Effect of polyethylene microplastics on antibiotic resistance genes: A comparison based on different soil types and plant types.

Microplastics (MPs) and antibiotic resistance genes (ARGs) are two types of contaminants that are widely present in the soil environment. MPs can act as carriers of microbes, facilitating the colonization and spread of ARGs and thus posing potential hazards to ecosystem safety and human health. In the present study, we explored the microbial networks and ARG distribution characteristics in different soil types (heavy metal (HM)-contaminated soil and agricultural soil planted with different plants: Bidens pilosa L., Ipomoea aquatica F., and Brassica chinensis L.) after the application of MPs and evaluated environmental factors, potential microbial hosts, and ARGs. The microbial communities in the three rhizosphere soils were closely related to each other, and the modularity of the microbial networks was greater than 0.4. Moreover, the core taxa in the microbial networks, including Actinobacteriota, Proteobacteria, and Myxococcota, were important for resisting environmental stress. The ARG resistance mechanisms were dominated by antibiotic efflux in all three rhizosphere soils. Based on the annotation results, the MP treatments induced changes in the relative abundance of microbes carrying ARGs, and the G1-5 treatment significantly increased the abundance of MuxB in Verrucomicrobia, Elusimicrobia, Actinobacteria, Planctomycetes, and Acidobacteria. Path analysis showed that changes in MP particle size and dosage may indirectly affect soil enzyme activities by changing pH, which affects microbes and ARGs. We suggest that MPs may provide surfaces for ARG accumulation, leading to ARG enrichment in plants. In conclusion, our results demonstrate that MPs, as potentially persistent pollutants, can affect different types of soil environments and that the presence of ARGs may cause substantial environmental risks.

Characteristics and clustering analysis of peripheral blood lymphocyte subsets in children with systemic lupus erythematosus complicated with clinical infection.

OBJECTIVES: Clinical infection is a common complication in children with systemic lupus erythematosus (SLE). However, few studies have investigated immune alterations in children with SLE complicated with clinical infection. We assessed lymphocyte subsets in children with SLE to explore the possibility of clinical infection. METHODS: We retrospectively analyzed the proportion of peripheral lymphocyte subsets in 140 children with SLE. Children with SLE were classified into different clusters according to the proportion of peripheral blood lymphocyte subsets: (CD3 + /CD4 + T cell, CD3 + /CD8 + T cell, CD3 + /CD4 + /CD8 + T cell, CD3 + /CD4-/CD8- T cell, CD19 + B cell, and CD3-/CD16 + /CD56 + NK cell). Differences in the proportion of lymphoid subsets, infection rates, and systemic lupus erythematosus disease activity index (SLEDAI) scores were compared between clusters. In addition, we grouped the subjects according to the presence or absence of infection. Proportions of lymphoid subsets, demographic variables, clinical presentation, and other laboratory variables were compared between the infected and uninfected groups. Finally, the diagnostic ability of lymphocyte subset ratios to distinguish secondary infection in children with SLE was predicted using an ROC curve. RESULTS: Cluster C2 had a higher proportion of B cells than Cluster C1, while Cluster C1 had a lower proportion of NK cells, CD3 + T cells, CD3 + /CD4 + T cells, CD3 + /CD8 + T cells, and CD3 + /CD4-/CD8- T cells. Infection rates and SLEDAI scores were higher in Cluster C2 than in Cluster C1. The infected children had a higher proportion of B cells and a lower proportion of CD3 + T cells, CD3 + /CD4 + T cells, CD3 + /CD8 + T cells, and CD3 + /CD4-/CD8- T cells. There were no significant differences in lymphoid subsets between children in Cluster C2 and the infected groups. The area under the ROC curve of B lymphocytes in predicting SLE children with infection was 0.842. The area under the ROC curve was 0.855 when a combination of B cells, NK cells, CD4 + T cells, and CD8 + T cells was used to predict the outcome of coinfection. CONCLUSIONS: A high percentage of B cells and a low percentage of CD3 + T cells, CD3 + /CD4 + T cells, CD3 + /CD8 + T cells, CD3 + /CD4 + /CD8 + T cells, and CD3 + /CD4-/CD8- T cells may be associated with infection in children with SLE. B cells was used to predict the outcome of coinfection in children with SLE. Key Points • A high percentage of B cells and a low percentage of CD3 + T cells, CD3 + /CD4 + T cells, CD3 + /CD8 + T cells, CD3 + /CD4 + /CD8 + T cells, and CD3 + /CD4-/CD8- T cells may be associated with infection in children with SLE • B cells was used to predict the outcome of coinfection in children with SLE.

Potential impact of polyethylene microplastics on the growth of water spinach (Ipomoea aquatica F.): Endophyte and rhizosphere effects.

Microplastic contamination has received much attention, especially in agroecosystems. However, since edible crops with different genetic backgrounds may present different responses to microplastics, more research should be conducted and focused on more edible crops. In the current study, pot experiments were conducted to investigate the potential impact of polyethylene microplastic (PE) (particle sizes: 0.5 µm and 1.0 µm, addition levels: 0 (control), 0.5% and 1.0% (w/w)) addition on the physiological and biochemical variations of I. aquatica F.. The results indicated that PE addition caused an increase in the soil pH and NH4+-N and soil organic matter contents, which increased by 10.1%, 29.9% and 50.1% when PE addition at A10P0.5 level (10 g (PE) kg-1 soil, particle size: 0.5 µm). While, PE exposure resulted in a decrease in soil available phosphorus and total phosphorus contents, which decreased by 53.9% and 10.5% when PE addition at A10P0.5 level. In addition, PE addition altered the soil enzyme activities. Two-way ANOVA indicated that particle size had a greater impact on the variations in soil properties and enzyme activities than the addition level. PE addition had a strong impact on the rhizosphere microbial and root endophyte community diversity and structure of I. aquatica F.. Two-way ANOVA results indicated that the particle size and addition level significantly altered the α-diversity indices of both rhizosphere microbial and root endophyte (P < 0.05, P < 0.01 or P < 0.001). Moreover, PE was adsorbed by I. aquatica F., which was clearly observed in the transverse roots and significantly increased the H2O2, ·O2-, malondialdehyde and ascorbic acid contents in both the roots and aerial parts of I. aquatica F., leading to a decrease in I. aquatica F. biomass. Overall, the current study enriches the understanding of the effect of microplastics on edible crops.

Peripheral blood lymphocyte subsets in children with nephrotic syndrome: a retrospective analysis.

BACKGROUND: Nephrotic syndrome (NS) in children is widely believed to be associated with severe changes in the immune system. Based on lymphocyte subset analysis, we examined the pathogenesis of immune deficiencies in children with NS with varying steroid sensitivity. METHODS: Our study utilized flow cytometry to retrospectively analyze the ratios of lymphocyte subsets in 204 children with nephrotic syndrome and 19 healthy children. RESULTS: Compared with healthy children, the ratio of CD4 + /CD8 + in onset and remission was decreased in SRNS group (p < 0.05), and CD19 + B lymphocytes were increased in onset (p < 0.05). Compared with onset, the proportion of CD19 + B lymphocytes decreased in SRNS, while the proportion of CD19 + B lymphocytes increased in SDNS, p < (0.01). The ratio of CD8 + T/CD19 + B in onset in SDNS group was significantly higher than that in SSNS and SRNS groups (p < 0.01) and healthy control group (p < 0.05). Compared with onset, the ratio of CD8 + T/CD19 + B in SDNS group decreased significantly (p < 0.01), while the ratio of CD8 + T/CD19 + B in SRNS group increased significantly (p < 0.01). The proportion of CD56 + CD16 + NK cells was significantly reduced in children with INS (p < 0.01). CONCLUSION: CD8 + T lymphocytes may be involved in the mechanism of lymphocyte subsets disorder during onset of SDNS, while CD19 + B lymphocytes may be involved in the mechanism of lymphocyte subsets disorder during relapse of SDNS. The CD8 + T/CD19 + B ratio may predict the degree of frequent recurrence. There is a certain degree of lymphoid subsets disorder in children with NS.

Long Intergenic Non-Coding 00162 as Diagnostic Biomarker for Early-Stage Pancreatic Cancer.

OBJECTIVE: Pancreatic cancer (PC) is the fourth leading cause of cancer death due to insufficient diagnostic methods in early stage of PC. Growing evidence has shown that long intergenic non-coding RNAs (LINCRNAs) is a biomarker of the early-stage of PC. However, the expression level and diagnostic value of LINC00162 remains unclear. METHODS: LINC00162 expression was detected in peripheral blood samples from 155 subjects (52 healthy controls, 52 benign pancreatic disease (BPD) persons and 51 PC patients) by quantitative reverse transcription real-time polymerase chain reaction. Receiver operating characteristic (ROC) analysis was used to evaluate the diagnostic value of LINC00162, carcinoembryonic antigen (CEA) and cancer antigen 199 (CA199). RESULTS: Our data indicated that the LINC00162 expression was upregulated in PC patients compared with healthy controls and BPD (all P<0.001). Furthermore, PC patients with advanced pathological grades, positive lymph node metastasis and positive distant metastasis showed higher LINC00162 levels (all P<0.001). In addition, the area under the ROC curve (AUC) found that the LINC00162 had higher diagnostic ability than CEA and CA199 in distinguishing the early-stage PC patients (AUC: LINC00162 versus(vs) CEA vs CA199=0.932 vs 0.669 vs 0.725). CONCLUSION: In summary, the LINC00162 may be a noninvasive and efficient marker for identifying patients with the early-stage PC. Further validation studies with a large number of patients and long-term follow-up patients are needed to confirm the potential diagnostic value and clinical utility of LINC00162 in patients with PC.

Testis-specific protein Y-encoded 1 regulates androgen receptor expression through the MAPK/ERK pathway in male hepatocellular carcinoma.

OBJECTIVES: To analyze the mechanism of testis-specific protein Y-encoded 1 (TSPY1) in male hepatocellular carcinoma (HCC). METHODS: This experimental study was carried out at Guangxi Medical University's First Affiliated Hospital, Guangxi, China, between January 2016 and December 2019. The expression of TSPY1, androgen receptor (AR), messenger ribonucleic acids (mRNAs), and proteins were detected by qRT-PCR and Western blotting. The co-localization and interaction of TSPY1 and AR were observed by immunofluorescence assay and co-immunoprecipitation. Hepatocellular carcinoma cells overexpressing and silencing TSPY1 were constructed, and the expression and phosphorylation levels of TSPY1, AR, and mitogen-activated protein kinases/extracellular signal-regulated kinases (MAPK/ERK) signaling pathway-related key molecules ERK1/2, p38, and JNK were also detected. RESULTS: The expression levels of TSPY1, AR mRNAs, and proteins were highly positively correlated in HCC cells in different metastatic potentials with a high correlation coefficient of R=0.929 and R=0.884. Testis-specific protein Y-encoded 1 and AR were then co-localized in the nucleus of HCC cells, and TSPY1 and AR can interact with each other. In addition, the expression of AR and phosphorylation of ERK1/2 were enhanced in TSPY1 overexpressed Huh7 cells. They were reduced in HCCLM3 cells with TSPY1 knockdown expression. In addition, in response to blocking MAPK/ERK signaling activity, AR was reduced in expression. CONCLUSION: These findings suggested that there was a positive correlation between TSPY1 expression and AR in male HCC cells, and high TSPY1 expression stimulates AR expression, MAPK/ERK signaling pathway may be involved in its mechanism.

Long non-coding RNA LINC01793 as a potential diagnostic biomarker of hepatitis B virus-related hepatocellular carcinoma.

BACKGROUND: There is growing evidence that long non-coding RNAs (lncRNAs) play important roles in the progression of hepatocellular carcinoma (HCC) and may serve as diagnostic markers. This study investigates the diagnostic efficiency of the long intergenic non-protein-coding RNA 1793 (LINC01793) in hepatitis B virus (HBV)-related HCC. METHODS: Bioinformatics methods were used to screen the aberrantly expressed lncRNAs in HCC tissues based on The Cancer Genome Atlas (TCGA). Quantitative reverse transcription polymerase chain reaction was performed to assess the expression of the candidate lncRNAs in tissues, cells and whole blood samples of patients with HBV-related HCC, liver cirrhosis (LC), chronic hepatitis (CHB), and healthy controls. Then, the correlations between LINC01793 and clinical characteristics were analyzed. Finally, the diagnostic value of LINC01793 was explored based on the receiver operating characteristic curve. RESULTS: LINC01793 was remarkably upregulated in the HCC tissues and cells. It was highly expressed in the whole blood of the HBV-related HCC patients, unlike in that of the healthy controls and of the CHB and LC patients. Subsequent analysis revealed that high LINC01793 was related to the Barcelona Clinic Liver Cancer (P = 0.007), tumor invasion (P = 0.042), the number of tumors (P = 0.031) and serum level of alanine aminotransferase(p = 0.022). The areas under the curve of LINC01793, for distinguishing HCC from healthy controls, CHB and LC patients, were 0.824, 0.767 and 0.756, respectively. In addition, the combination of LINC01793 with alpha fetoprotein (AFP) had a stronger diagnostic value than LINC01793 or AFP alone in AFP-negative HCC patients. CONCLUSION: High expression of LINC01793 is correlated with adverse clinical characteristics and can serve as a non-invasive biomarker of HCC.

Diagnostic value of long noncoding RNA LINC01485 in patients with colorectal cancer.

BACKGROUND: Long noncoding RNAs (lncRNAs) were considered as transcription noise without biological functions. However, accumulated evidence shows that lncRNAs are expressed heterogeneously in tumor tissues. This study aims to identify the specific expression of lncRNAs in colorectal cancer patients and to perform verification analysis. METHODS: The differentially expressed lncRNAs and mRNAs in colorectal cancer and normal tissues were screened by bioinformatics methods. Subsequently, the qRT-PCR method was used to verify the expression of differential lncRNAs in tumor tissues and blood samples. Concurrently ROC curves were used to analyze the diagnostic efficacy of lncRNAs. Moreover, the correlation between lncRNAs and clinicopathological features was also analyzed. Finally, functional annotation analysis was performed for lncRNAs. RESULTS: Eleven lncRNAs differentially expressed in colorectal cancer tissues and normal tissues were screened. In the validation tissue sample set, FOXD3-AS1 was down-regulated in colorectal cancer tissues (P < 0.001), while LINC01485 was up-regulated in colorectal cancer tissues compared with the adjacent tissues (P < 0.05). In a further verification of the whole blood sample set, LINC01485 showed high sensitivity and specificity (sensitivity = 98.33%, specificity = 84.00%) in differentiating colorectal cancer patients from healthy controls (P < 0.001). Simultaneously, there was no difference in the expression of LINC01485 in other gastrointestinal tumors (hepatocellular carcinoma, esophageal cancer, gastric cancer, and pancreatic cancer) and healthy controls. LINC01485 is significantly related to the clinical staging, lymph node metastasis, and distant metastasis of colorectal cancer. CONCLUSIONS: The expression, diagnostic efficiency, and functional analysis of the lncRNA file of colorectal cancer reveals the important role of LINC01485 in colorectal cancer and provides an important clinical reference value for the early diagnosis and targeted therapy of colorectal cancer.

Diagnostic value of platelet-lymphocyte ratio and hemoglobin-platelet ratio in patients with rectal cancer.

BACKGROUND: This study aimed to investigate the diagnostic value of platelet-lymphocyte ratio (PLR) and hemoglobin-platelet ratio (HPR) combined or not with carcinoembryonic antigen (CEA) in rectal cancer. METHODS: We recruited 235 patients pathologically diagnosed with rectal cancer, 113 patients with benign rectal diseases, and 229 healthy control patients in this retrospective analysis. Then, the correlation between PLR, HPR, and clinicopathological findings was analyzed. Receiver operating characteristic (ROC) curve was used to assess the diagnostic value of PLR and HPR combined or not with CEA in rectal cancer patients. RESULTS: The levels of PLR, HPR, and CEA were higher in rectal cancer patients than those in the subjects with benign rectal diseases (P < .001) and the healthy controls (P < .001). Platelet-lymphocyte ratio and HPR were associated with lymph node metastasis and tumor stage, rather than serosa invasion, distant metastasis, or tumor size. PLR or HPR combined with CEA produced larger area under curve (AUC) (AUCPLR+CEA  = 0.75, 95% CI = 0.70-0.79, AUCHPR+CEA  = 0.76, 95% CI = 0.71-0.80) than PLR (P < .0001), HPR (P < .0001), or CEA (P = .024) alone. CONCLUSION: Our results suggest that PLR or HPR combined with CEA can increase diagnostic efficacy and may be a useful diagnostic marker for patients with rectal cancer.

Genetic polymorphisms in complement receptor 1 gene and its association with HBV-related liver disease: A case-control study.

BACKGROUND: Several investigators have reported that complement receptor 1 (CR1) likely play a role in the pathogenesis of tumors, autoimmune and inflammatory diseases. However, the association of genetic polymorphisms of CR1 with risk of hepatitis B virus (HBV)-related liver disease remains unexplored. METHODS: In a case-control study of 399 HBV-related liver disease patients and 227 healthy controls, we genotyped two SNPs in CR1 (rs3811381 and rs2274567) and assessed their associations with risk of HBV-related liver disease. RESULTS: No significant differences were observed in the frequency distribution of genotypes or alleles between CR1 rs3811381 and rs2274567 polymorphisms in patients and controls. However, stratification analysis indicated that these two CR1 polymorphisms may contribute to the risk of HBV- hepatocellular carcinoma (HCC) and chronic hepatitis B (CHB) in subgroups of males, alcohol drinkers and nonsmokers. Further, our results showed that the rs3811381 polymorphism may contribute to HBV-HCC risk in subgroups of older and younger subjects, while the G allele, AG and the combined AG + GG genotypes of rs2274567 may be risk factors for HBV-HCC in younger subjects. In addition, our results indicated that subjects who carried the rs3811381 G allele and the rs2274567 AG genotype were at decreased risk of HBV- liver cirrhosis (LC) in subgroups of females. CONCLUSIONS: Our results support the hypothesis that the CR1 gene rs3811381 and rs2274567 polymorphisms may contribute to HBV-HCC and HBV-CHB risk, particularly in subgroups of males, alcohol drinkers, nonsmokers, while these two CR1 polymorphisms were found to associate with decreased risk of HBV-LC, particularly in females. Further validation of these results is warranted.

Glycoprofiling of Early Gastric Cancer Using Lectin Microarray Technology.

BACKGROUND: Recently, studies have reported that protein glycosylation plays an important role in the occurrence and development of cancer. Gastric cancer is a common cancer with high morbidity and mortality owing to most gastric cancers are discovered only at an advanced stage. Here, we aim to discover novel specific serum glycanbased biomarkers for gastric cancer. METHODS: A lectin microarray with 50 kinds of tumor-associated lectin was used to detect the glycan profiles of serum samples between early gastric cancer and healthy controls. Then lectin blot was performed to validate the differences. RESULTS: The result of the lectin microarray showed that the signal intensities of 13 lectins showed significant differences between the healthy controls and early gastric cancer. Compared to the healthy, the normalized fluorescent intensities of the lectins PWA, LEL, and STL were significantly increased, and it implied that their specifically recognized GlcNAc showed an especially elevated expression in early gastric cancer. Moreover, the binding affinity of the lectins EEL, RCA-II, RCA-I, VAL, DSA, PHA-L, UEA, and CAL were higher in the early gastric cancer than in healthy controls. These glycan structures containing GalNAc, terminal Galß 1-4 GlcNAc, Tri/tetraantennary N-glycan, ß-1, 6GlcNAc branching structure, α-linked fucose residues, and Tn antigen were elevated in gastric cancer. While the two lectins CFL GNL reduced their binding ability. In addition, their specifically recognized N-acetyl-D-galactosamine structure and (α-1,3) mannose residues were decreased in early gastric cancer. Furthermore, lectin blot results of LEL, STL, PHA-L, RCA-I were consistent with the results of the lectin microarray. CONCLUSIONS: The findings of our study clarify the specific alterations for glycosylation during the pathogenesis of gastric cancer. The specific high expression of GlcNAc structure may act as a potential early diagnostic marker for gastric cancer.

Reduced N-acetylglucosaminyltransferase III expression via Smad3 and Erk signaling in TGF-ß1-induced HCC EMT model.

N-acetylglucosaminyltransferase III (GnT-III), encoded by the MGAT3 glycogene, is thought to be a tumor metastatic suppressor. Our previous studies found that the mRNA expression level of GnT-III decreased in a hepatocyte growth factor (HGF)-induced hepatocellular carcinoma (HCC) epithelial-mesenchymal transition (EMT) model. However, the molecular mechanism of GnT-III expression is unclear. In the present study, we established an HCC EMT model using the classic inducer transforming growth factor-ß1 (TGF-ß1) and focused on the Smad3 and Erk signaling pathways. Results showed that GnT-III gene expression and its catalytic product bisecting GlcNAc structure decreased and phosphorylation of both Smad3 and Erk1/2 was up-regulated in TGF-ß1-treated MHCC97-L cells, while GnT-III mRNA expression and bisecting GlcNAc structure increased after blocking the activities of Smad3 and Erk signaling pathways. These findings suggested that GnT-III gene expression is modulated by the growth factor signaling pathways in the EMT model and that GnT-III may be a potential drug target for HCC treatment.

Glycosylation patterns and PHA-E-associated glycoprotein profiling associated with early hepatic encephalopathy in Chinese hepatocellular carcinoma patients.

Hepatic encephalopathy (HE) as a severe neuropsychiatric complication is commonly present in the end stage of Hepatocellular Carcinoma (HCC). However, widely accepted biomarkers for diagnosing early HE are still absent. Here, we screened glycosylation patterns of serum proteins from Chinese HCC patients with or without early HE by lectin microarray. Then, phaseolus vulgaris erythroagglutinin (PHA-E) as a lectin binding with bisecting GlcNAc structure which was significantly decreased in sera from Chinese HCC patients with early HE, was chosen to perform lectin affinity chromatography, following by in-gel digestion, Mass Spectrometry (MS) analysis and bioinformatics analysis. Here we found, 13 lectins showed statistically significant reduction suggesting GalNAc, terminal α-1,3 Man, bisecting GlcNAc, (GlcNAc)n, O-GlcNAc, Neu5Ac, tetra-antennary complex-type N-glycan and GalNAc α/ß1-3/6 Gal were decreased in serum glycoproteins from Chinese HCC patients with early HE. Furthermore, a total of 141 PHA-E-associated glycoproteins were identified in MS, of which 12 serum glycoproteins only in Chinese HCC patients without early HE and 26 serum glycoproteins only in Chinese HCC patients with early HE. In addition, bioinformatics analysis revealed the PHA-E-associated serum glycoproteins only in Chinese HCC patients with early HE might be related to early HE occurrence through p38 MAPK signaling pathway and MAPK/ERK signaling pathway. Collectively, this was the first glycomics study of serum proteins in HCC patients with early HE and it could provide a database for discovering and developing serum biomarkers to identify and predict early HE in HCC patients.

Type conversion of secretomes in a 3D TAM2 and HCC cell co-culture system and functional importance of CXCL2 in HCC.

Macrophages play important roles in the tumor microenvironment, driving cancer progression and metastasis, particularly in hepatocellular carcinoma (HCC). However, few studies have assessed the exact secretome composition in HCC. In the present study, the impact of different phenotype of macrophages on HCC cells was investigated. Alternatively activated macrophages (M2) were found to significantly increase the proliferation, migration, and invasion abilities of SMMC7721 cells (all P < 0.05). M2 were then co-cultured with SMMC7721 cells to reconstruct the tumor microenvironment. Conditioned medium from 3D single cultures of M2, SMMC7721 cells, and their co-culture system were analyzed using quantitative proteomics via iTRAQ labeling combined with mass spectrometric analysis. Secretome analysis revealed a total of 159 differential secreted proteins in the co-culture system compared to the single culture systems, with 63 being up-regulated (>1.3-fold) and 96 down-regulated (<0.7-fold). CXCL2 was confirmed to have higher expression in the co-culture system and HCC tissues, and was selected for further investigation. Functional effects data suggested that recombinant human CXCL2 significantly enhanced the migration, invasion ability of SMMC7721 cells, and weakened adhesion ability. While CXCL2 neutralization and CXCR2 blockage significantly inhibited the effects of CXCL2 on SMMC7721 cells, indicating that CXCL2 may play pivotal role in HCC metastasis.

The Effects of RANTES Polymorphisms on Susceptibility to HIV-1 Infection and Disease Progression: Evidence from an Updated Meta-Analysis.

Associations of regulated on activation, normal T cell expressed and secreted (RANTES) -403G/A, -28C/G, and In1.1T/C polymorphisms with HIV-1 infection and the progression of HIV-1 disease have been widely reported with inconsistent results. To clarify this situation, we performed an updated meta-analysis of all available studies from PubMed, EMBASE, and the China National Knowledge Infrastructure. A total of 24 eligible studies involving more than 10,000 subjects were included. By using the healthy controls, we found that -403G/A polymorphism was significantly associated with reduced susceptibility to HIV-1 infection in G/A+A/A versus GG (odds ratio [OR] = 0.755, 95% confidence interval [CI] = 0.581-0.982); and a significantly decreased risk was also found for -28C/G polymorphisms (G vs. C, OR = 0.804, 95% CI = 0.696-0.927; G/G+C/G vs. C/C, OR = 0.826, 95% CI = 0.704-0.969). Whereas for In1.1T/C polymorphism, increased risk of HIV-1 infection was revealed (C vs. T, OR = 1.216, 95% CI = 1.047-1.430; T/C vs. T/T, OR = 1.68, 95% CI = 1.263-2.234; T/C+T/T vs. C/C, OR = 1.466, 95% CI = 1.147-1.875). Subgroup analyses by ethnicity showed significant association among Asians, but not among Caucasians. When HIV-1-exposed seronegative (HESN) controls were used, no significant association was detected. Moreover, -403G/A and -28C/G polymorphisms were also not associated with long-term nonprogressive HIV-1 infection (all p > .05). This meta-analysis suggests that RANTES -403G/A and -28C/G polymorphisms confer possible protection against HIV-1 infection, whereas In1.1T/C polymorphism may increase risk of HIV-1 infection, especially in Asians. These results may contribute to finding a theoretical basis for effective control strategies against HIV/AIDS. Further investigations are needed to validate our conclusions.

Genetic polymorphisms in hypoxia-inducible factor-1a gene and its association with HBV-related hepatocellular carcinoma in a Chinese population.

Previous studies have demonstrated that hypoxia-inducible factor-1a (HIF-1a) may play a vital role in the pathogenesis of hepatocellular carcinoma (HCC). However, the relationship between HIF-1a polymorphisms and HCC has not been thoroughly investigated. The aim of this study is to determine whether HIF-1a polymorphisms are associated with HCC through a case-control study. Two polymorphisms in the HIF-1a gene (rs11549465 and rs115494657) were examined in 157 hepatitis B virus (HBV)-related HCC patients and 173 healthy controls using the polymerase chain reaction-restriction fragment length polymorphism method. DNA sequencing was used to validate genotype results. There were no significant differences in the genotype and allele frequencies of HIF-1a rs11549465 and rs115494657 polymorphisms between the HBV-related HCC patients and healthy controls. However, the data revealed that subjects with the CG haplotype have a higher susceptibility to HBV-related HCC [odds ratio (OR)=2.327, 95% confidence interval (CI)=1.578-4.721, P=0.008]. In contrast, the CA haplotype was associated with a significantly decreased risk of HBV-related HCC (OR=0.416, 95% CI=0.172-0.910, P=0.025). HIF-1a rs11549465 and rs115494657 polymorphisms appeared to be irrelevant to HBV-related HCC. However, the HIF-1a CG and CA haplotypes might be a risk factor and a protective marker, respectively, for HBV-related HCC in a Chinese population. Further investigations with a larger sample size may be required to validate the genetic effects of HIF-1a polymorphisms on HBV-related HCC.

Establishing reference values for blood urea nitrogen and serum creatinine in Chinese Han ethnic adult men.

BACKGROUND: The aim was to calculate the two-sided 95th percentile reference values for blood urea nitrogen (BUN) and serum creatinine (SCr) in Chinese Han ethnic adult men. METHODS: Serum samples were collected from Chinese Han ethnic adult men aged 20 - 69 years. After screening based on the inclusion and exclusion criteria, a total of 1575 individuals were enrolled in our study. BUN and SCr values were measured on an automatic analyzer (Dade Behring, USA). The data was analyzed and calculated using nonparametric statistical methods. RESULTS: BUN and SCr values were not normally distributed. The reference values were in the range 3.3 - 7.5 mmol/L for BUN and 64 - 113 micromol/L for SCr. BUN levels were significantly lower in the smoking group than the non-smoking group (Z = -4.52, p < 10(-5)). An increase with age was observed in BUN levels (r(s) = 0.172, p < 0(-5)) and lower SCr levels were weakly associated with the older subjects (r(s) = -0.071, p = 0.005). Moreover, it was found that higher Body Mass Index (BMI) tended toward higher levels of SCr (r(s) = 0.118, p < 10(-5)). CONCLUSIONS: The reference values established for BUN and SCr exhibit a slight deviation compared to those developed in previous studies. We propose reference values of BUN for smokers and non-smokers be constructed, and age- and BMI-specific reference values be applied in clinical laboratories.

Association of PvuII and XbaI polymorphisms in estrogen receptor alpha gene with the risk of hepatitis B virus infection in the Guangxi Zhuang population.

BACKGROUND AND OBJECTIVE: Available evidence has suggested that estrogen receptor alpha (ESR1) is implicated in the pathogenic process of hepatitis B infection. Therefore, we evaluated the association of PvuII (rs2234693) and XbaI (rs9340799) in ESR1 and HBV infection in Guangxi Zhuang populations. METHODS: A total of 389 subjects were divided into four groups: 112 patients with chronic hepatitis B (CHB), 65 patients with hepatitis B virus (HBV)-related liver cirrhosis (LC), 107 patients with HBV-related hepatocellular carcinoma (HCC), and 105 healthy controls. The polymerase chain reaction-restriction fragment length polymorphism strategy was used to detect ESR1 gene PvuII and XbaI polymorphisms. RESULTS: Compared with healthy controls, binary logistic regression analyses show that the CC genotype of PvuII was associated with a significantly increased susceptibility to CHB compared with the TT genotype (OR=1.760, 95% CI 1.316-2.831; p=0.044). The PvuII CC genotype was also associated with significantly increased risk of HBV-related LC (OR=1.921, 95% CI 1.342-2.478; p=0.043). Similarly, the subjects bearing the homozygous CC genotype of PvuII polymorphism also had more than a 1.7-fold increased risk for development of HCC (OR=1.748, 95% CI 1.313-2.787; p=0.010) compared with those bearing the TT genotype. Furthermore, the AC haplotype was associated with a significantly increased risk of HCC with an OR of 1.456 (p=0.003). In contrast, there were no significant differences in the genotype and allele of XbaI polymorphisms in the ESR1 gene between the groups of patients and healthy controls. In addition, ESR1 polymorphisms were not significantly associated with susceptibility to HBV-related HCC when using CHB and LC patients as references. CONCLUSION: We conclude that the CC genotype of PvuII in ESR1 is associated with an increased risk of CHB, HBV-related LC and HCC in Guangxi Zhuang populations.

Current evidences on XPC polymorphisms and gastric cancer susceptibility: a meta-analysis.

BACKGROUND: Reduced DNA repair capacities due to inherited polymorphisms may increase the susceptibility to cancers including gastric cancer. Previous studies investigating the association between Xeroderma Pigmentosum group C (XPC) gene polymorphisms and gastric cancer risk reported inconsistent results. We performed a meta-analysis to summarize the possible association. METHODS: All studies published up to January 2014 on the association between XPC polymorphisms and gastric cancer risk were identified by searching electronic databases PubMed, EMBASE, Cochrane library, and Chinese Biomedical Literature database (CBM). The association between XPC polymorphisms and gastric cancer risk was assessed by odds ratios (ORs) together with their 95% confidence intervals (CIs). RESULTS: Six studies with 1,355 gastric cancer cases and 2,573 controls were finally included in the meta-analysis. With respect to Lys939Gln polymorphism, we did not observe a significant association when all studies were pooled into the meta-analysis. When stratified by ethnicity, source of control, and study quality, statistical significant association was not detected in all subgroups. With respect to Ala499Val and PAT-/+polymorphisms, we also did not observe any significant association with gastric cancer risk in the pooled analysis. CONCLUSIONS: This meta-analysis based on current evidences suggested that the XPC polymorphisms (Lys939Gln, Val499Arg, and PAT-/+) did not contribute to gastric cancer risk. Considering the limited sample size and ethnicity included in the meta-analysis, further larger scaled and well-designed studies are needed to confirm our results. VIRTUAL SLIDES: The virtual slide(s) for this article can be found here: http://www.diagnosticpathology.diagnomx.eu/vs/1485880312555069.

Positive association between IL-16 rs11556218 T/G polymorphism and cancer risk: a meta-analysis.

BACKGROUND: Interleukin-16 (IL-16) is a multifunctional cytokine which plays a key role in inflammatory and autoimmune diseases as well as in cancer. Genetic polymorphisms of IL-16 have been implicated in susceptibility to cancer. However, associations remain inconclusive. The present meta-analysis was therefore carried out to establish a more conclusive association of IL-16 polymorphisms with cancer risk. MATERIALS AND METHODS: Relevant studies were searched through the PubMed, Embase, Web of Science, Google Scholar and Wan fang electronic databases updated in October 2013. Odds ratios (OR) and 95% confidence intervals (95% CI) were used to assess the association between IL-16 polymorphisms and cancer risk. RESULTS: Eight eligible studies (rs4778889 T/C: 8, rs11556218 T/G: 7, rs4072111 C/T: 6) that met our selection criteria were included. The meta-analysis indicated that rs11556218 T/G was associated with a significant increased risk of cancer (G vs. T, OR=1.321, 95% CI=1.142-1.528, P <0.001; TG vs. TT, OR=1.665, 95% CI=1.448-1.915, P<0.001; GG+TG vs. TT, OR=1.622, 95% CI=1.416-1.858, P<0.001),as well as nasopharyngeal carcinoma and colorectal cancer. Furthermore, in the subgroup of Chinese, significant associations were found between rs11556218 polymorphism and cancer risk. There was no statistically significant association between the other two variants (rs4778889, rs4072111) and risk of cancer. CONCLUSIONS: This meta-analysis suggests that the IL-16 rs11556218 polymorphism is associated with increased cancer risk. Large well-designed studies involving various cancer types and different populations are now needed.