Colloidal semiconductor quantum dots (QDs) have long established their versatility and utility for the visualization of biological interactions. On the single-particle level, QDs have demonstrated superior photophysical properties compared to organic dye molecules or fluorescent proteins, but it remains an open question as to which of these fundamental characteristics are most significant with respect to the performance of QDs for imaging beyond the diffraction limit. Here, we demonstrate significant enhancement in achievable localization precision in QD-labeled neurons compared to neurons labeled with an organic fluorophore. Additionally, we identify key photophysical parameters of QDs responsible for this enhancement and compare these parameters to reported values for commonly used fluorophores for super-resolution imaging.
Systemic perturbations can drive a neuroimmune cascade after surgical trauma, including affecting the blood–brain barrier (BBB), activating microglia, and contributing to cognitive deficits such as delirium. Delirium superimposed on dementia (DSD) is a particularly debilitating complication that renders the brain further vulnerable to neuroinflammation and neurodegeneration, albeit these molecular mechanisms remain poorly understood. Here, we have used an orthopedic model of tibial fracture/fixation in APPSwDI/mNos2−/− AD (CVN‐AD) mice to investigate relevant pathogenetic mechanisms underlying DSD. We conducted the present study in 6‐month‐old CVN‐AD mice, an age at which we speculated amyloid‐β pathology had not saturated BBB and neuroimmune functioning. We found that URMC‐099, our brain‐penetrant anti‐inflammatory neuroprotective drug, prevented inflammatory endothelial activation, breakdown of the BBB, synapse loss, and microglial activation in our DSD model. Taken together, our data link post‐surgical endothelial activation, microglial MafB immunoreactivity, and synapse loss as key substrates for DSD, all of which can be prevented by URMC‐099.
Living bio-nano systems for artificial photosynthesis are of growing interest. Typically, these systems use photoinduced charge transfer to provide electrons for microbial metabolic processes, yielding a biosynthetic solar fuel. Here, we demonstrate an entirely different approach to constructing a living bio-nano system, in which electrogenic bacteria respire semiconductor nanoparticles to support nanoparticle photocatalysis. Semiconductor nanocrystals are highly active and robust photocatalysts for hydrogen (H
2
) evolution, but their use is hindered by the oxidative side of the reaction. In this system,
Shewanella oneidensis
MR-1 provides electrons to a CdSe nanocrystalline photocatalyst, enabling visible light-driven H
2
production. Unlike microbial electrolysis cells, this system requires no external potential. Illuminating this system at 530 nm yields continuous H
2
generation for 168 h, which can be lengthened further by replenishing bacterial nutrients.
Persistent organic pollutants (POPs) are toxic synthetic chemicals prevalent in the environment that have been linked to serious health effects including various cancers, hypertension, and diabetes. Owing to their unique physicochemical properties, POP accumulation in the environment poses a serious risk to public health. Over the last few decades global climate change (GCC) has exacerbated increasing temperature and extreme weather events, which reduce the storage capacity of POPs in the environment and precipitate their global remobilization. If we remain unprepared to block GCC-associated release of POPs globally, our adaptation and resilience to climate change will be jeopardized. The Stockholm Convention, an international treaty that aims to reduce and eliminate POPs, is not fully enforceable due to a lack of environmental funds for governments of developing countries. One way to circumnavigate these financial hurdles is to create new markets for POP removal through the private sector. We recommend the International Finance Corporation, the private sector arm of the World Bank, reform its institutional regulations to consistently guarantee funding for proactive measures against POPs. We additionally recommend investing in local POP removal infrastructure projects that encourage economic growth.
Despite limited evidence for competent infection and viral replication of SARS-CoV-2 in the central nervous system (CNS), neurologic dysfunction is a common post-acute medical condition reported in “recovered” COVID-19 patients. To identify a potential noninfectious route for SARS-CoV-2-mediated neurological damage, we constructed colloidal nanocrystal quantum dots linked to micelles decorated with spike protein (COVID-QDs) as a biomimetic to interrogate how blood-brain barrier (BBB) dysregulation may subsequently induce neuroinflammation in the absence of infection. In transwell co-culture of endothelial bEnd.3 monolayers and primary neuroglia, we exposed only the bEnd.3 monolayers to COVID-QDs and examined by fluorescence microscopy whether such treatment led to (i) increased inflammation and leakage across the bEnd.3 monolayers, (ii) permeability of the COVID-QDs across the monolayers, and (iii) induction of neuroinflammation in neuroglial cultures. The results of our study provide evidence of neuroinflammatory hallmarks in cultured neurons and astrocytes without direct exposure to SARS-CoV-2-like nanoparticles. Additionally, we found that pre-treatment of our co-cultures with a small-molecule, broad-spectrum inhibitor of mixed lineage and leucine rich repeat kinases led to reversal of the observed dysregulation in endothelial monolayers and resulted in neuroglial protection. The results reported here may serve to guide future studies into the potential mechanisms by which SARS-CoV-2 mediates neurologic dysfunction.
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