Multiple Human Papillomavirus Infections among Chinese Women with and without Cervical Abnormalities: A Population-Based Multi-Center Cross-Sectional Study

Background: Despite an increase in the number of studies conducted in recent years on human papillomavirus (HPV) and cervical cancer epidemiology, the profile of multiple HPV infections remain obscure, particularly among Chinese women. During 2004–2005, a series of population-based HPV prevalence surveys were performed by Cancer Institute and Hospital of Chinese Academy of Medical Sciences (CIHCAMS) and International Agency for Research on Cancer (IARC). Based on these surveys, we evaluated the prevalence and risk factors of multiple HPV infections, and explored its association with cervical abnormalities among Chinese women. Methods: A total of 2374 women from three study centers underwent gynecological examinations with valid cytology and their HPV results were included in the analysis. Forty-four HPV types were detected using the GP5+/6+ PCR-based enzyme immunoassay. An unconditional logistic regression model was used to evaluate the effect of multiple HPV infections on cervical lesions and its risk factors adjusting for confounders. The between-groups difference was evaluated by a heterogeneity test based on the Q test. Results: One hundred and eleven women of multiple HPV infections was found among 2374 Chinese women with a prevalence of 5.28% (95% CI = 3.86–5.60%), which attributed to 28.98% (95% CI = 24.49–33.81%) of all of the 383 HPV-positive women. A significantly increased risk of multiple HPV infections was found in the older women (≥45 years; adjusted OR = 1.52, 95% CI = 1.02–2.27) and those having more than three sexual partners (adjusted OR = 2.10, 95% CI = 1.05–4.17) after adjustment for age-group, study area, and number of sexual partner. We also found that the risk of high-grade lesions was significantly higher than that of low-grade lesions with the multiple HPV infections (Pheterogeneity = 0.044), but not as significantly with the single HPV infection (Pheterogeneity = 0.108). Conclusion: Multiple HPV Infections, especially with high-risk HPV types, may be a substantial indicator either for public cervical cancer prevention or clinical implications

Evaluation of port efficiency in Shanghai Port and Busan Port based on three-stage DEA model with environmental concerns

The global green development has led many ports to impose measures to reduce emissions and improve port efficiency. As large-scale construction can do damage to the environment, it is not supported under the green strategy, which makes it more important to make full use of existing resources in the port competition. While, whether there is a relationship between emissions and port efficiency, and whether the relationship can reflect the problems in port management are vital factors need to be considered when making port development strategy. To solve the two problems, this paper takes the case of Shanghai Port and Busan Port, and uses the three-stage Data Envelopment Analysis (DEA) to evaluate the efficiency of the two ports respectively. Pollutant emissions from the ports are selected as an environmental variable in the second stage to examine their effects on the redundancy of input variables. The results indicate that the efficiency of Shanghai Port is insufficient due to excessive scale and pollutant emissions. Based on the results, some suggestions are given to improve the drawbacks. Furthermore, the use of the three-stage DEA to study the annual change in performance of a single target in this paper is also a novelty. First published online 20 November 201

Microbiota characterization of the green mussel Perna viridis at the tissue scale and its relationship with the environment

Research on the microbiota associated with marine invertebrates is important for understanding host physiology and the relationship between the host and the environment. In this study, the microbiota of the green mussel Perna viridis was characterized at the tissue scale using 16S rRNA gene high-throughput sequencing and compared with the microbiota of the surrounding environment. Different mussel tissues were sampled, along with two environmental samples (the mussel's attachment substratum and seawater). The results showed that the phyla Proteobacteria, Bacteroidetes, and Spirochaetae were dominant in mussel tissues. The bacterial community composition at the family level varied among the tissues of P. viridis. Although the microbiota of P. viridis clearly differed from that of the surrounding seawater, the composition and diversity of the microbial community of the foot and outer shell surface were similar to those of the substratum, indicating their close relationship with the substratum. KEGG prediction analysis indicated that the bacteria harbored by P. viridis were enriched in the degradation of aromatic compounds, osmoregulation, and carbohydrate oxidation and fermentation, processes that may be important in P. viridis physiology. Our study provides new insights into the tissue-scale characteristics of mussel microbiomes and the intricate connection between mussels and their environment

Jump-seq: Genome-Wide Capture and Amplification of 5-Hydroxymethylcytosine Sites

5-Hydroxymethylcytosine (5hmC) arises from the oxidation of 5-methylcytosine (5mC) by Fe2+ and 2-oxoglutarate-dependent 10–11 translocation (TET) family proteins. Substantial levels of 5hmC accumulate in many mammalian tissues, especially in neurons and embryonic stem cells, suggesting a potential active role for 5hmC in epigenetic regulation beyond being simply an intermediate of active DNA demethylation. 5mC and 5hmC undergo dynamic changes during embryogenesis, neurogenesis, hematopoietic development, and oncogenesis. While methods have been developed to map 5hmC, more efficient approaches to detect 5hmC at base resolution are still highly desirable. Herein, we present a new method, Jump-seq, to capture and amplify 5hmC in genomic DNA. The principle of this method is to label 5hmC by the 6-N3-glucose moiety and connect a hairpin DNA oligonucleotide carrying an alkyne group to the azide-modified 5hmC via Huisgen cycloaddition (click) chemistry. Primer extension starts from the hairpin motif to the modified 5hmC site and then continues to “land” on genomic DNA. 5hmC sites are inferred from genomic DNA sequences immediately spanning the 5-prime junction. This technology was validated, and its utility in 5hmC identification was confirmed

Rosiglitazone Inhibits Transforming Growth Factor-β1 Mediated Fibrogenesis in ADPKD Cyst-Lining Epithelial Cells

BACKGROUND: Interstitial fibrosis plays an important role in progressive renal dysfunction in autosomal dominant polycystic kidney disease (ADPKD). In our previous studies, we confirmed that PPAR-γ agonist, rosiglitazone could protect renal function and prolong the survival of a slowly progressive ADPKD animal model by reducing renal fibrosis. However, the mechanism remains unknown. METHODS: Primary culture epithelial cells pretreated with TGF-β1 were incubated with rosiglitazone. Extracellular matrix proteins were detected using real-time PCR and Western blotting. MAPK and Smad2 phosphorylation were measured with western blot. ERK1/2 pathway and P38 pathway were inhibited with the specific inhibitors PD98059 and SB203580. The Smad2 pathway was blocked with the siRNA. To address whether PPAR-γ agonist-mediated inhibition of TGF-β1-induced collagen type I expression was mediated through a PPAR-γ dependent mechanism, genetic and pharmaceutical approaches were used to block the activity of endogenous PPARγ. RESULTS: TGF-β1-stimulated collagen type I and fibronectin expression of ADPKD cyst-lining epithelia were inhibited by rosiglitazone in a dosage-dependent manner. Smad2, ERK1/2 and P38 pathways were activated in response to TGF-β1; however, TGF-β1 had little effect on JNK pathway. Rosiglitazone suppressed TGF-β1 induced Smad2 activation, while ERK1/2 and P38MAPK signals remained unaffected. Rosiglitazone could also attenuate TGF-β1-stimulated collagen type I and fibronectin expression in primary renal tubular epithelial cells, but had no effect on TGF-β1-induced activation of Smad2, ERK1/2 and P38 pathways. There was no crosstalk between the Smad2 and MAPK pathways in ADPKD cyst-lining epithelial cells. These inhibitory effects of rosiglitazone were reversed by the PPARγ specific antagonist GW9662 and PPARγ siRNA. CONCLUSION: ADPKD cyst-lining epithelial cells participate in TGF-β1 mediated fibrogenesis. Rosiglitazone could suppress TGF-β1-induced collagen type I and fibronectin expression in ADPKD cyst-lining epithelia through modulation of the Smad2 pathway. Our study may provide therapeutic basis for clinical applications of rosiglitazone in retarding the progression of ADPKD

A novel COMP mutation in a pseudoachondroplasia family of Chinese origin

<p>Abstract</p> <p>Background</p> <p>Pseudoachondroplasia (PSACH) is caused exclusively by mutations in the gene for cartilage oligomeric matrix protein (<it>COMP</it>). Only a small number of studies have documented the clinical phenotype and genetic basis in Chinese PSACH patients.</p> <p>Case presentation</p> <p>We investigated a four-generation PSACH pedigree of Chinese Han origin. Two patients and two unaffected individuals were recruited for clinical evaluation and molecular genetic analysis. The genomic DNA was extracted from peripheral blood leukocytes. Polymerase chain reaction (PCR) was adopted to amplify the 8-19 exons of <it>COMP </it>gene. Then the products were sequenced bi-directionally for screening mutation. Clinical evaluation revealed that PSACH patients in this pedigree had a severe disproportionate short stature (-10SD). A heterozygous TGTCCCTGG insertion in exon 13, between nucleotide 1352T and 1353G, were identified in the patients except the unaffected individuals, which resulted in a three-amino-acid insertion (451V_452P ins VPG) in the sixth calmodulin-like repeat of the <it>COMP </it>protein.</p> <p>Conclusion</p> <p>This c. 1352_1353ins TGTCCCTGG is a novel mutation responsible for severe familial PSACH.</p

Efficacy of Short-Term High-Dose Statin in Preventing Contrast-Induced Nephropathy: A Meta-Analysis of Seven Randomized Controlled Trials

Background: A few studies focused on statin therapy as specific prophylactic measures of contrast-induced nephropathy have been published with conflicting results. In this meta-analysis of randomized controlled trials, we aimed to assess the effectiveness of shor-term high-dose statin treatment for the prevention of CIN and clinical outcomes and re-evaluate of the potential benefits of statin therapy. Methods: We searched PubMed, OVID, EMBASE, Web of science and the Cochrane Central Register of Controlled Trials databases for randomized controlled trials comparing short-term high-dose statin treatment versus low-dose statin treatment or placebo for preventing CIN. Our outcome measures were the risk of CIN within 2–5 days after contrast administration and need for dialysis. Results: Seven randomized controlled trials with a total of 1,399 patients were identified and analyzed. The overall results based on fixed-effect model showed that the use of short-term high-dose statin treatment was associated with a significant reduction in risk of CIN (RR = 0.51, 95 % CI 0.34–0.76, p = 0.001; I 2 = 0%). The incidence of acute renal failure requiring dialysis was not significant different after the use of statin (RR = 0.33, 95 % CI 0.05–2.10, p = 0.24; I 2 = 0%). The use of statin was not associated with a significant decrease in the plasma C-reactive protein level (SMD 20.64, 95 % CI: 21.57 to 0.29, P = 0.18, I 2 = 97%)