gebhart/patrepeval huggingface dataset:
Overexpression of a Na + /H + antiporter confers salt tolerance on a freshwater cyanobacterium, making it capable of growth in sea water (2002)

The salt tolerance of a freshwater cyanobacterium, Synechococcus sp. PCC 7942, transformed with genes involved in the synthesis of a Na(+)/H(+) antiporter, betaine, catalase, and a chaperone was examined. Compared with the expression of betaine, catalase, and the chaperone, the expression of the Na(+)/H(+) antiporter gene from a halotolerant cyanobacterium (ApNhaP) drastically improved the salt tolerance of the freshwater cyanobacterium. The Synechococcus cells expressing ApNhaP could grow in BG11 medium containing 0.5 M NaCl as well as in sea water, whereas those expressing betaine, catalase, and the chaperone could not grow under those conditions. The coexpression of ApNhaP with catalase or ApNhaP with catalase and betaine did not further enhance the salt tolerance of Synechococcus cells expressing ApNhaP alone when grown in BG11 medium containing 0.5 M NaCl. Interestingly, the coexpression of ApNhaP with catalase resulted in enhanced salt tolerance of cells grown in sea water. These results demonstrate a key role of sodium ion exclusion by the Na(+)/H(+) antiporter for the salt tolerance of photosynthetic organisms.
Principles of color technology (1981)

Second edition of a standard work covering all the major advances in colour applied to the use of colorants in the industrial and creative production of coloured materials. Emphasis has been put on new developments including more extensive coverage of: metamerism; non-colour problems - quality control, techniques of sampling and sample preparation, and application of simple statistics; methods of instrument selection. Besides the book covers fundamentals such as the role of light, description of colour in objective, numerical terms and practical industrial applications of colour technology. -- ICCROM
Proinflammatory cytokine expression profile in degenerated and herniated human intervertebral disc tissues (2010)

Greater IFNgamma positivity, macrophage presence, and cellularity in herniated IVDs suggests a pattern of Th1 lymphocyte activation in this pathology. Remarkable pathologic IVD tissue expression of IL-17 is a novel finding that contrasts markedly with low levels of IL-17 in autopsy control tissue. These findings suggest involvement of Th17 lymphocytes in the pathomechanism of disc degeneration.
Chemokine Receptor Ccr2 Deficiency Reduces Renal Disease and Prolongs Survival in MRL/lpr Lupus-Prone Mice (2005)

MRL/MpJ-Fas(lpr)/J (MRL/lpr) mice represent a well-established mouse model of human systemic lupus erythematosus. MRL/lpr mice homozygous for the spontaneous lymphoproliferation mutation (lpr) are characterized by systemic autoimmunity, massive lymphadenopathy associated with proliferation of aberrant T cells, splenomegaly, hypergammaglobulinemia, arthritis, and fatal immune complex-mediated glomerulonephritis. It was reported previously that steady-state mRNA levels for the chemokine (C-C motif) receptor 2 (Ccr2) continuously increase in kidneys of MRL/lpr mice. For examining the role of Ccr2 for development and progression of immune complex-mediated glomerulonephritis, Ccr2-deficient mice were generated and backcrossed onto the MRL/lpr genetic background. Ccr2-deficient MRL/lpr mice developed less lymphadenopathy, had less proteinuria, had reduced lesion scores, and had less infiltration by T cells and macrophages in the glomerular and tubulointerstitial compartment. Ccr2-deficient MRL/lpr mice survived significantly longer than MRL/lpr wild-type mice despite similar levels of circulating immunoglobulins and comparable immune complex depositions in the glomeruli of both groups. Anti-dsDNA antibody levels, however, were reduced in the absence of Ccr2. The frequency of CD8+ T cells in peripheral blood was significantly lower in Ccr2-deficient MRL/lpr mice. Thus Ccr2 deficiency influenced not only monocyte/macrophage and T cell infiltration in the kidney but also the systemic T cell response in MRL/lpr mice. These data suggest an important role for Ccr2 both in the general development of autoimmunity and in the renal involvement of the lupus-like disease. These results identify Ccr2 as an additional possible target for the treatment of lupus nephritis.
SuperBook (1987)

The goals and methods of the text browser, SuperBook, are compared with those of hypertext systems in general. SuperBook, intended to provide improved access to text existing in electronic form, employs cognitive tools arising from human computer interaction research, such as full-text indexing, adaptive aliasing, and dynamic views of hierarchical information. Superbook automatically preprocesses on-line text written for paper publication, and produces a multi-window display, including a dynamic table of contents, pages of text, and a history of search words. Although SuperBook and hypertext share common goals of improved search and navigation, SuperBook is designed for accessing existing documents while most hypertext systems are better suited for authoring new information structures. Further studies are needed to evaluate the effectiveness of each of these kinds of systems.
Classification of Intrinsically Disordered Regions and Proteins (2014)

Characterization of unannotated and uncharacterized protein segments is expected to lead to the discovery of novel functions as well as provide important insights into existing biological processes. In addition, it is likely to shed new light on molecular mechanisms of diseases that are not yet fully understood. The classical concept implies that protein sequence defines structure, which in turn determines function; that is, function can be inferred from the sequence and its structure. Even when protein sequences diverge during evolution, for example, after gene duplication, the overall fold of their structures remains roughly the same. Therefore, structural similarity between proteins can reveal distant evolutionary relationships that are not easily detectable using sequence-based methods.
INTERLEUKIN-6 (IL-6) INDUCES THE PROLIFERATION OF SYNOVIAL FIBROBLASTIC CELLS IN THE PRESENCE OF SOLUBLE IL-6 RECEPTOR (1995)

A number of investigators have reported that there are detectably elevated levels of interleukin-6 (IL-6) and soluble IL-6 receptor (sIL-6R) in the synovial fluids of rheumatoid arthritis (RA) patients. However, the precise role of IL-6 and sIL-6R in the pathogenesis of RA remains unclear. In the present study we examined whether IL-6 and/or sIL-6R could induce the proliferation of synovial fibroblastic cells (SFC) obtained from a RA patient. Co-existence of IL-6 and sIL-6R induced SFC proliferation without needing any further stimulation. This proliferation was completely blocked by either anti-IL-6 or anti-sIL-6 antibody. In contrast, neither IL-6 nor sIL-6R alone induced SFC proliferation. Although sIL-6R alone could not induce SFC proliferation, it did however augment IL-1 beta-induced SFC proliferation in a dose-dependent manner, but not tumour necrosis factor alpha-, platelet-derived growth factor-AB- or b-fibroblast growth factor-induced proliferation. This augmentation was completely neutralized by the addition of anti-IL-6 or anti-sIL-6R antibodies. This may be explained by the fact that an amount of IL-6 sufficient to induce SFC proliferation in the presence of sIL-6R was found to be detectable in the IL-1 beta-stimulated-culture supernatant. This evidence suggests that IL-6 is very likely to be involved in synovial cell proliferation in the synovium of RA patients in co-operation with sIL-6R.
The permeability of the wall fabric of Escherichia coli and Bacillus subtilis (1996)

To study the overall structure of the peptidoglycan fabric of the sacculi of gram-negative and gram-positive walls, actively growing cultures of Escherichia coli and Bacillus subtilis were treated with boiling sodium dodecyl sulfate solutions. The sacculi were then treated with enzymes to eliminate proteins and nucleic acids. These intact saccoli were probed with fluorescein-labeled dextrans with a range of known molecular weights. The penetration of the probes could be monitored by the negative-staining appearance in the fluorescence microscope. At several chosen times, the molecular weight fraction that allowed barely observable entry of the fluorescein-labeled probe and the molecular weight fraction that penetrated to achieve almost, but not quite, the concentration of probe in the solution external to the sacculi were determined. From three pairs of times and molecular weights that met one or the other of these two criteria, the effective pore size could be calculated. The minimum size of protein molecule that could diffuse through the pores was also calculated. Two mathematical models, which gave essentially the same results, were used to interpret the experimental data: one for the permeation of random coils through a surface containing holes and the other for rigid spheres diffusing through water-filled cylindrical pores. The mean estimate of the effective hole radius in walls from E. coli is 2.06 nm, and that of the effective hole size in walls from B. subtilis is 2.12 nm. These results are supported by experiments in which the loss of preloaded cells was monitored. Various fluorescein-labeled dextran samples were mixed with samples of intact cell walls, held for a long time, and then diluted. The efflux of the dextrans was monitored. Neither large nor small dextrans stained under these conditions. Only with dextran samples of a sufficiently small size were the sacculi filled during the preincubation period, and only with the largest of these could the probe not escape quickly. From the pore (or mesh) size, it can be concluded that the wall fabric of both organisms has few imperfections and that the major passageway is through the smallest possible pore, or "tessera," formed by the maximal cross-linking of the peptides from glycan chain to glycan chain compatible with the degree of rotational flexibility of the chains of repeating disaccharides of N-acetyl muramic acid and N-acetyl glucosamine. A tessera is composed of two chains of eight saccharides cross-linked by two octapeptides. The size of a globular hydrophilic molecule, if it did not bind to wall components, that could pass freely through the meshwork of an unstretched sacculus of either organism is roughly 25 kDa. We stress that this is only a rough estimate, and it may be possible for proteins of less than 50 kDa to pass through the native wall during normal growth conditions.
Alterations of the blood‐brain barrier after transplantation of autonomic ganglia into the mammalian central nervous system (1986)

Abstract Autonomic (superior cervical) ganglia, the vessels of which are freely permeable to macromolecules, from mature rat donors (allografts or autografts) were transplanted to different sites in the central nervous system (CNS). Minimal trauma was caused by grafts into the IVth ventricle while grafts to intraparenchymal locations such as cerebral cortex and spinal cord were necessarily traumatic and produced glial scarring. Postoperative periods were between 4 weeks and 30 months. A potentially significant aspect of neural transplantation is the functional vascular connections between host and graft. It is highly likely that grafting procedures alter the bloodbrain barrier (BBB) in the recipient brain. In order to determine permanent BBB changes, the glycoprotein horseradish peroxidase (HRP) (M.W. 40,000) was injected intravascularly for circulation periods ranging between 50 seconds and 90 minutes. Protein exudatation was monitored by using the chromagens DAB and the highly sensitive TMB. All autonomic ganglia transplants, regardless of postoperative or HRP circulation times, were permeable to the injected protein; no qualitative differences were found between allografts and autografts. The blood‐borne protein traversed the autonomic graft and infiltrated into the host brain for distances between 200 μm in intraparenchymal grafts to over 1 mm in intraventricular grafts; a smaller exudate was found in the intraparenchymal model than in the intraventricular site probably due to glial scarring, that impeded the protein movement in the interstitial spaces. Significantly, TMB demonstrated that the systemic protein entered the cerebrospinal fluid. HRP was detected on the ventricular floor and in the perivascular spaces of the microvasculature. Transplantation of an autonomic ganglion into the brain provides a biological portal that bypasses normal barriers to macromolecules. The vascular and extracellular confluences between host and graft could provide direct access for systemically administered substances to enter brain regions where they, normally, would be excluded.
Synphilin-1 is present in Lewy bodies in Parkinson's disease (2000)

Alpha-synuclein is believed to play an important role in Parkinson's disease (PD). Mutations in the alpha-synuclein gene are responsible for familial forms of PD and alpha-synuclein protein is a major component of Lewy bodies in patients with sporadic PD. Synphilin-1 is a novel protein that we have previously found to associate in vivo with alpha-synuclein. We now show that synphilin-1 is present in Lewy bodies of patients with PD. Our data suggest that synphilin-1 could play a role in Lewy body formation and the pathogenesis of PD.
Distinct genomic copy number in mitochondria of different mammalian organs (1990)

This study shows that mitochondria in liver, kidney, heart, and brain of the mouse have a distinct mitochondrial density. It also demonstrates that the mtDNA copy number per mitochondrion is organ-specific. A reliable method of determining mitochondrial density per organ is by stereological analysis of tissue sections while mtDNA quantitation is by the use of radiolabelled mtDNA probe. This is the first study in which a comprehensive examination of mitochondrial density and quantitation of mitochondrial genomes in mouse organs have been done. In summary the variability is not only in mitochondrial density but also in genomic copy number in mitochondria of various tissues.
Single Molecule Detection of Glycosaminoglycan Hyaluronic Acid Oligosaccharides and Depolymerization Enzyme Activity Using a Protein Nanopore (2012)

Glycosaminoglycans are biologically active anionic carbohydrates that are among the most challenging biopolymers with regards to their structural analysis and functional assessment. The potential of newly introduced biosensors using protein nanopores that have been mainly described for nucleic acids and protein analysis to date, has been here applied to this polysaccharide-based third class of bioactive biopolymer. This nanopore approach has been harnessed in this study to analyze the hyaluronic acid glycosamiglycan and its depolymerization-derived oligosaccharides. The translocation of a glycosaminoglycan is reported using aerolysin protein nanopore. Nanopore translocation of hyaluronic acid oligosaccharides was evidenced by the direct detection of translocated molecules accumulated into the arrival compartment using high-resolution mass spectrometry. Anionic oligosaccharides of various polymerization degrees were discriminated through measurement of the dwelling time and translocation frequency. This molecular sizing capability of the protein nanopore device allowed the real-time recording of the enzymatic cleavage of hyaluronic acid polysaccharide. The time-resolved detection of enzymatically produced oligosaccharides was carried out to monitor the depolymerization enzyme reaction at the single-molecule level.
The inhibition of lysyl oxidase in vivo by isoniazid and its reversal by pyridoxal. Effect on collagen cross-linking in the chick embryo (1984)

Isonicotinic acid hydrazide (isoniazid) causes a large increase in the salt-solubility of collagen when injected into chick embryos; this change is accompanied by the inactivation of lysyl oxidase (EC 1.4.3.13), the enzyme responsible for initiating cross-link formation in collagen and elastin. In addition, isoniazid markedly decreases the liver content of pyridoxal phosphate. The depletion of pyridoxal phosphate takes approx. 6 h, whereas the inhibition of lysyl oxidase and the increase in collagen solubility occur more slowly. A reversal of these effects of isoniazid can be produced by the subsequent injection of a stoichiometric amount of pyridoxal, supporting the role of pyridoxal as a cofactor for lysyl oxidase. Treatment of chick embryos with beta-aminopropionitrile, an irreversible inhibitor of lysyl oxidase, causes an inhibition of the enzyme, which begins to recover within 24 h but which is not affected by the administration of pyridoxal; with isoniazid inhibition, however, lysyl oxidase activity does not show any sign of recovery by 48 h. It is proposed that isoniazid may cause the inhibition of lysyl oxidase by competing for its obligatory cofactor, pyridoxal phosphate. The potential clinical implications in the therapeutic control of fibrosis are briefly discussed.
Vascular damage from smoking: disease mechanisms at the arterial wall (1998)

The products of tobacco combustion are absorbed into the systemic circulation. Absorbed nicotine stimulates the release of catecholamines, whilst other products (perhaps including nicotine) injure the arterial endothelium and promote atherogenesis. Free radicals and aromatic compounds diminish the endothelial synthesis of nitric oxide, causing impaired endothelium-dependent relaxation of arteries, the earliest clinical sign of endothelial dysfunction. Smoking alters the shear forces and rheology at the endothelial surface and these changes enhance the effects of products of tobacco combustion to upregulate leucocyte adhesion molecules on the endothelial surface. The increased oxidation of low density lipoprotein (LDL) in smokers has synergistic effects to promote monocyte adhesion and monocyte migration into the subintimal space. Continued stimulation of intimal cells by oxidized LDL leads to the development of atherosclerosis. Many of these effects are ameliorated by high concentrations of vitamin C. Smoking also potentiates thrombosis at the dysfunctional endothelium by increasing the concentration of plasma fibrinogen and altering the activity of platelets. All these proatherogenic effects of smoking to injure the endothelium also are observed, albeit to lesser extent, in passive smokers.
Introduction (1999)

The idea for this book arose from an international research symposium of the same title which took place at Middlesex Business School in January 1998. The symposium was created so that academics specialising in this field could meet and discuss their work in specific terms as well as debating broader yet related issues such as the use of methodologies and research design, and the problems and politics surrounding research efforts in health care. Rarely are such opportunities available within many of the mainstream management conferences that this group may contribute to, and one outcome is that further such opportunities are now planned for the future.
AIDS and Homophobia: A Perspective for AIDS Educators. (1989)

Many health professionals have been known to refer to AIDS as affecting only those in high risk groups, comprised of gay men and intravenous drug users: Those other poor, innocent people (hemophiliacs, newborns) they were just minding their own business when they got what the homosexuals and IV drug users got. AIDS is never simply discussed as a medical condition caused by a virus. It is almost always discussed as a valueladen human condition. Is there an AIDS educator out there who has
Differential mitochondrial distribution in human pronuclear embryos leads to disproportionate inheritance between blastomeres: relationship to microtubular organization, ATP content and competence (2000)

It has been suggested that mitochondrial DNA defects that effect metabolic capacity may be a proximal cause of failures in oocyte maturation, fertilization, or early embryonic development. Here, the distribution of mitochondria was examined by scanning laser confocal microscopy in living human pronuclear oocytes and cleavage stage embryos, followed either by measurements of the net ATP content of individual blastomeres or anti-tubulin immunofluorescence to determine the relationship between mitochondrial distribution and microtubular organization. The results indicate that specific patterns of perinuclear mitochondrial aggregation and microtubular organization are related, and that asymmetrical mitochondrial distributions at the pronuclear stage can result in some proportion of blastomeres with reduced mitochondrial inheritance and diminished ATP generating capacity. While the inability to divide appears to be a development consequence for an affected blastomere, for the embryo, reduced competence may occur during cleavage if several blastomeres inherit a mitochondrial complement inadequate to support normal cellular functions. The findings provide a possible epigenetic explanation for the variable developmental ability expressed within cohorts of morphologically normal early cleavage stage human embryos obtained by in-vitro fertilization.
VASE-encoded peptide modifies NCAM- and L1-mediated neurite outgrowth (1997)

Interactions between the neural cell adhesion molecule (NCAM) with NCAM-expressing neurons (trans-interaction) stimulate outgrowth of neurites. The extent of NCAM-triggered neurite outgrowth depends on the presence of 10 amino acids derived from the variable alternatively spliced exon (VASE or pi-exon) in the fourth immunoglobulin-like domain of NCAM (Ig4): NCAM with VASE reduces and without VASE enhances neurite outgrowth in cis- or trans-interaction. We have investigated the role of VASE in neurite outgrowth by characterizing the receptors at the cell surface of cultured cerebellar neurons. Results from experiments with L1 and NCAM antibodies and with cerebellar neurons derived from wild-type or NCAM-deficient mice show that substrate-coated Ig4 with VASE (Ig4+) or without VASE (Ig4-) stimulates neurite outgrowth by a trans-interaction with L1 and that Ig4- promotes neurite outgrowth more strongly than Ig4+ by a transinteraction with NCAM.
Quantum Optics with Superconducting Circuits: From Single Photons to Schrodinger Cats (2013)

Over the last decade and a half, superconducting circuits have advanced to the point where we can generate and detect highly-entangled states, and perform universal quantum gates. Meanwhile, the coherence properties of these systems have improved more than 10,000-fold. I will describe recent experiments, such as the latest advance in coherence using a three-dimensional implementation of qubits interacting with microwave cavities, called “3D circuit QED.” The control and strong interactions possible in superconducting circuits make it possible to generate non-classical states of light, including large superpositions known as “Schrodinger cat” states. This field has many interesting prospects both for applications in quantum information processing, and fundamental investigations of the boundary between the macroscopic classical world and the microscopic world of the quantum.