Human DNA AI Model to Predict COVID-19 Symptomatic or Asymptomatic Percentages

The current paper proposes to use convolutional neural networks (CNN) to analyze human genome single nucleotide variants (SNVs) from nuclear deoxyribonucleic acid (DNA) and mitochondrial deoxyribonucleic acid (mtDNA) presented as a 2D image structure to understand if the answer to COVID-19 severities can be found in the human genome. That methodology was implemented with 447 Mexican population samples. From the results, two main groups were formed divided into symptomatic and asymptomatic cases composed of 80.986% and 19.014% respectively and the model was validated through an online survey of individuals, giving a 91.89% of accuracy.

SECONDARY MITOCHONDRIAL DYSFUNCTION

Mitochondria are the most vital organelle in the cell because of its multitask properties. They are well known for the production of energy in the form of adenosine triphosphate (ATP) through oxidative phosphorylation (OXPHOS), which involves multiple complexes and cofactors. Mitochondria in addition to ATP production, also perform other vital functions like generation of reactive oxygen species (ROS), antioxidants, apoptosis, signaling and hormone actions. Because of their multiple actions, it is quite expected that their dysfunction will result in the number of effects. Since most vital organs exclusively depend on ATP to perform their functions, therefore impediment in its supply resulting from mitochondrial dysfunction will be detrimental and have a widespread spectrum. Neurodegenerative disorders, Huntington’s disease, cardiovascular disease (CVD), epilepsy, aging, metabolic syndrome, diabetes, autism, muscular atrophy, lou gehrig’s disease, neoplasia, down syndrome are few instances where mitochondrial dysfunction is the basic cause in pathogenesis. Mitochondrial disorders are either Primary or secondary disorders. Primary mitochondrial disease or disorder (PMD) has mitochondrial or nuclear deoxyribonucleic acid (mt DNA or nDNA) mutation affecting oxidative phosphorylation (OXPHOS). While Secondary mitochondrial dysfunction (SMD) does not involve OXPHOS but is the result of mutations in non OXPHOS genes. Secondary mitochondrial dysfunction (SMD) can also be acquired secondary to adverse factors those cause oxidative stress. All this highlights the role of mitochondria and makes it a new therapeutic target in managing these disorders. The present review has briefly discussed the secondary mitochondrial dysfunctional disorders and the approach to tackle it.

A potential role as a suppressor protein of Regucalcin in the development of human carcinogenesis

Regucalcin was discovered in 1978 as a calcium-binding protein. After that, regucalcin was demonstrated to play a multifunctional role as a suppressor protein in signal transduction in various types of cell and tissues. The regucalcin gene (rgn) is localized on the X chromosome. Regucalcin was found to suppress nuclear deoxyribonucleic acid (DNA) and ribonucleic acid (RNA) synthesis in liver cells. Overexpression of endogenous regucalcin possessed suppressive effects on proliferation in the modeled rat hepatoma cells by inhibiting G1 and G2/M cell cycle arrests. Suppressed regucalcin gene expression was found to be associated with progression of hepatocarcinogenesis by proteosome analysis. Moreover, regucalcin mRNA expression was found to suppress in various human normal and tumor tissues including hepatocellular carcinoma, kidney transitional cell carcinoma, brain malignant meningioma, and lung non-small cell carcinoma of human subjects. Suppressed regucalcin gene expression may be a key in development of carcinogenesis. Development of the regucalcin gene deliver system will be expected as a novel gene therapy in clinical aspects for cancer treatment.

Involvement of Regucalcin in Protein Synthesis and Proteolysis: Regulation of the Enzyme Activity in the Cytoplasm and Nucleus

<p>Regucalcin was discovered in 1978 as a novel calcium-binding protein. The name, regucalcin, was proposed for this calcium-binding protein, which regulates various Ca^2+- or Ca²⁺/calmodulin-dependent enzyme activations. The regucalcin gene (gene symbol;rgn) is localized on the X chromosome. Regucalcin has been demonstrated to play a multifunctional role in the regulation of intracellular calcium homeostasis, signal transduction, gene expression, cell proliferation and apoptosis in various types of cells and tissues. The cytoplasmic regucalcin translocases to the nucleus and suppresses nuclear deoxyribonucleic acid (DNA) and ribonucleic acid (RNA) synthesis. Moreover, regucalcin has been shown to reveal a suppressive effect on protein synthesis and a stimulatory effect on protein degradation. Regucalcin has been found to inhibit aminoacyl-tRNA synthetase and activate thiol protease. Â Regucalcin may play a suppressive role in the regulation of protein turnover in cells.</p>

Procreation by Cloning: Crafting Anticipatory Guidelines

To clone humans is deliberately to generate two or more individuals who share the same nuclear deoxyribonucleic acid (DNA). Using animals, researchers have performed two basic types of cloning that will eventually yield commercial benefits. Embryo twinning involves separating the individual cells of an embryo and allowing each to cleave for later transfer to a uterus. Cloning by nuclear transfer involves removing the nuclei from embryonic cells or fetal or adult somatic (body) cells and fusing those nuclei with enucleated donor egg cells. Although for the purposes of commercial biotechnology these techniques do not raise undue concern when attempted with animals, embryo twinning, embryo nuclear transfer, fetal somatic cell nuclear transfer, and adult somatic cell nuclear transfer all provoke intense ethical discussions when considered for human use.