gebhart/patrepeval huggingface dataset:
Allopurinol Reduces Neointimal Hyperplasia in the Carotid Artery Ligation Model in Spontaneously Hypertensive Rats (2006)

Uric acid and oxidative stress promote cardiovascular diseases, including atherosclerosis and hypertension. Xanthine oxidase, through which uric acid is generated, is a free-radical generating enzyme. The aim of the current study was to investigate whether allopurinol, an inhibitor of xanthine oxidase activity, affects vascular remodeling and vascular smooth muscle cell (VSMC) proliferation. In the carotid artery ligation model using spontaneously hypertensive rats (SHR), treatment with allopurinol induced a reduction in the neointima/media ratio by 27% (38.5+/-34.3% in the control group and 28.1 20.8% in the allopurinol-treated group, respectively, p<0.01) without alterations in vascular circumference at 3 weeks after ligation when compared to the control. Allopurinol lowered the serum uric acid concentration (147.0+/-3.6 micromol/l in the control group and 16.1+/-3.6 micromol/l in the allopurinol-treated group, respectively p<0.01) and xanthine oxidase activity, but not the blood pressure. In an in vitro study, high concentrations of uric acid (100 and 200 micromol/l) stimulated VSMC growth, but there was no stimulation of these cells by a low concentration of uric acid (50 micromol/I) or by any of three concentrations of xanthine (50, 100 and 200 micromol/l). In addition, allopurinol (5 micromol/I) had no effect on the cell growth. In conclusion, uric acid is a potent stimulator of VSMC proliferation, and allopurinol prevented vascular remodeling in SHR at least in part by inhibiting uric acid concentration.
Ventilatory and Hemodynamic Effects of Continuous Positive Airway Pressure in Left Heart Failure (1997)

The ventilatory and hemodynamic effects of continuous positive airway pressure (CPAP) delivered via a face mask (at 0, 5, and 10 cm H2O, and after a return to 0 cm H2O) were studied in nine patients with acute left heart failure (pulmonary artery occlusion pressure [PAOP] > or = 18 mm Hg, and cardiac index [CI] < or = 2.8 L/min/m2). CPAP at 10 cm H2O induced an improvement in lung compliance (60 +/- 10 ml/cm H2O to 87 +/- 20 ml/cm H2O, p < 0.05) and in lung and airway resistance (5.7 +/- 1.0 cm H2O/L/s to 3.4 +/- 1.0 cm H2O/L/s, p < 0.05), a reduction in work of breathing (18 +/- 3 J/min to 12 +/- 2 J/min, p < 0.05), and in the pressure-time index of the respiratory muscles (279 +/- 22 cm H2O/s/min to 174 +/- 25 cm H2O/s/min, p < 0.05), without significant changes in breathing pattern. Despite a significant reduction in the negative swings in intrathoracic pressure (15.2 +/- 1.9 cm H2O to 10.8 +/- 1.8 cm H2O, p < 0.001), no significant change was observed in CI or stroke volume during CPAP. However, mean transmural filling pressures decreased significantly with CPAP, suggesting a better cardiac performance. Neither the level of stroke volume nor of PAOP, was predictive of changes in CI or in stroke volume. In patients with respiratory insufficiency caused by congestive heart failure (CHF), CPAP reduces respiratory muscle effort without altering cardiac output. The slight decrease in mean transmural left and right atrial pressures suggests an improvement in cardiac performance.
Translation Inhibitors Sensitize Prostate Cancer Cells to Apoptosis Induced by Tumor Necrosis Factor-related Apoptosis-inducing Ligand (TRAIL) by Activating c-Jun N-terminal Kinase (2003)

Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) induces apoptosis in several human tumors both in vitro and in vivo, however, some tumors remain resistant for poorly understood reasons. Using a quantitative DNA fragmentation assay for apoptosis, we have shown that human prostate cancer cells are resistant to a wide range of TRAIL doses up to 500 ng/ml. However, translation inhibitors, such as anisomycin, cycloheximide, emetine, harringtonine, and puromycin, unlike several transcription inhibitors, significantly sensitized PC3-neomycin (PC3-neo) cells to TRAIL-induced apoptosis. These effects were inhibited in PC3 cells engineered to express bcl2 (PC3-bcl2). Translation inhibitors led to activation of c-Jun N-terminal kinase (JNK), which plays a role in this sensitization process because inhibition of JNK activation resulted in protection against TRAIL plus translation inhibitor-induced apoptosis. JNK activation may be required for this process, but it is not sufficient because activation of JNK using an MEKK2 expression vector did not mimic the sensitizing effect of translation inhibitors. Other stress-activated protein kinases, such as ERK and p38, play an insignificant role in determining the apoptotic sensitivity. We conclude that activation of JNK is required for sensitization of PC3 cells to TRAIL-induced apoptosis by translation inhibitors in cells that are otherwise TRAIL-resistant. However, in addition to JNK activation, other aspects of translation inhibition such as the suppressed activity of apoptosis-inhibitory proteins or activation of other signal transduction pathways must also be involved.
Polysome-profiling in small tissue samples (2017)

Polysome-profiling is commonly used to study translatomes and applies laborious extraction of efficiently translated mRNA (associated with >3 ribosomes) from a large volume across many fractions. This property makes polysome-profiling inconvenient for larger experimental designs or samples with low RNA amounts. To address this, we optimized a non-linear sucrose gradient which reproducibly enriches for efficiently translated mRNA in only one or two fractions, thereby reducing sample handling 5-10-fold. The technique generates polysome-associated RNA with a quality reflecting the starting material and, when coupled with smart-seq2 single-cell RNA sequencing, translatomes in small tissues from biobanks can be obtained. Translatomes acquired using optimized non-linear gradients resemble those obtained with the standard approach employing linear gradients. Polysome-profiling using optimized non-linear gradients in serum starved HCT-116 cells with or without p53 showed that p53 status associates with changes in mRNA abundance and translational efficiency leading to changes in protein levels. Moreover, p53 status also induced translational buffering whereby changes in mRNA levels are buffered at the level of mRNA translation. Thus, here we present a polysome-profiling technique applicable to large study designs, primary cells and frozen tissue samples such as those collected in biobanks.
Down-regulation of pituitary receptors for luteinizing hormone-releasing hormone (LH-RH) in rats by LH-RH antagonist Cetrorelix. (1996)

Antagonists of luteinizing hormone-releasing hormone (LH-RH), unlike the LH-RH agonists, suppress gonadotropins and sex steroid secretion immediately after administration, without initial stimulatory effects. [Ac-D-Nal(2)1,D-Ph(4Cl)2,D-Pal(3)3,D-Cit6,D-Ala10]LH-R H (SB-75; Cetrorelix) is a modern, potent antagonistic analog of LH-RH. In this study, the binding characteristics of receptors for LH-RH in membrane fractions from rat anterior pituitaries were investigated after a single injection of Cetrorelix at a dose of 100 microg per rat. To determine whether the treatment with Cetrorelix can affect the concentration of measurable LH-RH binding sites, we applied an in vitro method to desaturate LH-RH receptors by chaotropic agents such as manganous chloride (MnCl2) and ammonium thiocyanate (NH4SCN). Our results show that the percentages of occupied LH-RH receptors at 1, 3, and 6 h after administration of Cetrorelix were approximately 28%, 14%, and 10%, respectively, of total receptors. At later time intervals, we could not detect occupied LH-RH binding sites. Ligand competition assays, following in vitro desaturation, demonstrated that rat pituitary LH-RH receptors were significantly (P < 0.01) down-regulated for at least 72 h after administration of Cetrorelix. The lowest receptor concentration was found 3-6 h after Cetrorelix treatment and a recovery in receptor number began within approximately 24 h. The down-regulation of LH-RH binding sites induced by Cetrorelix was accompanied by serum LH and testosterone suppression. Higher LH-RH receptor concentrations coincided with elevated serum hormone levels at later time intervals. Our results indicate that administration of LH-RH antagonist Cetrorelix produces a marked down-regulation of pituitary receptors for LH-RH and not merely an occupancy of binding sites.
General Deviants: An Analysis of Perturbations in Compressed Sensing (2010)

We analyze the Basis Pursuit recovery of signals with general perturbations. Previous studies have only considered partially perturbed observations Ax + e. Here, x is a signal which we wish to recover, A is a full-rank matrix with more columns than rows, and e is simple additive noise. Our model also incorporates perturbations E to the matrix A which result in multiplicative noise. This completely perturbed framework extends the prior work of Candes, Romberg, and Tao on stable signal recovery from incomplete and inaccurate measurements. Our results show that, under suitable conditions, the stability of the recovered signal is limited by the noise level in the observation. Moreover, this accuracy is within a constant multiple of the best-case reconstruction using the technique of least squares. In the absence of additive noise, numerical simulations essentially confirm that this error is a linear function of the relative perturbation.
Avoiding Loss of Catalytic Activity of Pd Nanoparticles Partially Embedded in Nanoditches in SiC Nanowires (2009)

Nanoditches from selective etching of periodically twinned SiC nanowires were employed to hinder the migration and coalescence of Pd nanoparticles supported on the nanowires, and thus to improve their catalytic stability for total combustion of methane. The results show that the etched Pd/SiC catalyst can keep the methane conversion of almost 100% while the unetched one has an obvious decline in the catalytic activity from 100 to 82% after ten repeated reaction cycles. The excellent catalytic stability originates from the limitation of the nanoditches to the migration and growth of Pd nanoparticles.
Single-crystal magnetotunnel junctions (2001)

We have grown epitaxial single-crystal magnetotunnel junctions using Fe(001) substrates, MgO(001) spacers and Fe top electrodes. We have used scanning tunneling microscopy and atomic force microscopy to measure the tunneling characteristics as a function of position and demonstrated that local tunneling can be obtained such that the buried MgO can be characterized with nm resolution. Local I(V) curves revealed that most of the area had intrinsic tunneling properties corresponding to the proper MgO tunneling barrier. A small fraction of the scanned areas showed localized spikes in the tunneling current which are most likely caused by defects in the MgO.
Comparison of the antinociceptive effect between the cyclic dipeptide cyclo (Tyr(Et)-homoarginine) and the linear dipeptide Boc-Tyr(Et)-homoarginine-OMe in rats. (1984)

The antinociceptive effect of the cyclic dipeptide cyclo[Tyr(Et)- homoarginine] (C.TEHA) was examined utilizing the tail flick test and the digitus pinching test in rats in comparison with the linear dipeptide Boc-Tyr(Et)-homoarginine-OMe (B.TEHM). Though both dipeptides administered into the lateral, 3rd and 4th cerebroventricles produced antinociceptive effects equipotent to morphine, except for the 4th cerebroventricular administration of B.TEHM, the administration into the spinal subarachnoid space was without effect. The effect of B.TEHM was completely antagonized by the pretreatment of naloxone (i.p.) when administered into the 3rd cerebroventricle where its effect was demonstrated to be the most potent. However, naloxone had no significant effect on C.TEHA administered into the 3rd cerebroventricle in both tests. It was concluded that both dipeptides act on the upper brain stem, especially around the 3rd cerebroventricle. Moreover, it was also thought that the effect of B.TEHM may be involved in the brain opioid system, and that of C.TEHA can be produced via a naloxone-resistant opioid system or a non-opioid system.
Acceleration of MR parameter mapping using annihilating filter‐based low rank hankel matrix (ALOHA) (2016)

Given that many diagnostic errors are caused by the systematic distortion of images, ALOHA may have a great potential for clinical applications. Magn Reson Med 76:1848-1864, 2016. © 2016 International Society for Magnetic Resonance in Medicine.
Inflammatory and Immune Reactions Associated with Stratum Corneum and Neutrophils in Sterile Pustular Dermatoses (2000)

In this review we present our own experimental findings as well as those from the literature related to the pathomechanisms for the inflammatory changes in psoriasis and its related diseases. A growing body of evidence has indicated that T cell-mediated immunity plays an important role in triggering and maintenance of psoriatic lesions. It has been revealed that lymphokines produced by activated T cells in psoriatic lesions have a strong influence on the proliferation of the epidermis. Characteristic neutrophil accumulation under the stratum corneum can be observed in the highly inflamed areas of psoriatic lesions. These neutrophils are chemotactically attracted and activated there by synergistic action of chemokines, IL-8 and Gro-alpha released by stimulated keratinocytes, and particularly by C5a/C5a des arg produced via the alternative complement pathway activation. We demonstrated that the infiltrating neutrophils adhere to iC3b-opsonized corneocytes to produce active oxygen and probably lysosomal enzymes. From a close relationship observed between neutrophil accumulation and high mitotic ratio of the lesional epidermis, we think that these stimulated neutrophils influence the growth and differentiation of epidermal keratinocytes. Aberrant expression of HLA-DR on neutrophils suggests their activation of infiltrating T cells in the presence of bacterial superantigen. These T cells in turn influence the transepidermal neutrophil migration through the effect of their cytokines on the keratinocyte production of proinflammatory mediators including IL-8 and C3. In this review we discuss the pivotal roles played by stratum corneum and neutrophils in several skin diseases, where neutrophils accumulate beneath the stratum corneum in a sterile condition.
A Formidable Foe Is Sabotaging Your Results: What You Should Know about Biofilms and Wound Healing (2017)

Biofilm represents a protected mode of growth for bacteria, allowing them to evade standard diagnostic techniques and avoid eradication by standard therapies. Although only recently discovered, biofilm has existed for millennia and complicates nearly every aspect of medicine. Biofilm impacts wound healing by allowing bacteria to evade immune responses, prolonging inflammation and disabling skin barrier function. It is important to understand why problem wounds persist despite state-of-the-art treatment, why they are difficult to accurately diagnose, and why they recur. The aim of this article is to focus on current gaps in knowledge related to problem wounds, specifically, biofilm infection.
Protein Kinase C-related Kinase and ROCK Are Required for Thrombin-induced Endothelial Cell Permeability Downstream from Gα12/13 and Gα11/q (2008)

Increase in vascular permeability occurs under many physiological conditions such as wound repair, inflammation, and thrombotic reactions and is central in diverse human pathologies, including tumor-induced angiogenesis, ocular diseases, and septic shock. Thrombin is a pro-coagulant serine protease, which causes the local loss of endothelial barrier integrity thereby enabling the rapid extravasation of plasma proteins and the local formation of fibrin-containing clots. Available information suggests that thrombin induces endothelial permeability by promoting actomyosin contractility through the Rho/ROCK signaling pathway. Here we took advantage of pharmacological inhibitors, knockdown approaches, and the emerging knowledge on how permeability factors affect endothelial junctions to investigate in detail the mechanism underlying thrombin-induced endothelial permeability. We show that thrombin signals through PAR-1 and its coupled G proteins Galpha(12/13) and Galpha(11/q) to induce RhoA activation and intracellular calcium elevation, and that these events are interrelated. In turn, this leads to the stimulation of ROCK, which causes actin stress-fiber formation. However, this alone is not sufficient to account for thrombin-induced permeability. Instead, we found that protein kinase C-related kinase, a Rho-dependent serine/threonine kinase, is activated in endothelial cells upon thrombin stimulation and that its expression is required for endothelial permeability and the remodeling of cell-extracellular matrix and cell-cell adhesions. Our results demonstrate that the signal initiated by thrombin bifurcates at the level of RhoA to promote changes in the cytoskeletal architecture through ROCK, and the remodeling of focal adhesion components through protein kinase C-related kinase. Ultimately, both pathways converge to cause cell-cell junction disruption and provoke vascular leakage.
Vehicle wheel detector using 2D filter banks (2004)

Detecting vehicles from a moving vehicle is an important task. In this paper a new vehicle detector is introduced. The new vehicle detector employs the use of the ubiquitous wheel. Every car has wheels; this wheel detector finds wheels and infers vehicle location from the wheel detection. Views from an omnidirectional camera are used to generate side view images. These images are processed using a difference of Gaussian filter bank. The responses from the filter bank are applied to a precomputed set of principle components. The principle component responses are compared against a Gaussian mixture model of wheels and Gaussian model roadbed. Wheel candidates are chosen and tracked. Initial experimental results along with analysis are shown.
Stimulation of bone formation and prevention of bone loss by prostaglandin E EP4 receptor activation (2002)

Bone remodeling, comprising resorption of existing bone and de novo bone formation, is required for the maintenance of a constant bone mass. Prostaglandin (PG)E2 promotes both bone resorption and bone formation. By infusing PGE2 to mice lacking each of four PGE receptor (EP) subtypes, we have identified EP4 as the receptor that mediates bone formation in response to this agent. Consistently, bone formation was induced in wild-type mice by infusion of an EP4-selective agonist and not agonists specific for other EP subtypes. In culture of bone marrow cells from wild-type mice, PGE2 induced expression of core-binding factor alpha1 (Runx2/Cbfa1) and enhanced formation of mineralized nodules, both of which were absent in the culture of cells from EP4-deficient mice. Furthermore, administration of the EP4 agonist restored bone mass and strength normally lost in rats subjected to ovariectomy or immobilization. Histomorphometric analysis revealed that the EP4 agonist induced significant increases in the volume of cancellous bone, osteoid formation, and the number of osteoblasts in the affected bone of immobilized rats, indicating that activation of EP4 induces de novo bone formation. In addition, osteoclasts were found on the increased bone surface at a density comparable to that found in the bone of control animals. These results suggest that activation of EP4 induces bone remodeling in vivo and that EP4-selective drugs may be beneficial in humans with osteoporosis.
Technology Could Cut CO2 Cost Sharply for Enhanced Oil Recovery (2014)

Technology Update As oil fields throughout the world are reaching maturity and requiring the use of secondary and tertiary recovery techniques, oil companies are looking for new processes and technologies to extract more oil from these aging fields. In the next 20 years, an estimated 50% of waterflooded fields will need to shift to enhanced oil recovery (EOR). Carbon dioxide (CO2) has proved to be an almost ideal EOR medium for a broad range of reservoir types and conditions, yielding increases in recovery of up to 15% of oil initially in place. Most of the experience with commercial CO2 EOR has been gained in onshore oil fields in the United States, particularly in the Permian Basin of Texas, where nearby sources of natural CO2 gas and an extensive CO2 transport infrastructure are available. “Onshore CO2 flooding is economical at CO2 costs of around USD 35 to 40 per tonne and an oil price of more than USD 75 per barrel,” said Richard Doidge, director of the TriGen CO2 removal technology program at Maersk Oil. “Where natural CO2 sources are not readily available, CO2 may today be sourced from petrochemical and pre- or post-combustion capture plants, for example. However, these capture methods typically yield CO2 prices of USD 80 to 120 per tonne, which would make CO2 flooding uneconomical.” A ready but limited source of lowcost CO2 can be obtained from facilities, such as ethanol, petrochemical, and gasto- liquids plants, but the bulk of globally emitted industrial CO2 comes from power production and heavy industries, such as steelmaking and cement production. There are three main approaches to removing or “scrubbing” CO2 from feed or flue gases: precombustion, post-combustion, and combustion. Because of the oxygen required in the combustion mixture, the combustion methods are usually called oxy-fuel processes. The efficiency of these processes depends on, among other factors, the concentration of CO2 in the feed or flue gas and the pressure at which the contaminated gas is treated.
A High-Throughput Automated Technique for Counting Females of Heterodera glycines using a Fluorescence-Based Imaging System. (2010)

The soybean cyst nematode (SCN), Heterodera glycines, is the most damaging pathogen of soybean. Methods to phenotype soybean varieties for resistance to SCN are currently very laborious and time consuming. Streamlining a portion of this phenotyping process could increase productivity and accuracy. Here we report an automated method to count SCN females using a fluorescence-based imaging system that is well suited to high-throughput SCN phenotyping methods used in greenhouse screening. For optimal automated imaging, females were washed from roots at 30 days post-inoculation into small Petri dishes. Using a Kodak Image Station 4000MM Pro, the Petri dishes were scanned using excitation and emission wavelengths of 470 nm and 535 nm, respectively. Fluorescent images were captured and analyzed with Carestream Molecular Imaging Software for automated counting. We demonstrate that the automated fluorescent-based imaging system is just as accurate (r(2) ≥ 0.95) and more efficient (>50% faster) than manual counting under a microscope. This method can greatly improve the consistency and turnaround of data while reducing the time and labor commitment associated with SCN female counting.
Control of cyclic chromosome replication in Escherichia coli (1991)

The biochemical basis for cyclic initiation of bacterial chromosome replication is reviewed to define the processes involved and to focus on the putative oscillator mechanism which generates the replication clock. The properties required for a functional oscillator are defined, and their implications are discussed. We show that positive control models, but not negative ones, can explain cyclic initiation. In particular, the widely accepted idea that DnaA protein controls the timing of initiation is examined in detail. Our analysis indicates that DnaA protein is not involved in the oscillator mechanism. We conclude that the generations of a single leading to cyclic initiation is separate from the initiation process itself and propose a heuristic model to focus attention on possible oscillator mechanisms.