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1.
Science ; 367(6482): 1097-1104, 2020 03 06.
Article in English | MEDLINE | ID: mdl-32139537

ABSTRACT

Wide-band gap metal halide perovskites are promising semiconductors to pair with silicon in tandem solar cells to pursue the goal of achieving power conversion efficiency (PCE) greater than 30% at low cost. However, wide-band gap perovskite solar cells have been fundamentally limited by photoinduced phase segregation and low open-circuit voltage. We report efficient 1.67-electron volt wide-band gap perovskite top cells using triple-halide alloys (chlorine, bromine, iodine) to tailor the band gap and stabilize the semiconductor under illumination. We show a factor of 2 increase in photocarrier lifetime and charge-carrier mobility that resulted from enhancing the solubility of chlorine by replacing some of the iodine with bromine to shrink the lattice parameter. We observed a suppression of light-induced phase segregation in films even at 100-sun illumination intensity and less than 4% degradation in semitransparent top cells after 1000 hours of maximum power point (MPP) operation at 60°C. By integrating these top cells with silicon bottom cells, we achieved a PCE of 27% in two-terminal monolithic tandems with an area of 1 square centimeter.

2.
Expert Opin Pharmacother ; 18(10): 965-972, 2017 Jul.
Article in English | MEDLINE | ID: mdl-28443349

ABSTRACT

INTRODUCTION: Tardive dyskinesia (TD) is an iatrogenic movement disorder most commonly observed in patients with psychotic disorders who are treated with dopamine blocking antipsychotic medications. Treatment options are limited, and recommendations for treatment are based on a relative scarcity of evidence. Areas covered: After briefly highlighting current mechanistic theories of TD, this review will discuss the evidence for a number of medications of several different classes that have been studied for the treatment of TD since the 1970s with an emphasis on placebo controlled trials when possible. We used a Pubmed search of primary studies, reviews, and metaanalyses on the topic of TD treatment in order to cover this topic. Expert opinion: Treatment of TD is difficult given limited data and incomplete understanding of the mechanism. Treatment of TD must be evaluated on an individual basis with careful weight given to severity of symptoms. We suggest the use of atypical versus conventional antipsychotics whenever possible and would recommend trials with one or more of a number of additional agents starting with valbenazine.


Subject(s)
Antipsychotic Agents/adverse effects , Dopamine Antagonists/adverse effects , Schizophrenia/drug therapy , Tardive Dyskinesia/drug therapy , Antipsychotic Agents/administration & dosage , Antipsychotic Agents/therapeutic use , Dopamine Antagonists/administration & dosage , Dopamine Antagonists/therapeutic use , Humans , Tardive Dyskinesia/chemically induced
5.
J Am Chem Soc ; 134(9): 4100-3, 2012 Mar 07.
Article in English | MEDLINE | ID: mdl-22339401

ABSTRACT

A major challenge in nanomaterial science is to develop approaches that ensure that when administered in vivo, nanoparticles can be targeted to their requisite site of action. Herein we report the first approach that allows for cell-specific uptake of nanomaterials by a process involving reprogramming of the behavior of the ubiquitous protein corona of nanomaterials. Specifically, judicious surface modification of quantum dots with a small molecule that induces a protein-misfolding event in a component of the nanoparticle-associated protein corona renders the associated nanomaterials susceptible to cell-specific, receptor-mediated endocytosis. We see this chemical approach as a new and general method for exploiting the inescapable protein corona to target nanomaterials to specific cells.


Subject(s)
Apolipoprotein B-100/chemistry , Lipoproteins/chemistry , Nanostructures/chemistry , Animals , Cadmium Compounds/chemistry , Cholesterol/analogs & derivatives , Cholesterol/chemistry , Macrophages/chemistry , Mice , Molecular Weight , Protein Folding , Quantum Dots , Selenium Compounds/chemistry , Sulfides/chemistry , Zinc Compounds/chemistry
7.
Chembiochem ; 10(8): 1344-7, 2009 May 25.
Article in English | MEDLINE | ID: mdl-19396893

ABSTRACT

Attacking Alzheimer's by ACAT: The aggregation of beta-amyloid peptides, especially Abeta(42), into senile plaques is a hallmark of Alzheimer's disease (AD). We show that the fungal natural products beauveriolides I and III can potently decrease Abeta secretion from cells expressing human amyloid precursor protein; this offers a potential new scaffold for the development of compounds with proven bioavailability for the treatment of AD.


Subject(s)
Amyloid beta-Peptides/metabolism , Depsipeptides/pharmacology , Alzheimer Disease/drug therapy , Animals , CHO Cells , Cell Line , Cricetinae , Cricetulus , Depsipeptides/chemical synthesis , Depsipeptides/chemistry , Depsipeptides/metabolism , Humans , Plaque, Amyloid/metabolism
8.
Biochemistry ; 45(23): 7162-70, 2006 Jun 13.
Article in English | MEDLINE | ID: mdl-16752907

ABSTRACT

The proatherogenic properties of the cholesterol 5,6-secosterols (atheronal-A and atheronal-B), recently discovered in atherosclerotic arteries, have been investigated in terms of their effects on monocyte/macrophage function. A fluorescent analogue of atheronal-B (1) (50 microM), when cultured in either aqueous buffer (PBS) or in media containing fetal calf serum (10%), is rapidly taken-up into cultured macrophage (J774.1 or RAW 264.7) cells and accumulates at perinuclear sites (within 1 h). Co-incubation of macrophage cells (J774.1) with atheronal-A (25 microM) and atheronal-B (25 microM) when complexed with low-density lipoprotein (LDL) (100 microg/mL) leads to a significant upregulation of scavenger receptor class A (approximately 3-fold increase relative to LDL alone, p < 0.05) but not CD36, showing that cultured macrophages respond to LDL-complexed atheronals in a manner highly analogous to acetylated LDL rather than oxidized LDL. Both atheronal-A and atheronal-B in solution exhibit a dose-dependent (0-25 microM) induction of chemotaxis of cultured macrophages (p < 0.001). When complexed with LDL (100 microg/mL), atheronal-A (but not atheronal-B) induces a dose-dependent (0-25 microM, p < 0.05) upregulation of the cell-surface adhesion molecule endothelial (E)-selectin on vascular endothelial cells (HUVECs). LDL (100 microg/mL) complexed atheronal-B (25 microM) but not atheronal-A induces cultured human monocytes (THP-1) to differentiate into macrophage cell lineage. When these in vitro data are taken together with the already known effects of cholesterol 5,6-secosterols on foam cell formation and macrophage cytotoxicity, the atheronals possess biological effects that if translated to an in vivo setting could lead to the recruitment, entrapment, dysfunction, and ultimate destruction of macrophages, with the major leukocyte player in inflammatory artery disease. As such, the atheronal molecules may be a new association, in the already complex inter-relationship, between inflammation, cholesterol oxidation, the tissue macrophage, and atherosclerosis.


Subject(s)
Atherosclerosis/chemically induced , Cholesterol/analogs & derivatives , Cholesterol/metabolism , Ozone/metabolism , Animals , Cell Line , Cholesterol/toxicity , Endothelium, Vascular/cytology , Endothelium, Vascular/drug effects , Endothelium, Vascular/metabolism , Humans , Macrophages/drug effects , Macrophages/metabolism , Magnetic Resonance Spectroscopy , Mice , Receptors, Scavenger/metabolism , Spectrometry, Mass, Matrix-Assisted Laser Desorption-Ionization
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