Intraband Transition of HgTe Nanocrystals for Long-Wave Infrared Detection at 12 µm.

The synthesis of n-doped HgTe colloidal quantum dots was optimized to produce samples with a 1Se-1Pe intraband transition in the long-wave infrared (8-12 µm). The spin-orbit splitting of 1Pe states places the 1Se-1Pe1/2 transition around 10 µm. The narrow line width of 130 cm-1 at 300 K is limited by the size distribution. This narrowing leads to an absorption coefficient about 5 times stronger than is possible with the HgTe CQD interband transition at similar energies. From 300 to 80 K, the intraband transition blueshifts by 90 cm-1, while the interband transition redshifts by 350 cm-1. These shifts are assigned to the temperature dependence of the band structure. With ∼2 electrons/dot doping at 80 K, a photoconductive film of 80 nm thickness on a quarter wave reflector substrate showed a detectivity (D*) of ∼107 Jones at 500 Hz in the 8-12 µm range.

Room-Temperature 15% Efficient Mid-Infrared HgTe Colloidal Quantum Dot Photodiodes.

Mid-infrared HgTe colloidal quantum dot photovoltaic devices previously achieved background-limited infrared photodetection at cryogenic temperatures but also decreased from 20 to 1% efficiency from 150 to 300 K. The reduced quantum efficiency was tentatively attributed to the carrier diffusion length being much shorter than the device thickness of ∼400 nm at room temperature. Here, the carrier diffusion length is measured and is found to peak at 215 nm at 200 K and decrease only to 180 nm at 295 K. It is therefore not the cause of the much larger reduced quantum efficiency. Instead, it is shown that the efficiency drops due to the series resistance. With the device size reduced to 50 by 50 µm, the room-temperature quantum efficiency reaches 10 and 15% for HgTe colloidal quantum dot devices with 2400 cm-1 (4.2 µm) and 2675 cm-1 (3.7 µm) cutoff, respectively. These small-area devices achieve background-limited photodetection at 150 K and a detectivity above 109 Jones at room temperature with a cutoff at 2675 cm-1 (3.7 µm).

Mid-infrared HgTe Colloidal Quantum Dot LEDs.

Mid-infrared HgTe colloidal quantum dot electroluminescent devices are demonstrated. With emission at 4 µm, devices achieved an external quantum efficiency of ∼10-3 and power conversion efficiency of ∼10-4 under biases of a few volts. The power conversion efficiency benefited from lowering the transparent electrode resistance through the incorporation of a metal conductive grid. The average power emitted was about 16 µW at 2 V bias with 50% duty cycle and a 1 mm2 device. The room-temperature electroluminescence efficiency at low current was limited by the photoluminescence efficiency of the quantum dots, while the diode structure provided efficient electron-hole recombination.

Structure/function studies and the effects of memantine in monkeys with experimental glaucoma.

Purpose. The scanning laser polarimetry with variable corneal compensation (GDx VCC) methodology was established and verified in monkeys with experimental glaucoma (ExpG). Terminal GDx parameters were correlated with axon counts and electrophysiologic measures. The effects of memantine on these parameters were investigated. Methods. ExpG was induced in monkeys and intraocular pressure monitored weekly. Some monkeys received memantine in their diet before and after ExpG induction (1-10 months). GDx VCC scans, stereophotographs, and multifocal visual evoked potential (mfVEP) data were collected at baseline and every 6 to 8 weeks until euthanasia. Optic nerves were prepared for axon counting and other morphologic analysis. Results. There was no difference in IOP elevation exposure between memantine-treated and no-memantine-treated monkeys. The percentage of the optic nerve area composed of connective tissue septa was significantly greater in ExpG eyes than in Fellow eyes. There was a strong positive correlation between axon counts and terminal GDx parameter measures. Animals not receiving memantine exhibited significantly lower mfVEP amplitudes in ExpG eyes compared with the ipsilateral baseline or the final value in the Fellow eye. ExpG eyes from memantine-treated animals had higher overall mean amplitudes that were not significantly different relative to the ipsilateral baseline and final amplitudes in the Fellow eye. Conclusions. The authors' studies confirm that GDx VCC can be utilized in monkey ExpG studies to detect early retinal structural changes and that these changes are highly correlated with optic nerve axon counts. These structural changes may or may not lead to central functional changes as shown by the mfVEP in response to investigational therapies.

Surgical lowering of elevated intraocular pressure in monkeys prevents progression of glaucomatous disease.

Recent reports from large clinical trials have clearly demonstrated that lowering intraocular pressure (IOP) in persons with ocular hypertension has a beneficial effect on reducing the progression of glaucomatous disease. Few studies of this effect have been conducted in controlled laboratory settings, however, none have been conducted using non-human primates, the model of experimental glaucoma considered most similar to the human disease. Using data collected retrospectively from a trabeculectomy study using 16 cynomolgous monkeys with experimental ocular hypertension, we evaluated both the threshold of elevated IOP required to cause clinically observable damage to the optic nerve head and also if lowering IOP below this threshold prevents further damage. An index of the level of elevated IOP experienced by experimental eyes (the Pressure Insult) was calculated as the slope of the difference in cumulative IOP between experimental and control eyes during four intervals of time over the course of the experiment, while damage to the optic nerve head was evaluated by measuring the Cup:Disc ratio for each eye from stereoscopic photographs taken at the end of each interval. An increase in the Cup:Disc ratio was significantly associated with both the maximum IOP obtained in the experimental eye during each interval (r=0.573, P<0.001) and the Pressure Insult (r=0.496, P<0.001). Pressure Insult values less than 11 mm Hg Days/Day were not associated with glaucomatous damage in monkey eyes, whereas values greater than 11 showed a significant correlation with increasing Cup:Disc ratios (P<0.001). Trabeculectomy to reduce the Pressure Insult below 11 was correlated with an attenuation of the rate of progression of the Cup:Disc ratio in eyes that had exhibited damage before surgery. These results contribute further to our understanding of this model of experimental glaucoma by demonstrating a threshold at which IOP needs to be elevated to stimulate damage, while also providing corroborating evidence that lowering IOP in ocular hypertensive monkeys can attenuate the progression of glaucomatous disease.

Crystal structure of the molecular chaperone HscA substrate binding domain complexed with the IscU recognition peptide ELPPVKIHC.

HscA, a specialized bacterial Hsp70-class molecular chaperone, interacts with the iron-sulfur cluster assembly protein IscU by recognizing a conserved LPPVK sequence motif. We report the crystal structure of the substrate-binding domain of HscA (SBD, residues 389-616) from Escherichia coli bound to an IscU-derived peptide, ELPPVKIHC. The crystals belong to the space group I222 and contain a single molecule in the asymmetric unit. Molecular replacement with the E.coli DnaK(SBD) model was used for phasing, and the HscA(SBD)-peptide model was refined to Rfactor=17.4% (Rfree=21.0%) at 1.95 A resolution. The overall structure of HscA(SBD) is similar to that of DnaK(SBD), although the alpha-helical subdomain (residues 506-613) is shifted up to 10 A relative to the beta-sandwich subdomain (residues 389-498) when compared to DnaK(SBD). The ELPPVKIHC peptide is bound in an extended conformation in a hydrophobic cleft in the beta-subdomain, which appears to be solvent-accessible via a narrow passageway between the alpha and beta-subdomains. The bound peptide is positioned in the reverse orientation of that observed in the DnaK(SBD)-NRLLLTG peptide complex placing the N and C termini of the peptide on opposite sides of the HscA(SBD) relative to the DnaK(SBD) complex. Modeling of the peptide in the DnaK-like forward orientation suggests that differences in hydrogen bonding interactions in the binding cleft and electrostatic interactions involving surface residues near the cleft contribute to the observed directional preference.