Introduction Despite the broad spectrum of neurological symptomatic manifestation in COVID19 patients, the brain tissue susceptibility and permissiveness to SARS-Cov2 infection is yet uncertain. This critical appraisal aims at bridging the gap by consolidating the body of evidence for meticulous evaluation of molecular neuropathological pathways and CSF diagnostic signatures of SARS-Cov2 infection in the central nervous system (CNS) that will underpin further strategic approach for neuroprotection and treatment of neurological COVID19 Methods and Analysis We have developed the protocol of this review according to the provisions of Joanna Briggs Institute Reviewer Manual for Evidence Synthesis ,2015 and Arksey and O Malley Methodological Framewotk ,2005.The articles for this review will be sourced from several electronic databases including EMBASE, PubMed, Scopus, Web of Science (WOS), Cochrane, Crossref Metadata and Semantic scholar. Herein we generated the search strategy using the medical subject headings [ MeSH Terms] , term in all field bibliography at all permutations in conjunctions with boolean operators Ethical Clearance and Dissemination plan Herein the review will not involve the human participants henceforth the ethical clearance approval is not applicable .We will disseminate the final findings of this review to scientific conferences at local and international level. The manuscript for final findings will be published on reputable journal of neuroscience. Keywords: Molecular, Neuropathology, CSF biomarkers, SARS-Cov2
Acinetobacter baumannii, has emerged as a critical nosocomial pathogen with the ability to develop resistance to all available antimicrobials, including colistin. Metabolomics tools may aid in the observation of the low molecular weight compounds in biochemical pathways yielding additional information about drug-resistant bacteria. The objective of this work was to compare the differential expression of metabolites between colistin-susceptible and resistant clinical strains of A. baumannii. The Q-TOF LC/MS method was used together with multivariate data analysis, Annotation of identified metabolites was performed along with the analysis of the metabolic pathways. Our results revealed that colistin-susceptible and colistin-resistant A. baumannii Strains have different metabolic profiles. Some of the identified metabolites were found to be involved in multiple biochemical pathways, such as cell wall biosynthesis and recycling, astaxanthin biosynthesis, and nucleotide metabolism. Cell wall recycling and nucleic acid degradation-related metabolites were up-regulated in colistin-sensitive strains. The lipid profile was down-regulated in colistin-resistant strains. On the other hand, a virulence factor that can serve as a drug target was found to be up-regulated in resistant strains. Our findings can provide a basis for further research on the elucidation of metabolites' role in resistance mechanisms and the determination of novel drug targets that would aid in the development of effective therapeutics against A. baumannii.
Biofilm-associated infections are characterized by the chronicity, recurrence, and the requirement of a prolonged administration of multiple drugs. Several non-pathogenic and pathogenic species of microorganism including Mycobacteria spp form biofilm. Mycobacterial biofilms present a unique composition. Instead of exopolysaccharides in other bacteria, proteins are essential compounds of the biofilm matrix in mycobacteria. To tackle mycobacterial infections, a detailed understanding of the biofilm-forming mechanisms is crucial. In this present study, all available Mycobacterial proteins involved in the biofilm were selected. Their sequences were retrieved and characterized through the determination of their physicochemical properties, secondary structure, 3D structure, subcellular localization, conserved domain, ubiquitination sites, and virulence potentiality. Furthermore, druggability testing was undertaken after excluding proteins with homology to human proteins to identify possible drug targets. The results showed that they possess functionally important domains and families. All of the selected hypothetical proteins were stable. Six of them were classified as soluble and the remaining as transmembrane proteins. A sole protein was found to lack ubiquitination sites. Additionally, three of these were discovered to be virulent. Moreover, host non-homology results indicated eight pathogen-specific proteins that might be potential therapeutic targets. Among them, D-alanyl-D-alanine carboxypeptidase is a druggable target that is inhibited by beta-lactam antibiotics. The remainder of the proteins were categorized as new targets. In conclusion, this study may increase our knowledge of pathogenesis and host adaptation, drug resistance, and identification of drug and vaccine targets against infections caused by Mycobacteria. It can also guide new research.
Candida species are commonly encountered strains associated with a wide range of infections. Unlike bacterial pathogens, fungal pathogens treatment is difficult and the development of resistance has been increasing at an alarming rate. In this study, the antifungal and antibiofilm effect of thyme oil, rosemary oil, mint oil, citronella oil, was tested on Candida albicans, Candida tropicalis, Candida kefyr, Candida glabrata, Candida parapsilosis isolated from clinical samples. The agar disc diffusion method was employed to determine the antifungal effect of the essential oils, and the inhibition of biofilm formation was assessed using microtiter biofilm inhibition assay. The results indicated that all the essential oils inhibited Candida strains and their biofilm in varying degrees. The highest antifungal activity in all isolates was observed in the thyme oil (>50mm), while rosemary oil showed the highest antibiofilm effect (>77%) in all tested strains. These findings led us to assume that the active components found in essential oils might be potential antifungal agents, adding to the repertoire of therapeutic options for the treatment of candidiasis.
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