gebhart/patrepeval huggingface dataset:
Markov Random Fields for Improving 3D Mesh Analysis and Segmentation (2008)

Mesh analysis and clustering have became important issues in order to improve the efficiency of common processing operations like compression, watermarking or simplification. In this context we present a new method for clustering / labeling a 3D mesh given any field of scalar values associated with its vertices (curvature, density, roughness etc.). Our algorithm is based on Markov Random Fields, graphical probabilistic models. This Bayesian framework allows (1) to integrate both the attributes and the geometry in the clustering, and (2) to obtain an optimal global solution using only local interactions, due to the Markov property of the random field. We have defined new observation and prior models for 3D meshes, adapted from image processing which achieve very good results in terms of spatial coherency of the labeling. All model parameters are estimated, resulting in a fully automatic process (the only required parameter is the number of clusters) which works in reasonable time (several seconds).
Wang et al 2018 "Nuclear entry and export of FIH are mediated by HIF1α and exportin1, respectively" (2021)

Data supporting the repeat of Figure 3A, Wang et al 2018, Journal of Cell Science, "Nuclear entry and export of FIH are mediated by HIF1α and exportin1, respectively" Microscopy images and mycoplasma testing results.
Vitronectin decreases microvascular endothelial cell apoptosis (1998)

Angiogenesis after tissue injury occurs in a matrix environment consisting of fibrin, fibronectin, and vitronectin as the major extracellular matrix (ECM) constituents. ECM-integrin interactions is critical for angiogenesis and failure to bind a ligand to certain integrin receptors (alpha[v]beta3 or alpha[v]beta5) inhibits angiogenesis. The ligand that binds to alpha(v)beta3 or alpha(v)beta5 integrin receptors during microvascular angiogenesis has not been identified. Our hypothesis is that provisional matrix molecules provide the environmental context cues to microvascular endothelial cells and promote angiogenesis by decreased programmed cell death. Using cultured human microvascular endothelial cells, we show that vitronectin, in comparison to growth on alternative provisional matrix molecules (fibronectin, fibrinogen plus thrombin), collagen I, and basement membrane molecules (collagen IV), significantly reduces microvascular endothelial cell death in vitro. This reduction was observed using morphologic criteria, TdT-mediated dUTP nick end labeling (TUNEL) assay, histone release into the cytoplasm, and thymidine release into the supernatant. Though our data confirm that vitronectin may bind to more than one integrin receptor to reduce MEC apoptosis, binding to the alpha(v) component appears to be the critical integrin subcomponent for reducing apoptosis.
Droplets and Bubbles in Microfluidic Devices (2015)

Precise, tunable emulsions and foams produced in microfluidic geometries have found wide application in biochemical analysis and materials synthesis and characterization. Superb control of the volume, uniformity, and generation rate of droplets and bubbles arises from unique features of the microscale behavior of fluid interfaces. Fluid interfaces confined within microfluidic channels behave quite differently than their counterparts in unbounded flows. Confinement inhibits capillary instabilities so that breakup occurs by largely quasi-static mechanisms. The three-dimensional flow near confined interfaces in rectangular geometries and feedback effects from resistance changes in the entire microfluidic network play important roles in regulating the interfacial deformation. Timescales for transport of surfactants and particles to interfaces compete with flow timescales at the microscale, providing further opportunity for tuning the interfacial coverage and properties of individual droplets and bubbles.
Evolving Concepts of Apoptosis in Idiopathic Pulmonary Fibrosis (2006)

Idiopathic pulmonary fibrosis (IPF) is a chronic, relentlessly progressive fibrosing disease of the lung of unknown etiology. Significant progress has been made in recent years in elucidating key aspects of the pathobiology of IPF. Insights into disease pathogenesis have come from studies of cell biology, growth factor/cytokine signaling, animal models of pulmonary fibrosis, and human IPF cells and tissue. A consistent finding in the ultrastructural pathology of IPF is alveolar epithelial cell injury and apoptosis. Another consistent finding in the histopathology of human IPF, described as usual interstitial pneumonia, is the accumulation of aggregates of myofibroblasts in fibroblastic foci. The extent or profusion of fibroblastic foci in lung biopsies is strongly correlated with increased mortality in patients with IPF. There is emerging evidence that myofibroblasts in IPF/usual interstitial pneumonia, both in the in vivo microenvironment and during the process of differentiation in vitro, acquire resistance to apoptosis. Here, we review the current evidence and mechanisms for this apparent "apoptosis paradox" in the pathogenesis of IPF.
Failure of SCID-X1 gene therapy in older patients (2005)

Gene therapy has been shown to be a highly effective treatment for infants with typical X-linked severe combined immunodeficiency (SCID-X1, gammac-deficiency). For patients in whom previous allogeneic transplantation has failed, and others with attenuated disease who may present later in life, the optimal treatment strategy in the absence of human leukocyte antigen (HLA)-matched donors is unclear. Here we report the failure of gene therapy in 2 such patients, despite effective gene transfer to bone marrow CD34(+) cells, suggesting that there are intrinsic host-dependent restrictions to efficacy. In particular, there is likely to be a limitation to initiation of normal thymopoiesis, and we therefore suggest that intervention for these patients should be considered as early as possible.
The New Element Californium (Atomic Number 98) (1950)

Definite identification has been made of an isotope of the element with atomic number 98 through the irradiation of ${\mathrm{Cm}}^{242}$ with about 35-Mev helium ions in the Berkeley Crocker Laboratory 60-inch cyclotron. The isotope which has been identified has an observed half-life of about 45 min. and is thought to have the mass number 244. The observed mode of decay of ${98}^{244}$ is through the emission of alpha-particles, with energy of about 7.1 Mev, which agrees with predictions. Other considerations involving the systematics of radioactivity in this region indicate that it should also be unstable toward decay by electron capture.The chemical separation and identification of the new element was accomplished through the use of ion exchange adsorption methods employing the resin Dowex-50. The element 98 isotope appears in the ekadysprosium position on elution curves containing berkelium and curium as reference points---that is, it precedes berkelium and curium off the column in like manner that dysprosium precedes terbium and gadolinium. The experiments so far have revealed only the tripositive oxidation state of eka-dysprosium character and suggest either that higher oxidation states are not stable in aqueous solutions or that the rates of oxidation are slow.The successful identification of so small an amount of an isotope of element 98 was possible only through having made accurate predictions of the chemical and radioactive properties.
Angiotensin-(1–7) inhibits growth of cardiac myocytes through activation of themasreceptor (2005)

Peptide hormones such as ANG II and endothelin contribute to cardiac remodeling after myocardial infarction by stimulating myocyte hypertrophy and myofibroblast proliferation. In contrast, angiotensin-(1-7) [ANG-(1-7)] infusion after myocardial infarction reduced myocyte size and attenuated ventricular dysfunction and remodeling. We measured the effect of ANG-(1-7) on protein and DNA synthesis in cultured neonatal rat myocytes to assess the role of the heptapeptide in cell growth. ANG-(1-7) significantly attenuated either fetal bovine serum- or endothelin-1-stimulated [(3)H]leucine incorporation into myocytes with no effect on [(3)H]thymidine incorporation. [d-Ala(7)]-ANG-(1-7), the selective ANG type 1-7 (AT(1-7)) receptor antagonist, blocked the ANG-(1-7)-mediated reduction in protein synthesis in cardiac myocytes, whereas the AT(1) and AT(2) angiotensin peptide receptors were ineffective. Serum-stimulated ERK1/ERK2 mitogen-activated protein kinase activity was significantly decreased by ANG-(1-7) in myocytes, a response that was also blocked by [d-Ala(7)]-ANG-(1-7). Both rat heart and cardiac myocytes express the mRNA for the mas receptor, and a 59-kDa immunoreactive protein was identified in both extracts of rat heart and cultured myocytes by Western blot hybridization with the use of an antibody to mas, an ANG-(1-7) receptor. Transfection of cultured myocytes with an antisense oligonucleotide to the mas receptor blocked the ANG-(1-7)-mediated inhibition of serum-stimulated MAPK activation, whereas a sense oligonucleotide was ineffective. These results suggest that ANG-(1-7) reduces the growth of cardiomyocytes through activation of the mas receptor. Because ANG-(1-7) is elevated after treatment with angiotensin-converting enzyme inhibitors or AT(1) receptor blockers, ANG-(1-7) may contribute to their beneficial effects on cardiac dysfunction and ventricular remodeling after myocardial infarction.
House Banks in Out-of-court Reorganization: Evidence from Austria (2020)

The main purpose of this article is to study the role of house banks in out-of-court reorganization. Banks are traditionally one of the most important financial resources for firms. Especially in financially difficult times like those we now face due to the coronavirus, it can make a difference whether a bank supports its clients and accompanies firms through a crisis or not. With the help of relationship lending theory, we review the existing literature on this topic. Next, based on empirical findings from Austrian banks, we derive implications for corporate practice. The empirical study covers a sample of 658 firm reorganizations in Austria. The data were collected anonymously by different banks processing the cases in their workout departments between January 2011 and December 2013. Correlation analysis and logistic regression were applied to analyze the data. The findings indicate that house banks, despite their relationship of trust, must be critical in their assessment of reorganization projects due to the danger of zombie lending. The four most important prerequisites for completing an out-of-court reorganization were a new loan, an open and proactive communication policy on the part of the distressed company, management changes, and a financial contribution from existing shareholders. The findings show that bank-supported out-of-court reorganization has a high probability of success. A recommendation to entrepreneurs is to respond rapidly to financial distress and maintain open communication with stakeholders, in particular banks. The findings indicate that the implementation of Directive (EU) 2019/1023 on preventive restructuring frameworks in the European Union is crucial to enable bank-led reorganizations.
The Role of NFAT in Osteoclast Formation (2007)

Osteoclasts are cells of monocyte-macrophage origin that degrade bone matrix. Receptor activator of NF-kappaB ligand (RANKL) induces osteoclast formation in the presence of macrophage-colony-stimulating factor (M-CSF) and costimulatory signals. RANKL induces activation of the TNF receptor-associated factor 6 (TRAF6) and c-Fos pathways, which lead to the osteoclast-specific event, that is, autoamplification of nuclear factor of activated T cells (NFAT)c1, the master transcription factor for osteoclast differentiation. Autoamplification of NFATc1 is dependent on the calcium signaling of immunoglobulin-like receptors associated with immunoreceptor tyrosine-based activation motif (ITAM)-harboring adaptors. In addition to the calcineurin-NFATc1 axis, calcium signaling activates the calmodulin-dependent kinase pathway, which also plays a critical role in osteoclast formation. Such advances in the understanding of the molecular mechanism of osteoclast differentiation are expected to lead to novel therapeutic approaches to bone diseases.
Pore structure and swelling behavior of porous hydrogels prepared via a thermal reverse‐casting technique (2011)

Abstract In this work, we investigated the design and fabrication of porous polyacrylamide hydrogels via a thermal reverse‐casting technique. The porous hydrogels were prepared by the free‐radical crosslinking polymerization of the monomer solution within the space of an agarose gel, which after the setting of the chemical gel, was removed to allow for the formation of an interconnected porosity pathway. Two different agarose/monomer solution ratios were selected to modulate the porosity of the hydrogels, and the as‐obtained samples were characterized in terms of their chemical structure, morphology, thermal properties, and swelling behavior in different ionic strength solutions. The results of this study demonstrate that the reverse‐casting process enhanced the solvent‐retaining capability of the hydrogels and that their swelling ratio increased with increasing concentration of the agarose solution in the initial formulation. All of these results finally demonstrate that the pore structure features played a key role in defining the swelling behavior of the hydrogels. © 2011 Wiley Periodicals, Inc. J Appl Polym Sci, 2011
An adaptive Volterra predistorter for the linearization of RF high power amplifiers (2002)

An efficient digital baseband predistortion linearizer is presented to compensate for nonlinear distortions induced by RF high power amplifiers in wireless communication systems. The proposed approach utilizes an indirect learning architecture with a fast recursive least squares (RLS) filtering algorithm, implemented using V-vector algebra, to update the coefficients of a Volterra-based predistorter. There is no requirement for an initial identification of the nonlinear characteristics of HPA as in linearizers based on conventional pth-order inverse methods. Simulation results show that that good performance and low computational complexity are achieved in the linearization of both narrow and wide bandwidth systems.
Characterization of the Polyomavirus Late Polyadenylation Signal (1995)

The polyomavirus late polyadenylation signal is used inefficiently during the late phase of a productive viral infection. Inefficient polyadenylation serves an important purpose for viral propagation, as it allows a splicing event that stabilizes late transcripts (G. R. Adami, C. W. Marlor, N. L. Barrett, and G. G. Carmichale, J. Virol. 63:85-93, 1989; R. P. Hyde-DeRuyscher and G. G. Carmichael, J. Virol. 64:5823-5832, 1990). We have recently shown that late-strand readthrough transcripts serve as natural antisense molecules to downregulate early-strand RNA levels at late times in infection (Z. Liu, D. B. Batt, and G. G. Carmichael, Proc. Natl. Acad. Sci. USA 91:4258-4262, 1994). Thus, poor polyadenylation contributes to the early-late switch by allowing the formation of more stable late RNAs and by forming antisense RNA to early RNAs. The importance of late poly(A) site inefficiency in the viral life cycle has prompted us to map the cis elements of this site. Since the polyomavirus late site proved a poor substrate for in vitro polyadenylation, we used an in vivo assay which allowed us to map the cis sequences required for its function. In this assay, various fragments containing the AAUAAA and different surrounding sequences were placed 1.4 kb upstream of a second, wild-type signal. The second signal served to stabilize transcripts that are not processed at the upstream site, allowing accurate quantitation of relative poly(A) site use by an RNase protection assay. Processing was primary at the upstream site when a large fragment surrounding the poly(A) signal (50 nucleotides [nt] upstream and 90 nt downstream) was tested in this assay, demonstrating that this fragment contains the essential cis elements. Deletion analysis of this fragment revealed that most but not all upstream sequences can be removed with little effect on polyadenylation efficiency, indicating the absence of a strong stimulatory upstream element. Deletion of all but 25 nt downstream of the AAUAAA reduced polyadenylation activity only by half, demonstrating that processing can occur at this site despite the lack of downstream sequences. Thus, the core cis element for polyadenylation is quite small, with most important cis-acting elements lying within 19 nt upstream and 25 nt downstream of the AAUAAA sequence. This core contains the AAUAAA hexanucleotide, an upstream A/U-rich element, and three identical repeats of a 6-nt sequence, UAUUCA. Polyadenylation was eliminated or greatly reduced when either the AAUAAA or the three repeats were mutated.
Sialyllactose-mediated Cell Interaction during Granulosa Cell Differentiation (1995)

The present study was designed to prove the carbohydrate-binding proteins interacting with cell surface sialyllactosylceramide (GM3, NeuAc alpha 2-->3Gal beta 1-->4Glc beta 1-->1'Cer), which is highly expressed during differentiation of rat ovarian granulosa cells. As a specific ligand for the sialyllactose (SL)-binding proteins on granulosa cells, we used a radioiodinated multivalent SL-linked albumin (Alb-(SL)17). The specific association of the ligand to the putative proteins on the intact cells was competitively inhibited by GM3 more effectively than other gangliosides, sialyllactotetraosylceramide, sialylneolactotetraosylceramide, and several glycoproteins with N-linked oligosaccharides. However, the proteins had no specificity for the side chain (N-acetyl or N-glycolyl forms) of sialic acid in GM3. Scatchard analysis of Alb-(SL)17 binding showed high (Kd = 6.4 x 10(-10)M) and low (Kd = 3.1 x 10(-8)M) affinity population of binding sites. By direct binding of 125I-Alb-(SL)17 to SL-binding proteins on Western blots, the putative proteins with molecular masses of 35, 18, and 14 kDa were detected. The interaction of the multivalent derivative with these binding proteins was differently modulated by Ca2+ and Mn2+. The SL-binding proteins occurred in immature granulosa cells and progressively decreased during differentiation, whereas their endogenous ligand GM3 increased. These results indicate that relatively low molecular weight SL-binding proteins exist on the surface of immature granulosa cells and that they may serve as receptor sites for newly synthesized GM3 during differentiation.
iMOSFLM: a new graphical interface for diffraction-image processing withMOSFLM (2011)

iMOSFLM is a graphical user interface to the diffraction data-integration program MOSFLM. It is designed to simplify data processing by dividing the process into a series of steps, which are normally carried out sequentially. Each step has its own display pane, allowing control over parameters that influence that step and providing graphical feedback to the user. Suitable values for integration parameters are set automatically, but additional menus provide a detailed level of control for experienced users. The image display and the interfaces to the different tasks (indexing, strategy calculation, cell refinement, integration and history) are described. The most important parameters for each step and the best way of assessing success or failure are discussed.
Activation of protein kinase C family members by the novel polyphosphoinositides PtdIns-3,4-P2 and PtdIns-3,4,5-P3. (1994)

The effect of phosphoinositides on the activity of protein kinase C (PKC) isotypes was investigated. PKC alpha, beta I, beta II, gamma, delta, epsilon, eta, and zeta were expressed in baculovirus-infected insect cells and purified by column chromatography. The calcium-activated PKC isotypes alpha, beta I, beta II, and gamma were not significantly activated by any of the phosphoinositides investigated (phosphatidylinositol-4-phosphate (PtdIns-4-P), PtdIns-3-P, PtdIns-4,5-P2, PtdIns-3,4-P2, and PtdIns-3,4,5-P3) when added in the presence of concentrations of phosphatidylserine that give maximal stimulation. The calcium-insensitive PKC isotypes delta, epsilon, and theta also showed little response to PtdIns-3-P, PtdIns-4-P, or PtdIns-4,5-P2 when these lipids were added in the presence of phosphatidylserine. In contrast, PtdIns-3,4-P2 and PtdIns-3,4,5-P3 caused a 5-15-fold stimulation of these enzymes compared with phosphatidylserine alone. 50% maximal stimulation of PKC epsilon by PtdIns-3,4,5-P3 occurred when this lipid was present at about 1% of the carrier PtdIns-4,5-P2 (about 100 nM). These lipids had little effect on baculovirus-expressed PKC zeta, which was constitutively active. A short chain version of PtdIns-3,4,5-P3, dioctanoyl-PtdIns-3,4,5-P3, activated PKC delta, epsilon, and eta in the absence of other lipids, whereas a short chain version of PtdIns-4,5-P2, dihexanoyl-PtdIns-4,5-P2, did not. Since PtdIns-3,4-P2 and PtdIns-3,4,5-P3 are nominally absent in unstimulated cells and appear within seconds to minutes of stimulation by various cell activators, these lipids could act as second messengers to activate PKC delta, epsilon, or eta in vivo.
MRI as a marker for disease heterogeneity in multiple sclerosis (2005)

The inflammatory activity and destructiveness of the multiple sclerosis process are to some degree independent of each other, and the successive evaluation of both of these variables can strengthen prediction of clinical outcome in individual patients.
Prolonged subcutaneous administration of 852A, a novel systemic toll‐like receptor 7 agonist, to activate innate immune responses in patients with advanced hematologic malignancies (2012)

The toll-like receptor (TLR) 7 agonist 852A, a small-molecule imidazoquinoline, stimulates plasmacytoid dendritic cells to produce multiple cytokines. We conducted a Phase II study of 852A in patients with recurrent hematologic malignancies. The primary objective was assessing the activity of 852A administered subcutaneously twice weekly for 12 weeks. Secondary objectives were assessing the safety of 852A and its ability to activate the immune system with prolonged dosing. Patients with relapsed hematologic malignancies of any age with adequate organ function were eligible. Patients initiated dosing at 0.6 mg/m(2) twice weekly and escalated by 0.2 mg/m(2) after every two doses as tolerated to a target dose of 1.2 mg/m(2) . Patients with responses or stable disease were eligible for additional cycles. Seventeen patients (15 males) entered the study: 6 with AML, 5 ALL, 4 NHL, 1 Hodgkin's lymphoma, and 1 multiple myeloma. The mean age was 41 years (12-71 years). The median number of prior chemotherapy regimens was 5 (range = 1-14). Thirteen patients completed all 24 injections. Grade 3-4 toxicities included nausea, dyspnea, fever, myalgia, malaise, and cough. Responses included one complete response (ALL), one partial response (AML), two stable disease (AML and NHL), and 9 progressive disease. This is the first in-human hematologic malignancy trial of a subcutaneously (SC) delivered TLR7 agonist using a prolonged dosing schedule. 852A was safely administered up to 1.2 mg/m(2) twice weekly with evidence of sustained tolerability and clinical activity in hematologic malignancies. Systemic TLR agonists for the treatment of hematologic malignancies warrant further study.