gebhart/patrepeval huggingface dataset:
Dendritic cells and immune-based therapies. (1996)

The dendritic cell (DC) lineage of white blood cells specializes in capturing antigens and stimulating T-dependent immunity. Because of their efficacy in inducing T cell responses in vivo without other adjuvants, DCs can be considered "nature's adjuvant." DCs are the least abundant of leukocytes, but methods for generating large numbers of DCs are being developed. Ex vivo, DCs develop from CD34+ progenitors cultured in the presence of a combination of granulocyte-macrophage colony-stimulating factor (GM-CSF) and tumor necrosis factor-alpha (TNF-alpha). This kind of work is stimulating interest in charging DCs with clinically relevant antigens and inducing active immunity in patients. Targeting antigens to DCs may become feasible also because of the identification of distinct antigen receptors such as DEC-205, a DECalectin with 10 contiguous, C-type lectin domains. DEC-205 can mediate adsorptive uptake and presentation via DCs. AIDS is another disease for which DCs should be considered in designing new therapies, since DCs can play a major role in promoting HIV-1 replication. Many HIV-1 isolates induce syncytia between DCs and CD4+ memory T cells. These syncytia in turn are the site for a productive infection with HIV-1, possibly because requisite transcription factors like NF-kappaB and Sp1 are separately provided by DCs and T cells, respectively. Further attention to the DC lineage should provide new avenues for manipulating the immune system in several clinical contexts.
Heparan sulfate proteoglycans from mouse mammary epithelial cells: localization on the cell surface with a monoclonal antibody. (1985)

Mouse mammary epithelial cells, of the normal murine mammary gland (NMuMG) cell line, bear a heparan sulfate-rich proteoglycan (HSPG) on their surfaces. A hybridoma (281-2) secreting a monoclonal antibody that recognizes this HSPG was produced by fusion of SP-2/0 myeloma cells with spleen cells from rats immunized with NMuMG cells. The 281-2 monoclonal antibody is directed against the core protein of the cell surface HSPG, as demonstrated by (a) recognition of the isolated proteoglycan but not its glycosaminoglycan chains, (b) co-localization of 281-2-specific antigen and radioactive cell surface HSPG on gradient polyacrylamide gel electrophoresis and on isopycnic centrifugation, and (c) abolition of immunofluorescent staining of the NMuMG cell surface by the intact, but not the protease-digested ectodomain of the cell surface HSPG. The antibody is specific for cell surface HSPG and does not recognize the HSPG that accumulates extracellularly beneath the basal cell surface. Therefore, the 281-2 antibody may be used to isolate the cell surface HSPG and to explore its distribution in tissues.
A thymus-specific member of the HMG protein family regulates the human T cell receptor C alpha enhancer. (1991)

The human T cell-specific transcription factor TCF-1 alpha plays a key role in the tissue-specific activation of the T cell receptor (TCR) C alpha enhancer and binds to pyrimidine-rich elements (5'-PyCTTTG-3') present in a variety of other T cell-specific control regions. Using amino acid sequence information derived from the DNA affinity-purified protein, we have now isolated cDNA clones encoding TCF-1 alpha. The TCF-1 alpha cDNA contains a single 68-amino-acid domain that is homologous to a region conserved among high-mobility group (HMG) and nonhistone chromosomal proteins. Expression of full-length and mutant cDNA clones in bacteria reveal that the single HMG motif, which is predicted to contain two extended alpha-helical segments, is sufficient to direct the sequence-specific binding of TCF-1 alpha to DNA. Northern blot experiments demonstrate further that TCF-1 alpha mRNA is highly tissue specific, found primarily in the thymus or T cell lines. The immature CEM T cell line expresses relatively low levels of TCF-1 alpha mRNA, which are increased upon activation of these cells by phorbol esters. Interestingly, the cloned TCF-1 alpha protein is a potent transcriptional activator of the human TCR alpha enhancer in nonlymphoid cell lines, whereas the activity of the endogenous protein in T cell lines is strongly dependent on an additional T cell-specific protein that interacts with the core enhancer. TCF-1 alpha is currently unique among the newly emerging family of DNA-binding regulatory proteins that share the HMG motif in that it is a highly tissue-specific RNA polymerase II transcription factor.
Purifying antibody-plasminogen activator conjugates (1992)

ADVERTISEMENT RETURN TO ISSUEArticleNEXTPurifying antibody-plasminogen activator conjugatesChristoph Bode, Marschall S. Runge, and Edgar HaberCite this: Bioconjugate Chem. 1992, 3, 4, 269–272Publication Date (Print):July 1, 1992Publication History Published online1 May 2002Published inissue 1 July 1992https://doi.org/10.1021/bc00016a001RIGHTS & PERMISSIONSArticle Views55Altmetric-Citations5LEARN 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 PDF (476 KB) Get e-Alertsclose Get e-Alerts
Relative benefit-risk comparing diclofenac to other traditional non-steroidal anti-inflammatory drugs and cyclooxygenase-2 inhibitors in patients with osteoarthritis or rheumatoid arthritis: a network meta-analysis (2015)

The benefit-risk profile of diclofenac was comparable to other treatments used for pain relief in OA and RA; benefits and risks vary in individuals and need consideration when making treatment decisions.
Development of intelligent cruise control system (1999)

This paper describes a intelligent control system for cruise driving vehicle. With the steady increase in the number of automobiles on the road, it has become ever more important to merge traffic flow efficiently to optimize utilization of existing road capacity. Based on the idea that minimize fuel cost air pollution and accept driver's need for driving, we have developed a intelligent control system for cruise driving vehicle. The system with intelligent controller for cruise driving is fully implemented in a open road and verify its performance.
IEEE 802.11 Wireless LAN: can we use it for multimedia? (1998)

The IEEE P802.11 committee developed the 802.11 Wireless LAN standard to cover wireless networks for fixed, portable, and moving stations within a local area. This standard addresses the need for wireless connectivity to stations, equipment, or automatic machinery that requires rapid deployment and may be portable, handheld, or mounted on moving vehicles. It can function totally wireless or connected to a wired network. Most people familiar with the standard expect to use it in providing wireless networks for personal computers or stations connected to the global wired infrastructure through access points. Now that the 802.11 standard is finally here, it will energize the wireless LAN market and result in the proliferation of low cost wireless connectivity in the office and home. Study groups are working on higher rates at 2.4 GHz and at 5 GHz for future inclusion into the standard. These higher rates will make it even more practical to employ this standard for multimedia traffic.
Transthyretin: Its Response to Malnutrition and Stress Injury. Clinical Usefulness and Economic Implications (2002)

Serum transthyretin is an ideal marker for monitoring patients who are malnourished or have metabolic consequences of acute stress injury because it has a short half-life, it measures the level of metabolic deficit, the response to nutritional metabolic support, and because it is a prognostic indicator. Mounting clinical evidence indicates that the use of transthyretin to assess and monitor a patient's nutritional status results in improved treatment outcomes and lower overall healthcare costs.
Palladium-Catalyzed Hydroarylation of 1,3-Dienes with Boronic Esters via Reductive Formation of π-Allyl Palladium Intermediates under Oxidative Conditions (2010)

A palladium-catalyzed reductive cross-coupling of 1,3-dienes with boronic esters in which a pi-allyl Pd species is generated directly from a 1,3-diene via a Pd-catalyzed aerobic alcohol oxidation is reported. Both the scope of the process and the origin of a highly selective 1,2-addition are discussed.
A region and data hiding based error concealment scheme for images (2001)

Traditional error concealment systems for still images compressed in the discrete cosine transform (DCT) domain and transmitted over lossy channels are not suitable for JPEG2000 compressed images. In this paper a novel error concealment scheme for images compressed in wavelet domain is proposed. It is based on data hiding techniques to reconstruct missing data of the region-of-interest (ROI). The ROI and region-of-background (ROB) of images are transformed into the wavelet domain using the shape-adaptive wavelet transform and coded with the rate-distortion optimized coder. Embedded data are truncated from the coded bitstream of the ROI and embedded into the wavelet coefficients of the ROB. A fragile watermark is embedded into the ROI to detect errors. When a data loss occurs in the bitstream of the ROI, embedded data are extracted for reconstruction. Experiments show the efficiency of this scheme. It is also shown that this scheme has the capability of detecting and correcting malicious tampers in the ROI.
The SAPASI Is Valid and Responsive to Psoriasis Disease Severity Changes in a Multi‐Center Clinical Trial (1999)

We developed a structured Psoriasis Area Severity Index (PASI)-like instrument, the Self-administered PASI (SAPASI), that allows subjects to assess accurately the severity of their psoriasis. The major limitation of our previous SAPASI validity studies is that all were performed in a single academic center, raising questions about the generalizability of the instrument. We administered the SAPASI to 182 subjects in a 12-week, multicenter, double-blind clinical trial of topical tazarotene for psoriasis. On the same day, investigators blind to the SAPASI rating determined the degree of erythema, induration, scale, body surface area (BSA) affected, and overall lesion severity of the subjects' psoriasis. Using these data, we calculated an investigator PASI-Equivalent. Correlation analysis shows that for both initial and final assessments of psoriasis severity, the SAPASI score reflects the PASI-Equivalent score in a significant way (p = .0001), although the correlation is a modest one (r = 0.3 to 0.5). Significant (p = .0001), modest correlations were found between the subjects' reported BSAs and the investigators' reported BSAs. To assess responsiveness, the proportional changes of the SAPASI and PASI-Equivalent were found to be modestly significantly correlated (r = 0.2, p = .04). The results of this study support the general validity of the SAPASI and demonstrate that the SAPASI can detect changes in disease severity in a clinical trial. Significant correlations were also observed between SAPASI components and their investigator-reported counterparts in this multicenter trial. To the best of our knowledge, the current study represents the first multicenter validity study performed on a psoriasis severity instrument, and clearly demonstrates the value of this instrument in assessing the psoriasis severity in a population.
Reduced oxygen tension increases hematopoiesis in long-term culture of human stem and progenitor cells from cord blood and bone marrow. (1992)

Growth of hematopoietic stem and progenitor cells found in the mononuclear cell (MNC) fraction of human cord blood and bone marrow was evaluated under atmospheres containing reduced (5%) and normal (20%) oxygen tension. Cord blood MNC were grown in suspension and on preestablished irradiated bone marrow stromal layers, whereas bone marrow MNC were used to initiate one-step long-term bone marrow cultures (LTBMC). Reduced oxygen tension resulted in a substantial increase in both the number and frequency of colony-forming cells observed in all three types of long-term hematopoietic cultures (LTHC) studied. At various time points under low oxygen, progenitor cell numbers were as much as 12-fold, 3-fold, and 4-fold higher for granulocyte-macrophage colony-forming units (CFU-GM), erythroid burst-forming units (BFU-E), and granulocyte erythrocyte macrophage megakaryocyte colony-forming units (CFU-GEMM), respectively. In addition to these numerical increases, progenitor cells were maintained for 1-2 weeks longer under low oxygen conditions. Reduced oxygen tension also increased total cell numbers by as much as fivefold in cord blood suspension cultures, but this effect on total cell numbers was less pronounced in cultures containing a stromal layer. The rate of irradiated stromal layer degeneration, as judged by cell counts and microscopic examination, was reduced under low oxygen. Finally, the beneficial effect of reduced oxygen was comparable to the effect of an irradiated stromal layer for maintaining cord blood progenitor cells in LTHC. These results indicate that low oxygen, which better approximates the in vivo environment, enhances the growth and maintenance of both stromal and progenitor cells for a longer period of time in vitro.
Densification of amorphous silicon prepared by hydrogen-ion-beam-assisted evaporation (1996)

Hydrogenated amorphous silicon films were deposited by ion-beam-assisted evaporation onto substrates maintained at 120 °C. The influence of the substrate bias was studied. By combined infrared spectrometry and thermal desorption spectrometry experiments, it is inferred that the bombardment of the growing a-Si:H film by energetic hydrogen ions produces a densification of the material without modification of the Si:H bonding.
1,25-Dihydroxyvitamin D3 and IL-2 Combine to Inhibit T Cell Production of Inflammatory Cytokines and Promote Development of Regulatory T Cells Expressing CTLA-4 and FoxP3 (2009)

The active form of vitamin D, 1,25-dihydroxyvitamin D(3) (1,25(OH)(2)D(3)), has potent immunomodulatory properties that have promoted its potential use in the prevention and treatment of infectious disease and autoimmune conditions. A variety of immune cells, including macrophages, dendritic cells, and activated T cells express the intracellular vitamin D receptor and are responsive to 1,25(OH)(2)D(3.) Despite this, how 1,25(OH)(2)D(3) regulates adaptive immunity remains unclear and may involve both direct and indirect effects on the proliferation and function of T cells. To further clarify this issue, we have assessed the effects of 1,25(OH)(2)D(3) on human CD4(+)CD25(-) T cells. We observed that stimulation of CD4(+)CD25(-) T cells in the presence of 1,25(OH)(2)D(3) inhibited production of proinflammatory cytokines including IFN- gamma, IL-17, and IL-21 but did not substantially affect T cell division. In contrast to its inhibitory effects on inflammatory cytokines, 1,25(OH)(2)D(3) stimulated expression of high levels of CTLA-4 as well as FoxP3, the latter requiring the presence of IL-2. T cells treated with 1,25(OH)(2)D(3) could suppress proliferation of normally responsive T cells, indicating that they possessed characteristics of adaptive regulatory T cells. Our results suggest that 1,25(OH)(2)D(3) and IL-2 have direct synergistic effects on activated T cells, acting as potent anti-inflammatory agents and physiologic inducers of adaptive regulatory T cells.
A fluorescent protein biosensor of myosin II regulatory light chain phosphorylation reports a gradient of phosphorylated myosin II in migrating cells. (1995)

Phosphorylation of the regulatory light chain by myosin light chain kinase (MLCK) regulates the motor activity of smooth muscle and nonmuscle myosin II. We have designed reagents to detect this phosphorylation event in living cells. A new fluorescent protein biosensor of myosin II regulatory light chain phosphorylation (FRLC-Rmyosin II) is described here. The biosensor depends upon energy transfer from fluorescein-labeled regulatory light chains to rhodamine-labeled essential and/or heavy chains. The energy transfer ratio increases by up to 26% when the regulatory light chain is phosphorylated by MLCK. The majority of the change in energy transfer is from regulatory light chain phosphorylation by MLCK (versus phosphorylation by protein kinase C). Folding/unfolding, filament assembly, and actin binding do not have a large effect on the energy transfer ratio. FRLC-Rmyosin II has been microinjected into living cells, where it incorporates into stress fibers and transverse fibers. Treatment of fibroblasts containing FRLC-Rmyosin II with the kinase inhibitor staurosporine produced a lower ratio of rhodamine/fluorescein emission, which corresponds to a lower level of myosin II regulatory light chain phosphorylation. Locomoting fibroblasts containing FRLC-Rmyosin II showed a gradient of myosin II phosphorylation that was lowest near the leading edge and highest in the tail region of these cells, which correlates with previously observed gradients of free calcium and calmodulin activation. Maximal myosin II motor force in the tail may contribute to help cells maintain their polarized shape, retract the tail as the cell moves forward, and deliver disassembled subunits to the leading edge for incorporation into new fibers.
Regularization Theory and Neural Networks Architectures (1995)

We had previously shown that regularization principles lead to approximation schemes that are equivalent to networks with one layer of hidden units, called regularization networks. In particular, standard smoothness functionals lead to a subclass of regularization networks, the well known radial basis functions approximation schemes. This paper shows that regularization networks encompass a much broader range of approximation schemes, including many of the popular general additive models and some of the neural networks. In particular, we introduce new classes of smoothness functionals that lead to different classes of basis functions. Additive splines as well as some tensor product splines can be obtained from appropriate classes of smoothness functionals. Furthermore, the same generalization that extends radial basis functions (RBF) to hyper basis functions (HBF) also leads from additive models to ridge approximation models, containing as special cases Breiman's hinge functions, some forms of projection pursuit regression, and several types of neural networks. We propose to use the term generalized regularization networks for this broad class of approximation schemes that follow from an extension of regularization. In the probabilistic interpretation of regularization, the different classes of basis functions correspond to different classes of prior probabilities on the approximating function spaces, and therefore to different types of smoothness assumptions. In summary, different multilayer networks with one hidden layer, which we collectively call generalized regularization networks, correspond to different classes of priors and associated smoothness functionals in a classical regularization principle. Three broad classes are (1) radial basis functions that can be generalized to hyper basis functions, (2) some tensor product splines, and (3) additive splines that can be generalized to schemes of the type of ridge approximation, hinge functions, and several perceptron-like neural networks with one hidden layer.
Approximate loop shaping in PID parameter adaptation (2012)

SUMMARY This paper discusses the use of H‐infinity approximation for the online adaptation of PID controller parameters. For a frequency loop‐shaping control objective, it is possible to adapt the PID parameters directly with linear model estimation algorithms. Standard least squares algorithms are common solutions for this problem, but their estimates exhibit a well‐known strong dependence on the properties of the excitation. This drawback becomes more pronounced for systems where the modeling mismatch is large, as is frequently the case in PID control. In an alternative formulation of the estimation problem, we use a filter‐bank to decompose the error signal to different components and minimize approximately the H‐infinity norm of the sensitivity‐weighted error operator. This approach results in a more consistent estimate of the optimal PID parameters, at the expense of higher excitation requirements. It also allows for the computation of a ‘health indicator’ to describe the confidence in the estimated parameters. The practical implication of this observation is that PIDs can be tuned more reliably, even in cases of large mismatch between the target and the feasible loop shapes. It also suggests a general theme where a min–max optimization of an operator error provides an advantage over signal error optimization. The key aspects of the algorithm are illustrated by numerical examples. Copyright © 2012 John Wiley &amp; Sons, Ltd.
Immune response to p53 is dependent upon p53/HSP70 complexes in breast cancers. (1992)

Overexpression of the p53 protein, resulting from gene mutations that increase protein stability, has been detected in greater than 25% of primary human breast cancers. In addition, approximately 10% of breast cancer patients have circulating antibodies to the p53 protein. In this study, the anti-p53 humoral response is correlated with the presence and type of mutant p53 protein expressed in the tumor. In a series of 60 breast cancer patients, 0 of 30 tumors with normal, low-level p53 expression induced anti-p53 antibodies, whereas 7 (23%) of 30 tumors with p53 overexpression elicited a specific anti-p53 antibody response. These 7 patients had anti-p53 antibodies that recognized wild-type p53 and a variety of mutant p53 proteins. A comparison of p53 mutations revealed that antibody-negative tumors had mutations exclusively in exons 7 and 8, whereas antibody-positive tumors had mutations primarily in exons 5 and 6. Moreover, all antibody-eliciting tumors contained complexes between p53 and a 70-kDa heat shock protein, whereas none of the antibody-negative tumors contained this complex. This study implicates a 70-kDa heat shock protein in the antigenic presentation of p53.