gebhart/patrepeval huggingface dataset:
Purification and Characterization of the Soluble Methane Monooxygenase of the Type II Methanotrophic Bacterium Methylocystis sp. Strain WI 14 (1999)

Methane monooxygenase (MMO) catalyzes the oxidation of methane to methanol as the first step of methane degradation. A soluble NAD(P)H-dependent methane monooxygenase (sMMO) from the type II methanotrophic bacterium WI 14 was purified to homogeneity. Sequencing of the 16S rDNA and comparison with that of other known methanotrophic bacteria confirmed that strain WI 14 is very close to the genus Methylocystis. The sMMO is expressed only during growth under copper limitation (<0.1 microM) and with ammonium or nitrate ions as the nitrogen source. The enzyme exhibits a low substrate specificity and is able to oxidize several alkanes and alkenes, cyclic hydrocarbons, aromatics, and halogenic aromatics. It has three components, hydroxylase, reductase and protein B, which is involved in enzyme regulation and increases sMMO activity about 10-fold. The relative molecular masses of the native components were estimated to be 229, 41, and 18 kDa, respectively. The hydroxylase contains three subunits with relative molecular masses of 57, 43, and 23 kDa, which are present in stoichiometric amounts, suggesting that the native protein has an alpha(2)beta(2)gamma(2) structure. We detected 3.6 mol of iron per mol of hydroxylase by atomic absorption spectrometry. sMMO is strongly inhibited by Hg(2+) ions (with a total loss of enzyme activity at 0.01 mM Hg(2+)) and Cu(2+), Zn(2+), and Ni(2+) ions (95, 80, and 40% loss of activity at 1 mM ions). The complete sMMO gene sequence has been determined. sMMO genes from strain WI 14 are clustered on the chromosome and show a high degree of homology (at both the nucleotide and amino acid levels) to the corresponding genes from Methylosinus trichosporium OB3b, Methylocystis sp. strain M, and Methylococcus capsulatus (Bath).
Acoustically driven programmable liquid motion using resonance cavities (2009)

Performance and utility of microfluidic systems are often overshadowed by the difficulties and costs associated with operation and control. As a step toward the development of a more efficient platform for microfluidic control, we present a distributed pressure generation scheme whereby independently tunable pressure sources can be simultaneously controlled by using a single acoustic source. We demonstrate how this scheme can be used to perform precise droplet positioning as well as merging, splitting, and sorting within open microfluidic networks. We further show how this scheme can be implemented for control of continuous-flow systems, specifically for generation of acoustically tunable liquid gradients. Device operation hinges on a resonance-decoding and rectification mechanism by which the frequency content in a composite acoustic input is decomposed into multiple independently buffered output pressures. The device consists of a bank of 4 uniquely tuned resonance cavities (404, 484, 532, and 654 Hz), each being responsible for the actuation of a single droplet, 4 identical flow-rectification structures, and a single acoustic source. Cavities selectively amplify resonant tones in the input signal, resulting in highly elevated local cavity pressures. Fluidic-rectification structures then serve to convert the elevated oscillating cavity pressures into unidirectional flows. The resulting pressure gradients, which are used to manipulate fluids in a microdevice, are tunable over a range of approximately 0-200 Pa with a control resolution of 10 Pa.
Structure-function studies of a colony stimulating factor (CSF-1). (1982)

CSF-1 is a glycoprotein growth factor which specifically stimulates the survival, proliferation, and differentiation of cells of the mononuclear phagocytic lineage. In this study, microgram amounts of radiolabeled murine L-cell and human urinary CSF-1 were isolated in pure form and used to investigate the nature and extent of CSF-1 glycosylation and the requirement of the carbohydrate moiety for its biological and antibody-binding activities. The molecular weight of the preparations examined varied between approximately 47,000 and approximately 76,000. Reduction and alkylation halved the molecular weight of all preparations, reflecting within each the existence of two similar subunits. Exhaustive treatment of reduced and alkylated CSF-1 with endo-beta-N-acetylglucosaminidase D, but not endo-beta-N-acetylglucosaminidase H, gave rise to a molecule of Mr approximately 16,500 of which the polypeptide portion accounted for approximately 15,500. Whereas the parent molecule bound concanavalin A, the product did not, indicating that heterogeneity in the saccharide component could explain the observed variation in the molecular weight of CSF-1. These results also suggest that the two polypeptide chains in the dimeric CSF-1 molecule are very similar and possibly even identical. Because of the specificity of endo-beta-N-acetylglucosaminidase D, it is concluded that the carbohydrate moieties are Asn-linked "complex-type" units. Examination of the effects of endo-alpha-N-acetyl-D-galactosaminidase treatment on the molecular weight of reduced and alkylated CSF-1 failed to provide evidence for the existence of O-glycosidically linked oligosaccharides. Treatment of native CSF-1 with endo-beta-N-acetylglucosaminidase D was almost as efficient in removing carbohydrate as in the case of the reduced and alkylated subunits. Removal did not cause loss of antibody binding, receptor binding, or biological activity.
An experimental study on spinal cord injury treatmen with fetal spinal cord transplantation and methylprednisolone therapy (2002)

Objective:To find out the synergistic action of fetal spinal cord transplantation(FST) and methylprednisolone (MP)treatment in spinal cord injury therapy.Method:50 male SD rats were divided evenly into 5 groups,In Group A～D,semisection was done at the right half of T12 spinal cord of each rat.Group A were treated with the combination of large dose MP and FST;Group B were treated with large dose MP only;Group C accepted FST;and no therapy was given to Group D;Group E served as blank control.Spinal cord somatosensory evoked poteneial(SSEP) examination and behavior observation were performed 24 hours and 2 months after treatment.Nerve fibre number at injured cord cross section in the 5 groups was treated with statistics analysis .Result:There was significant difference in and nerve fibres SSEP examination between Group A and Group B,C,D( P 0.05).No obvious behavior changes were found except partial sensory recovery in Group A.Conclusion:The combination of large dose MP therapy and FST have synergistic effects.
Tumor hypoxia: A target for selective cancer therapy (2003)

Tumor hypoxia has been considered to be a potential therapeutic problem because it renders solid tumors more resistant to sparsely ionizing radiation (IR) and chemotherapeutic drugs. Moreover, recent laboratory and clinical data have shown that tumor hypoxia is also associated with a more malignant phenotype and poor survival in patients suffering from various solid tumors. Therefore, selective targeting of hypoxic tumor cells has been explored, and since severe hypoxia (pO(2) < 0.33%, 2.5 mmHg) does not occur in normal tissue, tumor hypoxia could be exploited for therapeutic advantage. However, the following three characteristics of hypoxic tumor regions present obstacles in targeting hypoxic cells. First, it is difficult to deliver a sufficient amount of drug to a region that is remote from blood vessels. Second, one must specifically target hypoxic tumor cells while sparing normal well-oxygenated tissue from damage. Finally, the severely hypoxic tumor cells to be attacked have often stopped dividing. Therefore, high delivery efficiency, high specificity and selective cytotoxicity are all necessary to target and combat hypoxic tumor cells. The current review describes progress on the biological aspects of tumor hypoxia and provides a compilation of the recent molecular approaches used to target hypoxic tumors. These approaches include our work with a unique hypoxia-targeting protein drug, TOP3, with which we have sought to address the above three difficulties.
Sequencing of DNA by Free-Solution Capillary Electrophoresis Using a Genetically Engineered Protein Polymer Drag-Tag (2008)

We demonstrate the first use of a non-natural, genetically engineered protein polymer drag-tag to sequence DNA fragments by end-labeled free-solution electrophoresis (ELFSE). Fluorescently labeled DNA fragments resulting from the Sanger cycle sequencing reaction were separated by free-solution capillary electrophoresis, with much higher resolution and cleaner results than previously reported for this technique. With ELFSE, size-based separation of DNA in the absence of a sieving matrix is enabled by the end-on attachment of a polymeric "drag-tag" that modifies the charge-to-friction ratio of DNA in a size-dependent fashion. Progress in ELFSE separations has previously been limited by the lack of suitable large, monodisperse drag-tags. To address this problem, we designed, constructed, cloned, expressed, and purified a non-natural, genetically engineered 127mer protein polymer for use as an ELFSE drag-tag. The Sanger cycle sequencing reaction is performed with the drag-tag covalently attached to the sequencing primer, a major advance over previous strategies for ELFSE sequencing. The electrophoretic separation is diffusion-limited, without significant adsorption of the drag-tag to capillary walls. Although the read length (at about 180 bases) is still short, our results provide evidence that larger protein polymer drag-tags, currently under development, could extend the read length of ELFSE to more competitive levels. ELFSE offers the possibility of very rapid DNA sequencing separations without any of the difficulties associated with viscous polymeric sieving networks and hence will be amenable to implementation in microchannel and chip-based electrophoresis systems.
[Changes of serum BAFF and IL-21 levels in patients with systemic lupus erythematosus and their clinical significance]. (2007)

The levels of serum BAFF and IL-21 level are increased in the patients with SLE. The dysfunction and synergistic effect of T and B lymphocytes play different roles in the patients with different organ damage and pathoprocess respectively.
Nonviral Vectors for Cancer Gene Therapy: Prospects for Integrating Vectors and Combination Therapies (2005)

Gene therapy has the potential to improve the clinical outcome of many cancers by transferring therapeutic genes into tumor cells or normal host tissue. Gene transfer into tumor cells or tumor-associated stroma is being employed to induce tumor cell death, stimulate anti-tumor immune response, inhibit angiogenesis, and control tumor cell growth. Viral vectors have been used to achieve this proof of principle in animal models and, in select cases, in human clinical trials. Nevertheless, there has been considerable interest in developing nonviral vectors for cancer gene therapy. Nonviral vectors are simpler, more amenable to large-scale manufacture, and potentially safer for clinical use. Nonviral vectors were once limited by low gene transfer efficiency and transient or steadily declining gene expression. However, recent improvements in plasmid-based vectors and delivery methods are showing promise in circumventing these obstacles. This article reviews the current status of nonviral cancer gene therapy, with an emphasis on combination strategies, long-term gene transfer using transposons and bacteriophage integrases, and future directions.
Germ-line p53 mutations in 15 families with Li-Fraumeni syndrome. (1995)

Germ-line mutations of the tumor-suppressor gene p53 have been observed in some families with the Li-Fraumeni syndrome (LFS), a familial cancer syndrome in which affected relatives develop a diverse set of early-onset malignancies including breast carcinoma, sarcomas, and brain tumors. The analysis of the p53 gene in LFS families has been limited, in most studies to date, to the region between exon 5 and exon 9. In order to determine the frequency and distribution of germ-line p53 mutations in LFS, we sequenced the 10 coding exons of the p53 gene in lymphocytes and fibroblast cell lines derived from 15 families with the syndrome. Germ-line mutations were observed in eight families. Six mutations were missense mutations located between exons 5 and 8. One mutation was a nonsense mutation in exon 6, and one mutation was a splicing mutation in intron 4, generating aberrant shorter p53 RNA(s). In three families, a mutation of the p53 gene was observed in the fibroblast cell line derived from the proband. However, the mutation was not found in affected relatives in two families and in the blood from the one individual, indicating that the mutation probably occurred during cell culture in vitro. In four families, no mutation was observed. This study indicates that germ-line p53 mutations in LFS are mostly located between exons 5 and 8 and that approximately 50% of patients with LFS have no germ-line mutations in the coding region of the p53 gene.(ABSTRACT TRUNCATED AT 250 WORDS)
Trophoblastic apoptosis in mice with preterm delivery and its suppression by urinary trypsin inhibitor (1997)

We demonstrated that trophoblastic apoptosis occurs in the placentas of a mouse model with preterm delivery induced by lipopolysaccharide. We postulated that apoptosis may lead to placental abruption, and its development may be prevented by treatment with urinary trypsin inhibitor.
RSEARCH: Finding homologs of single structured RNA sequences (2003)

RSEARCH outperforms primary sequence programs in finding homologs of structured RNA sequences.
Novel Pyrrolopyrimidine-Based α-Helix Mimetics: Cell-Permeable Inhibitors of Protein−Protein Interactions (2010)

There is considerable interest in developing non-peptidic, small-molecule α-helix mimetics to disrupt α-helix-mediated protein−protein interactions. Herein, we report the design of a novel pyrrolopyrimidine-based scaffold for such α-helix mimetics with increased conformational rigidity. We also developed a facile solid-phase synthetic route that is amenable to divergent synthesis of a large library. Using a fluorescence polarization-based assay, we identified cell-permeable, dual MDMX/MDM2 inhibitors, demonstrating that the designed molecules can act as α-helix mimetics.
A Novel Toxinotyping Scheme and Correlation of Toxinotypes with Serogroups of Clostridium difficile Isolates (1998)

Two hundred nineteen Clostridium difficile isolates from 22 serogroups were screened for changes in the genes coding for toxin B (tcdB) and toxin A (tcdA). Parts of the toxin genes were amplified, and the PCR fragments were checked for length polymorphisms and cut with several restriction enzymes to monitor restriction fragment length polymorphisms (RFLPs). For 47 strains (21%), differences in the toxin genes were found compared to the toxin genes of reference strain VPI 10,463. Polymorphisms were usually observed in both toxin genes. RFLPs were more commonly found in the tcdB gene, in which a single restriction enzyme could give up to five different patterns. Restriction sites seemed to be less heterogeneous in the tcdA gene, in which for most enzymes only two different RFLPs were recognized. However, deletions were observed in tcdA, and four new types of shortened tcdA genes are described. According to the changes in their toxin genes, variant strains could be divided into 10 groups (toxinotypes I to X). A toxinotype was characterized by similar patterns of changes in the toxin genes and in other regions of the pathogenicity locus and also similar pulsed-field gel electrophoresis patterns. Variant toxinotypes were found in 9 of the 22 serogroups studied, and some toxinotypes were clearly associated with specific serogroups. Toxinotype VIII is characteristic for all strains of serogroup F. Other serogroups in which variant toxinotypes were commonly found are A1, A15, E, and X. Testing of variability in C. difficile toxin genes not only might be useful as a molecular typing system but also could have implications in diagnostics and pathogenesis.
Botnet cluster identification (2014)

Botnets are a group of computers infected with a specific sub-set of a malware family and controlled by one individual, called botmaster. This kind of networks are used not only, but also for virtual extorsion, spam campaigns and identity theft. They implement different types of evasion techniques that make it harder for one to group and detect botnet traffic. This thesis introduces one methodology, called CONDENSER, that outputs clusters through a self-organizing map and that identify domain names generated by an unknown pseudo-random seed that is known by the botnet herder(s). Aditionally DNS Crawler is proposed, this system saves historic DNS data for fast-flux and double fastflux detection, and is used to identify live C&Cs IPs used by real botnets. A program, called CHEWER, was developed to automate the calculation of the SVM parameters and features that better perform against the available domain names associated with DGAs. CONDENSER and DNS Crawler were developed with scalability in mind so the detection of fast-flux and double fast-flux networks become faster. We used a SVM for the DGA classififer, selecting a total of 11 attributes and achieving a Precision of 77,9% and a F-Measure of 83,2%. The feature selection method identified the 3 most significant attributes of the total set of attributes. For clustering, a Self-Organizing Map was used on a total of 81 attributes. The conclusions of this thesis were accepted in Botconf through a submited article. Botconf is known conferênce for research, mitigation and discovery of botnets tailled for the industry, where is presented current work and research. This conference is known for having security and anti-virus companies, law enforcement agencies and researchers.
Serum C-Reactive Protein as Independent Prognostic Variable in Patients with Ovarian Cancer (2008)

Serum CRP can be seen as a novel, widely available independent prognostic variable of ovarian cancer.
Cultures of Proliferating Vascular Smooth Muscle Cells from Adult Human Aorta (2003)

Abnormal proliferation of human vascular smooth muscle cells (hVSMCs) is a central event in the development of atherosclerosis (1-3) As a result, there is considerable interest in the establishment of hVSMC cultures as a mode1 of this disease process However, it has been noted in the past (4,5) that hVSMCs, especially when cultured by the enzyme-dispersal technique (hVSMC,(ED)), grow poorly in culture compared to VSMCs from other species (e.g., rat) This has limited their use for cell-culture studies. We have recently reported that the reduced proliferative capacity of hVSMC(ED) from adult aorta can be attributed to the endogenous production of active TGF-β(6,7). We (6-8) and others (9-11) have shown that TGF-β; is a potent inhibtior of smooth muscle cell proliferation. Moreover, recent studies in animal models of atherosclerosis (12) have suggested that TGF-P plays a pivotal role in regulation of vessel wall architecture (13). We have also shown that hVSMCs derived by the alternative method of explanting (hVSMC(EX)) have a greater proliferative capacity than the hVSMC(ED) (14) In accordance with our hypotheses, the cells grown from explanted tissue did not produce TGF-β; (14).
Leucine Zipper Dimerized Bivalent and Bispecific scFv Antibodies from a Semi-synthetic Antibody Phage Display Library (1996)

This report describes the construction of leucine zipper-based dimerization cassettes for the conversion of recombinant monomeric scFv antibody fragments to bivalent and bispecific dimers. A truncated murine IgG3 hinge region and a Fos or Jun leucine zipper were cloned into four scFv fragments previously isolated from a synthetic antibody phage display library. Cysteine residues flanking the zipper region were introduced to covalently link dimerized scFv fragments. The secreted fusion proteins were shown to spontaneously and efficiently form stable Fos-Fos or Jun-Jun homodimers in the Escherichia coli periplasm at levels comparable to their monovalent counterparts. The bivalent (scFv)2 fragments performed well in enzyme-linked immunosorbent assay, flowcytometric, and immunohistochemical analysis. Fos and Jun homodimer (scFv)2 antibodies with different specificities could be reduced, reshuffled, and reoxidized to form preparations of functional bispecific (scFv)2 Fos-Jun heterodimers. These Fos and Jun fusion protein cassettes provide a universal basis for the construction of dimeric scFv antibodies with enhanced avidity or dual specificity.
Identification and sequencing of theChoristoneura biennisentomopoxvirus DNA polymerase gene (1991)

A degenerate oligonucleotide probe corresponding to a highly conserved amino acid sequence in several DNA polymerases was used to locate the DNA polymerase gene in the Choristoneura biennis entomopoxvirus. Southern blot analysis of the entomopoxvirus genome using the degenerate oligonucleotide probe showed specific interaction between the probe and an eight kilobasepair EcoRI fragment from the entomopoxvirus genome. Sequencing this EcoRI fragment revealed an open reading frame 2892 nucleotides in length, capable of encoding a protein about 115 kilodaltons. Homology search of this open reading frame against other proteins indicated a high degree of homology in four distinct regions with DNA polymerases from other organisms. The highest degree of homology (24.9% at the amino acid level) was found between the vaccinia DNA polymerase gene and the entomopoxvirus open reading frame.
Exacerbation of antigen-induced arthritis after challenge with intravenous antigen. (1983)

The occurrence and morphology of flare-up of arthritis after intravenous (i.v.) antigen administration was investigated in mice with on-going antigen-induced arthritis (AIA). Intravenous injection of 300 micrograms methylated bovine serum albumin (mBSA) in mice with unilateral arthritis induced by mBSA, elicited 6 weeks previously, caused clear flare-up of the smouldering joint inflammation without affecting the contralateral non-arthritic knee joint. Histological signs of the flare-up reaction were already present at 6 hr after i.v. challenge and lasted for at least 4 days. Characteristic features are the presence of large numbers of granulocytes just beneath the synovial lining layer, inflammatory foci in adjacent periarticular tissues, and deposits of fibrin-like material in the joint space. Variations in the severity of the preceding arthritis and in the interval (4-12 weeks) between AIA induction and i.v. challenge had no major influence on the occurrence and degree of the flare-up phenomenon. Since exacerbations of joint inflammation are seen in rheumatoid arthritis, this phenomenon may be of importance in this disease.