42 research outputs found
Electronic Raman scattering and photoluminescence from LaSrMnO exhibiting giant magnetoresistance
Raman and Photoluminescence (PL) experiments on correlated metallic
LaSrMnO have been carried out using different excitation
wavelengths as a function of temperature from 15 K to 300 K. Our data suggest a
Raman mode centered at 1800 cm and a PL band at 2.2 eV. The intensities
of the two peaks decrease with increasing temperature. The Raman mode can be
attributed to a plasmon excitation whose frequency and linewidths are
consistent with the measured resistivities. The PL involves intersite
electronic transitions of the manganese ions.Comment: 10 pages + 4 eps figures, Revtex 3.0, figures available on reques
Hole concentration and phonon renormalization in Ca-doped YBa_2Cu_3O_y (6.76 < y < 7.00)
In order to access the overdoped regime of the YBa_2Cu_3O_y phase diagram, 2%
Ca is substituted for Y in YBa_2Cu_3O_y (y = 7.00,6.93,6.88,6.76). Raman
scattering studies have been carried out on these four single crystals.
Measurements of the superconductivity-induced renormalization in frequency
(Delta \omega) and linewidth (\Delta 2\gamma) of the 340 cm^{-1} B_{1g} phonon
demonstrate that the magnitude of the renormalization is directly related to
the hole concentration (p), and not simply the oxygen content. The changes in
\Delta \omega with p imply that the superconducting gap (\Delta_{max})
decreases monotonically with increasing hole concentration in the overdoped
regime, and \Delta \omega falls to zero in the underdoped regime. The linewidth
renormalization \Delta 2\gamma is negative in the underdoped regime, crossing
over at optimal doping to a positive value in the overdoped state.Comment: 18 pages; 5 figures; submitted to Phys. Rev. B Oct. 24, 2002 (BX8292
Carrier relaxation, pseudogap, and superconducting gap in high-Tc cuprates: A Raman scattering study
We describe results of electronic Raman-scattering experiments in differently
doped single crystals of Y-123 and Bi-2212. The comparison of AF insulating and
metallic samples suggests that at least the low-energy part of the spectra
originates predominantly from excitations of free carriers. We therefore
propose an analysis of the data in terms of a memory function approach.
Dynamical scattering rates and mass-enhancement factors for the carriers are
obtained. In B2g symmetry the Raman data compare well to the results obtained
from ordinary and optical transport. For underdoped materials the dc scattering
rates in B1g symmetry become temperature independent and considerably larger
than in B2g symmetry. This increasing anisotropy is accompanied by a loss of
spectral weight in B2g symmetry in the range between the superconducting
transition at Tc and a characteristic temperature T* of order room temperature
which compares well with the pseudogap temperature found in other experiments.
The energy range affected by the pseudogap is doping and temperature
independent. The integrated spectral loss is approximately 25% in underdoped
samples and becomes much weaker towards higher carrier concentration. In
underdoped samples, superconductivity related features in the spectra can be
observed only in B2g symmetry. The peak frequencies scale with Tc. We do not
find a direct relation between the pseudogap and the superconducting gap.Comment: RevTeX, 21 pages, 24 gif figures. For PostScript with embedded eps
figures, see http://www.wmi.badw-muenchen.de/~opel/k2.htm
The delivery of personalised, precision medicines via synthetic proteins
Introduction:
The design of advanced drug delivery systems based on synthetic and su-pramolecular chemistry has been very successful. Liposomal doxorubicin (Caelyx®), and liposomal daunorubicin (DaunoXome®), estradiol topical emulsion (EstrasorbTM) as well as soluble or erodible polymer systems such as pegaspargase (Oncaspar®) or goserelin acetate (Zoladex®) represent considerable achievements.
The Problem:
As deliverables have evolved from low molecular weight drugs to biologics (currently representing approximately 30% of the market), so too have the demands made of advanced drug delivery technology. In parallel, the field of membrane trafficking (and endocytosis) has also matured. The trafficking of specific receptors i.e. material to be recycled or destroyed, as well as the trafficking of protein toxins has been well characterized. This, in conjunction with an ability to engineer synthetic, recombinant proteins provides several possibilities.
The Solution:
The first is using recombinant proteins as drugs i.e. denileukin diftitox (Ontak®) or agalsidase beta (Fabrazyme®). The second is the opportunity to use protein toxin architecture to reach targets that are not normally accessible. This may be achieved by grafting regulatory domains from multiple species to form synthetic proteins, engineered to do multiple jobs. Examples include access to the nucleocytosolic compartment. Herein the use of synthetic proteins for drug delivery has been reviewed
Identification of regulatory variants associated with genetic susceptibility to meningococcal disease.
Non-coding genetic variants play an important role in driving susceptibility to complex diseases but their characterization remains challenging. Here, we employed a novel approach to interrogate the genetic risk of such polymorphisms in a more systematic way by targeting specific regulatory regions relevant for the phenotype studied. We applied this method to meningococcal disease susceptibility, using the DNA binding pattern of RELA - a NF-kB subunit, master regulator of the response to infection - under bacterial stimuli in nasopharyngeal epithelial cells. We designed a custom panel to cover these RELA binding sites and used it for targeted sequencing in cases and controls. Variant calling and association analysis were performed followed by validation of candidate polymorphisms by genotyping in three independent cohorts. We identified two new polymorphisms, rs4823231 and rs11913168, showing signs of association with meningococcal disease susceptibility. In addition, using our genomic data as well as publicly available resources, we found evidences for these SNPs to have potential regulatory effects on ATXN10 and LIF genes respectively. The variants and related candidate genes are relevant for infectious diseases and may have important contribution for meningococcal disease pathology. Finally, we described a novel genetic association approach that could be applied to other phenotypes
Subtelomeric deletion of chromosome 10p15.3: clinical findings and molecular cytogenetic characterization.
We describe 19 unrelated individuals with submicroscopic deletions involving 10p15.3 characterized by chromosomal microarray (CMA). Interestingly, to our knowledge, only two individuals with isolated, submicroscopic 10p15.3 deletion have been reported to date; however, only limited clinical information is available for these probands and the deleted region has not been molecularly mapped. Comprehensive clinical history was obtained for 12 of the 19 individuals described in this study. Common features among these 12 individuals include: cognitive/behavioral/developmental differences (11/11), speech delay/language disorder (10/10), motor delay (10/10), craniofacial dysmorphism (9/12), hypotonia (7/11), brain anomalies (4/6) and seizures (3/7). Parental studies were performed for nine of the 19 individuals; the 10p15.3 deletion was de novo in seven of the probands, not maternally inherited in one proband and inherited from an apparently affected mother in one proband. Molecular mapping of the 19 individuals reported in this study has identified two genes, ZMYND11 (OMIM 608668) and DIP2C (OMIM 611380; UCSC Genome Browser), mapping within 10p15.3 which are most commonly deleted. Although no single gene has been identified which is deleted in all 19 individuals studied, the deleted region in all but one individual includes ZMYND11 and the deleted region in all but one other individual includes DIP2C. There is not a clearly identifiable phenotypic difference between these two individuals and the size of the deleted region does not generally predict clinical features. Little is currently known about these genes complicating a direct genotype/phenotype correlation at this time. These data however, suggest that ZMYND11 and/or DIP2C haploinsufficiency contributes to the clinical features associated with 10p15 deletions in probands described in this study