Identification of Novel ARSB Genes Necessary for p-Benzoquinone Biosynthesis in the Larval Oral Secretion Participating in External Immune Defense in the Red Palm Weevil.

External secretions, composed of a variety of chemical components, are among the most important traits that endow insects with the ability to defend themselves against predators, parasites, or other adversities, especially pathogens. Thus, these exudates play a crucial role in external immunity. Red palm weevil larvae are prolific in this regard, producing large quantities of p-benzoquinone, which is present in their oral secretion. Benzoquinone with antimicrobial activity has been proven to be an active ingredient and key factor for external immunity in a previous study. To obtain a better understanding of the genetic and molecular basis of external immune secretions, we identify genes necessary for p-benzoquinone synthesis. Three novel ARSB genes, namely, RfARSB-0311, RfARSB-11581, and RfARSB-14322, are screened, isolated, and molecularly characterized on the basis of transcriptome data. To determine whether these genes are highly and specifically expressed in the secretory gland, we perform tissue/organ-specific expression profile analysis. The functions of these genes are further determined by examining the antimicrobial activity of the secretions and quantification of p-benzoquinone after RNAi. All the results reveal that the ARSB gene family can regulate the secretory volume of p-benzoquinone by participating in the biosynthesis of quinones, thus altering the host's external immune inhibitory efficiency.

Functional conservation and division of two single-carbohydrate-recognition domain C-type lectins from the nipa palm hispid beetle Octodonta nipae (Maulik).

As an invasive pest, the complete and effective innate immune system is crucial for the nipa palm hispid beetle Octodonta nipae (Maulik) to adjust to new environments. C-type lectins (CTLs) are large families of carbohydrate-binding proteins that possess one or more characteristic carbohydrate-recognition domains (CRD) and function as pattern-recognition receptors, which play important roles in mediating humoral and cellular immunity. In the present study, for the first time, we report two CTL-Ss (single-CRD CTLs) from O. nipae (Maulik) (designated OnCTL1 and OnCTL2). The two CTL-Ss share high identity at conserved amino acids associated with conserved carbohydrate binding sites Gln-Pro-Asp (QPD) motifs and clearly show a 1:1 orthologous relationship in insects, which endow them with functional conservation and diversification. mRNA abundance analysis showed that OnCTL1 was upregulated upon Staphylococcus aureus and Escherichia coli challenge at 6 and 12 h, while OnCTL2 underwent no changes upon E. coli challenge and was even downregulated after S. aureus infection. Knockdown of OnCTL1 significantly decreased the transcripts of two key serine proteases (prophenoloxidase activating factors), OnPPAF1 and OnPPAF3, followed by the reduction of haemolymph phenoloxidase activity; it also increased the expression of Defensin2B. In contrast, silencing of OnCTL2 significantly decreased the expression of Defensin2B and Attacin3C, the encapsulation index, and the phagocytosis rate compared to the dsEGFP group. The spreading results showed that more irregularly shaped plasmatocytes and lower levels of aggregation were found in OnCTL2-silenced pupae than in the dsOnCTL1 and dsEGFP groups. We can infer from the results of this study that the two OnCTLs play important roles in the immune system and generate a functional division: OnCTL1 seems to function more in humoral immunity including mediating bacterial recognition and activating the phenoloxidase cascade, and OnCTL2 plays a greater role in enhancing cellular immunity. These observations could replenish information on the functional diversification of insect CTLs, and also provide valuable information to unravel the immunity in O. nipae.

Increased lysyl oxidase-like 2 associates with a poor prognosis in non-small cell lung cancer.

BACKGROUND: Lysyl oxidase-like 2 (LOXL2) is a member of the lysyl oxidase family and is associated with invasiveness and metastasis in breast cancer. However, its relevance in non-small cell lung cancer (NSCLC) remained largely unknown. METHODS: LOXL2 protein levels in a cohort of NSCLC and adjacent normal lung tissues were evaluated and analyzed their clinicopathologic and prognostic significance. RESULTS: It was found that cytoplasmic and nuclear LOXL2 levels were higher in lung adenocarcinoma (AD) and squamous cell carcinoma (SCC) tissues than in paired adjacent normal tissues. High LOXL2 levels were associated with p-TNM stage, and cytoplasmic, but not nuclear, LOXL2 levels were an independent prognostic factor in lung AD and SCC patients. CONCLUSION: These results demonstrate that elevated LOXL2 levels are positively associated with poor prognosis in NSCLC patients. LOXL2 might, therefore, serve as a novel prognostic biomarker and potential therapeutic target in NSCLC patients.

Prognostic significance of TP53 expression for patients with hepatocellular carcinoma: a meta-analysis.

BACKGROUND: Various studies evaluated the relationship between p53 expression and the clinical outcome in patients with hepatocellular carcinoma (HCC), but yielded conflicting results. METHODS: Electronic databases updated to Dec 2013 were searched to find relevant studies. A meta-analysis was conducted with eligible studies which quantitatively evaluated the relationship between p53 expression and survival of patients with HCC. Survival data were aggregated and quantitatively analyzed. RESULTS: We performed a meta-analysis of 24 studies that evaluated the correlation between p53 expression and survival in patients with HCC. Combined hazard ratios (HRs) suggested that p53 expression had an unfavorable impact on overall survival (OS) [HR =1.64, 95% confidence interval (CI): 1.40-1.85], and disease free survival (DFS) (HR =1.57, 95% CI: 1.26-1.87) in patients with HCC. CONCLUSIONS: p53 expression indicates a poor prognosis for patients with HCC.

Prognostic value of vascular endothelial growth factor A expression in gastric cancer: a meta-analysis.

Vascular endothelial growth factor A (VEGF-A) is considered as a prime mediator of angiogenesis and has been implicated in carcinogenesis and metastasis. Various studies examined the relationship between VEGF-A overexpression with the clinical outcome in patients with gastric cancer, but yielded conflicting results. Electronic databases updated to September 2013 were searched to find relevant studies. A meta-analysis was conducted with eligible studies which quantitatively evaluated the relationship between VEGF-A overexpression and survival of patients with gastric cancer. Survival data were aggregated and quantitatively analyzed. We performed a meta-analysis of 20 studies that evaluated the correlation between VEGF-A overexpression and survival in patients with gastric cancer. Combined hazard ratios suggested that VEGF-A overexpression had an unfavorable impact on overall survival (OS) (hazard ratio [HR] = 1.57; 95% confidence interval [CI], 1.30­1.84) and disease-free survival (DFS) (HR = 1.85; 95% CI, 1.39­2.32) in patients with gastric cancer. No significant heterogeneity (P = 0.487) was observed among 16 studies for OS and among 7 studies for DFS (P = 0.435). VEGF-A overexpression indicates a poor prognosis for overall survival and disease-free survival in patients with gastric cancer.

TP53 immunohistochemical expression is associated with the poor outcome for hepatocellular carcinoma: evidence from a meta-analysis.

Various studies examined the relationship between p53 expression with the clinical outcome in patients with hepatocellular carcinoma (HCC), but yielded conflicting results. Electronic databases updated to July 2013 were searched to find relevant studies. A meta-analysis was conducted with eligible studies which quantitatively evaluated the relationship between p53 expression and survival of patients with HCC. Survival data were aggregated and quantitatively analyzed. We performed a meta-analysis of 24 studies that evaluated the correlation between p53 expression and survival in patients with HCC. Combined hazard ratios suggested that p53 expression had an unfavorable impact on overall survival (OS) (HR (hazard ratio) = 1.55, 95 % CI (confidence interval) 1.36-1.74) and disease-free survival (DFS) (HR = 1.54, 95 % CI 1.21-1.88) in patients with HCC. No significant heterogeneity was observed among 20 studies for OS (P = 0.786) and among 11 studies for DFS (P = 0.698). P53 expression indicates a poor prognosis for patients with hepatocellular carcinoma.

VEGF is associated with the poor survival of patients with prostate cancer: a meta-analysis.

BACKGROUND: Vascular endothelial growth factor (VEGF) is considered as a prime mediator of angiogenesis, and has been implicated in carcinogenesis and metastasis. Various studies examined the relationship between VEGF overexpression with the clinical outcome in patients with prostate cancer, but yielded conflicting results. METHODS: Electronic databases updated to July 2013 were searched to find relevant studies. A meta-analysis was conducted with eligible studies which quantitatively evaluated the relationship between VEGF status and survival of patients with prostate cancer. Survival data were aggregated and quantitatively analyzed. RESULTS: We performed a meta-analysis of 9 studies that evaluated the correlation between VEGF overexpression and survival in patients with prostate cancer. Combined hazard ratios suggested VEGF overexpression had an unfavorable impact on overall survival (OS) [hazard ratio (HR) =1.54, 95% CI (confidence interval): 1.25-1.83], but not disease free survival (DFS) (HR=1.23, 95% CI: 0.99-1.47) in patients with prostate cancer. No significant heterogeneity was observed among all studies. CONCLUSIONS: VEGF overexpression indicates a poor prognosis for patients with prostate cancer.

TP53 mutation is associated with a poor outcome for patients with hepatocellular carcinoma: evidence from a meta-analysis.

BACKGROUND: Various studies examined the relationship between p53 mutation with the clinical outcome in patients with hepatocellular carcinoma (HCC), but yielded conflicting results. METHODS: Electronic databases updated to July 2013 were searched to find relevant studies. A meta-analysis was conducted with eligible studies which quantitatively evaluated the relationship between p53 mutation and survival of patients with HCC. Survival data were aggregated and quantitatively analyzed. RESULTS: We performed a meta-analysis of 9 studies that evaluated the correlation between p53 mutation and survival in patients with HCC. Combined hazard ratios suggested that p53 mutation had an unfavorable impact on overall survival (OS) [hazard ratio (HR) =1.46, 95% confidence interval (CI): 1.15-1.76], and disease free survival (DFS) (HR =2.57, 95% CI: 1.46-3.68) in patients with HCC. The significant heterogeneity (P=0.035) was observed among 8 studies for OS, however no significant heterogeneity (P=0.597) was observed among 5 studies for DFS. CONCLUSIONS: p53 mutation indicates a poor prognosis for patients with hepatocellular carcinoma.

CYP1A1 Ile462Val polymorphism contributes to lung cancer susceptibility among lung squamous carcinoma and smokers: a meta-analysis.

Many studies have examined the association between the CYP1A1 Ile462Val gene polymorphisms and lung cancer risk in various populations, but their results have been inconsistent. To assess this relationship more precisely, a meta-analysis was performed. Ultimately, 43 case-control studies, comprising 19,228 subjects were included. A significantly elevated lung cancer risk was associated with 2 Ile462Val genotype variants (for Val/Val vs Ile/Ile: OR = 1.22, 95% CI = 1.08-1.40; for (Ile/Val +Val/Val) vs Ile/Ile: OR = 1.15, 95% CI = 1.07-1.23) in overall population. In the stratified analysis, a significant association was found in Asians, Caucasians and lung SCC, not lung AC and lung SCLC. Additionally, a significant association was found in smoker population and not found in non-smoker populations. This meta-analysis suggests that the Ile462Val polymorphisms of CYP1A1 correlate with increased lung cancer susceptibility in Asian and Caucasian populations and there is an interaction with smoking status, but these associations vary in different histological types of lung caner.

CYP1A1 MspI polymorphisms and lung cancer risk: an updated meta-analysis involving 20,209 subjects.

Published data describing the association between CYP1A1 MspI gene polymorphism and lung cancer risk are inconclusive. To determine a more conclusive relationship, we performed an updated meta-analysis of all eligible studies and conducted the subgroup analysis by stratification according to the ethnicity source, histological types of lung cancer, gender and smoking status of case and control populations. A total of 51 studies comprising 20,209 subjects were included in the analysis. A significantly elevated lung cancer risk was associated with two variant genotypes (for TT vs CC: OR=1.24, 95% CI=1.11-1.40; for CT and TT combined vs CC: OR=1.19, 95% CI=1.12-1.27) in the overall population. In the stratified analysis, significantly higher risks associated with lung cancer were found in Asians, Caucasians, lung SCC, lung AC and the male population. In contrast, negligible risks were found in the mixed population, lung SCLC and the female population. Additionally, a significant association was found in the smoker population, whereas no association was found in non-smoker populations. This meta-analysis suggests that the MspI polymorphisms of CYP1A1 correlate with increased lung cancer susceptibility, and that there is an interaction between the CYP1A1 polymorphism and smoking. However, the associations vary in different ethnic populations, histological types of lung cancer and the gender of case and control populations.

Cytomegalovirus infection and coronary heart disease risk: a meta-analysis.

The chronic inflammatory process including cytomegalovirus (CMV) infection has been hypothesized to induce the progression of atherosclerosis in coronary heart disease (CHD). Numbers studies were conducted to analyze the association between CMV infection and risk of CHD, but no clear consensus had been reached. To assess this relationship more precisely, a meta-analysis was performed. The electronic databases PubMed, Embase, and CNKI were searched; data were extracted and analyzed independently by two investigators. Ultimately, 55 studies, involving 9,000 cases and 8,608 controls from six prospective studies (all with a nested case-control design) and 49 retrospective case-control studies were included. Overall, people exposed to CMV infection had an odds ratio (OR) of 1.67 (95% CI, 1.56-1.79) for CHD risk, relative to those not exposed. CMV infection was clearly identified as a risk factor for CHD in both prospective studies (OR, 1.31; 95% CI, 1.132-1.517) and retrospective studies (OR, 1.79; 95% CI, 1.659-1.939), and in both Asian group (OR, 2.69; 95% CI, 2.304-3.144) and non-Asian group (OR, 1.48; 95% CI, 1.371-1.600). Interestingly, in the subgroup analyses by detection methods of CMV, the increased risk (OR, 8.121) was greater among studies using polymerase chain reaction than the risk (OR, 1.561) among studies using enzyme-linked immunosorbent assay. In conclusion, this meta-analysis suggested that CMV infection is associated with an increased risk for CHD, especially among Asian populations.

Intercellular adhesion molecule 1 gene K469E polymorphism is associated with coronary heart disease risk: a meta-analysis involving 12 studies.

Coronary atherosclerosis is a leading cause of coronary heart disease (CHD). Atherosclerotic lesion is a complex polygenic disease in which gene-environment interactions play a critical role in disease onset and progression. The ICAM1 gene-E469K polymorphism has been reported to be associated with CHD, but results were conflicting. A systematic review and meta-analysis of the published studies were performed to gain a clearer understanding of this association. The PubMed, Embase, and CNKI databases were searched for case-control studies published up to August 2011. Data were extracted and pooled odds ratios (OR) with 95% confidence intervals (CI) were calculated. Twelve eligible studies, comprising 2,157 cases and 1,952 controls, were included in the meta-analysis. The pooled result showed that the ICAM1 gene-E469K polymorphism was significantly associated with an increased risk of CHD (OR = 1.496, 95% CI = 1.363-1.642, for the allele K vs. allele E; OR = 1.919, 95% CI = 11.635-2.253, for the K allele carriers vs. EE). Subgroup analysis supported the results in the Asian populations and in the Caucasian populations. This meta-analysis suggests that the ICAM1 gene K469E polymorphism is associated with CHD risk and the K allele is a more significant risk factor for developing CHD among Asian and Caucasians populations.

APE1 Asp148Glu gene polymorphism and lung cancer risk: a meta-analysis.

Many studies have examined the association between the APE1 T1349G (Asp148Glu) gene polymorphisms and lung cancer risk in various populations, but their results have been inconsistent. To assess this relationship more precisely, a meta-analysis was performed. The PubMed, Embase, Web of Science, and CNKI database was searched for case-control studies published up to June 2010. Data were extracted and pooled odds ratios (OR) with 95% confidence intervals (CI) were calculated. Ultimately, ten studies, comprising 2,696 lung cancer cases and 3,948 controls were included. Overall, for the G allele carriers (TG + GG) versus homozygote TT, the pooled OR was 1.037 (95% CI = 0.928-1.159 P = 0.001 for heterogeneity), for GG versus TT the pooled OR was 0.997 (95% CI = 0.861-1.154 P = 0.005 for heterogeneity). In the stratified analysis by ethnicity, significantly risks were not found among Asians or Caucasians. However, in the subgroup analyses by smoking status, significantly risks were found among smokers not in non-smokers. This meta-analysis suggested that the APE1 T1349G (Asp148Glu) polymorphism was not associated with lung cancer risk among Asians or Caucasians. But, the APE1 G allele was an increased risk factor for developing lung cancer among smokers.

[Ischemic myocardial viability assessment with interleaved T1-T2* magnetic resonance imaging].

OBJECTIVE: To investigate the value of ischemic myocardial viability assessment using interleaved T1-T2* magnetic resonance imaging. METHODS: The left anterior descending coronary arteries (LAD) were occluded for 2 hours, followed by 1-hour reperfusion in 7 pigs. The hearts were then removed and perfused with a mixture of pig blood and crystalloid solution in 1:1 ratio. T1 relaxation times of the myocardium were measured with a TurboFLASH inversion-recovery sequence. The contrast agent, Gadolinium diethylenetriamine pentaacetic acid (Gd-DTPA) was then injected as a bolus into the aortic perfusion line (0.05 mmol/kg body wt). The first pass of the contrast agent through the heart was followed using the interleaved T1-T2* imaging sequence. Once the concentration of Gd-DTPA was in an equilibrium state, T1 relaxation times were measured again. RESULTS: The percentage recovery of T2* intensity (PRT2*) at the maximum T1 intensity measured during the first pass of the contrast agent with the interleaved T1-T2* imaging was statistically different in normal myocardium (37 +/- 11)%, infarct rim (90 +/- 15)% and infarct core (100 +/- 5)%, F = 66.585, P = 0.000. Moreover, the infarcted regions shown on PR(T2)* maps matched well with the infarcted myocardium measured by TTC staining. The median of T(1) relaxation time in normal region, infarct rim and infarct core was 531 ms, 541 ms and 1298 ms, respectively (H = 6.284, P = 0.043). However, normal region could not be differentiated from infarct rim with T1 relaxation times (q = 0.082, P = 0.775). CONCLUSION: Infarcted myocardium and ischemic myocardial viability can be correctly identified and evaluated by the interleaved T1-T2* magnetic resonance imaging in this model.