gebhart/patrepeval huggingface dataset:
Changes in Emiliania huxleyi fatty acid profiles during infection with E. huxleyi virus 86: physiological and ecological implications (2009)

Fatty acids profiles of Emiliania huxleyi strain CCMP1516 were determined in a virusinduced culture crash with E. huxleyi virus 86 (EhV-86). As cell numbers declined in the infected cultures due to virus lysis, a concomitant decrease in fatty acids was observed in the particulate fraction. The composition of fatty acids within infected E. huxleyi cells was restructured, with a shift from polyunsaturated to monounsaturated and saturated fatty acids (respective distributions changing from 70:10:20% at the start of the experiment to 44:24:32% at the final time point). In particular, decreases were seen in the major fatty acid 22:6(n-3) and in 18:5(n-3), whereas greatest increases were seen in 18:1(n-9) and 22:0. The increase in the amount and restructuring of the fatty acid pool in E. huxleyi was indicative of a combination of specific and non-specific effects of virus infection. Specific effects primarily included induction of metabolic pathways such as the synthesis of components involved in virus replication, the production of virions and signal transduction via sphingolipid biosynthesis. Non-specific effects due to stress were likely mediated by reactive oxygen species. Changes in the composition of virus-infected E. huxleyi are of significance to the food web since grazing on virus-infected blooms will decrease the amount of essential polyunsaturated fatty acids passed on to higher trophic levels. Consequently, this could decrease the overall productivity of marine ecosystems.
Grading the commercial optical biosensor literature—Class of 2008: ‘The Mighty Binders’ (2009)

Optical biosensor technology continues to be the method of choice for label-free, real-time interaction analysis. But when it comes to improving the quality of the biosensor literature, education should be fundamental. Of the 1413 articles published in 2008, less than 30% would pass the requirements for high-school chemistry. To teach by example, we spotlight 10 papers that illustrate how to implement the technology properly. Then we grade every paper published in 2008 on a scale from A to F and outline what features make a biosensor article fabulous, middling or abysmal. To help improve the quality of published data, we focus on a few experimental, analysis and presentation mistakes that are alarmingly common. With the literature as a guide, we want to ensure that no user is left behind.
Recombinant Genomes Which Express Chloramphenicol Acetyltransferase in Mammalian Cells (1982)

We constructed a series of recombinant genomes which directed expression of the enzyme chloramphenicol acetyltransferase (CAT) in mammalian cells. The prototype recombinant in this series, pSV2-cat, consisted of the beta-lactamase gene and origin of replication from pBR322 coupled to a simian virus 40 (SV40) early transcription region into which CAT coding sequences were inserted. Readily measured levels of CAT accumulated within 48 h after the introduction of pSV2-cat DNA into African green monkey kidney CV-1 cells. Because endogenous CAT activity is not present in CV-1 or other mammalian cells, and because rapid, sensitive assays for CAT activity are available, these recombinants provided a uniquely convenient system for monitoring the expression of foreign DNAs in tissue culture cells. To demonstrate the usefulness of this system, we constructed derivatives of pSV2-cat from which part or all of the SV40 promoter region was removed. Deletion of one copy of the 72-base-pair repeat sequence in the SV40 promoter caused no significant decrease in CAT synthesis in monkey kidney CV-1 cells; however, an additional deletion of 50 base pairs from the second copy of the repeats reduced CAT synthesis to 11% of its level in the wild type. We also constructed a recombinant, pSV0-cat, in which the entire SV40 promoter region was removed and a unique HindIII site was substituted for the insertion of other promoter sequences.
Therapy of Experimental Pseudomonas Infections with a Nonreplicating Genetically Modified Phage (2004)

Bacteriophage therapy of bacterial infections has received renewed attention owing to the increasing prevalence of antibiotic-resistant pathogens. A side effect of many antibiotics as well as of phage therapy with lytic phage is the release of cell wall components, e.g., endotoxins of gram-negative bacteria, which mediate the general pathological aspects of septicemia. Here we explored an alternative strategy by using genetically engineered nonreplicating, nonlytic phage to combat an experimental Pseudomonas aeruginosa infection. An export protein gene of the P. aeruginosa filamentous phage Pf3 was replaced with a restriction endonuclease gene. This rendered the Pf3 variant (Pf3R) nonreplicative and concomitantly prevented the release of the therapeutic agent from the target cell. The Pf3R phage efficiently killed a wild-type host in vitro, while endotoxin release was kept to a minimum. Treatment of P. aeruginosa infections of mice with Pf3R or with a replicating lytic phage resulted in comparable survival rates upon challenge with a minimal lethal dose of 3. However, the survival rate after phage therapy with Pf3R was significantly higher than that with the lytic phage upon challenge with a minimal lethal dose of 5. This higher survival rate correlated with a reduced inflammatory response elicited by Pf3R treatment relative to that with the lytic phage. Therefore, this study suggests that the increased survival rate of Pf3R-treated mice could result from reduced endotoxin release. Thus, the use of a nonreplicating modified phage for the delivery of genes encoding proteins toxic to bacterial pathogens may open up a new avenue in antimicrobial therapy.
SOS1 mutations are rare in human malignancies: Implications for Noonan syndrome patients (2007)

Germ line gain-of-function mutations in several members of the RAS/ERK pathway, including PTPN11, KRAS, and RAF1, cause the autosomal dominant genetic disorder Noonan Syndrome (NS). NS patients are at increased risk of leukemia/myeloproliferative disease and possibly some solid tumors, such as neuroblastoma. Recently, SOS1 gain of function mutations have also been shown to cause NS. Somatic PTPN11, KRAS, and RAF1 mutations occur (although at different frequencies) in a variety of sporadic neoplasms, but whether SOS1 mutations are associated with human cancer has not been evaluated. We sequenced DNA from a total of 810 primary malignancies, including pancreatic, lung, breast, and colon carcinomas, and acute myelogenous leukemia, as well as several neuroblastoma cell lines. From this large, diverse series, missense SOS1 mutations were identified in a single pancreatic tumor, one lung adenocarcinoma, and a T-cell acute lymphoblastic leukemia cell line. Our findings suggest that SOS1 is not a significant human oncogene in most cancers. Furthermore, NS patients with SOS1 mutations may not be at increased risk of developing cancer.
Phage Displayed Antibodies to Heat Stable Alkaline Phosphatase: Framework Region as a Determinant of Specificity (2002)

Human antibodies against specific targets of tumor cells are the most desirable molecules for possible immunotherapy. They could be developed by using the combinatorial antibody library displayed on a phage. We selected four human antibody fragments (scFv) binding to the oncoplacental antigen Heat Stable Alkaline Phosphatase (HSAP, the placental isozyme of alkaline phosphatase) from a synthetic human antibody library. Characterization of these scFvs showed they bound HSAP with moderate affinity but did not have isozyme specificity, as determined by binding to cell lines exhibiting differential expression of isozymes of alkaline phosphatase. The V(H) sequences of two of these scFvs were similar and although both bound to HSAP only one was cross-reactive with albumin. The sequences revealed a difference in the framework region (FR1) of these antibodies, indicating a role for this region in the determination of specificity. This is also significant considering that the heavy chains generated the diversity of the synthetic library used in this study, and only a single light chain showing binding to BSA was used for the entire library.
Synthesis of a Zwitterionic Silane and Its Application in the Surface Modification of Silicon-Based Material Surfaces for Improved Hemocompatibility (2010)

A phosphorylcholine-like silane coupling agent bearing zwitterionic molecular structure was synthesized and studied. The chemical structure of this silane coupling agent was characterized by FTIR, 1H NMR and 31P NMR. The zwitterionic structure was successfully constructed onto the surface of silicon as a self-assembled layer (SAL). Static water contact angle, and atomic force microscopy (AFM) were used to investigate the wettability and surface topography of the modified silicon surfaces. Static water contact angle results indicated that the hydrophilicity of the surfaces could be effectively improved by the modification with this zwitterionic silane coupling agent. The changes of the topography and water contact angle of the modified surfaces with different incubation periods in PBS solution were also measured to evaluate the stability of the SALs. Blood compatibility of the modified surfaces were evaluated by testing the full-blood activated partial thromboplastin time (APTT), prothrombin time (PT), and thrombin time (TT), as well as by observing the adhered blood platelets onto the surface. The modified surfaces showed prolonged clotting time and fewer adherent platelets, revealing that the blood compatibility was evidently improved by the modification using this zwitterionic silane.
COMMD Proteins, a Novel Family of Structural and Functional Homologs of MURR1 (2005)

MURR1 is a multifunctional protein that inhibits nuclear factor kappaB (NF-kappaB), a transcription factor with pleiotropic functions affecting innate and adaptive immunity, apoptosis, cell cycle regulation, and oncogenesis. Here we report the discovery of a new family of proteins with homology to MURR1. These proteins form multimeric complexes and were identified in a biochemical screen for MURR1-associated factors. The family is defined by the presence of a conserved and unique motif termed the COMM (copper metabolism gene MURR1) domain, which functions as an interface for protein-protein interactions. Like MURR1, several of these factors also associate with and inhibit NF-kappaB. The proteins designated as COMMD or COMM domain containing 1-10 are extensively conserved in multicellular eukaryotic organisms and define a novel family of structural and functional homologs of MURR1. The prototype of this family, MURR1/COMMD1, suppresses NF-kappaB not by affecting nuclear translocation or binding of NF-kappaB to cognate motifs; rather, it functions in the nucleus by affecting the association of NF-kappaB with chromatin.
<title>Optical synergetic computers for pattern recognition</title> (1993)

Using the concept that pattern recognition can be conceived as pattern formation, and using the mathematical methods of synergetics for the treatment of the spontaneous formation of spatial, temporal or spatio-temporal patterns, we study several laser configurations in which both, competition and pre-processing, allow one to deal with the problem of pattern recognition.
Erythromycin breath test as an assay of glucocorticoid-inducible liver cytochromes P-450. Studies in rats and patients. (1989)

The major P-450IIIA gene family member present in human liver is HLp which, like its rat liver orthologue P-450p, is inducible by glucocorticoids and catalyzes erythromycin N-demethylation. To develop a practical method to estimate the amounts of HLp in patients [14C]N-methyl erythromycin was injected into rats that had been pretreated with dexamethasone or with inducers of other forms of cytochrome P-450. The rate of demethylation of this substrate, measured simply as 14CO2 in the breath, correlated well with the concentrations of immunoreactive P-450p protein (r = 0.70), holocytochrome P-450p (r = 0.70), or with erythromycin N-demethylase activity (r = 0.90) determined in the liver microsomes prepared from each rat. Next, [14C]N-methyl erythromycin was administered to 30 patients and there was a sixfold interindividual variation in breath 14CO2 production seemingly unrelated to medications, smoking status or age. However, the average breath test values were twofold greater in female as compared to male patients (P less than 0.01). Breath 14CO2 production rose in patients retested after treatment with the P-450IIIA inducers dexamethasone (P less than 0.05) or rifampicin (P less than 0.05) and was decreased after treatment with the HLp inhibitor triacetyloleandomycin (P less than 0.05). We conclude that the erythromycin breath test provides a convenient assay of P-450IIIA cytochromes in rats and in some patients.
Nanoelectropulse-driven membrane perturbation and small molecule permeabilization (2006)

Megavolt-per-meter electric pulses as short as 3 ns alter the structure of the plasma membrane and permeabilize the cell to small molecules. The dose responses of cells to unipolar and bipolar pulses ranging from 3 ns to 30 ns duration support the hypothesis that a field-driven charging of the membrane dielectric causes the formation of pores on a nanosecond time scale, and that the anionic phospholipid PS migrates electrophoretically along the wall of these pores to the external face of the membrane.
Molecular Mechanisms and Regulation of Iron Transport (2003)

Iron homeostasis is primarily maintained through regulation of its transport. This review summarizes recent discoveries in the field of iron transport that have shed light on the molecular mechanisms of dietary iron uptake, pathways for iron efflux to and between peripheral tissues, proteins implicated in organellar transport of iron (particularly the mitochondrion), and novel regulators that have been proposed to control iron assimilation. The transport of both transferrin-bound and nontransferrin-bound iron to peripheral tissues is discussed. Finally, the regulation of iron transport is also considered at the molecular level, with posttranscriptional, transcriptional, and posttranslational control mechanisms being reviewed.
Mining Quality Phrases from Massive Text Corpora (2015)

Text data are ubiquitous and play an essential role in big data applications. However, text data are mostly unstructured. Transforming unstructured text into structured units (<i>e.g.</i>, semantically meaningful phrases) will substantially reduce semantic ambiguity and enhance the power and efficiency at manipulating such data using database technology. Thus mining quality phrases is a critical research problem in the field of databases. In this paper, we propose a new framework that extracts quality phrases from text corpora integrated with phrasal segmentation. The framework requires only limited training but the quality of phrases so generated is close to human judgment. Moreover, the method is scalable: both computation time and required space grow linearly as corpus size increases. Our experiments on large text corpora demonstrate the quality and efficiency of the new method.
Inhibition of growth and induction of apoptosis in human hepatoma cell line by tanshinone IIA (2003)

Objective To investigate the effect of tanshinone ⅡA on growth and apoptosis in human hepatoma cell line BEL 7402 in vitro . Methods The human hepatoma cell line BEL 7402 was treated with tanshinone ⅡA at various concentrations for 72 h. Cytotoxicity was evaluated by MTT assay, apoptosis related alterations in morphology ascertained by cytochemical staining(Hoechst 33258) and transmission electron microscopy(TEM). Apoptotic rate was quantified by flow cytometry (FCM). Results Tanshinone ⅡA inhibited the growth of hepatoma cells in a dose dependent manner, with IC 50 values of 6.28 μg/ml. After treatment with 1～10 μg/ml tanshinone ⅡA for 72 h, BEL 7402 cell apoptosis with nuclear chromatin concentration and fragmentation as well as cell shrinkage and the formation of apoptotic bodies were observed. FCM analysis showed hypodiploid peaks on histogram and the apoptotic rates at 5 μg/ml concentration for 12, 24, 36, 48 and 72 h were (2.32±0.16)%, (3.01±0.35)%, (3.87± 0.43 )%, (6.73±0.58)% and (20.85±1.74)% respectively, which were all significantly higher than that of control group (1.07±0.13)%. Conclusion Tanshinone ⅡA can induce the apoptosis of human hepatoma cell line BEL 7402 in vitro , which may be related to the mechanism of growth inhibition of the human hepatoma cell line.
Ghrelin, Peptide YY, Glucose-Dependent Insulinotropic Polypeptide, and Hunger Responses to a Mixed Meal in Anorexic, Obese, and Control Female Adolescents (2005)

To determine whether peptide YY (PYY), ghrelin, glucose-dependent insulinotropic polypeptide (GIP), and satiety responses to food intake are impaired in anorexia or obesity, we studied 30 female adolescents with anorexia nervosa [body mass index (BMI) 16.3 kg/m2], obesity (BMI 34.3 kg/m2), or normal weight (BMI 20.2 kg/m2). PYY, ghrelin, GIP, insulin, and glucose concentrations and four markers of satiety were measured for 240 min after a mixed meal. The area under the curve for glucose was similar in obese (OB) and normal-weight control (C) subjects but was 15% lower in anorexic (AN) subjects. The area under the curve for insulin was 47% lower in AN and 87% higher in OB subjects, compared with C subjects. After the meal, PYY increased significantly in C (+41%, P < 0.05) but not in AN or OB adolescents. Ghrelin concentrations were highest in AN subjects and lowest in the OB group, compared with C subjects and fell significantly by 25% in all three groups. GIP concentrations were lower in AN subjects throughout the test and increased in all three groups after the mixed meal. AN adolescents reported being less hungry than OB and C adolescents. There was a negative correlation between fasting ghrelin (but not PYY or GIP) and BMI and insulin (r2= 0.33) and a positive correlation between the decrease in hunger 15 min after the meal and PYY concentrations at 15 min (r2= 0.20). In conclusion, the blunted PYY response to a meal in OB adolescents suggests that PYY plays a role in the pathophysiology of obesity. Ghrelin is unlikely to play a causal role in anorexia nervosa or obesity. The lower GIP observed in AN subjects despite a similar caloric intake may appropriately prevent an excessive insulin response in these patients.
Nocturnal Dyspnea and Atrial Fibrillation Predict Cheyne-Stokes Respirations in Patients With Congestive Heart Failure (1995)

Cheyne-Stokes respirations and nonspecific sleep-disordered breathing are common in unselected patients with congestive heart failure, and Cheyne-Stokes respirations are predicted by a history of nocturnal dyspnea and the presence of atrial fibrillation. Techniques designed to modify the nocturnal breathing pattern of patients with congestive heart failure may be applicable to a large portion of the congestive heart failure population.
VDAC-dependent permeabilization of the outer mitochondrial membrane by superoxide induces rapid and massive cytochrome c release (2001)

Enhanced formation of reactive oxygen species (ROS), superoxide (O2*-), and hydrogen peroxide (H2O2) may result in either apoptosis or other forms of cell death. Here, we studied the mechanisms underlying activation of the apoptotic machinery by ROS. Exposure of permeabilized HepG2 cells to O2*- elicited rapid and massive cytochrome c release (CCR), whereas H2O2 failed to induce any release. Both O2*- and H2O2 promoted activation of the mitochondrial permeability transition pore by Ca2+, but Ca2+-dependent pore opening was not required for O2*--induced CCR. Furthermore, O2*- alone evoked CCR without damage of the inner mitochondrial membrane barrier, as mitochondrial membrane potential was sustained in the presence of extramitochondrial ATP. Strikingly, pretreatment of the cells with drugs or an antibody, which block the voltage-dependent anion channel (VDAC), prevented O2*--induced CCR. Furthermore, VDAC-reconstituted liposomes permeated cytochrome c after O2*- exposure, and this release was prevented by VDAC blocker. The proapoptotic protein, Bak, was not detected in HepG2 cells and O2*--induced CCR did not depend on Bax translocation to mitochondria. O2*--induced CCR was followed by caspase activation and execution of apoptosis. Thus, O2*- triggers apoptosis via VDAC-dependent permeabilization of the mitochondrial outer membrane without apparent contribution of proapoptotic Bcl-2 family proteins.
Intermolecular association and trans-phosphorylation of different neu-kinase forms permit SH2-dependent signaling and oncogenic transformation. (1995)

The neu oncogene encodes a 185 kDa receptor tyrosine kinase. A single point mutation (Val664-->Glu) within the p185neu transmembrane region results in higher efficiency of receptor dimerization, constitutive activity of tyrosine kinase and cellular transformation. The oncogenic potential of this mutated form of p185neu (termed Tneu) can be inactivated by site-directed alteration of a lysine residue in the conserved catalytic domain. In this report, we have utilized the physical and functional interaction of a full-length kinase-deficient neu protein (T757) and truncated kinase-active Tneu forms to determine critical protein domains for Tneu oligomerization and the resultant biological consequences. Analysis of various truncated Tneu mutants confirmed that the transmembrane region was crucial for p185 dimerization. Receptor association facilitates intermolecular phosphorylation of kinase-deficient mutant T757 by truncated kinase-active p185 proteins, and the trans-phosphorylated kinase-deficient T757 was able to associate in vitro with proteins containing SH2 domains. Receptor-receptor interactions resulted in enhanced signal transduction potential and transformation of cell-lines co-expressing different neu-kinase forms. These studies emphasize a novel feature of protein-protein interaction and the functional significance of p185 dimerization, intermolecular phosphorylation and signaling which may result in cellular transformation.
Flow level detection and filtering of low-rate DDoS (2012)

The recently proposed TCP-targeted Low-rate Distributed Denial-of-Service (LDDoS) attacks send fewer packets to attack legitimate flows by exploiting the vulnerability in TCP’s congestion control mechanism. They are difficult to detect while causing severe damage to TCP-based applications. Existing approaches can only detect the presence of an LDDoS attack, but fail to identify LDDoS flows. In this paper, we propose a novel metric – Congestion Participation Rate (CPR) – and a CPR-based approach to detect and filter LDDoS attacks by their intention to congest the network. The major innovation of the CPR-base approach is its ability to identify LDDoS flows. A flow with a CPR higher than a predefined threshold is classified as an LDDoS flow, and consequently all of its packets will be dropped. We analyze the effectiveness of CPR theoretically by quantifying the average CPR difference between normal TCP flows and LDDoS flows and showing that CPR can differentiate them. We conduct ns-2 simulations, test-bed experiments, and Internet traffic trace analysis to validate our analytical results and evaluate the performance of the proposed approach. Experimental results demonstrate that the proposed CPR-based approach is substantially more effective compared to an existing Discrete Fourier Transform (DFT)-based approach – one of the most efficient approaches in detecting LDDoS attacks. We also provide experimental guidance to choose the CPR threshold in practice.