We review methods in the study of nucleotide correlation in DNA sequence, and demonstrate two basic properties of the correlation through statistical analysis, namely, the short-range dominance of nucleotide correlation in most DNA sequences and the coarse-grained evolutionary dependence of the short-range correlation in coding sequences. A corresponding evolutionary mechanism is suggested. By the use of spectral analysis a large inhomogeneity in long-range base correlations for different sequences is indicated. Some results on three-dimensional DNA walks are reported. The linguistic differences between coding and noncoding sequences are also indicated.
Textual analysis of typical microbial genomes reveals that they have the statistical characteristics of a DNA sequence of a much shorter length. This peculiar property supports an evolutionary model in which a genome evolves by random mutation but primarily grows by random segmental duplication. That genomes grew mostly by duplication is consistent with the observation that repeat sequences in all genomes are widespread and intragenomic and intergenomic homologous genes are preponderant across all life forms.
BackgroundHepatocellular carcinoma (HCC) is one of the most lethal human tumors with extensive intratumor heterogeneity (ITH). Serine protease 3 (PRSS3) is an indispensable member of the trypsin family and has been implicated in the pathogenesis of several malignancies, including HCC. However, the paradoxical effects of PRSS3 on carcinogenesis due to an unclear molecular basis impede the utilization of its biomarker potential. We hereby explored the contribution of PRSS3 transcripts to tumor functional heterogeneity by systematically dissecting the expression of four known splice variants of PRSS3 (PRSS3-SVs, V1~V4) and their functional relevance to HCC.MethodsThe expression and DNA methylation of PRSS3 transcripts and their associated clinical relevance in HCC were analyzed using several publicly available datasets and validated using qPCR-based assays. Functional experiments were performed in gain- and loss-of-function cell models, in which PRSS3 transcript constructs were separately transfected after deleting PRSS3 expression by CRISPR/Cas9 editing.ResultsPRSS3 was aberrantly differentially expressed toward bipolarity from very low (PRSS3Low) to very high (PRSS3High) expression across HCC cell lines and tissues. This was attributable to the disruption of PRSS3-SVs, in which PRSS3-V2 and/or PRSS3-V1 were dominant transcripts leading to PRSS3 expression, whereas PRSS3-V3 and -V4 were rarely or minimally expressed. The expression of PRSS3-V2 or -V1 was inversely associated with site-specific CpG methylation at the PRSS3 promoter region that distinguished HCC cells and tissues phenotypically between hypermethylated low-expression (mPRSS3-SVLow) and hypomethylated high-expression (umPRSS3-SVHigh) groups. PRSS3-SVs displayed distinct functions from oncogenic PRSS3-V2 to tumor-suppressive PRSS3-V1, -V3 or PRSS3-V4 in HCC cells. Clinically, aberrant expression of PRSS3-SVs was translated into divergent relevance in patients with HCC, in which significant epigenetic downregulation of PRSS3-V2 was seen in early HCC and was associated with favorable patient outcome.ConclusionsThese results provide the first evidence for the transcriptional and functional characterization of PRSS3 transcripts in HCC. Aberrant expression of divergent PRSS3-SVs disrupted by site-specific CpG methylation may integrate the effects of oncogenic PRSS3-V2 and tumor-suppressive PRSS3-V1, resulting in the molecular diversity and functional plasticity of PRSS3 in HCC. Dysregulated expression of PRSS3-V2 by site-specific CpG methylation may have potential diagnostic value for patients with early HCC.
This work presents a novel rapid and sensitive label-free electrochemical method for the detection of bacteria on surface nanostructures. A simple electrochemical deposition and calcination method is employed to prepare different gold nanostructures on FTO substrate. The sensor based on nanostructure gold exhibits excellent linear relation between E. coli DH5α bacteria and the changes of ΔR, especially FTO-GEDC-D30, with a correction coefficient R = 0.998. Both the spectrophotometric (OD methods) and fluorescence-staining methods also verified the reliability of electrochemical impedance spectroscopy (EIS) methods for evaluating the antibacterial activity of the gold nanostructure.
The aim of this study was to investigate the role of soil and rice pollution on human renal dysfunction. The participants were 97 inhabitants (46 men and 51 women) who are aged 50 to 60 years old and have been living in Xiaogan (Hubei, China) from birth. We collected samples of soil, rice, and urinary correspondingly. Urinary N-acetyl-β-D-glucosaminidase (NAG) and β-2-microglobulin (βMG) were used as indicators of renal dysfunction, and urinary cadmium (U-Cd) was used as indicator of total internal cadmium exposure. We made a hypothesis that soil cadmium concentration (S-Cd) and rice cadmium concentration (R-Cd) could be used as indicators of environmental cadmium exposure. Correlation and path analysis were used to estimate the relationships among the levels of rice cadmium (R-Cd), soil cadmium (S-Cd), urinary cadmium (U-Cd), and renal damage indicators (NAG and βMG). Our results showed that there was positive significant relationship between S-Cd (R-Cd, U-Cd), and U-NAG (U-βMG). The standard multiple regression describing the relationship between S-Cd (R-Cd, U-Cd) and U-NAG was Y = 1.26X-6.53X + 9.32, where Y is U-NAG, X is U-Cd, X is S-Cd. The equation of U-βMG was Y = 49.32X + 3085.99X + 143.42, where Y is U-βMG, X is U-Cd, X is R-Cd. It is obvious that the effect of S-Cd and R-Cd on NAG or U-βMG cannot be ignored. Through our study, we can find that the effects of S-Cd on renal health even as significant as R-Cd. To protect people from the damage of cadmium pollution, it is vital to monitor the situation of soil and rice cadmium pollution.
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