238 research outputs found
THE IRAQI CONFLICT: AN ASSESSMENT OF POSSIBLE WAR CRIMES AND THE CALL FOR ADOPTION OF AN INTERNATIONAL CRIMINAL CODE AND PERMANENT INTERNATIONAL CRIMINAL TRIBUNAL
Colossal magnetostriction and negative thermal expansion in the frustrated antiferromagnet ZnCr2Se4
A detailed investigation of ZnCr2Se4 is presented which is dominated by
strong ferromagnetic exchange but orders antiferromagnetically at T_N = 21 K.
Specific heat C and thermal expansion Delta L/L exhibit sharp first-order
anomalies at the antiferromagnetic transition. T_N is strongly reduced and
shifted to lower temperatures by external magnetic fields and finally is fully
suppressed suggesting a field induced quantum critical behavior close to 60
kOe. Delta L/L(T) is unusually large and exhibits negative thermal expansion
below 75 K down to T_N indicating strong frustration of the lattice.
Magnetostriction Delta L/L(H) reveals colossal values (0.5x10^{-3}) comparable
to giant magnetostriction materials. Electron-spin resonance, however, shows
negligible spin-orbital coupling excluding orbitally induced Jahn-Teller
distortions. The obtained results point to a spin-driven origin of the
structural instability at T_N explained in terms of competing ferromagnetic and
antiferromagnetic exchange interactions yielding strong bond frustration.Comment: 5 pages 4 figure
Spin-driven Phonon Splitting in Bond-frustrated ZnCr2S4
Utilizing magnetic susceptibility, specific heat, thermal expansion and IR
spectroscopy we provide experimental evidence that the two subsequent
antiferromagnetic transitions in ZnCr_2S_4 at T_N1 = 15 K and T_N2= 8 K are
accompanied by significant thermal and phonon anomalies. The anomaly at T_N2
reveals a strong temperature hysteresis typical for a first-order
transformation. Due to strong spin-phonon coupling both magnetic phase
transitions induce a splitting of phonon modes, where at T_N1 the
high-frequency and at T_N2 the low-frequency modes split. The anomalies and
phonon splitting observed at T_N2 are strongly suppressed by magnetic field.
Regarding the small positive Curie-Weiss temperature Theta= 8 K, we argue that
this scenario of two different magnetic phases with concomitant different
magneto-elastic couplings results from the strong competition of ferromagnetic
and antiferromagnetic exchange of equal strength.Comment: 4 pages, 4 figure
Spin-driven Phase Transitions in ZnCrSe and ZnCrS Probed by High Resolution Synchrotron X-ray and Neutron Powder Diffraction
The crystal and magnetic structures of the spinel compounds ZnCrS and
ZnCrSe were investigated by high resolution powder synchrotron and
neutron diffraction. ZnCrSe exhibits a first order phase transition at
K into an incommensurate helical magnetic structure. Magnetic
fluctuations above are coupled to the crystal lattice as manifested by
negative thermal expansion. Both, the complex magnetic structure and the
anomalous structural behavior can be related to magnetic frustration.
Application of an external magnetic field shifts the ordering temperature and
the regime of negative thermal expansion towards lower temperatures. Thereby,
the spin ordering changes into a conical structure. ZnCrS shows two
magnetic transitions at K and K that are accompanied by
structural phase transitions. The crystal structure transforms from the cubic
spinel-type (space group \={3}) at high temperatures in the paramagnetic
state, via a tetragonally distorted intermediate phase (space group /
) for into a low temperature orthorhombic phase
(space group ) for . The cooperative displacement of
sulfur ions by exchange striction is the origin of these structural phase
transitions. The low temperature structure of ZnCrS is identical to the
orthorhombic structure of magnetite below the Verwey transition. When applying
a magnetic field of 5 T the system shows an induced negative thermal expansion
in the intermediate magnetic phase as observed in ZnCrSe.Comment: 11 pages, 13 figures, to be published in PR
Human-Computer Music Performance: From Synchronized Accompaniment to Musical Partner
Live music performance with computers has motivated many research projects in science, engineering, and the arts. In spite of decades of work, it is surprising that there is not more technology for, and a better understanding of the computer as music performer. We review the development of techniques for live music performance and outline our efforts to establish a new direction, Human-Computer Music Performance (HCMP), as a framework for a variety of coordinated studies. Our work in this area spans performance analysis, synchronization techniques, and interactive performance systems. Our goal is to enable musicians to ncorporate computers into performances easily and effectively through a better understanding of requirements, new techniques, and practical, performance-worthy implementations. We conclude with directions for future work
Corseto: A Kinesthetic Garment for Designing, Composing for, and Experiencing an Intersubjective Haptic Voice
We present a novel intercorporeal experience - an intersubjective haptic voice. Through an autobiographical design inquiry, based on singing techniques from the classical opera tradition, we created Corsetto, a kinesthetic garment for transferring somatic reminiscents of vocal experience from an expert singer to a listener. We then composed haptic gestures enacted in the Corsetto, emulating upper-body movements of the live singer performing a piece by Morton Feldman named Three Voices. The gestures in the Corsetto added a haptics-based \u27fourth voice\u27 to the immersive opera performance. Finally, we invited audiences who were asked to wear Corsetto during live performances. Afterwards they engaged in micro-phenomenological interviews. The analysis revealed how the Corsetto managed to bridge inner and outer bodily sensations, creating a feeling of a shared intercorporeal experience, dissolving boundaries between listener, singer and performance. We propose that \u27intersubjective haptics\u27 can be a generative medium not only for singing performances, but other possible intersubjective experiences
The adenovirus E4orf4 protein targets PP2A to the ACF chromatin-remodeling factor and induces cell death through regulation of SNF2h-containing complexes
The adenovirus E4 open-reading-frame 4 (E4orf4) protein regulates the progression of viral infection and when expressed individually it induces non-classical apoptosis in transformed cells. Here we show that E4orf4 associates with the ATP-dependent chromatin-remodeling factor ACF that consists of a sucrose non fermenting-2h (SNF2h) ATPase and an Acf1 regulatory subunit. Furthermore, E4orf4 targets protein phosphatase 2A (PP2A) to this complex and to chromatin. Obstruction of SNF2h activity inhibits E4orf4-induced cell death, whereas knockdown of Acf1 results in enhanced E4orf4-induced toxicity in both mammalian and yeast cells, and Acf1 overexpression inhibits E4orf4′s ability to downregulate early adenovirus gene expression in the context of viral infection. Knockdown of the Acf1 homolog, WSTF, inhibits E4orf4-induced cell death. Based on these results we suggest that the E4orf4–PP2A complex inhibits ACF and facilitates enhanced chromatin-remodeling activities of other SNF2h-containing complexes, such as WSTF–SNF2h. The resulting switch in chromatin remodeling determines life versus death decisions and contributes to E4orf4 functions during adenovirus infection
The Cytosolic Tail of the Golgi Apyrase Ynd1 Mediates E4orf4-Induced Toxicity in Saccharomyces cerevisiae
The adenovirus E4 open reading frame 4 (E4orf4) protein contributes to regulation of the progression of virus infection. When expressed individually, E4orf4 was shown to induce non-classical transformed cell-specific apoptosis in mammalian cells. At least some of the mechanisms underlying E4orf4-induced toxicity are conserved from yeast to mammals, including the requirement for an interaction of E4orf4 with protein phosphatase 2A (PP2A). A genetic screen in yeast revealed that the Golgi apyrase Ynd1 associates with E4orf4 and contributes to E4orf4-induced toxicity, independently of Ynd1 apyrase activity. Ynd1 and PP2A were shown to contribute additively to E4orf4-induced toxicity in yeast, and to interact genetically and physically. A mammalian orthologue of Ynd1 was shown to bind E4orf4 in mammalian cells, confirming the evolutionary conservation of this interaction. Here, we use mutation analysis to identify the cytosolic tail of Ynd1 as the protein domain required for mediation of the E4orf4 toxic signal and for the interaction with E4orf4. We also show that E4orf4 associates with cellular membranes in yeast and is localized at their cytoplasmic face. However, E4orf4 is membrane-associated even in the absence of Ynd1, suggesting that additional membrane proteins may mediate E4orf4 localization. Based on our results and on a previous report describing a collection of Ynd1 protein partners, we propose that the Ynd1 cytoplasmic tail acts as a scaffold, interacting with a multi-protein complex, whose targeting by E4orf4 leads to cell death
An Alzheimer-associated TREM2 variant occurs at the ADAM cleavage site and affects shedding and phagocytic function
Sequence variations occurring in the gene encoding the triggering receptor expressed on myeloid cells 2 (TREM2) support an essential function of microglia and innate immunity in the pathogenesis of Alzheimer's disease (AD) and other neurodegenerative disorders. TREM2 matures within the secretory pathway, and its ectodomain is shed on the plasma membrane. Missense mutations in the immunoglobulin (Ig)-like domain such as p.T66M and p.Y38C retain TREM2 within the endoplasmic reticulum and reduce shedding as well as TREM2-dependent phagocytosis. Using mass spectrometry, we have now determined the cleavage site of TREM2. TREM2 is shed by proteases of the ADAM (a disintegrin and metalloproteinase domain containing protein) family C-terminal to histidine 157, a position where an AD-associated coding variant has been discovered (p.H157Y) in the Han Chinese population. Opposite to the characterized mutations within the Ig-like domain, such as p.T66M and p.Y38C, the p.H157Y variant within the stalk region leads to enhanced shedding of TREM2. Elevated ectodomain shedding reduces cell surface full-length TREM2 and lowers TREM2-dependent phagocytosis. Therefore, two seemingly opposite cellular effects of TREM2 variants, namely reduced versus enhanced shedding, result in similar phenotypic outcomes by reducing cell surface TREM2
Tyrphostins that suppress the growth of human papilloma virus 16‐immortalized human keratinocytes
ABSTRACT Human papilloma virus 16 (HPV16) is considered to be the causative agent for cervical cancer, which ranks second to breast cancer in women's malignancies. In an attempt to develop drugs that inhibit the malignant transformation of HPV16-immortalized epithelial cells, we examined the effect of tyrphostins on such cells. We examined the effect of tyrphostins from four different families on the growth of HPV16-immortalized human keratinocytes (HF-1) cells. We found that they alter their cell cycle distribution, their morphology, and induce cell death by apoptosis. The effects of tyrphostins on HF-1 cells are different from their effects on normal keratinocytes. Growth suppression by AG555 and AG1478 is accompanied by 30% apoptosis in HF-1 cells, but this is not observed in normal keratinocytes. Tyrphostin treatment produces distinctive morphological changes in HF-1 cells and in normal keratinocytes; however, the culture organization of normal keratinocytes is less disrupted. These differential effects of the tyrphostins on HPV16-immortalized keratinocytes compared with their effects on normal keratinocytes suggests that these compounds are suitable candidates for the treatment of papilloma. Previous and present results indicate that group 1 tyrphostins, which inhibit Cdk2 activation, and group 2 tyrphostins, represented by AG1478, a potent epidermal growth factor receptor kinase inhibitor, induce cell cycle arrest; and, in the case of HF-1 cells, apoptosis and differentiation. Cells accumulate in the G 1 phase of the cell cycle at the expense of S and G 2 ϩ M. These compounds block the growth of normal keratinocytes without inducing apoptosis or differentiation, causing them to accumulate in G 1 . AG17, which belongs to group 4, exerts its antiproliferative effect mainly by increasing the fractions of cells in G 1 with a concomitant decrease in the fraction of cells in S and G 2 ϩ M
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