Comparison of immune activation of the COVID vaccines : ChAdOx1, BNT162b2, mRNA-1273, BBIBP-CorV, and Gam-COVID-Vac from serological human samples in Hungary showed higher protection after mRNA-based

To gain insight into the different protective mechanisms of approved vaccines, this study focuses on the comparison of humoral and cellular immune responses of five widely used vaccines including ChAdOx1 (AZD1222, AstraZeneca), BNT162b2 (Pfizer), mRNA-1273 (Moderna), BBIBP-CorV (Sinopharm), and Gam-COVID-Vac (Sputnik V).Isolated plasma from 95 volunteers' blood samples was used to measure anti-SARS-CoV-2 humoral and cellular immune responses. Positive controls were recovered patients from COVID-19 (unvaccinated). Specific quantification kits for anti-nucleocapsid IgG, anti-Spike protein IgG, neutralizing antibodies as well as specific SARS-CoV-2 antigens for T-cell activation were used and Spearman correlation and matrix analyses were performed to compare overall immune responses.Nucleocapsid antibodies were significantly higher for the BBIBP-CorV and convalescent group when compared to other vaccines. In contrast, subjects vaccinated with BNT162b2 and mRNA-1273 presented significantly higher anti-spike IgG. In fact, 9.1% of convalescent, 4.5% of Gam-COVID-Vac, 28.6% of ChAdOx1, and 12.5% of BBIBP-CorV volunteers did not generate anti-spike IgG. Similarly, a positive correlation was observed after the neutralization assay. T-cell activation studies showed that mRNA-based vaccines induced a T-cell driven immune response in all cases, while 55% of convalescents, 8% of BNT162b1, 12,5% of mRNA-1273, 9% of Gam-COVID-Vac, 57% of ChAdOx1, and 56% of BBIBP-CorV subjects presented no cellular response. Further correlation matrix analyses indicated that anti-spike IgG and neutralizing antibodies production, and T-cell activation follow the same trend after immunization.RNA-based vaccines induced the most robust adaptive immune activation against SARS-CoV-2 by promoting a significantly higher T-cell response, anti-spike IgG and neutralization levels. Vector-based vaccines protected against the virus at a comparable level to convalescent patients

Osteo-Chondroprogenitor–Specific Deletion of the Selenocysteine tRNA Gene, Trsp, Leads to Chondronecrosis and Abnormal Skeletal Development: A Putative Model for Kashin-Beck Disease

Kashin-Beck disease, a syndrome characterized by short stature, skeletal deformities, and arthropathy of multiple joints, is highly prevalent in specific regions of Asia. The disease has been postulated to result from a combination of different environmental factors, including contamination of barley by mold mycotoxins, iodine deficiency, presence of humic substances in drinking water, and, importantly, deficiency of selenium. This multifunctional trace element, in the form of selenocysteine, is essential for normal selenoprotein function, including attenuation of excessive oxidative stress, and for the control of redox-sensitive molecules involved in cell growth and differentiation. To investigate the effects of skeletal selenoprotein deficiency, a Cre recombinase transgenic mouse line was used to trigger Trsp gene deletions in osteo-chondroprogenitors. Trsp encodes selenocysteine tRNA[Ser]Sec, required for the incorporation of selenocysteine residues into selenoproteins. The mutant mice exhibited growth retardation, epiphyseal growth plate abnormalities, and delayed skeletal ossification, as well as marked chondronecrosis of articular, auricular, and tracheal cartilages. Phenotypically, the mice thus replicated a number of the pathological features of Kashin-Beck disease, supporting the notion that selenium deficiency is important to the development of this syndrome

Proteomic mapping of differentially vulnerable pre-synaptic populations identifies regulators of neuronal stability in vivo.

Synapses are an early pathological target in many neurodegenerative diseases ranging from well-known adult onset conditions such as Alzheimer and Parkinson disease to neurodegenerative conditions of childhood such as spinal muscular atrophy (SMA) and neuronal ceroid lipofuscinosis (NCLs). However, the reasons why synapses are particularly vulnerable to such a broad range of neurodegeneration inducing stimuli remains unknown. To identify molecular modulators of synaptic stability and degeneration, we have used the Cln3-/- 33 mouse model of a juvenile form of NCL. We profiled and compared the molecular composition of anatomically-distinct, differentially-affected pre-synaptic populations from the Cln3-/- 35 mouse brain using proteomics followed by bioinformatic analyses. Identified protein candidates were then tested using a Drosophila CLN3 model to study their ability to modify the CLN3-neurodegenerative phenotype in vivo. We identified differential perturbations in a range of molecular cascades correlating with synaptic vulnerability, including valine catabolism and rho signalling pathways. Genetic and pharmacological targeting of key ‘hub’ proteins in such pathways was sufficient to modulate phenotypic presentation in a Drosophila CLN3 model. We propose that such a workflow provides a target rich method for the identification of novel disease regulators which could be applicable to the study of other conditions where appropriate models exist

SICOT contribution to natural disaster assistance: the triage.

Journal ArticleSCOPUS: ar.jinfo:eu-repo/semantics/publishe