gebhart/patrepeval huggingface dataset:
THE GENERATION OF Ca2+ SIGNALS IN PLANTS (2004)

The calcium ion is firmly established as a ubiquitous intracellular second messenger in plants. At their simplest, Ca(2+)-based signaling systems are composed of a receptor, a system for generating the increase in [Ca(2+)]cyt, downstream components that are capable of reacting to the increase in [Ca(2+)]cyt, and other cellular systems responsible for returning [Ca(2+)]cyt to its prestimulus level. Here we review the various mechanisms responsible for generating the stimulus-induced increases in [Ca(2+)]cyt known as Ca(2+) signals. We focus particularly on the mechanisms responsible for generating [Ca(2+)]cyt oscillations and transients and use Nod Factor signaling in legume root hairs and stimulus-response coupling in guard cells to assess the physiological significance of these classes of Ca(2+) signals.
Object-oriented chemical process modeling in Omola (2003)

An object-oriented approach to modeling chemical processes with control systems in the modeling language Omola is discussed. The basic elements in this modeling methodology are modularization, model encapsulation, hierarchical decomposition, parameterization and inheritance. Models have an internal structure of model components, like terminals, parameters and behavior descriptions. The model behavior can be described by equations or as a connected structure of submodels. Models and model components are represented as objects in single inheritance object class hierarchies. Chemical processes and control systems can be described with the same basic concepts. The object-oriented model representation is implemented in the Omola simulation environment, called OmSim. An exothermic tank reactor example is successfully modeled and simulated.< <ETX xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink">&gt;</ETX>
Isotope‐Reinforced Polyunsaturated Fatty Acids Protect Yeast Cells from Oxidative Stress (2010)

Polyunsaturated fatty acids (PUFAs) are exquisitely sensitive to autoxidation damage. The enhanced vulnerability of PUFAs to such autoxidation stems from the labile nature of the bis‐allylic hydrogen atoms. PUFAs synthesized to contain Deuterium atoms uniquely at the bis‐allylic sites (termed isotope‐reinforced PUFAs) would be expected to be more resistant to autoxidation reactions due to the isotope effect. This hypothesis was tested by making use of yeast coq mutants with defects in biosynthesis of coenzyme Q (CoQ, or ubiquinone). CoQ plays a well‐known role in respiratory energy metabolism and also functions as a lipid soluble chain terminating antioxidant. Although yeast cannot synthesize PUFAs, they are able to incorporate exogenously supplied PUFAs. Yeast coq mutants incubated in the presence of linolenic acid (C18:3) exhibit profound loss of viability as ascertained by greater than 99% loss of colony formation at 4 hours. In contrast, the coq mutants treated with the isotope‐reinforced linolenic acid (bis‐allylic D4‐C18:3) retain 80–90% viability, a value similar to wild‐type or CoQ‐replete yeast. These results indicate that isotope reinforced PUFAs are stabilized as compared to standard PUFAs, and the coq mutant yeast cells containing the D4‐linolenic acid are protected against the toxic effects of lipid autoxidation products. This research was supported by NIH GM45952.
A gaze-responsive self-disclosing display (1990)

An information display system is described which uses eye-tracking to monitor user looking about its graphics screen. The system analyzes the user's patterns of eye movements and fixations in real-time to make inferences about what item or collection of items shown holds most relative interest for the user. Material thus identified is zoomed-in for a closer look, and described in more detail via synthesized speech.
Fecal Microbiota Transplantation Inducing Remission in Crohn’s Colitis and the Associated Changes in Fecal Microbial Profile (2014)

Inflammatory bowel disease (IBD) is a chronic relapsing disorder of the intestine of unclear etiology. Increasing evidence has pointed to intestinal dysbiosis as a potential factor in a genetically susceptible individual. Fecal microbiota transplantation (FMT) has been used to treat inflammatory bowel disease with variable degrees of success. Herein, we report a patient with Crohn's colitis, previously failing an immunosuppressant, who achieved clinical, endoscopic, and histologic remission after a single fecal microbiota transplantation infusion. We have further characterized the changes in the fecal microbiota associated with this observation.
Boron neutron capture therapy research at the MIT research reactor (1994)

Abstract The concept of neutron capture cancer therapy, originally suggested by Locher (l), is relatively straightforward. A compound containing a suitable neutron capture agent, e.g. 10B, is introduced into the patient. The compound must have been developed to selectively concentrate in tumor. Then the tumor and surrounding tissue are irradiated with neutrons. Neutron induced 10B(n,α) 7Li reactions, with a positive Q value of about 2.3 MeV, produce highly energetic alpha and lithium ions with a combined range of around 12 micrometers. The high linear energy transfer (LET) and the short combined range of the two ions assure that the cell killing will be efficient and highly localized, i.e., within the range of about one cell diameter. Thus the 10B(n,α) reaction can be thought of as a microscopic scalpel which can destroy tumor cells while sparing adjacent healthy cells.
An Optimized CFSE‐based T‐cell Suppression Assay to Evaluate the Suppressive Capacity of Regulatory T‐Cells Induced by Human Tolerogenic Dendritic Cells (2010)

In autoimmune diseases or transplant graft rejection, a therapy that will prevent or reduce the present immune activation is highly desired. Ex vivo generated tolerogenic dendritic cells (DC) are considered to have a strong potential as cellular therapy for these diseases. One of the mechanisms of immune suppression mediated by tolerogenic DC is the induction of regulatory T-cells (Treg). Consequently, the efficacy of such DC to induce Treg will reflect their tolerogenic capacity. Because no specific markers have been described for human induced (i)Treg yet, the Treg can only be appreciated by functionality. Therefore, we have optimized an in vitro suppression assay to screen for human DC-induced-Treg activity. IL-10-generated tolerogenic DC were used to induce Treg that were previously shown to effectively suppress the proliferation of responder T-cells stimulated with allogeneic mature DC (mDC). Our results show that the suppressive capacity of IL-10 DC-induced Treg measured in the suppression assay increases with the iTreg dose and decreases with higher numbers of antigen-presenting cells (APC) as T-cell stimulation. Lowering the ratio between responder T-cells and stimulator mDC present in the coculture clearly improved the read-out of the suppression assay. Furthermore, mDC-primed T-cells in the suppression assay were shown to be an essential control condition. In conclusion, we recommend titrations of both APC and iTreg in the suppression assay and to include a negative control condition with T-cells primed by mDC, to distinguish specific and functional suppression by iTreg from possible generalized suppressive activity.
Chronic inflammation, chronic obstructive pulmonary disease, and lung cancer (2009)

The relationships between inflammation, airflow obstruction, and lung cancer are complex. Deregulated inflammation is complicit in the pathogenesis of chronic obstructive pulmonary disease and lung cancer, but the overlap of signaling events is not yet fully understood. Tobacco exposure is an important risk factor that confers long-term risk of lung disease. Diagnostic sensitivity of detecting lung cancer may improve with the utilization of genetic profiling in combination with pathologic evaluation of airway epithelium. Additional research is required to understand the role of epithelial-to-mesenchymal transition in chronic inflammatory lung diseases and lung carcinogenesis.
Acid-Induced Structural Modifications of Unsaturated Fatty Acids and Phenolic Olive Oil Constituents by Nitrite Ions:  A Chemical Assessment (2004)

The structural modifications of the unsaturated fatty acid components of triglycerides in extra virgin olive oil (EVOO) following exposure to nitrite ions in acidic media were determined by two-dimensional (2D) NMR spectroscopy, aided by (15)N labeling and GC analysis, allowing investigation of the matrix without fractionation steps. In the presence of excess nitrite ions in a 1% sulfuric acid/oil biphasic system, extensive double bond isomerization of the oleic/linoleic acid components of triglycerides was observed associated with nitration/oxidation processes. Structurally modified species were identified as E/Z-nitroalkene, 1,2-nitrohydroxy, and 3-nitro-1-alkene(1,5-diene) derivatives based on (1)H, (13)C, and (15)N 2D NMR analysis in comparison with model compounds. Minor constituents of EVOO, including phenolic compounds and tocopherols, were also substantially modified by nitrite-derived nitrating species, even under milder reaction conditions relevant to those occurring in the gastric compartments. Novel nitrated derivatives of tyrosol, hydroxytyrosol, and oleuropein (6-8) were identified by LC/MS analysis of the polar fraction of EVOO and by comparison with synthetic samples. Overall, these results provide the first systematic description at the chemical level of the consequences of exposing EVOO to nitrite ions at acidic pH and offer an improved basis for further investigations in the field of toxic nitrosation/nitration reactions and dietary antinitrosating agents.
An Orally Available Small-Molecule Inhibitor of c-Met, PF-2341066, Exhibits Cytoreductive Antitumor Efficacy through Antiproliferative and Antiangiogenic Mechanisms (2007)

The c-Met receptor tyrosine kinase and its ligand, hepatocyte growth factor (HGF), have been implicated in the progression of several human cancers and are attractive therapeutic targets. PF-2341066 was identified as a potent, orally bioavailable, ATP-competitive small-molecule inhibitor of the catalytic activity of c-Met kinase. PF-2341066 was selective for c-Met (and anaplastic lymphoma kinase) compared with a panel of >120 diverse tyrosine and serine-threonine kinases. PF-2341066 potently inhibited c-Met phosphorylation and c-Met-dependent proliferation, migration, or invasion of human tumor cells in vitro (IC(50) values, 5-20 nmol/L). In addition, PF-2341066 potently inhibited HGF-stimulated endothelial cell survival or invasion and serum-stimulated tubulogenesis in vitro, suggesting that this agent also exhibits antiangiogenic properties. PF-2341066 showed efficacy at well-tolerated doses, including marked cytoreductive antitumor activity, in several tumor models that expressed activated c-Met. The antitumor efficacy of PF-2341066 was dose dependent and showed a strong correlation to inhibition of c-Met phosphorylation in vivo. Near-maximal inhibition of c-Met activity for the full dosing interval was necessary to maximize the efficacy of PF-2341066. Additional mechanism-of-action studies showed dose-dependent inhibition of c-Met-dependent signal transduction, tumor cell proliferation (Ki67), induction of apoptosis (caspase-3), and reduction of microvessel density (CD31). These results indicated that the antitumor activity of PF-2341066 may be mediated by direct effects on tumor cell growth or survival as well as antiangiogenic mechanisms. Collectively, these results show the therapeutic potential of targeting c-Met with selective small-molecule inhibitors for the treatment of human cancers.
Reliability of the Mismatch Negativity in the Responses of Individual Listeners (2001)

The mismatch negativity (MMN) was recorded from 12 normal adults during four biweekly sessions. Responses were elicited by a synthetically generated speech contrast (/dalpha/-/galpha/) that all listeners discriminated with at least 90 percent accuracy. Standard and deviant waveforms were replicable across sessions for all listeners; however, replicability of the derived difference waveforms was poor. Of greater importance, the MMN identification rate was too low (29%) to allow reliability to be evaluated. The implications that these findings may have on clinical applicability are discussed.
Functional mapping of cytotactin: proteolytic fragments active in cell-substrate adhesion. (1988)

Cytotactin is an extracellular matrix glycoprotein with a restricted distribution during development. In electron microscopic images, it appears as a hexabrachion with six arms extending from a central core. Cytotactin binds to other extracellular matrix proteins including a chondroitin sulfate proteoglycan (CTB proteoglycan) and fibronectin. Although cytotactin binds to a variety of cells including fibroblasts and neurons, in some cases it causes cells in culture to round up and it inhibits their migration. To relate these various effects of cytotactin on cell behavior to its binding regions, we have examined its ability to support cell-substrate adhesion and have mapped its cell-binding function onto its structure. In a cell-substrate adhesion assay, fibroblasts bound to cytotactin but remained round. In contrast, they both attached and spread on fibronectin. Neither neurons nor glia bound to cytotactin in this assay. In an assay in which cell-substrate contact was initiated by centrifugation, however, neurons and glia bound well to cytotactin; this binding was blocked by specific anti-cytotactin antibodies. The results suggest that neurons and glia can bind to cytotactin-coated substrates and that these cells, like fibroblasts, possess cell surface ligands for cytotactin. After applying methods of limited proteolysis and fractionation, these assays were used to map the binding functions of cytotactin onto its structure. Fragments produced by limited proteolysis were fractionated into two major pools: one (fraction I) contained disulfide-linked oligomers of a 100-kD fragment and two minor related fragments, and the second (fraction II) contained monomeric 90- and 65-kD fragments. The 90- and 65-kD fragments in fraction II were closely related to each other and were structurally and immunologically distinct from the fragments in fraction I. Only components in fraction I were recognized by mAb M1, which binds to an epitope located in the proximal portion of the arms of the hexabrachion and by a polyclonal antibody prepared against a 75-kD CNBr fragment of intact cytotactin. A mAb (1D8) and a polyclonal antibody prepared against a 35-kD CNBr fragment of cytotactin only recognized components present in fraction II. In cell-binding experiments, fibroblasts, neurons, and glia each adhered to substrates coated with fraction II, but did not adhere to substrates coated with fraction I. Fab fragments of the antibody to the 35-kD CNBr fragment strongly inhibited the binding of cells to cytotactin, supporting the conclusion that fraction II contains a cell-binding region. In addition, Fab fragments of this antibody inhibited the binding of cytotactin to CTB pr
Intravenous immunoglobulin treatment in multiple sclerosis Effect on relapses (1998)

We conducted a double-blind, placebo-controlled study of 40 patients (aged 19 to 60 years) with clinical definite relapsing remitting (RR) MS and brain MRI confirmed. Patients were randomly assigned to receive a loading dose of immunoglobulin IgG (0.4 g/kg/body weight per day for 5 consecutive days), followed by single booster doses (0.4 g/kg/body weight) or placebo once every 2 months for 2 years. The primary outcome measures were change in the yearly exacerbation rate (YER), proportion of exacerbation-free patients, and time until first exacerbation. Neurologic disability, exacerbation severity, and changes in brain MRI lesion score were the secondary outcome measures, all determined at baseline, 1 year, and on completion. Treated patients showed a reduction in YER from 1.85 to 0.75 after 1 year and 0.42 after 2 years versus 1.55 to 1.8 after 1 year and to 1.4 after 2 years in the placebo group (p = 0.0006, overall), reflecting a 38.6% reduction in relapse rate. Six patients in the IVIg group were exacerbation free throughout the 2-year period of the study, whereas none were exacerbation free in the placebo group. The median time to first exacerbation was 233 days in the IVIg group versus 82 days in the placebo group (p = 0.003). Neurologic disability as measured by the Expanded Disability Status Scale (EDSS score) decreased by 0.3 in the IVIg group and increased by 0.15 in the placebo group. Total lesion score evaluated by brain MRI did not show a significant difference between groups. Side effects were minor and occurred in only 19 of 630 (3.0%) infusions administered in both groups. Our results suggest that IVIg may be safe and effective in reducing the frequency of exacerbations in RR-MS.
Localization of an immunodominant domain on baculovirus-produced parvovirus B19 capsids: correlation to a major surface region on the native virus particle (1992)

An immunodominant region on baculovirus-produced parvovirus B19 VP2 capsids was localized between amino acids 259 and 426 by mapping the binding sites of a panel of monoclonal antibodies which recognize determinants on the particles. The binding sites of three monoclonal antibodies were fine-mapped within this antigenic domain. Six VP2-specific monoclonal antibodies recognized determinants common to both the empty capsids and native parvovirus. The defined antigenic region is most probably exposed on the native B19 virion and corresponds to part of the threefold spike on the surface of canine parvovirus particles.
A 0.5 V SIMOX-MTCMOS circuit with 200 ps logic gate (2002)

Multi-threshold CMOS (MTCMOS) circuit technology combining low-Vth CMOS logic gates and high-Vth MOSFETs is suitable for 1 V LSIs for battery-operated portable equipment. Improvements in MTCMOS device technology promise to lead to higher operating frequencies. However, higher frequencies will increase power consumption even if the supply voltage is 1 V. To reduce the power consumption, it is necessary to lower the supply voltage below 1 V, without sacrificing speed. A circuit consisting of depletion-mode MOSFETs operates with 200 mV supply. However, it cannot be applied to an LSI with more than 1 k gates because active-mode leakage current is too large. In addition, the circuit needs backgate bias, which is much larger than the supply voltage, to increase the threshold voltage and to reduce the leakage current in the sleep mode. To generate the large back-gate bias, multiple supply voltages or a boost circuit are required. The proposed low supply-voltage MTCMOS circuit with SIMOX technology uses enhancement-mode MOSFFTs and contains no boost circuit. High-speed operation of this SIMOX-MTCMOS circuit at 0.5 V supply is obtained by use of low-Vth CMOS logic gates consisting of fully-depleted body-floating MOSFETs.
Autologous biograft and mesenchymal stem cells in treatment of the diabetic foot. (2006)

Closing and healing of the non-healing diabetic ulcer was achieved by using the given combined therapy.
The Effects of Fuel Composition and Fuel Additives on Intake System Detergency of Japanese Automobile Engine (1979)

&lt;div class="htmlview paragraph"&gt;The effects of fuel composition and additives (antioxidant and detergent) on intake system cleanliness have been studied using Japanese automobile engines equipped with EGR systems. The following conclusions were obtained.&lt;/div&gt; &lt;div class="htmlview paragraph"&gt;Cleanliness of the intake system (carburetor and intake manifold) is influenced remarkably by the fuel characteristics, namely the olefin content and the type of antioxidant.&lt;/div&gt; &lt;div class="htmlview paragraph"&gt;The detergent gives a large improvement in the cleanliness of carburetors and intake manifolds, but shows little or no effect on the intake valves.&lt;/div&gt; &lt;div class="htmlview paragraph"&gt;A carrier oil used together with the detergent does reduce the deposit formation especially on the intake valves.&lt;/div&gt; &lt;div class="htmlview paragraph"&gt;The increase of the aromatic content appears to augment the deposits on the cylinder head.&lt;/div&gt;
Blood coagulation at the site of microvascular injury: effects of low-dose aspirin (2001)

The sequence of coagulant reactions in vivo following vascular injury is poorly characterized. Using quantitative immunoassays, the time courses were evaluated for activation of prothrombin, factor (F)V, FXIII, fibrinogen (Fbg) cleavage, and FVa inactivation in bleeding-time blood collected at 30-second intervals from 12 healthy subjects both before and after aspirin ingestion. Prothrombin decreased at a maximum rate of 14.2 +/- 0.6 nM per second to 10% of initial values at the end of bleeding. Significant amounts of alpha-thrombin B chain appeared rapidly at 90 seconds of bleeding and increased at a maximum rate of 0.224 +/- 0.03 nM per second to a peak value of 38 nM. Kinetics of prethrombin 2 generation was almost identical. Prothrombinase concentration reached a peak value of 22 pM at 150 seconds and then decreased to 9 pM at the end of bleeding. Prothrombin fragment 1.2 (F1.2) was produced explosively (0.673 +/- 0.05 nM per second), whereas thrombin-antithrombin III (TAT) complexes were generated at a much slower rate (0.11 +/- 0.008 nM per second; P =.002). FVa light chain was detectable 30 seconds later than the heavy chain (150 seconds) and was produced at a slightly slower rate (0.027 +/- 0.001 nM per second) when compared with the heavy chain (0.032 +/- 0.002 nM per second; P =.041). The 30 000 fragment (residues 307-506) of FVa heavy chain produced by activated protein C appeared as early as at 90 seconds and increased with time. Fbg was removed from the blood shed with a high rate of 0.047 +/- 0.02 microM/s and became undetectable at approximately 180 seconds of bleeding. The velocity of FXIII activation correlated with thrombin B-chain formation. A 7-day aspirin administration (75 mg/d) resulted in significant reductions in maximum rates of (1) prothrombin removal (by 29%; P =.008); generation of alpha-thrombin B-chain (by 27.2%; P =.022), and prethrombin 2 (by 26%; P =.014); formation of F1.2 (by 31.4%; P =.009) and TAT (by 30.3%; P = 0.013); (2) release of FVa heavy chain (by 25%; P =.003) and FVa light chain (by 29.6%; P =.007); (3) Fbg depletion from solution (by 30.5%; P =.002); and (4) FXIII activation (by 28.6%; P =.003). Total amounts of the proteins studied, collected at every interval, also significantly decreased following aspirin ingestion. These results indicate that low-dose aspirin impairs thrombin generation and reactions catalyzed by this enzyme at the site of the injury.