Alginate-Capped Silver Nanoparticles as a Potent Anti-mycobacterial Agent Against Mycobacterium tuberculosis

Tuberculosis (TB) is a leading cause of death from a single infectious agent, Mycobacterium tuberculosis (Mtb). Although progress has been made in TB control, still about 10 million people worldwide develop TB annually and 1.5 million die of the disease. The rapid emergence of aggressive, drug-resistant strains and latent infections have caused TB to remain a global health challenge. TB treatments are lengthy and their side effects lead to poor patient compliance, which in turn has contributed to the drug resistance and exacerbated the TB epidemic. The relatively low output of newly approved antibiotics has spurred research interest toward alternative antibacterial molecules such as silver nanoparticles (AgNPs). In the present study, we use the natural biopolymer alginate to serve as a stabilizer and/or reductant to green synthesize AgNPs, which improves their biocompatibility and avoids the use of toxic chemicals. The average size of the alginate-capped AgNPs (ALG-AgNPs) was characterized as nanoscale, and the particles were round in shape. Drug susceptibility tests showed that these ALG-AgNPs are effective against both drug-resistant Mtb strains and dormant Mtb. A bacterial cell-wall permeability assay showed that the anti-mycobacterial action of ALG-AgNPs is mediated through an increase in cell-wall permeability. Notably, the anti-mycobacterial potential of ALG-AgNPs was effective in both zebrafish and mouse TB animal models in vivo. These results suggest that ALG-AgNPs could provide a new therapeutic option to overcome the difficulties of current TB treatments.

Two-dimensional numerical studies of particle motion and deposition in the channel of diesel particulate filters

A numerical investigation on the soot laden flow of gas in a partial diesel particulate filter (PDPF) is presented based on solving the momentum equations for a continuous phase in the Euler frame and the motion equations for the dispersed phase in the Lagrangian frame. The interaction between the gas phase and the particles is considered as a one-way coupling for dilute particle concentration, while the interaction between particles and porous wall is implemented through user-definedsubroutines. To accurately track motion of nanoscale particles, the Brownian excitation and drag force as well as partial slip are taken into account in the particulate motion equation. Two methods are used to verify the gas flow model and reasonable agreements for both comparisons are observed. The effects of inlet velocity, wall permeability and particle size on the filtration efficiency and deposition distribution of the particles along with wall surface of inlet channel are quantitatively studied. The results show that (i) wall permeability plays the primary role in determining the filtration efficiency of PDPF, (ii) both upstream velocity and particle size have an effect on the initial deposition position of particles and (iii) filtration efficiency of PDPF is not markedly proportional to gas flow into inlet channels at a low wall permeability.

Gut Microbiota as a Potential Player in Mn-Induced Neurotoxicity

Manganese (Mn) is an essential metal, which at high exposures causes neurotoxic effects and neurodegeneration. The neurotoxic effects of Mn are mediated by neuroinflammation, oxidative and endoplasmic reticulum stress, mitochondrial dysfunction, and other mechanisms. Recent findings have demonstrated the potential impact of Mn overexposure on gut microbiota dysbiosis, which is known to contribute to neurodegeneration via secretion of neuroactive and proinflammatory metabolites. Therefore, in this review, we discuss the existing data on the impact of Mn exposure on gut microbiota biodiversity, bacterial metabolite production, and gut wall permeability regulating systemic levels. Recent data have demonstrated that Mn exposure may affect gut microbiota biodiversity by altering the abundance of Shiegella, Ruminococcus, Dorea, Fusicatenibacter, Roseburia, Parabacteroides, Bacteroidetes, Firmicutes, Ruminococcaceae, Streptococcaceae, and other bacterial phyla. A Mn-induced increase in Bacteroidetes abundance and a reduced Firmicutes/Bacteroidetes ratio may increase lipopolysaccharide levels. Moreover, in addition to increased systemic lipopolysaccharide (LPS) levels, Mn is capable of potentiating LPS neurotoxicity. Due to the high metabolic activity of intestinal microflora, Mn-induced perturbations in gut microbiota result in a significant alteration in the gut metabolome that has the potential to at least partially mediate the biological effects of Mn overexposure. At the same time, a recent study demonstrated that healthy microbiome transplantation alleviates Mn-induced neurotoxicity, which is indicative of the significant role of gut microflora in the cascade of Mn-mediated neurotoxicity. High doses of Mn may cause enterocyte toxicity and affect gut wall integrity through disruption of tight junctions. The resulting increase in gut wall permeability further promotes increased translocation of LPS and neuroactive bacterial metabolites to the systemic blood flow, ultimately gaining access to the brain and leading to neuroinflammation and neurotransmitter imbalance. Therefore, the existing data lead us to hypothesize that gut microbiota should be considered as a potential target of Mn toxicity, although more detailed studies are required to characterize the interplay between Mn exposure and the gut, as well as its role in the pathogenesis of neurodegeneration and other diseases.

Dietary Influences on the Microbiota–Gut–Brain Axis

Over unimaginable expanses of evolutionary time, our gut microbiota have co-evolved with us, creating a symbiotic relationship in which each is utterly dependent upon the other. Far from confined to the recesses of the alimentary tract, our gut microbiota engage in complex and bi-directional communication with their host, which have far-reaching implications for overall health, wellbeing and normal physiological functioning. Amongst such communication streams, the microbiota–gut–brain axis predominates. Numerous complex mechanisms involve direct effects of the microbiota, or indirect effects through the release and absorption of the metabolic by-products of the gut microbiota. Proposed mechanisms implicate mitochondrial function, the hypothalamus–pituitary–adrenal axis, and autonomic, neuro-humeral, entero-endocrine and immunomodulatory pathways. Furthermore, dietary composition influences the relative abundance of gut microbiota species. Recent human-based data reveal that dietary effects on the gut microbiota can occur rapidly, and that our gut microbiota reflect our diet at any given time, although much inter-individual variation pertains. Although most studies on the effects of dietary macronutrients on the gut microbiota report on associations with relative changes in the abundance of particular species of bacteria, in broad terms, our modern-day animal-based Westernized diets are relatively high in fats and proteins and impoverished in fibres. This creates a perfect storm within the gut in which dysbiosis promotes localized inflammation, enhanced gut wall permeability, increased production of lipopolysaccharides, chronic endotoxemia and a resultant low-grade systemic inflammatory milieu, a harbinger of metabolic dysfunction and many modern-day chronic illnesses. Research should further focus on the colony effects of the gut microbiota on health and wellbeing, and dysbiotic effects on pathogenic pathways. Finally, we should revise our view of the gut microbiota from that of a seething mass of microbes to one of organ-status, on which our health and wellbeing utterly depends. Future guidelines on lifestyle strategies for wellbeing should integrate advice on the optimal establishment and maintenance of a healthy gut microbiota through dietary and other means. Although we are what we eat, perhaps more importantly, we are what our gut microbiota thrive on and they thrive on what we eat.

Microorganisms Photocatalytic Inactivation on Ag3PO4 Sub-microcrystals Under WLEDs Light Source

In this article, we report the silver orthophosphate (Ag3PO4) photocatalytic inactivation properties on strains Gram-positive Saprophyte B. subtilis, a diploid fungus Candida albicans and Gram-negative Pseudomonas aeruginosa, using as irradiation source white-light-emitting diodes (WLEDs) with luminous flux (Φ v) of 1.3 x 103 Lumens and relative power density of 15 mW m− 2. Microorganisms death curves and the kinetic constants (Kd) indicated that the inhibitory effect of the Ag3PO4 under WLEDs irradiation is well pronounced to C. albicans (6.6 x 10− 2 min− 1) in relation to P. augenosas (4.6 x 10− 2 min− 1) and B. subitilis (2.5 x 10− 2 min− 1). Decimal reduction time (Dt) were 34.4 min to C. albicans, 50.1 min P. augenosas and 92.1 min to B.subitilis The micrographs obtained by scanning electron microscopy with field emission gun (SEM-FEG) demonstrated that there was cell wall permeability and consequently total rupture in the C. albicans, suggesting the lipid peroxidation phenomenon and protein oxidation promoted by the presence of reactive oxygen species (ROS). Furthermore, it was observed the Ag3PO4 when irradiated by WLEDs demonstrates important sporicidal activity in related to B. subtilis, promoting the endospore wall rupture.