gebhart/patrepeval huggingface dataset:
Sal-like protein 4 (SALL4), a stem cell biomarker in liver cancers (2012)

SALL4's expression is an indicator of stem cells, a prognostic marker in liver cancers, correlates with cell and tumor growth, with resistance to 5-FU, and its suppression results in differentiation and slowed tumor growth. SALL4 is a novel therapeutic target for liver cancers.
Characterization of cellular sources for non-quantal ACh release in mouse airways (2016)

Acetylcholine (ACh) is the major transmitter to induce contraction of the airway smooth muscle (ASM). In addition to the quantal vesicular ACh release after stimulation of parasympathetic neurons, non-quantal ACh (nqACh) release is observed in tracheal preparations after eserine treatment, which is capable to induce ASM contraction. In order to identify which cell population in the airways contributes to nqACh synthesis, expression of the choline acetyltransferase (ChAT), high affinity choline transporter-1 (CHT1), and the low-affinity choline transporter-like family (CTL1 – 5) was evaluated by RT-PCR in primary isolated vagal and dorsal root ganglia, parasympathetic neurons, tracheal epithelial cells, lymphocytes, granulocytes, and in a smooth muscle and fibroblast cell line. All evaluated cell populations expressed ChAT-, CHT1- or CTL-mRNA, respectively. ACh release was functionally investigated by using M3WT4 cells, a reporter cell line overexpressing muscarinic M3 receptors. An increase in [Ca2+]i was induced in M3WT4 cells by supernatants of eserine-treated tracheal preparations and inhibited by atropine co-application. However, supernatants of eserine-treated isolated cell populations or cells co-cultured cells with M3WT4 cells, respectively, had no effect on [Ca2+]i levels. To address the question if mast cells might contribute to nqACh release, organ bath experiments with tracheas of mast cell-deficient B6.Cg-KitW-sh/HNihrJaeBsmGlliJ mice (kindly provided by Frank Petersen, Leibniz Forschungszentrum Borstel, ARCN) were performed. ASM contraction in response to eserine in mast cell-deficient mice was unaltered in comparison to wild-type mice. In conclusion, we were able to show that many different cell populations located in the trachea express transporters and/or enzymes associated with nqACh release. The fact that we were not able identify the major source of nqACh may be due to a low sensitivity of the M3WT4 cell assay. Alternatively, the possibility that the effect of nqACh-dependent ASM contraction is the sum of low-level ACh released from different cell populations has to be discussed.
Late reverberant spectral variance estimation using acoustic channel equalization (2015)

In many single- and multi-channel speech dereverberation methods an estimate of the late reverberant spectral variance (LRSV) is required. Contrary to LRSV estimators based on room acoustical properties, such as reverberation time, or based on isotropic models of the reverberant sound field, in this paper we propose to use acoustic channel equalization with estimated room impulse responses (RIRs) for LRSV estimation. Unlike the typical application of acoustic channel equalization, where the objective is to estimate the anechoic or the early reverberant speech component, here the late reverberant part of the estimated RIR is set as the target response. The combination of the proposed LRSV estimator with a beamformer and a spectral gain aims at a tradeoff between the performance of acoustic channel equalization and the robustness of methods based on models of the reverberant sound field. The performance, evaluated for different levels of RIR estimation error, is compared to the results obtained using a maximum likelihood estimator (MLE) of the LRSV, based on an isotropic model of the reverberant sound field, and to a state-of-the-art acoustic channel equalization method. Experimental results for different acoustic scenarios show that for medium levels of RIR estimation errors the proposed method outperforms acoustic channel equalization as well as the maximum-likelihood LRSV estimator in terms of instrumental speech quality measures.
A single germline VH gene segment of normal A/J mice encodes autoantibodies characteristic of systemic lupus erythematosus. (1986)

These experiments tested the hypothesis that unmutated germline genes from normal mice can encode autoantibodies. We found that the unmutated VHIdCR gene segment, which encodes a large proportion of antiarsonate antibodies in A/J mice, also encodes antibodies with the ability to bind to DNA and cytoskeletal proteins. After Ars immunization, at a time when the VHIdCR gene segment mutates and antibody affinity for the hapten increases, reactivity with the autoantigens was lost. Six antibodies obtained after immunization with Ars bound both the Ars and DNA. Results of competitive inhibition assays suggested that the same variable region site in the antibodies bound to both Ars and DNA. The properties of the individual germline-encoded antibodies, which include reactivity to both DNA and cytoskeletal proteins, suggest that autoantibodies characteristic of SLE might be a subset of antibodies encoded by unmutated germline V genes.
Discovery of Fragment-Derived Small Molecules for in Vivo Inhibition of Ketohexokinase (KHK) (2017)

Increased fructose consumption and its subsequent metabolism have been implicated in hepatic steatosis, dyslipidemia, obesity, and insulin resistance in humans. Since ketohexokinase (KHK) is the principal enzyme responsible for fructose metabolism, identification of a selective KHK inhibitor may help to further elucidate the effect of KHK inhibition on these metabolic disorders. Until now, studies on KHK inhibition with small molecules have been limited due to the lack of viable in vivo pharmacological tools. Herein we report the discovery of 12, a selective KHK inhibitor with potency and properties suitable for evaluating KHK inhibition in rat models. Key structural features interacting with KHK were discovered through fragment-based screening and subsequent optimization using structure-based drug design, and parallel medicinal chemistry led to the identification of pyridine 12.
The assumed light direction for perceiving shape from shading (2008)

Figure 1: The shading of an object’s surface depends on the light source direction. The light is directed from the viewpoint in the left image, from 22 deg above the viewpoint in the middle image, and from 44 deg above the viewpoint in the right image. The object is positioned identically in each of the three views. In this paper, we present an experiment designed to test how shape perception is affected by changing the angle of the light direction. We found the lighting used in the center image led to the most accurate estimations of 3D shape. Recovering 3D shape from shading is an ill-posed problem that the visual system can solve only by making use of additional information such as the position of the light source. Previous research has shown that people tend to assume light is above and slightly to the left of the object [Sun and Perona 1998]. We present a study to investigate whether the visual system also assumes the angle between the light direction and the viewing direction. We conducted a shape perception experiment in which subjects estimated surface orientation on smooth, virtual 3D shapes displayed monocularly using local Lambertian shading without cast shadows. We varied the angle between the viewing direction and the light direction within a range +/- 66 deg (above/below), and subjects indicated local surface orientation by rotating a gauge figure to appear normal to the surface [Koenderink et al. 1992]. Observer settings were more accurate and precise when the light was positioned above rather than below the viewpoint. Additionally, errors were minimized when the angle between the light direction and the viewing direction was 20-30 deg. Measurements of surface slant and tilt error support this result. These findings confirm the light-from-above prior and provide evidence that the angle between the viewing direction and the light direction is assumed to be 20-30 deg above the viewpoint. Keywords: Shape-from-shading, light-from-above, shape perception, Lambertian shading. 1
Education case report: CAMPEP Medical Physics PhD education program within Engineering (2023)

Medical physics doctoral programs have large variations in organization, administration and financing. Blending a medical physics stream into an engineering graduate program has advantages of pre-existing financial and educational infrastructures. A case study of the accredited program at Dartmouth was carried out, analyzing operational, financial, educational and outcome features. The support structures provided by each institutional partner were outlined, including engineering school, graduate school, and radiation oncology. The initiatives undertaken by founding faculty were reviewed, along with allocated resources, financial model, and peripheral entrepreneurship activities, each with quantitative outcome metrics. Currently 14 PhD students are enrolled, supported by 22 faculty across both engineering and clinical departments. The total peer-reviewed publications are ≈75/year, while the conventional medical physics fraction of this is about 14/year. Following program formation, a significant rise was seen in jointly published papers between engineering and medical physics faculty, up from 5.6 to 13.3 papers/year, with students publishing an average of 11.3/person with 5.7/person as first author. Student support was predominantly via federal grants, with a stable $5.5million/year, using about $610K/year supporting student stipends and tuition. First year funding, recruiting and staff support were via engineering school. Faculty teaching effort was supported by agreement with each home department, and student services were provided by engineering and graduate schools. Student outcomes were exceptional, with high numbers of presentations, awards, and residency placements at research universities. The lack of financial and student support in medical physics can be mitigated by this hybrid design of blending medical physics doctoral students into an engineering graduate program, providing complementary strengths. Future growth in medical physics programs might consider following this pathway, strengthening research collaborations for clinical physics and engineering faculty, as long as there is vested commitment to teach by the faculty and department leadership.
Don Luigi Sturzo—Christian Democrat (1945)

The future government of Italy portends a challenge of enormous magnitude for the Catholic Church. Subject as it has been to periodic attacks for reactionism, the Church has been hard pressed to throw off the stigma of its association with Franco in Spain and its willingness to deal with Mussolini's Fascist régime. In the light of these accusations, coupled with rather widespread doubt whether church orthodoxy is compatible with political democracy, it seems altogether appropriate to examine the political theories of one of the leading exponents of liberal Catholicism—Don Luigi Sturzo. A little over twenty years ago, foreign correspondents, eagerly seeking a label for the “mystery man of Italian politics,” referred to him as a clerical socialist. If the term “clerical socialism” is synonymous with Christian socialism, such a characterization might be a proper one for this Sicilian priest. Certainly Sturzo was a champion of the Christian socialist movement which urged the correction of economic injustices but decried the materialism of the Marxists. He approved of the Guild of St. Mathew's sympathy for the unionism and socialism of the nineties and the Roman Catholic Social Guild. The latter found its incentive in the papal encyclical Rerum Novarum and the “scholastic traditions in restraint of usury and economic injustice.” Both of these organizations were associated with Christian socialism. But, although Christian socialism and clerical socialism have occasionally been placed in the same category, the latter is too ambiguous a term to permit a precise classification.
Supplementary Figures 1-9, Table 1 from hsa-miR-191 Is a Candidate Oncogene Target for Hepatocellular Carcinoma Therapy (2023)

Supplementary Figures 1-9, Table 1 from hsa-miR-191 Is a Candidate Oncogene Target for Hepatocellular Carcinoma Therapy
Conductive Atomic Force Microscope Nanopatterning of Epitaxial Graphene on SiC(0001) in Ambient Conditions (2011)

Conductive atomic force microscope (cAFM) nanopatterning is demonstrated on epitaxial graphene on SiC (0001) under ambient conditions. Nanopatterning kinetics and chemistry suggest that ambient cAFM nanopatterning induces local oxidization with the surface, interface, and bulk layers of epitaxial graphene on SiC (0001) playing distinct roles in the depth profile of the final nanopatterned structure.
NEAT1 is Required for the Expression of the Liver Cancer Stem Cell Marker CD44 (2020)

CD44, a cancer stem cell (CSC) marker, is required for maintaining CSC properties in hepatocellular carcinoma (HCC). Nuclear enriched abundant transcript 1 (NEAT1), a long noncoding RNA (lncRNA), is an oncogenic driver in HCC. In the present study, we investigated the significance of the <i>NEAT1</i> gene in association with CD44 expression in liver CSCs of human HCC cell lines. The CSC properties were evaluated by spheroid culture, CSC marker expression, and sensitivity to anti-cancer drugs. The expression of both NEAT1 variant 1 (NEAT1v1) and variant 2 (NEAT1v2) as well as CD44 was significantly increased in the spheroid culture, compared with that in monolayer culture. Overexpression of Neat1v1, but not Neat1v2, enhanced the CSC properties, while knockout of the NEAT1 gene suppressed them. CD44 expression was increased by the overexpression of Neat1v1 and abrogated by NEAT1 knockout. The overexpression of NEAT1v1 restored the CSC properties and CD44 expression in NEAT1-knockout cells. NEAT1v1 expression in HCC tissues was correlated with poor prognosis and CD44 expression. These results suggest that NEAT1v1 is required for CD44 expression. To our surprise, NEAT1v1 also restored the CSC properties even in CD44-deficient cells, suggesting that NEAT1v1 maintains the properties of CSCs in a CD44-independent manner.
Inhibition of yes‐associated protein down‐regulates PD‐L1 (CD274) expression in human malignant pleural mesothelioma (2018)

Although tumour PD-L1 (CD274) expression had been used as a predictive biomarker in checkpoint immunotherapy targeting the PD1/PD-L1 axis in various cancers, the regulation of PD-L1 (CD274) expression is unclear. Yes-associated protein (YAP), an important oncogenic protein in Hippo signalling pathway, reportedly promotes cancer development. We investigated whether inhibition of YAP down-regulates PD-L1 (CD274) in human malignant pleural mesothelioma (MPM). Western blotting showed that 2 human MPM cell lines (H2052 and 211H) had increased PD-L1 protein expression compared to H290, MS-1 and H28 cells. In H2052 and 211H cells, PD-L1 mRNA expression was significantly increased compared to other MPM cell lines; YAP knockdown by small interfering RNA decreased PD-L1 protein and mRNA expression. Forced overexpression of the YAP gene increased PD-L1 protein expression in H2452 cells. Chromatin immunoprecipitation (ChIP) assay showed the precipitation of PD-L1 enhancer region encompassing 2 putative YAP-TEAD-binding sites in H2052 cells. We found that, in human MPM tissue microarray samples, YAP and PD-L1 concurrently expressed in immunohistochemistry stain (n = 70, P < .05, chi-square). We conclude that PD-L1 is correlated with YAP expression, and inhibition of YAP down-regulates PD-L1 expression in human MPM. Further study of how YAP regulates PD-L1 in MPM is warranted.
Studies of Human MDR1-MDR2 Chimeras Demonstrate the Functional Exchangeability of a Major Transmembrane Segment of the Multidrug Transporter and Phosphatidylcholine Flippase (1999)

P-glycoprotein (P-gp), encoded by the MDR1 gene, is a plasma membrane transporter which effluxes a large number of structurally nonrelated hydrophobic compounds. The molecular basis of the broad substrate recognition of P-gp is not well understood. Despite the 78% amino acid sequence identity of the MDR1 and MDR2 transporter, MDR2, which has been identified as a phosphatidylcholine transporter, does not transport most MDR1 substrates. The structural and functional differences between MDR1 and MDR2 provide an opportunity to identify the residues essential for the broad substrate spectrum of MDR1. Using an approach involving exchanging homologous segments of MDR1 and MDR2 and site-directed mutagenesis, we have demonstrated that MDR1 residues Q330, V331, and L332 in transmembrane domain 6 are sufficient to allow an MDR2 backbone in the N-terminal half of P-gp to transport several MDR1 substrates, including bisantrene, colchicine, vinblastine, and rhodamine-123. These studies help define some residues important for multidrug transport and indicate the close functional relationship between the multidrug transporter (MDR1) and phosphatidylcholine flippase (MDR2).
SPPL3 regulation of Ca2+ homeostasis modulates NFAT activation during antigen-receptor stimulation in lymphocytes (50.11) (2010)

Abstract During T cell receptor signaling, activation of several transcription factors initiates new gene expression, leading to the generation of specific T cell responses. One important event in this pathway involves store-operated calcium entry (SOCE) through Ca2+-release-activated-Ca2+ (CRAC) channels, which activates the key transcription factor NFAT. Induction of this Ca2+-dependent signaling necessitates tight regulation of intracellular Ca2+ levels, and while the identification of STIM1 and CRACM1 has significantly helped elucidate how SOCE is achieved, other players in this pathway and alternative unknown pathways also controlling Ca2+ levels are not well understood. Here, we have used an expression cloning screen to identify signal peptide peptidase like 3 (SPPL3) as a novel activator of NFAT. Interestingly, SPPL3 is a polytopic membrane protein which localizes to the ER or Golgi compartment. Using Ca2+-sensitive dyes, we determined that SPPL3 overexpression elevated basal intracellular Ca2+ levels, dampened the thapsigargin-stimulated release of ER Ca2+ stores, and enhanced Ca2+ influx. SPPL3-mediated NFAT activation was blocked by the SOCE inhibitor SKF 96365 and a dominant negative CRACM1. By influencing intracellular Ca2+ levels, SPPL3 appears to be a novel regulator of calcium homeostasis that can positively modulate antigen receptor-mediated activation of NFAT.
Method for removing a foulant from a gas stream with minimal external refrigeration (2023)

A process for removing a foulant from a gas stream. The gas stream is cooled in a series of heat exchangers, causing a portion of the foulant to desublimate and become entrained in a cryogenic liquid. This foulant slurry stream is pressurized, cooled, and separated into a pressurized foulant solid stream and the cryogenic liquid stream. The pressurized foulant solid stream is melted to produce a liquid foulant stream. Heat exchange processes, both internal and external, are provided that close the heat balance of the process. In this manner, the foulant is removed from the gas stream.
Swapped genetic code blocks viral infections and gene transfer (2022)

Abstract Removing cellular transfer RNAs (tRNAs), making their cognate codons unreadable, creates a genetic firewall that prevents viral replication and horizontal gene transfer. However, numerous viruses and mobile genetic elements encode parts of the translational apparatus, including tRNAs, potentially rendering a genetic-code-based firewall ineffective. In this paper, we show that such horizontally transferred tRNA genes can enable viral replication in Escherichia coli cells despite the genome-wide lack of three codons and the previously essential cognate tRNAs and release factor 1. By repurposing viral tRNAs, we then develop recoded cells bearing an amino-acid-swapped genetic code that reassigns two of the six serine codons to leucine during translation. This amino-acid-swapped genetic code renders cells completely resistant to viral infections by mistranslating viral proteomes and prevents the escape of synthetic genetic information by engineered reliance on serine codons to produce leucine-requiring proteins. Finally, we also repurpose the third free codon to biocontain this virus-resistant host via dependence on an amino acid not found in nature.
Curcumin stimulates proliferation, stemness acting signals and migration of 3T3-L1 preadipocytes (2011)

In the present study, the potential of curcumin to stimulate proliferation, stemness acting signals and migration of 3T3-L1 preadipocytes and the associated molecular mechanisms were investigated. Low concentrations of curcumin stimulated cell proliferation, whereas high concentrations were cytotoxic to 3T3-L1 cells. In particular, application of 0.02 µM of curcumin for 24 h resulted in significantly increased cell proliferation and was determined to be the optimal treatment for this study. In a colony-forming cell assay, cells treated with 0.02 µM of curcumin showed an approximately 1.5-fold increase in colony formation. Curcumin treatment up-regulated the proliferation-related marker proteins coupled with increased cell growth, telomerase activity and overexpression of stemness acting signals, which was associated with activation of the phosphoinositide 3-kinase (PI3K) pathway. In addition, curcumin significantly inactivated p38 mitogen-activated protein kinases (MAPK) and stress-activated protein kinase/c-Jun N-terminal kinases (SARK/JNK), coupled with inhibition of p53 and p21 tumor suppressor gene products. In addition, curcumin significantly increased cell migration through activation of migration-associated transcription factors. Therefore, these results clearly show that activation of cell proliferation by curcumin is associated with improved stem cell potency in 3T3-L1 preadipocytes.
Subarachnoid hemorrhage-negative Terson syndrome after intracranial artery treatment with a flow diverter device (2020)

This is the first reported case of vitreous hemorrhage and sub-ILM hemorrhage that should be considered to be Terson syndrome, after flow diverter stents treatment in the absence of SAH.
Development of P-Doped SiO[sub 2] as Proton Exchange Membrane for Microfuel Cells (2005)

Phosphorus-doped silicon dioxide (PSG) thin films with improved ionic conductivity were deposited via plasma-enhanced chemical vapor deposition for application as a thin-film proton exchange membrane (PEM) in microfabricated fuel cells. More than three orders of magnitude improvement in the ionic conductivity is obtained by P doping of low-temperature deposited . The area resistance of thick film of PSG is comparable to a thick film of Nafion. Application of these PSG films as PEM in microfuel cells yielded more than one order of magnitude improvement in power density compared to low-temperature, undoped membranes.
Evaluation of low contrast detectability performance using two-alternative forced choice method on computed tomography dose reduction algorithms (2012)

Today lowering patient radiation dose while maintaining image quality in Computed Tomography has become a very active research field. Various iterative reconstruction algorithms have been designed to improve/maintain image quality for low dose patient scans. Typically radiation dose variation will result in detectability variation for low contrast objects. This paper assesses the low contrast detectability performance of the images acquired at different dose levels and obtained using different image generation algorithms via two-alterative forced choice human observer method. Filtered backprojection and iterative reconstruction algorithms were used in the study. Results showed that for the objects and scan protocol used, the iterative algorithm employed in this study has similar low contrast detectability performance compared to filtered backprojection algorithm at a 4 times lower dose level. It also demonstrated that well controlled human observer study is feasible to assess the image quality of a CT system.