gebhart/patrepeval huggingface dataset:
THE ROLE OF MONOCYTE CHEMOATTRACTANT PROTEIN-1 (MCP-1) IN THE PATHOGENESIS OF COLLAGEN-INDUCED ARTHRITIS IN RATS (1997)

Collagen-induced arthritis was produced in rats by intradermal immunization with type II collagen and the expression and production of monocyte chemoattractant protein-1 (MCP-1) were examined by immunohistochemistry, enzyme-linked immunosorbent assay (ELISA), and Northern blot analysis. Two to three weeks after the immunization, the hindfeet showed swelling and redness, followed by the development of severe arthritis, particularly in the ankle joints. During this period, prominent infiltration of neutrophils and macrophages was observed. Sandwich ELISA and Northern blot analysis revealed that MCP-1 concentrations in the joint lavages and MCP-1 mRNA levels in the joint tissues both peaked at 2 weeks after the immunization. By immunohistochemistry, various types of cells, particularly neutrophils, macrophages, synovial cells, and vascular endothelial cells, stained positively for MCP-1. Finally, injection of a neutralizing monoclonal antibody against rat MCP-1 significantly decreased the number of exudate macrophages in the lesions and reduced the ankle swelling by about 30 per cent compared with controls. These results suggest that MCP-1 plays a critical role in this model in the recruitment of monocytes and in the development of arthritis.
Pulmonary Retention of Ultrafine and Fine Particles in Rats (1992)

In aerosol research, particle size has been mainly considered in the context of the role it plays in particle deposition along the respiratory tract. The possibility that the primary particle size may affect the fate of particles after they are deposited was explored in this study. Rats were exposed for 12 wk to aerosolized ultrafine (integral of 21 nm diameter) or fine (integral of 250 nm diameter) titanium dioxide (TiO2) particles. Other rats were exposed to TiO2 particles of various sizes (12, 21, 230, and 250 nm) by intratracheal instillation. After the rat lungs were extensively lavaged, analysis of particle content in the lavaged lungs, lavage fluid, and of lymphatic nodes was performed. Electron and light microscopy was also performed using unlavaged lungs. Both acute instillation and subchronic inhalation studies showed that ultrafine particles (integral of 20 nm) at equivalent masses access the pulmonary interstitium to a larger extent than fine particles (integral of 250 nm). An increasing dose in terms of particle numbers and a decreasing particle size promoted particle access into the interstitium. The translocation of particles into the interstitium appeared to be a function of the number of particles, and the process appeared to be related to the particle size, the delivered dose, and the delivered dose rate. A net effect of the preferential translocation of the smaller particles into the interstitium was a prolongation in their lung retention. After the 12-wk inhalation exposure, pulmonary clearance of ultrafine particles was slower (t1/2 = 501 days) than of larger particles (t1/2 = 174 days).(ABSTRACT TRUNCATED AT 250 WORDS)
Synthesis and characterization of a self‐crosslinkable polymer from cardanol: Autooxidation of poly(cardanyl acrylate) to crosslinked film (1993)

Abstract Cardanyl acrylate (CA), a monomer that yields crosslinkable copolymers, was synthesized by the reaction of cardanol with acryloyl chloride. A linear polymer was obtained by solution polymerization of the monomer in toluene using 0.8% azobisisobutyronitrile as initiator. Upon removal of solvent, the polymer undergoes crosslinking on exposure to air (or UV light) to give an insoluble transparent film. However, in bulk and suspension polymerization the polymer undergoes in situ crosslinking in the absence of any crosslinking agent. The polymer was characterized by IR, NMR, DSC, and GPC. The crosslinking reaction of soluble polymer on exposure to air at ambient conditions was explained by the hydroperoxide theory. © 1993 John Wiley &amp; Sons, Inc.
Microfabrication of freestanding porous silicon particles containing spectral barcodes (2006)

Abstract A method to microfabricate micron‐scale freestanding porous silicon photonic crystal particles is described. An electrochemically prepared film of porous silicon on a crystalline silicon substrate is patterned with an SU8‐25 photoresist, and the unmasked porous silicon is removed with a chlorine plasma reactive ion etch. Porous microparticles are then removed from the substrate by electropolishing. Scanning electron microscopy and microscopic reflection spectroscopy are used to characterize the geometry and optical properties of the freestanding particles. (© 2007 WILEY‐VCH Verlag GmbH &amp; Co. KGaA, Weinheim)
Refined physical mapping of chromosome 16-specific low-abundance repetitive DNA sequences (1993)

Repetitive DNA sequences have been implicated in the origin of several disease phenotypes, including fragile X syndrome, myotonic dystrophy, and spinal bulbar atrophy. In addition, a complex family of chromosome 16-specific low-abundance repetitive (CH16LAR) DNA sequences have been mapped by fluorescence in situ hybridization to regions of chromosome 16 that undergo breakage/rearrangement in acute nonlymphocytic leukemia (ANLL) cells. It has been hypothesized that these repetitive sequences are causally related to the chromosome rearrangements found in ANLL. Here, we further refine the mapping of CH16LAR sequences with respect to the ANLL inversion breakpoints, using a panel of somatic cell hybrids containing 51 different chromosome 16 breakpoints. These studies indicate that CH16LAR sequences at 16p13 are in close proximity to the ANLL short-arm breakpoint region. However, the region containing the highest density of CH16LAR sequences on the long arm appears to be distal to the region where the ANLL long-arm breakpoint has been mapped. These studies further show that CH16LAR sequences map in close proximity to FRA16D and FRA16A.
An engineered disulfide bond in dihydrofolate reductase (1987)

Substitution of cysteine for proline-39 in Escherichia coli dihydrofolate reductase by oligonucleotide-directed mutagenesis positions the new cysteine adjacent to already existing cysteine-85. When the mutant protein is expressed in the E. coli cytosol, the cysteine sulfur atoms are found, by X-ray crystallographic analysis, to be in van der Waals contact but not covalently bonded to one another. In vitro oxidation by dithionitrobenzoate results in formation of a disulfide bond between residues 39 and 85 with a geometry close to that of the commonly observed left-handed spiral. Comparison of 2.0-A-refined crystal structures of the oxidized (cross-linked) and reduced (un-cross-linked) forms of the mutant enzyme shows that the conformation of the enzyme molecule was not appreciably affected by formation of the disulfide bond but that details of the molecule's thermal motion were altered. The disulfide-cross-linked enzyme is at least 1.8 kcal/mol more stable with respect to unfolding, as measured by guanidine hydrochloride denaturation, than either the wild-type or the reduced (un-cross-linked) mutant enzyme. Nevertheless, the cross-linked form is not more resistant to thermal denaturation. Moreover, the appearance of intermediates in the guanidine hydrochloride denaturation profile and urea-gradient polyacrylamide gels indicates that the folding/unfolding pathway of the disulfide-cross-linked enzyme has changed significantly.
A G-Quadruplex Ligand with 10000-Fold Selectivity over Duplex DNA (2007)

ADVERTISEMENT RETURN TO ISSUEPREVCommunicationNEXTA G-Quadruplex Ligand with 10000-Fold Selectivity over Duplex DNAIsabelle M. Dixon, Frédéric Lopez, Agueda M. Tejera, Jean-Pierre Estève, Maria A. Blasco, Geneviève Pratviel, and Bernard MeunierView Author Information Laboratoire de Chimie de Coordination, CNRS, 205 route de Narbonne, 31077 Toulouse Cedex 4, France, INSERM IFR 31, Institut Louis Bugnard, Hôpital Rangueil, TSA 50032, 31059 Toulouse Cedex 9, France, Spanish National Cancer Center, Melchor Fernández Almagro 3, 28029 Madrid, Spain, INSERM U 531, Institut Louis Bugnard, Hôpital Rangueil, TSA 50032, 31059 Toulouse Cedex 9, France, and Palumed, BP 28262, 31682 Labège Cedex, France Cite this: J. Am. Chem. Soc. 2007, 129, 6, 1502–1503Publication Date (Web):January 20, 2007Publication History Received2 August 2006Published online20 January 2007Published inissue 1 February 2007https://pubs.acs.org/doi/10.1021/ja065591thttps://doi.org/10.1021/ja065591trapid-communicationACS PublicationsCopyright © 2007 American Chemical SocietyRequest reuse permissionsArticle Views3991Altmetric-Citations166LEARN ABOUT THESE METRICSArticle Views are the COUNTER-compliant sum of full text article downloads since November 2008 (both PDF and HTML) across all institutions and individuals. These metrics are regularly updated to reflect usage leading up to the last few days.Citations are the number of other articles citing this article, calculated by Crossref and updated daily. Find more information about Crossref citation counts.The Altmetric Attention Score is a quantitative measure of the attention that a research article has received online. Clicking on the donut icon will load a page at altmetric.com with additional details about the score and the social media presence for the given article. Find more information on the Altmetric Attention Score and how the score is calculated. Share Add toView InAdd Full Text with ReferenceAdd Description ExportRISCitationCitation and abstractCitation and referencesMore Options Share onFacebookTwitterWechatLinked InRedditEmail Other access optionsGet e-AlertscloseSupporting Info (1)»Supporting Information Supporting Information SUBJECTS:G-Quadruplex,Genetics,Peptides and proteins,Pyrroles,Selectivity Get e-Alerts
Energy, the world and the nuclear contribution (1985)

By the year 2030 the world's population will have increased from its present 4 billion (four thousand million) or thereabouts to some 8 billion. Some studies propose a higher figure; few suggest anything lower, Figure 1. The question is, of course, how much per capita energy will be needed - demanded - required, indeed - for the then doubled world's population. Resolution of this question poses the two further questions namely, what rates of GDP growth will be achieved, nation by nation and area by area; and what energy/GDP coefficient will underwrite, and be necessary for, this growth.
Transmission dynamics of the COVID‐19 outbreak and effectiveness of government interventions: A data‐driven analysis (2020)

Using the parameterized susceptible-exposed-infectious-recovered model, we simulated the spread dynamics of coronavirus disease 2019 (COVID-19) outbreak and impact of different control measures, conducted the sensitivity analysis to identify the key factor, plotted the trend curve of effective reproductive number (R), and performed data fitting after the simulation. By simulation and data fitting, the model showed the peak existing confirmed cases of 59 769 arriving on 15 February 2020, with the coefficient of determination close to 1 and the fitting bias 3.02%, suggesting high precision of the data-fitting results. More rigorous government control policies were associated with a slower increase in the infected population. Isolation and protective procedures would be less effective as more cases accrue, so the optimization of the treatment plan and the development of specific drugs would be of more importance. There was an upward trend of R in the beginning, followed by a downward trend, a temporary rebound, and another continuous decline. The feature of high infectiousness for severe acute respiratory syndrome coronavirus 2(SARS-CoV-2) led to an upward trend, and government measures contributed to the temporary rebound and declines. The declines of R could be exploited as strong evidence for the effectiveness of the interventions. Evidence from the four-phase stringent measures showed that it was significant to ensure early detection, early isolation, early treatment, adequate medical supplies, patients' being admitted to designated hospitals, and comprehensive therapeutic strategy. Collaborative efforts are required to combat the novel coronavirus, focusing on both persistent strict domestic interventions and vigilance against exogenous imported cases.
Wild-type p53 suppresses growth of human prostate cancer cells containing mutant p53 alleles. (1991)

Evidence supporting a broad role for the inactivation of the p53 gene in human tumorigenesis has been provided by studies showing that the p53 gene is mutated in many human cancers. In this study, we report on the mutational status of the p53 gene in prostate cancer cells and provide functional evidence that the wild-type p53 gene may have a role in suppressing prostatic tumorigenesis. Sequence analysis of exons 5-8 of the p53 gene reveals that three of five prostate cancer cell lines (TSUPr-1, PC3, DU145) contain mutations which alter the amino acid sequence of this most highly conserved portion of the gene. One of two primary prostatic cancer specimens examined also contained a mutation in this region. Transfection of the wild-type p53 gene versus a mutated p53 gene into two cell lines with p53 mutations results in reduced colony formation. Wild-type p53 gene expression is apparently incompatible with continued growth of these tumor cells inasmuch as none of the colonies which formed after wild-type transfections retain the transfected p53 sequences. Immunocytochemical data indicate that prostate carcinoma cells expressing the transfected wild-type p53 gene are growth arrested because they exhibit a reduced level of thymidine incorporation into DNA. This study is the first report of p53 gene mutations in prostate cancer cells and suggests a functional role for the p53 gene in suppressing prostatic tumorigenesis.
Expression of interleukin‐1 receptors and their role in interleukin‐1 actions in murine microglial cells (2002)

Interleukin (IL)-1 is an important mediator of acute brain injury and inflammation, and has been implicated in chronic neurodegeneration. The main source of IL-1 in the CNS is microglial cells, which have also been suggested as targets for its action. However, no data exist demonstrating expression of IL-1 receptors [IL-1 type-I receptor (IL-1RI), IL-1 type-II receptor (IL-1RII) and IL-1 receptor accessory protein (IL-1RAcP)] on microglia. In the present study we investigated whether microglia express IL-1 receptors and whether they present target or modulatory properties for IL-1 actions. RT-PCR analysis demonstrated lower expression of IL-1RI and higher expression of IL-1RII mRNAs in mouse microglial cultures compared with mixed glial or pure astrocyte cultures. Bacterial lipopolysaccharide (LPS) caused increased expression of IL-1RI, IL-1RII and IL-1RAcP mRNAs, induced the release of IL-1beta, IL-6 and prostaglandin-E2 (PGE2), and activated nuclear factor kappaB (NF-kappaB) and the mitogen-activated protein kinases (MAPKs) p38, and extracellular signal-regulated protein kinase (ERK1/2), but not c-Jun N-terminal kinase (JNK) in microglial cultures. In comparison, IL-1beta induced the release of PGE2, IL-6 and activated NF-kappaB, p38, JNK and ERK1/2 in mixed glial cultures, but failed to induce any of these responses in microglial cell cultures. IL-1beta also failed to affect LPS-primed microglial cells. Interestingly, a neutralizing antibody to IL-1RII significantly increased the concentration of IL-1beta in the medium of LPS-treated microglia and exacerbated the IL-1beta-induced IL-6 release in mixed glia, providing the first evidence that microglial IL-1RII regulates IL-1beta actions by binding excess levels of this cytokine during brain inflammation.
A novel high-frequency quasi-SOI power MOSFET for multi-gigahertz applications (2002)

We have fabricated a high-efficiency quasi-SOI power MOSFET for multi-gigahertz applications. The device was formed by reversed silicon wafer direct bonding which enables easy use of a high-resistivity substrate. The breakdown voltage of the quasi-SOI power MOSFET is more than twice that of a conventional SOI power MOSFET. Fmax of the quasi-SOI power MOSFET is 11.0 GHz, about 15% higher than that of the SOI power MOSFET. The fabricated device has the excellent power added efficiency of 68% at a 2 GHz under 3.6 V operation.
Cleavage of arginyl-arginine and lysyl-arginine from the C-terminus ofpro-hormone peptides by human germinal angiotensin I-converting enzyme (ACE) and the C-domain of human somatic ACE (1997)

Mammalian germinal angiotensin I-converting enzyme (gACE) is a single-domain dipeptidyl carboxypeptidase found exclusively in male germ cells, which has almost identical sequence and enzymic properties with the C-domain of the two-domain somatic ACE. Mutant mice that do not express gACE are infertile, suggesting a role for the enzyme in the processing of undefined peptides involved in fertilization. A number of spermatid peptides [e.g. cholecystokinin (CCK) and gastrin] are processed from pro-hormones by endo- and exo-proteolytic cleavages which might generate substrates for gACE. We have shown that peptide hormone intermediates with Lys/Arg-Arg at the C-terminus are high-affinity substrates for human gACE. gACE from human sperm cleaved Arg-Arg from the C-terminus of the CCK5-GRR (GWMDFGRR), a peptide corresponding to the C-terminus of a CCK-gastrin prohormone intermediate. Hydrolysis of CCK5-GRR by recombinant human C-domain ACE was Cl- dependent, with maximal activity achieved in 5-10 mM NaCl at pH 6.4. C-Domain ACE cleaved Lys/Arg-Arg from the C-terminus of dynorphin-(1-7), a pro-TRH peptide KRQHPGKR, and two insect peptides FSPRLGKR and FSPRLGRR. C-Domain ACE displayed high affinity towards all these substrates with Vmax/Km values between 14 and 113 times greater than the Vmax/Km for the conversion of the best known ACE substrate, angiotensin I, into angiotensin II. In conclusion, we have identified a new class of substrates for human gACE, and we suggest that gACE might be an alternative to carboxypeptidase E for the trimming of basic dipeptides from the C-terminus of intermediates generated from pro-hormones by subtilisin-like convertases in human male germ cells.
Visualizing and quantifying protein secretion using aRenilla luciferase-GFP fusion protein (2000)

We have shown previously that an engineered form of Renilla luciferase (SRUC) can be secreted as a functional enzyme by mammalian cells, and that fusing wild-type Renilla luciferase with the green fluorescent protein from Aequorea victoria (GFP) yields a chimeric protein retaining light-emission properties similar to that of unfused Renilla luciferase and GFP. In the work presented here, SRUC was fused with GFP to determine whether it could be used to both visualize and quantify protein secretion in mammalian cells. Simian COS-7 and Chinese hamster ovary (CHO) cells were transiently transfected with gene constructs encoding a secreted or an intracellular version of a Renilla luciferase-GFP fusion protein. Renilla luciferase activity was measured from COS-7 cell lysates and culture media, and GFP activity was detected in CHO cells using fluorescence microscopy. Data indicated that the SRUC-GFP fusion protein was secreted as a chimeric protein that had both Renilla luciferase and GFP activity. This fusion protein could be a useful marker for the study of protein secretion in mammalian cells.
Kinetics and cellular localisation of putrescine uptake in human lung tissue. (1993)

These results show that the human lung possesses an active uptake system for putrescine, and probably also cystamine, which is located in both cell types of the alveolar epithelium. These findings may be used to develop tests for the assessment of the alveolar epithelium.
Human homologue of maid: A dominant inhibitory helix-loop-helix protein associated with liver-specific gene expression (2000)

The helix-loop-helix (HLH) family of transcriptional regulatory proteins are key regulators in numerous developmental processes. The class I HLH proteins, such as E12 are ubiquitously expressed. Class II HLH proteins, such as MyoD, are expressed in a tissue-specific manner. Class I and II heterodimers can bind to E-boxes (CANNTG) and regulate lineage commitments of embryonic cells. In an attempt to identify partners for the E12 protein that may exert control during liver development, we performed the yeast 2-hybrid screen using an expression complementary DNA library from human fetal liver. A novel dominant inhibitory HLH factor, designated HHM (human homologue of maid), was isolated and characterized. HHM is structurally related to the Id family and was highly expressed in brain, pituitary gland, lung, heart, placenta, fetal liver, and bone marrow. HHM physically interacted with E12 in vitro and in mammalian cells. Comparison of the dominant inhibitory effects of HHM and Id2 on the binding of E12/MyoD dimer to an E-box element revealed a weaker inhibition by HHM. However, HHM but not Id2 specifically inhibited the luciferase gene activation induced by hepatic nuclear factor 4 (HNF4) promoter. The HHM was transiently expressed during stem-cell-driven regeneration of the liver at the stage in which the early basophilic foci of hepatocytes started to appear. These results suggest that HHM is a novel type of dominant inhibitory HLH protein that might modulate liver-specific gene expression.
Molecular basis for a polymorphism involving Fc receptor II on human monocytes. (1989)

IgG Fc receptor II (Fc gamma RII) on human monocytes is polymorphic with respect to its appearance on gels after isoelectric focusing and with respect to its ability to mediate T lymphocyte proliferation induced by murine anti-CD3 mAb of the IgG1 isotype (i.e., its ability to bind murine IgG1). To determine the molecular basis for this polymorphism, we isolated total cellular RNA from PBMC of responders and nonresponders (defined by Leu-4-induced [3H] thymidine incorporation) and synthesized corresponding cDNA. Sequences encoding the extracellular domain of Fc gamma RII were then amplified using the Taq polymerase chain reaction. Amplified DNA fragments were cloned into pUC vectors, and sequenced. Analysis of clones from two nonresponders revealed a single base change (G for A) at position 519, which would result in the substitution of a histidine for an arginine at residue 133 in the mature Fc gamma RII protein. These findings suggest that the polymorphism involving human monocyte Fc gamma RII results from allelic variation of a single gene.