gebhart/patrepeval huggingface dataset:
Glycine‐Like Modulation of N‐Methyl‐d‐Aspartate Receptors by a Monoclonal Antibody That Enhances Long‐Term Potentiation (1991)

We have identified a monoclonal antibody, B6B21, that significantly elevates long-term potentiation when applied to CA1 pyramidal cell apical dendrites in rat hippocampal slices and characterized its binding to N-methyl-D-aspartate-receptor complexes using extensively washed hippocampal membranes. Five micrograms of affinity-purified B6B21 per 100 micrograms of membranes gave a two- to threefold elevation in N-[1-(2-thienyl)cyclohexyl]-3,4-[3H]piperidine ([3H]TCP) binding. When [3H]TCP binding was stimulated by the combined addition of maximal concentrations of glutamate, glycine, and magnesium, B6B21 no longer stimulated [3H]TCP binding. Like glycine, B6B21 enhanced the effect of N-methyl-D-aspartate and glutamate in stimulating [3H]TCP binding. Moreover, B6B21 reversed 7-chlorokynurenic acid inhibition of [3H]TCP binding, but it had no effect on the inhibition of [3H]TCP binding by D-(-)-2-amino-5-phosphonovaleric acid. B6B21 increased the rate of association and dissociation of [3H]TCP, but had no effect on equilibrium binding. Glutamate, but not glycine, however, increased B6B21-enhancement of [3H]TCP association and dissociation. B6B21 binding at strychnine-insensitive glycine sites was confirmed by direct measurement of [3H]glycine binding. These results suggest that B6B21 binds directly to N-methyl-D-aspartate receptors and displays properties similar to glycine.
Ruthenium(II)-bipyrimidine complexes. Spectroscopic and electrochemical properties of a novel series of compounds (1977)

ADVERTISEMENT RETURN TO ISSUEPREVArticleNEXTRuthenium(II)-bipyrimidine complexes. Spectroscopic and electrochemical properties of a novel series of compoundsMax Hunziker and Andreas LudiCite this: J. Am. Chem. Soc. 1977, 99, 22, 7370–7371Publication Date (Print):October 1, 1977Publication History Published online1 May 2002Published inissue 1 October 1977https://pubs.acs.org/doi/10.1021/ja00464a054https://doi.org/10.1021/ja00464a054research-articleACS PublicationsRequest reuse permissionsArticle Views995Altmetric-Citations117LEARN 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-Alertsclose Get e-Alerts
Macrophage migration inhibitory factor: a counter-regulator of glucocorticoid action and critical mediator of septic shock. (1997)

Recent studies have led to the discovery of a mediator that acts as an endogenous counter-regulator of glucocorticoid action within the immune system. Isolated as a product of anterior pituitary cells, this protein was found to have the sequence of macrophage migration inhibitory factor (MIF), one of the first cytokine activities to be described. Macrophages and T cells release MIF in response both to various inflammatory stimuli and upon incubation with low concentrations of glucocorticoids. The glucocorticoid-induced secretion of MIF is tightly regulated and decreases at high, anti-inflammatory steroid concentrations. Once secreted, MIF "overrides" the anti-inflammatory and immunosuppressive effects of steroids on macrophage and T-cell cytokine production. The physiological role of MIF thus appears to be to counter-balance steroid inhibition of the inflammatory response. Anti-MIF antibodies fully protect animals from experimentally induced gram-negative or gram-positive septic shock, an effect that may be the result of the increased anti-inflammatory effects of glucocorticoids after neutralization of endogenous MIF. Anti-MIF therapeutic strategies are presently under development and may prove to be a means to modulate cytokine production in septic shock as well as in other inflammatory disease states.
Transient appearance of CRES protein during spermatogenesis and caput epididymal sperm maturation (1995)

In previous studies we identified an epididymal gene that exhibits homology to the cystatin family of cysteine protease inhibitors. The expression of this gene, termed CRES (cystatin-related epididymal and spermatogenic), was shown to be highly restricted to the proximal caput epididymal epithelium with less expression in the testis and no expression in the 24 other tissues examined. In this report, studies were carried out to examine CRES gene expression in the testis as well as to characterize the CRES protein in the testis and epididymis. In situ hybridization experiments revealed that within the testis CRES gene expression is stage-specific during spermatogenesis and is exclusively expressed by the round spermatids of Stages VII-VIII and the early elongating spermatids of Stages IX and X. Immunohistochemical studies demonstrated that CRES protein was transiently expressed in both the testis and epididymis. Within the testis the protein was localized to the elongating spermatids, whereas within the epididymis CRES protein was exclusively synthesized by the proximal caput epithelium and then secreted into the lumen. Surprisingly, the secreted CRES protein had completely disappeared from the epididymal lumen by the distal caput epididymidis. Western blot analysis of testicular and epididymal proteins showed that the CRES antibody specifically recognized a predominant 19 kDa CRES protein and a less abundant 14 kDa form. These observations suggest that the CRES protein performs a specialized role during sperm development and maturation.
N-formimidoyl analogues of distamycin (1996)

Novel N-formimidoyl analogues of distamycin, bearing a second positive charge (3–5) or a single positive charge (6) at the N-terminus, were synthesised and assayed for their DNA affinity and anti-herpes activity.
PRINCIPLES THAT DETERMINE THE STRUCTURE OF PROTEINS (1984)

The Hippo pathway was initially discovered in Drosophila melanogaster as a key regulator of tissue growth. It is an evolutionarily conserved signaling cascade regulating numerous biological processes, including cell growth and fate decision, organ size ...Read More
Activation of the First Component of Complement (1987)

Exhausted CD8 T (Tex) cells are a distinct cell lineage that arise during chronic infections and cancers in animal models and humans. Tex cells are characterized by progressive loss of effector functions, high and sustained inhibitory receptor expression, ...Read More
Expression of myogenic regulatory proteins (myogenin and MyoD1) in small blue round cell tumors of childhood. (1995)

The distinction of rhabdomyosarcoma (RMS) from other small blue round cell tumors of childhood, such as Ewing's sarcoma/peripheral primitive neuroectodermal tumor (pPNET) and neuroblastoma, continues to present a diagnostic challenge to pathologists. The recent recognition of the master role of myogenic regulatory proteins in skeletal muscle commitment and differentiation, and the availability of monoclonal antibodies to two of them (myogenin and MyoD1), has prompted us to test their diagnostic utility in routinely processed, formalin-fixed, and deparaffinized tissue. Preliminary studies had demonstrated that, with the use of heat-induced epitope retrieval techniques, expression of myogenin and MyoD1 could be documented specifically in nuclei of fetal skeletal muscle by the respective antibodies. We performed a retrospective immunohistochemical analysis on 72 cases of small blue round cell tumors, including 33 RMSs, 1 metastatic myogenous Wilms' tumor, 26 Ewing's sarcomas/pPNETs, and 12 neuroblastomas. Nuclear expression of myogenin and MyoD1 were both found in 30/33 non-overlapping cases of RMS, with no significant differences in the sensitivity with respect to histological subtypes, and in 1/1 case of myogenous Wilms' tumor. None of the neuroblastomas or Ewing's sarcomas/pPNETs demonstrated positive nuclear staining with either antibody. However, most of the neuroblastomas, and occasional Ewing's sarcomas/pPNETs, showed variable fibrillary, cytoplasmic immunoreactivity with antibody to MyoD1. We conclude that, with the use of microwave-based epitope retrieval, antibodies to myogenin and MyoD1 are both useful markers for the identification of RMS among other small blue round cell tumors of childhood, but antibodies to myogenin have technical advantages over those to MyoD1, as the latter may cross-react with an unknown cytoplasmic antigen in non-muscle cells and tumors.
Design of axial-flux permanent-magnet low-speed machines and performance comparison between radial-flux and axial-flux machines (2005)

This thesis presents an alternative approach to the analytical design of surface-mounted axialflux permanent-magnet machines. Emphasis has been placed on the design of axial-flux machines with a one-rotor-two-stators configuration. The design model developed in this study incorporates facilities to include both the electromagnetic design and thermal design of the machine as well as to take into consideration the complexity of the permanent-magnet shapes, which is a typical requirement for the design of high-performance permanent-magnet motors. A prototype machine with rated 5 kW output power at 300 min-1 rotation speed has been designed and constructed for the purposesof ascertaining the results obtained from the analytical design model. A comparative study of low-speed axial-flux and low-speed radial-flux permanent-magnet machines is presented. The comparative study concentrates on 55 kW machines with rotation speeds 150 min-1, 300 min-1 and 600 min-1 and is based on calculated designs. A novel comparison method is introduced. The method takes into account the mechanical constraints of the machine and enables comparison of the designed machines, with respect to the volume, efficiency and cost aspects of each machine. It is shown that an axial-flux permanent-magnet machine with one-rotor-two-stators configuration has generally a weaker efficiency than a radial-flux permanent-magnet machine if for all designs the same electric loading, air-gap flux density and current density have been applied. On the other hand, axial-flux machines are usually smaller in volume, especially when compared to radial-flux machines for which the length ratio (axial length of stator stack vs. air-gap diameter)is below 0.5. The comparison results show also that radial-flux machines with alow number of pole pairs, p &lt; 4, outperform the corresponding axial-flux machines.
Splice Variants of the Human EP3 Receptor for Prostaglandin E2 (1995)

The EP3 receptor for prostaglandin E2 (PGE2) mediates various biological activities such as uterine contraction, inhibition of gastric acid secretion, presynaptic inhibition of neurotransmitter release and potentiation of platelet aggregation. In an attempt to understand the molecular basis of this diversity of biological function, we cloned full-length cDNAs encoding EP3 receptors for PGE2 from human uterus cDNA libraries. Seven cDNA variants were identified which code for six distinct EP3-receptor isoforms. Sequencing revealed that the receptor isoforms differ in their intracellular C-terminal domains. Southern blot experiments indicate that the isoforms are generated by alternative splicing. The EP3-receptor gene is expressed in various tissues with high expression in kidney and pancreas, as demonstrated by Northern blot analysis. All receptors, stably expressed in baby hamster kidney (BHK) cells, bind PGE2 specifically with similar Kd of 2.2-5.8 nM. The binding of [3H]PGE2 is competed with by unlabelled prostaglandins in the order sulprostone (a PGE2-like agonist) approximately PGE2 >> PGF2 alpha > Iloprost (a prostacyclin analogue) > PGD2, which is specific for EP3 receptors. Analysis of the signal-transduction pathways demonstrated that all receptors respond with inhibition of forskolin-induced cAMP accumulation with an IC50 of 0.1-3 nM PGE2. In addition, some isoforms induce an increase in intracellular free calcium ([Ca2+]i) at PGE2 concentrations greater than or equal to 10 nM. These results may offer an explanation for the different physiological responses observed in various tissues following activation of EP3 receptors.
The 68-kilodalton E1 protein of bovine papillomavirus is a DNA binding phosphoprotein which associates with the E2 transcriptional activator in vitro (1991)

The E1 open reading frame of bovine papillomavirus type 1 encodes factors necessary for extrachromosomal maintenance of the viral genome in transformed cells. To facilitate biochemical characterization of the gene products encoded by this open reading frame, we have expressed the full-length E1 protein in a baculovirus-insect cell system. This protein was found to be phosphorylated and localized to the nucleus of infected cells. The E1 protein alone has affinity for DNA but appears to lack specificity for viral sequences. In addition, we present evidence that the E1 protein interacts with the virally encoded transcriptional activator E2 in vitro. These results are consistent with a model in which the E1 protein, as part of a complex with E2, interacts with specific DNA sequences in the viral genome.
Establishment of a Human Pancreatic Tumor Xenograft Model (1998)

Adenocarcinoma of the pancreas is currently the fifth leading cause of death in the United States. It remains generally incurable by available treatment modalities. We report here on the characterization of a permanent pancreatic cell line (KCI-MOH1), established as a xenograft in severe combined immune deficient (SCID) mice, from a 74 year-old African American male patient diagnosed with pancreatic cancer. Sections from paraffin-embedded tumors excised from SCID mice revealed typical adenocarcinoma of the pancreas. Karyotypic analysis of cultured cells derived from tumors grown in SCID mice revealed a male karyotype with multiple clonal aberrations: 42, XY, add (3)(p11.2), der(7) t(7;12) (p22;q12), -10, -12, add (14)(p11), -18, add (20)(q13)-22/84, idemx2. Immunostaining of KCI-MOH1 tissues shows strong expression of p53 and p21 proteins. The xenograft model was established by transplanting the KCI-MOH1 cells subcutaneously (s.c.) in SCID mice. When the s.c. tumor was transplanted in vivo to other SCID mice, the success rate was 100%, with a doubling time of 8.5 days. The SCID mouse xenograft model was used to test the efficacy of selected standard chemotherapeutic drugs (taxol, gemcitabine, 5-fluorouracil, and Ara-C) and novel biological agents (Bryostatin 1 and Auristatin-PE). Results show that gemcitabine, Ara-C, and Bryostatin 1 were active against KCI-MOH1. The xenograft described herein can be used as an animal model to facilitate the development of novel therapeutic agents against human pancreatic cancers.
Controlled modification of heterojunction band lineups by diffusive intralayers (1990)

We explore the effects of ultrathin Au intralayers at the interfaces of the lattice-matched heterojunctions ZnSe–Ge and GaP–Si, and compare them to earlier results with Al intralayers. Au intralayers do not chemically react with the semiconductors and diffuse strongly into both sides of the junction, whereas Al intralayers react and remain localized to the interface. Not only do the intralayer metals diffuse differently, but they cause the semiconductor components to interdiffuse differently. Comparison gives insight concerning interface-localized effects on the valence band discontinuity.
Acute and sublethal effects of two insecticides on earthworms (Lumbricus terrestris L.) under laboratory conditions (2003)

Earthworms (Lumbricus terrestris L.) were exposed to commercial formulations of endosulfan and aldicarb for 2, 7, and 15 days, and the LC(10), LC(25), and LC(50) were determined. Worms were then exposed to LC(10), LC(25), and LC(50) concentrations of endosulfan and LC(10) and LC(25) concentrations of aldicarb. The growth rate and total protein content were determined and related to endosulfan and aldicarb residues in soil and earthworms. Aldicarb was more toxic than endosulfan under the experimental conditions. The residues of endosulfan and aldicarb caused a significant reduction in the growth rate and total protein content of earthworms. The residues of endosulfan and aldicarb were monitored in soil and earthworms after 2, 7, and 15 days of exposure. The residues remaining in the soil after the experiments ranged between 37.75% and 68.54% of the applied concentration for endosulfan and between 10.13% and 67.71% of the applied concentration for aldicarb. Small amounts of both insecticides were detected in worms, and accumulation was more important for endosulfan. This study proposes the use of growth rate and total protein content as biomarkers for contamination by endosulfan and aldicarb.
Protein deprivation: its effects on fever and plasma iron during bacterial infection in rabbits. (1979)

1. The effects of chronic dietary protein deprivation on fever and host plasma iron reduction in bacterially infected rabbits (Oryctolagus cuniculus) were investigated. 2. Injection with Pasteurella multocida, a Gram-negative bacterium pathogenic to rabbits, led to an attenuated 24 hr fever in the protein-deprived rabbits (0.26 degrees C) compared with the 24 hr fever in the control rabbits (1.43 degrees C). 3. Plasma iron concentration remained relatively high in the protein-deprived rabbits as measured 24 hr after injection with bacteria. Total iron binding capacity did not change in the protein-deprived rabbits as measured 24 hr after injection with bacteria. 4. Inoculation of the rabbits with endogenous pyrogen from donor rabbits resulted in fever and reduction in plasma iron concentration that was of equal magnitude in the protein-deprived and control rabbits. 5. There were no differences in the concentration of total circulating leukocytes or in the differential count between the protein-deprived and control rabbits before and 24 hr after injection with bacteria. 6. These data support the hypothesis that chronic protein deprivation in rabbits results in a diminished synthesis or release, or both, of endogenous pyrogen from circulating leukocytic phagocytes, resulting in an attenuated fever and a relative hyperferremia during infection.
Design and Synthesis of a Stable Supramolecular Trigonal Prism Formed by the Self-Assembly of a Linear Tetrakis(Zn2+−cyclen) Complex and Trianionic Trithiocyanuric Acid in Aqueous Solution and Its Complexation with DNA (Cyclen = 1,4,7,10-Tetraazacyclododecane) (2009)

A new supramolecular complex, {(Zn(4)L(4))(3)-(TCA(3-))(4)}(12+), was designed and synthesized by the 3:4 self-assembly of a linear tetrakis(Zn(2+)-cyclen) complex (Zn(4)L(4))(8+) and trianionic trithiocyanurate (TCA(3-)) in aqueous solution (cyclen = 1,4,7,10-tetraazacyclododecane). The {(Zn(4)L(4))(3)-(TCA(3-))(4)}(12+) complex, which should have a trigonal prism configuration, was found to be very stable in aqueous solution at neutral pH and 25 degrees C, as evidenced by (1)H NMR titration, potentiometric pH and UV titrations, and MS measurements. The complex does not dissociate into the starting building blocks in the presence of Zn(2+)-binding anions such as phosphates and double-stranded DNA. The results of the competitive binding assays with ethidium bromide and calf-thymus DNA, thermal melting experiments, gel mobility shift assays, and dynamic light-scattering data strongly indicated that the trigonal prism functions as a polycationic template to induce the aggregation of double-stranded DNA.
Palladium-catalyzed cyanation of aryl and heteroaryl iodides with copper(I) cyanide (1999)

T. Sakamoto and K. Ohsawa, J. Chem. Soc., Perkin Trans. 1, 1999, 2323 DOI: 10.1039/A903345I
bcl-xLx is the major bcl-x mRNA form expressed during murine development and its product localizes to mitochondria (1994)

Most examples of cell death in animals are controlled by a genetic program that is activated within the dying cell. The apoptotic process is further regulated by a set of genes that act as repressors of cell death. Of these, bcl-2 is expressed in a variety of embryonic and postnatal tissues which suggests a critical role for bcl-2 in organogenesis and tissue homeostasis. Surprisingly, mutant mice with targeted disruption of bcl-2 appear normal at birth and complete maturation of lymphoid tissues before succumbing to fulminant lymphopenia and polycystic renal disease by 2-5 weeks of age. This suggests that there may be genes other than bcl-2 that can regulate apoptosis during development. To begin to investigate this possibility, we have cloned and characterized the murine bcl-x gene, whose human counterpart displays striking homology to bcl-2. The predicted murine bcl-xL gene product exhibits a high level of amino acid identity (97%) to its human counterpart. Just like Bcl-2, the murine bcl-xL gene product can act as a dominant inhibitor of cell death upon growth factor withdrawal. In addition, the bulk of the bcl-xL product localizes to the periphery of mitochondria as assessed by a bcl-xL-tag expression system, suggesting that both Bcl-2 and Bcl-xL proteins prevent cell death by a similar mechanism. bcl-xL is the most abundant bcl-x mRNA species expressed in embryonic and adult tissues. The levels of bcl-xL mRNA appear higher than those of bcl-2 during embryonal development and in several adult organs including bone marrow, brain, kidney and thymus. In addition to bcl-xL, we have identified another form of bcl-x mRNA, bcl-x beta, that results from an unspliced bcl-x transcript. bcl-x beta mRNA is expressed in various embryonic and postnatal tissues. Surprisingly, the expression of bcl-xS (a negative regulator of programmed cell death) was undetectable by a sensitive S1-nuclease assay and polymerase chain reaction analysis of mouse tissues. Based on its tissue and developmental patterns of expression, it appears that bcl-x may play an important role in the regulation of cell death during development and tissue homeostasis.