73 research outputs found
Ballistic heat transport of quantum spin excitations as seen in SrCuO2
Fundamental conservation laws predict ballistic, i.e., dissipationless
transport behaviour in one-dimensional quantum magnets. Experimental evidence,
however, for such anomalous transport has been lacking ever since. Here we
provide experimental evidence for ballistic heat transport in a S=1/2
Heisenberg chain. In particular, we investigate high purity samples of the
chain cuprate SrCuO2 and observe a huge magnetic heat conductivity
. An extremely large spinon mean free path of more than a
micrometer demonstrates that is only limited by extrinsic
scattering processes which is a clear signature of ballistic transport in the
underlying spin model
The thermal conductivity of alternating spin chains
We study a class of integrable alternating (S1,S2) quantum spin chains with
critical ground state properties. Our main result is the description of the
thermal Drude weight of the one-dimensional alternating spin chain as a
function of temperature. We have identified the thermal current of the model
with alternating spins as one of the conserved currents underlying the
integrability. This allows for the derivation of a finite set of non-linear
integral equations for the thermal conductivity. Numerical solutions to the
integral equations are presented for specific cases of the spins S1 and S2. In
the low-temperature limit a universal picture evolves where the thermal Drude
weight is proportional to temperature T and central charge c.Comment: 15 pages, 1 figur
Heat conductivity of the spin-Peierls compounds TiOCl and TiOBr
We report experimental results on the heat conductivity \kappa of the S=1/2
spin chain compounds TiOBr and TiOCl for temperatures 5K<T<300K and magnetic
fields up to 14. Surprisingly, we find no evidence of a significant magnetic
contribution to \kappa, which is in stark contrast to recent results on S=1/2
spin chain cuprates. Despite this unexpected result, the thus predominantly
phononic heat conductivity of these spin-Peierls compounds exhibits a very
unusual behavior. In particular, we observe strong anomalies at the phase
transitions Tc1 and Tc2. Moreover, we find an overall but anisotropic
suppression of \kappa in the intermediate phase which extends even to
temperatures higher than Tc2. An external magnetic field causes a slight
downshift of the transition at Tc1 and enhances the suppression of \kappa up to
Tc2. We interprete our findings in terms of strong spin-phonon coupling and
phonon scattering arising from spin-driven lattice distortions.Comment: 6 pages, 3 figure
Spinon heat transport and spin-phonon interaction in the antiferromagnetic spin-1/2 Heisenberg chain cuprates Sr2CuO3 and SrCuO2
We have investigated the thermal conductivity \kappa_mag of high-purity
single crystals of the spin chain compound Sr2CuO3 which is considered an
excellent realization of the one-dimensional spin-1/2 antiferromagnetic
Heisenberg model. We find that the spinon heat conductivity \kappa_mag is
strongly enhanced as compared to previous results obtained on samples with
lower chemical purity. The analysis of \kappa_mag allows to compute the spinon
mean free path l_mag as a function of temperature. At low-temperature we find
l_mag\sim0.5\mum, corresponding to more than 1200 chain unit cells. Upon
increasing the temperature, the mean free path decreases strongly and
approaches an exponential decay ~1/T*exp(T*/T) which is characteristic for
umklapp processes with the energy scale k_B T*. Based on Matthiesen's rule we
decompose l_mag into a temperature-independent spinon-defect scattering length
l0 and a temperature dependent spinon-phonon scattering length l_sp(T). By
comparing l_mag(T) of Sr2CuO3 with that of SrCuO2, we show that the spin-phonon
interaction, as expressed by l_sp is practically the same in both systems. The
comparison of the empirically derived l_sp with model calculations for the
spin-phonon interaction of the one-dimensional spin-1/2 XY model yields
reasonable agreement with the experimental data.Comment: revised version, accepted by: Journal of Statistical Mechanics:
theory and experimen
Silymarin Targets β-Catenin Signaling in Blocking Migration/Invasion of Human Melanoma Cells
Metastatic melanoma is a leading cause of death from skin diseases, and is often associated with activation of Wnt/β-catenin signaling pathway. We have examined the inhibitory effect of silymarin, a plant flavanoid from Silybum marianum, on cell migration of metastasis-specific human melanoma cell lines (A375 and Hs294t) and assessed whether Wnt/β-catenin signaling is the target of silymarin. Using an in vitro invasion assay, we found that treatment of human melanoma cell lines with silymarin resulted in concentration-dependent inhibition of cell migration, which was associated with accumulation of cytosolic β-catenin, while reducing the nuclear accumulation of β-catenin (i.e., β-catenin inactivation) and reducing the levels of matrix metalloproteinase (MMP) -2 and MMP-9 which are the down-stream targets of β-catenin. Silymarin enhanced: (i) the levels of casein kinase 1α, glycogen synthase kinase-3β and phosphorylated-β-catenin on critical residues Ser45, Ser33/37 and Thr41, and (ii) the binding of β-transducin repeat-containing proteins (β-TrCP) with phospho forms of β-catenin in melanoma cells. These events play important roles in degradation or inactivation of β-catenin. To verify whether β-catenin is a potent molecular target of silymarin, the effect of silymarin was determined on β-catenin-activated (Mel 1241) and β-catenin-inactivated (Mel 1011) melanoma cells. Treatment of Mel 1241 cells with silymarin or FH535, an inhibitor of Wnt/β-catenin pathway, significantly inhibited cell migration of Mel 1241 cells, which was associated with the elevated levels of casein kinase 1α and glycogen synthase kinase-3β, and decreased accumulation of nuclear β-catenin and inhibition of MMP-2 and MMP-9 levels. However, this effect of silymarin and FH535 was not found in Mel 1011 melanoma cells. These results indicate for the first time that silymarin inhibits melanoma cell migration by targeting β-catenin signaling pathway
Oral acantholytic squamous cell carcinoma shares clinical and histological features with angiosarcoma
<p>Abstract</p> <p>Background</p> <p>acantholytic squamous cell carcinomas (ASCC) and intraoral angiosarcoma share similar histopathological features. Aim of this study was to find marker for a clear distinction.</p> <p>Methods</p> <p>Four oral acantholytic squamous cell carcinomas and one intraoral angiosarcoma are used to compare the eruptive intraoral growth-pattern, age-peak, unfavourable prognosis and slit-like intratumorous spaces in common histological staining as identical clinical and histopathological features. Immunohistochemical staining for pancytokeratin, cytokeratin, collagen type IV, γ2-chain of laminin-5, endothelial differentiation marker CD31 and CD34, F VIII-associated antigen, Ki 67-antigen, β-catenin, E-cadherin, α-smooth-muscle-actin and Fli-1 were done.</p> <p>Results</p> <p>Cytokeratin-immunoreactive cells can be identified in both lesions. The large vascularization of ASCC complicates the interpretation of vascular differential markers being characteristic for angiosarcoma. Loss of cell-cell-adhesion, monitored by loss of E-cadherin and β-catenin membrane-staining, are indetified as reasons for massive expression of invasion-factor ln-5 in ASCC and considered responsible for unfavourable prognosis of ASCC. Expression of Fli-1 in angiosarcoma and cellular immunoreaction for ln-5 in ASCC are worked out as distinguishing features of both entities.</p> <p>Conclusion</p> <p>Fli-1 in angiosarcoma and ln-5 in ASCC are distinguishing features.</p
PTTG1 Attenuates Drug-Induced Cellular Senescence
As PTTG1 (pituitary tumor transforming gene) abundance correlates with adverse outcomes in cancer treatment, we determined mechanisms underlying this observation by assessing the role of PTTG1 in regulating cell response to anti-neoplastic drugs. HCT116 cells devoid of PTTG1 (PTTG1−/−) exhibited enhanced drug sensitivity as assessed by measuring BrdU incorporation in vitro. Apoptosis, mitosis catastrophe or DNA damage were not detected, but features of senescence were observed using low doses of doxorubicin and TSA. The number of drug-induced PTTG1−/− senescent cells increased ∼4 fold as compared to WT PTTG1-replete cells (p<0.001). p21, an important regulator of cell senescence, was induced ∼3 fold in HCT116 PTTG1−/− cells upon doxorubicin or Trichostatin A treatment. Binding of Sp1, p53 and p300 to the p21 promoter was enhanced in PTTG1−/− cells after treatment, suggesting transcriptional regulation of p21. p21 knock down abrogated the observed senescent effects of these drugs, indicating that PTTG1 likely suppresses p21 to regulate drug-induced senescence. PTTG1 also regulated SW620 colon cancer cells response to doxorubicin and TSA mediated by p21. Subcutaneously xenografted PTTG1−/− HCT116 cells developed smaller tumors and exhibited enhanced responses to doxorubicin. PTTG1−/− tumor tissue derived from excised tumors exhibited increased doxorubicin-induced senescence. As senescence is a determinant of cell responses to anti-neoplastic treatments, these findings suggest PTTG1 as a tumor cell marker to predict anti-neoplastic treatment outcomes
Migratory marker expression in fibroblast foci of idiopathic pulmonary fibrosis
BACKGROUND: Fibroblast foci (FF) are considered a relevant morphologic marker of idiopathic pulmonary fibrosis/usual interstitial pneumonia (IPF/UIP), and are recognised as sites where fibrotic responses are initiated and/or perpetuated in this severe disease. Despite their relevance, the cellular and molecular mechanisms responsible for the formation of FF and their role in tissue remodelling are poorly defined. In previous studies we have provided evidence of abnormal activation of the wnt-signaling-pathway in IPF/UIP that is centred on FF and the overlying epithelium. This important morphogenetic pathway is able to trigger epithelial-mesenchymal-transition (EMT), a mechanism involved in developmental and metastatic processes, which is also potentially involved in pulmonary fibrosis. METHODS: Since EMT is characterised by enhancement of migratory potential of cells, we investigated the molecular profile of FF in 30 biopsies of IPF/UIP and a variety of control samples, focussing on the immunohistochemical expression of three molecules involved in cell motility and invasiveness, namely laminin-5-γ2-chain, fascin, and heat-shock-protein-27. RESULTS: We provide evidence that in UIP these three molecules are abnormally expressed in discrete clusters of bronchiolar basal cells precisely localised in FF. These cellular clusters expressed laminin-5-γ2-chain and heat-shock-protein-27 at very high levels, forming characteristic three-layered lesions defined as "sandwich-foci" (SW-FF). Upon quantitative analysis SW-FF were present in 28/30 UIP samples, representing more than 50% of recognisable FF in 21/30, but were exceedingly rare in a wide variety of lung pathologies examined as controls. In UIP, SW-FF were often observed in areas of microscopic honeycombing, and were also found at the interface between normal lung tissue and areas of dense scarring. CONCLUSION: These molecular abnormalities strongly suggest that SW-FF represent the leading edge of pulmonary remodelling, where abnormal migration and re-epithelialisation take place, and that abnormal proliferation and migration of bronchiolar basal cells have a major role in the remodelling process characterising IPF/UIP. Further investigations will assess their possible use as reliable markers for better defining the UIP-pattern in difficult cases
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