Carbon quantum dots (CDs) are a relatively new class of carbon nanomaterials which have been studied very much in the last fifteen years to improve their already favorable properties.

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Cardiovascular disease (CVD) has threatened human lives for decades, and a technique for estimating and healing is still needed. There has been increasing interest in finding CVD diagnostic biomarkers to predict risk. Cardiac troponin I (cTnI) has proven to be a significant biomarker for acute myocardial infarction detection. An immunoassay based biosensor for cTnI can play an important role in diagnosis of CVD. Over the past decades, various methodologies regarding cTnI detection have been studied, including colorimetric, fluorescence, paramagnetic, electrochemical, and surface plasmon resonance. This review will focus more on recent strategies about surface immobilized cTnI detection.

Herein, we describe how cantilever-free scanning probes can be used to deposit precursor material and subsequently irradiate the precursor to initiate polymerization, resulting in a 3D lithographic method wherein the position, height and diameter of each feature can be tuned independently. Specifically, acrylate and methacrylate monomers were patterned onto thiol terminated glass and subsequently exposed to UV light produced brush polymers by a photoinduced radical acrylate polymerization reaction. Here, we report the first examples of glycan arrays, comprised of methacrylate brush polymers that are side-chain functionalized with a-glucose, by this new lithographic approach. Their binding with fluorophore labeled concanavalin A (ConA) was assayed by fluorescence microscopy. The fluorescence of these brush polymers was compared to glycan arrays composed of monolayers of a-mannosides and a-glucosides prepared by combining polymer pen lithography (PPL) with the thiol-ene photochemical reaction or the copper-catalyzed azidealkyne cycloaddition. At high ConA concentration, the fluorescence signal of the brush polymer was nearly 20 times greater than that of the glycan monolayers, and the brush polymer arrays had a detection limit nearly two orders of magnitude better than their monolayer counterparts. Because of the ability of this method to control precisely the polymer length, the relationship between limit of detection and multivalency could be explored, and it was found that the longer polymers (136 nm) are an order of magnitude more sensitive towards ConA binding than the shorter polymers (8 nm) and that binding affinity decreased systematically with length. These glycan arrays are a new tool to study the role of multivalency on carbohydrate recognition, and the photopolymerization route towards forming multivalent glycan scaffolds described herein, is a promising route to create multiplexed glycan arrays with nanoscale feature dimensions.

The last decades have witnessed a growing global burden of Alzheimer's disease (AD). Evidence indicates that the onset and progression of AD is associated with β-amyloid (Aβ) peptide fibrillation. As such, there is a strong passion with discovering potent Aβ fibrillation inhibitors that can be developed into anti-amyloiddogenic agents for AD treatment. Current challenges that have arisen with this development involve with Aβ oligomer toxicity suppression and Blood Brain Barrier penetration capability. Considering most natural or biological events, one would observe that there is usually a "seed" to direct natural materials to assemble in response to a certain stimulation. Inspired by this, several materials or compounds, including nanoparticle, peptide or peptide mimics, and organic molecules, have been designed for the purpose of redirecting or impeding Aβ aggregation. Achieving these tasks requires comprehensive understanding on (1) initial Aβ assembly into insoluble deposits, (2) main concerns with fibrillation inhibition, and (3) current major methodologies to disrupt the aggregation. Herein, the objective of this review is to address these three areas, and enable the pathway for a promising therapeutic agent design for AD treatment.

Cisplatin [cis-diamminedichloroplatinum(II)]/oxaliplatin [1,2-diamminocyclohexane(trans-1)oxolatoplatinum(II)] toxicity is enhanced by functional gap junctions between treated cells, implying that inhibition of gap junctions may decrease cytotoxic activity of these platinum-based agents. This study investigates the effect of gap junction modulation by cisplatin/oxaliplatin on cytotoxicity in a transformed cell line. The effects were explored using junctional channels expressed in transfected HeLa cells and purified hemichannels. Junctional channels showed a rapid, dose-dependent decrease in dye coupling with exposure to cisplatin/oxaliplatin. With longer exposure, both compounds also decreased connexin expression. Both compounds inhibit the activity of purified connexin hemichannels, over the same concentration range that they inhibit junctional dye permeability, demonstrating that inhibition occurs by direct interaction of the drugs with connexin protein. Cisplatin/oxaliplatin reduced the clonogenic survival of HeLa cells at low density and high density in a dose-dependent manner, but to a greater degree at high density, consistent with a positive effect of gap junctional intercellular communication (GJIC) on cytotoxicity. Reduction of GJIC by genetic or pharmacological means decreased cisplatin/oxaliplatin toxicity. At low cisplatin/oxaliplatin concentrations, where effects on connexin channels are minimal, the toxicity increased with increased cell density. However, higher concentrations strongly inhibited GJIC, and this counteracted the enhancing effect of greater cell density on toxicity. The present results indicate that inhibition of GJIC by cisplatin/ oxaliplatin decreases their cytotoxicity. Direct inhibition of GJIC and reduction of connexin expression by cisplatin/oxaliplatin may thereby compromise the effectiveness of these compounds and be a factor in the development of resistance to this class of chemotherapeutic agents.

The force dependence of the copper-free Huisgen cycloaddition between an alkyne and a surface-bound azide was examined in elastomeric nanoreactors. These studies revealed that pressure and chain length are critical factors that determine the reaction rate. These experiments demonstrate the central role of pressure and surface structure on interfacial processes that are increasingly important in biology, materials science, and nanotechnology.

Amyloid-β peptide (Aβ) fibrillation is pathologically associated with alzheimer’s disease (AD), and this has resulted in the development of an Aβ inhibitor which is essential for the treatment of AD. However, the design of potent agents which can target upstream secretases, inhibit Aβ toxicity and aggregation, as well as cross the blood-brain barrier remains challenging. In, this research carbon dots for AD treatment were investigated in vitro using experimental and computational methods for the first time. the results presented here demonstrate a novel strategy for the discovery of novel antiamyloidogenic agents for AD treatments.