gebhart/patrepeval huggingface dataset:
Hybrid-scanning optical-resolution photoacoustic microscopy for in vivo vasculature imaging (2010)

Recently developed optical-resolution photoacoustic microscopy (OR-PAM), which is based on the detection of optical absorption contrast, is complementary to other optical microscopy modalities such as optical confocal microscopy, optical coherence tomography, and multiphoton microscopy. A hybrid optical-mechanical scanning configuration increases the imaging speed of OR-PAM significantly, facilitating many demanding biomedical applications. With a high-pulse-repetition-rate laser, the hybrid-scanning OR-PAM can acquire one-dimensional depth-resolved images (A-lines) at 5 kHz and two-dimensional B-scan images containing 800 A-lines at 6.25 Hz. We demonstrated in vivo in a mouse three-dimensional imaging of the iris vasculature in 128 s for an 800x800x200 data set and of the ear vasculature in 256 s for an 800x1600x200 data set.
GREEN FLUORESCENT PROTEIN (1995)

Several bioluminescent coelenterates use a secondary fluorescent protein, the green fluorescent protein (GFP), in an energy transfer reaction to produce green light. The most studied of these proteins have been the GFPs from the jellyfish Aequorea victoria and the sea pansy Renilla reniformis. Although the proteins from these organisms are not identical, they are thought to have the same chromophore, which is derived from the primary amino acid sequence of GFP. The differences are thought to be due to changes in the protein environment of the chromophore. Recent interest in these molecules has arisen from the cloning of the Aequorea gfp cDNA and the demonstration that its expression in the absence of other Aequorea proteins results in a fluorescent product. This demonstration indicated that GFP could be used as a marker of gene expression and protein localization in living and fixed tissues. Bacterial, plant and animal (including mammalian) cells all express GFP. The heterologous expression of the gfp cDNA has also meant that it could be mutated to produce proteins with different fluorescent properties. Variants with more intense fluorescence or alterations in the excitation and emission spectra have been produced.
Modular Automated Transport Frequently Asked Questions (FAQ) (2001)

1 General Questions 1 1.1 Why is MAIT divided into cabins, carriers and tracks ? . . . . . . . . . . . . . 1 1.2 What have MAIT and PRT in common? . . . . . . . . . . . . . . . . . . . . 6 1.3 What is the difference between MAIT and a Dual mode systems? . . . . . . . 7 1.4 What is the difference between MAIT and integrated transport systems? . . . 7 1.5 What is the difference between MAIT and GRT ? . . . . . . . . . . . . . . . 7 1.6 Who is in charge of MAIT , is MAIT not a big monopoly? . . . . . . . . . . . 8
Involvement of the Glucocorticoid Receptor in the Pathogenesis of Rheumatoid Arthritis (2002)

The glucocorticoid receptor (GR) is a ligand-inducible transcription factor which controls the expression of several genes. Its cognate ligand, the glucocorticoids, induces receptor activation by binding to the cytoplasmic located receptor, ultimately leading to translocation of the receptor/hormone complex into the nucleus and the regulation of gene activity. Because glucocorticoids are widely used for suppression of inflammation in rheumatoid arthritis (RA), we investigated whether the expression level of GR is correlated with RA. We designed a study to detect the total amount of GR in lymphocytes of untreated RA patients, glucocorticoid-treated RA patients, and healthy controls. We observed a significant change in the expression levels of GR. Untreated RA patients exhibited a significantly higher amount of GR than the healthy controls, whereas glucocorticoid-treated RA patients showed a strongly decreased receptor density. These results seem to reflect a functional dysregulation of the HPA axis and may lead to a better understanding of the pathogenesis of RA.
A New Redox Cofactor in Eukaryotic Enzymes: 6-Hydroxydopa at the Active Site of Bovine Serum Amine Oxidase (1990)

An active site, cofactor-containing peptide has been obtained in high yield from bovine serum amine oxidase. Sequencing of this pentapeptide indicates: Leu-Asn-X-Asp-Tyr. Analysis of the peptide by mass spectrometry, ultraviolet-visible spectroscopy, and proton nuclear magnetic resonance leads to the identification of X as 6-hydroxydopa. This result indicates that, contrary to previous proposals, pyrroloquinoline quinone is not the active site cofactor in mammalian copper amine oxidases. Although 6-hydroxydopa has been implicated in neurotoxicity, the data presented suggest that this compound has a functional role at an enzyme active site.
Aspirin Use and the Risk for Colorectal Cancer and Adenoma in Male Health Professionals (1994)

These results support laboratory, clinical, and other epidemiologic evidence that regular use of aspirin is associated with a decreased risk for colorectal cancer.
Diacylglycerol Kinase ζ (DGKζ) and Casitas b-Lineage Proto-Oncogene b–Deficient Mice Have Similar Functional Outcomes in T Cells but DGKζ-Deficient Mice Have Increased T Cell Activation and Tumor Clearance (2018)

Targeting negative regulators downstream of the T cell receptor (TCR) represents a novel strategy to improve cancer immunotherapy. Two proteins that serve as critical inhibitory regulators downstream of the TCR are diacylglycerol kinase ζ (DGKζ), a regulator of Ras and PKC-θ signaling, and Casitas b-lineage proto-oncogene b (Cbl-b), an E3 ubiquitin ligase that predominantly regulates PI(3)K signaling. We sought to compare the signaling and functional effects that result from deletion of DGKζ, Cbl-b, or both (double knockout, DKO) in T cells, and to evaluate tumor responses generated in a clinically relevant orthotopic pancreatic tumor model. We found that whereas deletion of Cbl-b primarily served to enhance NF-κB signaling, deletion of DGKζ enhanced TCR-mediated signal transduction downstream of Ras/Erk and NF-κB. Deletion of DGKζ or Cbl-b comparably enhanced CD8<sup>+</sup> T cell functional responses, such as proliferation, production of IFNγ, and generation of granzyme B when compared with WT T cells. DKO T cells demonstrated enhanced function above that observed with single knockout T cells after weak, but not strong, stimulation. Deletion of DGKζ, but not Cbl-b, however, resulted in significant increases in numbers of activated (CD44<sup>hi</sup>) CD8<sup>+</sup> T cells in both non-treated and tumor-bearing mice. DGKζ-deficient mice also had enhanced control of pancreatic tumor cell growth compared to Cbl-b-deficient mice. This represents the first direct comparison between mice of these genotypes and suggests that T cell immunotherapies may be better improved by targeting TCR signaling molecules that are regulated by DGKζ as opposed to molecules regulated by Cbl-b.
Novel One-Mask Self-Heating Pillar Phase Change Memory (2006)

A novel Pillar phase change memory based on fully integrated test arrays in 180nm CMOS technology has been successfully fabricated. A current-confining Pillar structure leads to a self-heating at the center of the chalcogenide layer, and needs only one additional mask level for its fabrication. Switching characteristics with write currents less than 900μA at 75nm diameter and multilevel operation are reported
Determination and prediction of digestible and metabolizable energy from chemical analysis of corn coproducts fed to finishing pigs1 (2011)

Twenty corn coproducts from various wet- and dry-grind ethanol plants were fed to finishing pigs to determine DE and ME and to generate equations predicting DE and ME based on chemical analysis. A basal diet comprised corn (97.05%), limestone, dicalcium phosphate, salt, vitamins, and trace minerals. Twenty test diets were formulated by mixing the basal diet with 30% of a coproduct, except for dried corn solubles and corn oil, which were included at 20 and 10%, respectively. There were 8 groups of 24 finishing gilts (n = 192; BW = 112.7 ± 7.9 kg). Within each group, gilts were randomly assigned to 1 of 5 test diets or the basal diet for a total of 4 replications per diet per group. Two groups of gilts were used for each set of coproducts, resulting in 8 replications per coproduct and 32 replications of the basal diet. The experiment was conducted as a completely randomized design. Gilts were placed in metabolism crates and offered 3 kg daily of their assigned test diet for 13 d, with total collection of feces and urine during the last 4 d. Ingredients were analyzed for DM, GE, CP, ether extract, crude fiber, NDF, ADF, total dietary fiber (TDF), ash, AA, and minerals, and in vitro OM digestibility was calculated for each ingredient. The GE was determined in the diets, feces, and urine to calculate DE and ME for each ingredient. The DE and ME of the basal diet were used as covariates among groups of pigs. The DE of the coproducts ranged from 2,517 kcal/kg of DM (corn gluten feed) to 8,988 kcal/kg of DM (corn oil), and ME ranged from 2,334 kcal/kg of DM (corn gluten feed) to 8,755 kcal/kg of DM (corn oil). By excluding corn oil and corn starch from the stepwise regression analysis, a series of DE and ME prediction equations were generated. The best fit equations were as follows: DE, kcal/kg of DM = -7,471 + (1.94 × GE) - (50.91 × ether extract) + (15.20 × total starch) + (18.04 × OM digestibility), with R(2) = 0.90, SE = 227, and P < 0.01; ME, kcal/kg of DM = (0.90 × GE) - (29.95 × TDF), with R(2) = 0.72, SE = 323, and P < 0.01. Additional equations for DE and ME included NDF in the instance that TDF data were not available. These results indicate that DE and ME varied substantially among corn coproducts and that various nutritional components can be used to accurately predict DE and ME in corn coproducts for finishing pigs.
Interdependence of Backbone Flexibility, Residue Conservation, and Enzyme Function:  A Case Study on β1,4-Galactosyltransferase-I (2003)

Beta1,4-galactosyltransferase-I (beta4Gal-T1) catalyzes the transfer of a galactose from UDP-galactose to N-acetylglucosamine. A recent crystal structure determination of the substrate-bound enzyme reveals a large conformational change, which creates binding sites for the oligosaccharide and alpha-lactalbumin, when compared to the ligand-free structure. The conformational changes take place in a 21-residue-long loop (I345-H365) and in a smaller loop containing a tryptophan residue (W314) flanked by glycines (Y311-G316; Trp loop). A series of molecular dynamics simulations carried out with an implicit solvent model and with explicit water successfully identify flexibility in the two loops and in another interacting loop. These observations are confirmed by limited proteolysis experiments that reveal an intrinsic flexibility of the long loop. The multiple simulation runs starting with the substrate-free structure show that the long loop moves toward its conformation in the ligand-bound structure; however, it gets stabilized in an intermediate position. The Trp loop moves in the opposite direction to that of the long loop, making contacts with residues in the long loop. Remarkably, when the Trp loop is restrained in its starting conformation, no large conformational change takes place in the long loop, indicating residue communication of flexibility. Sequence and structural analysis of the beta4Gal-T1 family with 37 known sequences reveals that in contrast to the unconserved long loop, which undergoes a much larger conformational change, the Trp loop including the glycines is highly conserved. These observations lead us to propose a new functional mechanism that may be conserved by evolution to perform a variety of functions.
Expression of USP22 and Survivin is an indicator of malignant behavior in hepatocellular carcinoma (2015)

Hepatocellular carcinoma (HCC) is the most common primary malignant liver tumor type, ranking as the third leading cause of all cancer-related deaths in the world. The post-surgical 5-year survival rate is low, largely due to the high recurrence rate. Therefore, the identification of target molecules that control the biological characteristics of HCC is of great importance. Ubiquitin-specific protease 22 (USP22) is a newly discovered deubiquitinating enzyme and is a cancer stem cell marker that plays a role in tumorigenesis, therapy resistance and cell cycle progression. Survivin is a member of the inhibitor of apoptosis protein (IAP) family and is known to function either as an inhibitor for apoptosis or as a regulator of cell division. Levels of survivin are correlated with the aggressiveness of tumors and a poor prognosis in various cancers including HCC. In the present study, we examined the USP22 expression and its association with survivin expression and clinicopathological features in HCC. First, we examined the expression of USP22 and survivin in 151 HCC cases by immunohistochemistry. High expression of USP22 and survivin was frequently observed in HCC cases, in comparison with normal adjacent liver tissues. Expression of USP22 and survivin was well correlated with malignant behavior including tumor size, stage and differentiation in HCC cases. Importantly, HCC patients with high expression of USP22 and survivin showed poor prognosis. USP22 expression was well correlated with survivin expression in HCC cases. This correlation was confirmed in HCC cell lines and tissues by RT-PCR and western blot analysis. Next, to investigate the biological role of USP22 in HCC, we examined the effect of USP22 knockdown on the cell growth and the expression of cell cycle-related protein including survivin in HCC cells. USP22 siRNA suppressed cell growth. Moreover, USP22 siRNA decreased survivin expression together with upregulation of CDK inhibitor, p21 and downregulation of cyclin B. These findings suggest that USP22 may be involved in HCC progression in cooperation with survivin. We suggest that USP22 can be useful as a new prognostic marker and therapeutic target in HCC patients.
Elucidating the Effects of a Rare-Earth Oxide Shell on the Luminescence Dynamics of Er3+:Y2O3Nanoparticles (2012)

Rare-earth (RE) (Er3+ and Yb3+, Er3+)-doped yttrium oxide (Y2O3) core–shell particles were synthesized in this work using a two-step process where the cores were formed by molten salt synthesis while the shell was deposited by a sol–gel process. The cores were 100–150 nm, and a shell layer, up to 12 nm thick, was controllable based on the mass ratio between the RECl3 salts and the Er3+:Y2O3 (1 mol %) particles. A passive Y2O3 shell layer, at an optimal thickness around 8 nm, passivated the surface quenching sites and resulted in a 53% increase in photoluminescence lifetimes and visible separation in Stark splitting. Optically active shell layers, such as Yb2O3 and Yb3+:Y2O3, not only passivated the quenching sites but also facilitated energy transfer between the spatially controlled RE ions. Furthermore, the effect of surface passivation on the upconversion luminescence was determined through the purposed dynamic processes to corroborate the effect of the hydroxyl groups on energy dissipation. The addition of a passive shell layer or a sensitizer reduced the upconversion to a two-photon process due to a decreased branching ratio at the 4I11/2 energy level. Yb2O3 is deemed the most effective shell material due to the largest increase photoluminescence intensity at 1535 nm as a function of the pump power and the lifetime of the 4S3/2 radiative transition, important in upconversion luminescence. The increased lifetime and low pump power achieved with Er3+:Y2O3|Yb2O3 core–shell phosphors hold promise in lighting devices for improved overall device efficiency.
Uncialamycin, A New Enediyne Antibiotic (2005)

[structure: see text] Laboratory cultures of an undescribed streptomycete obtained from the surface of a British Columbia lichen produce uncialamycin (1), a new enediyne antibiotic. The structure of uncialamycin (1) has been elucidated by analysis of spectroscopic data. Uncialamycin (1) exhibits potent in vitro antibacterial activity against gram-positive and gram-negative human pathogens, including Burkholderia cepacia, a major cause of morbidity and mortality in patients with cystic fibrosis.
Tumor Necrosis Factor-α–Converting Enzyme (ADAM17) Mediates GPIbα Shedding From Platelets In Vitro and In Vivo (2004)

Interaction of the platelet receptor glycoprotein (GP) Ib-V-IX with von Willebrand factor exposed at a site of vascular injury is an essential step in the initiation of a hemostatic plug. Proteolytic cleavage (shedding) of the GPIbalpha subunit was first described >25 years ago, the protease mediating this event as well as its physiological function, however, have not been elucidated. We reported recently that shedding of GPIbalpha induced by platelet storage or mitochondrial injury involves a platelet-derived metalloproteinase(s). Here we show that GPIbalpha shedding in response to mitochondrial injury or physiological activation is inhibited in platelets obtained from chimeric mice, which express inactive tumor necrosis factor-alpha converting enzyme (TACE(DeltaZn/DeltaZn)) in blood cells only. Shedding was also inhibited in mouse and human platelets in the presence of 2 potent TACE inhibitors: TAP1 and TMI-1. Our data further suggest that TACE is important in the regulation of GPIbalpha expression in vivo because we observed an approximately 90% reduction in soluble GPIbalpha (glycocalicin) in plasma of TACE(DeltaZn/DeltaZn) chimeras as well as significantly increased levels of GPIbalpha on circulating platelets. In contrast, shedding of P-selectin from activated platelets was not affected by the mutation in TACE. Damaged TACE(DeltaZn/DeltaZn) platelets were further characterized by a markedly improved post-transfusion recovery and hemostatic function in mice. In conclusion, our data demonstrate that TACE is expressed in platelets and that it is the key enzyme mediating shedding of GPIbalpha.
Toxic effect of blood components on perinatal rat subventricular zone cells and oligodendrocyte precursor cell proliferation, differentiation and migration in culture (2009)

The germinal matrix of human brain gives rise to oligodendrocytes and astrocytes after mid-gestation. Hemorrhage in the germinal matrix of premature infants is associated with suppressed cell proliferation. We hypothesize that soluble blood constituents have an adverse effect on the proliferation of cultured rat subventricular zone (SVZ) cells and the proliferation, migration, and differentiation of oligodendrocyte progenitor cells (OPC). Using caspase 3 activation and lactate dehydrogenase release assays, rat plasma, serum, thrombin, and kallikrein killed SVZ cells when grown in the presence (but not absence) of platelet derived growth factor. Plasma and serum killed OPC at 1:1 to 1:100 dilutions. Using a bromodeoxyuridine incorporation assay OPC proliferation was reduced by plasma, serum, thrombin and plasmin. Blood proteins also suppressed OPC migration in a concentration dependent manner. However, differentiation of OPC into myelin basic protein expressing cells was suppressed only by thrombin. We conclude that soluble blood components, particularly thrombin, have an adverse effect on maturing SVZ cells and OPC derived from newborn rat brain.
Mapping of chromosomal gains and losses in prostate cancer by comparative genomic hybridization (1995)

Comparative genomic hybridization (CGH) allows detection of chromosomal imbalances in whole genomes in a comprehensive manner. With this approach, ten cases of prostate cancer (seven primary tumors and three metastases) were analyzed. Frequent chromosomal gains detected by CGH involved chromosome arms 7q, 8q, 9q, and 16p, and chromosomes 20 and 22, as well as frequent losses of chromosome arms 16q and 18q, in at least three of the ten cases. Overrepresentation of chromosome arm 9q has not been described in published reports. The CGH data were compared with results of a loss of heterozygosity (LOH) study, in which complete allelotyping was performed in the same prostate tumors with 74 different polymorphic markers. In general, a high concordance between the CGH and LOH results was observed (92%). Tumors revealing discrepancies by CGH and LOH analysis were investigated further by interphase cytogenetics, and the resulting picture regarding the genomic alterations is discussed in detail.
Inhibition of C5a des Arg-induced neutrophil alveolitis in transgenic mice expressing C-reactive protein (1994)

C-reactive protein (CRP) is the classic acute phase reactant in man with serum levels elevated up to 1,000-fold after the onset of inflammation. CRP inhibits chemotaxis of complement (C5a)-stimulated neutrophils in vitro and rabbits with elevated serum CRP levels exhibit diminished neutrophil infiltration and vascular permeability in a model of C5a-induced alveolitis. To specifically evaluate the effect of CRP on C5a-induced neutrophil inflammation in vivo, experiments were performed in transgenic mice capable of expressing rabbit CRP in an inducible fashion. After direct instillation of a known inflammatory agent (C5a des Arg) into the airways, transgenic mice with high plasma levels of CRP showed significantly diminished infiltration of neutrophils into bronchoalveolar lavage fluid (BALF) and a significant reduction of BALF total protein levels compared with normal mice. These data indicate that CRP can diminish lung injury by a reduction in neutrophil influx and protein leakage into alveoli following complement-induced inflammation.
Characterization of a spontaneous mutation to a beta-thalassemia allele. (1986)

We have studied a nuclear family containing a single child with severe beta-thalassemia intermedia, a Greek-Cypriot mother with hematological findings of beta-thalassemia trait, and a Polish father who is hematologically normal. Since both the child and her father were heterozygous for a DNA polymorphism within the beta-globin gene, it was possible to clone and sequence the beta-globin gene identical by descent from both the child and her father. A nonsense mutation in codon 121 (GAA----TAA) was found in the beta-globin gene of the child, while the same gene from her father lacked this mutation and was normal. This mutation has not been previously observed among over 200 beta-thalassemia genes characterized in Caucasians. Since the mutation eliminates an EcoRI site in the beta-globin gene, we could show that the mutation is not present in genomic DNA of the father. To rule out germinal mosaicism, sperm DNA of the father was also digested with EcoRI, and the mutant EcoRI fragment was not observed under conditions that would detect the mutation if it were present in at least 2% of sperm cells. Routine HLA and blood group testing supported stated paternity. In addition, studies with 17 DNA probes that detect multiple allele polymorphisms increased the probability of stated paternity to at least 10(8):1. These data provide evidence that the G----T change in codon 121 of the beta-globin gene in the child is the result of a spontaneous mutation that occurred during spermatogenesis in a paternal germ cell.
In vitromodel for penetration of sensory nerve fibres on a Matrigel basement membrane: implications for possible application to intractable pruritus (2009)

Membrane-associated MMP-2 contributes to penetration of nerve fibres into Matrigel through modulation by axonal guidance molecules and/or ECM. These findings provide insight for understanding the development of intractable pruritus involving epidermal nerve density.