gebhart/patrepeval huggingface dataset:
Complete amino acid sequence of puroindoline, a new basic and cystine‐rich protein with a unique tryptophan‐rich domain, isolated from wheat endosperm by Triton X‐114 phase partitioning (1993)

A new basic protein has been isolated from wheat endosperm by Triton X-114 phase partitioning. It contains five disulfide bridges and is composed of equal amounts of a polypeptide chain of 115 amino acid residues and of the same chain with a C-terminus dipeptide extension. The most striking sequence feature is the presence of a unique tryptophan-rich domain so that this protein isolated from wheat seeds has been named puroindoline. The similar phase partitioning behavior in Triton X-114 of this basic cystine-rich protein and of purothionins suggests that puroindoline may also be a membranotoxin that might play a role in the defense mechanism of plants against microbial pathogens.
The quaternary structure of streptavidin in urea (1991)

We report on the interactions of urea and guanidinium salts with streptavidin. Gel filtration chromatography in 0, 4, 6, and 7 M urea indicates that the streptavidin tetramer remains intact in urea. Biotin alters the electrophoretic mobility of streptavidin whether or not 6 M urea is present. The intrinsic fluorescence of streptavidin is increased and blue-shifted in 6 M urea. The fluorescence changes indicate the absence of unfolding. A conformational response to urea is possible, but much of the fluorescence change is due to urea binding as a weak biotin analog (Ka approximately 1.3 M-1). The resistance to structural perturbation by urea reflects the structural stability of streptavidin's anti-parallel beta-barrel motif. Unfolding is sluggish in 6 M guanidinium hydrochloride (half-time, approximately 50 days). After guanidinium thiocyanate unfolding, streptavidin can be refolded, but the unfolding and refolding transitions are centered at different concentrations of perturbant. Slow unfolding, with a 15th power dependence on guanidinium thiocyanate concentration, may be partially responsible for the noncoincidence of the unfolding and refolding processes. Nonequilibrium behavior is also seen in 6 M urea, as native streptavidin does not unfold and guanidinium thiocyanate unfolded streptavidin does not refold. Refolding does occur at lower concentrations of urea. Guanidinium thiocyanate only slowly unfolds the biotin-streptavidin complex. In the presence of biotin, unfolded streptavidin does not refold in 6 M guanidinium thiocyanate or in 6 M urea.
Variability of Plasma HDL Subclass Concentrations in Men and Women Over Time (1997)

Plasma HDL subclasses were examined by gradient gel electrophoresis in repeated samples to assess variability over time. Absorbance of the protein stain was used as an index of mass concentrations at 0.01-nm intervals within five HDL subclasses: HDL3c (7.2 to 7.8 nm), HDL3b (7.8 to 8.2 nm), HDL3a (8.2 to 8.8 nm), HDL2a (8.8 to 9.7 nm), and HDL2b (9.7 to 12 nm). Three separate longitudinal studies of men showed that repeated samples of HDL over time were correlated most strongly within HDL2b, somewhat less within HDL2a, and more weakly within HDL3a, HDL3b, and HDL3c. As in men, repeated samples in women from two studies were significantly correlated within the HDL2b, HDL2a, and HDL3b intervals. Plasma HDL2b levels were significantly more stable in men than in women. Although the variability of HDL subclass measurements includes both methodological and physiological sources, differences in laboratory measurement error do not appear to explain the differences in correlations among subclasses. Specifically, analysis of 288 replications from frozen aliquots suggested that laboratory error had the least effect on correlations involving HDL3 subclasses and only slightly greater effect on correlations involving HDL2 subclasses. Our results suggest that for plasma sampled over time, the stability of HDL subclass levels increases with particle size. Prior reports of subclass-specific correlations between HDL and other variables (eg, diet, exercise, and other lipids) are unlikely to be artifacts of laboratory precision but could arise from subclass differences in variability that are physiological.
Body Iron Stores Are Associated With Serum Insulin and Blood Glucose Concentrations: Population study in 1,013 eastern Finnish men (1997)

Mildly elevated body iron stores are associated with statistically significant elevations in glucose homeostasis indexes.
An Adaptive and Optimized Switching Observer for Sensorless Control of an Electromagnetic Valve Actuator in Camless Internal Combustion Engines (2013)

Abstract In this paper, the design and operation of a special electromagnetic actuator as a variable engine valve actuator are presented. Further, this paper describes a feasible approximated velocity switching estimator based on measurements of current and input voltage to achieve sensorless control. The proposed concept allows a reduced‐order observer to be conceived and yields a specific control strategy with an acceptable performance. In general, this approach represents a viable strategy to build reduced‐order observers for estimating the velocity of systems through the measurement of input current and voltage. The robustness of the velocity tracking is explored using a minimum variance approach. The effect of the noise is minimized, and the position can be achieved through an adaptive and optimized structure by combining this particular velocity estimator and an observer based on the electromechanical system. Position control is achieved through an inversion of the model. This approach avoids a more complex structure for the observer and yields an acceptable performance as well as eliminating bulky position‐sensor systems. In addition, a control strategy is presented and discussed. Computer simulations of the sensorless control structure are presented in which the positive effects of the observer with optimized parameter setting are visible in the closed‐loop control.
Immunological heterogeneity of human monocyte subsets prepared by counterflow centrifugation elutriation. (1986)

Human peripheral blood mononuclear cells were separated into three fractions by means of counterflow centrifugation elutriation (CCE). The first fraction, eluted at a flow rate of 24 ml/min, was composed of lymphocytes with less than 2% contaminating esterase-positive cells. The cells in this fraction were incapable of responding to either soluble antigen (tetanus toxoid) or particulate antigen (cytomegalovirus-infected fibroblasts) unless recombined with accessory cells. The second fraction, eluted at a flow rate of 28 ml/min, was composed predominantly (72%) of small Ia, leu M3, and esterase-positive monocytes, which stained weakly with leu 10 antibody. Cells in this fraction efficiently presented soluble and particulate antigens to monocyte-depleted lymphocytes. Of the remaining cells, 87% were large esterase-positive monocytes that labelled strongly with Ia, leu M3, and leu 10. These cells were less efficient in antigen presentation than the small monocytes. However, lymphocytes activated with antigen-pulsed large monocytes exhibited more suppressor cell activity than those activated with antigen-pulsed small monocytes.
Accurate Laboratory Boresight Alignment Of Transmitter/Receiver Optical Axes (1986)

An apparatus and procedure for the boresight alignment of the transmitter and receiver optical axes of a laser radar system are described. This accurate technique is applicable to both shared and dual aperture systems. A laser autostigmatic cube interferometer (LACI) is utilized to align a paraboloid in autocollimation. The LACI pinhole located at the paraboloid center of curvature becomes the far field receiver track and transmit reference point when illuminated by the transmit beam via a fiber optic pick-off/delay line. Boresight alignment accuracy better than 20 prad is achievable.
Interference of propamidine with binding of the fifth component of complement to surface-fixed C3b, and with C5 activation. (1979)

The effects of propamidine and their dose dependency, on utilization of the third and fifth complement components in immune haemolysis have been compared. While C3 utilization is not disturbed that of C5 is markedly inhibited by propamidine in concentrations as low as 0.5 mM. Both, binding of C5 to surface-fixed C3b and cleavage of C5 by convertases C42 and C3bBb, are also inhibited in the presence of propamidine. Since neither C3 cleavage by these enzymes nor even C5 cleavage by the cobra venom factor-supported convertase CFVBb is significantly reduced a general convertase-inhibiting effect of propamidine is ruled out. Rather the effect on utilization of C5 is the result of interference with binding of C5 is the result of interference with binding of C5 to C3b and hence impairment of its accessibility to the convertases. These findings thus further support the role of surface fixed C3b in C5 activation proposed earlier.
Effects of interferons and cytokines on melanoma cells. (1993)

This review summarizes recent information on the effects of immunomodulatory cytokines on human melanoma cells. The action of interferon (IFN)-alpha, -beta, and -gamma has been extensively examined in melanoma and melanocyte cultures in vitro, and increasing information on the action of other cytokines is now available. All IFNs revealed a dose-dependent antiproliferative effect on melanoma cells with the highest growth inhibition caused by IFN-beta. Proliferation was also inhibited by interleukin (IL) 1-alpha and -beta, and tumor necrosis factor (TNF)-alpha. For IL-4, both growth-stimulatory and -inhibitory properties have been reported. Cellular differentiation in terms of melanin synthesis, formation of dendritelike structures, and antigenic changes was not affected by IFN-alpha or -beta. IFN-gamma, however, induced a more dedifferentiated and biologically more aggressive phenotype of melanoma cells. Histocompatibility antigen (HLA) class I molecules were found upregulated by all IFNs and by TNF-alpha, associated with a marked increase of melanoma cell lysis by tumor infiltrating lymphocytes in vitro. HLA class II molecules were de novo expressed or enhanced by IFN-gamma and TNF-alpha. The adhesion molecules ICAM-1, LFA-3, and VLA-2 were upregulated by IFN-gamma, TNF-alpha, and IL-1-beta, whereas melanoma-associated antigens were hardly affected by cytokines. It seems that both antiproliferative and immunomodulatory effects may contribute to the antitumoral activity of cytokines in vivo. In vivo application of cytokines as well as combinations with cytotoxic drugs, therefore, may be promising for future treatment strategies.
Lipopolysaccharide Induces Rac1-dependent Reactive Oxygen Species Formation and Coordinates Tumor Necrosis Factor-α Secretion through IKK Regulation of NF-κB (2001)

Reactive oxygen species (ROS) are important second messengers generated in response to many types of environmental stress. In this setting, changes in intracellular ROS can activate signal transduction pathways that influence how cells react to their environment. In sepsis, a dynamic proinflammatory cellular response to bacterial toxins (e.g. lipopolysaccharide or LPS) leads to widespread organ damage and death. The present study demonstrates for the first time that the activation of Rac1 (a GTP-binding protein), and the subsequent production of ROS, constitutes a major pathway involved in NFkappaB-mediated tumor necrosis factor-alpha (TNFalpha) secretion following LPS challenge in macrophages. Expression of a dominant negative mutant of Rac1 (N17Rac1) reduced Rac1 activation, ROS formation, NFkappaB activation, and TNFalpha secretion following LPS stimulation. In contrast, expression of a dominant active form of Rac1 (V12Rac1) mimicked these effects in the absence of LPS stimulation. IKKalpha and IKKbeta were both required downstream modulators of LPS-activated Rac1, since the expression of either of the IKK dominant mutants (IKKalphaKM or IKKbetaKA) drastically reduced NFkappaB-dependent TNFalpha secretion. Moreover, studies using CD14 blocking antibodies suggest that Rac1 induces TNFalpha secretion through a pathway independent of CD14. However, a maximum therapeutic inhibition of LPS-induced TNFalpha secretion occurred when both CD14 and Rac1 pathways were inhibited. Our results suggest that targeting both Rac1- and CD14-dependent pathways could be a useful therapeutic strategy for attenuating the proinflammatory cytokine response during the course of sepsis.
EphA2 enhances the proliferation and invasion ability of LNCaP prostate cancer cells (2014)

EphA2 is persistently overexpressed and functionally changed in numerous human cancers. However, to the best of our knowledge, the role that EphA2 plays in prostate cancer is not entirely clear. To investigate the roles of EphA2 in the development and progression of prostate cancer, the present study initially evaluated the roles of the EphA2 protein in LNCaP prostate cancer cells using recombinant plasmid, western blot analysis, flow cytometry, Matrigel invasion chamber and the cell counting kit-8 assay. An immunohistochemistry assay was also conducted to observe the effects of EphA2 in prostate cancer tissues. The results demonstrated that the LNCaP human prostate cancer cells that were transfected with pcDNA3.1(+) plasmid-mediated pcDNA3.1(+)-EphA2, markedly enhanced the cell growth and invasion <i>in vitro</i>. Additionally, EphA2 was overexpressed in prostate cancer specimens and the expression of EphA2 was significantly associated with Gleason grade, total prostate-specific antigen, advanced clinical stage and lymph node metastasis. Collectively, these results demonstrate that EphA2 is involved in malignant cell behavior and is a potential therapeutic target in human prostate cancer.
A New Sampling Scheme for Slice Based Volume Rendering (2010)

In this paper we present a novel approach to generate proxy geometry for slice based volume rendering. The basic idea is derived from the behavior of a ray-caster and is a simple extension of the well known 2D object-aligned texture stack based technique. From this our novel scheme inherits the advantage that it enables hardware-based volume rendering for devices that do not support 3D textures. On these devices previous object-aligned 2D texture based approaches suffered from disturbing view angle dependent stack-switching artifacts which are avoided by our novel method. Our approach also shows benefits compared to the widely used view aligned slicing algorithm as it avoids jagged boundary artifacts and increases performance.
ITOMP: Incremental Trajectory Optimization for Real-Time Replanning in Dynamic Environments (2012)

We present a novel optimization-based algorithm for motion planning in dynamic environments. Our approach uses a stochastic trajectory optimization framework to avoid collisions and satisfy smoothness and dynamics constraints. Our algorithm does not require a priori knowledge about global motion or trajectories of dynamic obstacles. Rather, we compute a conservative local bound on the position or trajectory of each obstacle over a short time and use the bound to compute a collision-free trajectory for the robot in an incremental manner. Moreover, we interleave planning and execution of the robot in an adaptive manner to balance between the planning horizon and responsiveness to obstacle. We highlight the performance of our planner in a simulated dynamic environment with the 7-DOF PR2 robot arm and dynamic obstacles.
Small-Molecule Antagonists for CXCR2 and CXCR1 Inhibit Human Melanoma Growth by Decreasing Tumor Cell Proliferation, Survival, and Angiogenesis (2009)

Together, these studies show that selectively targeting CXCR2/CXCR1 with orally active small-molecule inhibitors is a promising therapeutic approach for inhibiting melanoma growth and angiogenesis.
Estimated burden of keratitis--United States, 2010. (2014)

Keratitis, inflammation of the cornea, can result in partial or total loss of vision and can result from infectious agents (e.g., microbes including bacteria, fungi, amebae, and viruses) or from noninfectious causes (e.g., eye trauma, chemical exposure, and ultraviolet exposure). Contact lens wear is the major risk factor for microbial keratitis; outbreaks of Fusarium and Acanthamoeba keratitis have been associated with contact lens multipurpose solution use, and poor contact lens hygiene is a major risk factor for a spectrum of eye complications, including microbial keratitis and other contact lens-related inflammation. However, the overall burden and the epidemiology of keratitis in the United States have not been well described. To estimate the incidence and cost of keratitis, national ambulatory-care and emergency department databases were analyzed. The results of this analysis showed that an estimated 930,000 doctor's office and outpatient clinic visits and 58,000 emergency department visits for keratitis or contact lens disorders occur annually; 76.5% of keratitis visits result in antimicrobial prescriptions. Episodes of keratitis and contact lens disorders cost an estimated $175 million in direct health care expenditures, including $58 million for Medicare patients and $12 million for Medicaid patients each year. Office and outpatient clinic visits occupied over 250,000 hours of clinician time annually. Developing effective prevention messages that are disseminated to contact lens users and investigation of additional preventive efforts are important measures to reduce the national incidence of microbial keratitis.
Dengue-specific subviral nanoparticles: design, creation and characterization (2013)

VLPs armed with EDIII may be potentially useful in diagnostic, therapeutic and prophylactic applications.
Long-term Safety of Asenapine in Pediatric Patients Diagnosed With Bipolar I Disorder: A 50-Week Open-Label, Flexible-Dose Trial (2016)

Asenapine was generally well tolerated in pediatric patients with BP-1 during ≤50 weeks of open-label treatment; among predefined TEAEs of interest, the combination of somnolence/sedation/hypersomnia was the most common. Trial registration ClinicalTrials.gov: NCT01349907.
In Vitro Release by Aspergillus fumigatus of Galactofuranose Antigens, 1,3-β- d -Glucan, and DNA, Surrogate Markers Used for Diagnosis of Invasive Aspergillosis (2006)

Aspergillus markers are becoming increasingly important for the early diagnosis of invasive aspergillosis. The kinetics of release of these surrogate markers, however, is largely unknown. We investigated the release of beta-(1-5)-galactofuranosyl (galf) antigens (Platelia Aspergillus), 1,3-beta-D-glucan (BG) (Fungitell), and DNA (PCR) in an in vitro model of Aspergillus fumigatus. The results showed that release is correlated to the growth phase of the fungus, which depends on available nutrients. Whereas galf antigens and BG are released during logarithmic growth, DNA is released only after mycelium breakdown. During early logarithmic growth, galf antigens seem to be released somewhat earlier than BG. Furthermore, galf antigen concentrations of more than 120,000 times the serum cutoff value (0.5 ng/ml) can be measured, while BG concentrations reach a value only 978 times the serum cutoff value (60 pg/ml). During lytical growth, release of galf antigens further increased to a maximum level, which depended on pH. After that, the concentration of galf antigens stayed high (pH 7.4) or decreased to zero within 4 days (pH 5.0). In contrast to galf antigens, BG concentration decreased after 1 day of growth. The decrease of galf components seems to be due to the enzyme beta-galactofuranosidase, which is able to destroy galf epitopes and whose activity fluctuates in the culture filtrates in parallel with galf antigen concentration. Fungal DNA seems to be released only due to autolysis caused by nutrient limitation. In conclusion, several factors clearly influence the release of surrogate markers in vitro. These same factors might also play a role at the infection site of Aspergillus disease in humans.
Group III nitride-based UV light emitting devices (2003)

The effect of the non-radiative recombination center at or around the dislocations on the performance of the AlGaN-based UV light emitting diode (LED) is discussed. For high-efficiency emission, it is necessary to reduce the density of dislocations to less than 5 × 107 cm–2.
Adenoviral-Directed Expression of the Type 1A Angiotensin Receptor Promotes Cardiomyocyte Hypertrophy via Transactivation of the Epidermal Growth Factor Receptor (2002)

Angiotensin II (Ang II) may cause cardiac hypertrophy via type 1 Ang II receptors (AT(1)) on cardiomyocytes and through growth factors released from cardiac fibroblasts. Whereas cardiomyocyte-specific AT(1) receptor expression produces cardiac hypertrophy and remodeling in vivo, delineation of the signals that mediate growth to Ang II is challenging because the prevailing in vitro model (cultured neonatal cardiomyocytes) expresses low levels of AT(1) receptor and responds inconsistently to Ang II. In this study, when AT(1A) receptors were expressed using adenovirus in cultured neonatal cardiomyocytes, Ang II stimulated a robust hypertrophy that was not secondary to the release of cardiac fibroblast-derived factors, specifically endothelin-1. Hypertrophy was accompanied by the induction of the immediate-early response genes, c-fos and c-jun, and reexpression of atrial natriuretic peptide (ANP). Ang II-induced activation of an ANP promoter-reporter was inhibited by the dominant/negative mutants, GalphaqI and N17Ras, indicating that hypertrophic signaling by the AT(1A) receptor is via heterotrimeric G protein coupling and downstream Ras pathways. AT(1A)-mediated cardiomyocyte hypertrophy and mitogen-activated protein kinase (MAPK) activation were inhibited by the MAPK kinase inhibitor, PD98059, and the epidermal growth factor (EGF) receptor kinase antagonist, AG1478, but not by PKC inhibitor, bisindolylmaleimide-1. Moreover, Ang II-induced MAPK activation was prevented by treatment with a matrix metalloproteinase inhibitor, consistent with the tyrosine phosphorylation of the EGF receptor in response to AT(1A) receptor activation. These data unequivocally demonstrate that Ang II can directly promote cardiac myocyte growth via AT(1A) receptors expressed on these cells and reveal for the first time the important contribution of EGF receptor-transactivated MAPK signaling to this process.
Blocking extracellular activation of myostatin as a strategy for treating muscle wasting (2018)

Many growth factors are intimately bound to the extracellular matrix, with regulated processing and release leading to cellular stimulation. Myostatin and GDF11 are closely related members of the TGFβ family whose activation requires two proteolytic cleavages to release the growth factor from the prodomain. Specific modulation of myostatin and GDF11 activity by targeting growth factor-receptor interactions has traditionally been challenging. Here we demonstrate that a novel strategy for blocking myostatin and GDF11, inhibition of growth factor release, specifically and potently inhibits signaling both in vitro and in vivo. We developed human monoclonal antibodies that selectively bind the myostatin and GDF11 precursor forms, including a subset that inhibit myostatin proteolytic activation and prevent muscle atrophy in vivo. The most potent myostatin activation-blocking antibodies promoted robust muscle growth and resulted in significant gains in muscle performance in healthy mice. Altogether, we show that blocking the extracellular activation of growth factors is a potent method for preventing signaling, serving as proof of concept for a novel therapeutic strategy that can be applied to other members of the TGFβ family of growth factors.