Genetics & Molecular Biology

Extracellular vesicles as drug delivery vehicles

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Extracellular vesicles (EVs) are discharged film encased nano-sized particles (40– 1,000 nm) that convey natural data between cells. The atomic organization of these subcellular particles incorporates development factor receptors, ligands bond proteins, mRNA, miRNAs, lncRNA and lipids that are gotten from giver cells. Various investigations exhibited that foundational microorganism determined EVs are the key middle person of tissue repair and recovery in different creature sickness models. What’s more, the synthesis of these particles is known to be modified in tumor and sickness pathology recommending them for valuable in indicative and restorative purposes. Their endogenous source and organic properties offer advantages over traditional medication conveyance frameworks (DDS, for example, liposome, manufactured nanoparticles and incited the further use of EVs as medication conveyance vehicles for concoction drugs, hereditary materials and proteins. The substance of EVs can be productively adjusted by concoction, organic or physical means. Consequently, EVs can be an inventive DDS as it can beat physical and natural boundaries and securely convey restorative medications to target tissues.

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Spectrum of CFTR Mutations in the Algerian Population: Molecular and Computational Analysis

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Little has been reported on the occurrence of cystic fibrosis in Algerian population. In order to contribute to the few existing data we undertook this study. The aim was in first instance to detect genetics alteration in the CFTR gene of 21 CF Algerian patients by sequencing. 14 different mutations were detected one of them
has never been described. Among these mutations the c.680T>G (L227R) which seems to be specific to the Algerian population, it was in silico studied to determine its impact at a molecular level.

For more: https://www.scitechnol.com/peer-review/spectrum-of-cftr-mutations-in-the-algerian-population-molecular-and-computational-analysis-mN5B.php?article_id=4698

Contact us: editor.jgdgr@scitechnol.org (or) editor.jgdgr@scitechnol.com

Anti-Ige (Omalizumab) Improved Trombotic Emboli by Elevating Activated Protein C, Protein S, and Antithrombin III in a Case of Prothrombin G20210A Mutation: Long Term Follow-Up

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Plasma protein C levels were significantly lower compared to patients without acute rejection at the time of rejection, specifically antibody mediated rejection. In a parallel mammer Endothelial Protein C Receptor (EPCR) expression was found higher in tubules and arteries of rejection patients than in control patients [3] and activation of the inflammatory/coagulation cascades has been suggested in the pathogenesis of the rejection.

For more: https://www.scitechnol.com/peer-review/antiige-omalizumab-improved-trombotic-emboli-by-elevating-activated-protein-c-protein-s-and-antithrombin-iii-in-a-case-of-prothrom-A28q.php?article_id=4699

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If humans are related to chimps, how can we account for this difference?

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Scientists have concluded that 96–98% of human genome is similar to that of the chimp. As humans and chimps gradually evolved from a common ancestor, their DNA passed from generation to generation. Much of the similarity lies in the regions of the DNA that result in proteins It seems logical that if a protein performs a certain function in one organism, and that function is necessary in other organisms, then the same protein would be utilized by multiple organisms.

For more related information, visit us on https://www.scitechnol.com/journal-genetics-gene-therapy.php

SciTechnol

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SciTechnol is an online publisher that enjoys global presence with International Journals on Clinical, Medical, Environmental, Pharmaceutical, Neurosciences, Environmental Science, and Business Management. SciTechnol offers a meaningful platform to the global scientific community to discuss and share knowledge while disseminating research findings globally.

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The Genomic Novel and Priority Mapping Tool: Using Empathic Design to Develop Innovative Patient-Centered Decision-Making Tools for the Genomic Testing Experience

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The volume and complexity of data discussed between a genetic counselor and patient and the unavoidable generation of incidental findings related to whole exome sequencing (WES) or whole genome sequencing (WGS) have created challenges for patients and their providers. Gone are the days when a genetic counselor could focus on discussing one or a handful of gene testing results with their patients. Instead, healthcare providers are presented with the challenge of figuring out how to disclose multiple potentially clinically meaningful results, many of which could not have been anticipated.

For more: https://www.scitechnol.com/peer-review/the-genomic-novel-and-priority-mapping-tool-using-empathic-design-to-develop-innovative-patientcentered-decisionmaking-tools-for-t-vdKF.php?article_id=4683

Contact us: editor.jgdgr@scitechnol.org (or) editor.jgdgr@scitechnol.com

Severe Expressive-Language Delay and Congenital Malformations in a Boy with Microduplication 7q11.23 Diagnosed by Molecular Cytogenetic Analysis

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Williams-Beuren syndrome (WBS) (MIM 194050) is an autosomal dominant disorder affecting 1 in 7,500 to 1 in 20,000 births due to sporadic de novo chromosomal microdeletions at 7q11.23 detectable by fluorescence in situ hybridization (FISH). As with many other genomic disorders, the common recurrent 1.55- Mb microdeletion occurs by nonallelic homologous recombination (NAHR)  between numerous low copy repeats (LCRs) flanking the commonly deleted region. Inversion of the same segment has been found in 27% of affected individuals with an atypical WBS phenotype and in 33% of transmitting parents, suggesting that the presence of this structural variant in the population may be associated with WBS or may predispose to genomic rearrangements.

For more: https://www.scitechnol.com/peer-review/severe-expressivelanguage-delay-and-congenital-malformations-in-a-boy-with-microduplication-7q1123-diagnosed-by-molecular-cytogene-46Xx.php?article_id=4700

Contact us: editor.jgdgr@scitechnol.org (or) editor.jgdgr@scitechnol.com