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MiRNAs regulate both physiological and pathological heart functions. Altered expression of miRNAs is associated with cardiovascular diseases (CVDs), making miRNAs attractive therapeutic strategies for the diagnosis and treatment of heart diseases. A recent publication defined, for the first time, the term theranoMiRNA, meaning the miRNAs that may be used both for diagnosis and treatment. The use of in silico tools may be considered fundamental for these purposes, clarifying several molecular aspects, suggesting future directions for in vivo studies. This study aims to explore different bioinformatic tools in order to clarify miRNA interactions with candidate genes, demonstrating the need to use a computational approach when establishing the most probable associations between miRNAs and target genes. This study focused on the functions of miR-133a-3p, miR-21-5p, miR-499a-5p, miR-1-3p, and miR-126-3p, providing an up-to-date overview, and suggests future lines of research in the identification of theranoMiRNAs related to CVDs. Based on the results of the present study, we elucidated the molecular mechanisms that could be linked between miRNAs and CVDs, confirming that these miRNAs play an active role in the genesis and development of heart damage. Given that CVDs are the leading cause of death in the world, the identification of theranoMiRNAs is crucial, hence the need for a definition of in vivo studies in order to obtain further evidence in this challenging field of research. [ABSTRACT FROM AUTHOR]

Background: Pancreatitis is an inflammatory disorder resulting from the autoactivation of trypsinogen in the pancreas. The genetic basis of the disease is an old phenomenon, and evidence is accumulating for the involvement of synonymous/non-synonymous codon variants in disease initiation and progression. Results: The present study envisaged a panel of 26 genes involved in pancreatitis for their codon choices, compositional analysis, relative dinucleotide frequency, nucleotide disproportion, protein physical properties, gene expression, codon bias, and interrelated of all these factors. In this set of genes, gene length was positively correlated with nucleotide skews and codon usage bias. Codon usage of any gene is dependent upon its AT and GC component; however, AGG, CGT, and CGA encoding for Arg, TCG for Ser, GTC for Val, and CCA for Pro were independent of nucleotide compositions. In addition, Codon GTC showed a correlation with protein properties, isoelectric point, instability index, and frequency of basic amino acids. We also investigated the effect of various evolutionary forces in shaping the codon usage choices of genes. Conclusions: This study will enable us to gain insight into the molecular signatures associated with the disease that might help identify more potential genes contributing to enhanced risk for pancreatitis. All the genes associated with pancreatitis are generally associated with physiological function, and mutations causing loss of function, over or under expression leads to an ailment. Therefore, the present study attempts to envisage the molecular signature in a group of genes that lead to pancreatitis in case of malfunction. [ABSTRACT FROM AUTHOR]

The overexpression of SARS-CoV-2 primary receptors and co-receptors (ACE2, TMPRSS2, FURIN, and CD147) enhance the likeliness of SARS-CoV-2 infection. The genes for same receptors are overexpressed in the periodontal tissues of periodontitis patients. On the other hand, BMAL1 is recognized to play a crucial role in regulating pulmonary inflammation and enhancing susceptibility to viral infection. Silenced BMAL1 disrupts circadian transcriptional regulations, enhances vulnerability to SARS-CoV-2 infections, and may trigger the further production of TNF-α and other pro-inflammatory cytokines that propagate the cytokine storm and exacerbate periodontal inflammation. Therefore ACE2, TMPRSS2, FURIN, CD147, and BMAL1 are the crossroads between SARS-CoV-2 and Periodontitis genes. The enhanced expression of ACE2, TMPRSS2, FURIN, and CD147 and the diminished expression of BMAL1 may be a strategy to check both ailments simultaneously. In gene manipulation techniques, oligos are introduced, which contain all the necessary information to manipulate gene expression. The data are derived from the studies on genes' molecular patterns, including nucleotide composition, dinucleotide patterns, relative synonymous codon usage, codon usage bias, codon context, and rare and abundant codons. Such information may be used to manipulate the overexpression and underexpression of the genes at the time of SARS-CoV-2 infection and periodontitis to mitigate both ailments simultaneously; it can be explored to uncover possible future treatments. [ABSTRACT FROM AUTHOR]

Azoreductase is a reductive enzyme that efficiently biotransformed textile azo dyes. This study demonstrated the heterologous overexpression of the azoreductase gene in Escherichia coli for the effective degradation of Remazol Red-R and Acid-Blue 29 dyes. The AzK gene of Klebsiella pneumoniae encoding a ≈22 kDa azoreductase enzyme was cloned into the pET21+C expression vector. The inoculum size of 1.5%, IPTG concentration of 0.5 mM, and incubation time of 6 h were optimized by response surface methodology a statistical tool. The crude extract showed 76% and 74%, while the purified enzyme achieved 94% and 93% decolorization of RRR and AB-29, respectively in 0.3 h. The reaction kinetics showed that RRR had a K m and V max value of 0.058 mM and 1416 U mg−1, respectively at an NADH concentration of 10 mM. HPLC and GC-MS analyses showed that RRR was effectively bio-transformed by azoreductase to 2-[3-(hydroxy-amino) benzene-1-sulfonyl and AB-29 to aniline and 3-nitrosoaniline. This study explored the potential of recombinant azoreductase isolated from K. pneumoniae in the degradation of toxic textile azo dyes into less toxic metabolites. [Display omitted] • Azoreductase gene overexpression in E. coli for effective degradation of azo dyes. • Optimization of protein expression and decolorization using RSM. • Purified enzyme decolorized 94 and 93% of RRR and AB-29, respectively in 0.3 h. • HPLC and GCMS confirmed effective degradation of azo dyes into simple compounds. [ABSTRACT FROM AUTHOR]

Inflammatory bowel disease (IBD) is an inflammatory disorder of the gastrointestinal tract. The present study attempted to understand the codon usage preferences in genes associated with IBD progression. Compositional analysis, codon usage bias (CUB), Relative synonymous codon usage (RSCU), RNA structure, and expression analysis were performed to obtain a comprehensive picture of codon usage in IBD genes. Compositional analysis of 62 IBD-associated genes revealed that G and T are the most and least abundant nucleotides, respectively. ApG, CpA, and TpG dinucleotides were overrepresented or randomly used, while ApC, CpG, GpT, and TpA dinucleotides were either underrepresented or randomly used in genes related to IBD. The codons influencing the codon usage the most in IBD genes were CGC and AGG. A comparison of codon usage between IBD, and pancreatitis (non-IBD inflammatory disease) indicated that only codon CTG codon usage was significantly different between IBD and pancreatitis. At the same time, there were codons ATA, ACA, CGT, CAA, GTA, CCT, ATT, GCT, CGG, TTG, and CAG for whom codon usage was significantly different for IBD and housekeeping gene sets. The results suggest similar codon usage in at least two inflammatory disorders, IBD and pancreatitis. The analysis helps understand the codon biology, factors affecting gene expression of IBD-associated genes, and the evolution of these genes. The study helps reveal the molecular patterns associated with IBD. [ABSTRACT FROM AUTHOR]

Cyclohexyl thiosemicarbazone derivatives ( C1 – 14 ) were synthesized, characterized and evaluated against HER-2 over expressed breast cancer cells. The synthesized compounds were screened in vitro against four breast cancer cell lines; SKBr-3, MCF-7, MDA-MB-468 and MDA-MB-231. All the compounds showed activity against HER-2 over expressed SKBr-3 cells with (IC 50 = 25.6 ± 0.07 μM–61.6 ± 0.4 μM). The most active compounds inhibit ALDH + breast cancer stem cells more effectively than the cancer stem cells specific agent Salinomycin. Immunohistochemistry staining also confirmed that these compounds inhibit the expression of HER-2 on SKBr-3 cells. Compound C2 significantly inhibited the cell migration and cell adhesion of breast cancer cell lines. Compound C2 was found to most active compound of this series targeting HER-2 over expressed breast cancer cells. [ABSTRACT FROM AUTHOR]