Finite-width Gaussian sum rules for 0−+0^{-+} pseudoscalar glueball based on correction from instanton-gluon interference to correlation function

Based on correction from instanton-gluon interference to correlation function, the properties of the $0^{-+}$ pseudoscalar glueball is investigated in a family of finite-width Gaussian sum rules. In the framework of semiclassical expansion for quantum chromodynamics $(\textrm{QCD})$ in the instanton liquid background, the contribution arising from the the interference between instantons and the quantum gluon fields is calculated, and included in the correlation function together with pure-classical contribution from instantons and the perturbative one. The interference contribution is turned to be gauge-invariant, free of infrared divergence, and has a great role to restore the positivity of the spectra of the full correlation function. The negligible contribution from vacuum condensates is excluded in our correlation function to avoid the double counting. Instead of the usual zero-width approximation for the resonances, the usual Breit-Wigner form with a suitable threshold behavior for the spectral function of the finite-width resonances is adopted. A consistency between the subtracted and unsubtracted sum rules is very well justified. The values of the mass, decay width and coupling constants for the $0^{-+}$ resonance in which the glueball fraction is dominant are obtained, and agree with the phenomenological analysis.Comment: 18 pages, 10 figure

Replication of a Gene-Diet Interaction at CD36, NOS3 and PPARG in Response to Omega-3 Fatty Acid Supplements on Blood Lipids: A Double-Blind Randomized Controlled Trial.

BACKGROUND: Modulation of genetic variants on the effect of omega-3 fatty acid supplements on blood lipids is still unclear. METHODS: In a double-blind randomized controlled trial, 150 patients with type 2 diabetes (T2D) were randomized into omega-3 fatty acid group (n = 56 for fish oil and 44 for flaxseed oil) and control group (n = 50) for 180 days. All patients were genotyped for genetic variants at CD36 (rs1527483), NOS3 (rs1799983) and PPARG (rs1801282). Linear regression was used to examine the interaction between omega-3 fatty acid intervention and CD36, NOS3 or PPARG variants for blood lipids. FINDINGS: Significant interaction with omega-3 fatty acid supplements was observed for CD36 on triglycerides (p-interaction = 0.042) and PPAGR on low-density lipoprotein-cholesterol (p-interaction = 0.02). We also found a significant interaction between change in erythrocyte phospholipid omega-3 fatty acid composition and NOS3 genotype on triglycerides (p-interaction = 0.042), total cholesterol (p-interaction = 0.013) and ratio of total cholesterol to high-density lipoprotein cholesterol (p-interaction = 0.015). The T2D patients of CD36-G allele, PPARG-G allele and NOS3-A allele tended to respond better to omega-3 fatty acids in improving lipid profiles. The interaction results of the omega-3 fatty acid group were mainly attributed to the fish oil supplements. INTERPRETATION: This study suggests that T2D patients with different genotypes at CD36, NOS3 and PPARG respond differentially to intervention of omega-3 supplements in blood lipid profiles

Effects of n-3 fatty acid supplements on glycemic traits in Chinese type 2 diabetic patients: A double-blind randomized controlled trial.

SCOPE: To investigate the effects of n-3 fatty acid supplements, both marine and plant-based, on glycemic traits in Chinese type 2 diabetes patients. METHOD AND RESULTS: In a double-blind randomized controlled trial, 185 recruited Chinese type 2 diabetes patients were randomized to either fish oil (FO, n = 63), flaxseed oil (FSO, n = 61), or corn oil group (served as control group, n = 61) for 180 days. The patients were asked to take corresponding oil capsules (four capsules/day), which totally provided 2 g/day of eicosapentaenoic acid + docosahexaenoic acid in FO group and 2.5 g/day of alpha-linolenic acid in FSO group. No group × time interaction was observed for homeostatic model assessment of insulin resistance, fasting insulin, or glucose. Significant group × time interaction (P = 0.035) was observed for glycated hemoglobin A1c (HbA1c), with HbA1c decreased in FO group compared with corn oil group (P = 0.037). We also found significant group × time interactions for lipid traits, including LDL cholesterol (P = 0.043), total cholesterol (P = 0.021), total cholesterol/HDL cholesterol (P = 0.009), and triacylglycerol (P = 0.003), with the lipid profiles improved in FO group. No significant effects of FSO on glycemic traits or blood lipids were observed. CONCLUSIONS: Marine n-3 PUFA supplements may improve glycemic control and lipid profiles among Chinese type 2 diabetic patients.National Basic Research Program of China (973 Program: 2015CB553604)This is the author accepted manuscript. The final version is available from Wiley via http://dx.doi.org/10.1002/mnfr.20160023

Hybrid pooling and channel attention‐based single‐shot detector for printed circuit board defect detection

Abstract Automatic defect detection is a key but challenging technology for managing printed circuit board (PCB) production quality. In recent years, deep neural networks (DNNs) have attracted considerable attention for PCB defect detection. However, due to the complexity, diversity, and small‐scale characteristics of defects, it remains a challenge. In this letter, a single‐shot detector (SSD)‐based defects detection method is proposed. This method treats the test and template image as a single image with two channels. In order to reduce the information loss caused by the traditional pooling methods, a new pooling method combining three types of pooling features is proposed. To further improve the detection performance, the channel attention (CA) mechanism is introduced into the detection network. Our proposed method achieves 99.64% mean average precision (mAP) on the DeepPCB dataset, which surpasses the state‐of‐the‐art methods

Replication of a Gene-Diet Interaction at CD36, NOS3 and PPARG in Response to Omega-3 Fatty Acid Supplements on Blood Lipids: A Double-Blind Randomized Controlled Trial

Background: Modulation of genetic variants on the effect of omega-3 fatty acid supplements on blood lipids is still unclear. Methods: In a double-blind randomized controlled trial, 150 patients with type 2 diabetes (T2D) were randomized into omega-3 fatty acid group (n = 56 for fish oil and 44 for flaxseed oil) and control group (n = 50) for 180 days. All patients were genotyped for genetic variants at CD36 (rs1527483), NOS3 (rs1799983) and PPARG (rs1801282). Linear regression was used to examine the interaction between omega-3 fatty acid intervention and CD36, NOS3 or PPARG variants for blood lipids. Findings: Significant interaction with omega-3 fatty acid supplements was observed for CD36 on triglycerides (p-interaction = 0.042) and PPAGR on low-density lipoprotein-cholesterol (p-interaction = 0.02). We also found a significant interaction between change in erythrocyte phospholipid omega-3 fatty acid composition and NOS3 genotype on triglycerides (p-interaction = 0.042), total cholesterol (p-interaction = 0.013) and ratio of total cholesterol to high-density lipoprotein cholesterol (p-interaction = 0.015). The T2D patients of CD36-G allele, PPARG-G allele and NOS3-A allele tended to respond better to omega-3 fatty acids in improving lipid profiles. The interaction results of the omega-3 fatty acid group were mainly attributed to the fish oil supplements. Interpretation: This study suggests that T2D patients with different genotypes at CD36, NOS3 and PPARG respond differentially to intervention of omega-3 supplements in blood lipid profiles. Keywords: Diabetes, Genetic variants, Interaction, Omega-3 fatty acids, Randomized controlled tria

SLCO1B1 and SLC19A1 Gene Variants and Irinotecan-Induced Rapid Response and Survival: A Prospective Multicenter Pharmacogenetics Study of Metastatic Colorectal Cancer

<div><p>Background</p><p>Rapid response to chemotherapy in metastatic colorectal cancer (mCRC) patients (response within 12 weeks of chemotherapy) may increase the chance of complete resection and improved survival. Few molecular markers predict irinotecan-induced rapid response and survival. Single-nucleotide polymorphisms (SNPs) in solute carrier genes are reported to correlate with the variable pharmacokinetics of irinotecan and folate in cancer patients. This study aims to evaluate the predictive role of 3 SNPs in mCRC patients treated with irinotecan and fluoropyrimidine-containing regimens.</p> <p>Materials and Methods</p><p>Three SNPs were selected and genotyped in 137 mCRC patients from a Chinese prospective multicenter trial (NCT01282658). The chi-squared test, univariate and multivariable logistic regression model, and receiver operating characteristic analysis were used to evaluate correlations between the genotypes and rapid response. Kaplan-Meier survival analysis and Cox proportional hazard models were used to evaluate the associations between genotypes and survival outcomes. Benjamini and Hochberg False Discovery Rate correction was used in multiple testing</p> <p>Results</p><p>Genotype GA/AA of SNP rs2306283 of the gene <i>SLCO1B1</i> and genotype GG of SNP rs1051266 of the gene <i>SLC19A1</i> were associated with a higher rapid response rate (odds ratio [OR] =3.583 and 3.521, 95%CI =1.301-9.871 and 1.271-9.804, <i>p</i>=0.011 and p=0.013, respectively). The response rate was 70% in patients with both genotypes, compared with only 19.7% in the remaining patients (OR = 9.489, 95%CI = 2.191-41.093, Fisher's exact test <i>p</i>=0.002). Their significances were all maintained even after multiple testing (all <i>p</i>_<i>c</i> < 0.05). The rs2306283 GA/AA genotype was also an independent prognostic factor of longer progression-free survival (PFS) (hazard ratio = 0.402, 95%CI = 0.171-0.945, <i>p</i>=0.037). None of the SNPs predicted overall survival.</p> <p>Conclusions</p><p>Polymorphisms of solute carriers’ may be useful to predict rapid response to irinotecan plus fluoropyrimidine and PFS in mCRC patients.</p> <p>Trial Registry</p><p><a href="http://clinicaltrials.gov" target="_blank">ClinicalTrials.gov</a> NCT01282658</p> <p><a href="http://www.clinicaltrials.gov/ct2/show/nct01282658" target="_blank"><u>http://www.clinicaltrials.gov/ct2/show/NCT01282658</u></a></p> </div

PFS (A, D, G), IR-TTF (B, E, H) and OS (C, F, I) in patients according to rs2306283, rs1051266 and rs4149056 genotypes (log-rank test).

<p>PFS (A, D, G), IR-TTF (B, E, H) and OS (C, F, I) in patients according to rs2306283, rs1051266 and rs4149056 genotypes (log-rank test).</p