gebhart/patrepeval huggingface dataset:
The Vα14 invariant natural killer T cell TCR forces microbial glycolipids and CD1d into a conserved binding mode (2010)

Invariant natural killer T cells (iNKT cells) rapidly produce effector cytokines. In this study, we report the first crystal structures of the iNKT cell T cell receptor (TCR) bound to two natural, microbial glycolipids presented by CD1d. Binding of the TCR induced CDR3-α-dependent structural changes in the F' roof of CD1d; these changes resemble those occurring in the absence of TCR engagement when the highly potent synthetic antigen α-galactosylceramide (α-GalCer) binds CD1d. Furthermore, in the Borrelia burgdorferi α-galactosyl diacylglycerol-CD1d complex, TCR binding caused a marked repositioning of the galactose sugar into an orientation that closely resembles α-GalCer. The TCR-dependent reorientation of the sugar, together with the induced CD1d fit, may explain the weaker potency of the microbial antigens compared with α-GalCer. We propose that the TCR of iNKT cells binds with a conserved footprint onto CD1d, regardless of the bound glycolipid antigen, and that for microbial antigens this unique binding mode requires TCR-initiated conformational changes.
Two Syngeneic Cell Lines from Human Breast Tissue: The Aneuploid Mammary Epithelial (Hs578T) and the Diploid Myoepithelial (Hs578Bst) Cell Lines 2 (1977)

We characterized two human cell lines (Hs578T and Hs578Bst), which provide several unique features that should be useful in the study of breast disease. Hs578T, derived from a carcinosarcoma, is epithelial in origin. Hs578Bst, established from normal tissue peripheral to the tumor, is myoepithelial in origin. This is the first report of companion cell lines, one malignant and one normal, established from the same organ.
Release of the neuronal glycoprotein ICAM-5 in serum after hypoxic-ischemic injury (2000)

Intercellular adhesion molecule (ICAM)-5 (telencephalin) is unique among the ICAMs, because it is only expressed in somatodendritic membranes of telencephalic neurons. To investigate the fate of ICAM-5 during focal brain injury, we induced hypoxia-ischemia (HI) damage in adult mice by right common carotid artery ligation followed by hypoxia. ICAM-5 was detectable in serum within a 48-hour window after HI injury. In HI brain, dendritic ICAM-5 immunoreactivity was abolished, but it was present in the neuropil and soma of hippocampal pyramidal, dentate granule, and some cortical and striatal neurons. After HI injury, levels of ICAM-5 protein and messenger RNA initially increased, and ICAM-5 messenger RNA expression then decreased, although protein levels continued to increase. Because HI injury induces microglial activation with increases in CD11a/CD18 (lymphocyte function antigen [LFA]-1) counterreceptors to ICAM-5, we investigated whether modulation of interactions between LFA-1 receptors and brain ICAM-5 during HI injury are associated with changes in levels of serum ICAM-5. Intracerebroventricular administration of lipopolysaccharide to activate microglia before HI injury resulted in elevated serum ICAM-5 levels compared with those in mice with only HI injury. Pretreatment with anti-LFA-1 antibodies before HI injury or LFA-1 receptor knockout mice with HI injury had markedly reduced levels of serum ICAM-5. Lipopolysaccharide levels increased, whereas LFA-1 receptor blockade or LFA-1 knockout decreased HI injury in the first 12 hours. These data suggest that during the necrotic phase of HI injury, serum ICAM-5 may be a potential marker for somatodendritic neuronal damage. Ann Neurol 2000;48:590–602
Methods and protocols for prediction of immunogenic epitopes (2006)

T-cell recognition of peptide/major histocompatibility complex (MHC) is a prerequisite for cellular immunity. Recently, there has been an influx of bioinformatics tools to facilitate the identification of T-cell epitopes to specific MHC alleles. This article examines existing computational strategies for the study of peptide/MHC interactions. The most important bioinformatics tools and methods with relevance to the study of peptide/MHC interactions have been reviewed. We have also provided guidelines for predicting antigenic peptides based on the availability of existing experimental data.
Treatment of hyponatraemic seizures with intravenous 29.2% saline. (1986)

Five patients with severe hyponatraemia and epileptiform seizures were given 50 ml of 29.2% saline (250 mmol) through a central venous catheter over 10 minutes to control seizures rapidly, reduce cerebral oedema, and diminish the incidence of permanent neuronal damage. The saline controlled seizures in all patients, increasing the mean serum sodium concentration by 7.4 (SD 1.14) mmol(mEq)/l and decreasing the mean serum potassium concentration by 0.62 (0.5) mmol(mEq)/l. Further saline and frusemide were then administered over 10 (2) hours, raising the serum sodium concentration by 2.14 (0.49) mmol/l/h until it reached 133 (2.35) mmol/l. A total of 790 (139) mmol saline was infused and a negative fluid balance of 3.34 (0.75) litres achieved. Four patients survived without neurological abnormality. One patient, who was not treated immediately and suffered a prolonged episode of status epilepticus, was left with a permanent neurological defect.
Exogenous OX40 Stimulation during Lymphocytic Choriomeningitis Virus Infection Impairs Follicular Th Cell Differentiation and Diverts CD4 T Cells into the Effector Lineage by Upregulating Blimp-1 (2013)

T cell costimulation is a key component of adaptive immunity to viral infection but has also been associated with pathology because of excessive or altered T cell activity. We recently demonstrated that the TNFR family costimulatory molecule OX40 (CD134) is critically required to sustain antiviral T cell and Ab responses that enable control of viral replication in the context of chronic lymphocytic choriomeningitis virus (LCMV) infection. In this study, we investigated whether reinforcing OX40 stimulation through an agonist Ab had the potential to prevent LCMV persistence. We observed that anti-OX40 injection early after LCMV clone 13 infection increased CD8 T cell-mediated immunopathology. More strikingly, OX40 stimulation of virus-specific CD4 T cells promoted expression of the transcriptional repressor Blimp-1 and diverted the majority of cells away from follicular Th cell differentiation. This occurred in both acute and chronic infections, and resulted in dramatic reductions in germinal center and Ab responses to the viral infection. The effect of the OX40 agonist was dependent on IL-2 signaling and the timing of OX40 stimulation. Collectively, our data demonstrate that excessive OX40 signaling can result in deleterious consequences in the setting of LCMV infection.
Extracellular Matrix and Control of Proliferation of Vascular Endothelial Cells (1980)

Bovine vascular endothelial cells plated at low cell density in the presence of high (10%) concentrations of serum and maintained on plastic tissue culture dishes proliferate slowly. If the cultures were exposed to fibroblast growth factors (FGF), the cells proliferated actively and, after a week, a monolayer composed of closely apposed and highly contact-inhibited mononucleated cells formed. In contrast to cultures maintained on plastic, cultures maintained on dishes coated with an extracellular matrix produced by corneal endothelial cells proliferated rapidly and no longer required FGF to reach confluence. Addition of FGF to such cultures did not decrease the mean doubling time, which was already at a minimum (18 h), nor did it result in a higher final cell density, which was already at a maximum (700-1,000 cells/mm(2)). Likewise, although human umbilical vein endothelial cells plated at low density on plastic did not proliferate, they proliferated rapidly when plated on dishes coated with an extracellular matrix. However, unlike bovine vascular endothelial cells, they still required FGF if the cultures were to become confluent. The ability of plasma vs. serum to sustain cell proliferation was analyzed using low density bovine-vascular endothelial cell cultures maintained either on plastic or on dishes coated with an extracellular matrix. Cells plated on plastic had a lower growth rate when exposed to plasma than to serum. In both cases, FGF was required for the cultures to become confluent. In contrast, when cells were plated on an extracellular matrix, they proliferated equally well, regardless of whether they were exposed to plasma or serum, and no longer required FGF to become confluent. Because the growth rate of the cultures maintained on an extracellular matrix was a direct function of the serum or plasma concentrations to which they were exposed, it is likely that the extracellular matrix had a permissive rather than a direct mitogenic effect on the cells. Therefore, one can conclude that the simple change of substrate from plastic to extracellular matrix will restore the sensitivity of vascular endothelial cells to physiological agents present in plasma or serum.
Mitogen-activated Protein (MAP) Kinase Regulates Production of Tumor Necrosis Factor-α and Release of Arachidonic Acid in Mast Cells (1997)

Aggregation of the high affinity IgE receptor (FcepsilonRI) in a mast cell line resulted in activation of the p42 and the stress-activated p38 mitogen-activated protein (MAP) kinases. Selective inhibition of these respective kinases with PD 098059 and SB 203580 indicated that p42 MAP kinase, but not p38 MAP kinase, contributed to the production of the cytokine, tumor necrosis factor-alpha, and the release of arachidonic acid in these cells. Neither kinase, however, was essential for FcepsilonRI-mediated degranulation or constitutive production of tumor growth factor-beta. Studies with SB 203580 and the p38 MAP kinase activator anisomycin also revealed that p38 MAP kinase negatively regulated activation of p42 MAP kinase and the responses mediated by this kinase.
Hepatic Fibrogenesis (2007)

Hepatic fibrogenesis represents a wound-healing response of liver to a variety of insults, ultimately leading to decompensated cirrhosis in many patients and accounting for extensive morbidity and mortality worldwide. The net accumulation of extracellular matrix (ECM) in liver injury arises from increased synthesis by activated hepatic stellate cells and other hepatic fibrogenic cell types, as well as from bone marrow and circulating fibrocytes. Concurrently, degradation of ECM by matrix metalloproteinases (MMPs) fails to keep pace with increased synthesis, in part due to sustained expression of MMP inhibitors (e.g., tissue inhibitors of metalloproteinases). A growing list of circulating, paracrine, and autocrine mediators have been identified that amplify the fibrogenic response of liver. Combined with accelerating knowledge about signaling pathways and genetic determinants, major advances are anticipated in new diagnostics and therapies that will transform the care of patients with chronic liver diseases in the coming years.
Effect of Matrigel and laminin peptide YIGSR on tumor growth and metastasis. (1993)

Basement membrane has a variety of effects on tumor cells and promotes malignant behavior. Tumor cell growth is enhanced both in vitro and in vivo in mice in the presence of basement membrane. This has led to the ability to grow various tumors including human biopsy specimens in nude mice. Furthermore, low cell numbers can be used when coinjected with Matrigel, a basement membrane extract. The basement membrane glycoprotein laminin is important in promoting invasive behavior and the level of a 32/67 kDa laminin receptor has been shown to correlate with malignancy. A sequence of five amino acids, tyrosine-isoleucine-glycine-serine-arginine (YIGSR) has been shown to recognize this receptor and to reduce experimental metastases (tail vein injection resulting in colonization of the lung) and subcutaneous tumor growth. This peptide is active in both models either when coinjected or when daily intraperitoneal injections are given after tumor growth has initiated. YIGSR does not effect cell arrest but does inhibit angiogenesis which is necessary for tumor growth. YIGSR also appears to have an additional antitumor effect via its interaction with a specific receptor. YIGSR-adherent cells established after 30 successive selections on YIGSR-coated dishes in vitro formed more lung colonies after intravenous injection and larger tumors after subcutaneous injection than the parent B16F10 melanoma cells. The YIGSR-non-adherent cells formed fewer lung colonies and smaller subcutaneous tumors. These data demonstrate the importance of laminin-tumor cell interactions in malignancies and suggest that a short sequence from laminin has multiple effects in reducing tumor growth and spread.(ABSTRACT TRUNCATED AT 250 WORDS)
Efficient cooperative backup with decentralized trust management (2012)

Existing backup systems are unsatisfactory: commercial backup services are reliable but expensive while peer-to-peer systems are cheap but offer limited assurance of data reliability. This article introduces Friendstore, a system that provides inexpensive and reliable backup by giving users the choice to store backup data only on nodes they trust (typically those owned by friends and colleagues). Because it is built on trusted nodes, Friendstore is not burdened by the complexity required to cope with potentially malicious participants. Friendstore only needs to detect and repair accidental data loss and to ensure balanced storage exchange. The disadvantage of using only trusted nodes is that Friendstore cannot achieve perfect storage utilization. Friendstore is designed for a heterogeneous environment where nodes have very different access link speeds and available disk spaces. To ensure long-term data reliability, a node with limited upload bandwidth refrains from storing more data than its calculated maintainable capacity. A high bandwidth node might be limited by its available disk space. We introduce a simple coding scheme, called XOR(1,2), which doubles a node's ability to store backup information in the same amount of disk space at the cost of doubling the amount of data transferred during restore. Analysis and simulations using long-term node activity traces show that a node can reliably back up tens of gigabytes of data even with low upload bandwidth.
Expression of Pro‐Inflammatory Cytokine and Chemokine mRNA Upon Experimental Spinal Cord Injury in Mouse: an In Situ Hybridization Study (1997)

Injury to the spinal cord induces a complex cascade of cellular reactions at the local lesion area: secondary cell death and inflammatory reactions as well as scar and cavity formation take place. In order to investigate the molecular features underlying this local wounding response and to determine their pathophysiological implications, we studied the expression pattern of pro-inflammatory and chemoattractant cytokines in an experimental spinal cord injury model in mouse. We show by in situ hybridization that transcripts for the pro-inflammatory cytokines TNF alpha and IL-1 as well as the chemokines MIP-1alpha and MIP-1beta are upregulated within the first hour following injury. In this early phase, the expression of the pro-inflammatory cytokines is restricted to cells in the surroundings of the lesion area probably resident CNS cells. While TNF alpha is expressed in a very narrow time window, IL-1 can be detected in a second phase in a subset of polymorphonuclear granulocytes which immigrate into the spinal cord around 6 h. Message for the chemokines MIP-1alpha and beta is expressed in a generalized way in the grey matter of the entire spinal cord around 24 h and gets again restricted to the cellular infiltrate at the lesion site at 4 days following injury. Interestingly, our data suggest that resident CNS cells, most probably microglial cells, and not peripheral inflammatory cells, are the main source for cytokine and chemokine mRNAs. The defined cytokine pattern observed indicates that the inflammatory events upon lesioning the CNS are tightly controlled. The very early expression of pro-inflammatory cytokine and chemokine messages may represent an important element of the recruitment of inflammatory cells. Additional pathophysiological consequences of the specific cytokine pattern observed remain to be determined.
Comparison of host response to polypropylene and non‐cross‐linked porcine small intestine serosal‐derived collagen implants in a rat model (2005)

Biologically derived implant material induced a less pronounced inflammatory response and differences in collagen deposition. At 30 days tensile strength was weaker in the biological implant group but was equivalent by 90 days. These differences may have implications for the in vivo performance of the materials.
Genetic Engineering Using Homologous Recombination (2002)

In the past few years, in vivo technologies have emerged that, due to their efficiency and simplicity, may one day replace standard genetic engineering techniques. Constructs can be made on plasmids or directly on the Escherichia coli chromosome from PCR products or synthetic oligonucleotides by homologous recombination. This is possible because bacteriophage-encoded recombination functions efficiently recombine sequences with homologies as short as 35 to 50 base pairs. This technology, termed recombineering, is providing new ways to modify genes and segments of the chromosome. This review describes not only recombineering and its applications, but also summarizes homologous recombination in E. coli and early uses of homologous recombination to modify the bacterial chromosome. Finally, based on the premise that phage-mediated recombination functions act at replication forks, specific molecular models are proposed.
Acid-sensing ion channel 3 matches the acid-gated current in cardiac ischemia-sensing neurons (2000)

Cardiac afferents are sensory neurons that mediate angina, pain that occurs when the heart receives insufficient blood supply for its metabolic demand (ischemia). These neurons display enormous acid-evoked depolarizing currents, and they fire action potentials in response to extracellular acidification that accompanies myocardial ischemia. Here we show that acid-sensing ion channel 3 (ASIC3), but no other known acid-sensing ion channel, reproduces the functional features of the channel that underlies the large acid-evoked current in cardiac afferents. ASIC3 and the native channel are both especially sensitive to pH, interact similarly with Ca(2+), and gate rapidly between closed, open, and desensitized states. Particularly important is the ability of ASIC3 and the native channel to open at pH 7, a value reached in the first few minutes of a heart attack. The steep activation curve suggests that the channel opens when four protons bind. We propose that ASIC3, a member of the degenerin channel (of Caenorhabditis elegans)/epithelial sodium channel family of ion channels, is the sensor of myocardial acidity that triggers cardiac pain, and that it might be a useful pharmaceutical target for treating angina.
N-Phosphonomethyl Dipeptides and Their Phosphonate Prodrugs, a New Generation of Neutral Endopeptidase (NEP, EC 3.4.24.11) Inhibitors (1994)

Inhibitors of the zinc protease neutral endopeptidase (NEP, EC 3.4.24.11) offer significant therapeutic interest as antihypertensives due to their ability to potentiate the biological action of the circulating natriuretic hormone ANF (atrial natriuretic factor). N-Phosphonomethyl dipeptides bearing a central (4-phenyl)phenylalanine residue have been designed to exert potent and selective NEP inhibition. In particular, (S)-3-[N-[2- [(phosphonomethyl)amino]-3-(4-biphenylyl)propionyl]amino]propionic acid (10a) (CGS 24592) displayed high inhibitory potency in vitro (IC50 = 1.9 +/- 0.1 nM) and a long plasma half-life in rats but lacked oral bioavailability. This drawback was overcome by using esterase-sensitive (acyloxy)alkyl phosphonates. More remarkable, several diaryl phosphonate derivatives of 10a also performed as effective prodrugs. Specifically, the structurally simple diphenyl phosphonate 18 (CGS 25462) induced potent inhibition of NEP ex vivo for at least 8 h after oral administration to rats (30 mg/kg). Its antihypertensive effect was demonstrated in DOCA-salt rats. At 30 mg/kg orally, 18 caused a significant reduction in mean arterial pressure measuring -35 +/- 7 mmHg at 5-h postdosing. The alpha-aminomethyl phosphonate 18 represents a new generation of selective NEP inhibitors that combine high potency, long duration of action, and oral bioavailability. Therefore, it holds promise as a novel therapeutic agent for the treatment of human hypertension and congestive heart failure.
Electrical Sintering of Silver Nanoparticle Ink Studied by In-Situ TEM Probing (2011)

Metallic nanoparticle inks are used for printed electronics, but to reach acceptable conductivity the structures need to be sintered, usually using a furnace. Recently, sintering by direct resistive heating has been demonstrated. For a microscopic understanding of this Joule heating sintering method, we studied the entire process in real time inside a transmission electron microscope equipped with a movable electrical probe. We found an onset of Joule heating induced sintering and coalescence of nanoparticles at power levels of 0.1-10 mW/μm³. In addition, a carbonization of the organic shells that stabilize the nanoparticles were found, with a conductivity of 4 10⁵ Sm⁻¹.
Ionic Liquid and Microwave-Assisted Organic Synthesis: A "Green" and Synergic Couple (2007)

In the present century an ever-growing number of papers have been published describing the use of ionic liquids (ILs) on Microwave-Assisted Organic Synthesis (MAOS). In general, these works have shown evident advantages of this couple (IL/MAOS) respect to the conventional synthetic procedures for the generation of fast, efficient and environmental friendly synthetic methodologies. This review focuses on the advances in the developing of innovative applications of ILs/MAOS.
Larval Diets Containing Dyes for Tagging Pink Bollworm Moths Internally123 (1971)

Larvae of Pectinophora gossypiella (Saunders) developed on diets containing Calco Oil Red N-1700® dye and produced moths that were visibly dyed throughout their lives. At concentrations of 0.015-0.00% dye (wt/v) in the diet, there were no effects on the rate of development or adult longevity, fecundity, or mating.
Lung Adenocarcinoma with Anaplastic Lymphoma Kinase (ALK) Rearrangement Presenting as Carcinoma of Unknown Primary Site: Recognition and Treatment Implications (2016)

We report on patients with lung adenocarcinoma and ALK rearrangements originally diagnosed as CUP who were identified using a molecular cancer classifier assay. Although ALK inhibitors treatment experience is limited, this newly identifiable group of lung cancer patients should be considered for therapy according to guidelines for stage IV ALK-positive NSCLC.
On the utility of pooling biological samples in microarray experiments (2005)

Over 15% of the data sets catalogued in the Gene Expression Omnibus Database involve RNA samples that have been pooled before hybridization. Pooling affects data quality and inference, but the exact effects are not yet known because pooling has not been systematically studied in the context of microarray experiments. Here we report on the results of an experiment designed to evaluate the utility of pooling and the impact on identifying differentially expressed genes. We find that inference for most genes is not adversely affected by pooling, and we recommend that pooling be done when fewer than three arrays are used in each condition. For larger designs, pooling does not significantly improve inferences if few subjects are pooled. The realized benefits in this case do not outweigh the price paid for loss of individual specific information. Pooling is beneficial when many subjects are pooled, provided that independent samples contribute to multiple pools.