gebhart/patrepeval huggingface dataset:
Staphylococcal protein A binding to the Fab fragments of mouse monoclonal antibodies. (1984)

Two mouse IgG1 monoclonal antibodies specific for the Lewis(a) human blood group antigen were purified on protein A-Sepharose by using buffers of decreasing pH for elution. Unlike other IgG1 antibodies that eluted at pH 7.0 to 6.0, these antibodies could only be eluted at pH 4.0 to 3.0. The Fab and F(ab')2 fragments of these antibodies also eluted at pH 4.0 to 3.0, although the Fc fragment of one eluted at pH 6.0. This interaction of protein A with Fab was not due to anti-protein A antibody activity, because the presence of Lewis(a) trisaccharide did not prevent the binding of Fab to protein A-Sepharose and because Fab that had bound to solid phase hapten could still be recognized by protein A. Thus, certain mouse IgG1 antibodies possess determinants in their Fab portion recognized by protein A, allowing for the purification of such Fab fragments on protein A-Sepharose.
Determination of trace elements in oils by plasma emission spectroscopy (1982)

Abstract An analytical method for the determination of phosphorus and other elements at low concentrations in edible oils has been developed using a plasma emission spectrometer. The method is fast because it eliminates the ashing process in sample preparation and because the actual measurement takes less than 1 min. Reproducibility and accuracy of the measurement are good and very low detection limits have been observed, e.g., 0.5 ppm for phosphorus and 5 ppb for copper. However, the long‐term stability of the instrument cannot as yet be guaranteed and a procedure that prescribes regular measurement of samples of known concentration is essential as a means of detecting any drift in the output signal.
Review of cases of nosocomial Lassa fever in Nigeria: the high price of poor medical practice (1995)

This outbreak illustrates the high price exacted by the practice of modern medicine, particularly use of parenteral injections and surgery, without due attention to good medical practice. High priority must be given to education of medical staff in developing countries and to guidelines for safe operation of clinics and hospitals. Failure to do so will have far reaching, costly, and ultimately devastating consequences.
A study of the volatile organic compounds exhaled by lung cancer cells in vitro for breath diagnosis (2007)

Abstract BACKGROUND. The specific volatile organic compounds (VOCs) exhaled by lung cancer cells in the microenvironment are the source biomarkers of lung cancer and also serve as direct evidence that the diagnosis of lung cancer by breath is possible. However, to the authors' knowledge, few articles published to date have provided accurate VOCs in the microenvironment, thereby leading to different points of view with regard to searching for biomarkers in the breath from lung cancer patients In this article, an innovative pathologic analysis method of lung cancer and the early diagnosis of lung cancer at the cellular level were introduced for this purpose. METHODS. Solid‐phase microextraction combined with gas chromatography is used as the detection system to determine the VOCs in the culture medium of several target cells, including different kinds of lung cancer cells, bronchial epithelial cells, tastebud cells, osteogenic cells, and lipocytes. As a result, each kind of cells has a unique chromatogram. There are 4 special VOCs that were found to exist in all culture mediums of lung cancer cells, which are the metabolic products of lung cancer cells and can be viewed as markers of lung cancer. RESULTS. The authors were able to determine a correlation between VOCs in the metabolic products of lung cancer cells and VOCs in the breath of lung cancer patients, some of whom had stage I and II disease, and eventually hope to certify the biomarkers in the breath of lung cancer patients. CONCLUSIONS. This research is significant and provides the basis for the noninvasive detection and the breath diagnosis of lung cancer using an electronic nose. Cancer 2007; 110:835–44. © 2007 American Cancer Society.
The formation of paranemic and plectonemic joints between DNA molecules by the recA and single-stranded DNA-binding proteins of Escherichia coli. (1985)

During the initial pairing events in the transfer of a strand from a linear duplex to a homologous single-stranded circular DNA by the recA and single-stranded DNA-binding proteins of Escherichia coli, two types of structure are formed that are distinguishable by their stability in the presence of protein denaturants. One type which is resistant to 5.2 M guanidinium chloride is most likely a D-loop that depends only on heteroduplex base pairing for its stability. These D-loops form rapidly when the ends of the linear duplex are homologous with the single-stranded DNA but do not form when the ends are heterologous. The second type appears to require protein, in addition to base pairing, for stability since it is rapidly dissociated by treatment with 5.2 M guanidinium chloride. These unstable structures form even when the ends of the duplex are not homologous with the circular single-stranded DNA. The stability and topological properties of the stable and unstable structures are consistent with those of plectonemic and paranemic joints, respectively (Bianchi, M., Das Gupta, C., and Radding, C. M. (1983) Cell 34, 931-939). The plectonemic joints can be generated in situ from paranemic joints by the addition of a restriction enzyme that cleaves in the region of homology, thus producing free homologous ends. Omission of single-stranded DNA-binding protein results in a large decrease in the rate of formation of both paranemic and plectonemic joints.
Central Proinflammatory Cytokines and Pain Enhancement (2005)

Enhanced pain is a component of the 'sickness response' which is an evolutionarily adaptive constellation of responses that enhance the survival of the host. Proinflammatory cytokines mediate these sickness behaviors, and whether proinflammatory cytokines are involved in exaggerated pain has become an intriguing question. Studies suggest that spinal cord glial cells (astrocytes and microglia) are activated in conditions that lead to enhanced pain. Not only is glial activation associated with enhanced pain, but it is also integral to the induction and maintenance of these pain states. Proinflammatory cytokines can be released by activated astrocytes and microglia within the central nervous system. This review will discuss the role of proinflammatory cytokines in experimental models of prolonged pain states. Administration of exogenous proinflammatory cytokines facilitates pain, and agents that antagonize proinflammatory cytokine actions have been shown to block and/or reverse enhanced pain. These findings suggest that blocking the synthesis and/or release of proinflammatory cytokines may be viable strategies for the treatment of pathological pain. Gene therapy to augment the endogenous anti-inflammatory cytokine, interleukin-10, is one of the more promising therapies currently under study.
First trimester maternal serum AFP and total hCG in aneuploidies other than trisomy 21 (2000)

Total human chorionic gonadotropin (hCG) and alpha-fetoprotein (AFP) were measured in maternal serum at 10-14 weeks of gestation from 53 pregnancies affected by trisomy 18, 42 cases with trisomy 13, 46 with Turner's syndrome and 13 with other sex aneuploides. The only significant association was the finding of reduced levels of total hCG in cases of trisomy 18 and 13. The association of increased levels of AFP in cases of trisomy 18 with ventral wall defects and the slight increase in AFP in cases of sex chromosomal anomalies other than Turner's syndrome was found. AFP and total hCG are not likely to replace the markers free beta-hCG and PAPP-A in first trimester screening for chromosomal anomalies.
Hsp47 a novel collagen binding serpin chaperone, autoantigen and therapeutic target (2005)

Hsp47 was originally discovered as a cell surface collagen binding protein, colligin, and was later shown to be an endoplasmic reticulum (ER) resident protein with collagen binding properties in chick fibroblasts. Hsp47 has been termed J6, gp46, CB48 and CBP2 in various other organisms and has been mapped to human chromosome 11q13.5 a known "hot spot" in a number of human cancers. Hsp47 has been shown to be constitutively expressed with collagens; it is heat inducible and binds to both helical and non-helical forms of collagens. Hsp47 binds closely to procollagen in the ER, but dissociates from it in the cis-Golgi to allow fibril formation. Hsp47 is over-expressed in many fibrotic diseases including: glomerulosclerosis, pulmonary fibrosis, liver cirrhosis, cicatricial pemphigoid, epidermolysis bullosa acquista and keloids. Hsp47 is associated with fibrosis following myocardial infarction and has been localized in artherosclerotic arteries. Among a number of rheumatoid conditions, Hsp47 manifests properties of an autoantigen and in some cancers appears to be a biomarker. The unique properties of Hsp47 in modulating collagen production and its location to the cell membrane in many forms of cancer have designated Hsp47 as a potential biomarker and/or therapeutic target for a number of conditions and diseases.
Overexpression of cathepsin f, matrix metalloproteinases 11 and 12 in cervical cancer (2005)

Novel undetected CC promoting genes have been identified. Increased transcription of these genes may result in overexpression of proteins, such as CTSF, MMP11 and MMP12 which could contribute to the pathogenesis of CC.
Three-Dimensional Computer Reconstructions of Brain Lesions from Surface Contours Provided by Computed Tomography: A Prospectus (1982)

We present a prospectus on the use of computer graphics for the three-dimensional reconstruction and visualization of brain lesions from computed tomographic head examinations, including an algorithm that utilizes surface contour information to reconstruct and display three-dimensional anatomical sites. We provide examples of the use of this algorithm. We offer an algorithm for estimation of the volume and surface area of anatomical sites. The advantages and disadvantages for the clinical use of these algorithms are discussed.
GLK Transcription Factors Coordinate Expression of the Photosynthetic Apparatus in Arabidopsis (2009)

Chloroplasts of photosynthetic organisms harness light energy and convert it into chemical energy. In several land plants, GOLDEN2-LIKE (GLK) transcription factors are required for chloroplast development, as glk1 glk2 double mutants are pale green and deficient in the formation of the photosynthetic apparatus. We show here that glk1 glk2 double mutants of Arabidopsis thaliana accumulate abnormal levels of chlorophyll precursors and that constitutive GLK gene expression leads to increased accumulation of transcripts for antenna proteins and chlorophyll biosynthetic enzymes. To establish the primary targets of GLK gene action, an inducible expression system was used in combination with transcriptome analysis. Following induction, transcript pools were substantially enriched in genes involved in chlorophyll biosynthesis, light harvesting, and electron transport. Chromatin immunoprecipitation experiments confirmed the direct association of GLK1 protein with target gene promoters, revealing a putative regulatory cis-element. We show that GLK proteins influence photosynthetic gene expression independently of the phyB signaling pathway and that the two GLK genes are differentially responsive to plastid retrograde signals. These results suggest that GLK genes help to coregulate and synchronize the expression of a suite of nuclear photosynthetic genes and thus act to optimize photosynthetic capacity in varying environmental and developmental conditions.
Human dendritic cell (DC)-based anti-infective therapy: engineering DCs to secrete functional IFN-gamma and IL-12. (1998)

An imbalance in the Th1- and Th2-type cytokine responses may allow certain microbes to modify the host response to favor their own persistence. We now show that infection/pulsing of human CD34+ peripheral blood hemopoietic progenitor cell-derived dendritic cells (DCs) with Leishmania donovani promastigotes, Histoplasma capsulatum, and Mycobacterium kansasii impairs the constitutive production of IL-12 from these cells. Thus, strategies aimed at modulating a dysregulated Th1/Th2 response to infection would be of great interest. To both augment the host immune response and deliver potent immunomodulatory cytokines such as IL-12 and IFN-gamma, our goal is to develop a therapeutic strategy using genetically modified, microbial Ag-pulsed DCs. Toward developing such immunotherapies, we used retrovirus-mediated somatic gene transfer techniques to engineer human DCs to secrete biologically active IL-12 and IFN-gamma. DCs pulsed with microbial antigens (e.g., leishmania and histoplasma Ags) were capable of inducing proliferative responses in autologous CD4+ lymphocytes. CD4+ lymphocytes cocultured with IL-12-transduced autologous DCs had enhanced Ag-specific proliferative responses compared with CD4+ lymphocytes cocultured with nontransduced or IFN-gamma- transduced DCs. In this cell culture model system we demonstrate that IL-12 has a negative effect on IL-4 secretion that is independent of its ability to induce IFN-gamma secretion. Taken together, these results indicate that IL-12-transduced DCs may be specifically suited in inducing or down-modulating Ag-specific Th1 or Th2 responses, respectively, and thus may be useful as adjunctive therapy in those intracellular infections in which a dominant Th1 response is critical for the resolution of infection.
Characterization of Human FSH Isoforms Reveals a Nonglycosylatedβ -Subunit in Addition to the Conventional Glycosylatedβ -Subunit (2001)

Human FSH consists of a mixture of isoforms that can be separated on the basis of differences in negative charge conferred by variations in the numbers of sialic acid residues that terminate oligosaccharide branches. Western analysis of human FSH isoforms separated by chromatofocusing revealed the presence of two human FSHbeta isoforms that differed in size. A low mol wt human FSHbeta isoform was associated with all FSH isoform fractions. A high mol wt human FSHbeta isoform was associated with the more acidic fractions and increased in relative abundance as the pI decreased. Characterization of representative human FSHbeta isoforms by mass spectrometry and automated Edman degradation revealed a low mol wt isoform that was not glycosylated. A high mol wt isoform was N-glycosylated at Asn residues 7 and 24. These results indicate that pituitary human FSH consists of two classes of molecules: those that possess a nonglycosylated beta-subunit and those that possess a glycosylated beta-subunit. Glycoprotein hormones are known to be elliptical molecules, and the beta-subunit oligosaccharides project outward from the short diameter, thereby increasing it. It is interesting to speculate that this change in shape might affect ultrafiltration rates, leading to differences in delivery rates to target tissues and elimination by filtration in the kidney.
Differential effects of Th1 and Th2 derived cytokines on NGF synthesis by mouse astrocytes (1996)

During the course of brain injury and inflammation there is an increased secretion of neurotrophic substances by astrocytes. We have examined the effect of the Th2-derived cytokine IL-10 and the Th1-derived cytokines Il-2 and IFN-gamma on the secretion of NGF by mouse astrocytes. IL-10 induced a dose-dependent increase in NGF secretion which was blocked by anti-IL-10 antibody. In contrast, the Th1-derived cytokines IFN-gamma and IL-2 did not induce NGF synthesis. Moreover, INF-gamma completely inhibited the increase in NGF secretion induced by IL-10 whereas it had no effect on the induction of NGF by TNF-alpha. These results indicate that IL-10 similarly to other Th2-derived cytokines may provide a neurotrophic support to injured neurons via the induction of NGF synthesis, whereas the Th1-derived cytokine IFN-gamma antagonizes this effect.
Properties of Osteoconductive Biomaterials: Calcium Phosphates (2002)

Bone is formed by a series of complex events involving the mineralization of extracellular matrix proteins rigidly orchestrated by cells with specific functions of maintaining the integrity of the bone. Bone, similar to other calcified tissues, is an intimate composite of the organic (collagen and noncollagenous proteins) and inorganic or mineral phases. The bone mineral idealized as calcium hydroxyapatite, Ca10 (PO4)(6)(OH)2, is a carbonatehydroxyapatite, approximated by the formula: (Ca,X)(10)(PO4,HPO4,CO3)(6)(OH,Y)2, where X are cations (magnesium, sodium, strontium ions) that can substitute for the calcium ions, and Y are anions (chloride or fluoride ions) that can substitute for the hydroxyl group. The current author presents a brief review of CaP biomaterials that now are used as grafts for bone repair, augmentation, or substitution. Commercially-available CaP biomaterials differ in origin (natural or synthetic), composition (hydroxyapatite, beta-tricalcium phosphate, and biphasic CaP), or physical forms (particulates, blocks, cements, coatings on metal implants, composites with polymers), and in physicochemical properties. CaP biomaterials have outstanding properties: similarity in composition to bone mineral; bioactivity (ability to form bone apatitelike material or carbonate hydroxyapatite on their surfaces), ability to promote cellular function and expression leading to formation of a uniquely strong bone-CaP biomaterial interface; and osteoconductivity (ability to provide the appropriate scaffold or template for bone formation). In addition, CaP biomaterials with appropriate three-dimensional geometry are able to bind and concentrate endogenous bone morphogenetic proteins in circulation, and may become osteoinductive (capable of osteogenesis), and can be effective carriers of bone cell seeds. Therefore, CaP biomaterials potentially are useful in tissue engineering for regeneration of hard tissues.
Human cytomegalovirus UL36-38 and US3 immediate-early genes: temporally regulated expression of nuclear, cytoplasmic, and polysome-associated transcripts during infection (1991)

During permissive in vitro infection, the human cytomegalovirus (HCMV) UL36-38 and US3 immediate-early (IE) regions give rise to multiple distinct species of RNA in a temporally regulated manner. We have compared the temporally regulated expression of the UL36-38 and US3 regions with that of the well-characterized major IE (MIE) region. Northern (RNA) blot hybridizations with antisense RNA probes were used to examine RNA isolated from infected cells at IE, early, and late times after infection and from cells infected in the presence of anisomycin (used to block de novo viral protein synthesis) or in the presence of phosphonoformate (used to block HCMV DNA synthesis). Different US3 region transcripts were expressed in the cytoplasm during the IE and late phases of infection, with kinetics similar to those of the MIE region. In contrast, various cytoplasmic transcripts from the UL36-38 region were expressed during each of the IE, early, and late phases of infection, including some expressed from IE through late times. The levels of steady-state RNA from the US3 and MIE regions were increased dramatically by infection in the presence of anisomycin, predominantly because of an increase in multiply spliced transcripts. Two of the three UL36-38 IE transcripts were largely unaffected by anisomycin and were expressed abundantly throughout infection, but a third, multiply spliced UL36-38 IE transcript was abundant only during infection in the presence of anisomycin. Nuclear, cytoplasmic, and polysome-associated transcripts from the three IE regions were not significantly different qualitatively or quantitatively. These results suggest that posttranscriptional controls at the levels of nuclear retention or polysome exclusion of transcripts are not operative for the IE region genes. Overall, these results indicate common features of expression of US3, MIE, and UL36-38, in addition to distinctive expression of the UL36-38 region during all temporal phases of expression.
Universal Amplification, Next-Generation Sequencing, and Assembly of HIV-1 Genomes (2012)

Whole HIV-1 genome sequences are pivotal for large-scale studies of inter- and intrahost evolution, including the acquisition of drug resistance mutations. The ability to rapidly and cost-effectively generate large numbers of HIV-1 genome sequences from different populations and geographical locations and determine the effect of minority genetic variants is, however, a limiting factor. Next-generation sequencing promises to bridge this gap but is hindered by the lack of methods for the enrichment of virus genomes across the phylogenetic breadth of HIV-1 and methods for the robust assembly of the virus genomes from short-read data. Here we report a method for the amplification, next-generation sequencing, and unbiased de novo assembly of HIV-1 genomes of groups M, N, and O, as well as recombinants, that does not require prior knowledge of the sequence or subtype. A sensitivity of at least 3,000 copies/ml was determined by using plasma virus samples of known copy numbers. We applied our novel method to compare the genome diversities of HIV-1 groups, subtypes, and genes. The highest level of diversity was found in the env, nef, vpr, tat, and rev genes and parts of the gag gene. Furthermore, we used our method to investigate mutations associated with HIV-1 drug resistance in clinical samples at the level of the complete genome. Drug resistance mutations were detected as both major variant and minor species. In conclusion, we demonstrate the feasibility of our method for large-scale HIV-1 genome sequencing. This will enable the phylogenetic and phylodynamic resolution of the ongoing pandemic and efficient monitoring of complex HIV-1 drug resistance genotypes.
Motion artifacts in MRI: A complex problem with many partial solutions (2015)

Subject motion during magnetic resonance imaging (MRI) has been problematic since its introduction as a clinical imaging modality. While sensitivity to particle motion or blood flow can be used to provide useful image contrast, bulk motion presents a considerable problem in the majority of clinical applications. It is one of the most frequent sources of artifacts. Over 30 years of research have produced numerous methods to mitigate or correct for motion artifacts, but no single method can be applied in all imaging situations. Instead, a "toolbox" of methods exists, where each tool is suitable for some tasks, but not for others. This article reviews the origins of motion artifacts and presents current mitigation and correction methods. In some imaging situations, the currently available motion correction tools are highly effective; in other cases, appropriate tools still need to be developed. It seems likely that this multifaceted approach will be what eventually solves the motion sensitivity problem in MRI, rather than a single solution that is effective in all situations. This review places a strong emphasis on explaining the physics behind the occurrence of such artifacts, with the aim of aiding artifact detection and mitigation in particular clinical situations.