Controlled In Situ PbSe Quantum Dot Growth around Single-Walled Carbon Nanotubes: A Noncovalent PbSe-SWNT Hybrid Structure

We developed a simple method of synthesizing noncovalently linked hybrids of PbSe quantum dots (QDs) and single-walled carbon nanotubes (SWNTs). The PbSe QDs grow around the SWNTs without any linker molecule or chemical modification of the SWNTs. We are able to control the size and shape of the QDs attached to the SWNTs by varying the synthesis conditions and elucidate the three-dimensional (3D) morphology and atomic structure of the half-ring-shaped PbSe QDs bonded to the SWNTs using scanning transmission electron microscopy (STEM) tomography and high-resolution transmission electron microscopy (HRTEM). The PbSe QDs not only assemble on the SWNT bundles, but they actually grow around them. The growth of the PbSe QDs around SWNT sidewalls is favored over the growth of spherical particles in solution, probably due to dipole stabilization by the large π-electron system of the SWNTs

Ischemic lesions of striatum elicit secondary changes in ipsilateral substantia nigra.

<p>(A) Color coding of the relative frequency of “ischemic” voxels in the primary ischemic lesion of striatal stroke patients (n = 12) who subsequently developed secondary midbrain changes. Cd: Caudate nucleus (n_max = 11); Pu: putamen (n_max = 10). (B) Color coding of the relative frequency of voxels showing secondary changes in midbrain in these patients. SNC: substantia nigra, pars compacta (n_max = 9). SNR: substantia nigra, pars reticulata. Numbers ranging from -12.5 to +21.2 denote Talairach y-coordinates.</p

Subacute hyperintensity in ipsilateral midbrain at a delayed time point after striatal stroke.

<p>(A, B) MRI scans of two exemplary patients showing primary ischemic lesion confined to striatum (A) or involving striatum (B) in axial diffusion-weighted (DWI, left) and coronal T2-weighted (T2) imaging (white arrows; 2^nd from left). On the right side, coronal views through the midbrain display the development of an ipsilateral hyperintense lesion occuring between days 6 to 10 after stroke (red arrows). Note that corticospinal degeneration (blue arrows in B) associated with cortical involvement is detectable before the emergence of these secondary exofocal changes in midbrain. (C) Frequency of the anatomic distributions of the primary ischemic lesions (12 striatal stroke and 4 control stroke patients). Lesions are overlayed on the ICBM human brain template. Infarcts associated with secondary midbrain changes are coded in red, infarcts not associated with midbrain changes are coded in blue. Only frequencies of at least 25% are displayed. (D) Localization of secondary exofocal midbrain changes (n = 12 striatal stroke patients). For the purpose of this illustration, secondary lesions (day 10 or latest available scan before day 10) were adjusted to and superimposed on coronal and transverse T1-weighted images of a single patient.</p

Baseline characteristics of study participants.

<p>Baseline characteristics of study participants.</p

MRI findings in striatal stroke patients and control stroke patients.

<p>Clear evidence of a secondary lesion is denoted by “+”. “++” denotes especially large secondary lesions. Patients 1 through 12 showed clear evidence for delayed midbrain changes (DWI and T2) in ipsilateral substantia nigra occurring between days 6 and 10. Despite heavy motion artifacts, scans of patients 13 through 15 still showed some evidence for secondary midbrain changes (+). Several patients missed scans (n.d.). The primary reason for this was that patients had either been transferred to a rehabilitation center or discharged. Control stroke patients (patients 17 through 20) did not show evidence of secondary midbrain changes. Note that cortical involvement or the overall size of the infarct did not affect the development of secondary midbrain changes. Normalization of ADC was observed at late measurements in single patients (days 72, 90, and 144).</p><p>MRI findings in striatal stroke patients and control stroke patients.</p

Multimass Velocity-Map Imaging with the Pixel Imaging Mass Spectrometry (PImMS) Sensor: An Ultra-Fast Event-Triggered Camera for Particle Imaging

We present the first multimass velocity-map imaging data acquired using a new ultrafast camera designed for time-resolved particle imaging. The PImMS (Pixel Imaging Mass Spectrometry) sensor allows particle events to be imaged with time resolution as high as 25 ns over data acquisition times of more than 100 μs. In photofragment imaging studies, this allows velocity-map images to be acquired for multiple fragment masses on each time-of-flight cycle. We describe the sensor architecture and present bench-testing data and multimass velocity-map images for photofragments formed in the UV photolysis of two test molecules: Br₂ and <i>N</i>,<i>N</i>-dimethylformamide