gebhart/patrepeval huggingface dataset:
Arbovirus Plaquing in Two Simian Kidney Cell Lines (1969)

SUMMARY A total of 212 arbovirus serotypes, representing 29 arbovirus serogroups, were screened for their plaque-forming ability and titrated in two continuous simian kidney cell lines (VERO and LLC-MK2). Plaquing data were obtained with 205 viruses in either one or both of these cell lines; seven viruses failed to plaque in either line. Both cell lines were susceptible to 169 arbovirus serotypes. Seventeen viruses failed to plaque in VERO and 18 in LLC-MK2. Plaques appeared as early as 2 days, and as late as 18 days (Triniti virus in VERO) Plaque diameters ranged from 1 to 28 mm. during a 24-day observation period.
Interleukin-1 receptor antagonist decreases bone loss and bone resorption in ovariectomized rats. (1994)

Interleukin-1 (IL-1), a cytokine produced by bone marrow cells and bone cells, has been implicated in the pathogenesis of postmenopausal osteoporosis because of its potent stimulatory effects on bone resorption in vitro and in vivo. To investigate whether IL-1 plays a direct causal role in post ovariectomy bone loss, 6-mo-old ovariectomized rats were treated with subcutaneous infusions of IL-1 receptor antagonist (IL-1ra), a specific competitor of IL-1, for 4 wk, beginning either at the time of surgery or 4 wk after ovariectomy. The bone density of the distal femur was measured non invasively by dual-energy X-ray absorptiometry. Bone turnover was assessed by bone histomorphometry and by measuring serum osteocalcin, a marker of bone formation, and the urinary excretion of pyridinoline cross-links, a marker of bone resorption. Ovariectomy caused a rapid increase in bone turnover and a marked decrease in bone density which were blocked by treatment with 17 beta estradiol. Ovariectomy also increased the production of IL-1 from cultured bone marrow cells. Ovariectomy induced-bone loss was significantly decreased by IL-1ra treatment started at the time of ovariectomy and completely blocked by IL-1ra treatment begun 4 wk after ovariectomy. In both studies IL-1ra also decreased bone resorption in a manner similar to estrogen, while it had no effect on bone formation. In contrast, treatment with IL-1ra had no effect on the bone density and the bone turnover of sham-operated rats, indicating that IL-1ra specifically blocked estrogen-dependent bone loss. In conclusion, these data indicate that IL-1, or mediators induced by IL-1, play an important causal role in the mechanism by which ovariectomy induces bone loss in rats, especially following the immediate post ovariectomy period.
Phenotypic Effects of Wild-Type and Mutant SOD1 Expression in N9 Murine Microglia at Steady State, Inflammatory and Immunomodulatory Conditions (2019)

Accumulation of mutated superoxide dismutase 1 (mSOD1) in amyotrophic lateral sclerosis (ALS) involves injury to motor neurons (MNs), activation of glial cells and immune unbalance. However, neuroinflammation, besides its detrimental effects, also plays beneficial roles in ALS pathophysiology. Therefore, the targeting of microglia to modulate the release of inflammatory neurotoxic mediators and their exosomal dissemination, while strengthening cell neuroprotective properties, has gained growing interest. We used the N9 microglia cell line to identify phenotype diversity upon the overexpression of wild-type (WT; hSOD1<sup>WT</sup>) and mutated G93A (hSOD1<sup>G93A</sup>) protein. To investigate how each transduced cell respond to an inflammatory stimulus, N9 microglia were treated with lipopolysaccharide (LPS). Glycoursodeoxycholic acid (GUDCA) and dipeptidyl vinyl sulfone (VS), known to exert neuroprotective properties, were tested for their immunoregulatory properties. Reduced Fizz1, IL-10 and TLR4 mRNAs were observed in both transduced cells. However, in contrast with hSOD1<sup>WT</sup>-induced decreased of inflammatory markers, microglia transduced with hSOD1<sup>G93A</sup> showed upregulation of pro-inflammatory (TNF-α/IL-1β/HMGB1/S100B/iNOS) and membrane receptors (MFG-E8/RAGE). Importantly, their derived exosomes were enriched in HMGB1 and SOD1. When inflammatory-associated miRNAs were evaluated, increased miR-146a in cells with overexpressed hSOD1<sup>WT</sup> was not recapitulated in their exosomes, whereas hSOD1<sup>G93A</sup> triggered elevated exosomal miR-155/miR-146a, but no changes in cells. LPS stimulus increased M1/M2 associated markers in the naïve microglia, including MFG-E8, miR-155 and miR-146a, whose expression was decreased in both hSOD1<sup>WT</sup> and hSOD1<sup>G93A</sup> cells treated with LPS. Treatment with GUDCA or VS led to a decrease of TNF-α, IL-1β, HMGB1, S100B and miR-155 in hSOD1<sup>G93A</sup> microglia. Only GUDCA was able to increase cellular IL-10, RAGE and TLR4, together with miR-21, while decreased exosomal miR-155 cargo. Conversely, VS reduced MMP-2/MMP-9 activation, as well as upregulated MFG-E8 and miR-146a, while producing miR-21 shuttling into exosomes. The current study supports the powerful role of overexpressed hSOD1<sup>WT</sup> in attenuating M1/M2 activation, and that of hSOD1<sup>G93A</sup> in switching microglia from the steady state into a reactive phenotype with low responsiveness to stimuli. This work further reveals GUDCA and VS as promising modulators of microglia immune response by eliciting common and compound-specific molecular mechanisms that may promote neuroregeneration.
Different Sensitivity of RecombinantAspergillus nigerPhytase (r-PhyA) andEscherichia colipH 2.5 Acid Phosphatase (r-AppA) to Trypsin and Pepsinin Vitro (1999)

Proteolysis of two purified recombinant enzymes, namely, the Aspergillus niger phytase (r-PhyA) and the Escherichia coli pH 2.5 acid phosphatase (r-AppA), by pepsin and trypsin was investigated in this study. After r-PhyA and r-AppA were incubated with different concentrations of pepsin or trypsin, their residual phytase activities and amounts of inorganic phosphorus released from soybean meal were determined. Both enzymes retained more than 85% of their original activities at the trypsin/phytase ratios (w/w) 0.001 and 0. 005, while r-AppA and r-PhyA lost 60 and 20% of the original activity at the ratio of 0.01 or 0.025, respectively. In contrast, there was a 30% increase in phytase activity after r-AppA was incubated with pepsin at the ratios of 0.005 or 0.01. Meanwhile, r-PhyA lost 58 to 77% of its original activity under the same conditions. Trypsin and pepsin affected the hydrolysis of phytate phosphorus from soybean meal by r-AppA and r-PhyA in a similar way to their residual phytase activities. All of these in vitro proteolyses were confirmed by SDS-PAGE analysis. Our results demonstrate different sensitivities of r-AppA and r-PhyA to trypsin and pepsin, suggesting active trypsin resistant r-PhyA and pepsin resistant r-AppA polypeptides.
The acute respiratory distress syndrome following isolated severe traumatic brain injury (2016)

Prognostic/epidemiologic study, level III.
Arginine deprivation, growth inhibition and tumour cell death: 3. Deficient utilisation of citrulline by malignant cells (2003)

Arginine deprivation causes death of up to 80% of cancer cell lines in vitro, but in the body, citrulline would be available as a convertible source of this amino acid in vivo. Some tumour cell lines, notably the vast majority of melanomas and hepatocellular carcinomas, tend to be deficient in argininosuccinate synthetase (EC 6.5.4.3.), and therefore cannot recycle citrulline to arginine. Argininosuccinate synthetase is present at levels that convert enough citrulline to arginine to allow limited growth in about half of a modest range of malignant cell types analysed in this study. Attempts to rescue cells that are unable to utilise citrulline with the immediate downstream product, argininosuccinate, had very limited success in a few tumour cell lines. Particularly noteworthy is the demonstration that argininosuccinate was totally incapable of rescuing cells that utilise citrulline efficiently, consistent with tight channelling (coupling) of argininosuccinate synthetase and argininosuccinate lyase in the urea cycle. The findings suggest that an excellent opportunity exists for further exploitation of arginine deprivation in the selective killing of tumour cells.
A Novel Cardiac-Restricted Target for Doxorubicin (1997)

Doxorubicin (Dox), a cardiotoxic antineoplastic drug, disrupts the cardiac-specific program of gene expression (Kurabayashi, M., Dutta, S., Jeyaseelan, R., and Kedes, L. (1995) Mol. Cell. Biol. 15, 6386-6397; Jeyaseelan, R., Poizat, C., Wu, H. Y., and Kedes, L. (1997) J. Biol. Chem. 272, 5828-5832). To determine whether this drug might interfere with the function of cardiac-specific regulatory pathways, we used a differential display strategy to clone from neonatal rat cardiomyocyte candidate mRNAs that were rapidly sensitive to Dox. We report here the identification of a constitutively expressed, cardiac-restricted, nuclear protein whose mRNA level is exquisitely sensitive to Dox. Hence we have named this protein cardiac adriamycin-responsive protein (CARP). CARP mRNA is present at the earliest stages of cardiac morphogenesis. It was detected by in situ hybridization within the cardiogenic plate of 7. 5-day post coitum (p.c.) embryos, and in 8.5-day p.c. embryos CARP transcripts are present in uniformly high levels in the myocardium. Throughout cardiac development, CARP expression is specific for the myocardium; endocardial cushions and valves exhibit only background levels of signal. Transcript levels persist but gradually decrease in neonatal, 2-week-old, and adult hearts. There were no stages when CARP mRNA could not be detected. The pattern and timing of CARP mRNA expression, including transient expression in the tongue at 14.5 days p.c., coincides with that of Nkx2.5/Csx (a putative homolog of tinman, the Drosophila melanogaster gene responsible for cardiac development). The cloned full-length 1749 nucleotide CARP cDNA encodes a 319-amino acid 40-kDa polypeptide containing five tandem ankyrin repeats. CARP appears to be the rat homolog of a previously reported human single-copy gene (C-193; Chu, W., Burns, D. K., Swerlick, R. A., and Presky, D. H. (1995) J. Biol. Chem. 270, 10236-10245), whose mRNA is inducible by cytokines only in human endothelial cells. CARP appears to function as a negative regulator of cardiac-specific gene expression. Overexpression of CARP in cardiomyocytes suppresses cardiac troponin C and atrial natriuretic factor transcription. Cotransfection experiments in HeLa cells indicate that CARP inhibits Nkx2.5 transactivation of atrial natriuretic factor promoter. When fused to a GAL4 DNA-binding domain, CARP has transcriptional inhibitory properties in noncardiac cells. CARP thus represents the first example of a cardiac-restricted transcriptional regulatory protein that is sensitive to Dox.
Fluorescent dyes specific for quadruplex DNA (1998)

Fluorescent dyes which are specific for duplex DNA have found a wide range of applications from staining gels to visualization of chromosomes. Porphyrin dyes have been found which are highly fluorescent in the presence of quadruplex but not duplex DNA. These dyes may offer a route to the specific detection of quadruplex DNA under biologically important conditions. There are three types of DNA quadruplex structures, and these may play important roles in telomere, centromere, triplet repeat, integration sites and other DNAs, and this first set of porphyrin dyes show some selectivity between the quadruplex types.
Targeting CD19 in B-cell lymphoma: emerging role of SAR3419 (2013)

Non-Hodgkin lymphoma symbolizes a heterogeneous group of diseases resulting from malignant transformation of lymphocytes with differing patterns of behavior and responses to treatment. The potential curability of non-Hodgkin lymphoma differs among the various histologic subtypes and is associated in part with the stage at presentation. CD19 antigen is a type I transmembrane glycoprotein belonging to the immunoglobulin Ig superfamily. CD19 is specifically expressed in normal and neoplastic B-cells. Recent study showed that in a mouse model, CD19 and c-Myc synergize functionally to accelerate B-cell lymphomagenesis, which is associated with increased disease severity. Specificity is the most important challenge in cancer therapeutics. Antibody-drug conjugates have the prospect of enhancing the therapeutic efficacy over unconjugated monoclonal antibodies through the selective delivery of cytotoxic agents to cancer cells. The ubiquitous expression of CD19 in these tumors, especially at an earlier stage and the property of efficient internalization, makes CD19 an attractive and affective target for antibody-drug conjugate therapy as compared to CD20. SAR3419 (huB4-DM4) is a novel antibody-drug conjugate that is composed of a humanized monoclonal IgG1 anti-CD19 antibody (huB4) attached to the potent cytotoxic drug, a maytansine derivative (DM4), through a cleavable disulfide cross-linking agent N-Succinimidyl-4-2-pyridyldithio butanoic acid (SPDB). The preclinical efficacy of maytansine derivative-anti-CD19 conjugate was demonstrated in our laboratory, and SAR3419 was found to be more effective than CHOP in a xenograft model. Phase I trials have also been conducted on the basis of preclinical studies that demonstrated promising antitumor activity with acceptable safety results in human B-cell lymphoma models. Additional trials are ongoing and will provide additional insight into the full potential of this novel drug.
Surface modeling with oriented particle systems (1992)

article Free Access Share on Surface modeling with oriented particle systems Authors: Richard Szeliski Digital Equipment Corp.,Cambridge Research Lab, One Kendall Square, Bldg. 700, Cambridge, MA Digital Equipment Corp.,Cambridge Research Lab, One Kendall Square, Bldg. 700, Cambridge, MAView Profile , David Tonnesen Dept.of Computer Science, University of Toronto, Toronto, Canada M5S 1A4 Dept.of Computer Science, University of Toronto, Toronto, Canada M5S 1A4View Profile Authors Info & Claims ACM SIGGRAPH Computer GraphicsVolume 26Issue 2July 1992 pp 185–194https://doi.org/10.1145/142920.134037Online:01 July 1992Publication History 189citation2,483DownloadsMetricsTotal Citations189Total Downloads2,483Last 12 Months78Last 6 weeks5 Get Citation AlertsNew Citation Alert added!This alert has been successfully added and will be sent to:You will be notified whenever a record that you have chosen has been cited.To manage your alert preferences, click on the button below.Manage my Alerts New Citation Alert!Please log in to your account Save to BinderSave to BinderCreate a New BinderNameCancelCreateExport CitationPublisher SiteeReaderPDF
Segmented Flow Reactors for Nanocrystal Synthesis (2012)

In the past decade microreactors have emerged as a compelling technology for the highly controlled synthesis of colloidal nanocrystals, offering multiple advantages over conventional batch synthesis methods (including improved levels of control, reproducibility, and automation). Initial work in the field employed simple continuous phase reactors that manipulate miscible streams of a single reagent phase. Recently, however, there has been increasing interest in segmented flow reactors that use an immiscible fluid to divide the reagent phase into discrete slugs or droplets. Key advantages of segmented flow include the elimination of velocity dispersion (a significant cause of polydispersity) and greatly reduced susceptibility to reactor fouling. In this progress report we review the operation of segmented flow microreactors, their application to the controlled synthesis of nanocrystals, and some of the principal challenges that must be addressed before they can become a mainstream technology for the controlled production of nanomaterials.
Specific immunosuppressive activity of epiglycanin, a mucin-like glycoprotein secreted by a murine mammary adenocarcinoma (TA3-HA). (1991)

Epiglycanin (Epi) is a mucin-like glycoprotein carrying multiple Thomsen Freidenreich (TF) and Tn determinants secreted by a murine mammary adenocarcinoma, TA3-Ha. As an attempt to further characterize immunoregulatory networks in the TA3-Ha animal model, we tested whether Epi causes active suppression of the cell-mediated immune response against TF determinants. In this study, we show that (a) s.c. injection of epiglycanin emulsified in either complete Freund's adjuvant or Ribi adjuvant containing trehalose dimycolate and monophosphoryl lipid A elicits a classical specific delayed-type hyperactivity response to TF haptens either naturally expressed on epiglycanin or as synthetic haptens conjugated to a protein carrier; (b) i.v. injection of as little as 500 ng of Epi induces specific immunosuppression to anti-Epi and anti-TF synthetic antigen delayed-type hyperactivity responses; (c) this immunosuppression can be abrogated by i.v. injection of cyclophosphamide prior to immunizations; (d) Epi-induced specific immunosuppression can be adoptively transferred by nylon wool-nonadherent cells 6 days following i.v. injection of Epi; (e) pretreatment of suppressor cell populations with anti-Thy-1, anti-L3T4, anti-Lyt-1, or anti-I-Jk but not anti-Lyt-2 monoclonal antibodies plus complement prior to adoptive transfer abolished immunosuppression; (f) i.v. injection of immunosuppressive amounts of Epi on Days 2 and 6 after transplantation of TA3-Ha cells increased the lethality of the tumor transplant. These results suggest that Epi-induced specific immunosuppression in the TA3-Ha animal model is mediated by Thy-1+, L3T4+, Lyt-1+2-, and I-Jk+ suppressor cells. The results are also consistent with the suggestion that this immunosuppression may enhance TA3-Ha tumor growth.
Processing of Clostridium difficile toxins (2008)

The pathogenicity of Clostridium difficile depends on the large clostridial glucosylating toxins A and B (TcdA and TcdB). The proteins accomplish their own uptake by a modular structure comprising a catalytic and a binding/translocation domain. Based on a proteolytic processing step solely the catalytic domain reaches the cytosol. Within the cells, the glucosyltransferases inactivate small GTPases by mono-O-glucosylation. Here, a short overview is given regarding latest insights into the intramolecular processing, which is mediated by an intrinsic protease activity.
Basic concepts of depression (2008)

This paper reviews concepts of depression, including history and classification. The original broad concept of melancholia included all forms of quiet insanity. The term depression began to appear in the nineteenth century, as did the modern concept of affective disorders, with the core disturbance now viewed as one of mood. The 1980s saw the introduction of defined criteria into official diagnostic schemes. The modern separation into unipolar and bipolar disorder was introduced following empirical research by Angst and Perris in the 1960s. The partially overlapping distinctions between psychotic and neurotic depression, and between endogenous and reactive depression, started to generate debate in the 1920s, with considerable multivariate research in the 1960s. The symptom element in endogenous depression currently survives in melancholia or somatic syndrome. Life stress is common in various depressive pictures. Dysthymia, a valuable diagnosis, represents a form of what was regarded earlier as neurotic depression. Other subtypes are also discussed.
Atomic arrangement and emission properties of GaAs(In, Sb)N quantum wells (2009)

Fine structure related to different types of atomic arrangements (short-range order, phase separation and quantum dots) was observed in high-spatial-resolution low-temperature photoluminescence (PL) spectra of GaAsInN, GaAsSbN and GaAsInSbN quantum wells (QWs) containing ∼1.5% N and emitting at 1.2–1.3 µm. Using photoreflectance and temperature-dependent PL spectroscopy, we measured the activation energies and band-tail width of localized states, associated with different atomic arrangements, to be 5–66 meV. We found that the emission intensity in these GaAs(In, Sb)N QWs weakly depends on carrier localization and that it is limited at cryogenic temperatures by exciton scattering by N interstitials, while at room temperature it is limited by an intrinsic non-radiative recombination channel having activation energy of ∼60 meV and capture time between 0.01 and 1 ps.
Sound-Induced Cochlear Ischemia/Hypoxia as a Mechanism of Hearing Loss. (1999)

This review will briefly examine evidence supporting the hypothesis that sound causes changes in cochlear blood flow, intracochlear oxygen levels, and the morphology of cochlear blood vessels. A survey of the literature shows that traditional histopathological studies provided such evidence and that decreased cochlear blood flow can be demonstrated and measured by laser Doppler flowmetry and by direct observation of cochlear microvessels. Oxygen levels also decline and possibly to a greater degree than blood flow. There is also evidence that in certain circumstances sound can increase blood flow. Reduced blood flow, or reduced oxygenation, is critically important in an organ system with high energy needs like the cochlea. Therefore, a second hypothesis, that sound-induced reduction in CBF represents a functional ischemia, will be explored in examining the relevance of traditional ischemia/reperfusion models to cochlear damage. It is found that reactive oxygen species (free radicals and oxidizing ions) are present in sound-induced hearing loss and thus there is evidence that an ischemia/reperfusion type of injury occurs during loud sound exposures.
Adenovirus-mediated wild-type p53 expression induces apoptosis and suppresses tumorigenesis of prostatic tumor cells. (1995)

The use of replication-deficient adenoviral vectors in gene therapy may become a powerful method to achieve efficient but safe transfer of anti-tumor agents. Introduction of the wild-type p53 gene into tumor cells has, in general, been associated with growth suppression. In this study, infection of androgen-independent human prostate Tsu-pr1 cells lacking functional p53 alleles resulted in high levels of p53 protein within 10-15 h. Cells infected with AdCMV.p53 detached from the substratum, condensed, and exhibited fragmentation of nuclear DNA into nucleosomal units consistent with the process of apoptosis. These effects were evident within 24 h after infection, and the majority of cells had undergone apoptosis by 48 h, whereas cells infected with AdCMV.NLS beta Gal continued to proliferate. Uninfected or AdCMV.NLS beta Gal-infected Tsu-pr1 cells formed tumors in nude mice within 3 weeks after implantation, whereas AdCMV.p53-infected cells failed to form tumors during this period. Therefore, adenoviral-mediated antitumor therapy using the p53 gene is an efficient method to inhibit prostate tumor growth, and agents that target the cellular programmed cell death pathway may be useful in clinical applications.