Nowadays, nanomaterials [NPs; size, 1-100 nm] have emerged as unique antimicrobial agents. Specially, several classes of antimicrobial NPs and nanosized carriers for antibiotic delivery have proven their efficacy for handling infectious diseases, including antibiotic-resistant ones, in vitro as well as in animal models, which can offer better therapy than classical drugs due to their high surface area-tovolume ratio, resulting in appearance of new mechanical, chemical, electrical, optical, magnetic, electro-optical, and magneto-optical properties, unlike from their bulk properties. Thus, scientifically NPs have been validated to be fascinating in fighting bacteria. In this chapter, we will discuss precise properties of microorganisms and their modifications among each strain specifically. The toxicity mechanisms vary from one stain to another. Even the NP's efficacy to treat against bacteria and drug-resistant bacteria and their defense mechanisms change according to strains in particular composition of cell walls, the enzymic composition, and so on. Thus, we provide an outlook on NPs in the microbial world and mechanism to overcome the drug resistance by tagging antibiotics in NPs and its future prospects for the scientific world.

No abstract

The SIN3 repressor complex and the NAD-dependent deacetylase SIRT3 control cell growth, and development as well as malignant transformation. Even then, a little known about cross-talks between these two chromatin modifiers or whether their interaction explored therapeutically. Here we describe the identification of a C21-steroidal derivative compound, 3-O-chloroacetyl-gagamine, A671, which potently suppresses the growth of mouse and human T-cell lymphoma and erythroleukemia in vitro and preclinical models. A671 exerts its anti-neoplastic effects by direct interaction with Histone deacetylase complex subunit SAP18, a component of the SIN3 suppressor complex. This interaction stabilizes and activates SAP18, leading to transcriptional suppression of SIRT3, consequently to inhibition of proliferation and cell death. The resistance of cancer cells to A671 correlated with diminished SAP18 activation and sustained SIRT3 expression. These results uncover the SAP18-SIN3-SIRT3 axis that can be pharmacologically targeted by a C21-steroidal agent to suppress T-cell lymphoma and other malignancies.

No abstract

No abstract