gebhart/patrepeval huggingface dataset:
Use of nitrate to control sulfide generation by sulfate-reducing bacteria associated with oily waste (1999)

Sulfide is a toxic and corrosive product of sulfate-reducing bacteria that can accumulate in oily waste streams to nuisance levels. Sludge associated with an oily waste stream was collected from a settling tank and used to assess sulfide generation activities. Methanogenesis was a predominant process in sludge in the absence of sulfate, and was suppressed by nitrate. Sulfate reduction and sulfide formation were evident when sulfate was available. Nitrate diminished sulfate reduction and prevented sulfide accumulation under freshwater, brackish, and saltwater conditions. Sodium-, potassium-, and calcium nitrate were equally effective in curtailing sulfide formation. The effects of nitrate on sulfate depletion were concentration-dependent, with 50 mM nitrate diminishing sulfate reduction, yet as little as 16 mM nitrate prevented sulfide accumulation. Sulfide was oxidized in nitrate-reducing incubations, and accumulation of sulfur or sulfate was observed. Nitrate reduction was accompanied by production of nitrite and nitrous oxide, which probably helped prevent sulfate reduction in extended incubations. Our results suggest that nitrate amendments control the formation of sulfide in oily waste streams both by preventing sulfate reduction and by stimulating anaerobic sulfide oxidation.
Palladium‐Catalyzed Allylic Fluorination (2011)

Mild and rapid: The title reaction is presented and its applicability to 18F radiolabeling is demonstrated (see scheme; TBAF=tetra-n-butylammonium fluoride, THF=tetrahydrofuran, dba=dibenzylideneacetone). The use of p-nitrobenzoate as the leaving group is significant to the success of this catalytic organometallic fluorination process. A range of allylic fluorides were synthesized by this method.
Induced electron transfer in ammineruthenium catechol and quinone complexes (1984)

ADVERTISEMENT RETURN TO ISSUEPREVArticleNEXTInduced electron transfer in ammineruthenium catechol and quinone complexesR. B. Salmonsen, A. Abelleira, M. J. Clarke, and S. D. PellCite this: Inorg. Chem. 1984, 23, 4, 385–387Publication Date (Print):February 1, 1984Publication History Published online1 May 2002Published inissue 1 February 1984https://pubs.acs.org/doi/10.1021/ic00172a001https://doi.org/10.1021/ic00172a001research-articleACS PublicationsRequest reuse permissionsArticle Views204Altmetric-Citations42LEARN 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 Get e-Alerts
The Thyroid Hormone Receptor β-Specific Agonist GC-1 Selectively Affects the Bone Development of Hypothyroid Rats (2005)

Treatment of hypothyroid rats with the TRbeta-specific agonist GC-1 partially reverts the skeletal development and maturation defects resultant of hypothyroidism. This finding suggests that TRbeta1 has an important role in bone development.
Spirochaetes (2001)

Abstract The spirochaetes are helically shaped or wave‐like, motile bacteria whose phylogenetic relationships are evident at the level of gross phenotypic characteristics. They are easily recognizable by their morphological properties, and possess some genomic features that are unique among the prokaryotes.
Melanoma-initiating cells exploit M2 macrophage TGFβ and arginase pathway for survival and proliferation (2014)

M2 macrophages promote tumor growth and metastasis, but their interactions with specific tumor cell populations are poorly characterized. Using a mouse model of spontaneous melanoma, we showed that CD34- but not CD34+ tumor-initiating cells (TICs) depend on M2 macrophages for survival and proliferation. Tumor-associated macrophages (TAMs) and macrophage-conditioned media protected CD34- TICs from chemotherapy in vitro. In vivo, while inhibition of CD115 suppressed the macrophage-dependent CD34- TIC population, chemotherapy accelerated its development. The ability of TICs to respond to TAMs was acquired during melanoma progression and immediately preceded a surge in metastatic outgrowth. TAM-derived transforming growth factor-β (TGFβ) and polyamines produced via the Arginase pathway were critical for stimulation of TICs and synergized to promote their growth.
Role of basic fibroblast growth factor in vascular lesion formation. (1991)

In the present study we investigated whether basic fibroblast growth factor (bFGF) plays a role in the proliferative response of smooth muscle cells (SMCs) to denuding injury. Rat carotid smooth muscle was found to express the mRNA for bFGF, and bFGF protein was found to be present in rat aorta by immunoblot analysis. Systemically administered bFGF was a potent mitogen for vascular SMCs in arteries denuded with a balloon catheter, increasing replication from 11.5% in controls to 54.8%. Denudation with a device (filament loop), which causes only minimal damage to medial SMCs, showed a similar increase in replication (1.3% versus 43.3%) after bFGF infusion. In unmanipulated vessels, however, SMCs were unresponsive to infused bFGF. Infusion of a "mitotoxin" (bFGF conjugated to saporin) caused a greater than 50% decrease in the number of viable SMCs in the arterial wall after balloon injury. Prolonged administration of bFGF (12 micrograms/day for 2 weeks) after balloon injury caused an approximately twofold increase in intimal thickening. These results show that bFGF, which is synthesized by the arterial wall, could be a potent mitogen for SMCs in vivo and suggest that any release of endogenous bFGF may be capable of stimulating SMC proliferation, which may subsequently lead to intimal lesion formation.
Methotrexate therapy for autoimmune hearing loss: A preliminary report (1994)

The management of autoimmune sensorineural hearing loss (SNHL) continues to challenge the otologist. Steroids and cyclophosphamide, the two traditional medications for this malady, are often associated with serious adverse reactions. In an effort to use a less toxic medication, the authors treated five autoimmune SNHL patients with low-dose oral methotrexate. Methotrexate has been found to be very effective in rheumatoid arthritis patients with acceptable adverse reactions. Preliminary results from this study indicate that methotrexate has the potential of being effective for autoimmune SNHL and associated otologic symptoms. Tolerance has been very good and side effects have been minimal.
Metodología de trabajo cliente-proveedor en el sector de la automoción: elementos comunes y diferenciadores (2000)

Thoracic epidural blockade reduced mPAP and serum level of TNF-α and increased cGMP. The treatment reversed upregulated expression of CREB at mRNA and protein production.
Impact of modifications of heterocyclic bases in CpG dinucleotides on their immune-modulatory activity (2004)

Synthetic phosphorothioate oligodeoxynucleotides (ODN) bearing unmethylated CpG motifs can mimic the immune-stimulatory effects of bacterial DNA and are recognized by Toll-like receptor 9 (TLR9). Past studies have demonstrated that nucleotide modifications at positions at or near the CpG dinucleotides can severely affect immune modulation. However, the effect of nucleotide modifications to stimulate human leukocytes and the mechanism by which chemically modified CpG ODN induce this stimulation are not well understood. We investigated the effects of CpG deoxyguanosine substitutions on the signaling mediated by human TLR9 transfected into nonresponsive cells. ODN incorporating most of these substitutions stimulated detectable TLR9-dependent signaling, but this was markedly weaker than that induced by an unmodified CpG ODN. One of the most active ODN tested contained deoxyinosine for deoxyguanosine substitutions (CpI ODN), but its relative activity to induce cytokine secretion on mouse cells was much weaker than on human cells. The activity was dependent on TLR9, as splenocytes from mice genetically deficient in TLR9 did not respond to CpI ODN stimulation. It is surprising that CpI ODN were nearly as strong as CpG ODN for induction of human B cell stimulation but were inferior to CpG ODN in their ability to induce T helper cell type 1 effects. These data indicate that certain deoxyguanosine substitutions in CpG dinucleotides are tolerated to stimulate a TLR9-mediated immune response, but this response is insufficient to induce optimal interferon-alpha-mediated effects, which depend on the presence of an unmodified CpG dinucleotide. These studies provide a structure-activity relationship for TLR9 agonist compounds with diverse immune effects.
Mesenchymal Stem Cells in Autoimmune Disease (2004)

Autoimmune diseases afflict more than 3% of the U.S. population. Current therapy for mild to moderate cases is symptomatic, however advanced cases suffer high morbidity and mortality. Advanced patients have benefited from stem cell therapy in the form of bone marrow transplantation in conjunction with high-dose cytotoxic therapy. Broader application of stem cell therapy requires better understanding of how adult stem cells affect development and foster treatment of autoimmune pathologies, and of better ways to manipulate the host immune responses. While extensive research documents the role of hematopoietic stem cells (HSCs) in autoimmune disease, few studies have addressed if and how mesenchymal stem cells (MSCs) contribute to their etiopathology. Recent characterization of MSCs and their role in hematopoiesis and immune modulation suggest that their potential for cell therapy extends beyond their traditional accessory function in HSC engraftment. MSCs contribute significantly to tissue restructuring and immune functioning, in addition to facilitating durable, long-lasting stem cell engraftment. MSCs are relatively easy to obtain and expand in in vitro cultures, rendering them a prime candidate for genetic manipulations for stem cell therapy. They have the potential to differentiate into multiple lineages such as osteoblasts, adipose tissue, cartilage, tendon, and stromal cells. The role of MSCs for autoimmune disease therapy could thus be based both on immune function modulation and contribution to hematopoiesis. In this review, we examine the biology of MSCs, and their potential for cell therapy of autoimmune disease.
Chicken IgL variable region gene conversions display pseudogene donor preference and 5' to 3' polarity. (1990)

Chicken immunoglobulin variable region diversity is generated during B-cell development in the bursa of Fabricius by intrachromosomal gene conversion, resulting in the replacement of sequence blocks within the unique rearranged VL1 and VH1 genes with homologous sequences derived from V region pseudogene segments (psi V). In this report, the nucleotide sequences of 217 gene conversion events in 52 random IgL clones were analyzed to characterize the molecular mechanism of gene conversion. The frequency of psi VL usage as gene conversion donors is shown to depend on the proximity of the psi VL segment to VL1, extent of homology with VL1, and relative orientation of the psi VL segments. Gene conversion events are not observed in the 5' region of homology between psi VL segments and VL1, but are distributed throughout the remainder of the VL1 exon. The 5' ends of individual gene conversion events always begin in regions of homology between the donor psi VL and recipient VL1 gene, whereas the 3' ends can occur in regions of nonhomology and often have nucleotide insertions or deletions. These results suggest a 5' to 3' polarity in the gene conversion mechanism. The implications of our data are discussed in relation to current molecular models of gene conversion.
Improvement of Coronary Vasomotion With Eicosapentaenoic Acid Does Not Inhibit Acetylcholine-Induced Coronary Vasospasm in Patients With Variant Angina. (1995)

Impaired function of the endothelium may be a mechanism of the coronary vasospasm induced by acetylcholine. We examined whether purified eicosapentaenoic acid (EPA), a major component of fish oil, improves the coronary vasomotion in response to acetylcholine, and the effect of purified EPA on acetylcholine (ACh)-induced coronary vasospasm in 22 patients with variant angina. ACh was infused into the coronary artery both before and after 4 months of EPA treatment (EPA 1.8 g/day, n = 12). In the control group (n = 10) that did not receive EPA, the response of the coronary diameter to ACh did not change over time. In the EPA-treated group, the cholinergic response in non-spastic sites changed from vasoconstriction to vasodilation, while ACh-induced coronary vasospasm persisted at the spastic sites. Therefore, EPA treatment improved the coronary vasomotor responsiveness to ACh, but did not inhibit ACh-induced coronary vasospasm.
21.3: A New Patterning Method for Full‐Color Polymer Light‐Emitting Devices: Laser Induced Thermal Imaging (LITI) (2002)

Abstract We have developed a new color patterning method for the patterning of full color polymer light‐emitting devices. Laser Induced Thermal Imaging (LITI) involves the imagewise exposure of a thermal transfer film with a scanning near infrared laser. During the process, light emitting polymer (LEP) is transferred from a thermal film to a circuitized substrate. Using the technology, we fabricated a 3.6″ QVGA full color active matrix polymer light‐emitting device (PLED).
All-fiber gyroscope with inertial-navigation short-term sensitivity (1982)

We report new experimental data for an all-fiber gyroscope with a noise density of 0.004(deg/h)(2)/Hz. This is compatible with the requirements for inertial navigation. Noise contributions from the coherent Rayleigh backscatter when a phase-modulation bias scheme is used and also from acoustic vibrations are discussed.
Junio de 1996 (1997)

No hay resúmenes disponibles.&#x0D; &#x0D; ECA Estudios Centroamericanos, Vol. 52, No. 584, 1997: 625-643.
SOST Is a Ligand for LRP5/LRP6 and a Wnt Signaling Inhibitor (2005)

Sclerosteosis is an autosomal recessive disease that is characterized by overgrowth of bone tissue and is linked to mutations in the gene encoding the secreted protein SOST. Sclerosteosis shares remarkable similarities with "high bone mass" diseases caused by "gain-of-function" mutations in the LRP5 gene, which encodes a coreceptor for Wnt signaling proteins. We show here that SOST antagonizes Wnt signaling in Xenopus embryos and mammalian cells by binding to the extracellular domain of the Wnt coreceptors LRP5 and LRP6 and disrupting Wnt-induced Frizzled-LRP complex formation. Our findings suggest that SOST is an antagonist for Wnt signaling and that the loss of SOST function likely leads to the hyperactivation of Wnt signaling that underlies bone overgrowth seen in sclerosteosis patients.
Lethality of Auger Electrons from the Decay of Bromine-77 in the DNA of Mammalian Cells (1982)

A. I. Kassis, S. J. Adelstein, C. Haydock, K. S. R. Sastry, K. D. McElvany, M. J. Welch, Lethality of Auger Electrons from the Decay of Bromine-77 in the DNA of Mammalian Cells, Radiation Research, Vol. 90, No. 2 (May, 1982), pp. 362-373
Large-Scale Small-Molecule Screen Using Zebrafish Embryos (2009)

Zebrafish represents a versatile model organism with many molecular, morphological, and physiological similarities to mammals. Importantly, zebrafish are readily susceptible to perturbations by small molecules, including numerous pharmaceuticals in clinical use. Given these qualities, plus their small size and transparency, zebrafish embryos can be utilized for large-scale phenotype-based screens for small-molecule modifiers of biological processes. Thus, in a manner analogous to classical genetic screens, zebrafish chemical screens have the potential to reveal novel insights into complex biological pathways, as well as to identify lead compounds for novel therapeutics.
O-GlcNAc Modification Protects against Protein Misfolding and Aggregation in Neurodegenerative Disease (2019)

Post-translational modifications (PTMs) of proteins are becoming the focus of intense research due to their implications in a broad spectrum of neurodegenerative diseases. Various PTMs have been identified to alter the toxic profiles of proteins which play critical roles in disease etiology. In Alzheimer's disease (AD), dysregulated phosphorylation is reported to promote pathogenic processing of the microtubule-associated tau protein. Among the PTMs, the enzymatic addition of N-acetyl-d-glucosamine (GlcNAc) residues to Ser/Thr residues is reported to deliver protective effects against the pathogenic processing of both amyloid precursor protein (APP) and tau. Modification of tau with as few as one single O-GlcNAc residue inhibits its toxic self-assembly. This modification also has the same effect on the assembly of the Parkinson's disease (PD) associated α-synuclein (ASyn) protein. In fact, O-GlcNAcylation ( O-linked GlcNAc modification) affects the processing of numerous proteins implicated in AD, PD, amyotrophic lateral sclerosis (ALS), and Huntington's disease (HD) in a similar manner. As such, manipulation of a protein's O-GlcNAcylation status has been proposed to offer therapeutic routes toward addressing multiple neurodegenerative pathologies. Here we review the various effects that O-GlcNAc modification, and its modulated expression, have on pathogenically significant proteins involved in neurodegenerative disease.
Tudor‐SN interacts with and co‐localizes with G3BP in stress granules under stress conditions (2010)

SGs are mRNA containing cytoplasmic structures that are assembled in response to stress. Tudor-SN protein is a ubiquitously expressed protein. Here, Tudor-SN protein was found to physiologically interact with G3BP, which is the marker and effector of SG. The kinetics of the assembly of SGs in the living cells demonstrated that Tudor-SN co-localizes with G3BP and is recruited to the same SGs in response to different stress stimuli. Knockdown of endogenous Tudor-SN did not inhibit the formation of SGs, but retarded the aggregation of small SGs into large SGs. Thus Tudor-SN may not be an initiator as essential as G3BP for the formation of SGs, but affects the aggregation of SGs. These findings identify Tudor-SN as a novel component of SGs.
Proteasome inhibition by lipofuscin/ceroid during postmitotic aging of fibroblasts (2000)

We have studied the effects of hyperoxia and of cell loading with artificial lipofuscin or ceroid pigment on the postmitotic aging of human lung fibroblast cell cultures. Normobaric hyperoxia (40% oxygen) caused an irreversible senescence‐like growth arrest after about 4 wk and shortened postmitotic life span from 1–1/2 years down to 3 months. During the first 8 wk of hyperoxia‐induced ‘aging’, overall protein degradation (breakdown of [ 35 S]methionine metabolically radiolabeled cell proteins) increased somewhat, but by 12 wk and thereafter overall proteolysis was significantly depressed. In contrast, protein synthesis rates were unaffected by 12 wk of hyperoxia. Lysosomal cathepsin‐specific activity (using the fluorogenic substrate z‐FR‐MCA) and cytoplasmic proteasome‐specific activity (measured with suc‐LLVY‐MCA) both declined by 80% or more over 12 wk. Hyperoxia also caused a remarkable increase in lipofuscin/ceroid formation and accumulation over 12 wk, as judged by both fluorescence measurements and FACscan methods. To test whether the association between lipofuscin/ceroid accumulation and decreased proteolysis might be causal, we next exposed cells to lipofuscin/ceroid loading under normoxic conditions. Lipofuscin/ceroid‐loaded cells indeed exhibited a gradual decrease in overall protein degradation over 4 wk of treatment, whereas protein synthesis was unaffected. Proteasome specific activity decreased by 25% over this period, which is important since proteasome is normally responsible for degrading oxidized cell proteins. In contrast, an apparent increase in lysosomal cathepsin activity was actually caused by a large increase in the number of lysosomes per cell. To test whether lipofuscin/ceroid could in fact directly inhibit proteasome activity, thus causing oxidized proteins to accumulate, we incubated purified proteasome with lipofuscin/ceroid preparations in vitro. We found that proteasome is directly inhibited by lipofuscin/ceroid. Our results indicate that an accumulation of oxidized proteins (and lipids) such as lipofuscin/ceroid may actually cause further increases in damage accumulation during aging by inhibiting the proteasome.–Sitte, N., Huber, M., Grune, T., Ladhoff, A., Doecke, W.‐D., von Zglinicki, T., Davies, K. J. A. Proteasome inhibition by lipofuscin/ceroid during postmitotic aging of fibroblasts. FASEB J. 14, 1490–1498 (2000)
Surface proteins of Mycoplasma hyopneumoniae identified from an Escherichia coli expression plasmid library (1985)

A genomic library of Mycoplasma hyopneumoniae was constructed by cloning random DNA fragments approximately 300 base pairs long in a fusion expression plasmid, pEx29, containing the N terminus of the phage MS2 polymerase under the control of the PL promoter of phage lambda. Clones that produced fusion proteins carrying surface-specific antigenic determinants were identified by using antiserum raised in a pig by intranasal inoculation of viable mycoplasmas. Rabbit antisera produced against gel-purified fusion proteins synthesized in Escherichia coli were analyzed by Western blotting to identify antigenically related mycoplasma components. Distinct mycoplasma proteins termed P90, P68, P50, P30, and P26 were identified. Evidence for the surface location of P90, P68, and P50 was provided by their sensitivity to trypsin and their comigration with lactoperoxidase-catalyzed iodinated proteins of intact mycoplasmas. Immune electron microscopy, performed with antiserum against the hybrid MS2-mycoplasma protein produced in E. coli and corresponding to P90, also showed that its antigenic determinant is associated with the mycoplasma surface.
Stereochemistry of the Cyclization-Rearrangement of (+)-Copalyl Diphosphate to (−)-Abietadiene Catalyzed by Recombinant Abietadiene Synthase from Abies grandis (2000)

[reaction: see text] Syntheses and enzymatic cyclizations of 8alpha-hydroxy-17-nor copalyl diphosphate (8a), (15R)-[15-2H1] 8b, and (15R,17E)-[15-3H1,17-2H1] copalyl diphosphate ([2H,3H] 2) catalyzed by recombinant abietadiene synthase (rAS) gave 17-nor manoyl oxide (9a), (16E)-[16-2H1] 9b, and (15S,16R)-[16-2H1,16-3H1] abietadiene ([2H1,3H1] 4), respectively. These and other results indicate that conversion of CPP (2) to abietadiene (4) occurs by anti S(N)' cyclization to a sandaracopimar-15-en-8-yl carbocation intermediate (13+, 13beta-methyl) followed by hydrogen transfer and methyl migration suprafacially on the si face of the vinyl group.