gebhart/patrepeval huggingface dataset:
Hyperglycemia- and hyperinsulinemia-induced alteration of adiponectin receptor expression and adiponectin effects in L6 myoblasts (2005)

Adiponectin has been shown to regulate glucose and fatty acid uptake and metabolism in skeletal muscle. Here we investigated the role of the recently cloned adiponectin receptor (AdipoR) isoforms in mediating effects of both globular (gAd) and full-length (fAd) adiponectin, and their regulation by hyperglycemia (25 mM, 20 h) and hyperinsulinemia (100 nM, 20 h). We used L6 rat skeletal muscle cells, which were found to express both AdipoR1 and AdipoR2 mRNA in a ratio of over 6:1 respectively. Hyperglycemia and hyperinsulinemia both decreased AdipoR1 receptor expression by approximately 50%, while the latter induced an increase of approximately threefold in AdipoR2 expression. The ability of gAd to increase GLUT4 myc translocation, glucose uptake, fatty acid uptake and oxidation, as well as AMP-activated protein kinase (AMPK) and acetyl-CoA carboxylase (ACC) phosphorylation, was decreased by both hyperglycemia and hyperinsulinemia. Interestingly, hyperinsulinemia induced the ability of fAd to elicit fatty acid uptake and enhanced fatty acid oxidation in response to fAd. In summary, our results suggest that both hyperglycemia and hyperinsulinemia cause gAd resistance in rat skeletal muscle cells. However, hyperinsulinemia induces a switch toward increased fAd sensitivity in these cells.
[PTPL1, a proapoptotic protein tyrosine phosphatase in breast cancers]. (2004)

The protein tyrosine phosphatase L1 (PTPL1), also known as FAP1, has two major types of remarkable structural domains, in addition to its catalytic unit: a FERM domain which is responsible for its localization at the apical pole of the cell plasma membrane and 5 PDZ domains suggestive of numerous possibilities of protein partners and consequently of a role as a cargo protein or an integrator between different signalling pathways. In fact, though it was initially suggested, in 1995, that this enzyme acts as an inhibitor of Fas death receptor several recent studies indicate that PTPL1 plays many other roles. It dephosphorylates Ephrin B (ligand of Eph, a receptor triggering angiogenesis and axonal guidance), it interacts with numerous proteins associated to cytoskeleton plasticity and it is implicated in cytokinesis. We have demonstrated that its expression is regulated by antiestrogens in mammary cancer and shown, with stable antisense transfectants, that PTPL1 plays a key role in the mediation of the inhibitory effects of these antagonists on growth factor signalling by impeding the IRS-I/PI3-K/Akt survival pathway. Altogether PTPL1 has to be regarded as a unique marker of mammary tumor response to antiestrogens and a potential therapeutic target to activate apoptotic stimuli in tumor cells.
Superconducting Tunneling in Y-Ba-Cu-O System (1987)

Electron tunneling study on high- T c superconductor Y-Ba-Cu-O system with the onset transition temperature of about 95 K has been carried out. The observed energy gap is slightly larger than that expected from the BCS theory.
Effects of Electric Fields on Cholesterol Nonanoate Liquid Crystals (1966)

Abstract Effects of strong electric fields upon cholesteric liquid crystals have been studied. Increased intensity of light selectively scattered from the plane texture at d.c. and up to 3 kc have been found, as well as a temperature-dependent minimum in the average intensity as a function of frequency. An effect somewhat like hysteresis is shown by retention of the acquired brightness in the absence of field. Curious effects such as three classes of dark spots, some of which metamorphose into bars, light maltese crosses, and bright cross-hatchings are regularly observed. These effects taken together with the conditions of their appearance imply strong alignment such that the selective reflection of the cholesteric mesophase is greatly enhanced by the increased ordering of the planes of reflection within the mosphase. The complicated a.c. electric field effects are given a detailed, qualitative explanation.
Physical and biological characterization of erythroblast enhancing factor (EEF), a late acting erythropoietic stimulator in serum distinct from erythropoietin. (1983)

A factor with erythropoietic stimulating activity but distinct from erythropoietin (Ep) has been identified in normal human and mouse serum. Like Ep this factor causes a significant increase in the amount of 59Fe incorporated into heme in short term cultures of mouse marrow cells. However, dose response studies show that it acts synergistically rather than additively with erythropoietin. This factor has been partially purified using Sephadex G150 and chromatofocusing, and appears to be a protein with a molecular weight of 130,000 daltons and an isoelectric point of 4.8. Colcemid and time course studies indicate that this stimulator acts late in erythroid differentiation, primarily on erythroblasts. Benzidine staining studies suggest it may increase 59Fe uptake in hemoglobin-producing erythroblasts by enhancing their viability. Accordingly the term erythroblast enhancing factor (EEF) is proposed. Serum EEF levels have been found to be markedly reduced in polycythemic mice and EEF injected together with Ep into such animals has a synergistic effect in stimulating new red cell production. These findings strongly suggest that EEF acts as a positive regulator of terminal erythropoiesis in vivo.
Identification of genes differentially regulated by interferon α, β, or γ using oligonucleotide arrays (1998)

The pleiotropic activities of interferons (IFNs) are mediated primarily through the transcriptional regulation of many downstream effector genes. The mRNA profiles from IFN-alpha, -beta, or -gamma treatments of the human fibrosarcoma cell line, HT1080, were determined by using oligonucleotide arrays with probe sets corresponding to more than 6,800 human genes. Among these were transcripts for known IFN-stimulated genes (ISGs), the expression of which were consistent with previous studies in which the particular ISG was characterized as responsive to either Type I (alpha, beta) or Type II (gamma) IFNs, or both. Importantly, many novel IFN-stimulated genes were identified that were diverse in their known biological functions. For instance, several novel ISGs were identified that are implicated in apoptosis (including RAP46/Bag-1, phospholipid scramblase, and hypoxia inducible factor-1alpha). Furthermore, several IFN-repressed genes also were identified. These results demonstrate the usefulness of oligonucleotide arrays in monitoring mammalian gene expression on a broad and unprecedented scale. In particular, these findings provide insights into the basic mechanisms of IFN actions and ultimately may contribute to better therapeutic uses for IFNs.
Estimating block transfers and join sizes (1983)

In this paper we provide estimates of the number of sequential and random block accesses required for retrieving a number of records of a file when the distribution of records in blocks of secondary storage is not uniform. We show how these results apply to estimating sizes of joins and semi-joins. We prove that when the uniformity of placement assumption is not satisfied it often leads to pessimistic estimates of performance. Finally we show a recursive estimation of the probability distribution of the number of blocks containing a given number of records.
µ-Fractal based data perturbation algorithm for privacy protection (2012)

Many organizations publish anonymous medical data for sociology research, health research, education and other useful studies. Although attributes that clearly identify individuals, such as name and certain personal identity numbers are removed, the combination of some other information, like the date of birth, gender, post-code etc. can still be used to identify an individual. Existing data perturbation techniques are able to de-identify the data prior to publishing, but they suffer from making the process irreversible, so that the original data cannot be fully recovered. How to maintain the usability and utility of privacy-protected data as well as make the published data restorable for authorized users is a major issue. In this paper, we propose a novel robust data perturbation algorithm that can withstand brute force attacks, while the perturbed data pattern is indistinguishable from the original data pattern. A distinguishing feature of our data perturbation method is that, using fractal theory to derive perturbation vectors, it provides high privacy protection together with fully reversible data perturbation while maintaining maximal data utility. Experiments based on practical data confirm the desired operation of our data perturbation algorithm and its effectiveness. The results obtained from our experiments leads us to conclude that the proposed approach is able to computationally resist brute-force attacks as well as maintain the same data distribution type as that of original data.
ChloroP, a neural network‐based method for predicting chloroplast transit peptides and their cleavage sites (1999)

We present a neural network based method (ChloroP) for identifying chloroplast transit peptides and their cleavage sites. Using cross-validation, 88% of the sequences in our homology reduced training set were correctly classified as transit peptides or nontransit peptides. This performance level is well above that of the publicly available chloroplast localization predictor PSORT. Cleavage sites are predicted using a scoring matrix derived by an automatic motif-finding algorithm. Approximately 60% of the known cleavage sites in our sequence collection were predicted to within +/-2 residues from the cleavage sites given in SWISS-PROT. An analysis of 715 Arabidopsis thaliana sequences from SWISS-PROT suggests that the ChloroP method should be useful for the identification of putative transit peptides in genome-wide sequence data. The ChloroP predictor is available as a web-server at http://www.cbs.dtu.dk/services/ChloroP/.
Development, multiplexing, and application of ARMS tests for common mutations in the CFTR gene. (1992)

The amplification refractory mutation system (ARMS) is a simple, rapid and reliable method for the detection of any mutation involving single base changes or small deletions. We have applied ARMS methodology to the detection of mutations in the cystic fibrosis transmembrane conductance regulator (CFTR) gene. Single ARMS tests have been developed for 11 CFTR mutations found in the northwest of England. ARMS reactions for the most common mutations have been multiplexed to give a test which will detect the presence of the delta F508, G551D, G542X, and 621 + 1G----T mutations in a DNA sample. The multiplex test has been validated by the analysis of over 500 previously genotyped samples and has been found to be completely accurate. The rapid detection of the most common mutations has enabled early molecular confirmation of suspected cystic fibrosis in neonates, rapid typing of cystic fibrosis patients and their relatives, and testing of sperm and egg donors.
The extreme C terminus of herpes simplex virus DNA polymerase is crucial for functional interaction with processivity factor UL42 and for viral replication (1993)

The herpes simplex virus DNA polymerase is composed of two subunits, a large catalytic subunit (Pol) and a smaller subunit (UL42) that increases the processivity of the holoenzyme. The interaction between the two polypeptides is of interest both for the mechanism by which it enables the enzyme to synthesize long stretches of DNA processively and as a possible target for the rational design of novel antiviral drugs. Here, we demonstrate through a combination of insertion and deletion mutagenesis that the carboxy-terminal 35 amino acids of Pol are crucial for binding UL42. The functional importance of the interaction was confirmed by the finding that a pol mutant defective for UL42 binding retained polymerase activity, but did not synthesize longer DNA products in the presence of UL42. Moreover, several association-incompetent mutants failed to complement the replication of a pol null mutant in a transient transfection assay, confirming that the Pol-UL42 interaction is necessary for virus replication in vivo and therefore a valid target for directed drug design.
Effect of annealing time on bias stress and light-induced instabilities in amorphous indium–gallium–zinc-oxide thin-film transistors (2011)

Thermal post annealing was employed for amorphous indium–gallium–zinc-oxide (a-IGZO) thin-film transistors (TFTs) to optimize performance by a low-temperature process, in view of the envisaged role of a-IGZO in plastic electronics. The effect of annealing time at T = 250 and 280 °C on bias stress and light-induced instabilities was investigated. We find that long anneals are effective in reducing bias stress and light-induced instabilities, as well as hysteresis in the transfer characteristics. The time constant τ for positive bias stress and for negative bias stress increases after long anneal, attaining for positive bias stress the value of 1.05 × 106 s, the highest so far reported for these devices. The beneficial effect of long anneals appears to be because of a reorganization of the amorphous network, resulting in a more stable configuration.
IMPROVEMENT OF HGM-CSF EXPRESSION USING A FUSION SYSTEM BY DIRECTING PROTEIN TO THE PERIPLASMIC SPACE (2004)

Bacterial expression systems provide economic and logistic advantages
in manufacturing proteins for human therapeutic purposes. However, most
such proteins accumulate in insoluble biologically inactive form when
overexpressed in bacterial cells. This is the case while attempting to
produce recombinant human granulocyte-macrophage colony stimulating
factor (hGM-CSF) in E. coli. In this report, different strong promoters
are used to compare the yield of expression when the protein is
expressed as insoluble and soluble forms. The results obtained
indicated that the level of expression was independent of the nature of
promoter used. Moreover experimental data presented here suggest that
the fusion system which directs hGM-CSF to the periplasmic space not
only can prevent inclusion body formation but also improve the level of
expression significantly.
Role of Membrane Cofactor Protein (CD46) in Regulation of C4b and C3b Deposited on Cells (2002)

C4b and C3b deposited on host cells undergo limited proteolytic cleavage by regulatory proteins. Membrane cofactor protein (MCP; CD46), factor H, and C4b binding protein mediate this reaction, known as cofactor activity, that also requires the plasma serine protease factor I. To explore the roles of the fluid phase regulators vs those expressed on host cells, a model system was used examining complement fragments deposited on cells transfected with human MCP as assessed by FACS and Western blotting. Following incubation with Ab and complement on MCP(+) cells, C4b was progressively cleaved over the first hour to C4d and C4c. There was no detectable cleavage of C4b on MCP(-) cells, indicating that MCP (and not C4BP in the serum) primarily mediates this cofactor activity. C3b deposition was not blocked on MCP(+) cells because classical pathway activation occurred before substantial C4b cleavage. Cleavage, though, of deposited C3b was rapid (<5 min) and iC3b was the dominant fragment on MCP(-) and MCP(+) cells. Studies using a function-blocking mAb further established factor H as the responsible cofactor. If the level of Ab sensitization was reduced 8-fold or if Mg(2+)-EGTA was used to block the classical pathway, MCP efficiently inhibited C3b deposition mediated by the alternative pathway. Thus, for the classical pathway, MCP is the cofactor for C4b cleavage and factor H for C3b cleavage. However, if the alternative pathway mediates C3b deposition, then MCP's cofactor activity is sufficient to restrict complement activation.
Conservation and variability of wheat α/β-gliadin genes (1985)

We have sequenced two genomic clones for wheat alpha/beta-gliadin storage protein genes. Comparison with a known sequence reveals close homology between the three and confirms the previously suspected evolutionary relatedness of members of this gliadin family. The coding region can be divided into six domains. Two unusual structures were found within this region: (i) The P-boxes which are composed of 12 codons, six of which are for proline, that are tandemly repeated four or five times; and (ii) Two polyglutamine stretches which consist of 18-22 tandemly repeated glutamine codons in one case, and 7-28 in the second. Analysis of the P-box structures revealed that certain mutations were probably present in the hypothetical ancestral alpha/beta-gliadin gene prior to gene multiplication. None of the genes have introns. All of the genes appear to contain typical eukaryotic promoters and also possess the double polyadenylation signal of plants.
Failed Back Surgery Syndrome: 5-Year Follow-Up after Spinal Cord Stimulator Implantation (1991)

Spinal cord stimulation, in use for more than 20 years, has evolved into an easily implemented technique, with percutaneous methods for electrode placement. We have reviewed our experience with this technique in treating "failed back surgery syndrome," and have assessed patient and treatment characteristics as predictors of long-term outcome. A series of 50 patients with failed back surgery syndrome (averaging 3.1 previous operations), who underwent spinal cord stimulator implantation, was interviewed by impartial third parties, at mean follow-up intervals of 2.2 years and 5.0 years. Successful outcome (at least 50% sustained relief of pain and patient satisfaction with the result) was recorded in 53% of patients at 2.2 years and in 47% of patients at 5.0 years postoperatively. Ten of 40 patients who were disabled preoperatively returned to work. Improvements in activities of daily living were recorded in most patients for most activities; loss of function was rare. Most patients reduced or eliminated analgesic intake. Statistical analysis (including univariate and multivariate logistic regression) of patient characteristics as prognostic factors showed significant advantages for female patients and for those with programmable multi-contact implanted devices. These results, in patients with postsurgical lumbar arachnoid and epidural fibrosis and without surgically remediable lesions, compare favorably with the results in two separate series of patients with failed back surgery syndrome, in whom 1) surgical lesions were diagnosed and repeated operation performed; and 2) monoradicular pain syndromes were diagnosed and dorsal root ganglionectomies performed at our institution. This suggests the need for further assessment of selection criteria, critical analysis of treatment outcome, and prospective study of spinal cord stimulation and alternative approaches to failed back surgery syndrome.
Septic arthritis in patients with rheumatoid arthritis (2008)

There is an increasing number of rheumatoid patients who get septic arthritis. Chronic use of steroids is one of the important predisposing factors. The clinical picture of septic arthritis is different in immunocompromised patients like patients with rheumatoid arthritis. The diagnosis and management are discussed in this review article.
Herpes Simplex Virus Type 1 Glycoprotein E Mediates Retrograde Spread from Epithelial Cells to Neurites (2009)

In animal models of infection, glycoprotein E (gE) is required for efficient herpes simplex virus type 1 (HSV-1) spread from the inoculation site to the cell bodies of innervating neurons (retrograde direction). Retrograde spread in vivo is a multistep process, in that HSV-1 first spreads between epithelial cells at the inoculation site, then infects neurites, and finally travels by retrograde axonal transport to the neuron cell body. To better understand the role of gE in retrograde spread, we used a compartmentalized neuron culture system, in which neurons were infected in the presence or absence of epithelial cells. We found that gE-deleted HSV-1 (NS-gEnull) retained retrograde axonal transport activity when added directly to neurites, in contrast to the retrograde spread defect of this virus in animals. To better mimic the in vivo milieu, we overlaid neurites with epithelial cells prior to infection. In this modified system, virus infects epithelial cells and then spreads to neurites, revealing a 100-fold retrograde spread defect for NS-gEnull. We measured the retrograde spread defect of NS-gEnull from a variety of epithelial cell lines and found that the magnitude of the spread defect from epithelial cells to neurons correlated with epithelial cell plaque size defect, indicating that gE plays a similar role in both types of spread. Therefore, gE-mediated spread between epithelial cells and neurites likely explains the retrograde spread defect of gE-deleted HSV-1 in vivo.
Disulfide cross-linked protein represents a significant fraction of ALS-associated Cu, Zn-superoxide dismutase aggregates in spinal cords of model mice (2006)

Point mutations in Cu, Zn-superoxide dismutase (SOD1) cause a familial form of the neurodegenerative disease amyotrophic lateral sclerosis (ALS). Aggregates of mutant SOD1 proteins are observed in histopathology and are invoked in several proposed mechanisms for motor neuronal death; however, the significant stability and activity of the mature mutant proteins are not readily explained in such models. Recent biochemical studies suggest that it is the immature disulfide-reduced forms of the familial ALS mutant SOD1 proteins that play a critical role; these forms tend to misfold, oligomerize, and readily undergo incorrect disulfide formation upon mild oxidative stress in vitro. Here we provide physiological support for this mechanism of aggregate formation and show that a significant fraction of the insoluble SOD1 aggregates in spinal cord of the ALS-model transgenic mice contain multimers cross-linked via intermolecular disulfide bonds. These insoluble disulfide-linked SOD1 multimers are found only in the spinal cord of symptomatic transgenic animals, are not observed in unafflicted tissue such as brain cortex and liver, and can incorporate WT SOD1 protein. The findings provide a biochemical basis for a pathological hallmark of this disease; namely, incorrect disulfide cross-linking of the immature, misfolded mutant proteins leads to insoluble aggregates.