gebhart/patrepeval huggingface dataset:
Radiation Treatment Breaks and Ulcerative Mucositis in Head and Neck Cancer (2008)

Unplanned radiation treatment breaks and prolongation of the radiation treatment time are associated with lower survival and locoregional control rates when radiotherapy or concurrent chemoradiotherapy is used in the curative treatment of head and neck cancer. Treatment of head and neck cancer is intense, involving high-dose, continuous radiotherapy, and often adding chemotherapy to radiotherapy. As the intensity of treatment regimens has escalated in recent years, clinical outcomes generally have improved. However, more intensive therapy also increases the incidence of treatment-related toxicities, particularly those impacting the mucosal lining of the oral cavity, pharynx, and cervical esophagus, and results in varying degrees of ulcerative mucositis. Ulcerative mucositis is a root cause of unscheduled radiation treatment breaks, which prolongs the total radiation treatment time. Alterations in radiotherapy and chemotherapy, including the use of continuous (i.e., 7 days/week) radiotherapy to ensure constant negative proliferative pressure, may improve efficacy outcomes. However, these approaches also increase the incidence of ulcerative mucositis, thereby increasing the incidence of unplanned radiation treatment breaks. Conversely, the reduction of ulcerative mucositis to minimize unplanned breaks in radiotherapy may enhance not only tolerability, but also efficacy outcomes. Several strategies to prevent ulcerative mucositis in radiotherapy for head and neck cancer have been evaluated, but none have demonstrated strong efficacy. Continued investigation is needed to identify superior radiation treatment regimens, technology, and supportive care that reduce unplanned radiation treatment breaks with the goal of improving clinical outcomes in head and neck cancer.
8 × 2.5 Gbit/s WDM transmission over 6000km with wavelength add/drop multiplexing (1996)

Eight 2.5 Gbit/s NRZ data channels have been transmitted error free over a 6000 km straight line test-bed with a 75 km amplifier spacing. A wavelength add/drop function has been inserted in the link. Experimental results and calculations are compared.
Whose Public, Whose Order? Imperium, Region, and Normative Friction (2007)

Theories of international law and politics are a product of their times. They focus on the issues of the day (or of the immediate past) and their assumptions are often the assumptions of the society in which they were born. Perhaps that it is why so many international relations scholars were surprised by the end of the Cold War: Their theories were so informed by bipolarity that they were unable to see the actual changes that would transform the state system. As international relations scholars are re-assessing their theories in a post-Cold War world, lawyers may do the same concerning international legal jurisprudence. Throughout the Cold War, the New Haven School of policyoriented jurisprudence attempted to describe how law was actually used in the policymaking process and to suggest how it should be used towards the goals of securing human dignity and the spread of free societies.' But with the titanic struggle between competing world orders being replaced by parochial fights and feuds, whither the New Haven School? What insights does it have for today's world? Does the New Haven School's theory need to catch up to the practice of international law?
Structural studies on the carbohydrate portion of human antithrombin III. (1980)

Human antithrombin III has been shown to contain four identical N-glycosidically linked carbohydrate chain per molecule. These carbohydrate chains have been investigated by sugar and methylation analysis before and after removal of N-acetylneuraminic acid residues. The chains have been further investigated by Smith degradation, trifluoroacetolytic degradation, and degradation after chromium trioxide oxidation. As a result of these studies, the following structures is proposed for the carbohydrate chains in human antithrombin III: (formula: see text). NeuNAc, N-acetylneuraminic acid; Galp, galactopyranose; GlcNAcp, 2-acetamido-2-deoxyglucopyranose; Manp, mannopyranose are the abbreviations used in the structure.
LMO2 -Associated Clonal T Cell Proliferation in Two Patients after Gene Therapy for SCID-X1 (2003)

We have previously shown correction of X-linked severe combined immunodeficiency [SCID-X1, also known as gamma chain (gamma(c)) deficiency] in 9 out of 10 patients by retrovirus-mediated gamma(c) gene transfer into autologous CD34 bone marrow cells. However, almost 3 years after gene therapy, uncontrolled exponential clonal proliferation of mature T cells (with gammadelta+ or alphabeta+ T cell receptors) has occurred in the two youngest patients. Both patients' clones showed retrovirus vector integration in proximity to the LMO2 proto-oncogene promoter, leading to aberrant transcription and expression of LMO2. Thus, retrovirus vector insertion can trigger deregulated premalignant cell proliferation with unexpected frequency, most likely driven by retrovirus enhancer activity on the LMO2 gene promoter.
BRCA1 Inhibition of Estrogen Receptor Signaling in Transfected Cells (1999)

Mutations of the breast cancer susceptibility gene BRCA1 confer increased risk for breast, ovarian, and prostatic cancers, but it is not clear why the mutations are associated with these particular tumor types. In transient transfection assays, BRCA1 was found to inhibit signaling by the ligand-activated estrogen receptor (ER-alpha) through the estrogen-responsive enhancer element and to block the transcriptional activation function AF-2 of ER-alpha. These results raise the possibility that wild-type BRCA1 suppresses estrogen-dependent transcriptional pathways related to mammary epithelial cell proliferation and that loss of this ability contributes to tumorigenesis.
Mammary tissue damage during bovine mastitis: Causes and control1 (2008)

Mastitis, an inflammatory reaction of the mammary gland that is usually caused by a microbial infection, is recognized as the most costly disease in dairy cattle. Decreased milk production accounts for approximately 70% of the total cost of mastitis. Mammary tissue damage reduces the number and activity of epithelial cells and consequently contributes to decreased milk production. Mammary tissue damage has been shown to be induced by either apoptosis or necrosis. These 2 distinct types of cell death can be distinguished by morphological, biochemical, and molecular changes in dying cells. Both bacterial factors and host immune reactions contribute to epithelial tissue damage. During infection of the mammary glands, the tissue damage can initially be caused by bacteria and their products. Certain bacteria produce toxins that destroy cell membranes and damage milk-producing tissue, whereas other bacteria are able to invade and multiply within the bovine mammary epithelial cells before causing cell death. In addition, mastitis is characterized by an influx of somatic cells, primarily polymorphonuclear neutrophils, into the mammary gland. With more immune cells migrating into the mammary gland and the breakdown of the blood-milk barrier, damage to the mammary epithelium worsens. It is well known that breakdown of the extracellular matrix can lead to death of the epithelial cells. Meanwhile, polymorphonuclear neutrophils can harm the mammary tissue by releasing reactive oxygen intermediates and proteolytic enzymes. In vitro and in vivo studies suggest that the use of antioxidants and other protective compounds in mastitis control programs is worth investigating, because they may aid in alleviating damage to secretory cells and thus reduce subsequent milk loss.
Hybridization of synthetic oligodeoxyribonucleotides to ΦX174 DNA: the effect of single base pair mismatch (1979)

Oligodeoxyribonucleotides complementary to the DNA of the wild type (wt) bacteriophage phi chi 174 have been synthesized by the phosphotriester method. The oligomers, 11, 14, and 17 bases long, are complementary to the region of the DNA which accounts for the am-3 point mutation. When hybridized to am-3 DNA, the oligonucleotides form duplexes with a single base pair mismatch. The thermal stability of the duplexes formed between wt and am-3 DNAs has been measured. The am-3 DNA:oligomer duplexes dissociate at a temperature about 10 degrees C lower than the corresponding wt DNA:oligomer duplexes. This dramatic decrease in thermal stability due to a single mismatch makes it possible to eliminate the formation of the mismatched duplexes by the appropriate choice of hybridization temperature. These results are discussed with respect to the use of oligonucleotides as probes for the isolation of specific cloned DNA sequences.
Reconstruction of the Frank vectorcardiogram from standard electrocardiographic leads: diagnostic comparison of different methods (1990)

Three methods for reconstructing the Frank VCG from the standard 12-lead ECG were studied. The first was based on multivariate regression, the second on a model of the cardio-electrical activity, and the third method used a quasi-orthogonal set of ECG leads. The methods were evaluated on a test set of 90 cases by a numerical distance measure and by the agreement in diagnostic classification of the original and reconstructed VCGs. The original and reconstructed VCGs were presented separately and in random order to three referees. Eighteen of the original VCGs were presented three times to estimate the intra-observer agreement. Kappa statistics were used to quantify the agreement between diagnostic classifications. Separately, one referee was simultaneously presented the original VCG and its three reconstructions for all cases. Each reconstruction VCG was classified as either diagnostically 'same' as the original, 'borderline' or 'different'. The performance of the regression method and the model-based method was comparable. Both methods were preferable to the quasi-orthogonal method. The kappa values for the preferred methods indicated a good to excellent diagnostic agreement between the original and reconstructed VCGs. Only one out of ninety VCGs that were reconstructed with the regression method was classified as 'different' compared with the original VCGs; three VCGs were classified as 'different' with the model-based method. It was also found that estimation of similarity by a distance measure could not replace diagnostic evaluation by skilled observers.
T cell recognition of self-human histocompatibility leukocyte antigens (HLA)-DR peptides in context of syngeneic HLA-DR molecules. (1992)

It has been suggested that self major histocompatibility complex (MHC) peptides bound to self MHC molecules may be involved in the intrathymic induction of self tolerance. We studied the antigenicity of synthetic peptides derived from the first domain of DR beta 1*0101 chain in a DR beta 1*0101 responder. We found that a peptide corresponding to residues 21-42 of the beta chain could elicit the proliferation of autoreactive T cells. A T cell line (TCL-SUN) and 7 of 9 T cell clones (TCC) derived from TCL-SUN specifically recognized peptide 21-42 in the presence of APCs carrying the DR beta 1*0101 allele. DR beta 1*0101 positive APCs stimulated the TCCs in the absence of peptide, although the magnitude of the response was much lower than in cultures with peptide. This suggests that self DR1 molecules are continuously processed into peptides that are presented by the DR1 molecules on the surface of the cells. The data indicate that some T cells whose TCR binds to self MHC peptides presented by self MHC molecules are not deleted, although their ligand is continuously present. TCCs specific for peptide 21-42 presented in the context of DR1 were also stimulated by cells heterozygous for DR beta 1*0301 and 1601, indicating that some DR peptide-specific autoreactive T cells participate in alloreactivity.
DETECTION OF EPIDERMAL GROWTH FACTOR AND EPIDERMAL GROWTH FACTOR RECEPTOR IN COLORECTAL CANCERS (1993)

We immunohistochemically examined expression of EGF and EGF-R in 52 colorectal cancer tissues and 18 normal colon tissues. EGF and EGF-R positive rate were 22. 2% and 16. 7% in normal colon tissues,67. 3% and 61. 5% in colorectal cancers, The positive rate of EGF and EGF-R in colorcetal cancer significantly higher than that in normal tissues (P0. 05). the positive rate of EGF and EGF-R in advance cancers were higher than in early stage cancer. Expression of EGF or EGF-R was no relation to age,sex or location of cancer, Our results suggests that part colorectal cancer have overexpression of EGF and EGF-R,EGF and EGF-R autocrine may contribute to the growth of colorectal cancer.
Pharmacokinetics and efficacy of intravenous or intramuscular hepatitis B immunoglobulins in prophylaxis of hepatitis B after liver transplantation. (2010)

These results confirm an analogue efficacy and tolerance of iv- and im-HBIg combined with antivirals in prophylaxis of hepatitis B after LT. Anti-HBs titers three times higher than aimed and four weeks mean half-life could suggest the reduction of doses and the elongation of the interval of administration of im-HBIg.
The de-adhesive activity of matricellular proteins: is intermediate cell adhesion an adaptive state? (2001)

The process of cellular de-adhesion is potentially important for the ability of a cell to participate in morphogenesis and to respond to injurious stimuli. Cellular de-adhesion is induced by the highly regulated matricellular proteins TSP1 and 2, tenascin-C, and SPARC. These proteins induce a rapid transition to an intermediate state of adhesiveness characterized by loss of actin-containing stress fibers and restructuring of the focal adhesion plaque that includes loss of vinculin and alpha-actinin, but not of talin or integrin. This process involves intracellular signaling mediators, which are engaged in response to matrix protein-receptor interactions. Each of these proteins employs different receptors and signaling pathways to achieve this common morphologic endpoint. What is the function of this intermediate adhesive state and what is the physiologic significance of this action of the matricellular proteins? Given that matricellular proteins are expressed in response to injury and during development, one can speculate that the intermediate adhesive state is an adaptive condition that facilitates expression of specific genes that are involved in repair and adaptation. Since cell shape is maintained in weakly adherent cells, this state might induce survival signals to prevent apoptosis due to loss of strong cell adhesion, but yet allow for cell locomotion. The three matricellular proteins considered here might each preferentially facilitate one or more aspects of this adaptive response rather than all of these equally. Currently, we have only preliminary data to support the specific ideas proposed in this article. It will be interesting in the next several years to continue to elucidate the biological roles of the intermediate adhesive state induced by these matricellular proteins. and focal adhesions in a cell that nevertheless maintains a spread, extended morphology and integrin clustering. TSP1, tenascin-C, and SPARC induce the intermediate adhesive state, as shown by the red arrows. The significance of each adhesive state for cell behavior is indicated beneath the cells. The weak adhesive state would be consistent with cells undergoing apoptosis during remodeling or those undergoing cytokinesis. The strong adhesive state is characteristic of a differentiated, quiescent cell, whereas cells in the intermediate adhesive state would include those involved in responding to injury during wound healing or in tissue remodeling during morphogenesis.
The Chemistry of the Sulfur–Gold Interface: In Search of a Unified Model (2012)

Over the last three decades, self-assembled molecular films on solid surfaces have attracted widespread interest as an intellectual and technological challenge to chemists, physicists, materials scientists, and biologists. A variety of technological applications of nanotechnology rely on the possibility of controlling topological, chemical, and functional features at the molecular level. Self-assembled monolayers (SAMs) composed of chemisorbed species represent fundamental building blocks for creating complex structures by a bottom-up approach. These materials take advantage of the flexibility of organic and supramolecular chemistry to generate synthetic surfaces with well-defined chemical and physical properties. These films already serve as structural or functional parts of sensors, biosensors, drug-delivery systems, molecular electronic devices, protecting capping for nanostructures, and coatings for corrosion protection and tribological applications. Thiol SAMs on gold are the most popular molecular films because the resulting oxide-free, clean, flat surfaces can be easily modified both in the gas phase and in liquid media under ambient conditions. In particular, researchers have extensively studied SAMs on Au(111) because they serve as model systems to understand the basic aspects of the self-assembly of organic molecules on well-defined metal surfaces. Also, great interest has arisen in the surface structure of thiol-capped gold nanoparticles (AuNPs) because of simple synthesis methods that produce highly monodisperse particles with controllable size and a high surface/volume ratio. These features make AuNPs very attractive for technological applications in fields ranging from medicine to heterogeneous catalysis. In many applications, the structure and chemistry of the sulfur-gold interface become crucial since they control the system properties. Therefore, many researchers have focused on understanding of the nature of this interface on both planar and nanoparticle thiol-covered surfaces. However, despite the considerable theoretical and experimental efforts made using various sophisticated techniques, the structure and chemical composition of the sulfur-gold interface at the atomic level remains elusive. In particular, the search for a unified model of the chemistry of the S-Au interface illustrates the difficulty of determining the surface chemistry at the nanoscale. This Account provides a state-of-the-art analysis of this problem and raises some questions that deserve further investigation.
A putative origin of replication of plasmids derived from Epstein-Barr virus is composed of two cis-acting components. (1985)

A genetic element of Epstein-Barr virus, oriP, when present on recombinant plasmids allows those plasmids to replicate and to be maintained in cells that express the Epstein-Barr virus-encoded nuclear antigen EBNA-1. Here we define the DNA sequences required for oriP activity. Two noncontiguous regions of oriP are required in cis for activity. One consists of approximately 20 tandem, imperfect copies of a 30-base-pair (bp) sequence. The other required region, approximately 1,000 bp away, is at most 114 bp in length and contains a 65-bp region of dyad symmetry. When present together on a plasmid, these two components supported plasmid replication even when the distance between them was varied or their relative orientation was altered, or both. When present alone on a plasmid that expresses a selectable marker, the family of 30-bp repeats efficiently conferred a transient drug-resistant phenotype in human 143 cells that is dependent on the presence of EBNA-1. This result leads us to suggest that EBNA-1 interacts with the 30-bp repeated sequence to activate oriP. To test whether the 30-bp repeats might cause the increased transient expression of drug resistance by enhancing transcription, the family of 30-bp repeats was tested for the ability to activate the simian virus 40 early promoter present in plasmid pA10CAT2 (Laimins, et al., Proc. Natl. Acad. Sci. U.S.A. 79:6453-6457). In this assay, the 30-bp repeats could activate the simian virus 40 early promoter in Raji cells, an EBNA-positive Burkitt's lymphoma cell line, but not detectably an EBNA-positive 143 cells in which oriP also functions.
The omega-3 fatty acid docosahexaenoate reduces cytokine-induced expression of proatherogenic and proinflammatory proteins in human endothelial cells. (1994)

The mechanisms by which dietary fatty acids can modulate atherogenesis and inflammation are poorly understood. Induction in endothelial cells of adhesion molecules for circulating leukocytes and of inflammatory mediators by cytokines probably contributes to the early phases of atherogenesis and inflammation. We report here that incorporation into cellular lipids of docosahexaenoic acid (DHA), a specific fatty acid of the omega 3 family, decreases cytokine-induced expression of endothelial leukocyte adhesion molecules, secretion of inflammatory mediators, and leukocyte adhesion to cultured endothelial cells. DHA, but not eicosapentaenoic acid, decreased in a dose- and time-dependent fashion the expression of vascular cell adhesion molecule 1 (VCAM-1) induced by interleukin (IL)-1, tumor necrosis factor (TNF), IL-4, or bacterial lipopolysaccharide, with half-maximum inhibition at < 10 mumol/L. This reduction required prolonged (24- to 96-hour) exposure of endothelial cells to DHA and correlated with the degree of DHA incorporation into cellular lipids. DHA also limited cytokine-stimulated endothelial cell expression of E-selectin and intercellular adhesion molecule 1 and the secretion of IL-6 and IL-8 into the medium but not the surface expression of constitutive surface molecules. Cyclooxygenase inhibition did not block the effect of DHA on VCAM-1. In parallel with reduced surface VCAM-1 protein expression, DHA reduced VCAM-1 mRNA induction by IL-1 or TNF. DHA treatment also reduced the adhesion of human monocytes and of monocytic U937 cells to cytokine-stimulated endothelial cells. These properties of DHA may contribute to antiatherogenic and anti-inflammatory effects of omega 3 fatty acids.
Primary Structure Determination of Five Sialylated Oligosaccharides Derived from Bronchial Mucus Glycoproteins of Patients Suffering from Cystic Fibrosis (1984)

The structure of sialylated carbohydrate units of bronchial mucins obtained from cystic fibrosis patients was investigated by 600-MHz ‘H NMFt spectroscopy in conjunction with sugar analysis. After subjecting the mucins to alkaline borohydride degradation, sialylated oligosaccharide-alditols were isolated by anion-exchange chromatography and fractionated by high performance liquid chromatography. Five compounds could be obtained in a rather pure state; their structures were established as the following: A-1, Neu-
Tonic nicotinic modulation of serotoninergic transmission in the spinal cord (2001)

The spinal serotoninergic projection from the raphe magnus has been shown to modulate nociceptive inputs, and activation of this projection mediates nicotine-elicited analgesia. Here, we investigate the interactions between cholinergic and serotoninergic systems in the spinal cord, by conducting serotonin [5-hydroxytryptamine (5-HT)] efflux experiments on mouse spinal slices. At least three spinal populations of nicotinic receptors are distinguished that affect 5-HT release. The first could be directly located on serotoninergic terminals, is insensitive to nanomolar concentrations of methyllicaconitine (MLA), and may be subjected to a basal (not maximal) cholinergic tone. The second is tonically and maximally activated by endogenous acetylcholine, insensitive to nanomolar concentrations of MLA, and present on inhibitory neurons. The last is also present on inhibitory neurons but is sensitive to nanomolar concentrations of MLA and not tonically activated by acetylcholine. Multiple nicotinic acetylcholine receptor populations thus differentially exert tonic or not tonic control on 5-HT transmission in the spinal cord. These receptors may be major targets for nicotine effects on antinociception. In addition, the presence of a tonic nicotinic modulation of 5-HT release indicates that endogenous acetylcholine plays a role in the physiological regulation of descending 5-HT pathways to the spinal cord.