Background: Numerous studies have illustrated the association between Helicobacter pylori (H pylori) infection and acute coronary syndrome (ACS). However, the results are contradictory. Therefore, we conducted the meta-analysis to identify the association between H pylori and ACS. Methods: We performed a systematic search through electronic databases (Excerpta Medica Database, PubMed, Cochrane Library, and Web of Science). Pooled odds ratios (ORs) and 95% confidence intervals (CIs) were calculated with a random effect model. We also carried out the sensitivity analysis and publication bias. Results: Forty-four eligible studies involving 7522 cases and 8311 controls were included. The pooled result showed that H pylori infection was associated with an increase risk of ACS (OR = 2.03, 95% CI 1.66–2.47). In addition, similar results were obtained in subgroups of study quality, area, human development index, and H pylori detection method. The OR for developing countries was significantly higher than developed countries (OR = 2.58 vs OR = 1.69). Moreover, H pylori with cytotoxin-associated antigen A was also significantly associated with an increase risk of ACS (OR = 2.39, 95% CI 1.21–4.74). Conclusion: The meta-analysis suggested that H pylori infection was associated with an increased risk of ACS, especially in developing countries. H pylori is easily screened and can be treated with a wide range of drugs. Thus, more high-quality and well-designed studies are needed to confirm whether the treatment of H pylori is an effective way to reduce ACS risk.

Aim:To investigate whether plasma miR-19a can serve as a biomarker for esophageal squamous cell carcinoma (ESCC) diagnosis and prognosis. Materials & methods: Plasma samples from 89 ESCC, 45 benign lesion patients and 80 healthy controls were subjected to RT-qPCR analyses for miR-19a. In addition, plasma samples from 30 patients were collected before and after surgery for the same analyses. Results: Plasma miR-19a was significantly increased in ESCC patients compared with healthy controls. The sensitivity of miR-19a for early stages of ESCC was 68.09%. Combination of miR-19a and cytokeratin 19 fragment 21-1 (Cyfra21-1) further improved the sensitivity to 78.70%. Moreover, plasma miR-19a level was decreased in patients after surgery. Conclusion: Plasma miR-19a may serve as a potential biomarker that complements Cyfra21-1 in detecting early stages of ESCC. Esophageal cancer (EC) is one of the leading aggressive malignancies worldwide and is the fourth leading cause of cancer-related deaths in China [1]. The incidence of high-risk EC in China even exceeds 130 per 100,000 individuals [2,3]. The major pathological type of EC is esophageal squamous cell carcinoma (ESCC), which has been most frequently identified in Northern Iran and NorthCentral China [4]. Although there has been significant improvement in diagnosis and treatment, the overall 5-year survival rate remains only about 25-30% for patients who receive curative surgery [5,6], while the rate dropped to 13% for patients with lymph node meta stasis [7]. Early detection is critical for improving outcomes and reducing mortality of ESCC patients.Although biopsy and imaging examination have improved the detection rate of ESCC, these methods are invasive or require radiation, greatly limiting their applications [8,9].Currently, traditional tumor markers, such as cytokeratin 19 fragment (Cyfra) 21-1 and squamous cell carcinoma antigen, are used to diagnose and evaluate ESCC progression. However, they both exhibit a low sensitivity. Yamamoto reported that the sensitivity of Cyfra21-1 for the diagnosis of ESCC was only 47.9% [10]. Mealy showed that the sensitivity of squamous cell carcinoma antigen was about 32% [11]. The absence of sufficiently sensitive biomarkers limits early diagnosis. Therefore, there is an urgent need to identify novel, easy-to-assay biomarkers for early diagnosis and prognosis of ESCC to improve outcomes and reduce mortality of ESCC patients. miRNAs are small noncoding RNAs of 21-25 nucleotides in length that negatively regulate target genes [12] and play important roles in a wide range of physiological and pathological processes [13,14] Research Article Bai, Lin, Fang et al. are frequently located in cancer-associated genomic regions or in fragile sites, indicating that the potential great roles in tumorigenesis [15]. Since their discovery in 1993, emerging evidence shows that altered abundances of miRNAs are associated with cancer, such as ESCC [16][17][18], liver cancer [19][20][21] and breast cancer [22][23][24]. miRNAs are detectable in...

Background:Many studies have reported that the IL-1β + 3954C/T polymorphism (rs1143634) is related to myocardial infarction (MI). To classify the association between IL-1β + 3954C/T and MI susceptibility, we performed a meta-analysis.Methods:We retrieved relevant literature from electronic databases (Embase, PubMed, Cochrane, and Web of Science). Pooled odds ratios (ORs) and 95% confidence intervals (95% CIs) were calculated with a fixed effect model or a random effect model. Sensitivity analysis and publication bias results are also presented.Results:Nine eligible studies (2299 controls and 2203 cases) were included. The pooled results showed a significant relationship between MI and IL-1β + 3954C/T in an allelic comparison (T vs C: OR = 1.13, 95% CI 1.02–1.25, I2 = 0%, PH = .448) and in a dominant model (TC + TT vs CC: OR = 1.15, 95% CI 1.02–1.30, I2 = 0%, PH = .880). Ethnic subgroup analysis showed similar results in Caucasian populations: an allelic comparison (T vs C: OR = 1.16, 95% CI 1.04–1.29, I2 = 0%, PH = .701), homozygote model (TT vs CC: OR = 1.36, 95% CI 1.04–1.79, I2 = 0%, PH = .673), and dominant model (TC + TT vs CC: OR = 1.17, 95% CI 1.02–1.33, I2 = 0%, PH = .851). In addition, similar effects remained in subgroups analyses of high-quality studies and PCR-RFLP (restriction fragment length polymorphism) data.Conclusion:Our meta-analysis proved that IL-1β + 3954C/T is associated with MI susceptibility, especially among Caucasian populations.

We previously reported that overexpression of DHX32 contributes to the growth and metastasis of colorectal cancer (CRC). However, the underlying mechanism is not largely characterized. Herein, we reported that DHX32 in CRC cells upregulated expression of vascular endothelial growth factor A (VEGFA) at the transcription level through interacting with and stabilizing β-catenin. This promoted the recruitment of host endothelial cells to the tumor, and therefore, formation of microvessel in the tumor. Xenograft model revealed that depletion of DHX32 in CRC cells significantly reduced the microvessel density in the grafts and suppressed the growth of grafts. Furthermore, the expression level of DHX32 was positively associated with microvessel density in human CRC and poor outcome of CRC patients. Therefore, the report demonstrates that DHX32 is a pro-angiogenic factor, that inhibition of DHX32-β-catenin pathway can provide a strategy for CRC treatment, and that the expression level of DHX32 has the potential to serve as a biomarker for CRC diagnosis and prognosis.