisin/kexin type 9 E670G polymorphism and the risk of coronary artery disease and serum lipid levels: a meta-analysis.

BACKGROUND: Studies had investigated the associations between proprotein convertase subtilisin/kexin type 9 (PCSK9) E670G polymorphism and coronary artery disease (CAD) and lipid levels, but the results were controversial. Thus, we performed this meta-analysis to investigate the association between PCSK9 E670G polymorphism and lipid levels and the susceptibility to CAD. METHODS: All relevant articles according to the inclusion criteria were retrieved and included in the present meta-analysis. Odds ratios (ORs) with 95 % confidence interval (CI) were used to analyze the strength of the association between PCSK9 E670G polymorphism and the susceptibility to CAD. At the same time, the pooled standardized mean difference (SMD) with 95 % CI was used for the meta-analysis of PCSK9 E670G polymorphism and lipid levels. The publication bias was examined by using Begg's funnel plots and Egger's test. RESULTS: A total of seventeen studies met the inclusion criteria. For CAD association, the pooled effects indicated that the G allele carriers had higher risk of CAD than non-carriers in dominant genetic model (OR:1.601, 95 % CI: 1.314-1.951, P < 0.001), as well as in allelic genetic model (OR: 1.546, 95 % CI: 1.301-1.838, P < 0.001). When the subgroup analysis stratified by ethnicity and HWE was performed, the positive result existed in most of the subgroups. For lipid levels association, the pooled effects indicated that the G allele carriers had higher TC and LDL-C levels than the non-carriers (for TC, SMD: 0.126, 95 % CI: 0.023-0.229, P = 0.016; for LDL-C, SMD: 0.170, 95 % CI: 0.053-0.287, P = 0.004, respectively). There was no difference in the levels of TG and HDL-C between the G carriers and the non-carriers in the whole population (SMD: 0.031, 95 % CI: -0.048-0.110, P = 0.440; SMD: -0.123, 95 % CI: -0.251-0.006, P = 0.061, respectively). When the studies were stratified by ethnicity and type of study, the G carriers had higher TC levels than the non-carriers (SMD: 0.126, 95 % CI: 0.014-0.238, P = 0.027) in the non-Asian subgroup. The similar results existed in cohort subgroup. The association between PCSK9 E670G polymorphism and LDL-C levels was significant in all subgroups. Meanwhile, the G carriers had higher TG levels than the non-carriers (SMD: 0.113, 95 % CI: 0.012-0.214, P = 0.028) in the case-control subgroup. AG + GG genotypes had lower HDL-C levels than AA genotype in Asian subgroup (SMD: -0.224, 95 % CI: -0.423- -0.025, P = 0.027) and in case-control subgroup (SMD: -0.257, 95 % CI: -0.467--0.048, P = 0.016). CONCLUSIONS: The present meta-analysis concluded that PCSK9 E670G polymorphism was associated with CAD risk and lipid levels.

Interrogating chemical variation via layer-by-layer SERS during biofouling and cleaning of nanofiltration membranes with further investigations into cleaning efficiency.

Periodic chemical cleaning is an essential step to maintain nanofiltration (NF) membrane performance and mitigate biofouling, a major impediment in high-quality water reclamation from wastewater effluent. To target the important issue of how to clean and control biofouling more efficiently, this study developed surface-enhanced Raman spectroscopy (SERS) as a layer-by-layer tool to interrogate the chemical variations during both biofouling and cleaning processes. The fact that SERS only reveals information on the surface composition of biofouling directly exposed to cleaning reagents makes it ideal for evaluating cleaning processes and efficiency. SERS features were highly distinct and consistent with different biofouling stages (bacterial adhesion, rapid growth, mature and aged biofilm). Cleaning was performed on two levels of biofouling after 18 h (rapid growth of biofilm) and 48 h (aged biofilm) development. An opposing profile of SERS bands between biofouling and cleaning was observed and this suggests a layer-by-layer cleaning mode. In addition, further dynamic biochemical and infrastructural changes were demonstrated to occur in the more severe 48-h biofouling, resulting in the easier removal of sessile cells from the NF membrane. Biofouling substance-dependent cleaning efficiency was also evaluated using the surfactant sodium dodecyl sulfate (SDS). SDS appeared more efficient in cleaning lipid than polysaccharide and DNA. Protein and DNA were the predominant residual substances (irreversible fouling) on NF membrane leading to permanent flux loss. The chemical information revealed by layer-by-layer SERS will lend new insights into the optimization of cleaning reagents and protocols for practical membrane processes.

Associations of pregnancy-associated plasma protein-A level with essential hypertension and hypertensive disorders in pregnancy in Chinese population: a meta-analysis of 20 research studies involving 3332 individuals.

OBJECTIVE: To explore the associations between serum pregnancy-associated plasma protein-A (PAPP-A) level, and essential hypertension (EH) and hypertensive disorders in pregnancy (HDP) in Chinese population. METHODS: Pertinent studies were independently searched in PubMed, Embase, Cochrane Library, Chinese Biomedical Database (CBM), Wanfang databases and China National Knowledge Infrastructure (CNKI). The standardised mean difference (SMD) with 95% CIs was used to estimate the size of the effect. The subgroup analyses and meta-regression analysis were performed to identify the sources of heterogeneity among studies. Sensitivity analysis was conducted to assess the stability of the results. The publication bias between studies was examined by using Begg's funnel plots and Egger's test. RESULTS: A total of 20 studies involving 1493 patients and 1839 controls were included in the current meta-analysis. The PAPP-A level was significantly higher in EH patients than in controls (SMD=1.960, 95% CI 1.305 to 2.615, p<0.001), and significant associations were observed in all subgroups. The PAPP-A level was also significantly higher in HDP patients than in healthy pregnant women (SMD=2.249; 95% CI 1.324 to 3.173, p<0.001). The positive association between PAPP-A level and the risk of HDP was consistently observed in all subgroups except the subgroup with low NOS score. CONCLUSIONS: The present meta-analysis suggests that an elevated PAPP-A level may be associated with susceptibilities to EH and HDP.

The associations between the MCP-1 -2518 A/G polymorphism and ischemic heart disease and ischemic stroke: a meta-analysis of 28 research studies involving 21,524 individuals.

Epidemiologic studies have been performed to explore the relationship between MCP-1 polymorphism and ischemic heart disease (IHD) and ischemic stroke (IS). But, the results are not consistent. Because of the poor effect of each individual study, we've performed a systematic review and a meta-analysis. A comprehensive search was carried out from PubMed, Embase, Foreign Medical Journal Service (FMJS), China National Knowledge Infrastructure and Wanfang Data. Odds ratios (OR) with 95% confidence interval (CI) were used to evaluate the strength of associations between the MCP-1 A-2518G polymorphism (rs1024611) and IHD and IS susceptibilities. The pooled OR was calculated by the allelic model (G vs A), the additive model (GG vs AA), the dominant model (GG+GA vs AA) and the recessive model (GG vs AA+GA), respectively. The homogeneity among studies was checked using Cochrane Q statistic. The stability of results was checked by one-way sensitivity analysis. The publication bias between studies was examined by Begg's funnel plots and Egger's test. 28 eligible case-control studies met all the criteria and were involved in the present meta-analysis, including a total of 8,901 cases and 12,623 controls. Overall, the MCP-1 A-2518G polymorphism was significantly associated with the IHD susceptibility. The pooled OR was 1.27 (95% CI 1.09-1.48, P = 0.002) in the dominant model, 1.20 (95% CI 1.07-1.35, P = 0.001) in the allelic model, 1.25 (95% CI 1.05-1.50, P = 0.015) in the recessive model and 1.39 (95% CI 1.10-1.75, P = 0.005) in the additive model. At the same time, the MCP-1 A-2518G polymorphism was significantly associated with the IS susceptibility. The pooled OR was 1.72 (95% CI 1.12-2.65, P = 0.013) in the dominant model, 1.39 (95% CI 1.12-1.74, P = 0.003) in the allelic model, 1.59 (95% CI 1.30-1.93, P = 0.000) in the recessive model, and 2.33 (95% CI 1.76-3.08, P = 0.000) in the additive model, respectively. No significant publication bias was found in the present meta-analysis. The results of the present meta-analysis suggest that MCP-1 gene A-2518G polymorphism may be associated with the IHD and IS susceptibilities. But the positive result exists in relatively small sample size subgroup.

E-selectin gene polymorphisms and essential hypertension in Asian population: an updated meta-analysis.

OBJECTIVE: Epidemiological studies have shown that E-selectin gene polymorphisms (A561C and C1839T) may be associated with essential hypertension (EH), but the results are conflicting in different ethnic populations. Thus, we performed this meta-analysis to investigate a more authentic association between E-selectin gene polymorphisms and the risk of EH. METHODS: We searched the relevant studies for the present meta-analysis from the following electronic databases: PubMed, Embase, Cochrane Library, Google Scholar, Web of Science, Wanfang Data, and China National Knowledge Infrastructure (CNKI). Odds ratios (OR) with 95% confidence interval (CI) were used to evaluate the strength of the association between E-selectin gene polymorphisms and EH susceptibility. The pooled ORs were performed for dominant model, allelic model and recessive model. The publication bias was examined by Begg's funnel plots and Egger's test. RESULTS: A total of eleven studies met the inclusion criteria. All studies came from Asians. Ten studies (12 cohorts) evaluated the A561C polymorphism and EH risk, including 2,813 cases and 2,817 controls. The pooled OR was 2.280 (95%CI: 1.893-2.748, P<0.001) in dominant model, 5.284 (95%CI: 2.679-10.420, P<0.001) in recessive model and 2.359 (95%CI: 1.981-2.808, P = 0.001) in allelic model. Four studies (six cohorts) evaluated C1839T polymorphism and EH risk, including 1,700 cases and 1,681 controls. The pooled OR was 0.785 (95%CI: 0.627-0.983, P = 0.035) in dominant model, 1.250 (95%CI: 0.336-4.652, P = 0.739) in recessive model and 0.805 (95%CI: 0.649-0.999, P = 0.049) in allelic model. CONCLUSION: The current meta-analysis concludes that the C allele of E-selectin A561C gene polymorphism might increase the EH risk in Asian population, whereas the T allele of E-selectin C1839T gene polymorphism might decrease the EH risk.

The associations between endothelial lipase 584C/T polymorphism and HDL-C level and coronary heart disease susceptibility: a meta-analysis.

BACKGROUND: Studies had investigated the relationships between endothelial lipase (EL) 584C/T polymorphism and high density lipoprotein cholesterol (HDL-C) level and coronary heart disease (CHD), but the results were controversial. To investigate a more authentic associations between EL 584C/T polymorphism and HDL-C level, and the risk of CHD, we performed this meta-analysis. METHODS: We searched electric databases for all articles on the associations between EL 584C/T polymorphism and HDL-C level, and CHD risk. Odds ratios (ORs) with 95% confidence interval (CI) were used to evaluate the strength of the association between the EL 584C/T polymorphism and the CHD susceptibility. The pooled standardized mean difference (SMD) with 95% CI was used for the meta-analysis of EL 584C/T polymorphism and HDL-C level. Begg's funnel plots and Egger's test were used to examine the publication bias. RESULTS: For CHD association, the pooled OR was 0.829 (95% CI: 0.701-0.980, P = 0.028) for the dominant model and 0.882 (95% CI: 0.779-0.999, P = 0.049) for the allelic model. By meta-regression analysis, we found that only total sample size could influence the initial heterogeneity. When the subgroup analysis was carried out, we found that the protective effect only existed in the subgroups of relatively small sample size. Sensitivity analyses indicated that Tang's study influenced the overall results significantly. We calculated the pooled ORs again after excluding Tang's study and found the association between EL 584C/T polymorphism and the risk of CHD was not significant for any genetic model. For HDL-C level association, the carriers of 584 T allele had a higher HDL-C level than the non-carriers. The pooled SMD was 0.399 (95% CI: 0.094-0.704, P = 0.010). When the studies were stratified by ethnicity and total sample size, the positive effects existed in the Caucasians and in subgroups of larger sample size. No significant publication bias was found in the present meta-analysis. CONCLUSIONS: The results of the present meta-analysis suggest that the carriers of EL 584 T allele have a higher HDL-C level in Caucasian populations. Whereas, it might not be a protective factor for CHD.

High prevalence of BRCA1 and BRCA2 mutations in unselected Nigerian breast cancer patients.

Inherited mutations in the BRCA1 and BRCA2 genes are the strongest genetic predictors of breast cancer and are the primary causes of familial breast/ovarian cancer syndrome. The frequency, spectrum and penetrance of mutant BRCA1/BRCA2 alleles have been determined for several populations, but little information is available for populations of African ancestry, who suffer a disproportionate burden of early onset breast cancer. We have performed complete sequence analysis of all BRCA1 and BRCA2 exons and intron-exon boundaries for 434 Nigerian breast cancer patients from the University College Hospital in Ibadan, Nigeria. In contrast to previous suggestions that BRCA1/BRCA2 mutation frequencies are low or undetectable in African American populations, we find that Nigerian breast cancer patients have an exceptionally high frequency of BRCA1 and BRCA2 mutations (7.1 and 3.9%, respectively). Sixteen different BRCA1 mutations were detected, seven of which have never been reported previously, while thirteen different BRCA2 mutations were seen, six of which were previously unreported. Thus, our data support enrichment for genetic risk factors in this relatively young cohort. To improve breast cancer outcomes, we suggest that family-based models of risk assessment and genetic counseling coupled with interventions to reduce breast cancer risk should be broadly disseminated in Nigeria and other underserved and understudied populations.

Population differences in breast cancer: survey in indigenous African women reveals over-representation of triple-negative breast cancer.

PURPOSE: Compared with white women, black women experience a disproportionate burden of aggressive breast cancer for reasons that remain unknown and understudied. In the first study of its kind, we determined the distribution of molecular subtypes of invasive breast tumors in indigenous black women in West Africa. PATIENTS AND METHODS: The study comprised 507 patients diagnosed with breast cancer between 1996 and 2007 at six geographic regions in Nigeria and Senegal. Formalin-fixed and paraffin-embedded sections were constructed into tissue microarrays and immunostained with 15 antibodies. Five molecular subtypes were determined, and hierarchical cluster analysis was conducted to explore subgroups for unclassified cases. RESULTS: The mean (+/- standard deviation) age of 378 patients in the first cohort was 44.8 +/- 11.8 years, with the majority of women presenting with large (4.4 +/- 2.0 cm) high-grade tumors (83%) in advanced stages (72% node positive). The proportions of estrogen receptor (ER) -positive, progesterone receptor-positive, and human epidermal growth factor receptor 2 (HER2) -positive tumors were 24%, 20%, and 17%, respectively. Triple negativity for these markers was predominant, including basal-like (27%) and unclassified subtype (28%). Other subtypes were luminal A (27%), luminal B (2%), and HER2 positive/ER negative (15%). The findings were replicated in the second cohort of 129 patients. The unclassified cases could be grouped into a bad prognosis branch, with expression of vascular endothelial growth factor, B-cell lymphoma extra-large protein, and Cyclin E, and a good prognosis branch, with expression of B-cell lymphoma protein 2 and Cyclin D1. CONCLUSION: These findings underscore the urgent need for research into the etiology and treatment of the aggressive molecular subtypes that disproportionately affect young women in the African diaspora.

Evidence for an ancient BRCA1 mutation in breast cancer patients of Yoruban ancestry.

BACKGROUND: BRCA1 recurrent mutations have rarely been assessed in non-founder populations. Still, identifying such mutations could be important for designing genetic testing strategies for high-risk breast/ovarian cancer families in non-founder populations. OBJECTIVE: To determine whether the recurrent BRCA1 Y101X mutation identified in Yoruban breast cancer patients represents a single historical mutation event, and determine the prevalence of this mutation in a hospital based cohort. METHODS: 365 breast cancer patients and 177 controls of Yoruban ancestry from Nigeria, unselected for age of onset or family history were screened for the BRCA1 Y101X mutation. The haplotypes on which the Y101X mutation occurred were characterized using microsatellite markers and single-nucleotide polymorphisms (SNPs). Phase ambiguity was resolved using allele-specific PCR. RESULTS: The BRCA1 Y101X mutation was detected in four Yoruban patients with no documented family history of breast cancer among a cohort of 365 (1.1, 95% C.I. = 0.43-2.78%) unrelated Yoruban breast cancer patients. This study reveals the four Y101X mutations occur on a single, rare haplotype. Further characterization in a patient of European ancestry with a strong family history of breast/ovarian cancer revealed the same Y101X mutation on the same haplotype as those in the Yoruban carriers. These observations suggest the Y101X mutations identified in the Yoruban patients may have originated from a single mutation event. CONCLUSIONS: BRCA1 Y101X is the first reported recurrent mutation occurring in patients of African ancestry for which prevalence has been determined. Identification of this mutation in a woman of European ancestry with strong family history of breast/ovarian suggests further that this mutation occurred once, probably many generations ago.