gebhart/patrepeval huggingface dataset:
Allergen mimotopes in food enhance type I allergic reactions in mice (1999)

BIP1is a murine IgG antibody capable of enhancing the IgE binding to Bet v 1, the major birch pollen allergen. We have previously generated a mimotope of BIP1, designated Bet mim 1, from a constrained phage display peptide library. We demonstrated that oral immunization of BALB/c mice with the Bet mim 1 mimotope resulted in the induction of Bet v 1-specific IgG. The aim of this study was to test the influence of such an oral immunization with Bet mim 1 on a subsequent type I allergic response to Bet v 1. Phages displaying Bet mim 1 or control mimotopes, or PBS alone, were delivered to BALB/c mice by intragastric gavages prior to systemic sensitization with recombinant Bet v 1 and Al(OH)(3), an adjuvant inducing preferentially IgE antibody responses. Only mice fed with Bet mim 1-phages displayed substantially enhanced type I allergic skin reactivity to Bet v 1, as compared to mice pretreated with control mimotopes or PBS. A gastric digestion assay indicated that Bet v 1 and its homologue from apple, Mal d 1, were degraded within seconds under physiological conditions. In contrast, phage-displayed mimotopes were resistant to digestion. Our data indicate that allergen mimics in the diet that resist digestion, can induce allergen specific IgG able to enhance an allergic response. We therefore conclude that sensitization via the oral route may represent a mechanism for aggravating type I allergic reactions, probably leading to an earlier onset of symptoms even at lower allergen dosage.
Transplant of Bone Marrow and Muscle-Derived Connective Tissue Cultures in Diffusion Chambers for Bioassay of Bone Morphogenetic Protein (1993)

To promote a high concentration gradient, syngeneic bone marrow and muscle connective tissue cell cultures and subcultures were exposed to bone morphogenetic protein and associated noncollagenous bone matrix proteins (BMP/NCP) in vitro, transferred to diffusion chambers, and then transplanted into the anterior abdominal wall of isogeneic rats. Both muscle- and marrow-derived cells differentiated into cartilage and chondroosteoid on the inside of diffusion chambers. New bone developed on the vascularized outside surfaces in juxtaposition to avascular tissue on the inside. Levels of glycosaminoglycans (GAGs) and DNA synthesis in tissues inside the chambers were sharply elevated. These data, correlated with histologic observations, demonstrate that the BMP/NCP recruits mesenchymal-type cells for a skeletal tissue pathway of development. Muscle-derived cells, as distinguished from marrow-derived cells, originate in a nonosseous environment but differentiate into osteoprogenitor (osteogenic stem) cells and display levels of DNA synthesis almost as high as marrow stroma-derived cells. The rise in DNA synthesis was maximal in the interval from two to three weeks after transplantation. Whether the bone marrow stroma mesenchymal cell target for BMP is only the osteogenic stem cell population or also includes colony-forming units fibroblasts (CFU-F) remains to be investigated by experiments on established cell lines.
Acute Post-Surgical Pain Management: A Critical Appraisal of Current Practice (2006)

The Acute Pain Summit 2005 was convened to critically examine the perceptions of physicians about current methods used to control postoperative pain and to compare those perceptions with the available scientific evidence. Clinicians with expertise in treatment of postsurgical pain were asked to evaluate 10 practice-based statements. The statements were written to reflect areas within the field of acute-pain management, where significant questions remain regarding everyday practice. Each statement made a specific claim about the usefulness of a specific therapy (eg, PCA or epidural analgesia) or the use of pain-control modalities in specific patient populations (eg, epidural analgesia after colon resection). Members of the American Society of Regional Anesthesia and Pain Medicine (ASRA) were asked, via a Web-based survey, to rate their degree of agreement with each of the 10 statements; 22.8% (n = 632) of members responded. In preparation for the pain summit, a panel member independently conducted a literature search and summarized the available evidence relevant to each statement. Summit participants convened in December 2005. The assigned panel member presented the available evidence, and workshop participants then assigned a category for the level of evidence and recommendation for each statement. All participants then voted about each statement by use of the same accept/reject scale used earlier by ASRA members. This manuscript details those opinions and presents a critical analysis of the existing evidence supporting new and emerging techniques used to control postsurgical pain.
Study on the Apoptosis Mechanism Induced by T-2 Toxin (2013)

T-2 toxin is known to induce apoptosis in mammalian cells. The mechanism of apoptosis induced by T-2 toxin has been proposed to be linked with oxidative stress and mitochondrial pathway. In the current study, the toxic effect of T-2 on Hela, Bel-7402, and Chang liver cells was examined in dose-dependent and time-dependent manner by MTT assay. Caspase-3 was found to be up-regulated under T-2 toxin stress, which suggested that T-2 toxin induced cell apoptosis. Endogenous GSH and MDA levels in all three cell lines were found down- and up-regulated respectively, which indicated the link between toxic effect of T-2 toxin and intracellular oxidative stress. It was also found by MTT assay that NAC, which maintained the level of GSH in cells, could protect cells from death. Western-blot result showed that the level of both activated Caspase-8 and Caspase-9 increased when cells were treated by T-2 toxin. Caspase-9 was found to be activated earlier than Caspase-8. It was also found that p53 was up-regulated under T-2 toxin stress in the study. These results implied that the effect of T-2 toxin on cells was apoptosis rather than necrosis, and it was probably induced through mitochondrial pathway. To the best of our knowledge, the present study is the first to show that JunD is down-regulated in T-2 toxin induced apoptosis. By construction of an over-expression vector for the JunD gene, we observed that the survival ratio of JunD over-expressed cells obviously increased under T-2 toxin stress. These results suggested that the mechanism of T-2 induced cell death was closely connected with oxidative stress, and that JunD plays an important role in the defensive process against T-2 toxin stress.
A Versatile Platform for Single- and Multiple-Unnatural Amino Acid Mutagenesis in Escherichia coli (2013)

To site-specifically incorporate an unnatural amino acid (UAA) into target proteins in Escherichia coli, we use a suppressor plasmid that provides an engineered suppressor tRNA and an aminoacyl-tRNA synthetase (aaRS) specific for the UAA of interest. The continuous drive to further improve UAA incorporation efficiency in E. coli has resulted in several generations of suppressor plasmids. Here we describe a new, highly efficient suppressor plasmid, pUltra, harboring a single copy each of the tRNA and aaRS expression cassettes that exhibits higher suppression activity than its predecessors. This system is able to efficiently incorporate up to three UAAs within the same protein at levels up to 30% of the level of wild-type protein expression. Its unique origin of replication (CloDF13) and antibiotic resistance marker (spectinomycin) allow pUltra to be used in conjunction with the previously reported pEVOL suppressor plasmid, each encoding a distinct tRNA/aaRS pair, to simultaneously insert two different UAAs into the same protein. We demonstrate the utility of this system by efficiently incorporating two bio-orthogonal UAAs containing keto and azido side chains into ketosteroid isomerase and subsequently derivatizing these amino acid residues with two distinct fluorophores, capable of Förster resonance energy transfer interaction. Finally, because of its minimal composition, two different tRNA/aaRS pairs were encoded in pUltra, allowing the generation of a single plasmid capable of dual suppression. The high suppression efficiency and the ability to harbor multiple tRNA/aaRS pairs make pUltra a useful system for conducting single- and multiple-UAA mutagenesis in E. coli.
Chemical barriers to human immunodeficiency virus type 1 (HIV-1) infection: retrovirucidal activity of UC781, a thiocarboxanilide nonnucleoside inhibitor of HIV-1 reverse transcriptase (1997)

UC781, a thiocarboxanilide nonnucleoside inhibitor of human immunodeficiency virus type 1 (HIV-1) reverse transcriptase (RT), inhibited RT DNA polymerase activity in vitro with marked potency. Significant inhibition was noted at a 1:1 molar ratio of UC871 to RT, characteristic of a tight-binding inhibitor. Infectivity of the HIV-1(IIIB) laboratory strain was eliminated in a concentration-dependent manner following short exposure of isolated virion particles to UC781. Neither nevirapine nor certain other carboxanilide nonnucleoside inhibitors were effective in this manner. Endogenous reverse transcription in UC781-treated virus particles was markedly reduced. Treatment of chronically HIV-1-infected H9 cells with UC781 did not alter virus production, but the infectivity of the virus produced by the cells during drug exposure was markedly reduced. Moreover, the infectivity of nascent virus produced by the UC781-treated H9 cells after removal of exogenous drug was dramatically attenuated. Similarly, pretreatment of peripheral blood lymphocytes isolated from HIV-infected patients abolished the infectivity of virus produced by these cells after removal of exogenous drug, as measured by coculture experiments with uninfected cord blood mononuclear cells, indicating the utility of UC781 against a variety of clinical HIV samples. Importantly, preincubation of uninfected MT2 cells with UC781 rendered these cells refractory to subsequent HIV infection in the absence of extracellular drug, an effect that persisted for several days following removal of exogenous drug. These unique properties of UC781 indicate that this nonnucleoside inhibitor may have considerable promise for use in retrovirucidal formulations to minimize the spread of HIV from infected to noninfected individuals.
Delay test generation (1977)

Conflicting needs complicate the task of testing LSI chips. As system designs come to require better and more predictable performance, it becomes increasingly difficult to develop tests for application at the product I/O pins to verify that each internal device has been manufactured correctly.Any of numerous kinds of random manufacturing defect, though allowing correct dc operation, can cause a device to perform at a speed below that specified for it. This type of defect has led to the development of several testing methods that have become conventional. For numerous reasons, however, the conventional methods cannot be extended to LSI without certain design constraints.For the LSSD—level-sensitive scan design—constraints, dc fault-oriented testing has been extended to delay faults. The strategy is to delay-test each block input and/or output in both its longest and its shortest sensitizable delay paths. An algorithm for automatic generation of such delay tests has been developed, and extended to generate delay tests for designer-specified critical paths.
Interleukin‐2 injected around tumor‐draining lymph nodes in head and neck cancer (1991)

Twenty patients with recurrent, inoperable head and neck squamous cell carcinoma received perilymphatic injections of natural interleukin-2 (nIL-2) for 10 days. Ten patients received 200 units (U) of nIL-2; five 1,000 U; and five 5,000 U. Irrespective of the location of the recurrence, the injections were always performed 1.5 cm below the insertion of the sternocleidomastoid muscle on the mastoid. When the ipsilateral lymphatic chain was still present, they were performed on the same side as the tumor site, whereas when it had been stripped as a result of previous surgery, they were contralateral. Patients who had undergone bilateral neck dissection were injected on the tumor side. Whenever possible, the treatment was repeated after 45-day intervals. In 13 patients (65%) with bilateral or contralateral lymph nodes, complete or partial disappearance of the lesion was observed. Despite these marked responses, the tumor always relapsed, and subsequent IL-2 courses were poorly effective. There were no systemic disturbances during or after treatment, but only moderate local swelling and pain.
Mask material effects in cryogenic deep reactive ion etching (2007)

Cryogenic silicon etching in inductively coupled SF6∕O2 plasma has been studied, especially the behavior of mask materials. Suitability of eight different mask materials for cryogenic silicon deep reactive ion etching has been investigated. Three of the five photoresists suffered from cracking during cryogenic etching. We clarified the stages of the etching process and identified two mechanisms behind the cracking: thermal expansion mismatch and mechanical deformation from wafer clamping and backside helium pressure. Also thickness of the photoresist plays a role in cracking, but, contrary to common conception that all thick resists suffer from cracking in cryogenic etching, we found that SU-8 negative resist did not crack, even for very thick layers. This is explained to be due to its high cross-linking density. All three hard mask materials had high selectivities and were free of cracking problems. However, aluminum mask resulted in poor surface quality, while thermally grown SiO2 and amorphous Al2O3 deposited by atomic layer deposition showed smooth surfaces and sidewalls. Silicon dioxide had selectivity of 150:1, while Al2O3 selectivity was 66 000:1. This extreme selectivity of Al2O3 mask, combined with good surface quality, is shown to be highly beneficial in both shallow and through-wafer etching.
Experimental radiation pneumonitis. IV. Leakage of circulatory proteins onto the alveolar surface. (1980)

We have previously shown that the fall in lung compliance in radiation pneumonitis is mainly due to abnormality of the alveolar surface lining layer and speculated that this, in turn, is due to an increased amount of protein in the alveolar lining fluid layer. In the present study, this extra protein has been partially characterized, and the kinetics of permeation from the blood to the lung and the AF have been investigated by using intravenously injected of 125I-labeled albumin. Mice which had received 3000 rads to the thorax were used. A fourfold to fivefold increase in the total protein in AF obtained by pulmonary lavage was again found in mice irradiated 4 months previously, as compared to control littermates. With immunologic techniques and polyacrylamide disc-gel electrophoresis the excess protein in the alveolar lavage fluid was shown to be derived from the circulation. Following injection of 125I-labeled albumin into the tail vein, APR in the perfused, lavaged lung relative to radioactivity in simultaneously obtained blood rose to a plateau at 6 hr, which was approximately twice as high in irradiated mice as in controls. APR in the AF relative to that in simultaneously obtained blood rose rapidly and continued to rise throughout the period of study, reaching a level which was six times that in control mice at 24 hr. A major abnormality in radiation pneumonitis appears to be a large increase in permeability of the capillary and alveolar membranes to both small and large protein molecules. These abnormalities are not acute terminal events but probably persist for some weeks before death. It is speculated that leakage of plasma proteins onto the alveolar surface is responsible for the fall in compliance of the AF lining layer in radiation pneumonitis.
A brief survey of methods for preparing protein conjugates with dyes, haptens and crosslinking reagents (1992)

ADVERTISEMENT RETURN TO ISSUEPREVArticleNEXTA brief survey of methods for preparing protein conjugates with dyes, haptens and crosslinking reagentsMichael BrinkleyCite this: Bioconjugate Chem. 1992, 3, 1, 2–13Publication Date (Print):January 1, 1992Publication History Published online1 May 2002Published inissue 1 January 1992https://pubs.acs.org/doi/10.1021/bc00013a001https://doi.org/10.1021/bc00013a001research-articleACS PublicationsRequest reuse permissionsArticle Views7477Altmetric-Citations468LEARN 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
Target-oriented wave-equation least-squares migration/inversion with phase-encoded Hessian (2009)

Abstract Prestack depth migration produces blurred images resulting from limited acquisition apertures, complexities in the velocity model, and band-limited characteristics of seismic waves. This distortion can be partially corrected using the model-space least-squares migration/inversion approach, where a target-oriented wave-equation Hessian operator is computed explicitly and then inverse filtering is applied iteratively to deblur or invert for the reflectivity. However, one difficulty is the cost of computing the explicit Hessian operator, which requires storing a large number of Green's functions, making it challenging for large-scale applications. A new method to compute the Hessian operator for the wave-equation-based least-squares migration/inversion problem modifies the original explicit Hessian formula, enabling efficient computation of this operator. An advantage is that the method eliminates disk storage of Green's functions. The modifications, however, also introduce undesired crosstalk artifacts. Two different phase-encoding schemes, plane-wave-phase encoding and random-phase encoding, suppress the crosstalk. When the randomly phase-encoded Hessian operator is applied to the Sigsbee2A synthetic data set, an improved subsalt image with more balanced amplitudes is obtained.
Rapid protein release from Escherichia coli by chemical permeabilization under fermentation conditions (1992)

Overall protein release greater than 75% in less than 1 h can be attained by exposing exponentially growing Escherichia coli cells to 0.4 M guanidine plus 0.5% Triton X-100 at 37 degrees C in medium. Cell growth stops immediately upon addition of the chemicals, but the cells are not lysed. Guanidine concentrations lower than 0.2 M, in conjunction with 0.5% Triton X-100, do not release significant intracellular protein, nor do they inhibit cell growth. Under these conditions, the cells undergo an adaptation that confers resistance to protein release by further treatment with guanidine and Triton X-100. Cells treated with 0.2 M guanidine plus 0.5% Triton X-100 display intermediate behavior. Protein release is approximately 35%, and growth is temporarily interrupted by an extended lag phase. Subsequent resumption of cell growth results in resistant cells and no additional protein release. This resistance is shown to be reversible and is most likely due to physiological adaptation rather than genetic mutation.
The mechanism of islet amyloid polypeptide toxicity is membrane disruption by intermediate-sized toxic amyloid particles. (1999)

NIDDM is characterized by islet amyloid deposits and decreased beta-cell mass. Islet amyloid is derived from the locally expressed protein islet amyloid polypeptide (IAPP). While it is now widely accepted that abnormal aggregation of IAPP has a role in beta-cell death in NIDDM, the mechanism remains unknown. We hypothesized that small IAPP aggregates, rather than mature large amyloid deposits, are cytotoxic. Consistent with this hypothesis, freshly dissolved human (h)-IAPP was cytotoxic when added to dispersed mouse and human islet cells, provoking the formation of abnormal vesicle-like membrane structures in association with vacuolization and cell death. Human islet cell death occurred by both apoptosis and necrosis, predominantly between 24 and 48 h after exposure to h-IAPP. In contrast, the addition to dispersed islet cells of matured h-IAPP containing large amyloid deposits of organized fibrils was seldom associated with vesicle-like structures or features of cell death, even though the cells were often encased in the larger amyloid deposits. Based on these observations, we hypothesized that h-IAPP cytotoxicity is mediated by membrane damage induced by early h-IAPP aggregates. Consistent with this hypothesis, application of freshly dissolved h-IAPP to voltage-clamped planar bilayer membranes (a cell-free in vitro system) also caused membrane instability manifested as a marked increase in conductance, increased membrane electrical noise, and accelerated membrane breakage, effects that were absent using matured h-IAPP or rat IAPP solutions. Light-scattering techniques showed that membrane toxicity corresponded to h-IAPP aggregates containing approximately 25-6,000 IAPP molecules, an intermediate-sized amyloid particle that we term intermediate-sized toxic amyloid particles (ISTAPs). We conclude that freshly dissolved h-IAPP is cytotoxic and that this cytotoxicity is mediated through an interaction of ISTAPs with cellular membranes. Once ISTAPs mature into amyloid deposits comprising >10(6) molecules, the capacity of h-IAPP to cause membrane instability and islet cell death is significantly reduced or abolished. These data may have implications for the mechanism of cell death in other diseases characterized by local amyloid formation (such as Alzheimer's disease).
Review of therapeutic options and the management of patients with myelodysplastic syndromes (2013)

Myelodysplastic syndromes (MDS) are a poorly understood group of disorders caused by one or more genetic aberrations in the bone marrow-derived cell line responsible for hematopoiesis. Recent advances in genetic medicine have offered new insights into the epigenesis as well as the prognosis of MDS, but have not resulted in new or improved curative treatment options. Bone marrow transplantation, introduced before the advent of genetic medicine, is still the only potential cure. Advances in other medical and pharmaceutical areas have broadened the scope of supportive care and disease-modifying therapies, and treating physicians now have a broad range of disease management options depending on a patient's likely prognosis. There is now clear evidence that appropriate supportive care and therapeutic intervention can improve progression-free and overall survival of MDS patients.