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Etmopterus spinax (Linnaeus, 1758) and Etmopterus molleri (Whitley, 1939) are two bioluminescent deep-sea sharks, usually caught in large numbers as bycatch by deep-water fisheries. Yet, no study has ever involved population status of these two species using genetic tools. In order to investigate population genetic structure, diversity and connectivity of these two lanternsharks, 29 and 19 microsatellite loci were isolated from E. spinax DNA library for E. spinax and E. molleri, respectively. These loci were tested on 32 E. spinax individuals from the North Sea and seven E. molleri from the East China Sea. The number of alleles per locus ranged from 2 to 13. The observed heterozygosity ranged from 0.031 to 0.839 for E. spinax and from 0.000 to 1.000 for E. molleri, while the expected heterozygosity ranged from 0.031 to 0.903 and from 0.143 to 0.821, respectively. Almost all loci (24 and 16, respectively) were at Hardy–Weinberg equilibrium for both species and no linkage disequilibrium among loci was detected. These loci represent useful tools to better understand the population structure of these two species. Besides, they could also be suitable for other lanternsharks in general, as these latter remain largely understudied, specially in terms of understanding the basic science that will serve into their conservation.

Hepatitis B virus (HBV) as the main prevalent infectious agent, play important roles in inducing severe liver diseases. Previous studies demonstrated that during prolonged forms of hepatitis B infection including chronic, asymptomatic and occult forms, patients are unable to eradicate HBV from hepatocytes completely. The main mechanisms responsible for development of the forms of hepatitis B are yet to be identified. Investigators suggested that the various genetic and immunological parameters of the patients may are responsible for resulting in the prolonged infection forms. It has been evidenced that TLRs play key roles in inducing appropriate immune responses, against viral infections. Therefore, these molecules can be considered as crucial sensors for HBV detection to induce immune responses against this virus. It has also been documented that the TLR3 detects intracellular viral dsRNA and subsequently activates NF-κB via the TRIF pathway. Therefore, impaired TLR3 expression may result in inappropriate immune responses against HBV which is reported in prolonged forms of hepatitis B. This review collected the recent information regarding the important roles of TLR3 in immune responses against HBV and also the status of TLR3 expression and its genetic variations in prolonged forms of HBV infections.

The question about the nature of promoters in the transcriptional units containing SV-40 sequences in transformed cells was analyzed. It was found that the pulse-labeled RNA hybridizing to SV-40 DNA contains small but significant amounts of triphosphorylated 5′-ends detected as pppGp in alkaline hydrolyzates of this RNA. In another series of experiments the fragments of RNA containing triphosphorylated 5′-ends about 100 nucleotides in length have been isolated by hydroxyapatite chromatography. Some of them form hybrids with SV-40 DNA. The conclusion is drawn that at least some of SV-40 promoters are used for transcription initiation in SV-40 transformed cells.

Viral infection is still a serious global health problem that kills hundreds of thousands of people annually. Understanding the mechanism by which virus replicates, packages, and infects the host cells can provide new strategies to control viral infection. Long non-coding RNAs (lncRNAs) have been identified as critical regulators involved in viral infection process and antiviral response. A lot of host lncRNAs have been identified and shown to be involved in antiviral immune response during viral infection. However, our knowledge about lncRNAs expressed by viruses is still at its infancy. LncRNAs expressed by viruses are involved in the whole viral life cycle, including promoting genome replication, regulating gene expression, involvement in genome packaging, assembling new viruses and releasing virions to the host cells. Furthermore, they enhance the pathogenicity of viral infections by down-regulating the host cell’s antiviral immune response and maintain the viral latency through a refined procedure of genome integration. This review focuses on the regulatory roles of viral lncRNA in the life-cycle and pathogenicity of viruses. It gives an insight into the viral lncRNAs that can be utilized as therapeutic targets against viral diseases, and future researches aimed to identify and explore new viral lncRNAs and the mechanisms of their involvement in viral infection is encouraged.

The aim of this study was to assess the association of polymorphisms in the promoter region of the IL-10 gene with the risk of inflammatory bowel disease (IBD), including Crohn’s disease (CD) and ulcerative colitis (UC). Fifteen studies (3,693 cases and 4,574 controls) were included in a meta-analysis of association between IL-10 −1082G/A, −819C/T and −592C/A polymorphisms, and IBD, CD and UC using allele contrast and the recessive, dominant, and additive models. Hardy–Weinberg equilibrium was confirmed for each study. Heterogeneity and study quality were investigated using stratification analyses and sensitivity analyses. Polymorphism −1082G/A showed significant association with CD, with odds ratios (ORs) for the GG + GA genotype and GG versus AA genotype of 1.278 (1.004–1.627) and 1.238 (1.027–1.492) in all subjects. Significant associations were found in the Caucasian subgroup using the allele contrast, dominant, and additive models. C-allele carriers of the −819C/T polymorphism were at increased risk of IBD (OR 1.093, 95 % CI 1.004–1.190). Association with the −819C/T polymorphism was also found in Caucasians with CD (C vs. T: OR 1.104, 95 % CI 1.010–1.206; CC + CT vs. TT: OR 1.328, 95 % CI 1.006–1.754; CC vs. TT: OR 1.339, 95 % CI 1.008–1.778), and with UC (CC vs. CT + TT: OR 1.188, 95 % CI 1.019–1.385). No significant association was found between the −592C/A polymorphism and IBD, CD or UC. In conclusion, the meta-analysis demonstrated clear association between the IL-10 polymorphisms −1082G/A and −819C/T and the risk of IBD.

Medicinal effects of Crepidiastrum denticulatum have been previously reported. However, the genomic resources of this species and its applications have not been studied. In this study, based on the next generation sequencing method (Miseq sequencing system), we characterize the chloroplast genome of C. denticulatum which contains a large single copy (84,112 bp) and a small single copy (18,519 bp), separated by two inverted repeat regions (25,074 bp). This genome consists of 80 protein-coding gene, 30 tRNAs, and four rRNAs. Notably, the trnT_GGU is pseudogenized because of a small insertion within the coding region. Comparative genomic analysis reveals a high similarity among Asteraceae taxa. However, the junctions between LSC, SSC, and IRs locate in different positions within rps19 and ycf1 among examined species. Also, we describe a newly developed single nucleotide polymorphism (SNP) marker for C. denticulatum based on amplification‐refractory mutation system (ARMS) technique. The markers, inferred from SNP in rbcL and matK genes, show effectiveness to recognize C. denticulatum from other related taxa through simple PCR protocol. The chloroplast genome-based molecular markers are effective to distinguish a potentially medicinal species, C. denticulatum, from other related taxa. Additionally, the complete chloroplast genome of C. denticulatum provides initial genomic data for further studies on phylogenomics, population genetics, and evolutionary history of Crepidiastrum as well as other taxa in Asteraceae.

Studies investigating the association between glutathione S-transferase M1 (GSTM1) polymorphism and bladder cancer risk report conflicting results. The objective of this study was to quantitatively summarize the evidence for such a relationship. We performed a systematic search of the National Library of Medline and Embase databases. This meta-analysis included 26 case-control studies, which included 5029 bladder cancer cases and 6680 controls. The combined results based on all studies showed that the GSTM1 null genotype was associated with an increased risk of bladder cancer (OR = 1.46, 95% confidence interval [CI] = 1.35, 1.57). When stratifying for race, results were similar among Asians (OR = 1.60, 95% CI = 1.27, 2.01) and Caucasians (OR = 1.44, 95% CI = 1.33, 1.57) except Africans (OR = 1.25, 95% CI = 0.76, 2.06). When stratifying by the smoking, stage, grade, and histological type of bladder cancer, we found no statistical association. Our meta-analysis suggests that the GSTM1 null genotype is associated with a modest increase in the risk of bladder cancer.

Several evidences support that caveolin-1 is associated with mammary cell transformation and oncogenesis. We have previously reported that a cell line, named MCF10A-ST1 (ST1), which only expressed 30% Cav-1 compared with parental cells MCF10A (human mammary epithelial cell line) was isolated by gene trapping. The decreased expression of Cav-1 is sufficient for phenotypic transformation of MCF10A cells, which involved in the loss of anchorage-dependent growth and migration in nude mice with the existence of E2. The previous study in our lab on microarray assay showed that the expression of cyclin D1 (cell cycle protein) was up-regulated in ST1 cell line. Here, we not only confirmed the results by Western Blot but also demonstrated that Cav-1 down-regulation accelerate the progression of mammary cells from G1 phase into S phase by Flow Cytometry (FCM). This proposed that the Cav-1 down-regulation could change the progress of cell cycle in the mammary cells. Otherwise, microarray assay also showed that the transcription factor (c-Jun) was up-regulated. But, the original carcinoma gene (c-Fos) and transcription factor (AP-1) have not obviously changed compared with MCF10A. ST1 cells obtained the morigenicity in nude mice with the existence of E2, and the immunoprecipitation showed the interactions of Cav-1 with ERα in both MCF10A and ST1. ERα expression was increased as further down-regulation of Cav-1. So, we hypothesize that Cav-1 down-regulation could induce the activation of ERα-associated signaling pathway, in order to adjust the development and proliferation. By siRNA technology, the down regulation of Cav-1 could activate MAP kinase and Akt signaling pathway, including the phosphorylation of ERK1/2 and Akt. However, the mechanism of Cav-1 down-regulation in the early transformation and signaling transduction of mammary epithelial cells is unclear. Here, we report that down-regulation of caveolin-1 protein expression leads to deregulate estrogen receptor alpha (ERα) signaling and consequently early transformation in mammary epithelia.

Glutathione S-transferase genes, known to be highly polymorphic, are implicated in the process of phase II metabolism of many substrates, including xenobiotics, anticancer and anti-infective drugs. The detoxification activity is linked to individual genetic makeup. Therefore, the identification of alleles and genotypes in these genes within a population may help to better design genetic susceptibility and pharmacogenetic studies. We performed the present study to establish the frequencies of the GSTM1, GSTT1, and GSTP1 c. 313A > G (rs1695) polymorphisms in 206 individuals of the Malian healthy population. GSTM1 and GSTT1 were genotyped by using multiplex polymerase chain reaction, whereas genotypes of GSTP1 were identified by polymerase chain reaction followed by restriction fragment length polymorphism. The frequencies of GSTM1-null and GSTT1-null genotypes were respectively 24.3 and 41.3%. The observed genotype frequencies for GSTP1 were 25.73% homozygous wild-type AA, 49.03% heterozygous AG and 25.24% homozygous mutant GG. The frequency of GSTP1-A allele was 50.24% versus 49.76% for the GSTP1-G allele. The distribution of these three genes was homogeneous between men and women (p > 0.05). We found no statistical association between the presence of a particular profile of GSTM1 or GSTT1 with the genotypes of GSTP1 (p > 0.05). Nevertheless, we noticed that the majority of the individuals harboring the GSTM1-present or the GSTT1-present harbor also the GSTP1-AG genotype. In addition, the triple genotype GSTM1-present/GSTT1-present/AG was the most frequent with 25.2%. Our findings will facilitate future studies regarding genetic associations of multifactorial diseases and pharmacogenetic, thus opening the way to personalized medicine in our population.