gebhart/patrepeval huggingface dataset:
The World Economy (1998)

The effects of the financial turmoil in Asia are beginning to emerge in the industrialised economies, with a sharp decline in export sales to East Asia apparent in the most recently available trade statistics for Japan, the United States and Australia. Manufacturing output has fallen this year in both the United States and the UK, with external demand weakened further by the sustained rise in their real exchange rates over the past eighteen months. Firms in the major economies are facing greater price competition from Asian producers in their main markets. Imports have fallen sharply in the affected Asian economies, and domestic demand has been weak. This has also led to some weakness in most commodity markets. Global demand pressures have been further eased by the continuing downturn in Japan, where the economy is now on the verge of recession. This can only prolong the adjustment process for the smaller Asian economies as Japan is a key export market for them, and raises renewed risks of systemic failure within financial markets. Japan and the five smaller Asian economies directly affected by currency crises last year both account for around 7 per cent of total world trade.
Bcl-2 expression in chronic lymphocytic leukemia and its correlation with the induction of apoptosis and clinical outcome. (1996)

Transcriptional deregulation of the Bcl-2 gene has been demonstrated to extend cell viability via an inhibition of apoptotic cell death. Chronic lymphocytic leukemia (CLL) cells are inherently susceptible to apoptosis during short-term culture. Because increased expression of the Bcl-2 gene has been reported in CLL, we sought to correlate Bcl-2 protein expression with the in vitro propensity towards apoptosis and also clinical outcome. Immunoblot analysis of Bcl-2 protein revealed interpatient variability with nine of 42 (21%) cases demonstrating similar or greater expression than a t(14;18) containing lymphoma cell line and 18 of 42 (43%) cases demonstrating a level of expression similar to or less than that seen in normal peripheral blood lymphocytes. Bcl-2 expression did not correlate with clinical features, or with apoptosis, as measured by an in vitro DNA fragmentation assay. However, analysis of survival in the 33 untreated patients revealed significant differences based on the level of Bcl-2 expression, with higher expression being an adverse feature (P<0.02). This data suggests that Bcl-2 is important in the pathogenesis and progression of CLL and that quantitation of Bcl-2 protein may provide useful prognostic information.
Microfluidic squeezing for intracellular antigen loading in polyclonal B-cells as cellular vaccines (2015)

B-cells are promising candidate autologous antigen-presenting cells (APCs) to prime antigen-specific T-cells both in vitro and in vivo. However to date, a significant barrier to utilizing B-cells as APCs is their low capacity for non-specific antigen uptake compared to “professional” APCs such as dendritic cells. Here we utilize a microfluidic device that employs many parallel channels to pass single cells through narrow constrictions in high throughput. This microscale “cell squeezing” process creates transient pores in the plasma membrane, enabling intracellular delivery of whole proteins from the surrounding medium into B-cells via mechano-poration. We demonstrate that both resting and activated B-cells process and present antigens delivered via mechano-poration exclusively to antigen-specific CD8+T-cells, and not CD4+T-cells. Squeezed B-cells primed and expanded large numbers of effector CD8+T-cells in vitro that produced effector cytokines critical to cytolytic function, including granzyme B and interferon-γ. Finally, antigen-loaded B-cells were also able to prime antigen-specific CD8+T-cells in vivo when adoptively transferred into mice. Altogether, these data demonstrate crucial proof-of-concept for mechano-poration as an enabling technology for B-cell antigen loading, priming of antigen-specific CD8+T-cells, and decoupling of antigen uptake from B-cell activation.
Expression of the Nicotiana protein kinase (NPK1) enhanced drought tolerance in transgenic maize (2004)

Drought is one of the most important abiotic stresses affecting the productivity of maize. Previous studies have shown that expression of a mitogen‐activated protein kinase kinase kinase (MAPKKK) gene activated an oxidative signal cascade and led to the tolerance of freezing, heat, and salinity stress in transgenic tobacco. To analyse the role of activation of oxidative stress signalling in improving drought tolerance in major crops, a tobacco MAPKKK (NPK1) was expressed constitutively in maize. Results show that NPK1 expression enhanced drought tolerance in transgenic maize. Under drought conditions, transgenic maize plants maintained significantly higher photosynthesis rates than did the non‐transgenic control, suggesting that NPK1 induced a mechanism that protected photosynthesis machinery from dehydration damage. In addition, drought‐stressed transgenic plants produced kernels with weights similar to those under well‐watered conditions, while kernel weights of drought‐stressed non‐transgenic control plants were significantly reduced when compared with their non‐stressed counterparts.
Detection of Apolipoprotein E/Dimeric Soluble Amyloid β Complexes in Alzheimer's Disease Brain Supernatants (1997)

The inheritance of the apolipoprotein (apo) E4 allele is an important risk factor for late-onset Alzheimer's disease (AD). A major component of the Alzheimer's disease neuritic plaques is amyloid beta (A beta). We previously identified apoE/A beta complexes within neuritic plaques (1). It was not known if this interaction takes place before or after A beta peptides become incorporated into neuritic plaques. To address this question we sought evidence of apoE complexes with brain soluble A beta peptides in AD and control patients. In addition, numerous proteins have been shown to bind A beta peptides in vitro. It is not know if any of these bind brain sA beta in vivo. We found evidence for the presence of apoE/dimeric sA beta complexes in the AD brain and could not detect complexes with other A beta peptide binding proteins. The binding of sA beta to apoE may be one factor influencing its clearance from the brain and/or its conformational state.
Single-Molecule Spectroscopy and Dynamics at Room Temperature (1996)

ADVERTISEMENT RETURN TO ISSUEPREVArticleNEXTSingle-Molecule Spectroscopy and Dynamics at Room TemperatureX. Sunney XieView Author Information Environmental Molecular Sciences Laboratory, Pacific Northwest National Laboratory,† P.O. Box 999, Richland, Washington 99352 Cite this: Acc. Chem. Res. 1996, 29, 12, 598–606Publication Date (Web):December 11, 1996Publication History Received31 May 1996Published online11 December 1996Published inissue 11 December 1996https://doi.org/10.1021/ar950246mCopyright © 1996 American Chemical SocietyRIGHTS & PERMISSIONSArticle Views1042Altmetric-Citations136LEARN 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 InReddit Read OnlinePDF (320 KB) Get e-AlertsSUBJECTS:Computational chemistry,Fluorescence,Kinetics,Molecular structure,Molecules Get e-Alerts
Use of enzyme-loaded erythrocytes in in-vitro correction of arginase-deficient erythrocytes in familial hyperargininemia. (1976)

The capacity of arginase-deficient erythrocytes of patients with familial hyperargininemia to produce urea and to catabolize arginine can be increased in vitro by introducing human liver arginase into their erythrocytes. The results of this study on a specific human model show that it is possible to change the metabolic function of a genetically defective erythrocyte by incorporating exogenous human enzyme. The in vivo application of enzyme-loaded erythrocytes for enzyme replacement therapy of inborn metabolic errors in humans must await in vivo studies on animal models.
Limitations in Immunotherapy with CD3 Antibodies: Comment on the Article by Drs. Chatenoud and Bach (2005)

The Review of Diabetic Studies,2005,2,4,187-189.DOI:10.1900/RDS.2005.2.187Published:February 2006Type:CommentaryAuthors:Damien Bresson, and Matthias von Herrath Author(s) affiliations:Damien Bresson and Matthias von Herrath La Jolla Institute for Allergy and Immunology, Department of Developmental Immunology 3, 10355 Science Center Drive, San Diego, California 92121, USA. Abstract:The article by Drs. Chatenoud and Bach [1] is in many aspects sophisticated as well as surging. It summarizes the latest findings on immunotherapy of type 1 diabetes (T1D) regarding the application of CD3 antibodies by scrutinizing four prevailing concepts that could mislead the further development of such therapies. Inasmuch these concepts, i.e. antigenspecific therapies, initiation of immunotherapy before diabetes onset, combining several agents and, finally, caution regarding the generalization of results obtained from NOD mice, still remain burning issues in diabetes research, the article contributes valuably to the path of finding the optimal intervention strategy. The authors present criticism to the four concepts and take a clear stand of the promise of antigen-nonspecific immunotherapy in the establishment of long-term remission. Insofar, the article inspires to a more intensive discussion to include aspects that could be able to enrich the discussion on these critical concepts. Firstly, it is noticeable that the outcomes of several investigations do not confirm the role of anti-CD3 alone as a cure for T1D in humans [2-4]. If we act on this assumption, then either additional therapies and combinations will be needed or another holistic approach to cure the disease must be taken into consideration. Another critical issue in anti-CD3 therapy is the dose of administration. The dose that is currently being used in clinical trials is probably close to the maximum that can be ethically given. This is because of the initial cytokine release syndrome and the transient EBV reactivation that occurs in many patients due to the systemically immunosuppressive properties of anti- CD3 [5-8]. In order to avoid high doses, more frequent administrations of anti-CD3 or administration during the prediabetic phase could be beneficial, although we do not know whether this strategy will be safe. In this regard, we may consider why the NOD animal model could be misleading. Although anti-CD3 did not completely protect from diabetes when given to prediabetic NOD mice, it did in other diabetes models, such as the streptozotocin-treated CD1 mice [9] and the rat insulin promoter-lymphocytic choriomeningitis virus (RIPLCMV) model [10]. Therefore, maybe due to its multiple immune defects, the NOD mouse might not accurately reflect the immune status of the average prediabetic patient. Keywords:NilView:PDF (174.19 KB)
Ubiquitin Is Conjugated to the Cytoskeletal Protein α-Spectrin in Mature Erythrocytes (1995)

Ubiquitination of red blood cell (RBC) proteins was investigated by encapsulation of 125I-ubiquitin into human erythrocytes using a procedure of hypotonic dialysis, isotonic resealing, and reannealing. Incubation (37 degrees C, up to 2 h) of 125I-ubiquitin-loaded cells resulted in the recovery of 125I-ubiquitin with the cytosolic proteins (9.22 +/- 0.4 micrograms/ml RBC) and conjugated to membrane proteins (2.18 +/- 0.05 micrograms/ml RBC). This conjugation was time-dependent, and the predominant membrane protein band that became labeled showed an apparent molecular mass of 240 kDa on SDS-polyacrylamide gel electrophoresis (PAGE). Western blotting experiments with three different anti-ubiquitin antibodies revealed that this protein is also ubiquitinated in vivo. Cell-free experiments have shown that fraction II (a DEAE-bound protein fraction eluted by 0.5 M KCl) prepared from both mature erythrocytes and reticulocytes is able to conjugate ubiquitin to this protein. Ubiquitin conjugation was ATP-dependent (Km 0.09 mM), time-dependent, and fraction II-dependent (8 +/- 0.5 pmol of 125I-ubiquitin/h/mg of fraction II). Isolation of the major RBC membrane protein that is ubiquitinated was obtained by using biotinylated ubiquitin. Membrane proteins, once ubiquitinated with this derivative, were extracted and purified by affinity chromatography on immobilized avidin. The major components retained by the column were two peptides of molecular masses 220 and 240 kDa. Both proteins are recognized by a monoclonal anti-spectrin antibody, but only the 240-kDa component is detected by streptavidin peroxidase conjugate. That indeed the ubiquitinated membrane protein of 240-kDa is alpha-spectrin was confirmed by immunoaffinity chromatography using 125I-ubiquitin and a monoclonal anti-spectrin antibody. Antigen-antibody complexes were purified by protein A chromatography and analyzed by SDS-PAGE and autoradiography. Again two bands of 240 and 220 kDa were eluted (alpha- and beta-spectrin), but only one band corresponding to the electrophoretic mobility of alpha-spectrin was detected by autoradiography. Thus, alpha-spectrin is a substrate for the ATP-dependent ubiquitination system, suggesting that the cytoskeleton is covalently modified by ubiquitination both in reticulocytes and mature RBC.
Macrophages in gastrointestinal homeostasis and inflammation (2017)

Monocyte-derived mononuclear phagocytes, particularly macrophages, are crucial to maintain gastrointestinal homeostasis in the steady state but are also important for protection against certain pathogens. However, when uncontrolled, they can promote immunopathology. Broadly two subsets of macrophages can be considered to perform the vast array of functions to complete these complex tasks: resident macrophages that dominate in the healthy gut and inflammation-elicited (inflammatory) macrophages that derive from circulating monocytes infiltrating inflamed tissue. Here, we discuss the features of resident and inflammatory intestinal macrophages, complexities in identifying and defining these populations and the mechanisms involved in their differentiation. In particular, focus will be placed on describing their unique ontogeny as well as local gastrointestinal signals that instruct specialisation of resident macrophages in healthy tissue. We then explore the very different roles of inflammatory macrophages and describe new data suggesting that they may be educated not only by the gut microenvironment but also by signals they receive during development in the bone marrow. Given the high degree of plasticity of gut macrophages and their multifaceted roles in both healthy and inflamed tissue, understanding the mechanisms controlling their differentiation could inform development of improved therapies for inflammatory diseases such as inflammatory bowel disease (IBD).
Cloning and expression of the Photobacterium phosphoreum luminescence system demonstrates a unique lux gene organization. (1988)

The organization of the lux structural genes (A-E) in Photobacterium phosphoreum has been determined and a new gene designated as luxF discovered. The P. phosphoreum luminescence system was cloned into Escherichia coli using a pBR322 vector and identified by cross-hybridization with Vibrio fischeri lux DNA. The lux genes were located by specific expression of P. phosphoreum DNA fragments in the T7-phage polymerase/promoter system in E. coli and identification of the labeled polypeptide products. The luxA and luxB gene products (luciferase subunits) were shown to catalyze light emission in the presence of FMNH2, O2, and aldehyde. The luxC, luxD, and luxE gene products (fatty acid reductase subunits) responsible for aldehyde biosynthesis could be specifically acylated with 3H-labeled fatty acids. The order of the lux genes in P. phosphoreum was found to be luxCDABFE with luxF coding for a new polypeptide of 26 kDa. The presence of a new gene in the P. phosphoreum luminescence system between luxB and luxE as compared to the organization of the lux structural gene in V. fischeri and Vibrio harveyi (luxCDABE) demonstrates that the luminescent systems in the marine bacteria have significantly diverged. The discovery of the luxF gene provides the basis for elucidating the role of its gene product in the expression of luminescence in different marine bacteria.
Enhanced Oil Recovery - An Overview (2007)

Nearly 2.0 × 1012 barrels (0.3 × 1012 m3) of conventional oil and 5.0 × 1012 barrels (0.8 × 1012 m3) of heavy oil will remain in reservoirs worldwide after conventional recovery methods have been exhausted. Much of this oil would be recovered by Enhanced Oil Recovery (EOR) methods, which are part of the general scheme of Improved Oil Recovery (IOR). The choice of the method and the expected recovery depends on many considerations, economic as well as technological. This paper examines the EOR methods that have been tested in the field. Some of these have been commercially successful, while others are largely of academic interest. The reasons for the same are discussed. The paper examines thermal and non-thermal oil recovery methods. These are presented in a balanced fashion, with regard to commercial success in the field. Only a few recovery methods have been commercially successful, such as steam injection based processes in heavy oils and tar sands (if the reservoir offers favourable conditions for such applications) and miscible carbon dioxide for light oil reservoirs. Other recovery methods have been tested, and even produced incremental oil, but they have inherent limitations. The current EOR technologies are presented in a proper perspective, pointing out the technical reasons for the lack of success. Methods for improving oil recovery, in particular those concerned with lowering the interstitial oil saturation, have received a great deal of attention both in the laboratory and in the field. From the vast amount of literature on the subject, one gets the impression that it is relatively simple to increase oil recovery beyond secondary (assuming that the reservoir lends itself to primary and secondary recovery). It is shown that this is not the case. Many reservoirs suitable for steam injection and carbon dioxide have already been exploited and are approaching maturity. Other EOR methods suffer from limitations that have little to do with economics. Recovering incremental oil is complex and costly, and has been successful only for a few processes under exacting conditions. Nevertheless, EOR will continue to have an important place in oil production, in view of the escalating energy demand and the tight supply. It is suggested that much research is needed to develop technologies for recovering over two-thirds of the oil that will remain unrecovered in reservoirs. Key references are indicated.
Immune Defence in Mice Lacking Type I and/or Type II Interferon Receptors (1995)

Mice lacking the receptor for type I interferon (IFN-alpha beta, A129 mice), for type II interferon (IFN-gamma, G129 mice) or for both receptors (AG129 mice) have been generated by embryonic stem cell mediated gene targeting and inter-crossing A129 x G129, respectively. The role of the two IFN systems in controlling a range of infections has been studied using these mice. Type I IFN is shown to be responsible for the immune defence against most viral infections tested (Lymphocytic Choriomeningitis Virus, Semliki Forest Virus, Theiler's Virus, Vesicular Stomatitis Virus), type II IFN seems to be of little importance. In Vaccinia Virus and Theiler's Virus infection, however, both IFN systems were found to play a nonredundant role. IFN-gamma was critical for the defence against intracellular bacteria (Mycobacterium, Listeria) and parasites (Leishmania), whereas IFN-alpha beta was not. IFN-alpha beta is produced by virus-infected cells within hours and plays an important role in preventing virus spread early. Production of IFN-gamma on the other hand needs activation of the immune system and plays a major role later, i.e. mostly during the immune response. Data obtained with the mice described here show that both IFN systems seem to have evolved to complement each other in the host defence against a wide variety of infectious agents.
Tyrphostin-induced inhibition of p210bcr-abl tyrosine kinase activity induces K562 to differentiate (1993)

We report on the potency of two Tyrphostin tyrosine kinase blockers, AG 1112 and AG 568, to inhibit p210bcr-abl tyrosine kinase activity in K562 cells, concomitant with the induction of erythroid differentiation. AG 568 and especially AG 1112 represent a specific group of nontoxic protein tyrosine kinase blockers among more than 1,400 tested. These compounds possess therapeutic potential for purging Philadelphia chromosome-positive cells in preparation for autologous bone marrow transplantation in chronic myelogenous leukemia.
cDNA for the human beta 2-adrenergic receptor: a protein with multiple membrane-spanning domains and encoded by a gene whose chromosomal location is shared with that of the receptor for platelet-derived growth factor. (1987)

We have isolated and sequenced a cDNA encoding the human beta 2-adrenergic receptor. The deduced amino acid sequence (413 residues) is that of a protein containing seven clusters of hydrophobic amino acids suggestive of membrane-spanning domains. While the protein is 87% identical overall with the previously cloned hamster beta 2-adrenergic receptor, the most highly conserved regions are the putative transmembrane helices (95% identical) and cytoplasmic loops (93% identical), suggesting that these regions of the molecule harbor important functional domains. Several of the transmembrane helices also share lesser degrees of identity with comparable regions of select members of the opsin family of visual pigments. We have localized the gene for the beta 2-adrenergic receptor to q31-q32 on chromosome 5. This is the same position recently determined for the gene encoding the receptor for platelet-derived growth factor and is adjacent to that for the FMS protooncogene, which encodes the receptor for the macrophage colony-stimulating factor.
An X-linked Locus Influences the Amount of Circulating Interferon Induced in the Mouse by Herpes Simplex Virus Type 1 (1982)

Production of circulating interferon (IFN) was measured in inbred mouse strains following intravenous injection of herpes simplex virus type 1 (HSV-1). IFN titres reached maximal levels 2 to 3 h after injection of virus and a 10-fold difference was found between C57BL/6 mice and BALB/c, as high and low producers respectively. Mendelian analysis revealed that HSV-induced IFN production is governed by several loci, one of which is X-linked. The strain distribution pattern obtained from results in recombinant inbred lines and the results obtained in the congenic B6-C-H-28c-If-1(1) strain furthermore indicated an absence of close linkage to If-1. It is concluded that the levels of HSV-induced early IFN production are influenced by several autosomal loci and one X-linked locus.