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In the last decade, gold and silver nanomaterials have received considerable attention due to their attractive electronic and chemical properties and their potential applications in the development of new technologies. Recent advances in the study of various gold and silver nanomaterials have led to their utilization in a number of very important applications including biosensing, diagnostic imaging, and cancer diagnosis and therapy. This review surveys the various synthetic methods of gold and silver nanomaterials. Recent experimental studies focusing on the use of gold and silver nanomaterials in catalysis, food industry, and environmental conservation are also reviewed. This review also highlights the advantages of gold and silver nanomaterials in the development of fluorescence biosensors, glucose biosensors, nucleic acids-based biosensors, and protein-based biosensors. Moreover, the potent in vitro and in vivo anti-microbial and cyto-genotoxic effects of various gold and silver nanomaterials are underlined. Finally, recent advances in the employment of gold and silver nanomaterials as effective drug delivery vehicles and promising cancer therapeutic agents are summarized. Despite their use in remediating numerous medical and health-related conditions, the efficacy and safety of many gold and silver nanomaterials is still under some scrutiny. Needless to say, researchers are facing many challenges and obstacles in their ample attempts to synthesize nanomaterials that are relatively easy to design, inexpensive to fabricate, and effective in treating various diseases, but at the same time display a very low, if any, toxicity to the body. Future investigations should aim at overcoming such challenges in an attempt to design nanomaterials that will prove to be useful in diagnosing and treating life-threatening diseases while ensuring a high degree of efficacy and safety.

Peroxisome proliferator-activated receptor ␥1 (PPAR␥1) and liver X receptor ␣ (LXR␣) play pivotal roles in macrophage cholesterol homeostasis and inflammation, key biological processes in atherogenesis. Herein we identify adipocyte enhancer-binding protein 1 (AEBP1) as a transcriptional repressor that impedes macrophage cholesterol efflux, promoting foam cell formation, via PPAR␥1 and LXR␣ down-regulation. Contrary to AEBP1 deficiency, AEBP1 overexpression in macrophages is accompanied by decreased expression of PPAR␥1, LXR␣, and their target genes ATP-binding cassette A1, ATP-binding cassette G1, apolipoprotein E, and CD36, with concomitant elevation in IL-6, TNF-␣, monocyte chemoattractant protein 1, and inducible NO synthase levels. AEBP1, but not the C-terminally truncated DNA-binding domain mutant (AEBP1 ⌬Sty ), represses PPAR␥1 and LXR␣ in vitro. Expectedly, AEBP1-overexpressing transgenic (AEBP1 TG ) macrophages accumulate considerable amounts of lipids compared with AEBP1 nontransgenic macrophages, making them precursors for foam cells. Indeed, AEBP1-overexpressing transgenic macrophages exhibit diminished cholesterol efflux compared with AEBP1 nontransgenic macrophages, whereas AEBP1-knockout (AEBP1 ؊/؊ ) macrophages exhibit enhanced cholesterol efflux compared with wild-type (AEBP1 ؉/؉ ) macrophages. Our in vitro and ex vivo experimental data strongly suggest that AEBP1 plays critical regulatory roles in macrophage cholesterol homeostasis, foam cell formation, and proinflammation. Thereby, we speculate that AEBP1 may be critically implicated in the development of atherosclerosis, and it may serve as a molecular target toward developing antiinflammatory, antiatherogenic therapeutic approaches.atherogenesis ͉ cholesterol efflux ͉ liver X receptor ␣ ͉ peroxisome proliferator-activated receptor ␥

Nuclear factor B (NF-B) subunits comprise a family of eukaryotic transcription factors that are critically involved in cell proliferation, inflammation, and apoptosis. Under basal conditions, NF-B subunits are kept under inhibitory regulation by physical interaction with NF-B inhibitors (IB subunits) in the cytosol. Upon stimulation, IB subunits become phosphorylated, ubiquitinated, and subsequently degraded, allowing NF-B subunits to translocate to the nucleus and bind as dimers to B responsive elements of target genes. Previously, we have shown that AEBP1 enhances macrophage inflammatory responsiveness by inducing the expression of various proinflammatory mediators. Herein, we provide evidence suggesting that AEBP1 manifests its proinflammatory function by up-regulating NF-B activity via hampering IB␣, but not IB␤, inhibitory function through protein-protein interaction mediated by the discoidin-like domain (DLD) of AEBP1. Such interaction renders IB␣ susceptible to enhanced phosphorylation and degradation, subsequently leading to augmented NF-B activity. Collectively, we propose a novel molecular mechanism whereby NF-B activity is modulated by means of protein-protein interaction involving AEBP1 and IB␣. Moreover, our study provides a plausible mechanism explaining the differential regulatory functions exhibited by IB␣ and IB␤ in various cell types. We speculate that AEBP1 may serve as a potential therapeutic target for the treatment of various chronic inflammatory diseases and cancer.