gebhart/patrepeval huggingface dataset:
Peptidomimetic Src/Pretubulin Inhibitor KX-01 Alone and in Combination with Paclitaxel Suppresses Growth, Metastasis in Human ER/PR/HER2-Negative Tumor Xenografts (2012)

Src kinase is elevated in breast tumors that are ER/PR negative and do not overexpress HER2, but clinical trials with Src inhibitors have shown little activity. The present study evaluated preclinical efficacy of a novel peptidomimetic compound, KX-01 (KX2-391), that exhibits dual action as an Src and pretubulin inhibitor. KX-01 was evaluated as a single-agent and in combination with paclitaxel in MDA-MB-231, MDA-MB-157, and MDA-MB-468 human ER/PR/HER2-negative breast cancer cells. Treatments were evaluated by growth/apoptosis, isobologram analysis, migration/invasion assays, tumor xenograft volume, metastasis, and measurement of Src, focal adhesion kinase (FAK), microtubules, Ki67, and microvessel density. KX-01 inhibited cell growth in vitro and in combination with paclitaxel resulted in synergistic growth inhibition. KX-01 resulted in a dose-dependent inhibition of MDA-MB-231 and MDA-MB-157 tumor xenografts (1 and 5 mg/kg, twice daily). KX-01 inhibited activity of Src and downstream mediator FAK in tumors that was coincident with reduced proliferation and angiogenesis and increased apoptosis. KX01 also resulted in microtubule disruption in tumors. Combination of KX-01 with paclitaxel resulted in significant regression of MDA-MB-231 tumors and reduced metastasis to mouse lung and liver. KX-01 is a potently active Src/pretubulin inhibitor that inhibits breast tumor growth and metastasis. As ER/PR/HER2-negative patients are candidates for paclitaxel therapy, combination with KX-01 may potentiate antitumor efficacy in management of this aggressive breast cancer subtype.
High diagnostic performance of ELISA detection of antibodies to citrullinated antigens in rheumatoid arthritis (2003)

ELISA detection of antibodies to citrullinated antigens, especially a second generation anti-CCP, showed higher discriminative ability than other assays, including RF, and would be useful to aid the diagnosis of RA in clinical practice.
IB-MECA, an A3 adenosine receptor agonist prevents bone resorption in rats with adjuvant induced arthritis. (2006)

IB-MECA, a small highly bioavailable molecule, induces modulation of proteins which control survival and apoptosis resulting in the amelioration of the inflammatory process and the preservation of bone mass in AIA rats.
MicroRNA expression profiling of single whole embryonic stem cells (2006)

MicroRNAs (miRNAs) are a class of 17-25 nt non-coding RNAs that have been shown to have critical functions in a wide variety of biological processes during development. Recently developed miRNA microarray techniques have helped to accelerate research on miRNAs. However, in some instances there is only a limited amount of material available for analysis, which requires more sensitive techniques that can preferably work on single cells. Here we demonstrate that it is possible to analyse miRNA in single cells by using a real-time PCR-based 220-plex miRNA expression profiling method. Development of this technique will greatly facilitate miRNA-related research on cells, such as the founder population of primordial germ cells where rapid and dynamic changes occur in a few cells, and for analysing heterogeneous population of cells. In these and similar cases, our method of single cell analysis is critical for elucidating the diverse roles of miRNAs.
Microfluidic Library Screening for Mapping Antibody Epitopes (2007)

The capability to screen molecular libraries using disposable microfluidic devices provides the potential to simplify and automate reagent generation and to develop integrated bioanalytical systems for clinical diagnostics. Here, antibody epitopes were mapped using a disposable microfluidic device to screen a combinatorial peptide library composed of 5 x 108 members displayed on bacterial cells. On-chip library screening was achieved in a two-stage, continuous-flow microfluidic sorter that separates antibody-binding target cells captured on microspheres through dielectrophoretic funneling. The antibody fingerprints identified were comparable to those obtained using state-of-the-art commercial cell sorting instrumentation.
Design of Hologram for Brightness Enhancement in Color LCDs (1998)

Abstract Transmission holographic film for brightness enhancement in full color reflective LCDs is proposed. The hologram is attached to the front of the LCD. The goal is paper‐like brightness within the viewing zone under typical ambient lighting conditions. Optimum viewing and illumination angles have been identified. Modeling and measurements on holograms show that a viewing zone of 20° × 40° will provide a 12× film gain which is adequate to maintain a wide color gamut and brightness.
Chromosomal Instability in Peripheral Blood Lymphocytes and Risk of Prostate Cancer (2005)

Prostate cancer is an extremely complex disease, and it is likely that chromosomal instability is involved in the genetic mechanism of tumorigenesis. Several chromosomes have been labeled as "players" in the development of prostate cancer, among them chromosome 1 and X chromosome have been reported to harbor prostate cancer susceptibility loci. However, there is little information regarding the background levels of chromosome instability in these patients. In this pilot study, we examined spontaneous chromosome instability in short-term lymphocyte cultures from 126 study subjects, 61 prostate cancer patients, and 65 healthy controls. We evaluated chromosomal instability using a fluorescence in situ hybridization assay using two probes targeting specific regions on X chromosome and chromosome 1. Our results showed a significantly higher mean level of spontaneous breaks involving the X chromosome in patients compared with controls (mean +/- SE, 2.41 +/- 0.26 and 0.62 +/- 0.08, respectively; P < 0.001). Similarly, chromosome 1 spontaneous breaks were significantly higher among cases compared with controls (mean +/- SE, 1.95 +/- 0.24 and 1.09 +/- 0.16, respectively; P < 0.001). Using the median number of breaks in the controls as the cutoff value, we observed an odds ratio (95% confidence interval) of 15.53 (5.74 - 42.03; P < 0.001) for spontaneous X chromosome breaks and 3.71 (1.60 - 8.63; P < 0.001) for chromosome 1 breaks and risk of development of prostate cancer. In conclusion, our preliminary results show that spontaneous chromosome instability could be a risk factor for prostate cancer.
A Convenient Synthesis of Benzo[g]pyrrolo[3,2-c]quinoline-6,11-diones (2005)

Americanae nace como un proyecto conjunto que surge dentro de la Red Europea de Información y Documentación sobre América Latina (REDIAL), y que ha afrontado la Biblioteca de la Agencia Española de Cooperación Internacional para el Desarrollo (AECID). Esta nueva biblioteca virtual hace más accesibles los libros digitales de tema americanista a los investigadores y usuarios interesados de cualquier parte del mundo.
Spores of Bacillus subtilis: their resistance to and killing by radiation, heat and chemicals (2006)

A number of mechanisms are responsible for the resistance of spores of Bacillus species to heat, radiation and chemicals and for spore killing by these agents. Spore resistance to wet heat is determined largely by the water content of spore core, which is much lower than that in the growing cell protoplast. A lower core water content generally gives more wet heat-resistant spores. The level and type of spore core mineral ions and the intrinsic stability of total spore proteins also play a role in spore wet heat resistance, and the saturation of spore DNA with alpha/beta-type small, acid-soluble spore proteins (SASP) protects DNA against wet heat damage. However, how wet heat kills spores is not clear, although it is not through DNA damage. The alpha/beta-type SASP are also important in spore resistance to dry heat, as is DNA repair in spore outgrowth, as Bacillus subtilis spores are killed by dry heat via DNA damage. Both UV and gamma-radiation also kill spores via DNA damage. The mechanism of spore resistance to gamma-radiation is not well understood, although the alpha/beta-type SASP are not involved. In contrast, spore UV resistance is due largely to an alteration in spore DNA photochemistry caused by the binding of alpha/beta-type SASP to the DNA, and to a lesser extent to the photosensitizing action of the spore core's large pool of dipicolinic acid. UV irradiation of spores at 254 nm does not generate the cyclobutane dimers (CPDs) and (6-4)-photoproducts (64PPs) formed between adjacent pyrimidines in growing cells, but rather a thymidyl-thymidine adduct termed spore photoproduct (SP). While SP is formed in spores with approximately the same quantum efficiency as that for generation of CPDs and 64PPs in growing cells, SP is repaired rapidly and efficiently in spore outgrowth by a number of repair systems, at least one of which is specific for SP. Some chemicals (e.g. nitrous acid, formaldehyde) again kill spores by DNA damage, while others, in particular oxidizing agents, appear to damage the spore's inner membrane so that this membrane ruptures upon spore germination and outgrowth. There are also other agents such as glutaraldehyde for which the mechanism of spore killing is unclear. Factors important in spore chemical resistance vary with the chemical, but include: (i) the spore coat proteins that likely react with and detoxify chemical agents; (ii) the relative impermeability of the spore's inner membrane that restricts access of exogenous chemicals to the spore core; (iii) the protection of spore DNA by its saturation with alpha/beta-type SASP; and (iv) DNA repair for agents that kill spores via DNA damage. Given the importance of the killing of spores of Bacillus species in the food and medical products industry, a deeper understanding of the mechanisms of spore resistance and killing may lead to improved methods for spore destruction.
Multicolor Fluorescent Semiconducting Polymer Dots with Narrow Emissions and High Brightness (2013)

Fluorescent semiconducting polymer dots (Pdots) have attracted great interest because of their superior characteristics as fluorescent probes, such as high fluorescence brightness, fast radiative rates, and excellent photostability. However, currently available Pdots generally exhibit broad emission spectra, which significantly limit their usefulness in many biological applications involving multiplex detections. Here, we describe the design and development of multicolor narrow emissive Pdots based on different boron dipyrromethene (BODIPY) units. BODIPY-containing semiconducting polymers emitting at multiple wavelengths were synthesized and used as precursors for preparing the Pdots, where intraparticle energy transfer led to highly bright, narrow emissions. The emission full width at half-maximum of the resulting Pdots varies from 40 to 55 nm, which is 1.5-2 times narrower than those of conventional semiconducting polymer dots. BODIPY 520 Pdots were about an order of magnitude brighter than commercial Qdot 525 under identical laser excitation conditions. Fluorescence imaging and flow cytometry experiments indicate that the narrow emissions from these bright Pdots are promising for multiplexed biological detections.
[Study on the genetic association between DRB3 and DRB1 loci in the human MHC region and psychotic symptoms of schizophrenia]. (2003)

DRB1 locus seemed likely to be associated with psychotic symptoms as idea of reference and apathy. Further studies were necessary to reveal the relations between DRB1 gene or nearby locus with its susceptibility to schizophrenia.
Chemical modification of proteins: Selected methods and analytical procedures (1975)

The abundance of literature on this subject has been disseminated and logically laid out for use in the laboratory. It presents information on: chemical characterization of proteins and their derivatives; modification of protein side-chains: group-specific reagents; site-specific modification of native proteins with group-specific reagents; affinity labels; photoaffinity labels.
Autophagy Is a Tolerance-Avoidance Mechanism that Modulates TCR-Mediated Signaling and Cell Metabolism to Prevent Induction of T Cell Anergy (2018)

In response to activation, CD4<sup>+</sup> T cells upregulate autophagy. However, the functional consequences of that upregulation have not been fully elucidated. In this study, we identify autophagy as a tolerance-avoidance mechanism. Our data show that inhibition of autophagy during CD4<sup>+</sup> T cell activation induces a long-lasting state of hypo-responsiveness that is accompanied by the expression of an anergic gene signature. Cells unable to induce autophagy after T cell receptor (TCR) engagement show inefficient mitochondrial respiration and decreased turnover of the protein tyrosine phosphatase PTPN1, which translates into defective TCR-mediated signaling. In vivo, inhibition of autophagy during antigen priming induces T cell anergy and decreases the severity of disease in an experimental autoimmune encephalomyelitis mouse model. Interestingly, CD4<sup>+</sup> T cells isolated from the synovial fluid of juvenile idiopathic arthritis patients, while resistant to suboptimal stimulation-induced anergy, can be tolerized with autophagy inhibitors. We propose that autophagy constitutes a tolerance-avoidance mechanism, which determines CD4<sup>+</sup> T cell fate.
Effect of in vitro glucose and diabetic hyperglycemia on mouse kidney protein synthesis: relevance to diabetic microangiopathy. (2005)

To test the possible roles of diabetic hyperglycemia, we studied the in vitro effect of increasing glucose concentrations (5.0-27.5 mmol/L) on protein synthesis (PS) of the kidneys from "adult" male albino Swiss mice. In mouse kidney cortex slices, PS (3H-leucine incorporation into trichloroacetic acid-precipitable material), measured as cpm/mg protein/45 minutes, was already stimulated by 5.0 mmol/L of glucose (+24%, P < .05). At supraphysiologic glucose concentrations, PS was stimulated by 48% at 8.8 mmol/L of glucose and 31% at 13.6 mmol/L of glucose (P < .05, compared with the value observed at 5.0 mmol/L of glucose). However, the highest glucose levels (15.4 mmol/L and 27.5 mmol/L) were no longer effective. Other substrates (1.25 mmol/L or 6.26 mmol/L palmitic acid and 100 mcmol/L sorbitol) were without effect. Similar results were obtained when data were expressed as cpm/mg DNA/45 minutes. In contrast to adult mice, "young" mice showed the maximum stimulatory effect (+86%, P < .02), with a glucose concentration still in the nondiabetic range (6.6 mmol/L). However, in the "older" mice maximum stimulation was observed in the presence of high glucose concentrations (15.4 mmol/L and 27.5 mmol/L) with 52% (P < .02) and 26% (P < .05) increases, respectively, vs the value recorded at 5 mmol/L of glucose. With regard to the in vivo effect of diabetic hyperglycemia, the renal PS of 3-day streptozotocin diabetic mice was moderately increased, whereas the liver PS was markedly reduced. The effects of in vitro glucose and in vivo diabetic hyperglycemia, as modulated by both the concentration of glucose and the age, may lead to diabetic renal hypertrophy and the increased formation/accumulation of glycoproteins, thus contributing to microangiopathy.
Inter-limb musculoskeletal differences in competitive ten-pin bowlers: a preliminary analysis. (2011)

The femoral shaft of bowlers adapts by increasing bone area and cortical thickness without a change in vBMD, while the loaded radius adapts by increasing vBMD.
Evaluation of TNF-α and IL-1 Blockade in Collagen-Induced Arthritis and Comparison with Combined Anti-TNF-α/Anti-CD4 Therapy (2000)

We have evaluated the effects of anti-TNF-alpha, anti-IL-1, and combined anti-TNF-alpha/anti-CD4 therapy in collagen-induced arthritis. Blockade of TNF-alpha or IL-1 before disease onset delayed, but did not prevent, the induction of arthritis. When treatment was initiated after onset of arthritis, anti-TNF-alpha, anti-IL-1beta, and anti-IL-1R (which blocks IL-1alpha and IL-1beta) were all found to be effective in reducing the severity of arthritis, with anti-IL-1R and anti-IL-1beta showing greater efficacy than anti-TNF-alpha. Anti-IL-1beta was equally as effective as anti-IL-1R, indicating that IL-1beta plays a more prominent role than IL-1alpha in collagen-induced arthritis. An additive effect was observed between anti-TNF-alpha and anti-IL-1R in the prevention of joint erosion and in normalization of the levels of serum amyloid P. Combined anti-TNF-alpha/anti-CD4 therapy also caused normalization of serum amyloid P levels. The therapeutic effect of anti-TNF-alpha plus anti-CD4 was comparable to that of anti-TNF-alpha plus anti-IL-1R, suggesting that combined anti-TNF-alpha/anti-CD4 therapy prevents both TNF-alpha- and IL-1-mediated pathology. Anti-TNF-alpha treatment reduced IL-1beta expression in the joint and, conversely, anti-IL-1beta treatment reduced TNF-alpha expression. Combined anti-TNF-alpha/anti-CD4 treatment almost completely blocked the expression of IL-1beta, thereby confirming the ability of this form of combination therapy to prevent IL-1ss-mediated pathology.
The Multicenter Acellular Pertussis Trial: An Overview (1996)

A multicenter, randomized, double-blind study was undertaken in 2342 infants to evaluate the safety and immunogenicity of 13 acellular and 2 whole cell pertussis vaccines combined with diphtheria and tetanus toxoids. Vaccines were administered to infants at 2, 4, and 6 months of age. Sera were obtained before the first vaccination (age 2 months) and 1 month after the third vaccination (age 7 months). All of the acellular vaccines produced significant increases in antibody for included antigens; mean antibody levels often exceeded those obtained with the reference whole cell vaccine. The vaccines were well-tolerated. All acellular vaccines were associated with significantly fewer adverse reactions than the control whole cell vaccine.
DHSNet: Deep Hierarchical Saliency Network for Salient Object Detection (2016)

Traditional salient object detection models often use hand-crafted features to formulate contrast and various prior knowledge, and then combine them artificially. In this work, we propose a novel end-to-end deep hierarchical saliency network (DHSNet) based on convolutional neural networks for detecting salient objects. DHSNet first makes a coarse global prediction by automatically learning various global structured saliency cues, including global contrast, objectness, compactness, and their optimal combination. Then a novel hierarchical recurrent convolutional neural network (HRCNN) is adopted to further hierarchically and progressively refine the details of saliency maps step by step via integrating local context information. The whole architecture works in a global to local and coarse to fine manner. DHSNet is directly trained using whole images and corresponding ground truth saliency masks. When testing, saliency maps can be generated by directly and efficiently feed forwarding testing images through the network, without relying on any other techniques. Evaluations on four benchmark datasets and comparisons with other 11 state-of-the-art algorithms demonstrate that DHSNet not only shows its significant superiority in terms of performance, but also achieves a real-time speed of 23 FPS on modern GPUs.
Isolation and Characterization of Streptoverticillium Anticoagulant (SAC), a Novel Protein Inhibitor of Blood Coagulation Produced by Streptoverticillium cinnamoneum subsp. cinnamoneum (1994)

Three Streptoverticillium anticoagulants, SAC I, II, and III, which strongly inhibit human intrinsic blood coagulation, were each isolated in a homogeneous form from a culture fluid of Streptoverticillium cinnamoneum subsp. cinnamoneum IFO 12852. SAC I, II, and III are simple proteins with molecular weights of around 12,000, and with isoelectric points of 9.7, 9.7, and 9.9, respectively. Their amino acid compositions are similar and each SAC possesses two disulfide bonds. The COOH-terminal residue of each of these proteins is phenylalanine. Together with the similarity of their protein chemical properties, the results of NH2-terminal amino acid sequence analysis of these SAC proteins strongly suggested that the deletion of Ser-Leu and Ser-Leu-Tyr from the NH2-terminus of SAC I (Ser-Leu-Tyr-Ala-Pro-...) results in the generation of SAC II and III, respectively. The amount of each SAC necessary to double the partial thromboplastin time was around 5 micrograms/ml. SAC I inhibited activated human factor XII and human plasma kallikrein. It also inhibited, but to a lesser extent, activated factor X. The inhibition constants (Ki) of SAC I toward activated factor XII and plasma kallikrein were 5.3 x 10(-8) and 7.2 x 10(-9) M, respectively. The SACs also inhibited some microbial serine proteases such as subtilisin Carlsberg and, to a lesser extent, mammalian serine proteases including bovine trypsin and alpha-chymotrypsin. Of these three inhibitors, only SAC I inhibited metalloproteases such as thermolysin in addition to these serine proteases.
Retrovirally marked CD34-enriched peripheral blood and bone marrow cells contribute to long-term engraftment after autologous transplantation (1995)

We report here on a preliminary human autologous transplantation study of retroviral gene transfer to bone marrow (BM) and peripheral blood (PB)-derived CD34-enriched cells. Eleven patients with multiple myeloma or breast cancer had cyclophosphamide and filgrastim-mobilized PB cells CD34-enriched and transduced with a retroviral marking vector containing the neomycin resistance gene, and CD34-enriched BM cells transduced with a second marking vector also containing a neomycin resistance gene. After high-dose conditioning therapy, both transduced cell populations were reinfused and patients were followed over time for the presence of the marker gene and any adverse effects related to the gene-transfer procedure. All 10 evaluable patients had the marker gene detected at the time of engraftment, and 3 of 9 patients had persistence of the marker gene for greater than 18 months posttransplantation. The marker gene was detected in multiple lineages, including granulocytes, T cells, and B cells. The source of the marking was both the transduced PB graft and the BM graft, with a suggestion of better long-term marking originating from the PB graft. The steady-state levels of marking were low, with only 1:1000 to 1:10,000 cells positive. There was no toxicity noted, and patients did not develop detectable replication-competent helper virus at any time posttransplantation. These results suggest that mobilized PB cells may be preferable to BM for gene therapy applications and that progeny of mobilized peripheral blood cells can contribute long-term to engraftment of multiple lineages.
Discovery of a fusion kinase in EOL-1 cells and idiopathic hypereosinophilic syndrome (2003)

Idiopathic hypereosinophilic syndrome (HES) is a myeloproliferative disease of unknown etiology. Recently, it has been reported that imatinib mesylate (Gleevec), an inhibitor of Bcr-Abl kinase useful in the treatment of chronic myeloid leukemia, is also effective in treating HES; however, the molecular target of imatinib in HES is unknown. This report identifies a genetic rearrangement in the eosinophilic cell line EOL-1 that results in the expression of a fusion protein comprising an N-terminal region encoded by a gene of unknown function with the GenBank accession number NM_030917 and a C-terminal region derived from the intracellular domain of the platelet-derived growth factor receptor alpha (PDGFRalpha). The fusion gene was also detected in blood cells from two patients with HES. We propose naming NM_030917 Rhe for Rearranged in hypereosinophilia. Rhe-PDGFRalpha fusions result from an apparent interstitial deletion that links Rhe to exon 12 of PDGFRalpha on chromosome 4q12. The fusion kinase Rhe-PDGFRalpha is constitutively phosphorylated and supports IL-3-independent growth when expressed in BaF3 cells. Proliferation and viability of EOL-1 and BaF3 cells expressing Rhe-PDGFRalpha are ablated by the PDGFRalpha inhibitors imatinib, vatalanib, and THRX-165724.