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Purpose Pauwels type-3 femoral neck fractures are challenging injuries to manage with high rates of complications after internal fixation and no consensus has been reached regarding the optimal fixation construct. The current study aims to evaluate the effect of dynamic limited axial compression in parallel screws combined with medial buttress plate (SMBP) or lateral compression plate (LCP) fixation of Pauwels type-3 femoral neck fractures. Methods We performed a retrospective analysis of 51 cases of Pauwels type-3 femoral neck fractures who were fixed by SMBP or LCP. Specifically, the screw fixing the femoral head in the buttress plate was omitted. Postoperative complications and functional outcomes were mainly studied. Results With a mean follow-up of 19.9 months, the rate of neck shortening was higher in the LCP group than that in SMBP group (32.1% vs. 8.7%, p = 0.04). Neither nonunion nor avascular necrosis was observed in both groups. Good-to-excellent Harris hip score accounts for 95.2% in SMBP group and 89.3% in LCP group (p = 0.40). Moreover, older age, fracture comminution and compression plate fixation predispose to neck shortening. Conclusion Dynamic limited axial compression by SMBP or LCP fixation was effective to improve the functional outcome of patients with Pauwels type-3 femoral neck fractures.

Sigma non-opioid intracellular receptor 1 (sigma-1 receptor), a non-opioid transmembrane protein, is located on cellular mitochondrial membranes and endoplasmic reticulum. Current research has demonstrated that sigma-1 receptor is related to human degenerative diseases. This study is focused on the effects of sigma-1 receptor on the pathophysiological process of diminished ovarian reserve (DOR) and granulosa cells (GCs) apoptosis. Sigma-1 receptor concentration in follicular fluid (FF) and serum were negatively correlated with basal follicle-stimulating hormone (FSH) and positively correlated with anti-mullerian hormone (AMH), antral follicle count (AFC). Sigma-1 receptor reduction in GCs was accompanied by endoplasmic reticulum stress (ERS)-mediated apoptosis in women with DOR. Plasmid transfection was used to establish SIGMAR1-overexpressed and SIGMAR1-knockdown human granulosa-like tumor (KGN) cell and thapsigargin (TG) was used to induce ERS KGN cells. We found that KGN cells treated with endogenous sigma-1 receptor ligand dehydroepiandrosterone (DHEA) and sigma-1 receptor agonist PRE-084 showed similar biological effects to SIGMAR1-overexpressed KGN cells and opposite effects to SIGMAR1-knockdown KGN cells. DHEA may improve DOR patients' pregnancy outcomes by upregulating sigma-1 receptor and downregulating ERS-mediated apoptotic genes in GCs. Thus, sigma-1 receptor may be a potential ovarian reserve biomarker, and ligand-mediated sigma-1 receptor activation could be a future approach for DOR therapy.

Background Effect of serum calcium levels on prognosis of patients with coronary artery disease (CAD) is not well evaluated. We aimed to assess the associations of baseline serum calcium levels with both short-term and long-term outcomes in CAD patients. Methods This study included 3,109 consecutive patients with angiographically confirmed CAD. Patients were categorized into quartiles according to admission serum calcium. Multivariable regression analysis was used to determine the association of serum calcium with mortality. Results Compared to patients in the lowest quartile of serum calcium, patients in upper quartiles were presented with lower all-cause mortality (Hazard ratios [HRs] were −0.636 [95% CI: −0.424 to −0.954], −0.545 [95% CI: −0.351 to −0.846] and −0.641 [95% CI: −0.450 to −0.913] for three upper quartiles versus lowest quartile respectively), cardiovascular mortality (HRs 0.594 [0.368−0.961], 0.261 [0.124–0.551] and 0.407 [0.229–0.725]), and in-hospital mortality (Odd ratios [ORs] 0.391 [0.188–0.812], 0.231 [0.072–0.501] and 0.223 [0.093–0.534]). Consistent associations between serum calcium and long-term mortality were also obtained in subgroup analysis of ACS patients, stable CAD patients and discharged patients. Conclusions Serum calcium is inversely associated with CAD and can independently predict both in-hospital and long-term mortality among CAD patients.

Background The Global Registry of Acute Coronary Events (GRACE) risk score has been extensively validated to predict risk during hospitalization in patients with acute coronary syndrome (ACS). Recently, serum calcium has been suggested as an independent predictor for in-hospital mortality in patients with ST-segment elevation myocardial infarction; however, the relationship between the 2 has not been evaluated. Hypothesis The combination of GRACE risk score and serum calcium could provide better performance in risk prediction. Methods The study enrolled 2229 consecutive patients with ACS. Independent predictors were identified by a multivariate logistic regression model. The incremental prognostic value added by serum calcium to the GRACE score was evaluated by receiver operating characteristic, net reclassification improvement (NRI), and integrated discrimination improvement (IDI). Results Patients in the upper quartiles of serum calcium presented with lower in-hospital mortality (odds ratios for 3 upper quartiles vs lowest quartile, respectively: 0.443, 95% confidence interval [CI]: 0.206-0.953; 0.243, 95% CI: 0.090-0.654; and 0.210, 95% CI: 0.082-0.538). Area under the curve increased significantly after adding serum calcium to the GRACE score (0.685 vs 0.746; Z = 2.617, P = 0.009). Furthermore, inclusion of serum calcium in the GRACE score enhanced NRI (0.524; P = 0.009) and IDI (0.011; P = 0.003). Conclusions Lower serum calcium level on admission is a possible indicator of increased risk of in-hospital mortality in ACS patients. Inclusion of serum calcium in the GRACE score may lead to a more accurate prediction of this risk. Large prospective studies are needed to confirm this finding.

Objectives Calcium has a critical role in a spectrum of biological processes related to cardiovascular disease. This study aimed to evaluate associations of baseline serum calcium levels with both short-term and long-term outcomes in CAD patients. Materials and methods 3109 consecutive patients with angiography confirmed CAD, admitted to West China hospital of Sichuan University between July 2008 and September 2012 were enrolled and were categorized into quartiles according to admission serum calcium to determine the association of serum calcium level with in-hospital and long-term mortality by multivariable Logistic and Cox regression analysis respectively. Results The admission serum calcium was normally distributed with a mean level of 2.20±0.15 mmol/L. A total of 259 deaths, including 58 in-hospital deaths, occurred during a mean follow-up of 20 months. Patients in the upper quartiles of serum calcium, as compared to the lowest quartile of serum calcium, were presented with lower in-hospital mortality [HR was 0.391 (95% CI: 0.188–0.812), 0.231(95% CI: 0.072–0.501) and 0.223 (95% CI: 0.093–0.534) for three upper quartiles versus lowest quartile respectively] and long-term mortality [HR was 0.614 (95% CI: 0.434–0.869), 0.476(95% CI: 0.294–0.698) and 0.553 (95% CI: 0.349–0.777) respectively]. Similar association between serum calcium and long-term mortality as showed in total cohort were also obtained when restricting analyses to subgroups: stable CAD patients, ACS patients and discharged patients. Conclusions As a widely available clinical index, serum calcium was an independent predictor of both in-hospital and long-term mortality among CAD patients. Further studies are warranted to determine mechanisms and whether patients with hypocalcaemia could benefit from calcium supplement.

Background Cytochrome P450 (CYP)2C19 is expressed in vascular endothelium and metabolizes arachidonic acid to biologically active epoxyeicosatrienoic acids, which play a key role in regulating vascular tone. The aim of this study was to investigate whether the genetic functional variant 681G>A (*2) of cytochrome CYP2C19 is associated with adverse cardiovascular outcomes in Chinese patients with coronary artery disease (CAD). Methods Between July 2008 and September 2009, 654 consecutive patients with CAD were enrolled in this study. All participants underwent CYP2C19 genotyping. The primary study endpoint was a composite of cardiovascular death, nonfatal myocardial infarction, and nonfatal stroke. Secondary endpoints included the components of the primary endpoint, death from any cause, and recurrent revascularization. Results The baseline characteristics were well-balanced between carriers (heterozygous *1/*2, n =291; homozygous *2/*2, n =57) and non-carriers ( n =306) of the CYP2C19*2 variant. During the follow-up period (11.42±4.23 months), the primary endpoint occurred more frequently in homozygous *2/*2 than in non-carriers ( n =306) of CYP2C19*2 variant (12.28% versus 3.27%; adjusted hazard ratio [HR]=5.191; 95% confidence interval [CI]=1.936–13.917; P =0.001); however, no such increase was evident in heterozygous *1/*2 patients (4.12% versus 3.27%; adjusted HR=1.208; 95% CI 0.517–2.822; P =0.662). Conclusions The homozygous CYP2C19*2/*2 genotype is an independent determinant of adverse vascular events in Chinese patients with CAD.

Objectives: To assess the impact of different CYP2C19*2 polymorphisms on clinical outcomes and the effects of CYP2C19*2 polymorphism on predicting clinical outcomes in association with classic risk factors in patients with acute coronary syndromes (ACS). Methods: Between July 2008 and September 2009, 497 consecutive patients with ACS who were admitted to the West China Hospital of Sichuan University were enrolled and underwent CYP2C19*2 determination. The clinical outcomes were the composite of cardiovascular death, nonfatal myocardial infarction and nonfatal stroke. Results: Baseline characteristics were balanced between noncarrier, heterozygous and homozygous groups of the CYP2C19*2 variant. The clinical endpoint occurred more frequently in the homozygous group (HR 4.86, CI 1.62–14.56, p = 0.005). After multivariable analysis, the CYP2C19*2 genetic variant was an independent predictor of cardiovascular events (HR 5.96, CI 1.77–20.03, p = 0.0039) as well as GRACE score and Killip class. The combination of CYP2C19*2 with GRACE score and Killip class increases the potential to predict adverse outcomes. Conclusions: Homozygosity (A/A) for CYP2C19*2 mutant is an independent determinant of prognosis in patients with ACS. The combination of CYP2C19*2 polymorphism with classic risk factors may be a useful tool to predict the risk of cardiovascular events.

Background Sudden cardiac death (SCD) from cardiac arrest, one of the most common types of cardiac-related death, is most often triggered by ventricular arrhythmia (VA). It has been reported that aldosterone antagonists (AAs) have the benefit of reducing SCD in patients with heart failure (HF). It also has been indicated in animal experiments and clinical trials that AAs may have an antiarrhythmic effect. Hypothesis AAs have an effect on VA in patients with HF or coronary artery disease. Methods We searched the Cochrane Central Register of Controlled Trials, PubMed, Current Controlled Trials, and the National Research Register, and identified randomized controlled trials on the effect of AAs on VA. Results All together, 7 trials with a total of 8635 patients were identified and extracted. AAs reduced the risk of SCD in patients with HF by 21% (relative risk [RR]: 0.79, 95% confidence interval [CI]: 0.67–0.93). AAs significantly reduced the episodes of ventricular premature complexes (mean difference 705 ± 646 episodes per 24 hours). Risk of ventricular tachycardia was reduced by 72% (RR: 0.28, 95% CI: 0.10–0.77). Conclusions The additional administration of AAs in patients with HF or coronary artery disease shows a benefit in reducing the risk of SCD and may also be effective for reducing episodes of ventricular premature complexes and ventricular tachycardia. Copyright © 2010 Wiley Periodicals, Inc. The work was supported by grants from the Chinese National Nature Science Foundation (grant numbers 30600607 and 30770877, Beijing, China), and the National High-tech Research and Development Program of China (2006AA02A406, Beijing, China).

This study aimed to investigate the relationship between the number of oocytes retrieved and clinical outcomes in young women with normal ovarian reserve who were undergoing their first in vitro fertilization and embryo transfer (IVF-ET) cycle. The transfer strategy based on yielded oocytes was also discussed in this article.A total of 1567 patients who underwent first long protocol of IVF treatment in our reproductive medical center between January 2010 and June 2014 were categorized into five groups based on the retrieved oocyte number, namely, 4∼6, 7∼9, 10∼12, 13∼15, and ≥16. Baseline parameters were similar among the groups. Primary outcome was defined as the cumulative live birth rate (CLBR), and secondary outcomes included the rate of patients with high risks for ovarian hyperstimulation syndrome (OHSS).It was found that the CLBR increased with the number of oocytes, as well as the rate for high risks of OHSS. In fresh cycles, 10∼12 oocyte group demonstrated the highest implantation rate (53.32 %), clinical pregnancy rate (CPR) (73.13 %), and live birth rate (LBR) (61.14 %), with no significant differences. Moreover, both cumulative CPR (CCPR) and CLBR became significantly higher in the 10∼12 oocyte group, compared with 4∼6 and 7∼9 groups. However, when the retrieved oocytes increased to 13∼15 or ≥16, the cumulative results did not have a significant increase. Also, the high risk rate of OHSS was much lower in the 10∼12 group (11.53 %) than that in the 13∼15 group (29.97 %) and ≥16 group (77.30 %). Unconditional multivariate logistic regression analysis showed that when ≥10 oocytes were retrieved, the CLBR increased significantly (P 0.01). When oocyte number exceeded 16, the CPR of frozen embryo transfer cycle was much higher than that of fresh cycle (P 0.05).For young women with normal ovarian reserve, retrieving 10∼12 oocytes might result in optimized pregnancy outcomes in a fresh cycle with low OHSS risk and would not compromise cumulative outcomes. When ≥16 oocytes were retrieved, a "freeze-all" embryo strategy might be preferable.

The p73 gene is a structural and functional homolog of the p53 gene, which has a crucial role in mediating cell cycle arrest and apoptosis. Numerous previous studies have investigated the polymorphism of p73 G4C14-to-A4T14 at exon 2, as it was suggested to affect gene expression and result in functional significance. However, the correlation of this polymorphism with clinicopathological variables of patients with non-small cell lung cancer (NSCLC) remains to be elucidated. The aim of the present study was to examine the association between the gene polymorphism of p73 G4C14-to-A4T14 and the risk of developing NSCLC. The single-nucleotide polymorphisms of p73 G4C14-to-A4T14 were genotyped using polymerase chain reaction with confronting two-pair primers and direct DNA sequencing in 186 NSCLC patients and 196 cancer-free controls. χ(2)-tests and logistic regression analysis were used to analyze the experimental data, including the determination of odds ratio (OR), 95% confidence intervals (95% CIs) and P-values. The results demonstrated that the AT/AT genotype was associated with a significantly decreased risk of NSCLC (P=0.010; OR=0.370; 95% CI=0.170-0.806) compared with the GC allele genotypes including GC/GC and GC/AT. In addition, carriers of the AT allele exhibited a significantly reduced risk of NSCLC (P=0.038; OR=0.713; 95% CI=0.517-0.983) compared with non-carriers. In conclusion, these results indicated that the p73 G4C14-to-A4T14 polymorphism was a potential marker of NSCLC genetic susceptibility. However, further studies with a larger population are required in order to confirm these results.

Earthquake may increase the risk of hemodynamically unstable ventricular tachyarrhythmias (HUSVTs). However, it was unclear how these arrhythmias were triggered during the period of earthquake. Medical records of patients in the Cardiovascular (CV) Department of West China Hospital, Chengdu, Sichuan, China, during the month after the Wenchuan earthquake and the 2 control periods (1 month before the earthquake and April 12 through July 11, 2007) were reviewed. The HUSVT event rate/10,000 person-days was higher during the month after the earthquake than during the 2 control periods (67 events/10,000 person-days vs 7 and 14 events/10,000 person-days; p = 0.000006 and p = 0.0004, respectively). Most HUSVT events in the earthquake month occurred in afternoon hours, consistent with the temporal trend of strong seismic activities and different from the pattern of diurnal distribution of HUSVT events occurring in the control periods. In the subpopulation consisting of patients admitted to the CV Department before the earthquake who continued to be treated the CV Department during the earthquake period, all HUSVT events occurred during the interval after the earthquake in comparison to no HUSVT event during the interval before the earthquake. Hypokalemia without identifiable cause, acute myocardial ischemia, and heart failure without evidence of ischemia were associated with HUSVT events in the earthquake month. In conclusion, the earthquake and its aftershocks could trigger the occurrence of HUSVT events in hospitalized patients with heart disease.

In a recent issue of the Journal , Popp [(1)][1] reviewed the modern techniques to measure cardiac troponin (cTn) and the value of increased cTn as a marker of myocardial injury and predictor of future heart failure. More importantly, we have read and agree with the author’s hypothesis: “cTn…