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Exosome-derived miR-21 was independently associated with CD4 T cell decline in HIV-1-infected elite controllers (OR 0.369, 95% CI 0.137–0.994, p = 0.049). Also, a negative correlation between miR-21 expression and MCP-1 level was found (r = −0.649, p = 0.020), while no correlation between soluble biomarkers or cellular immune activation was found. Keywords: Exosomes, miRNAs, HIV-1, Elite controllers, Immune activation, Soluble biomarkers

Adulterating foods, such as milk powder (MP), is a common practice in countries with no rigid policy on food quality control. This study employs Fourier transform near-infrared and mid-infrared (FT-NIR, FT-MIR) spectroscopy and chemometric analysis to detect milk powder adulteration with corn starch (CS) and wheat flour (WF) from 0.00 to 30.00% w/w concentrations. Partial least square regression (PLSR) models were developed, optimized, and compared to quantify corn starch and wheat flour adulterations. According to the results, the root mean square error prediction (RMSEP) for FT-NIR and FT-MIR in corn starch was 0.74 and 1.69% w/w and 0.82 and 2.63% w/w for wheat flour, respectively. FT-NIR spectroscopy, rather than FT-MIR coupled with the appropriate chemometrics models represents a more valuable tool for simple, rapid, and nondestructive detection of adulterants in milk powder. The recent availability of portable instruments, combined with suitable chemometric tools, makes it possible to discriminate adulterated food samples in situ.

Cerebral autosomal recessive arteriopathy with subcortical infarcts and leukoencephalopathy (CARASIL) is an autosomal recessive vascular disorder caused by biallellic variants in HTRA1. Recently, it has been reported that several heterozygous mutations in HTRA1 are responsible for a milder late-onset cerebral small vessel disease (CSVD) with an autosomal dominant pattern of inheritance. The majority of them are missense that affects the Htr1A protease activity due to a dominant-negative effect caused by defective trimerization or monomer activation. The molecular mechanism related to the structural destabilization of the protein supports the practical utility of integrating computational stability predictors to prioritize candidate variants in this gene. In this work, we report a family with several members diagnosed with subcortical ischemic events and progressive cognitive impairment caused by the novel c.820C > G, p.(Arg274Gly) heterozygous variant in HTRA1 segregating in an autosomal dominant manner and propose its molecular mechanism by a three-dimensional model of the protein's structure., (Copyright © 2022 Elsevier Masson SAS. All rights reserved.)

Objective: Molecular epidemiology techniques in tuberculosis (TB) can identify high-risk strains that are actively transmitted. We aimed to implement a novel strategy to optimize the identification and control of multidrug-resistant (MDR) TB in a specific population., Methods: We developed a strain-specific PCR tailored from whole genome sequencing (WGS) data to track a specific MDR prevalent strain in Equatorial Guinea (EG-MDR)., Results: The PCR was applied prospectively on remnants of GeneXpert reaction mixtures owing to the lack of culture facilities in Equatorial Guinea. In 147 (93%) of 158 cases, we were able to differentiate between infection by the EG-MDR strain or by any other strain and found that 44% of all rifampicin-resistant TB cases were infected by EG-MDR. We also analysed 93 isolates obtained from Equatorial Guinea 15 years ago, before MDR-TB had become the problem it is today. We found that two of the scarce historical MDR cases were infected by EG-MDR. WGS revealed low variability-six single nucleotide polymorphisms acquired by this strain over 15 years-likely because of the lack in the country of a specific program to treat MDR-TB., Conclusions: Our novel strategy, which integrated WGS analysis and strain-specific PCRs, represents a low-cost, rapid and transferable strategy that allowed a prospective efficient survey and fast historical analysis of MDR-TB in a population., (Copyright © 2016 European Society of Clinical Microbiology and Infectious Diseases. Published by Elsevier Ltd. All rights reserved.)

Amyotrophic lateral sclerosis (ALS) is a common neurodegenerative disorder characterized mainly by a progressive loss of motor neurons. Glutamate excitotoxicity is likely the main cause of neuronal death, and Riluzole interferes with glutamate-mediated transmission. Thus, in such independent pathway, these effects may be partly due to inactivation of voltage-dependent sodium channels. Here we predict the structural model of the interaction and report the possible binding sites of Riluzole on Nav1.6 channel. The docked complexes were subjected to minimization and we further investigated the key interacting residues, binding free energies, pairing bridge determination, folding pattern, hydrogen bounding formation, hydrophobic contacts and flexibilities. Our results demonstrate that Riluzole interacts with the Nav1.6 channel, more specifically in the key residues TYR 1787, LEU 1843 and GLN 1799, suggesting possible cellular implications driven by these amino acids on Riluzole-Nav1.6 interaction, which may serve as an important output for a more specific and experimental drug design therapy against ALS., (Copyright © 2012 Elsevier Ltd. All rights reserved.)