gebhart/patrepeval huggingface dataset:
Internal Migration (2015)

Internal migration is associated with the redistribution of population within the borders of states and territories. The difficulties of measuring internal migration and generating comparable data are highlighted. Rarely are internal population movements simple origin‐to‐destination flows; they are made up of complex systems of return migration, repeat migration, or circular flows of people. The patterns of internal migration by urban and rural sector are examined, with emphasis on rural‐to‐urban movements, and the great transition to urban‐based societies is described. However, the other intersectoral migrations are also outlined, and particular attention is paid to the implications of rural‐to‐rural movements for the construction of the state. The processes of integration of migrants into the social and economic fabric of cities are discussed, as are the emerging linkages between internal and international migrations.
100 GHz binary counter using SQUID flip flops (1983)

A binary counter using bistable dc SQUID's as flip flop circuits is reviewed. Its potential for frequency division in the THz range and for ultra high accuracy A/D conversion are discussed.
Carnitine Treatment Inhibits Increases in Cerebral Carnitine Esters and Glutamate Detected by Mass Spectrometry After Hypoxia-Ischemia in Newborn Rats (2005)

Carnitine metabolic pathways are compromised in HI and hypoxia. The protective effect of carnitine treatment on HI injury may be attributable to maintaining mitochondrial function.
Dystrophic phenotype induced in vitro by antibody blockade of muscle α-dystroglycan-laminin interaction (1999)

ABSTRACT Alpha-dystroglycan is a glycoprotein expressed on the surface of skeletal muscle fibres and other cell types. In muscle, α-dystroglycan provides a link between the myofibre cytoskeleton through its indirect binding to dystrophin, and the basal lamina through its binding to laminin-2, a protein of the extracellular matrix. The disruption of this linkage between the myofibre cytoskeleton and the extracellular matrix is a common feature of Duchenne and other muscular dystrophies, though the pathogenic mechanisms leading to muscle wasting remain unknown. By treating primary mouse muscle cultures with a monoclonal antibody which blocks α-dystroglycan binding to laminin, we show here the induction of a dystrophic phenotype in vitro. The phenotype is inducible in differentiated cultures only, is characterised by reduced myotube size, myofibril disorganisation, loss of contractile activity, reduced spontaneous clustering of acetylcholine receptors and is reversed by addition of excess exogenous laminin-2. Thus, α-dystroglycan may be part of a signalling pathway for the maturation and maintenance of skeletal myofibres. Detailed knowledge of this signalling pathway may provide insights into the molecular pathology of the various inherited muscular dystrophies, and identify valuable pharmacological targets and new therapeutic strategies.
Mutations in nif genes that cause Klebsiella pneumoniae to be derepressed for nitrogenase synthesis in the presence of ammonium (1980)

Four Nif+ revertants from strains with polar insertions in nifL, were insensitive to ammonium and amino acid repression of nitrogenase synthesis. These strains have mutations located in or near the nifL region. The derepressed phenotype was dominant in a merodiploid containing a nif+ plasmid. These nif regulatory mutations also suppressed the Nif- phenotype of Gln- strains. Thus, regulation by fixed nitrogen (possible via glutamine synthetase) occurs on the nifLA operon but not on the other six nif operons.
Clinical evaluation of oral fluid samples for diagnosis of viral hepatitis (1992)

Oral fluid samples were compared with serum samples as a specimen source for hepatitis A, B, and C virus markers. Oral fluid was obtained with a treated absorbent pad and tested by using existing commercial enzyme immunoassays with only minor modifications. Compared with serum sampling the sensitivity and specificity of oral sampling were 100% (51 of 51 samples) and 98% (46 of 47 samples) for hepatitis A virus immunoglobulin M, 100% (29 of 29 samples) and 100% (29 of 29 samples) for hepatitis B virus surface antigen, and 100% (13 of 13 samples) and 100% (13 of 13 samples) for hepatitis C virus antibody, respectively. The decline of hepatitis A virus immunoglobulin M in oral samples was parallel to, though somewhat more rapid than, that of hepatitis A virus immunoglobulin M in serum samples. It is proposed that oral sampling represents a safer and more convenient procedure for reliable hepatitis virus testing than blood sampling and that it has wide application in patient and outbreak management.
Cryptococcus neoformans: the yeast that likes it hot (2006)

The ability of fungi to grow well at mammalian body temperatures is a fundamental characteristic of invasive human fungal pathogens. Cryptococcus neoformans, with its genetics, molecular biology, robust animal models and clinical importance, has become a premier fungal model system for molecular fungal pathogenesis studies. There has been over a half century of study into how C. neoformans grows at high temperatures. However, recently the understanding of high-temperature growth at a molecular level has dramatically accelerated. Many strategies have been used to identify genes and over a dozen genes have already been identified to be necessary for high-temperature growth. It is likely that there are many more to discover. It is clear that, as further studies understand how this encapsulated yeast is able to withstand the stresses of high temperature at a genetic and molecular basis, we will also know more about how it and other fungal pathogens have evolved into well-established human pathogens.
Conductance determined by transmission: probes and quantised constriction resistance (1989)

The domain of validity and the origin of different formulae relating conductance to transmissive behaviour is discussed. The large variety of possible measurement probes is emphasised. The quantised conductance of constrictions, studied in recent experiments, is treated. Theoretical discussions of that have stressed the supposedly unique role of G = (2e2/h)Tr(tt†) in this connection, regardless of the exact geometry or probe locations. This is shown to be incorrect, and a simple expression for the dependence of the 'quantised' conductance on the width of the wide region is given. We particularly emphasise the distinction between, on the one hand, experiments and discussions that are strictly limited to events at reservoirs and, on the other, those that have a concern with variations within the sample.
Focal expression of interleukin-2 does not break unresponsiveness to "self" (viral) antigen expressed in beta cells but enhances development of autoimmune disease (diabetes) after initiation of an anti-self immune response. (1995)

The participation of IL-2 in insulin-dependent (type 1) diabetes (IDDM) was analyzed in transgenic (tg) mice expressing the nucleoprotein (NP) of lymphocytic choriomeningitis virus and IL-2 under control of the rat insulin promoter focally in beta cells of the islets of Langerhans. Insertion and expression of the viral (self) gene or of the IL-2 gene alone did not lead to IDDM. Infiltration primarily of CD4 and B lymphocytes and increased expression of MHC class I and II molecules occurred in islets where IL-2 was expressed. By contrast, neither cellular infiltrates nor expression of MHC class I or II glycoproteins above base levels was noted in tgs expressing the viral protein alone. Double tg mice expressing both the viral protein and IL-2 in their islets displayed a modest increase in incidence of spontaneous diabetes compared with that of single transgenic mice expressing IL-2 alone. Breaking of immunological unresponsiveness or sensitization to self antigens did not occur. Neither cytotoxic T lymphocytes (CTL) nor antibodies directed against the viral tg (NP) were generated. However, after challenge with lymphocytic choriomeningitis virus, double tg mice developed anti-self (viral) CTL and IDDM (incidence > 95%) within 2 mo. The generation of virus ("self")-specific MHC-restricted CTL was dependent on CD4+ help. In contrast, viral inoculum to single tg mice expressing either the viral protein or IL-2 failed to enhance the incidence of IDDM over 30% for viral protein or 10% for IL-2 after an 8-mo observation period. Hence, in this autoimmune model in situ expression of IL-2 did not break unresponsiveness but markedly enhanced ongoing disease.
MAPPER: high throughput maskless lithography (2008)

MAPPER Lithography is developing a maskless lithography technology. The technology combines massively-parallel electron-beam writing with high speed optical data transport used in the telecommunication industry. The electron optics generates 13,000 electron beams that are focused on the wafer by electrostatic lens arrays which are manufactured by using MEMS manufacturing techniques. Each beam has its own optical column to avoid a central cross-over. This secures high throughput (> 10 wafers per hour) at high resolution (< 45 nm half pitch). The 13,000 e-beams are generated by splitting up a single electron beam that originates from a single electron source and are finally accelerated to 5 kV to expose the resist on the wafer. The e-beams are arranged in such a way that they form a rectangular slit with a width of 26 mm, the same width of a field in an optical stepper. During exposure the e-beams are deflected over 2 &mu;m perpendicular to the wafer stage movement. This means that with one scan of the wafer a full field of 26 mm x 33 mm can be exposed. During the simultaneous scanning of the wafer and deflection of the electron beams the beams are switched on and off by 13,000 light signals, one for each e-beam. The light beams are generated in a data system that contains the chip patterns in a bitmap format. This bitmap is divided over 13,000 data channels and streamed to the ebeams at 1-10 GHz. This paper will explain the design drivers behind the system and provide more detail on the current design. Finally, results of our technology Demonstrator are presented, showing the viability of MAPPER's concept.
A Synthetic HIV-1 Protease Inhibitor with Antiviral Activity Arrests HIV-Like Particle Maturation (1990)

A synthetic peptidemimetic substrate of the human immunodeficiency virus 1 (HIV-1) protease with a nonhydrolyzable pseudodipeptidyl insert at the protease cleavage site was prepared. The peptide U-81749 inhibited recombinant HIV-1 protease in vitro (inhibition constant Ki of 70 nanomolar) and HIV-1 replication in human peripheral blood lymphocytes (inhibitory concentration IC50 of 0.1 to 1 micromolar). Moreover, 10 micromolar concentrations of U-81749 significantly inhibited proteolysis of the HIV-1 gag polyprotein (p55) to the mature viral structural proteins p24 and p17 in cells infected with a recombinant vaccinia virus expressing the HIV-1 gag-pol genes. The HIV-1 like particles released from inhibitor-treated cells contained almost exclusively p55 and other gag precursors, but not p24. Incubation of HIV-like particles recovered from drug-treated cultures in drug-free medium indicated that inhibition of p55 proteolysis was at least partially reversible, suggesting that U-81749 was present within the particles.
Estimation of the Number of O-Linked Oligosaccharides per Heavy Chain of Human Serum IgA1 by Matrix-Assisted Laser Desorption Ionization Time-of-Flight Mass Spectrometry (MALDI-TOFMS) Analysis of the Hinge Glycopeptide (1996)

In our previous study, gas-phase hydrazinolysis was used to analyze the glycoform of the O-linked oligosaccharide of human serum IgA1. All O-linked oligosaccharide chains are known to be present in the hinge portion. However, the number of O-linked oligosaccharide chains on IgA1 remained unclear. In order to determine the number of linked sugar chains, we applied matrix-assisted laser desorption ionization time-of-flight mass spectrometry (MALDI-TOFMS) to the hinge glycopeptide prepared from human serum IgA1. MALDI-TOFMS did not show clear peaks, probably due to the microheterogeneity of the structure of each sugar chain. However, elimination of peripheral sialic acid and galactose residues by sequential treatment with neuraminidase and beta-galactosidase gave clear mass spectra with several sharp peaks. On the basis of these spectra, we conclude that IgA1 prepared from normal human serum carries different numbers of sugar chains. There are two major populations, one contains five GalNAc residues and the other four GalNAc residues. On the other hand, the hinge glycopeptide prepared from myeloma IgA1 was composed mainly of one population containing four GalNAc residues. Earlier, we reported incomplete glycosylation of IgA1 isolated from the serum of an IgA1 myeloma patient. In this experiment, the presence of four O-linked oligosaccharides per heavy chain of IgA1 from a myeloma patient was found. The reason why only four out of five sites on the hinge glycopeptide were fully glycosylated in the IgA1 from the IgA1 myeloma patient is not clear.
Antigenically related iron-regulated outer membrane proteins produced by different somatic serotypes of Pasteurella multocida (1988)

An 84-kilodalton outer membrane protein was expressed when Pasteurella multocida, somatic serotype 3, was grown in brain-heart infusion broth containing the iron chelator dipyridyl but not in brain-heart infusion broth alone. Antigenically related outer membrane proteins of various molecular masses were also expressed by P. multocida strains belonging to all of the other 15 somatic serotypes (somatic serotype 12 being the possible exception) as well as by isolates expressing somatic antigens representative of multiple somatic serotypes when grown under the same conditions of iron deprivation.
CARBOHYDRATE ANTIGENS OF PIG TISSUES REACTING WITH HUMAN NATURAL ANTIBODIES AS POTENTIAL TARGETS FOR HYPERACUTE VASCULAR REJECTION IN PIG-TO-MAN ORGAN XENOTRANSPLANTATION1 (1993)

Pig tissues were screened by immunofluorescence with lectins, mAb, and human natural antibodies for the presence of carbohydrate antigens, which may be potential targets for hyperacute vascular rejection in pig to man xenotransplantation. The unfucosylated monomorph linear B-antigen was found at the surface of all porcine vascular endothelial cells. This pig linear-B antigen reacts strongly with the anti-alpha Gal isolectin B4 from Griffonia simplicifolia 1 and with human natural anti-alpha Gal antibodies specifically purified by affinity chromatography on synthetic oligosaccharides containing the terminal nonreducing alpha Gal1-->3 beta Gal-R disaccharide. This antigenic activity is destroyed by treatment of pig tissues with alpha-galactosidase. The localization of this linear-B epitope on vascular endothelium and its reactivity with natural human anti-alpha Gal antibodies suggest that it may play a major role in the hyperacute vascular rejection of pig to man organ xenografts. The lectin from Maackia amurensis reacting with alpha NeuAc2-->3 beta Gal1-->4GlcNAc/Glc was also positive on pig vascular endothelium, but we do not know yet whether there are human natural antibodies reacting with the carbohydrate recognized by this lectin. Epithelial cells of pig renal proximal convoluted tubules, respiratory epithelium, pancreatic ducts, and epidermis express the linear-B antigen, but they are less likely to trigger a hyperacute vascular rejection because they are not directly exposed to the blood. The genetically defined pig A+/A- system controls the expression of A and H antigens in pig epithelial cells from renal distal and collecting tubules, biliary ducts, pancreatic ducts, large bronchi, and digestive mucosa. The pig A antigen may trigger an immune response in human O or B recipients if they are transplanted with organs from A+ pigs, but the pig A antigen is probably not involved in the hyperacute vascular rejection of a xenograft because it is not expressed on vascular endothelium.
<i>SEC31A-ALK</i> Fusion Gene in Lung Adenocarcinoma (2015)

Anaplastic lymphoma kinase (ALK) fusion is a common mechanism underlying pathogenesis of non-small cell lung carcinoma (NSCLC) where these rearrangements represent important diagnostic and therapeutic targets. In this study, we found a new ALK fusion gene, SEC31A-ALK, in lung carcinoma from a 53-year-old Korean man. The conjoined region in the fusion transcript was generated by the fusion of SEC31A exon 21 and ALK exon 20 by genomic rearrangement, which contributed to generation of an intact, in-frame open reading frame. SEC31A-ALK encodes a predicted fusion protein of 1,438 amino acids comprising the WD40 domain of SEC31A at the N-terminus and ALK kinase domain at the C-terminus. Fluorescence in situ hybridization studies suggested that SEC31A-ALK was generated by an unbalanced genomic rearrangement associated with loss of the 3'-end of SEC31A. This is the first report of SEC31A-ALK fusion transcript in clinical NSCLC, which could be a novel diagnostic and therapeutic target for patients with NSCLC.
Management of severe dengue (2012)

Objective: To determine the effect of inflammation and disease severity on midazolam pharmacokinetics (as surrogate marker of cytochrome 3A activity) and pharmacodynamics in critically ill children. Design: Analysis of prospectively collected pharmacokinetic and pharmacodynamic data from a midazolam study in critically ill children. Setting: Pediatric intensive care unit of a university hospital. Patients: Twenty-one critically ill children who needed midazolam for sedation. Interventions: None. Measurements and Main Results: We determined the relationship between inflammation (using C-reactive protein and leukocyte count as surrogate markers) and disease severity (Pediatric Logistic Organ Dysfunction and Pediatric Risk of Mortality scores) vs. the pharmacokinetics (clearance) and pharmacodynamics (COMFORT score, dose requirement) of midazolam. We found a significant negative correlation between disease severity and midazolam clearance corrected for body weight (r = −0.49, p = .02). Midazolam clearance was significantly lower in children with multiple organ failure (defined as Pediatric Logistic Organ Dysfunction ≥10, n = 11) compared with children without multiple organ failure (Pediatric Logistic Organ Dysfunction <10, n = 10) (median 0.14 [interquartile range, 0.11–0.23] vs. 0.28 [interquartile range, 0.14–0.43]) L/kg/h, p = .035). No other significant correlations were found. Conclusions: Results from this pilot study suggest that increased disease severity is associated with reduced midazolam clearance in critically ill children, most likely as a result of reduced cytochrome 3A activity. In contrast, reduced midazolam clearance does not seem to result in decreased midazolam dose requirements.
Comprehensive Study on the Chemical Structure of Dioxane Lignin from Plantation Eucalyptus globulus Wood (2001)

Results of a comprehensive study on the chemical structure of lignin from plantation Eucalyptus globulus Labill are presented. Lignin has been isolated by a modified mild acidolysis method and thoroughly characterized by functional group analysis, by a series of degradation techniques (nitrobenzene oxidation, permanganate oxidation, thioacidolysis, and Py-GC-MS), and (1)H and (13)C NMR spectroscopy. Plantation Eucalyptus globulus lignin was found to be of the S/G type with an extremely high proportion of syringyl (S) units (82-86%) and a minor proportion of p-hydrophenyl propane (H) units (roughly 2-3 mol %). Unknown C-6 substituted and 4-O-5' type syringyl substructures represent about 65% of lignin "condensed" structures. Eucalypt lignin showed high abundance of beta-O-4 (0.56/C(6)) structures and units linked by alpha-O-4 bonds (0.23/C(6)). The proportion of phenylcoumaran structures was relatively low (0.03/C(6)). Different kinds of beta-beta substructures (pino-/syringaresinol and isotaxiresinol types) in a total amount of 0.13/C(6) were detected. ESI-MS analysis revealed a wide molecular weight distribution of lignin with the center of gravity of mass distribution around 2500 u.
A nuclear factor induced by hypoxia via de novo protein synthesis binds to the human erythropoietin gene enhancer at a site required for transcriptional activation. (1992)

We have identified a 50-nucleotide enhancer from the human erythropoietin gene 3'-flanking sequence which can mediate a sevenfold transcriptional induction in response to hypoxia when cloned 3' to a simian virus 40 promoter-chloramphenicol acetyltransferase reporter gene and transiently expressed in Hep3B cells. Nucleotides (nt) 1 to 33 of this sequence mediate sevenfold induction of reporter gene expression when present in two tandem copies compared with threefold induction when present in a single copy, suggesting that nt 34 to 50 bind a factor which amplifies the induction signal. DNase I footprinting demonstrated binding of a constitutive nuclear factor to nt 26 to 48. Mutagenesis studies revealed that nt 4 to 12 and 19 to 23 are essential for induction, as substitutions at either site eliminated hypoxia-induced expression. Electrophoretic mobility shift assays identified a nuclear factor which bound to a probe spanning nt 1 to 18 but not to a probe containing a mutation which eliminated enhancer function. Factor binding was induced by hypoxia, and its induction was sensitive to cycloheximide treatment. We have thus defined a functionally tripartite, 50-nt hypoxia-inducible enhancer which binds several nuclear factors, one of which is induced by hypoxia via de novo protein synthesis.
384. AAV9 -Frataxin Reduces the Symptoms and Prolongs the Life of Friedreich Ataxia Mouse Models (2015)

Friedreich ataxia (FRDA) is a genetic disease due to increased repeats of the GAA trinucleotide in intron 1 of the frataxin gene. This mutation leads to a reduced expression of frataxin. We have produced an AAV9 coding for human frataxin (AAV9-hFXN). This AAV was delivered by intra-peritoneal injection to young conditionally knockout mice in which the frataxin gene had been knocked-out in some tissues during embryogenesis by breeding them with mice expressing the Cre recombinase gene under the MCK or the NSE promoter. In the first part of the study different doses of virus were tested from 6×1011 v.p. to 6×109 v.p. in NSE-cre mice and all leading to an increase in life spent of the mice. The higher and the lower dose were also tested in MCK-cre mice. A single administration of the AAV9-hFXN at 6×1011 v.p. more than doubled the life of these mice. In fact the MCK-cre mice treated with the AAV9-hFXN were sacrificed for further molecular investigations at the age of 29 weeks without apparent symptoms. Echography analysis of the heart function clearly indicated that the cardiac systolic function was better preserved in the mice that received 6×1011 v.p. of AAV9-hFXN. The human frataxin protein was detected by ELISA in the heart, brain, muscles, kidney and liver with the higher dose of virus in both mouse models. Thus gene therapy with an AAV9-hFXN is a potential treatment of FRDA.