Study of Highly Efficient Au/Pt Nanoparticles for Rapid Screening of Clostridium difficile.

This study synthesized core/shell gold-platinum nanoparticles and characterized their colorimetric properties; ultraviolet-visible spectroscopy revealed that the synthesized nanoparticles exhibited distinct colors from conventional gold nanoparticles. Furthermore, the nanoparticles were subjected to lateral flow assays using Protein A, and the results revealed that they outperformed conventional spherical gold nanoparticles in terms of color development. This improvement can be attributed to the distinct core/shell structures of our nanoparticles. Further evaluation revealed that these nanoparticles could facilitate the detection of Clostridium difficile Toxin B visually at an extremely low concentration (1 ng/mL) without the requirement for advanced instrumentation. This substantial improvement in sensitivity can be attributed to the meticulous design and nanoscale engineering of the structure of the nanoparticles.

Metal nanoparticles and nanoparticle composites are effective against Haemophilus influenzae, Streptococcus pneumoniae, and multidrug-resistant bacteria.

BACKGROUND: Treatment for lower respiratory tract infection caused by multidrug-resistant organisms (MDRO) are often limited. This study explored the activity of different metal nanoparticles against several respiratory pathogens including MDROs. METHODS: Clinical isolates of carbapenem-resistant Acinetobacter baumannii (CRAB), carbapenem-resistant Klebsiella pneumoniae (CRKP), Pseudomonas aeruginosa, Haemophilus influenzae, methicillin-resistant Staphylococcus aureus (MRSA), and Streptococcus pneumoniae were tested for in vitro susceptibilities to various antibiotics and nanoparticles. Minimum inhibitory concentrations (MICs) of silver-nanoparticle (Ag-NP), selenium-nanoparticle (Se-NP), and three composites solutions ND50, NK99, and TPNT1 (contained 5 ppm Ag-NP, 60 ppm ZnO-nanoparticle, and different concentrations of gold-nanoparticle or ClO2) were determined by broth microdilution method. RESULTS: Fifty isolates of each bacterial species listed above were tested. Ag-NP showed lower MICs to all species than Se-NP. The MIC50s of Ag-NP for CRAB, CRKP, P. aeruginosa, and H. influenzae were <3.125 ppm, 25 ppm, <3.125 ppm, and <3.125 ppm, respectively, while those for S. pneumoniae and MRSA were >50 ppm and 50 ppm. Among CRAB, CRKP and P. aeruginosa, the MIC50s of ND50, NK99, and TPNT1 for CRAB were the lowest (1/8 dilution, 1/8 dilution, and 1/8 dilution, respectively), and those for CRKP (>1/2 dilution, 1/2 dilution, and 1/2 dilution, respectively) were the highest. Both MRSA and S. pneumoniae showed high MIC50s to ND50, NK99, and TPNT1. CONCLUSIONS: Metal nanoparticles had good in vitro activity against Gram-negative bacteria. They might be suitable to be prepared as environmental disinfectants or inhaled agents to inhibit the growth of MDR Gram-negative colonizers in the lower respiratory tracts of patients with chronic lung diseases.

Nanoparticle composite TPNT1 is effective against SARS-CoV-2 and influenza viruses.

A metal nanoparticle composite, namely TPNT1, which contains Au-NP (1 ppm), Ag-NP (5 ppm), ZnO-NP (60 ppm) and ClO2 (42.5 ppm) in aqueous solution was prepared and characterized by spectroscopy, transmission electron microscopy, dynamic light scattering analysis and potentiometric titration. Based on the in vitro cell-based assay, TPNT1 inhibited six major clades of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) with effective concentration within the range to be used as food additives. TPNT1 was shown to block viral entry by inhibiting the binding of SARS-CoV-2 spike proteins to the angiotensin-converting enzyme 2 (ACE2) receptor and to interfere with the syncytium formation. In addition, TPNT1 also effectively reduced the cytopathic effects induced by human (H1N1) and avian (H5N1) influenza viruses, including the wild-type and oseltamivir-resistant virus isolates. Together with previously demonstrated efficacy as antimicrobials, TPNT1 can block viral entry and inhibit or prevent viral infection to provide prophylactic effects against both SARS-CoV-2 and opportunistic infections.

Mitochondrial dysfunction leads to impairment of insulin sensitivity and adiponectin secretion in adipocytes.

Adipocytes play an integrative role in the regulation of energy metabolism and glucose homeostasis in the human body. Functional defects in adipocytes may cause systemic disturbance of glucose homeostasis. Recent studies revealed mitochondrial abnormalities in the adipose tissue of patients with type 2 diabetes. In addition, patients with mitochondrial diseases usually manifest systemic metabolic disorder. However, it is unclear how mitochondrial dysfunction in adipocytes affects the regulation of glucose homeostasis. In this study, we induced mitochondrial dysfunction and overproduction of reactive oxygen species (ROS) by addition of respiratory inhibitors oligomycin A and antimycin A and by knockdown of mitochondrial transcription factor A (mtTFA), respectively. We found an attenuation of the insulin response as indicated by lower glucose uptake and decreased phosphorylation of Akt upon insulin stimulation of adipocytes with mitochondrial dysfunction. Furthermore, the expression of glucose transporter 4 (Glut4) and secretion of adiponectin were decreased in adipocytes with increased ROS generated by defective mitochondria. Moreover, the severity of insulin insensitivity was correlated with the extent of mitochondrial dysfunction. These results suggest that higher intracellular ROS levels elicited by mitochondrial dysfunction resulted in impairment of the function of adipocytes in the maintenance of glucose homeostasis through attenuation of insulin signaling, downregulation of Glut4 expression, and decrease in adiponectin secretion. Our findings substantiate the important role of mitochondria in the regulation of glucose homeostasis in adipocytes and also provide a molecular basis for the explanation of the manifestation of diabetes mellitus or insulin insensitivity in a portion of patients with mitochondrial diseases such as MELAS or MERRF syndrome.