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This paper describes a fast multi-channel radiation pyrometer that was developed for warm dense-matter experiments with intense heavy ion beams at the Gesellschaft für Schwerionenforschung mbH (GSI). The pyrometer is capable of measuring brightness temperatures from 2000 K to 50,000 K, at six wavelengths in the visible and near-infrared parts of the spectrum, with 5 ns temporal resolution, and several micrometers spatial resolution. The pyrometer's spectral discrimination technique is based on interference filters, which also act as mirrors to allow for simultaneous spectral discrimination of the same ray at multiple wavelengths.

This paper examines the reliability of a widely used method for temperature determination by multi-wavelength pyrometry. In recent warm dense matter experiments with ion-beam heated metal foils, we found that the statistical quality of the fit to the measured data is not necessarily a measure of the accuracy of the inferred temperature. We found a specific example where a second-best fit leads to a more realistic temperature value. The physics issue is the wavelength-dependent emissivity of the hot surface. We discuss improvements of the multi-frequency pyrometry technique, which will give a more reliable determination of the temperature from emission data.

This paper investigates prospects of utilizing a high-power laser-driven target-normal-sheath-acceleration proton beam for the experimental demonstration of the magnetic self-focusing phenomenon in charged particle beams. In the proposed concept, focusing is achieved by propagating a space-charge dominated ion beam through a stack of thin conducting and grounded foils separated by vacuum gaps. As the beam travels through the system, image charges build up at the foils and generate electric field that counteracts the beam's electrostatic self-field — a dominant force responsible for expansion of a high current beam. Once the electrostatic self-field is “neutralized” by the image charges, the beam currents magnetic self-field will do the focusing. The focal spot size and focal length depends on the choice of a number of foils and distance between foils. Considering the typical electrical current level of a target-normal-sheath-acceleration proton beam, we conclude that it is feasible to focus or collimate a beam within tens of millimeters distance, e.g., using 200–1000 Al foils, 0.5 µm thick each, with foil spacing ranging from 25 µm to 100 µm. These requirements are within technical capabilities of modern target fabrication, thus allowing the first possible demonstration of the pinch effect with heavy ion beams.

This paper describes a fast multi-channel radiation pyrometer that was developed for warmdense-matter experiments with intense heavy ion beams at Gesellschaft fur Schwerionenforschung mbH (GSI). The pyrometer is capable of measuring of brightness temperatures from 2000 K to 50000 K, at 6 wavelengths in visible and near-infrared parts of spectrum, with 5 nanosecond temporal resolution and several micrometers spatial resolution. The pyrometer's spectral discrimination technique is based on interference filters, which act as filters and mirrors to allow for simultaneous spectral discrimination of the same ray at multiple wavelengths.

CT pulmonary angiography is a standard diagnostic method for pulmonary embolism, but in pregnant women, this imaging test could expose mother and child to risks from radiation. A diagnostic algorithm allowed up to two thirds of pregnant women with suspected pulmonary embolism to safely avoid CT pulmonary angiography.

We recently demonstrated that acute myeloid leukemia (AML) cell lines and patient-derived blasts release exosomes that carry RNA and protein; following an in vitro transfer, AML exosomes produce proangiogenic changes in bystander cells. We reasoned that paracrine exosome trafficking may have a broader role in shaping the leukemic niche. In a series of in vitro studies and murine xenografts, we demonstrate that AML exosomes downregulate critical retention factors ( Scf , Cxcl12 ) in stromal cells, leading to hematopoietic stem and progenitor cell (HSPC) mobilization from the bone marrow. Exosome trafficking also regulates HSPC directly, and we demonstrate declining clonogenicity, loss of CXCR4 and c-Kit expression, and the consistent repression of several hematopoietic transcription factors, including c-Myb , Cebp-β and Hoxa-9 . Additional experiments using a model of extramedullary AML or direct intrafemoral injection of purified exosomes reveal that the erosion of HSPC function can occur independent of direct cell–cell contact with leukemia cells. Finally, using a novel multiplex proteomics technique, we identified candidate pathways involved in the direct exosome-mediated modulation of HSPC function. In aggregate, this work suggests that AML exosomes participate in the suppression of residual hematopoietic function that precedes widespread leukemic invasion of the bone marrow directly and indirectly via stromal components.

Increased expression of HBEGF in estrogen receptor-negative breast tumors is correlated with enhanced metastasis to distant organ sites and more rapid disease recurrence upon removal of the primary tumor. Our previous work has demonstrated a paracrine loop between breast cancer cells and macrophages in which the tumor cells are capable of stimulating macrophages through the secretion of colony-stimulating factor-1 while the tumor-associated macrophages (TAMs), in turn, aid in tumor cell invasion by secreting epidermal growth factor. To determine how the autocrine expression of epidermal growth factor receptor (EGFR) ligands by carcinoma cells would affect this paracrine loop mechanism, and in particular whether tumor cell invasion depends on spatial ligand gradients generated by TAMs, we generated cell lines with increased HBEGF expression. We found that autocrine HBEGF expression enhanced in vivo intravasation and metastasis and resulted in a novel phenomenon in which macrophages were no longer required for in vivo invasion of breast cancer cells. In vitro studies revealed that expression of HBEGF enhanced invadopodium formation, thus providing a mechanism for cell autonomous invasion. The increased invadopodium formation was directly dependent on EGFR signaling, as demonstrated by a rapid decrease in invadopodia upon inhibition of autocrine HBEGF/EGFR signaling as well as inhibition of signaling downstream of EGFR activation. HBEGF expression also resulted in enhanced invadopodium function via upregulation of matrix metalloprotease 2 (MMP2) and MMP9 expression levels. We conclude that high levels of HBEGF expression can short-circuit the tumor cell/macrophage paracrine invasion loop, resulting in enhanced tumor invasion that is independent of macrophage signaling.

In this work we explore photonic topological edge states arising in dielectric metasurface based on a deformed honeycomb lattice. We demonstrate numerically the effect of pseudo-spin locking of the edge states and verify its existence experimentally in microwave frequency range. Our findings thus demonstrate that open non-Hermitian metasurface can support the topological edge modes despite the radiative losses.

Leukemogenesis requires two classes of mutations, one that promotes proliferation and one that blocks differentiation. The erythroleukemia induced by Friend virus is a multistage disease characterized by an early proliferative stage driven by the interaction of the viral glycoprotein, gp55, with Sf-Stk and the EpoR, and a late block to differentiation resulting from retroviral insertion in the Pu.1 locus. We demonstrate here that activation of Stat3 by Sf-Stk in the early stage of disease is essential for the progression of erythroleukemia in the presence of differentiation signals induced by the EpoR, but is dispensable in the late stages of the disease. Furthermore, we identify Pu.1 as a Stat3 target gene in the early stages of erythroleukemia development. Our results support a model whereby the activation of Stat3 in the early stage of disease plays a pivotal role in regulating differentiation through the upregulation of Pu.1, thus inhibiting differentiation and favoring the expansion of infected erythroblasts and enhancing the pool of progenitors available for the acquisition of additional mutations, including insertional activation of Pu.1, resulting in full leukemic transformation.