208 research outputs found
Strong pinning of vortices by antiferromagnetic domain boundaries in CeCo(InCd)
We have studied the isothermal magnetization of
CeCo(InCd) with = 0.0075 and 0.01 down to 50 mK. Pronounced
field-history dependent phenomena occur in the coexistence regime of the
superconducting and antiferromagnetic phases. At low-fields, a phenomenological
model of magnetic-flux entry well explains implying the dominance of
bulk pinning effect. However, unless crystallographic quenched disorder is
hysteretic, the asymmetric peak effect (ASPE) which appears at higher fields
cannot be explained by the pinning of vortices due to material defects. Also
the temperature dependence of the ASPE deviates from the conventional scenario
for the peak effect. Comparison of our thermodynamic phase diagrams with those
from previous neutron scattering and magnetoresistance experiments indicates
that the pinning of vortices takes place at the field-history dependent
antiferromagnetic domain boundaries.Comment: 13 pages,4 figures, to be published in New Journal of Physic
Ferromagnetic Quantum Criticality in the Quasi-One-Dimensional Heavy Fermion Metal YbNi4P2
We present a new Kondo-lattice system, YbNi4P2, which is a clean
heavy-fermion metal with a severely reduced ferromagnetic ordering temperature
at T_C=0.17K, evidenced by distinct anomalies in susceptibility, specific-heat,
and resistivity measurements. The ferromagnetic nature of the transition, with
only a small ordered moment of ~0.05mu_B, is established by a diverging
susceptibility at T_C with huge absolute values in the ferromagnetically
ordered state, severely reduced by small magnetic fields. Furthermore, YbNi4P2
is a stoichiometric system with a quasi-one-dimensional crystal and electronic
structure and strong correlation effects which dominate the low temperature
properties. This is reflected by a stronger-than-logarithmically diverging
Sommerfeld coefficient and a linear-in-T resistivity above T_C which cannot be
explained by any current theoretical predictions. These exciting
characteristics are unique among all correlated electron systems and make this
an interesting material for further in-depth investigations.Comment: 14 pages, 6 figure
Superparamagnetic colloids in viscous fluids
The influence of a magnetic field on the aggregation process of superparamagnetic colloids has been well known on short time for a few decades. However, the influence of important parameters, such as viscosity of the liquid, has received only little attention. Moreover, the equilibrium state reached after a long time is still challenging on some aspects. Indeed, recent experimental measurements show deviations from pure analytical models in extreme conditions. Furthermore, current simulations would require several years of computing time to reach equilibrium state under those conditions. In the present paper, we show how viscosity influences the characteristic time of the aggregation process, with experimental measurements in agreement with previous theories on transient behaviour. Afterwards, we performed numerical simulations on equivalent systems with lower viscosities. Below a critical value of viscosity, a transition to a new aggregation regime is observed and analysed. We noticed this result can be used to reduce the numerical simulation time from several orders of magnitude, without modifying the intrinsic physical behaviour of the particles. However, it also implies that, for high magnetic fields, granular gases could have a very different behaviour from colloidal liquids
Easily Multiplexable Immunoplatform to Assist Heart Failure Diagnosis through Amperometric Determination of Galectin-3
This work reports the first electrochemical immunoassay involving magnetic microbeads (MBs) for the determination of galectin-3 (Gal-3), a Ξ²-galactosidase-binding lectin that acts as mediator of heart failure (HF). MBs-captured sandwich-type immune complexes and amperometric detection at disposable screen-printed carbon electrodes were used. The immunoplatform showed a detection limit of 8.3 pg mLβ1, good reproducibility, and excellent selectivity. The endogenous concentration of Gal-3 in human plasma from HF patients was determined with results in agreement with those obtained using ELISA. The multiplexing feasibility of the developed immunoplatform was demonstrated for the simultaneous determination of Gal-3 and N-terminal pro-brain natriuretic peptide (NT-proBNP).Fil: Piguillem Palacios, SofΓa Viviana. Consejo Nacional de Investigaciones CientΓficas y TΓ©cnicas. Centro CientΓfico TecnolΓ³gico Conicet - San Luis. Instituto de QuΓmica de San Luis. Universidad Nacional de San Luis. Facultad de QuΓmica, BioquΓmica y Farmacia. Instituto de QuΓmica de San Luis; Argentina. Universidad Complutense de Madrid; EspaΓ±aFil: MarΓa Gamella. Universidad Complutense de Madrid; EspaΓ±aFil: GarcΓa de Frutos, Pablo. INSTITUTO DE INVESTIGACIONES BIOMEDICAS AUGUST PI I SUNYER (IDIBAPS);Fil: Batlle, Montserrat. No especifΓca;Fil: YÑñez SedeΓ±o, Paloma. Universidad Complutense de Madrid; EspaΓ±aFil: Messina, GermΓ‘n Alejandro. Consejo Nacional de Investigaciones CientΓficas y TΓ©cnicas. Centro CientΓfico TecnolΓ³gico Conicet - San Luis. Instituto de QuΓmica de San Luis. Universidad Nacional de San Luis. Facultad de QuΓmica, BioquΓmica y Farmacia. Instituto de QuΓmica de San Luis; ArgentinaFil: FernΓ‘ndez Baldo, MartΓn Alejandro. Consejo Nacional de Investigaciones CientΓficas y TΓ©cnicas. Centro CientΓfico TecnolΓ³gico Conicet - San Luis. Instituto de QuΓmica de San Luis. Universidad Nacional de San Luis. Facultad de QuΓmica, BioquΓmica y Farmacia. Instituto de QuΓmica de San Luis; ArgentinaFil: Campuzano, Susana. Universidad Complutense de Madrid; EspaΓ±aFil: Pedrero, MarΓa. Universidad Complutense de Madrid; EspaΓ±aFil: PingarrΓ³n, JosΓ© M.. Universidad Complutense de Madrid; EspaΓ±
Endocrine Therapy Synergizes with SMAC Mimetics to Potentiate Antigen Presentation and Tumor Regression in Hormone Receptor-Positive Breast Cancer.
UNLABELLED: Immunotherapies have yet to demonstrate significant efficacy in the treatment of hormone receptor-positive (HR+) breast cancer. Given that endocrine therapy (ET) is the primary approach for treating HR+ breast cancer, we investigated the effects of ET on the tumor immune microenvironment (TME) in HR+ breast cancer. Spatial proteomics of primary HR+ breast cancer samples obtained at baseline and after ET from patients enrolled in a neoadjuvant clinical trial (NCT02764541) indicated that ET upregulated Ξ²2-microglobulin and influenced the TME in a manner that promotes enhanced immunogenicity. To gain a deeper understanding of the underlying mechanisms, the intrinsic effects of ET on cancer cells were explored, which revealed that ET plays a crucial role in facilitating the chromatin binding of RelA, a key component of the NF-ΞΊB complex. Consequently, heightened NF-ΞΊB signaling enhanced the response to interferon-gamma, leading to the upregulation of Ξ²2-microglobulin and other antigen presentation-related genes. Further, modulation of NF-ΞΊB signaling using a SMAC mimetic in conjunction with ET augmented T-cell migration and enhanced MHC-I-specific T-cell-mediated cytotoxicity. Remarkably, the combination of ET and SMAC mimetics, which also blocks prosurvival effects of NF-ΞΊB signaling through the degradation of inhibitors of apoptosis proteins, elicited tumor regression through cell autonomous mechanisms, providing additional support for their combined use in HR+ breast cancer. SIGNIFICANCE: Adding SMAC mimetics to endocrine therapy enhances tumor regression in a cell autonomous manner while increasing tumor immunogenicity, indicating that this combination could be an effective treatment for HR+ patients with breast cancer
Prognostic Impact of Array-based Genomic Profiles in Esophageal Squamous Cell Cancer
Background: Esophageal squamous cell carcinoma (ESCC) is a genetically complex tumor type and a major cause of cancer related mortality. Although distinct genetic alterations have been linked to ESCC development and prognosis, the genetic alterations have not gained clinical applicability. We applied array-based comparative genomic hybridization (aCGH) to obtain a whole genome copy number profile relevant for identifying deranged pathways and clinically applicable markers. Methods: A 32 k aCGH platform was used for high resolution mapping of copy number changes in 30 stage I-IV ESCC. Potential interdependent alterations and deranged pathways were identified and copy number changes were correlated to stage, differentiation and survival. Results: Copy number alterations affected median 19% of the genome and included recurrent gains of chromosome regions 5p, 7p, 7q, 8q, 10q, 11q, 12p, 14q, 16p, 17p, 19p, 19q, and 20q and losses of 3p, 5q, 8p, 9p and 11q. High-level amplifications were observed in 30 regions and recurrently involved 7p11 (EGFR), 11q13 (MYEOV, CCND1, FGF4, FGF3, PPFIA, FAD, TMEM16A, CTTS and SHANK2) and 11q22 (PDFG). Gain of 7p22.3 predicted nodal metastases and gains of 1p36.32 and 19p13.3 independently predicted poor survival in multivariate analysis. Conclusion: aCGH profiling verified genetic complexity in ESCC and herein identified imbalances of multiple central tumorigenic pathways. Distinct gains correlate with clinicopathological variables and independently predict survival, suggesting clinical applicability of genomic profiling in ESCC
Tissue microarray analysis reveals a tight correlation between protein expression pattern and progression of esophageal squamous cell carcinoma
BACKGROUND: The development of esophageal squamous cell carcinoma (ESCC) progresses a multistage process, collectively known as precursor lesions, also called dysplasia (DYS) and carcinoma in situ (CIS), subsequent invasive lesions and final metastasis. In this study, we are interested in investigating the expression of a variety of functional classes of proteins in ESCC and its precursor lesions and characterizing the correlation of these proteins with ESCC malignant progression. METHODS: Fas, FADD, caspase 8, CDC25B, fascin, CK14, CK4, annexin I, laminin-5Ξ³2 and SPARC were analyzed using immunohistochemistry on tissue microarray containing 205 ESCC and 173 adjacent precursor lesions as well as corresponding normal mucosa. To confirm the immunohistochemical results, three proteins, fascin, CK14 and laminin-5Ξ³2, which were overexpressed in ESCC on tissue microarray, were detected in 12 ESCC cell lines by Western blot assay. RESULTS: In ESCC and its precursor lesions, FADD, CDC25B, fascin, CK14, laminin-5Ξ³2 and SPARC were overexpressed, while Fas, caspase 8, CK4 and annexin I were underexpressed. The abnormalities of these proteins could be classified into different groups in relation to the stages of ESCC development. They were "early" corresponding to mild and moderate DYS with overexpression of fascin, FADD and CDC25B and underexpression of Fas, caspase 8, CK4 and annexin I, "intermediate" to severe DYS and CIS with overexpression of FADD and CK14, and "late" to invasive lesions (ESCC) and to advanced pTNM stage ESCC lesions with overexpression of CK14, laminin-5Ξ³2 and SPARC. CONCLUSION: Analyzing the protein expression patterns of Fas, FADD, caspase 8, CDC25B, fascin, CK14, CK4, annexin I, laminin-5Ξ³2 and SPARC would be valuable to develop rational strategies for early detection of lesions at risk in advance as well as for prevention and treatment of ESCC
Two Chromatin Remodeling Activities Cooperate during Activation of Hormone Responsive Promoters
Steroid hormones regulate gene expression by interaction of their receptors with hormone responsive elements (HREs) and recruitment of kinases, chromatin remodeling complexes, and coregulators to their target promoters. Here we show that in breast cancer cells the BAF, but not the closely related PBAF complex, is required for progesterone induction of several target genes including MMTV, where it catalyzes localized displacement of histones H2A and H2B and subsequent NF1 binding. PCAF is also needed for induction of progesterone target genes and acetylates histone H3 at K14, an epigenetic mark that interacts with the BAF subunits by anchoring the complex to chromatin. In the absence of PCAF, full loading of target promoters with hormone receptors and BAF is precluded, and induction is compromised. Thus, activation of hormone-responsive promoters requires cooperation of at least two chromatin remodeling activities, BAF and PCAF
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