gebhart/patrepeval huggingface dataset:
Preparing the wound bed 2003: focus on infection and inflammation. (2003)

Wound bed preparation is the promotion of wound closure through diagnosis of the cause, attention to patient-centered concerns, and correction of systemic and local factors that may delay healing. To enhance the evidence base that may be lacking, a review of relevant literature was conducted and combined with input from the International Wound Bed Preparation Advisory Board and the Canadian Chronic Wound Advisory Board to create an updated examination of practices. A template based on expert opinion of the clinical actions corresponding to each step in the paradigm of preparing the wound bed is presented and the effects of local factors (tissue debridement, infection or inflammation, moisture balance, and edge effect [TIME]) are discussed. This review differentiates increased bacterial burden/infection in the superficial and deep wound bed compartments from inflammation and provides a topical approach to treatment. Inflammatory conditions causing leg ulcers, including pyoderma gangrenosum and vasculitis are reviewed. The topical combination of silver with absorptive dressings has led to new therapeutic options for increased bacterial burden in the surface wound compartment. A compilation of the available systematic reviews for the treatment of infection has been included as a background for the expert opinion.
A hierarchy of invariant representations of 3D shape (2002)

The representation of geometrical 3D shape is discussed in this paper. A hierarchy of representations, which are invariant under weak perspective to either rigid or affine 3D transformations is described. These representations can be computed efficiently from a sequence of images with a linear and incremental algorithm. This hierarchy provides the means for adding a controlled amount of quantitative information to a symbolic representation. It also provides a library of representations, which may be used for different tasks (or purposes).< <ETX xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink">&gt;</ETX>
Analysis of established human carcinoma cell lines for lymphoreticular‐associated membrane receptors (1977)

Thirty-one different long-term established human carcinoma culture cell lines were examined for the presence or absence of receptors for the Fc portion of immunoglobulin G (IgG) ("Fc receptors"), the third component of complement (C3 receptors), sheep erythrocytes and mouse erythrocytes. Included in the catalogue of lines tested were adenocarcinoma of the adrenal cortex, colon, rectum, lung, liver, breast and kidney, and carcinomas of the uterine cervix, bladder and vulva. All lines were found to be consistently Fc receptor-negative, as assayed by rosette formation with sheep erythrocytes coated with subhemagglutinating amounts of anti-sheep erythrocyte antibodies, or bovine erythrocytes heavily coated with non-hemagglutinating anti-bovine erythrocyte antibodies. This is similar to results obtained with murine tumors: carcinomas are consistently Fc receptor-negative, while those lines which are Fc receptor-positive are invariably lymphoreticular in nature. The human carcinoma cell lines were also negative for complement (C3) receptors and spontaneous T and B rosette markers. It is proposed that, in most cases, rosette-forming cells found in primary human carcinomas are, as in the mouse or rat, representative of infiltrating non-malignant lymphoreticular cells.
Provable Methods for Training Neural Networks with Sparse Connectivity (2014)

We provide novel guaranteed approaches for training feedforward neural networks with sparse connectivity. We leverage on the techniques developed previously for learning linear networks and show that they can also be effectively adopted to learn non-linear networks. We operate on the moments involving label and the score function of the input, and show that their factorization provably yields the weight matrix of the first layer of a deep network under mild conditions. In practice, the output of our method can be employed as effective initializers for gradient descent.
Circadian Clock Mutants of Cyanobacteria (1994)

A diverse set of circadian clock mutants was isolated in a cyanobacterial strain that carries a bacterial luciferase reporter gene attached to a clock-controlled promoter. Among 150,000 clones of chemically mutagenized bioluminescent cells, 12 mutants were isolated that exhibit a broad spectrum of periods (between 16 and 60 hours), and 5 mutants were found that show a variety of unusual patterns, including arrhythmia. These mutations appear to be clock-specific. Moreover, it was demonstrated that in this cyanobacterium it is possible to clone mutant genes by complementation, which provides a means to genetically dissect the circadian mechanism.
High-speed, 100+W RF switches using GaAs MMICs (1992)

A low-loss, inductive gate bias network structure which allows a very high stacking level of FET devices for high-power RF switching applications is reported. The design, implementation, and performance of S- and C-band SPDT switches based on this structure are described. Multiple GaAs MMIC chips integrated into a suspended-substrate hybrid circuit are used. At S-band, switch risetimes/falltimes of less than 40 ns and an RF power handling capability of 300 W CW have been demonstrated. This input signal level could be maintained during the switch state transitions (hot-switching), while being switched between the two output ports at rates of up to 500 kHz.< <ETX xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink">&gt;</ETX>
The Escherichia coli MG1655 in silico metabolic genotype: Its definition, characteristics, and capabilities (2000)

The Escherichia coli MG1655 genome has been completely sequenced. The annotated sequence, biochemical information, and other information were used to reconstruct the E. coli metabolic map. The stoichiometric coefficients for each metabolic enzyme in the E. coli metabolic map were assembled to construct a genome-specific stoichiometric matrix. The E. coli stoichiometric matrix was used to define the system's characteristics and the capabilities of E. coli metabolism. The effects of gene deletions in the central metabolic pathways on the ability of the in silico metabolic network to support growth were assessed, and the in silico predictions were compared with experimental observations. It was shown that based on stoichiometric and capacity constraints the in silico analysis was able to qualitatively predict the growth potential of mutant strains in 86% of the cases examined. Herein, it is demonstrated that the synthesis of in silico metabolic genotypes based on genomic, biochemical, and strain-specific information is possible, and that systems analysis methods are available to analyze and interpret the metabolic phenotype.
Hormone Therapy Failure in Human Prostate Cancer: Analysis by Complementary DNA and Tissue Microarrays (1999)

The combination of cDNA and tissue microarray technologies enables rapid identification of genes associated with progression of prostate cancer to the hormone-refractory state and may facilitate analysis of the role of the encoded gene products in the pathogenesis of human prostate cancer.
Runx1 Controls Terminal Morphology and Mechanosensitivity of VGLUT3-expressing C-Mechanoreceptors (2013)

VGLUT3-expressing unmyelinated low-threshold mechanoreceptors (C-LTMRs) are proposed to mediate pleasant touch and/or pain, but the molecular programs controlling C-LTMR development are unknown. Here, we performed genetic fate mapping, showing that VGLUT3 lineage sensory neurons are divided into two groups, based on transient or persistent VGLUT3 expression. VGLUT3-transient neurons are large- or medium-diameter myelinated mechanoreceptors that form the Merkel cell-neurite complex. VGLUT3-persistent neurons are small-diameter unmyelinated neurons that are further divided into two subtypes: (1) tyrosine hydroxylase (TH)-positive C-LTMRs that form the longitudinal lanceolate endings around hairs, and (2) TH-negative neurons that form epidermal-free nerve endings. We then found that VGLUT3-persistent neurons express the runt domain transcription factor Runx1. Analyses of mice with a conditional knock-out of Runx1 in VGLUT3 lineage neurons demonstrate that Runx1 is pivotal to the development of VGLUT3-persistent neurons, such as the expression of VGLUT3 and TH and the formation of the longitudinal lanceolate endings. Furthermore, Runx1 is required to establish mechanosensitivity in C-LTMRs, by controlling the expression of the mechanically gated ion channel Piezo2. Surprisingly, both acute and chronic mechanical pain was largely unaffected in these Runx1 mutants. These findings appear to argue against the recently proposed role of VGLUT3 in C-LTMRs in mediating mechanical hypersensitivity induced by nerve injury or inflammation. Thus, our studies provide new insight into the genetic program controlling C-LTMR development and call for a revisit for the physiological functions of C-LTMRs.
Catalytic properties of the reverse transcriptases of human immunodeficiency viruses type 1 and type 2. (1991)

The enzyme reverse transcriptase (RT) is crucial in the early steps of the life cycle of retroviruses. We have expressed in bacteria the RTs from human immunodeficiency viruses (HIV) types 1 and 2 in order to study the structural-functional relationships of these two multifunctional enzymes that share a relatively high degree of amino acid sequence homology. For comparison purposes, we have analyzed several catalytic functions of both enzymes. The two HIV RTs show a high similarity in many aspects studied but exhibit profound differences in several other properties. For instance, the specific RNase H activity of HIV-2 RT is about 10 times lower than the corresponding activity of HIV-1 RT. There are also significant dissimilarities between some of the apparent Km values calculated for the DNA polymerizing functions of both enzymes. Furthermore, the heat stability of the DNA polymerizing activity of HIV-2 RT is about 15-fold higher than that of HIV-1 RT. On the other hand, the susceptibility of the RNase H activities of the two enzymes to heat inactivation was found to be similar. Other treatments also enable discrimination between the RNase H and DNA polymerizing catalytic properties of the two enzymes (although both reverse transcriptases respond similarily). Thus, the RNase H activity was inactivated by N-ethylmaleimide, suggesting the possible involvement of cysteine residues in performing this activity, whereas the DNA polymerizing functions of the two enzymes were fully resistant to this chemical modification. The zinc chelator 1,10-phenanthroline affected the DNA polymerase activities of both enzymes to a significantly higher extent than the RNase H activity. In all, the two HIV RTs were shown to be substantially different one from the other in several of their properties and also distinct from other RTs thus far studied.
Framework functionalisation triggers metal complex binding (2008)

Post-synthetic derivatisation of a porous material produces a functionalized material that binds the metal complex V(O)acac2, in contrast to the unfunctionalized precursor, which is inactive for complex binding.
Topography, Cell Response, and Nerve Regeneration (2010)

In the body, cells encounter a complex milieu of signals, including topographical cues, in the form of the physical features of their surrounding environment. Imposed topography can affect cells on surfaces by promoting adhesion, spreading, alignment, morphological changes, and changes in gene expression. Neural response to topography is complex, and it depends on the dimensions and shapes of physical features. Looking toward repair of nerve injuries, strategies are being explored to engineer guidance conduits with precise surface topographies. How neurons and other cell types sense and interpret topography remains to be fully elucidated. Studies reviewed here include those of topography on cellular organization and function as well as potential cellular mechanisms of response.
Context-sensitive synchronization-sensitive analysis is undecidable (2000)

Static program analysis is concerned with the computation of approximations of the runtime behavior of programs. Precise information about a program's runtime behavior is, in general, uncomputable for various different reasons, and each reason may necessitate making certain approximations in the information computed. This article illustrates one source of difficulty in static analysis of concurrent programs. Specifically, the article shows that an analysis that is simultaneously both context-sensitive and synchronization-sensitive (that is, a context-sensitive analysis that precisely takes into account the constraints on execution order imposed by the synchronization statements in the program) is impossible even for the simplest of analysis problems.
Localization of human eosinophil granule major basic protein, eosinophil cationic protein, and eosinophil-derived neurotoxin by immunoelectron microscopy. (1986)

By utilizing the colloidal gold particle technique, we localized eosinophil granule major basic protein, eosinophil cationic protein (ECP), and eosinophil-derived neurotoxin (EDN) in human nasal polyp sections by immunoelectron microscopy. Sections stained with affinity chromatography purified rabbit anti-human major basic protein, and subsequently with gold colloidal particle-goat anti-rabbit IgG, showed gold particles predominantly within granule cores, and not within other eosinophil organelles, plasma cells, mast cells, lymphocytes, or neutrophils. Sections stained with anti-ECP or anti-EDN showed gold particles concentrated over the granule matrix with fewer particles centrally. Control sections treated with preimmunization sera showed no staining of cells or organelles. These results verify the localization of major basic protein to the crystalloid core of the human eosinophil granule and show that ECP and EDN reside in the granule matrix. This technique provides a means of accurately locating the sites of major basic protein, ECP, and EDN deposition and thus of identifying eosinophil degranulation patterns in human disease.
In Vivo Role of p38 Mitogen-Activated Protein Kinase in Mediating the Anti-inflammatory Effects of CpG Oligodeoxynucleotide in Murine Asthma (2002)

DNA containing unmethylated CpG motifs is intrinsically immunostimulatory, inducing the production of a variety of cytokines and chemokines by immune cells. The strong Th1 response triggered by CpG oligodeoxynucleotide (ODN) inhibits the development of Th2-mediated allergic asthma in mice. This work documents that CpG ODN-induced IL-12 production plays a critical role in this process, because intrapulmonary CpG ODN inhibits allergic inflammation in wild-type but not IL-12(-/-) mice. CpG ODN rapidly localized to alveolar macrophages (AM), thereby triggering the phosphorylation of p38 mitogen-activated protein kinase (MAP kinase). AM cultured with CpG but not control ODN up-regulated IL-12 p40 expression and release, and these effects were blocked by the highly specific p38 MAP kinase inhibitor SB202190. Intrapulmonary administration of this inhibitor blocked the ability of CpG ODN to produce IL-12 in the lungs and reversed the anti-inflammatory effects of CpG ODN on allergic lung inflammation. These findings indicate that IL-12 production by AM is stimulated by intrapulmonary CpG ODN administration through a p38 MAP kinase-dependent process, and IL-12 is a key cytokine that mediates CpG ODN-induced protection against allergic lung inflammation.
Host Imprints on Bacterial Genomes—Rapid, Divergent Evolution in Individual Patients (2010)

Bacteria lose or gain genetic material and through selection, new variants become fixed in the population. Here we provide the first, genome-wide example of a single bacterial strain's evolution in different deliberately colonized patients and the surprising insight that hosts appear to personalize their microflora. By first obtaining the complete genome sequence of the prototype asymptomatic bacteriuria strain E. coli 83972 and then resequencing its descendants after therapeutic bladder colonization of different patients, we identified 34 mutations, which affected metabolic and virulence-related genes. Further transcriptome and proteome analysis proved that these genome changes altered bacterial gene expression resulting in unique adaptation patterns in each patient. Our results provide evidence that, in addition to stochastic events, adaptive bacterial evolution is driven by individual host environments. Ongoing loss of gene function supports the hypothesis that evolution towards commensalism rather than virulence is favored during asymptomatic bladder colonization.
Regulation of Murine Intestinal Inflammation by Reactive Metabolites of Oxygen and Nitrogen (2001)

Several reports have implicated reactive oxygen and nitrogen metabolites (RONS) in the initiation and/or progression of inflammatory bowel diseases (IBDs). We have investigated the role of three key RONS-metabolizing enzymes (inducible nitric oxide synthase [iNOS], superoxide dismutase [SOD], nicotinamide adenine dinucleotide phosphate [NADPH] oxidase) in a murine model of IBD. Mice genetically deficient ((-/-)) in either iNOS or the p47phox subunit of NADPH oxidase, transgenic (Tg) mice that overexpress SOD, and their respective wild-type (WT) littermates were fed dextran sulfate sodium (DSS) in drinking water for 7 days to induce colitis. In addition, the specific iNOS inhibitor 1400W was used in DSS-treated WT and p47phox(-/-) mice. WT mice responded to DSS feeding with progressive weight loss, bloody stools, elevated serum NO(X) and colonic mucosal injury with neutrophil infiltration. Both the onset and severity of colitis were significantly attenuated in iNOS(-/-) and 1400W-treated WT mice. While the responses to DSS did not differ between WT and p47phox(-/-) mice, enhanced protection was noted in 1400W-treated p47phox(-/-) mice. Interestingly, SOD(Tg) mice exhibited more severe colitis than their WT littermates. These findings reveal divergent roles for superoxide and iNOS-derived NO in intestinal inflammation.
Mechanisms for Electrical Degradation of GaN High-Electron Mobility Transistors (2006)

We have carried out systematic experiments of the electrical reliability of state-of-the-art GaN HEMTs. We have found that degradation is mostly driven by electric field and that there is a critical electric field below which negligible degradation is observed. Device degradation is associated with the appearance of prominent trapping behavior. Degradation is consistent with a model of defect formation in the AlGaN barrier as a result of the high electric field. We postulate that lattice defects are introduced by excessive stress associated with the inverse piezoelectric effect. Electron trapping at these defects reduces the extrinsic sheet carrier concentration and the maximum drain current
Different configurational states of beta-amyloid and their distributions relative to plaques and tangles in Alzheimer disease. (1990)

Antibodies have been raised against synthetic peptides corresponding to different parts of the beta-amyloid sequence. These antibodies stain different kinds of amyloid distributions in the hippocampal formation in Alzheimer disease, suggesting the existence of different states of aggregation and/or folding of beta-amyloid molecules. An antibody directed against the middle region of beta-amyloid stained mostly amyloid plaques without cores, whereas an antibody directed against the carboxyl-terminal region of beta-amyloid stained only amyloid plaques with cores. An antiserum directed against the amino terminus of beta-amyloid stained numerous tangle-bearing cells and bodies, as well as the neuritic component of plaques and neuropil threads. These antibodies, in conjunction with anti-tau antibodies, were used to demonstrate a close spatial relationship between amyloid deposits and neurofibrillary tangles.
α-Synuclein redistributes to neuromelanin lipid in the substantia nigra early in Parkinson's disease (2005)

The distribution and tempo of neuronal loss in Parkinson's disease correlates poorly with the characteristic and more widely spread intracellular changes associated with the disease process (Lewy bodies and Lewy neurites). To determine early intracellular changes in regions where cell loss is most marked (dopaminergic A9 substantia nigra) versus regions with Lewy bodies but where cell loss is limited, we assessed 13 patients with definite Parkinson's disease at various disease stages in comparison with controls. Using immunohistochemistry for alpha-synuclein, we confirmed the concentration of this protein in the soma of normal A9 neurons and in Lewy body pathology in brainstem catecholamine neurons in Parkinson's disease. Analysis of the degree of cell loss in brainstem catecholamine cell groups revealed that only the A9 substantia nigra had consistent significant cell loss early in the disease course with greater A9 cell loss correlating with increasing disease duration. To assess the earliest intracellular changes differentiating neurons more likely to degenerate, pigmented A9 and A10 neurons with and without obvious pathology were targeted, cell size and pigment density measured, and intracellular changes in alpha-synuclein location and lipid components analysed at both the light and electron microscope levels. There were no changes observed in healthy A10 neurons in Parkinson's disease compared with controls. Pigmented A9 neurons in later stages of degeneration with obvious Lewy body formation had a significant reduction in intracellular pigment, as previously described. In contrast, A9 neurons of normal morphological appearance and no characteristic pathology in Parkinson's disease exhibited significantly increased pigment density associated with a concentration of alpha-synuclein to the lipid component of the pigment and a loss of associated cholesterol. These changes in vulnerable but apparently healthy A9 neurons occurred without any change in cell size or in the amount of intracellular pigment compared with controls. The increase in pigment density is consistent with previously reported increases associated with oxidation and iron loading, reactions known to precipitate alpha-synuclein. The selectivity of the changes observed in A9 nigral neurons suggests that these early intracellular changes predispose these neurons to more rapid cell loss in Parkinson's disease. The increased concentration of neuronal alpha-synuclein and pigment in normal A9 neurons may already predispose these neurons to precipitate alpha-synuclein around pigment-associated lipid under oxidative conditions. Overall, these changes may trigger a cascade of events leading to larger intracellular aggregates of alpha-synuclein and the dispersement of protective pigment to precipitate cell death in Parkinson's disease.
Tunable Coupling of Superconducting Qubits (2003)

We study an LC circuit implemented using a current-biased Josephson junction (CBJJ) as a tunable coupler for superconducting qubits. By modulating the bias current, the junction can be tuned in and out of resonance and entangled with the qubits coupled to it. One can thus implement two-qubit operations by mediating entanglement. We consider the examples of CBJJ and charge-phase qubits. A simple recoupling scheme leads to a generalization to arbitrary qubit designs.