300 research outputs found
COVID-19 in Italian patients with rheumatic autoimmune systemic diseases
No abstract availabl
Chemokines in hyperthyroidism
The term “hyperthyroidism” indicates a condition due to an exaggerate production of thyroid hormone; the most frequent cause is Graves’ disease (GD). We review cytokines and chemokines in hyperthyroidism, with a special focus in GD. In GD, recruited Th1 lymphocytes are responsible for enhanced IFN-γ and TNF-α production, which in turn stimulates Th1 chemokines release from thyrocytes, initiating and perpetuating the autoimmune process. Circulating levels of these chemokines are associated with the active phase of GD. Additional studies are necessary to investigate whether Th1 chemokines could be a novel therapeutic target in this disease
Magnetoplasmonic design rules for active magneto-optics
Light polarization rotators and non-reciprocal optical isolators are
essential building blocks in photonics technology. These macroscopic passive
devices are commonly based on magneto-optical Faraday and Kerr polarization
rotation. Magnetoplasmonics - the combination of magnetism and plasmonics - is
a promising route to bring these devices to the nanoscale. We introduce design
rules for highly tunable active magnetoplasmonic elements in which we can
tailor the amplitude and sign of the Kerr response over a broad spectral range
Putative biomarkers for malignant pleural mesothelioma suggested by proteomic analysis of cell secretome
Background: Malignant pleural mesothelioma (MPM) a rare neoplasm linked to asbestos exposure is characterized by a poor prognosis. Soluble mesothelin is currently considered the most specific diagnostic biomarker. The aim of the study was to identify novel biomarkers by proteomic analysis of two MPM cell lines secretome. Materials and Methods: The protein patterns of MPM cells secretome were examined and compared to a non-malignant mesothelial cell line using two-dimensional gel electrophoresis coupled to mass spectrometry. Serum levels of candidate biomarkers were determined in MPM patients and control subjects. Results: Two up-regulated proteins involved in cancer biology, prosaposin and quiescin Q6 sulfhydryl oxidase 1, were considered candidate biomarkers. Serum levels of both proteins were significantly higher in MPM patients than control subjects. Combining the data of each receiver-operating characteristic analysis predicted a good diagnostic accuracy. Conclusion: A panel of the putative biomarkers represents a promising tool for MPM diagnosis
Immune and inflammatory cells in thyroid cancer microenvironment
A hallmark of cancer is the ability of tumor cells to avoid immune destruction. Activated immune cells in tumor microenvironment (TME) secrete proinflammatory cytokines and chemokines which foster the proliferation of tumor cells. Specific antigens expressed by cancer cells are recognized by the main actors of immune response that are involved in their elimination (immunosurveillance). By the recruitment of immunosuppressive cells, decreasing the tumor immunogenicity, or through other immunosuppressive mechanisms, tumors can impair the host immune cells within the TME and escape their surveillance. Within the TME, cells of the innate (e.g., macrophages, mast cells, neutrophils) and the adaptive (e.g., lymphocytes) immune responses are interconnected with epithelial cancer cells, fibroblasts, and endothelial cells via cytokines, chemokines, and adipocytokines. The molecular pattern of cytokines and chemokines has a key role and could explain the involvement of the immune system in tumor initiation and progression. Thyroid cancer-related inflammation is an important target for diagnostic procedures and novel therapeutic strategies. Anticancer immunotherapy, especially immune checkpoint inhibitors, unleashes the immune system and activates cytotoxic lymphocytes to kill cancer cells. A better knowledge of the molecular and immunological characteristics of TME will allow novel and more effective immunotherapeutic strategies in advanced thyroid cancer
Immunomodulation of CXCL10 secretion by hepatitis C virus: Could CXCL10 be a prognostic marker of chronic hepatitis C?
Chemokine (C-X-C motif) ligand (CXCL)10 and other CXCR3 chemokines are involved in the pathogenesis of acute and \u201cchronic hepatitis C virus (HCV) infection\u201d (CHC). Here, we review the scientific literature about HCV and CXCL10. The combination of circulating CXCL10 and single nucleotide polymorphisms (SNPs) in IL-28B can identify patients with acute HCV infection most likely to undergo spontaneous HCV clearance and those in need of early antiviral therapy. In CHC, the HCV and intrahepatic interferon- (IFN-) \u3b3 drive a raised CXCL10 expression by sinusoidal endothelium and hepatocytes, thereby inducing the recruitment of CXCR3-expressing T cells into the liver; thus, CXCL10 plays an important role in the development of necroinflammation and fibrosis. Increased CXCL10 was significantly associated with the presence of active vasculitis in HCV-associated cryoglobulinemia, or with autoimmune thyroiditis in CHC. Pretreatment CXCL10 levels are predictive of early virological response and sustained virological response (SVR) to IFN-\u3b1 and ribavirin and may be useful in the evaluation of candidates for therapy. The occurrence of SNPs adjacent to IL-28B (rs12979860, rs12980275, and rs8099917), and CXCL10 below 150 pg/mL, independently predicted the first phase viral decline and rapid virological response, which in turn independently predicted SVR. Directly acting antiviral agents-mediated clearance of HCV is associated with the loss of intrahepatic immune activation by IFN-\u3b1, associated by decreased levels of CXCL10. In conclusion, CXCL10 is an important marker of HCV clearance and successful therapy in CHC patients. Whether CXCL10 is a novel therapeutic target in CHC will be evaluated
Depth dependent magnetization profiles of hybrid exchange springs
We report on the magnetization depth profile of a hybrid exchange spring
system in which a Co/Pd multilayer with perpendicular anisotropy is coupled to
a CoFeB thin film with in-plane anisotropy. The competition between these two
orthogonal anisotropies promotes a strong depth dependence of the magnetization
orientation. The angle of the magnetization vector is sensitive both to the
strength of the individual anisotropies and to the local exchange constant, and
is thus tunable by changing the thickness of the CoFeB layer and by
substituting Ni for Pd in one layer of the Co/Pd stack. The resulting magnetic
depth profiles are directly probed by element specific x-ray magnetic circular
dichroism (XMCD) of the Co, Fe, and Ni layers located at different average
depths. The experimental results are corroborated by micromagnetic simulations
Full coherent control of nuclear spins in an optically pumped single quantum dot
Highly polarized nuclear spins within a semiconductor quantum dot (QD) induce
effective magnetic (Overhauser) fields of up to several Tesla acting on the
electron spin or up to a few hundred mT for the hole spin. Recently this has
been recognized as a resource for intrinsic control of QD-based spin quantum
bits. However, only static long-lived Overhauser fields could be used. Here we
demonstrate fast redirection on the microsecond time-scale of Overhauser fields
of the order of 0.5 T experienced by a single electron spin in an optically
pumped GaAs quantum dot. This has been achieved using full coherent control of
an ensemble of 10^3-10^4 optically polarized nuclear spins by sequences of
short radio-frequency (rf) pulses. These results open the way to a new class of
experiments using rf techniques to achieve highly-correlated nuclear spins in
quantum dots, such as adiabatic demagnetization in the rotating frame leading
to sub-micro K nuclear spin temperatures, rapid adiabatic passage, and spin
squeezing
Aggressive thyroid cancer: targeted therapy with sorafenib
Sorafenib (Nexavar), is a multikinase inhibitor, which has demonstrated both anti proliferative and anti-angiogenic properties in vitro and in vivo, inhibiting the activity of targets present in the tumoral cells [c-RAF (proto-oncogene serine/threonine-protein kinase), BRAF, (V600E)BRAF, c-KIT, and FMS-like tyrosine kinase 3] and in tumor vessels [c-RAF, vascular endothelial growth factor receptor (VEGFR)-2, VEGFR-3, and platelet-derived growth factor receptor β]. Sorafenib was initially approved for the treatment of hepatocellular carcinoma and advanced renal cell carcinoma. Experimental studies have demonstrated that sorafenib has both anti-proliferative and anti-angiogenic properties in vitro and in vivo, against thyroid cancer cells. Furthermore, several completed (or ongoing) studies have evaluated the long-term efficacy and tolerability of sorafenib in patients with papillary, follicular and medullary aggressive thyroid cancer. The results of the different studies showed good clinical responses and stabilization of the disease and suggested that sorafenib is a promising therapeutic option in patients with advanced thyroid cancer that is not responsive to traditional therapeutic strategies (such as radioiodine). Currently, USA Food and Drug Administration has approved the use of sorafenib for metastatic differentiated thyroid cancer
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