Squaraine dyes have significant potential for use in organic photovoltaic devices because their chemical and packing structure tunability leads to a broad solid state panchromaticity. Nevertheless, broadening of the spectrum does not always give rise to increasing power conversion efficiencies. Furthermore, the same processing strategy used to make devices from different squaraines does not lead to the same optimized performance. In this work, by varying the environmental conditions of a set of anilinic squaraines, we demonstrate that spin-cast thin films are made up of a complex set of states, with each state contributing differently to the overall device efficiency. We demonstrate crystallochromy in that small changes in the packing structure give rise to dramatically different absorption spectra. Through a remarkable comparison between squaraines in poly(methyl methacrylate) solid solution and squaraine:PC60BM blends, we also show long-range and orientational disorder broadening, which distorts the ability to correlate qualitative spectroscopic assessment with an understanding of the device mechanism. We conclude that a full quantitative assessment of the populations of each excited state must be carried out in order to make progress toward an improved understanding of each state's contribution to charge transfer at the bulk heterojunction interface.
Solution-processed bulk heterojunction
organic solar cells fabricated
with 1,3-bis[4-(
N,N
-diisopentylamino)-2,6-dihydroxyphenyl]squaraine
and phenyl-C61-butyric acid methyl ester were found to exhibit unexpectedly
low external quantum efficiency in the squaraine regions upon annealing.
X-ray diffraction (XRD), spectral response, and time-resolved microwave
absorption were all used to characterize the materials used and the
devices prepared from them. An explanation for the drop in efficiency
is proposed using Marcus–Hush theory to tie together the changes
in coherent crystal domain size found by XRD and the external quantum
efficiency results. Exciton dissociation at the interface was determined
to be the rate-limiting step in efficient current generation for these
devices.
Huntington’s
disease (HD) is a lethal autosomal
dominant
neurodegenerative disorder resulting from a CAG repeat expansion in
the huntingtin (HTT) gene. The product of translation
of this gene is a highly aggregation-prone protein containing a polyglutamine
tract >35 repeats (mHTT) that has been shown to colocalize with
histone
deacetylase 4 (HDAC4) in cytoplasmic inclusions in HD mouse models.
Genetic reduction of HDAC4 in an HD mouse model resulted in delayed
aggregation of mHTT, along with amelioration of neurological phenotypes
and extended lifespan. To further investigate the role of HDAC4 in
cellular models of HD, we have developed bifunctional degraders of
the protein and report the first potent and selective degraders of
HDAC4 that show an effect in multiple cell lines, including HD mouse
model-derived cortical neurons. These degraders act via the ubiquitin-proteasomal
pathway and selectively degrade HDAC4 over other class IIa HDAC isoforms
(HDAC5, HDAC7, and HDAC9).
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