gebhart/patrepeval huggingface dataset:
Development of a Simple, Noninvasive, Clinically Relevant Model of Pressure Ulcers in the Mouse (2004)

The formation of pressure ulcers and other skin wounds is considered to be a multifactorial process. Cycles of ischemia-reperfusion have been considered to be significant contributing factors in the pathogenesis of pressure ulcers. This study reports the development of a reproducible murine model of ischemia-reperfusion injury by the external application of magnets. Mice were sedated with 50% CO2:50% O2 for 50-60 s. Dorsal hair was shaved and the area cleaned. The skin was gently pulled and placed between two round ceramic magnetic plates (5 x 12 mm diameter, 2.4 g weight, 1000 G magnetic force). The resultant "pinch" procedure was designed to leave a 5-mm skin bridge between the magnets, creating 50 mm Hg pressure between the plates. Three 12-h ischemia-reperfusion cycles were employed to cause pressure ulcer formation. Animals tolerated the procedure well. They returned to normal activity a few minutes after magnet placement. The lesions reached their maximum at 10 days postinjury. Full-thickness skin loss with damage and necrosis of subcutaneous tissue (ulcer stage 3) was observed in all cases, reaching a mean stage score of 3.6 +/- 0.6 of based on a 0-5 scale for extent of injury by visual assessment. Thus, an inexpensive, reproducible murine pressure ulcer model was developed, which results in graded injury without long-term immobilization of the animals. This method will facilitate the development of new prevention and management strategies.
New classification of acute myeloid leukemia and precursor-related neoplasms: changes and unsolved issues. (2010)

The World Health Organization (WHO) classification of lympho-hematopoietic neoplasms is increasingly based on genetic criteria. Here, we focus on changes that, as compared to the 2001 edition, were introduced into the 2008 WHO classification of acute myeloid leukemia (AML) and related precursor neoplasms. The category of AML with recurrent genetic abnormalities was expanded to account for 60% of AML by adding three distinct entities, i.e., AML with t(6,9), inv(3), or t(1;22), and two provisional entities, i.e., AML with mutated NPM1 or CEBPA. These changes have greatly modified the approaches to diagnosis and prognostic stratification of AML patients. To emphasize the need of various parameters for diagnosis, including myelodysplasia (MD)-related cytogenetic abnormalities, history of myelodysplasia or myelodysplasia/myeloproliferative neoplasm, and multilineage dysplasia, the category of "AML with multilineage dysplasia" was re-named AML with MD-related changes. Finally, we describe the unique characteristics of myeloid proliferations associated with Down syndrome and blastic plasmacytoid dendritic cell neoplasm.
Optically Modulated Probe for Precision Near-Field Measurements (2010)

In this paper, the design and implementation of an accurate, sensitive, and cost-effective near-field (NF) probe are discussed. The probe is based on the modulated scatterer technique (MST), providing very low perturbation on the field to be measured. It consists of a commercial off-the-shelf (COTS) photodiode chip and an antenna acting as a scatterer. The optically modulated scatterer (OMS) essentially makes the NF measurements perturbation free. A matching network is added to the probe structure to increase its sensitivity. The radiation characteristics of the probe, including cross-polarization response and omnidirectional sensitivity, are both theoretically and experimentally investigated. Finally, the performance and reliability of the probe are studied by comparing the measured NF distributions to the simulated distributions.
Abnormal dendritic spines in fragile X knockout mice: Maturation and pruning deficits (1997)

Fragile X syndrome arises from blocked expression of the fragile X mental retardation protein (FMRP). Golgi-impregnated mature cerebral cortex from fragile X patients exhibits long, thin, tortuous postsynaptic spines resembling spines observed during normal early neocortical development. Here we describe dendritic spines in Golgi-impregnated cerebral cortex of transgenic fragile X gene (Fmr1) knockout mice that lack expression of the protein. Dendritic spines on apical dendrites of layer V pyramidal cells in occipital cortex of fragile X knockout mice were longer than those in wild-type mice and were often thin and tortuous, paralleling the human syndrome and suggesting that FMRP expression is required for normal spine morphological development. Moreover, spine density along the apical dendrite was greater in the knockout mice, which may reflect impaired developmental organizational processes of synapse stabilization and elimination or pruning.
Management of membranoproliferative glomerulonephritis type II with plasmapheresis (2002)

Membranoproliferative glomerulonephritis type II (MPGN II) is a rare kidney disease identified microscopically by electron-dense deposits surrounded by complement component C3 in glomerular basement membranes. MPGN II usually leads to renal failure, and patients with MPGN II experience a high rate of recurrence following renal transplantation. No treatment modalities have been proven successful if recurrence does occur. The sera of most patients with MPGN II contain complement C3 nephritic factor (C3NF), an IgG autoantibody directed against C3 convertase (C3bBb) that results in constitutive breakdown of C3. C3NF may be important in the pathogenesis of the disease. Since C3NF is IgG, we predicted that C3NF could be removed from the serum through plasmapheresis. We describe the use of long-term plasmapheresis to maintain good renal function in a 15-year-old girl with rapidly progressive recurrent MPGN II. After 73 plasmapheresis procedures over 63 weeks, her serum creatinine remained stable, and her creatinine clearance trended upward. Serial biopsies of the transplanted kidney demonstrated persistent MPGN II but no development of tubular atrophy. During the course of therapy, serum C3NF activity decreased; furthermore, C3NF activity was detected in the removed plasma. We have shown that plasmapheresis is a safe and effective method for delaying the onset of chronic renal failure in recurrent MPGN II. The efficacy may be due to the removal of serum C3NF.
Improving security using extensible lightweight static analysis (2002)

Most security attacks exploit instances of well-known classes of implementation flaws. Developers could detect and eliminate many of these flaws before deploying the software, yet these problems persist with disturbing frequency-not because the security community doesn't sufficiently understand them but because techniques for preventing them have not been integrated into the software development process. This article describes an extensible tool that uses lightweight static analysis to detect common security vulnerabilities (including buffer overflows and format string vulnerabilities).
Anti-viral immunity induced by recombinant nucleoprotein of influenza A virus. III. Delivery of recombinant nucleoprotein to the immune system using attenuated Salmonella typhimurium as a live carrier. (1990)

A plasmid encoding the influenza nucleoprotein gene from A/NT/60/68 virus was transduced into the attenuated Salmonella typhimurium aroA- strain SL3261. The bacterial vector expressing the viral gene product was able to induce both humoral and cell-mediated immune responses to the nucleoprotein antigen. CD4+ virus-specific T cells capable of proliferation were readily induced and, in some circumstances, class II major histocompatibility complex (MHC)-restricted cytotoxicity was detected. However, virus-specific class I MHC-restricted cytotoxic T lymphocytes (CTL) were not detected after such immunization. Mice immunized orally with the nucleoprotein-expressing bacteria mounted a strong anti-viral antibody response and spleen cells from such mice proliferated specifically to virus challenge in vitro, producing interferon-gamma (IFN-gamma) and interleukin-2 (IL-2). Orally immunized mice showed significant protection from challenge infection with influenza virus if the mice were also boosted intranasally before infection.
BMP4 induction of sensory neurons from human embryonic stem cells and reinnervation of sensory epithelium (2007)

In mammals, hair cells and auditory neurons lack the capacity to regenerate, and damage to either cell type can result in hearing loss. Replacement cells for regeneration could potentially be made by directed differentiation of human embryonic stem (hES) cells. To generate sensory neurons from hES cells, neural progenitors were first made by suspension culture of hES cells in a defined medium. The cells were positive for nestin, a neural progenitor marker, and Pax2, a marker for cranial placodes, and were negative for alpha-fetoprotein, an endoderm marker. The precursor cells could be expanded in vitro in fibroblast growth factor (FGF)-2. Neurons and glial cells were found after differentiation of the neural progenitors by removal of FGF-2, but evaluation of neuronal markers indicated insignificant production of sensory neurons. Addition of bone morphogenetic protein 4 (BMP4) to neural progenitors upon removal of FGF-2, however, induced significant numbers of neurons that were positive for markers associated with cranial placodes and neural crest, the sources of sensory neurons in the embryo. Neuronal processes from hES cell-derived neurons made contacts with hair cells in denervated ex vivo sensory epithelia and expressed synaptic markers, suggesting the formation of synapses. In a gerbil model with a denervated cochlea, the ES cell-derived neurons engrafted in the auditory nerve trunk and sent out neurites that grew toward the auditory sensory epithelium. These data indicate that hES cells can be induced to form sensory neurons that have the potential to treat neural degeneration associated with sensorineural hearing loss.
Nitrogen Fixation in Wheat Provided by Klebsiella pneumoniae 342 (2004)

In this report, all of the criteria necessary for the demonstration of nitrogen fixation in wheat (Triticum aestivum L.), the world's most important crop, are shown upon inoculation with a nitrogen-fixing bacterium, Klebsiella pneumoniae 342 (Kp342). Kp342 relieved nitrogen (N) deficiency symptoms and increased total N and N concentration in the plant. Nitrogen fixation was confirmed by 15N isotope dilution in the plant tissue and in a plant product, chlorophyll. All of these observations were in contrast to uninoculated plants, plants inoculated with a nitrogen-fixing mutant of Kp342, and plants inoculated with dead Kp342 cells. Nitrogenase reductase was produced by Kp342 in the intercellular space of the root cortex. Wild-type Kp342 and the nifH mutant colonized the interior of wheat roots in equal numbers on a fresh weight basis. The nitrogen fixation phenotype described here was specific to cv. Trenton. Inoculation of cvs. Russ or Stoa with Kp342 resulted in no relief of nitrogen deficiency symptoms.
Plasmid Localization and Organization of Melamine Degradation Genes in Rhodococcus sp. Strain Mel (2011)

Rhodococcus sp. strain Mel was isolated from soil by enrichment and grew in minimal medium with melamine as the sole N source with a doubling time of 3.5 h. Stoichiometry studies showed that all six nitrogen atoms of melamine were assimilated. The genome was sequenced by Roche 454 pyrosequencing to 13× coverage, and a 22.3-kb DNA region was found to contain a homolog to the melamine deaminase gene trzA. Mutagenesis studies showed that the cyanuric acid hydrolase and biuret hydrolase genes were clustered together on a different 17.9-kb contig. Curing and gene transfer studies indicated that 4 of 6 genes required for the complete degradation of melamine were located on an ∼265-kb self-transmissible linear plasmid (pMel2), but this plasmid was not required for ammeline deamination. The Rhodococcus sp. strain Mel melamine metabolic pathway genes were located in at least three noncontiguous regions of the genome, and the plasmid-borne genes encoding enzymes for melamine metabolism were likely recently acquired.
Tonic Control of Peripheral Cutaneous Nociceptors by Somatostatin Receptors (2001)

The peptide somatostatin [somatotropin release-inhibiting factor (SRIF)] is widely distributed in the body and exerts a variety of hormonal and neural actions. Several lines of evidence indicate that SRIF is important in nociceptive processing: (1) it is localized in a subset of small-diameter dorsal root ganglion cells; (2) activation of SRIF receptors results in inhibition of both nociceptive behaviors in animals and acute and chronic pain in humans; (3) SRIF inhibits dorsal horn neuronal activity; and (4) SRIF reduces responses of joint mechanoreceptors to noxious rotation of the knee joint. The goal of the present study is to show that cutaneous nociceptors are under the tonic inhibitory control of SRIF. This is accomplished using behavioral and electrophysiological paradigms. In a dose-dependent manner, intraplantar injection of the SRIF receptor antagonist cyclo-somatostatin (c-SOM) results in nociceptive behaviors in normal animals and enhancement of nociceptive behaviors in formalin-injected animals, and these actions can be blocked when c-SOM is coapplied with three different SRIF agonists. Furthermore, intraplantar injection of SRIF antiserum also results in nociceptive behaviors. Electrophysiological recordings using an in vitro glabrous skin-nerve preparation show increased nociceptor activity in response to c-SOM, and this increase is blocked by the same three SRIF agonists. Parallel behavioral and electrophysiological studies using the opioid antagonist naloxone demonstrate that endogenous opioids do not maintain a tonic inhibitory control over peripheral nociceptors, nor does opioid receptor antagonism influence peripheral SRIF effects on nociceptors. These findings demonstrate that SRIF receptors maintain a tonic inhibitory control over peripheral nociceptors, and this may contribute to mechanisms that control the excitability of these terminals.
Interactions with hydroxymethylglutaryl-coenzyme A reductase inhibitors (1995)

Drug-drug, drug-food, and drug-disease interactions involving hydroxymethylglutaryl-coenzyme A (HMG-CoA) reductase inhibitors are reviewed. The four available HMG-CoA reductase inhibitors-lovastatin, simvastatin, pravastatin, and fluvastatin-have different potentials for drug interactions, probably because of their different pharmacokinetic characteristics. Interactions of some of these cholesterol-lowering agents with cyclosporine, erythromycin, high-dose niacin, or gemfibrozil may produce myopathy with or without rhabdomyolysis. Interactions with other commonly prescribed agents, such as bile acid sequestrants, coumarin anticoagulants, and cardiovascular drugs, may alter the pharmacokinetics of either drug, but the clinical significance is generally minor. Food may affect plasma lovastatin concentrations, systemic pravastatin bioavailability, and the maximum serum concentration (Cmax) and time to achieve Cmax for fluvastatin. Hepatic dysfunction may influence the pharmacokinetics of pravastatin; all HMG-CoA reductase inhibitors are contraindicated in patients with liver disease or unexplained elevations in serum aminotransferases. Severe renal insufficiency may necessitate dosage modification in lovastatin recipients. Renal dysfunction seems to affect the pharmacokinetics of pravastatin, simvastatin, and fluvastatin only minimally, but caution is still warranted. Although the HMG-CoA reductase inhibitors rarely have severe adverse effects, they may interact, in some cases dangerously, with other drugs, with food, and with disease states.
Frameshift deletions of exons 3-7 and revertant fibers in Duchenne muscular dystrophy: mechanisms of dystrophin production. (1995)

Duchenne muscular dystrophy (DMD) patients with mutations that disrupt the translational reading frame produce little or no dystrophin. Two exceptions are the deletion of exons 3-7 and the occurrence of rare dystrophin-positive fibers (revertant fibers) in muscle of DMD patients. Antibodies directed against the amino-terminus and the 5' end of exon 8 did not detect dystrophin in muscle from patients who have a deletion of exons 3-7. However, in all cases, dystrophin was detected with an antibody directed against the 3' end of exon 8. The most likely method of dystrophin production in these cases is initiation at a new start codon in exon 8. We also studied two patients who have revertant fibers: one had an inherited duplication of exons 5-7, which, on immunostaining, showed two types of revertant fibers; and the second patient had a 2-bp nonsense mutation in exon 51, which creates a cryptic splice site. An in-frame mRNA that uses this splice site in exon 51 was detected. Immunostaining demonstrated the presence of the 3' end of exon 51, which is in agreement with the use of this mRNA in revertant fibers. The most likely method of dystrophin production in these fibers is a second mutation that restores the reading frame.
The clinical spectrum of catastrophic antiphospholipid syndrome in the absence and presence of lupus. (2007)

SLE is a poor prognostic factor in patients with CAPS and cyclophosphamide may be beneficial in those with SLE-CAPS.
Genetic transformation in Streptococcus pneumoniae: nucleotide sequence and predicted amino acid sequence of recP (1990)

We present the complete nucleotide sequence of recP, a locus required for high-efficiency recombination of chromosomal DNA during genetic transformation in Streptococcus pneumoniae. The sequence was determined by using plasmid DNA templates and synthetic oligonucleotide primers. The locus contained a single large open reading frame, ORF1, of 1,968 base pairs (bp). ORF1 is included within the recP locus previously mapped genetically and accounts for 94% of its extent. The predicted molecular weight of the largest polypeptide encoded within ORF1, 71,662, coincided with that measured previously (72,000) for the product of in vitro transcription-translation of the cloned recP locus. A Shine-Dalgarno sequence (AGAAAGGA; delta G = -17 kcal [ca. -71.1 kJ]) lay 6 bp upstream of ORF1. A sequence (TTGcat-17 bp-TATAAT) similar to the E. coli sigma-70 promoter consensus was located 52 bp upstream of ORF1. This putative promoter overlapped a structure consisting of two perfect inverted 10-bp repeats and a loop of 8 bp.
Shear Stress Induces Endothelial Differentiation From a Murine Embryonic Mesenchymal Progenitor Cell Line (2005)

This study demonstrates, for the fist time, endothelial differentiation in a mesenchymal progenitor CH3H/10T1/2 cell line resulting from shear exposure. Thus, this analysis may serve as a basis for further understanding the effect of shear on mesenchymal and vascular cell differentiation.
Polymorphisms in ion channel genes: emerging roles in pain (2010)

mechanism of seizure initiation, which is assumed to start at a single, well-defined location. In contrast, the present recordings show that the seizure activity can involve the interaction between different local populations of neurons, but most of the time this does not generalize to larger cortical territories. Another interesting finding is that microseizures always precede the occurrence of full-blown seizures. Consequently, as these events are invisible from macroelectrode recordings, the localization of the epileptic focus, both in space and time, may be biased by this invisibility. However, whether the localization of such microseizure activity is critical to the localization of the focus at scales relevant to surgery remains to be demonstrated.
Requirement of Type III TGF-β Receptor for Endocardial Cell Transformation in the Heart (1999)

Transforming growth factor-beta (TGF-beta) signaling is mediated by a complex of type I (TBRI) and type II (TBRII) receptors. The type III receptor (TBRIII) lacks a recognizable signaling domain and has no clearly defined role in TGF-beta signaling. Cardiac endothelial cells that undergo epithelial-mesenchymal transformation express TBRIII, and here TBRIII-specific antisera were found to inhibit mesenchyme formation and migration in atrioventricular cushion explants. Misexpression of TBRIII in nontransforming ventricular endothelial cells conferred transformation in response to TGF-beta2. These results support a model where TBRIII localizes transformation in the heart and plays an essential, nonredundant role in TGF-beta signaling.
Detection of Spores of Bacillus anthracis using the Polymerase Chain Reaction (1992)

Journal Article Detection of Spores of Bacillus anthracis using the Polymerase Chain Reaction Get access Mitchell Carl, Mitchell Carl Search for other works by this author on: Oxford Academic PubMed Google Scholar Richard Hawkins, Richard Hawkins Search for other works by this author on: Oxford Academic PubMed Google Scholar Nicholas Coulson, Nicholas Coulson Search for other works by this author on: Oxford Academic PubMed Google Scholar John Lowe, John Lowe Search for other works by this author on: Oxford Academic PubMed Google Scholar Donald L. Robertson, Donald L. Robertson Search for other works by this author on: Oxford Academic PubMed Google Scholar William M. Nelson, William M. Nelson Search for other works by this author on: Oxford Academic PubMed Google Scholar Richard W. Titball, Richard W. Titball Search for other works by this author on: Oxford Academic PubMed Google Scholar James N. Woody James N. Woody Search for other works by this author on: Oxford Academic PubMed Google Scholar The Journal of Infectious Diseases, Volume 165, Issue 6, June 1992, Pages 1145–1148, https://doi.org/10.1093/infdis/165.6.1145 Published: 01 June 1992 Article history Received: 30 October 1991 Revision received: 06 January 1992 Published: 01 June 1992
Synthetic sudies related to myoglobin: syntheses of bridged porphyrin systems (1976)

A. R. Battersby, D. G. Buckley, S. G. Hartley and M. D. Turnbull, J. Chem. Soc., Chem. Commun., 1976, 879 DOI: 10.1039/C39760000879
Generating network-based moving objects (2002)

Benchmarking spatiotemporal database systems requires the generation of suitable datasets simulating the typical behavior of moving objects. Previous approaches do not consider that in many applications the moving objects follow a given network. In this paper, the most important properties of network-based moving objects are presented. These properties are the basis for specifying and developing a new generator for spatiotemporal data. This generator combines a real network with user-defined properties of the resulting dataset. A framework for using and promoting the generator exists.
Outbreak of Carbapenem-Resistant Enterobacteriaceae Containing blaNDM-1, Ontario, Canada (2012)

We report a NDM-1-producing K. pneumoniae outbreak in Ontario, Canada. Implementation of standard infection control practices, including active screening was able to contain the spread of this organism in the hospital setting. Of concern is the potential loss of a travel history to identify patients that are at high risk of being colonized or infected with this organism and the lack of an accurate, cost-effective test that can be implemented in the hospital setting to identify these multidrug-resistant organisms.