Petrogenesis of synorogenic high-temperature leucogranites (Damara orogen, Namibia): Constraints from U–Pb monazite ages and Nd, Sr and Pb isotopes

Highlights: • Geochemical data from high-T leucogranites imply pure crustal melting. • New U–Pb monazite ages constrain intrusion time close to peak metamorphism. • Updated Sr–Nd–Pb isotope data imply metasedimentary sources. Two suites of leucogranites were emplaced at 508 ± 5.9 Ma in the Okombahe District of the Damara belt (Namibia) synchronous with the peak of regional high-temperature metamorphism. The Sr (87Sr/86Srinit: 0.707 to 0.711), Nd (εNdinit: − 4.5 to − 6.6), and Pb isotopic (206Pb/204Pb: 18.51–19.13; 207Pb/204Pb: 15.63–15.69; 208Pb/204Pb: 38.08–38.66) compositions indicate that these peraluminous S-type granites were derived from mid- to lower-crustal rocks, which are slightly different to the metapelitic rocks into which they intruded. Since the leucogranites are unfractionated and show no evidence for assimilation or contamination, they constrain the temperature and pressure conditions of their formation. Calculated Zr and LREE saturation temperatures of ca. 850 °C indicate high-temperature crustal melts. High Rb/Sr and low Sr/Ba ratios are consistent with biotite dehydration melting of pelitic source rocks. Qz–Ab–Or systematics reveal that melting and segregation for the least fractionated samples occurred at ca. 7 kbar corresponding to a mid-crustal level of ca. 26 km. However, there is no evidence for a mantle component that could have served as a local heat source for crustal melting. Therefore, the hot felsic magmas that formed close to the time of peak metamorphism are the result of long-lasting high temperature regional metamorphic conditions and intra-crustal collision

Selective-Area Growth of Heavily \u3cem\u3en\u3c/em\u3e–Doped GaAs Nanostubs on Si(001) by Molecular Beam Epitaxy

Using an aspect ratio trapping technique, we demonstrate molecular beam epitaxy of GaAs nanostubs on Si(001) substrates. Nanoholes in a SiO2 mask act as a template for GaAs-on-Si selective-area growth(SAG) of nanostubs 120 nm tall and ≤100 nm in diameter. We investigate the influence of growthparameters including substrate temperature and growth rate on SAG. Optimizing these parameters results in complete selectivity with GaAsgrowth only on the exposed Si(001). Due to the confined-geometry, strain and defects in the GaAs nanostubs are restricted in lateral dimensions, and surface energy is further minimized. We assess the electrical properties of the selectively grownGaAs nanostubs by fabricating heterogeneous p+–Si/n+–GaAs p–n diodes

Impact of Hapten Presentation on Antibody Binding at Lipid Membrane Interfaces

AbstractWe report the effects of ligand presentation on the binding of aqueous proteins to solid supported lipid bilayers. Specifically, we show that the equilibrium dissociation constant can be strongly affected by ligand lipophilicity and linker length/structure. The apparent equilibrium dissociation constants (KD) were compared for two model systems, biotin/anti-biotin and 2,4-dinitrophenyl (DNP)/anti-DNP, in bulk solution and at model membrane surfaces. The binding constants in solution were obtained from fluorescence anisotropy measurements. The surface binding constants were determined by microfluidic techniques in conjunction with total internal reflection fluorescence microscopy. The results showed that the bulk solution equilibrium dissociation constants for anti-biotin and anti-DNP were almost identical, KD(bulk)=1.7±0.2 nM vs. 2.9±0.1 nM. By contrast, the dissociation constant for anti-biotin antibody was three orders of magnitude tighter than for anti-DNP at a lipid membrane interface, KD=3.6±1.1 nM vs. 2.0±0.2 μM. We postulate that the pronounced difference in surface binding constants for these two similar antibodies is due to differences in the ligands’ relative lipophilicity, i.e., the more hydrophobic DNP molecules had a stronger interaction with the lipid bilayers, rendering them less available to incoming anti-DNP antibodies compared with the biotin/anti-biotin system. However, when membrane-bound biotin ligands were well screened by a poly(ethylene glycol) (PEG) polymer brush, the KD value for the anti-biotin antibody could also be weakened by three orders of magnitude, 2.4±1.1μM. On the other hand, the dissociation constant for anti-DNP antibodies at a lipid interface could be significantly enhanced when DNP haptens were tethered to the end of very long hydrophilic PEG lipopolymers (KD=21±10nM) rather than presented on short lipid-conjugated tethers. These results demonstrate that ligand presentation strongly influences protein interactions with membrane-bound ligands

Microwave properties of Nd_0.5Sr_0.5MnO_3: a key role of the (x^2-y^2)-orbital effects

Transmittance of the colossal magnetoresistive compound Nd_0.5Sr_0.5MnO_3 showing metal-insulator phase transition has been studied by means of the submm- and mm-wavelength band spectroscopy. An unusually high transparency of the material provided direct evidence for the significant suppression of the coherent Drude weight in the ferromagnetic metallic state. Melting of the A-type antiferromagnetic states has been found to be responsible for a considerable increase in the microwave transmission, which was observed at the transition from the insulating to the metallic phase induced by magnetic field or temperature. This investigation confirmed a dominant role of the (x^2-y^2)-orbital degree of freedom in the low-energy optical properties of Nd_0.5Sr_0.5MnO_3 and other doped manganites with planar (x^2-y^2)-orbital order, as predicted theoretically. The results are discussed in terms of the orbital-liquid concept.Comment: 8 pages, 3 figure

CRF Mediates Stress-Induced Pathophysiological High-Frequency Oscillations in Traumatic Brain Injury

Copyright © 2019 Narla et al. It is not known why there is increased risk to have seizures with increased anxiety and stress after traumatic brain injury (TBI). Stressors cause the release of corticotropin-releasing factor (CRF) both from the hypothalamic pituitary adrenal (HPA) axis and from CNS neurons located in the central amygdala and GABAergic interneurons. We have previously shown that CRF signaling is plastic, becoming excitatory instead of inhibitory after the kindling model of epilepsy. Here, using Sprague Dawley rats we have found that CRF signaling increased excitability after TBI. Following TBI, CRF type 1 receptor (CRFR1)-mediated activity caused abnormally large electrical responses in the amygdala, including fast ripples, which are considered to be epileptogenic. After TBI, we also found the ripple (120-250 Hz) and fast ripple activity (\u3e250 Hz) was cross-frequency coupled with θ (3-8 Hz) oscillations. CRFR1 antagonists reduced the incidence of phase coupling between ripples and fast ripples. Our observations indicate that pathophysiological signaling of the CRFR1 increases the incidence of epileptiform activity after TBI. The use for CRFR1 antagonist may be useful to reduce the severity and frequency of TBI associated epileptic seizures

Erythropoietin Modulates the Structure of Bone Morphogenetic Protein 2–Engineered Cranial Bone

The ideally engineered bone should have similar structural and functional properties to the native tissue. Although structural integrity is critical for functional bone regeneration, we know less about modulating the structural properties of the engineered bone elicited by bone morphogenetic protein (BMP) than efficacy and safety. Erythropoietin (Epo), a primary erythropoietic hormone, has been used to augment blood transfusion in orthopedic surgery. However, the effects of Epo on bone regeneration are not well known. Here, we determined the role of Epo in BMP2-induced bone regeneration using a cranial defect model. Epo administration improved the quality of BMP2-induced bone and more closely resembled natural cranial bone with a higher bone volume (BV) fraction and lower marrow fraction when compared with BMP2 treatment alone. Epo increased red blood cells (RBCs) in peripheral blood and also increased hematopoietic and mesenchymal stem cell (MSC) populations in bone marrow. Consistent with our previous work, Epo increased osteoclastogenesis both in vitro and in vivo. Results from a metatarsal organ culture assay suggested that Epo-promoted osteoclastogenesis contributed to angiogenesis because angiogenesis was blunted when osteoclastogenesis was blocked by alendronate (ALN) or osteoprotegerin (OPG). Earlier calcification of BMP2-induced temporary chondroid tissue was observed in the Epo+BMP group compared to BMP2 alone. We conclude that Epo significantly enhanced the outcomes of BMP2-induced cranial bone regeneration in part through its actions on osteoclastogenesis and angiogenesis.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/98479/1/ten%2Etea%2E2011%2E0742.pd

Compensatory Neural Reorganization in Tourette Syndrome

Children with neurological disorders may follow unique developmental trajectories whereby they undergo compensatory neuroplastic changes in brain structure and function that help them gain control over their symptoms [1, 2, 3, 4, 5, 6]. We used behavioral and brain imaging techniques to investigate this conjecture in children with Tourette syndrome (TS). Using a behavioral task that induces high levels of intermanual conflict, we show that individuals with TS exhibit enhanced control of motor output. Then, using structural (diffusion-weighted imaging) brain imaging techniques, we demonstrate widespread differences in the white matter (WM) microstructure of the TS brain that include alterations in the corpus callosum and forceps minor (FM) WM that significantly predict tic severity in TS. Most importantly, we show that task performance for the TS group (but not for controls) is strongly predicted by the WM microstructure of the FM pathways that lead to the prefrontal cortex and by the functional magnetic resonance imaging blood oxygen level-dependent response in prefrontal areas connected by these tracts. These results provide evidence for compensatory brain reorganization that may underlie the increased self-regulation mechanisms that have been hypothesized to bring about the control of tics during adolescence

Ploidy influences cellular responses to gross chromosomal rearrangements in saccharomyces cerevisiae

<p>Abstract</p> <p>Background</p> <p>Gross chromosomal rearrangements (GCRs) such as aneuploidy are key factors in genome evolution as well as being common features of human cancer. Their role in tumour initiation and progression has not yet been completely elucidated and the effects of additional chromosomes in cancer cells are still unknown. Most previous studies in which <it>Saccharomyces cerevisiae </it>has been used as a model for cancer cells have been carried out in the haploid context. To obtain new insights on the role of ploidy, the cellular effects of GCRs were compared between the haploid and diploid contexts.</p> <p>Results</p> <p>A total number of 21 haploid and diploid <it>S. cerevisiae </it>strains carrying various types of GCRs (aneuploidies, nonreciprocal translocations, segmental duplications and deletions) were studied with a view to determining the effects of ploidy on the cellular responses. Differences in colony and cell morphology as well as in the growth rates were observed between mutant and parental strains. These results suggest that cells are impaired physiologically in both contexts. We also investigated the variation in genomic expression in all the mutants. We observed that gene expression was significantly altered. The data obtained here clearly show that genes involved in energy metabolism, especially in the tricarboxylic acid cycle, are up-regulated in all these mutants. However, the genes involved in the composition of the ribosome or in RNA processing are down-regulated in diploids but up-regulated in haploids. Over-expression of genes involved in the regulation of the proteasome was found to occur only in haploid mutants.</p> <p>Conclusion</p> <p>The present comparisons between the cellular responses of strains carrying GCRs in different ploidy contexts bring to light two main findings. First, GCRs induce a general stress response in all studied mutants, regardless of their ploidy. Secondly, the ploidy context plays a crucial role in maintaining the stoichiometric balance of the proteins: the translation rates decrease in diploid strains, whereas the excess protein synthesized is degraded in haploids by proteasome activity.</p