gebhart/patrepeval huggingface dataset:
Role of the postnatal radial glial scaffold for the development of the dentate gyrus as revealed by reelin signaling mutant mice (2013)

During dentate gyrus development, the early embryonic radial glial scaffold is replaced by a secondary glial scaffold around birth. In contrast to neocortical and early dentate gyrus radial glial cells, these postnatal glial cells are severely altered with regard to position and morphology in reeler mice lacking the secreted protein Reelin. In this study, we focus on the functional impact of these defects. Most radial glial cells throughout the nervous system serve as scaffolds for migrating neurons and precursor cells for both neurogenesis and gliogenesis. Precursor cell function has been demonstrated for secondary radial glial cells but the exact function of these late glial cells in granule cell migration and positioning is not clear. No data exist concerning the interplay between granule neurons and late radial glial cells during dentate gyrus development. Herein, we show that despite the severe morphological defects in the reeler dentate gyrus, the precursor function of secondary radial glial cells is not impaired during development in reeler mice. In addition, selective ablation of Disabled-1, an intracellular adaptor protein essential for Reelin signaling, in neurons but not in glial cells allowed us to distinguish effects of Reelin signaling on radial glial cells from possible secondary effects based on defective granule cells positioning.
Attovial‐based antibody nanoarrays (2009)

Antibody array-based technology is a powerful emerging tool in proteomics, but to enable global proteome analysis, antibody array layouts with even higher density has to be developed. To this end, we have further developed the first generation of a nanoarray platform, based on attoliter-sized vials, attovials, which we have characterized and used for the detection of complement factor C1q in human serum samples. Finally, we demonstrated proof-of-concept for individual functionalization of the attovials with a recombinant antibody.
PMEPA1-AR DEGRADATION PATHWAY: A NEW MECHANISM FOR THE REGULATION OF ANDROGEN RECEPTOR IN PROSTATE CANCER (2009)

You have accessJournal of Urology1 Apr 2009PMEPA1-AR DEGRADATION PATHWAY: A NEW MECHANISM FOR THE REGULATION OF ANDROGEN RECEPTOR IN PROSTATE CANCER Eliza Raymundo, Li Hongyun, Linda Xu, Katsuaki Masuda, David G McLeod, Albert Dobi, and Shiv Srivastava Eliza RaymundoEliza Raymundo More articles by this author , Li HongyunLi Hongyun More articles by this author , Linda XuLinda Xu More articles by this author , Katsuaki MasudaKatsuaki Masuda More articles by this author , David G McLeodDavid G McLeod More articles by this author , Albert DobiAlbert Dobi More articles by this author , and Shiv SrivastavaShiv Srivastava More articles by this author View All Author Informationhttps://doi.org/10.1016/S0022-5347(09)61440-3AboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissionsReprints ShareFacebookLinked InTwitterEmail "PMEPA1-AR DEGRADATION PATHWAY: A NEW MECHANISM FOR THE REGULATION OF ANDROGEN RECEPTOR IN PROSTATE CANCER." The Journal of Urology, 181(4S), p. 510 © 2009 by American Urological AssociationFiguresReferencesRelatedDetails Volume 181Issue 4SApril 2009Page: 510 Advertisement Copyright & Permissions© 2009 by American Urological AssociationMetricsAuthor Information Eliza Raymundo More articles by this author Li Hongyun More articles by this author Linda Xu More articles by this author Katsuaki Masuda More articles by this author David G McLeod More articles by this author Albert Dobi More articles by this author Shiv Srivastava More articles by this author Expand All Advertisement PDF downloadLoading ...
Structure in differential transfer ionization: A Thomas resonance? (1996)

The differential cross section for Ar(e + , Ps e − )Ar ++ was measured for the first time. The outgoing Ps atom was detected in time correlation with the Ar ++ ion to identify this particular cross section. At an emission angle of 45°, a distinct dip in this transfer ionization, the formation of Ps combined with the ejection of an electron, was observed. The width of this structure is not wider than our effective angular acceptance of ±2.5°. No such feature is observed in the transfer reaction, usually referred to as Ps formation. Thomas scattering is suggested as a possible cause for this phenomenon.
Aquaporin-4–binding autoantibodies in patients with neuromyelitis optica impair glutamate transport by down-regulating EAAT2 (2008)

Neuromyelitis optica (NMO)-immunoglobulin G (IgG) is a clinically validated serum biomarker that distinguishes relapsing central nervous system (CNS) inflammatory demyelinating disorders related to NMO from multiple sclerosis. This autoantibody targets astrocytic aquaporin-4 (AQP4) water channels. Clinical, radiological, and immunopathological data suggest that NMO-IgG might be pathogenic. Characteristic CNS lesions exhibit selective depletion of AQP4, with and without associated myelin loss; focal vasculocentric deposits of IgG, IgM, and complement; prominent edema; and inflammation. The effect of NMO-IgG on astrocytes has not been studied. In this study, we demonstrate that exposure to NMO patient serum and active complement compromises the membrane integrity of CNS-derived astrocytes. Without complement, astrocytic membranes remain intact, but AQP4 is endocytosed with concomitant loss of Na(+)-dependent glutamate transport and loss of the excitatory amino acid transporter 2 (EAAT2) . Our data suggest that EAAT2 and AQP4 exist in astrocytic membranes as a macromolecular complex. Transport-competent EAAT2 protein is up-regulated in differentiating astrocyte progenitors and in nonneural cells expressing AQP4 transgenically. Marked reduction of EAAT2 in AQP4-deficient regions of NMO patient spinal cord lesions supports our immunocytochemical and immunoprecipitation data. Thus, binding of NMO-IgG to astrocytic AQP4 initiates several potentially neuropathogenic mechanisms: complement activation, AQP4 and EAAT2 down-regulation, and disruption of glutamate homeostasis.
Temperature dependence of ultrasonic backscattered energy in images compensated for tissue motion (2004)

Noninvasive temperature imaging would enhance the ability to uniformly heat tumors at therapeutic levels. Ultrasound is an attractive modality for this purpose. Previously, we predicted monotonic changes in ultrasonic backscattered energy (CBE) for certain sub wavelength scatterers. We measured CBE values similar to our predictions in bovine liver, turkey breast, and pork rib in 1D. Those measurements were corrected manually for changes in the axial position of scatterers with temperature. To investigate the effect of temperature on CBE in 2D, we imaged 1-cm thick samples of bovine liver during heating in a water bath from 37 to 50/spl deg/C. Images were formed by a Terason 2000 imager with a 7 MHz linear probe. Employing RF signals from the Terason 2000 (courtesy Teratech Corp.) permitted the use of cross-correlation as a similarity measure for automatic tracking of feature displacement as a function of temperature. Tissue motion across the specimen was non-uniform with typical total displacements of 0.5 to 1 mm in both axial and lateral directions. Tissue motion in 8 image regions was tracked from 37 to 50/spl deg/C in 0.5/spl deg/C steps. Motion compensated image regions were demodulated with the Hilbert transform and smoothed with a 3/spl times/3 running average filter before forming the backscattered energy at each pixel. Our measure of CBE compared means of both the positive and negative changes in the BE images. CBE changed monotonically by about 4 dB at 50/spl deg/C from its value at 37/spl deg/C. Relatively noise-free CBE curves from tissue volumes of less than 1 cm/sup 3/ supports the use of CBE for temperature estimation. Motion in 3D will affect CBE values, but because beam width in elevation is larger than the lateral width, effects of motion in elevation on CBE may be less. Thus, we expect CBE to support temperature estimation in 3D. Furthermore, because CBE exploits inherent tissue inhomogeneities, extension to in vivo applications is a genuine prospect.
CD26/dipeptidylpeptidase IV—chemokine interactions: double-edged regulation of inflammation and tumor biology (2016)

Post-translational modification of chemokines is an essential regulatory mechanism to enhance or dampen the inflammatory response. CD26/dipeptidylpeptidase IV, ubiquitously expressed in tissues and blood, removes NH2-terminal dipeptides from proteins with a penultimate Pro or Ala. A large number of human chemokines, including CXCL2, CXCL6, CXCL9, CXCL10, CXCL11, CXCL12, CCL3L1, CCL4, CCL5, CCL11, CCL14, and CCL22, are cleaved by CD26; however, the efficiency is clearly influenced by the amino acids surrounding the cleavage site and although not yet proven, potentially affected by the chemokine concentration and interactions with third molecules. NH2-terminal cleavage of chemokines by CD26 has prominent effects on their receptor binding, signaling, and hence, in vitro and in vivo biologic activities. However, rather than having a similar result, the outcome of NH2-terminal truncation is highly diverse. Either no difference in activity or drastic alterations in receptor recognition/specificity and hence, chemotactic activity are observed. Analogously, chemokine-dependent inhibition of HIV infection is enhanced (for CCL3L1 and CCL5) or decreased (for CXCL12) by CD26 cleavage. The occurrence of CD26-processed chemokine isoforms in plasma underscores the importance of the in vitro-observed CD26 cleavages. Through modulation of chemokine activity, CD26 regulates leukocyte/tumor cell migration and progenitor cell release from the bone marrow, as shown by use of mice treated with CD26 inhibitors or CD26 knockout mice. As chemokine processing by CD26 has a significant impact on physiologic and pathologic processes, application of CD26 inhibitors to affect chemokine function is currently explored, e.g., as add-on therapy in viral infection and cancer.
Estimates of the Energy Cost of Rifle Carriage in Biathlon Ski Skating (1987)

Elite biathletes now ski using skating techniques in place of the more traditional diagonal stride. Because of the more extreme flexion and extension of the trunk with these new techniques, it has become necessary to reevaluate the method of rifle carriage. This paper describes a model which evaluates the incremental mechanical power required to move the additional weight of the rifle through defined angular flexions and extensions of the trunk. By combining this model with actual observations of typical kinematics of trunk flexion, we can generate realistic estimates of the energy cost of rifle carriage. This approach is also used to evaluate the energy consequences of reduced rifle mass and of different rifle carriage strategies while moving with ski skating techniques. These results show that rotational kinetic energy changes are a minor part of the overall energy cost of rifle carriage, and that changes in the horizontal velocity of the rifle are the greatest source of increased cost of transport. The largest reductions in this cost, however, would come from reducing rifle mass because both potential and kinetic energies are affected. Additional but secondary reductions can be obtained by placing the rifle center of mass opposite the lumbosacral joint, thereby reducing horizontal and vertical excursions of the rifle.
FGF401 characterizing data from FGF401, A First-In-Class Highly Selective and Potent FGFR4 Inhibitor for the Treatment of FGF19-Driven Hepatocellular Cancer (2023)

&lt;p&gt;This file provides the full characterization of FGF401&lt;/p&gt;
Data from Blocking HSP90 Addiction Inhibits Tumor Cell Proliferation, Metastasis Development, and Synergistically Acts with Zoledronic Acid to Delay Osteosarcoma Progression (2023)

&lt;div&gt;Abstract&lt;p&gt;&lt;b&gt;Purpose:&lt;/b&gt; Despite recent improvements in therapeutic management of osteosarcoma, ongoing challenges in improving the response to chemotherapy warrants the development of new strategies to improve overall patient survival. Among them, HSP90 is a molecular chaperone involved in the maturation and stability of various oncogenic proteins leading to tumor cells survival and disease progression. We assessed the antitumor properties of a synthetic HSP90 inhibitor, PF4942847, alone or in combination with zoledronic acid in osteosarcoma.&lt;/p&gt;&lt;p&gt;&lt;b&gt;Experimental Design:&lt;/b&gt; The effects of PF4942847 were evaluated on human osteosarcoma cells growth and apoptosis. Signaling pathways were analyzed by Western blotting. The consequence of HSP90 therapy combined or not with zoledronic acid was evaluated in mice bearing HOS-MNNG xenografts on tumor growth, associated bone lesions, and pulmonary metastasis. The effect of PF4942847 on osteoclastogenesis was assessed on human CD14&lt;sup&gt;+&lt;/sup&gt; monocytes.&lt;/p&gt;&lt;p&gt;&lt;b&gt;Results:&lt;/b&gt; In osteosarcoma cell lines, PF4942847 inhibited cell growth in a dose-dependent manner (IC&lt;sub&gt;50&lt;/sub&gt; ±50 nmol/L) and induced apoptosis with an increase of sub-G&lt;sub&gt;1&lt;/sub&gt; fraction and cleaved PARP. These biologic events were accompanied by decreased expression of Akt, p-ERK, c-Met, and c-RAF1. When administered orally to mice bearing osteosarcoma tumors, PF4942847 significantly inhibited tumor growth by 80%, prolonged survival compared with controls, and inhibited pulmonary metastases by blocking c-Met, FAK, and MMP9 signaling. In contrast to 17-allylamino-17-demethoxygeldanamycin (17-AAG), PF4942847 did not induce osteoclast differentiation, and synergistically acted with zoledronic acid to delay osteosarcoma progression and prevent bone lesions.&lt;/p&gt;&lt;p&gt;&lt;b&gt;Conclusions:&lt;/b&gt; All these data provide a strong rationale for clinical evaluation of PF4942847 alone or in combination with zoledronic acid in osteosarcoma. &lt;i&gt;Clin Cancer Res; 22(10); 2520–33. ©2015 AACR&lt;/i&gt;.&lt;/p&gt;&lt;/div&gt;
AML Student Program Volunteer: Synthesis of Tin Phosphides. (2015)

Abstract not provided.
Synaptic Plasticity: Stairway to Memory (1995)

Since the idea that memory is associated with alterations in synaptic strength was accepted, studies on the cellular and molecular mechanisms responsible for the plastic changes in neurons have attracted wide interest in the scientific community. Recent studies on memory processes have also pointed out some unifying themes emerging from a wide range of nervous systems, suggesting that regardless of the species or brain regions, a common denominator for memory may exist. Thus, the present review attempted to create a hypothetical and universal synaptic model valid for a variety of nervous systems, ranging from molluscs to mammals. The cellular and molecular events leading to short- and long-term modifications of memory have been described in a sequential order, from the triggering signals to the gene expression, synthesis of new proteins and neuronal growth. These events are thought to represent the late phases of memory consolidation leading to persistent modifications in synaptic plasticity, thereby facilitating the permanent storage of acquired information throughout the individual's life.
Fast Three-Dimensional Modeling of Atomic Oxygen Undercutting of Protected Polymers (2004)

Covers advancements in spacecraft and tactical and strategic missile systems, including subsystem design and application, mission design and analysis, materials and structures, developments in space sciences, space processing and manufacturing, space operations, and applications of space technologies to other fields.
Single-Cell States in the Estrogen Response of Breast Cancer Cell Lines (2014)

Estrogen responsive breast cancer cell lines have been extensively studied to characterize transcriptional patterns in hormone-responsive tumors. Nevertheless, due to current technological limitations, genome-wide studies have typically been limited to population averaged data. Here we obtain, for the first time, a characterization at the single-cell level of the states and expression signatures of a hormone-starved MCF-7 cell system responding to estrogen. To do so, we employ a recently proposed model that allows for dissecting single-cell states from time-course microarray data. We show that within 32 hours following stimulation, MCF-7 cells traverse, most likely, six states, with a faster early response followed by a progressive deceleration. We also derive the genome-wide transcriptional profiles of such single-cell states and their functional characterization. Our results support a scenario where estrogen promotes cell cycle progression by controlling multiple, sequential regulatory steps, whose single-cell events are here identified.
Supplementary Figure S7 from &lt;i&gt;In Vivo&lt;/i&gt; Screening Unveils Pervasive RNA-Binding Protein Dependencies in Leukemic Stem Cells and Identifies ELAVL1 as a Therapeutic Target (2023)

&lt;p&gt;Supplemental Figure S7 shows the expression profile of TOMM34 in normal human bone marrow and across different AML and CML data sets. The effects of TOMM34 depletion on human primary AML cells in vitro and validation of TOMM34 knockdown and overexpression is shown.&lt;/p&gt;
Laser Extinction in Laminar Inverse Diffusion Flames - eScholarship (2005)

Measurements of line-of-sight laser extinction in a co-annular ethylene-air laminar inverse diffusion flame (IDF) were made to determine soot concentration. Extinction has frequently been used in the literature to measure soot concentration in normal diffusion flames (NDFs), but it has rarely been applied to IDFs. A coflow IDF contains a primary air flow surrounded by a fuel annulus. Soot particles form on the outside of IDFs, advect upward, and eventually quench without being oxidized. It has been proposed in the literature that IDFs will produce less near-flame soot than NDFs because, for flames of comparable fuel, size and flow rates, movement of soot outward into cool regions of an IDF limits its simultaneous exposure to the high temperatures and fuel pyrolysis products needed for soot growth. A two-dimensional soot concentration map of an IDF using experimental data confirms this hypothesis by showing integrated soot volume fractions to be an order of magnitude lower than those reported for NDFs in the literature. Computer simulations of particle temperature histories in an NDF and IDF of similar height lend support to these results.
Interleukin (IL) 4, in the absence of antigen stimulation, induces an anergy-like state in differentiated CD8+ TC1 cells: loss of IL-2 synthesis and autonomous proliferation but retention of cytotoxicity and synthesis of other cytokines. (1995)

Naive T cells in the periphery mainly secrete interleukin (IL) 2 upon activation. After stimulation in the presence of appropriate costimulators, both CD4+ and CD8+ T cells differentiate into effector cells secreting distinct T helper (Th) 1- and Th2-like cytokine patterns. Subsequent to differentiation, both CD4+ (Th1 and Th2) and CD8+ (TC1 and TC2) cells are stable and cannot be induced to differentiate into the opposite pattern or revert to the naive cytokine secretion pattern. We now show that IL-4 caused committed TC1 bulk populations or clones to lose the ability to synthesize IL-2. The cells retained the ability to secrete interferon (IFN) gamma, granulocyte/macrophage colony-stimulating factor, and tumor necrosis factor, did not synthesize any Th2 cytokines, and did not alter cell surface marker expression. IL-4 rapidly inhibited IL-2-synthesizing ability in the absence or presence of antigen-presenting cells, thus demonstrating that IL-4 acted directly on TC1 cells. The defect in IL-2 synthesis could not be reversed by subsequent stimulation with potent antigen-presenting cells in the presence of IL-2 and anti-IL-4, or with anti-CD3 plus anti-CD28 antibodies. Both IL-2+ and IL-2- TC1 cells were strongly cytotoxic toward allogeneic but not syngeneic targets. However, IL-2- TC1 cells were unable to proliferate unless exogenous IL-2 was provided. TC1 cells that lose IL-2 synthesis but retain IFN-gamma synthesis and cytotoxicity may be similar to the "anergic" cells induced by stimulation of CD4+ or CD8+ cells in the absence of costimulators. These results suggest that during a mixed type 1/type 2 response in vivo, IL-4 may induce the IL-2+ TC1-->IL-2-TC1 conversion, and thus curtail the expansion of the TC1 response without impairing short-term effector function.
The Expression of Chemokine Genes Correlates with Nuclear Factor-??B Activation in Human Pancreatic Cancer Cell Lines (2000)

Chemokines may regulate the process of immune cell infiltration that is often found in pancreatic cancer. In this study, we investigated the secretion of the chemokines [interleukin (IL)-8, monocyte chemoattractant protein (MCP)-1, and RANTES (regulated on activation, normal T cell expressed and secreted)] in human pancreatic cancer cell lines. The chemokine secretion in three pancreatic cancer cell lines (PANC-1, MIA PaCa-2, and BxPC-3) was evaluated by enzyme-linked immunosorbent assay (ELISA) and Northern blot, and the activation of nuclear factor-kappaB (NF-kappaB) and NF-IL6 was assessed by an electrophoretic gel mobility shift assay (EMSA). Without any stimulation, IL-8 secretion was detected in all cell lines, and MCP-1 secretion was detected in PANC-1 and MIA PaCa-2 cells. However, RANTES secretion was not detected in all cells. The addition of IL-1beta and tumor necrosis factor (TNF)-alpha strongly enhanced IL-8, MCP-1, and RANTES secretion; these responses were observed at the mRNA level as well as at the protein level. IL-1beta and TNF-alpha induced a rapid activation of nuclear factor (NF)-kappaB in PANC-1 cells, and the increase in chemokine mRNA expression correlated with NF-kappaB activation. The activation of NF-IL6 was modest. A blockade of NF-kappaB activation by TPCK markedly reduced the IL-1beta- and TNF-alpha-induced chemokine gene expression. Our findings indicate that chemokines are produced by pancreatic cancer cells, and suggest that these factors may contribute to the accumulation of tumor-associated immune cells. In addition, the transcriptional activation of chemokine genes in pancreatic cancer cells may be closely associated with NF-kappaB activation.
&lt;title&gt;Observations of MeV electrons and scattered light from intense subpicosecond laser-plasma interactions&lt;/title&gt; (1993)

In this paper we will present work in progress in our experimental investigation of the coupling of intense, sub-picosecond laser pulses with plasmas preformed on solid targets. (This situation is to be contrasted with the interaction of intense laser fields with solid-density matter, a subject which has generated considerable interest in the last several years.) We will discuss our characterization of the energy distribution of energetic electrons which escape a solid target irradiated by an intense laser. We have also performed experiments to study the excitation of parametric instabilities near the quarter-critical layer and second-harmonic generation near the critical layer in the plasma. We will discuss some preliminary scattered light spectroscopy measurements. Other topics related to this work are discussed.