gebhart/patrepeval huggingface dataset:
Interleukin‐17 as an Effector Molecule of Innate and Acquired Immunity against Infections (2007)

Interleukin (IL)-17 is a proinflammatory cytokine which induces differentiation and migration of neutrophils through induction of cytokines and chemokines including granulocyte-colony stimulating factor and CXCL8/IL-8. IL-17-producing CD4(+) T cells (Th17) have pivotal role in pathogenesis of autoimmune diseases. IL-17 is also involved in protective immunity against various infections. IL-17 has important role in induction of neutrophil-mediated protective immune response against extracellular bacterial or fungal pathogens such as Klebsiella pneumoniae and Candida albicans. Importance of IL-17 in protection against intracellular pathogens including Mycobacterium has also been reported. Interestingly, not only CD4(+) T cells but atypical CD4(-)CD8(-) T cells expressing T cell receptor (TCR) gammadelta produce IL-17, and IL-17 producing cells participate in both innate and acquired immune response to infections. Furthermore, neutrophil induction may not be the only mechanism of IL-17-mediated protective immunity. IL-17 seems to participate in host defense through regulation of cell-mediated immunity or induction of antimicrobial peptides such as beta-defensins. In this review, we summarize recent progress on the role of IL-17 in immune response against infections, and discuss possible application of IL-17 in prevention and treatment of infectious diseases.
Polybenzimidazoles. III (1964)

Abstract Polybenzimidazoles have been prepared from 2,3‐, 2,7‐, and 2,6‐naphthalenedicarboxylic acids, 1,1′ ‐ferrocenedicarboxylic acid, maleic acid, fumaric acid, 4,5‐imidazole‐dicarboxylic acid, perfluoroglutaric acid, perfluorosuberic acid, and 3,3′ ‐diaminobenzidine. A copolymer has been prepared from a mixture of terephthalic acid and 2,2′‐diphenic acid. Thermogravimetric curves have been obtained for most of these polymers.
NKT cell ligand α‐galactosylceramide blocks the induction of oral tolerance by triggering dendritic cell maturation (2004)

NKT cells play contradictory roles in vivo, both regulating autoimmunity and activating immunity to intracellular pathogens and tumors. In this study, we studied the effect of NKT cell activation on the induction of systemic tolerance by oral administration of antigen. Administration of alpha-galactosylceramide (alphaGC) at the time of oral ovalbumin (OVA) feeding completely blocked the OVA-specific tolerance induced by both high- and low-dose regimens in BALB/c mice. In the mesenteric lymph nodes (MLN) of alphaGC-treated mice, the proliferation of OVA-specific T cells was greater than that seen in the MLN of vehicle-treated mice in vivo. The administration of alphaGC triggered the full maturation of mesenteric dendritic cells (DC), which were in turn responsible for the enhanced division of OVA-specific T cells in vitro. To further determine whether the costimulation provided by DC in alphaGC-treated mice was responsible for the reversal of oral tolerance in vivo, mice were given alphaGC together with anti-CD80 and anti-CD86 blocking Ab. OVA-specific systemic tolerance was restored in mice given the blocking Ab, even when they simultaneously received alphaGC. Therefore, oral tolerance can be reversed via costimulation by DC that have been triggered to fully mature by the administration of alphaGC.
Tumor target prostate specific membrane antigen (PSMA) and its regulation in prostate cancer (2003)

Prostate specific membrane antigen (PSMA), is a unique membrane bound glycoprotein, which is overexpressed manifold on prostate cancer as well as neovasculature of most of the solid tumors, but not in the vasculature of the normal tissues. This unique expression of PSMA makes it an important marker as well as a large extracellular target of imaging agents. PSMA can serve as target for delivery of therapeutic agents such as cytotoxins or radionuclides. PSMA has two unique enzymatic functions, folate hydrolase and NAALADase and found to be recycled like other membrane bound receptors through clathrin coated pits. The internalization property of PSMA leads one to consider the potential existence of a natural ligand for PSMA. In this review we have discussed the regulation of PSMA expression within the cells, and significance of its expression in prostate cancer and metastasis.
Subtrigonal Phenol Injection for Urge Incontinence Secondary to Detrusor Instability in Females (1982)

Thirty female patients with urge incontinence or bypassing an indwelling urethral catheter have been treated by subtrigonal phenol injection. All were proven to have detrusor instability. The injection method is described. Seventy-six per cent of patients were rendered dry. The urodynamic changes are recorded.
Bicalutamide Functions as an Androgen Receptor Antagonist by Assembly of a Transcriptionally Inactive Receptor (2002)

Prostate cancers (PCa) that relapse after androgen deprivation therapy invariably express high levels of androgen receptor (AR) and AR-regulated genes. Most do not respond to secondary hormonal therapies, including AR antagonists, and the mechanisms of AR activation in these clinically androgen-independent tumors are unclear. Bicalutamide, the most widely used AR antagonist, is a competitive antagonist shown previously to stabilize AR association with cytosolic heat shock protein complexes. This study found nuclear AR expression in bicalutamide-treated androgen-independent PCa and found that bicalutamide could stimulate AR nuclear translocation. Moreover, specific DNA binding by the bicalutamide-liganded AR was demonstrated in vivo using a VP16-AR fusion protein and was confirmed by chromatin immunoprecipitation showing binding to the prostate-specific antigen enhancer in LNCaP PCa cells. Nonetheless, bicalutamide could not stimulate interactions between the AR N and C termini or recruitment of steroid receptor coactivator proteins (SRC-1 or -2), although SRC transfection augmented AR activity in the presence of dihydrotestosterone and inhibitory concentrations of bicalutamide. These results demonstrate that bicalutamide stimulates the assembly of a transcriptionally inactive AR on DNA and support altered coactivator (or corepressor) expression as a mechanism of bicalutamide-resistant androgen-independent PCa.
Quantification of biofilm structures by the novel computer program comstat (2000)

The structural organization of four microbial communities was analysed by a novel computer program, COMSTAT, which comprises ten features for quantifying three-dimensional biofilm image stacks. Monospecies biofilms of each of the four bacteria, Pseudomonas: putida, P. aureofaciens, P. fluorescens and P. aeruginosa, tagged with the green fluorescent protein (GFP) were grown in flow chambers with a defined minimal medium as substrate. Analysis by the COMSTAT program of four variables describing biofilm structure - mean thickness, roughness, substratum coverage and surface to volume ratio - showed that the four Pseudomonas: strains represent different modes of biofilm growth. P. putida had a unique developmental pattern starting with single cells on the substratum growing into micro-colonies, which were eventually succeeded by long filaments and elongated cell clusters. P. aeruginosa colonized the entire substratum, and formed flat, uniform biofilms. P. aureofaciens resembled P. aeruginosa, but had a stronger tendency to form micro-colonies. Finally, the biofilm structures of P. fluorescens had a phenotype intermediate between those of P. putida and P. aureofaciens. Analysis of biofilms of P. aureofaciens growing on 0.03 mM, 0.1 mM or 0.5 mM citrate minimal media showed that mean biofilm thickness increased with increasing citrate concentration. Moreover, biofilm roughness increased with lower citrate concentrations, whereas surface to volume ratio increased with higher citrate concentrations.
Association between High Levels of Expression of the TRK Gene and Favorable Outcome in Human Neuroblastoma (1993)

A high level of expression of the TRK proto-oncogene in a neuroblastoma is strongly predictive of a favorable outcome. A tumor with a functional nerve growth factor receptor may be dependent on the neurotrophin nerve growth factor for survival and may regress in its absence, allowing a new approach to the treatment of certain patients with neuroblastoma.
Long-term survival after liver transplantation in patients with familial amyloid polyneuropathy (2012)

This study provides Class III evidence that liver transplantation prolongs survival in patients with FAP Val30Met.
CHARACTERIZATION AND PROPERTIES OF THE HUMAN AND BOVINE LACTOTRANSFERRINS EXTRACTED FROM THE FAECES OF NEWBORN INFANTS (1982)

Human lactotransferrin was characterized in the faecal extracts from breastfed babies. Quantitative determination of human copro-lactotransferrin from birth for a period of up to 3 weeks showed that the daily elimination decreased from 35 to 5 mg. The amount of copro-lactotransferrin corresponding to the endogenous secretion was calculated to be from 0.5 to 1 mg per day. When a cow's milk diet supplemented by partially or completely iron-saturated human or bovine lactotransferrin was fed to the babies, the amounts of copro-lactotransferrin excreted depended on the origin and on the iron saturation of the lactoransferrin. In particular, the amount of bovine copro-lactotransferrin in the faeces averaged 200 mg per day. The human and bovine copro-lactotransferrins were isolated by ion-exchange chromatography or by affinity chromatography and were still able to bind iron. The fingerprints of native human and bovine lactotransferrins hydrolysed in vitro by infant's gastric or duodenal secretions showed that both proteins were not extensively digested. This demonstrates that these lactotransferrins ingested by babies are not completely destroyed and keep their ability to bind iron, and thus may supplement the bacteriostatic effects of the endogenous lactotransferrin in the intestinal tract.
Cloning of P2XM, a novel human P2X receptor gene regulated by p53. (1997)

Through cloning of functional p53-binding sites (p53-tagged sites) from the human genome, we isolated a novel gene inducible by wild-type p53. Its cDNA sequence contained an open reading frame encoding a 431-amino acid peptide that showed a significant homology with members of the P2X family. This protein also revealed a similarity to RP-2, a gene activated in thymocytes undergoing programmed cell death. Northern blot analysis showed that it was expressed predominantly in skeletal muscle. Hence, we designated the gene P2XM (P2X specifically expressed in skeletal muscle). P2XM was localized to chromosomal band 22q11, where frequent loss of heterozygosity has been observed in rhabdoid tumors. Although we detected no genetic alteration in the coding sequences, one of four rhabdomyosarcoma cell lines examined had completely lost expression of this gene. Furthermore, a minor splice variant lacking a part of exon 1 that would encode residues corresponding to transmembrane domain M1 was relatively more abundant in two of seven sarcoma cell lines, one of which was derived from a rhabdomyosarcoma, and the other was derived from an osteosarcoma. The results suggest that P2XM may play a significant role in the proliferation and/or differentiation of skeletal muscle cells and that its altered expression may be involved in the development of some sarcomas.
What is next generation sequencing? (2013)

Next generation sequencing (NGS), massively parallel or deep sequencing are related terms that describe a DNA sequencing technology which has revolutionised genomic research. Using NGS an entire human genome can be sequenced within a single day. In contrast, the previous Sanger sequencing technology, used to decipher the human genome, required over a decade to deliver the final draft. Although in genome research NGS has mostly superseded conventional Sanger sequencing, it has not yet translated into routine clinical practice. The aim of this article is to review the potential applications of NGS in paediatrics.
Hyperspectral and multispectral bioluminescence optical tomography for small animal imaging (2005)

For bioluminescence imaging studies in small animals, it is important to be able to accurately localize the three-dimensional (3D) distribution of the underlying bioluminescent source. The spectrum of light produced by the source that escapes the subject varies with the depth of the emission source because of the wavelength-dependence of the optical properties of tissue. Consequently, multispectral or hyperspectral data acquisition should help in the 3D localization of deep sources. In this paper, we describe a framework for fully 3D bioluminescence tomographic image acquisition and reconstruction that exploits spectral information. We describe regularized tomographic reconstruction techniques that use semi-infinite slab or FEM-based diffusion approximations of photon transport through turbid media. Singular value decomposition analysis was used for data dimensionality reduction and to illustrate the advantage of using hyperspectral rather than achromatic data. Simulation studies in an atlas-mouse geometry indicated that sub-millimeter resolution may be attainable given accurate knowledge of the optical properties of the animal. A fixed arrangement of mirrors and a single CCD camera were used for simultaneous acquisition of multispectral imaging data over most of the surface of the animal. Phantom studies conducted using this system demonstrated our ability to accurately localize deep point-like sources and show that a resolution of 1.5 to 2.2 mm for depths up to 6 mm can be achieved. We also include an in vivo study of a mouse with a brain tumour expressing firefly luciferase. Co-registration of the reconstructed 3D bioluminescent image with magnetic resonance images indicated good anatomical localization of the tumour.
PtK1 cells contain a nondiffusible, dominant factor that makes the Golgi apparatus resistant to brefeldin A. (1991)

Brefeldin A (BFA) was shown in earlier studies of numerous cell types to inhibit secretion, induce enzymes of the Golgi stacks to redistribute into the ER, and to cause the Golgi cisternae to disappear. Here, we demonstrate that the PtK1 line of rat kangaroo kidney cells is resistant to BFA. The drug did not disrupt the morphology of the Golgi complex in PtK1 cells, as judged by immunofluorescence using antibodies to 58- (58K) and 110-kD (beta-COP) Golgi proteins, and by fluorescence microscopy of live cells labeled with C6-NBD-ceramide. In addition, BFA did not inhibit protein secretion, not alter the kinetics or extent of glycosylation of the vesicular stomatitis virus (VSV) glycoprotein (G-protein) in VSV-infected PtK1 cells. To explore the mechanism of resistance to BFA, PtK1 cells were fused with BFA-sensitive CV-1 cells that had been infected with a recombinant SV-40 strain containing the gene for VSV G-protein and, at various times following fusion, the cultures were exposed to BFA. Shortly after cell fusion, heterokaryons contained one Golgi complex associated with each nucleus. Golgi membranes derived from CV-1 cells were sensitive to BFA, whereas those of PtK1 origin were BFA resistant. A few hours after fusion, most heterokaryons contained a single, large Golgi apparatus that was resistant to BFA and contained CV-1 galactosyltransferase. In unfused cells that had been perforated using nitrocellulose filters, retention of beta-COP on the Golgi was optimal in the presence of cytosol, ATP, and GTP. In perforated cell models of the BFA-sensitive MA104 line, BFA caused beta-COP to be released from the Golgi complex in the presence of nucleotides, and either MA104 or PtK1 cytosol. In contrast, when perforated PtK1 cells were incubated with BFA, nucleotides, and cytosol from either cell type, beta-COP remained bound to the Golgi complex. We conclude that PtK1 cells contain a nondiffusible factor, which is located on or very close to the Golgi complex, and confers a dominant resistance to BFA. It is possible that this factor is homologous to the target of BFA in cells that are sensitive to the drug.
A Low Power Micro Deep Brain Stimulation Device for Murine Preclinical Research (2013)

Deep brain stimulation has emerged as an effective medical procedure that has therapeutic efficacy in a number of neuropsychiatric disorders. Preclinical research involving laboratory animals is being conducted to study the principles, mechanisms, and therapeutic effects of deep brain stimulation. A bottleneck is, however, the lack of deep brain stimulation devices that enable long term brain stimulation in freely moving laboratory animals. Most of the existing devices employ complex circuitry, and are thus bulky. These devices are usually connected to the electrode that is implanted into the animal brain using long fixed wires. In long term behavioral trials, however, laboratory animals often need to continuously receive brain stimulation for days without interruption, which is difficult with existing technology. This paper presents a low power and lightweight portable microdeep brain stimulation device for laboratory animals. Three different configurations of the device are presented as follows: 1) single piece head mountable; 2) single piece back mountable; and 3) two piece back mountable. The device can be easily carried by the animal during the course of a clinical trial, and that it can produce non-stop stimulation current pulses of desired characteristics for over 12 days on a single battery. It employs passive charge balancing to minimize undesirable effects on the target tissue. The results of bench, in-vitro, and in-vivo tests to evaluate the performance of the device are presented.
Design and verification of secure systems (1981)

This paper reviews some of the difficulties that arise in the verification of kernelized secure systems and suggests new techniques for their resolution. It is proposed that secure systems should be conceived as distributed systems in which security is achieved partly through the physical separation of its individual components and partly through the mediation of trusted functions performed within some of those components. The purpose of a security kernel is simply to allow such a 'distributed' system to actually run within a single processor; policy enforcement is not the concern of a security kernel. This approach decouples verification of components which perform trusted functions from verification of the security kernel. This latter task may be accomplished by a new verification technique called 'proof of separability' which explicitly addresses the security relevant aspects of interrupt handling and other issues ignored by present methods.
Bioinspired pH-Responsive Polymers for the Intracellular Delivery of Biomolecular Drugs (2003)

The biotechnology and pharmaceutical industries have developed a wide variety of potential therapeutics based on the molecules of biology: DNA, RNA, and proteins. While these therapeutics have tremendous potential, effectively formulating and delivering them have also been a widely recognized challenge. A variety of viruses and toxins have evolved multi-functional biomolecules to solve this problem by directing cellular uptake and enhancing biomolecular transport to the cytoplasm from the low pH endosomal compartment. In the study reported here, we have designed and synthesized bio-inspired, pH-responsive polymeric carriers, which we call "encrypted polymers", that mimic the multi-functional design of biology. These encrypted polymers target and direct cellular uptake, as well as enhance cytosolic delivery by disrupting endosomal membranes in a pH-dependent fashion. We show that the encrypted polymeric carriers significantly enhance the delivery of oligonucleotides and peptides to the cytoplasm of cultured macrophages, demonstrating the potential of this approach for delivery of biotherapeutics and vaccines.
Representational difference analysis in a lupus-prone mouse strain results in the identification of an unstable region of the genome on chromosome 11 (2002)

BXSB mice develop a lupus-like autoimmune syndrome. We have previously identified several intervals that were linked to disease and, in an attempt to characterise lupus susceptibility genes within these intervals, we have sought to isolate differentially expressed genes. Representational difference analysis was used to compare gene expression between BXSB and C57BL/10 mice using spleen and thymus as a source of mRNA. The majority of differentially expressed sequences identified were immunoglobulin and gp70-related sequences, overexpression of these being characteristic of the disease. Among other isolated sequences were a sialyltransferase gene, a mouse tumour virus superantigen gene (Mtv-3), and the virus-related sequence, hitchhiker. In BXSB the sialyltransferase gene not only overexpressed spliced transcripts, but also produced high levels of unspliced mRNA. Further analysis demonstrated that the copy number of the three linked sequences: sialyltransferase, Mtv-3 and hitchhiker, was amplified in BXSB and that the structural organisation of this locus varies in different mouse strains. This locus consists of three parts, Mtv-3-hitchhiker-sialyltransferase, hitchhiker-sialyltransferase, and sialyltransferase alone. Different combinations of the regions are present in different mouse strains. Linkage analysis demonstrated that this region at the distal end of chromosome 11 is weakly linked to phenotypic markers of disease.
Rapid prenatal diagnosis using uncultured amniocytes and oligonucleotide array CGH (2008)

This study demonstrates the feasibility of prenatal genetic diagnosis using oligonucleotide array CGH analysis for direct analysis of amniocytes without culturing cells. The use of oligonucleotide arrays increases the sensitivity and accuracy of detection over previous bacterial artificial chromosome (BAC)-based arrays. Furthermore, the direct analysis allows for rapid array CGH results and shorter reporting time.
Mutation of MEF2A in an Inherited Disorder with Features of Coronary Artery Disease (2003)

The early genetic pathway(s) triggering the pathogenesis of coronary artery disease (CAD) and myocardial infarction (MI) remain largely unknown. Here, we describe an autosomal dominant form of CAD/MI (adCAD1) that is caused by the deletion of seven amino acids in transcription factor MEF2A. The deletion disrupts nuclear localization of MEF2A, reduces MEF2A-mediated transcription activation, and abolishes synergistic activation by MEF2A and by the transcription factor GATA-1 through a dominant-negative mechanism. The MEF2A protein demonstrates strong expression in the endothelium of coronary arteries. These results identify a pathogenic gene for a familial vascular disease with features of CAD and implicate the MEF2A signaling pathway in the pathogenesis of CAD/MI.