gebhart/patrepeval huggingface dataset:
Direct and indirect lactate oxidation in trained and untrained men (2013)

Lactate has been shown to be an important oxidative fuel. We aimed to quantify the total lactate oxidation rate (Rox) and its direct vs. indirect (glucose that is gluconeogenically derived from lactate and subsequently oxidized) components (mg·kg(-1)·min(-1)) during rest and exercise in humans. We also investigated the effects of endurance training, exercise intensity, and blood lactate concentration ([lactate]b) on direct and indirect lactate oxidation. Six untrained (UT) and six trained (T) men completed 60 min of constant load exercise at power outputs corresponding to their lactate threshold (LT). T subjects completed two additional 60-min sessions of constant load exercise at 10% below the LT workload (LT-10%), one of which included a lactate clamp (LC; LT-10%+LC). Rox was higher at LT in T [22.7 ± 2.9, 75% peak oxygen consumption (Vo2peak)] compared with UT (13.4 ± 2.5, 68% Vo2peak, P < 0.05). Increasing [lactate]b (LT-10%+LC, 67% Vo2peak) significantly increased lactate Rox (27.9 ± 3.0) compared with its corresponding LT-10% control (15.9 ± 2.2, P < 0.05). Direct and indirect Rox increased significantly from rest to exercise, and their relative partitioning remained constant in all trials but differed between T and UT: direct oxidation comprised 75% of total lactate oxidation in UT and 90% in T, suggesting the presence of training-induced adaptations. Partitioning of total carbohydrate (CHO) use showed that subjects derived one-third of CHO energy from blood lactate, and exogenous lactate infusion increased lactate oxidation significantly, causing a glycogen-sparing effect in exercising muscle.
Intestinal barrier in inflammatory bowel disease (2014)

A complex mucosal barrier protects as the first line of defense the surface of the healthy intestinal tract from adhesion and invasion by luminal microorganisms. In this review, we provide an overview about the major components of this protective system as for example an intact epithelium, the synthesis of various antimicrobial peptides (AMPs) and the formation of the mucus layer. We highlight the crucial importance of their correct functioning for the maintenance of a proper intestinal function and the prevention of dysbiosis and disease. Barrier disturbances including a defective production of AMPs, alterations in thickness or composition of the intestinal mucus layer, alterations of pattern-recognition receptors, defects in the process of autophagy as well as unresolved endoplasmic reticulum stress result in an inadequate host protection and are thought to play a crucial role in the pathogenesis of the inflammatory bowel diseases Crohn's disease and ulcerative colitis.
Variability of 11q23 rearrangements in hematopoietic cell lines identified with fluorescence in situ hybridization. (1993)

We mapped and ordered 17 cosmid, phage, and plasmid clones to chromosome 11, bands q22-q24, using fluorescence in situ hybridization (FISH). We then analyzed four hematopoietic cell lines with 11q23 rearrangements, Karpas 45, SUP-T13, RC-K8, and Karpas 422, using these probes. The studies showed that the translocation breakpoints of the Karpas 45 and SUP-T13 cell lines, which were derived from T-cell malignancies, were located in the same breakpoint cluster region of the MLL gene as the RS4; 11 cell line and patients with the t(9;11), t(11;19), and t(6;11) described previously. We confirmed that the translocation breakpoint of the RC-K8 cell line was located telomeric to the MLL gene, and found that the derivative 11 chromosome of the Karpas 422 cell line, which had been thought to contain a t(4;11) (q21;q23), was in fact formed through a deletion and an inverted tandem repeat of part of 11q.
Enabling high-temperature nanophotonics for energy applications (2012)

The nascent field of high-temperature nanophotonics could potentially enable many important solid-state energy conversion applications, such as thermophotovoltaic energy generation, selective solar absorption, and selective emission of light. However, special challenges arise when trying to design nanophotonic materials with precisely tailored optical properties that can operate at high-temperatures (> 1,100 K). These include proper material selection and purity to prevent melting, evaporation, or chemical reactions; severe minimization of any material interfaces to prevent thermomechanical problems such as delamination; robust performance in the presence of surface diffusion; and long-range geometric precision over large areas with severe minimization of very small feature sizes to maintain structural stability. Here we report an approach for high-temperature nanophotonics that surmounts all of these difficulties. It consists of an analytical and computationally guided design involving high-purity tungsten in a precisely fabricated photonic crystal slab geometry (specifically chosen to eliminate interfaces arising from layer-by-layer fabrication) optimized for high performance and robustness in the presence of roughness, fabrication errors, and surface diffusion. It offers near-ultimate short-wavelength emittance and low, ultra-broadband long-wavelength emittance, along with a sharp cutoff offering 41 emittance contrast over 10% wavelength separation. This is achieved via Q-matching, whereby the absorptive and radiative rates of the photonic crystal's cavity resonances are matched. Strong angular emission selectivity is also observed, with short-wavelength emission suppressed by 50% at 75° compared to normal incidence. Finally, a precise high-temperature measurement technique is developed to confirm that emission at 1,225 K can be primarily confined to wavelengths shorter than the cutoff wavelength.
Specific Interactions in Modified Chitosan Systems (2005)

This paper concerns the bulk and interfacial properties of a series of alkylated chitosans having different alkyl chain lengths grafted randomly along the main chitosan chain. Chitosan has a low degree of acetylation (5%); on chitosan derivatives, the role of the degree of grafting and of length of the alkyl chains are examined. The optimum alkyl chain length is C12 and the degree of grafting 5% to get physical gelation based on the formation of hydrophobic domains. The cross-linking is essentially controlled by the salt concentration: it is shown that 0.025 M AcONa is needed to screen electrostatic interchain repulsions. Hydrophobic interactions produce highly non-Newtonian behavior with large thinning behavior; this behavior is suppressed in the presence of cyclodextrins able to cap the hydrophobic alkyl chains. The interfacial properties of the chitosan derivatives were tested for the air/aqueous solution interfaces. Specifically, the role of their structure on the kinetic of film formation was examined showing that excess of external salt favors the stabilization of the interfacial film. The derivatives with a higher degree of substitution and longer alkyl chains are more efficient and give a higher elastic modulus compared to the model surfactant as a result of the chain properties.
Genome Analysis Reveals Interplay between 5′UTR Introns and Nuclear mRNA Export for Secretory and Mitochondrial Genes (2011)

In higher eukaryotes, messenger RNAs (mRNAs) are exported from the nucleus to the cytoplasm via factors deposited near the 5' end of the transcript during splicing. The signal sequence coding region (SSCR) can support an alternative mRNA export (ALREX) pathway that does not require splicing. However, most SSCR-containing genes also have introns, so the interplay between these export mechanisms remains unclear. Here we support a model in which the furthest upstream element in a given transcript, be it an intron or an ALREX-promoting SSCR, dictates the mRNA export pathway used. We also experimentally demonstrate that nuclear-encoded mitochondrial genes can use the ALREX pathway. Thus, ALREX can also be supported by nucleotide signals within mitochondrial-targeting sequence coding regions (MSCRs). Finally, we identified and experimentally verified novel motifs associated with the ALREX pathway that are shared by both SSCRs and MSCRs. Our results show strong correlation between 5' untranslated region (5'UTR) intron presence/absence and sequence features at the beginning of the coding region. They also suggest that genes encoding secretory and mitochondrial proteins share a common regulatory mechanism at the level of mRNA export.
Constitutive Activation of STAT5A Promotes Human Hematopoietic Stem Cell Self-Renewal and Erythroid Differentiation (2004)

Activation of the transcription factor signal transducer and activator of transcription (STAT)5 is involved in various aspects of hematopoiesis, affecting cell proliferation, differentiation, and cell survival. Constitutive activation of STAT5 has also been associated with leukemic transformation. We overexpressed the constitutively active mutant STAT5A(1*6) in human cord blood CD34+ cells and evaluated the effects on the hematopoietic potential of stem cells in a variety of in vitro and in vivo systems. The observed phenotypic changes were correlated with differential gene expression patterns induced by STAT5A(1*6). Our data indicate that a persistent activation of STAT5A in human hematopoietic stem and progenitor cells results in their enhanced self-renewal and diverts differentiation to the erythroid lineage.
An in vivo model of experimental arterial stenosis, intimal damage, and periodic thrombosis. (1991)

Coronary artery bypass grafts, angioplasty, and thrombolysis are beneficial procedures for patients with coronary artery disease. However, these procedures can fail by mechanisms related to interactions between platelets and the damaged arterial wall. An experimental model for studying some of the mechanisms of platelet interaction with endothelial- and medial-damaged stenosed arteries is described. Dogs or pigs are anesthetized, and the chest opened. The heart is exposed, the circumflex or left anterior descending coronary artery is dissected out, and an EMF or Doppler flow probe is placed on it. Distal to the flow probe, the artery is clamped with a vascular clamp to produce endothelial and/or medial injury. Then, an encircling plastic cylinder is placed around the outside of the injured artery, producing a "critical stenosis." Acute platelet thrombus formation begins to occur in the stenosed lumen, gradually increasing the amount of stenosis. This causes the coronary flow to decline and reach zero flow when the artery is completely occluded. Then, the thrombus is embolized into the distal circulation, and flow is restored to normal levels. This occurs repeatedly causing cyclic flow reductions (CFRs). These CFRs can be made larger and to occur more frequently by increasing in vivo platelet activity, by raising the plasma catecholamine levels, or by increasing the collagen exposed in the stenosed lumen by increased medial damage. If an effective dose of an antiplatelet agent is given, the CFRs will be decreased in size and frequency or abolished entirely. Aspirin and other agents abolish the CFRs in this model; however, CFRs can be renewed by infusions of catecholamines or platelet activating factor. Thus, the model may be useful for studying mechanisms that enhance or inhibit arterial thrombosis in stenosed arteries with endothelial and medial injury.
Structure and Chromosomal Localization of theRAE28/HPHIGene, a Human Homologue of thePotyhomeoticGene (2000)

The Polycomb group of (Pc-G) genes and trithorax group of genes are known to play a crucial role in the maintenance of the transcriptional repression state of Hox genes, probably through modification of the chromatin configuration. The rae28/mph1 gene is a mammalian homologue of the Drosophila polyhomeotic gene, which belongs to the Pc-G genes. As reported previously, we established mice deficient in the rae28/mph1 gene and showed that these homozygous animals displayed the developmental defects compatible with a human congenital disorder, CATCH22 syndrome. In this study we analyzed the structural organization of the human counterpart of the rae28/mph1 gene (RAE28/HPH1) and its processed pseudogene (psiPH), which are located on, respectively, human chromosome 12p13 and 12q13. The HPH1 gene consists of 15 exons spanning approximately 26 kb and its structural organization is well conserved between mouse and human. These genetic information of the RAE28/HPH1 gene may provide an important clue for further examination of its involvement in human congenital disorders related to CATCH22 syndrome.
Analysis ofcepAand otherBacteroides fragilisgenes reveals a unique promoter structure (2000)

There is little known about the sequences that mediate the initiation of transcription in Bacteroides fragilis, thus transcriptional start sites for 13 new genes were determined and a total of 23 promoter regions upstream of the start sites were aligned and similarities were noted. A region at about -7 contained a consensus sequence of TAnnTTTG and upstream in the region centered at about -33, another TTTG motif was found in the majority of promoters examined. Canonical, Escherichia coli, -10 and -35 consensus sequences were not readily apparent. Mutations within the -7 motif indicated the TTTG residues were essential since changes in this sequence reduced the promoter activity to that of a no promoter control in a chloramphenicol acetyl transferase transcriptional fusion model system. Additional fusion studies indicated that the -33 region was also necessary for full activity.
Cloning and mapping of variety-specific rice genomic DNA sequences: amplified fragment length polymorphisms (AFLP) from silver-stained Polyacrylamide gels (1996)

An efficient technique for cloning DNA from silver-stained denaturing polyacrylamide gels was developed to allow the isolation of specific bands obtained from selective restriction fragment amplification (SRFA). This method proved as reliable as cloning radioactively labelled SRFA bands from the same gels. Rice DNA was used as a template, both with and without [32P]dCTP, using the same PCR profiles. Amplified products were separated using denaturing polyacryamide gel electrophoresis and visualized either by silver staining of gels or by autoradiography of 32P-labelled products. We cloned specific polymorphic SRFA bands directly from the denaturing polyacrylamide gels with one round of PCR amplification and confirmed that the sequences of the bands from silver-stained gels were identical to the corresponding 32P-labelled bands. The bands that were chosen represented amplified fragment length polymorphisms (AFLPs) between japonica and indica rice varieties. We studied the ability of two cloned AFLP bands to serve as heritable genetic markers by mapping them as RFLPs in an interspecific rice population and found that they represented single-copy DNA at unique loci in the rice genome.
Inactivation of the inhA -Encoded Fatty Acid Synthase II (FASII) Enoyl-Acyl Carrier Protein Reductase Induces Accumulation of the FASI End Products and Cell Lysis of Mycobacterium smegmatis (2000)

The mechanism of action of isoniazid (INH), a first-line antituberculosis drug, is complex, as mutations in at least five different genes (katG, inhA, ahpC, kasA, and ndh) have been found to correlate with isoniazid resistance. Despite this complexity, a preponderance of evidence implicates inhA, which codes for an enoyl-acyl carrier protein reductase of the fatty acid synthase II (FASII), as the primary target of INH. However, INH treatment of Mycobacterium tuberculosis causes the accumulation of hexacosanoic acid (C(26:0)), a result unexpected for the blocking of an enoyl-reductase. To test whether inactivation of InhA is identical to INH treatment of mycobacteria, we isolated a temperature-sensitive mutation in the inhA gene of Mycobacterium smegmatis that rendered InhA inactive at 42 degrees C. Thermal inactivation of InhA in M. smegmatis resulted in the inhibition of mycolic acid biosynthesis, a decrease in hexadecanoic acid (C(16:0)) and a concomitant increase of tetracosanoic acid (C(24:0)) in a manner equivalent to that seen in INH-treated cells. Similarly, INH treatment of Mycobacterium bovis BCG caused an inhibition of mycolic acid biosynthesis, a decrease in C(16:0), and a concomitant accumulation of C(26:0). Moreover, the InhA-inactivated cells, like INH-treated cells, underwent a drastic morphological change, leading to cell lysis. These data show that InhA inactivation, alone, is sufficient to induce the accumulation of saturated fatty acids, cell wall alterations, and cell lysis and are consistent with InhA being a primary target of INH.
A DNA damage-activated checkpoint kinase phosphorylates tau and enhances tau-induced neurodegeneration (2010)

Hyperphosphorylation of the microtubule associated protein tau is detected in the brains of individuals with a range of neurodegenerative diseases including Alzheimer's disease (AD). An imbalance in phosphorylation and/or dephosphorylation of tau at disease-related sites has been suggested to initiate the abnormal metabolism and toxicity of tau in disease pathogenesis. However, the mechanisms underlying abnormal phosphorylation of tau in AD are not fully understood. Here, we show that the DNA damage-activated Checkpoint kinase 2 (Chk2) is a novel tau kinase and enhances tau toxicity in a transgenic Drosophila model. Overexpression of Drosophila Chk2 increases tau phosphorylation at Ser262 and enhances tau-induced neurodegeneration in transgenic flies expressing human tau. The non-phosphorylatable Ser262Ala mutation abolishes Chk2-induced enhancement of tau toxicity, suggesting that the Ser262 phosphorylation site is involved in the enhancement of tau toxicity by Chk2. In vitro kinase assays revealed that human Chk2 and a closely related checkpoint kinase 1 (Chk1) directly phosphorylate human tau at Ser262. We also demonstrate that Drosophila Chk2 does not modulate the activity of the fly homolog of microtubule affinity regulating kinase, which has been shown to be a physiological tau Ser262 kinase. Since accumulation of DNA damage has been detected in the brains of AD patients, our results suggest that the DNA damage-activated kinases Chk1 and Chk2 may be involved in tau phosphorylation and toxicity in the pathogenesis of AD.
Kinome expression profiling of human neuroblastoma tumors identifies potential drug targets for ultra high-risk patients (2017)

Neuroblastoma (NBL) accounts for >7% of malignancies in patients younger than 15 years. Low- and intermediate-risk patients exhibit excellent or good prognosis after treatment, whereas for high-risk (HR) patients, the estimated 5-year survival rates is still <40%. The ability to stratify HR patients that will not respond to standard treatment strategies is critical for informed treatment decisions. In this study, we have generated a specific kinome gene signature, named Kinome-27, which is able to identify a subset of HR-NBL tumors, named ultra-HR NBL, with highly aggressive clinical behavior that not adequately respond to standard treatments. We have demonstrated that NBL cell lines expressing the same kinome signature of ultra-HR tumors (ultra-HR-like cell lines) may be selectively targeted by the use of two drugs [suberoylanilide hydroxamic acid (SAHA) and Radicicol], and that the synergic combination of these drugs is able to block the ultra-HR-like cells in G2/M phase of cell cycle. The use of our signature in clinical practice will allow identifying patients with negative outcome, which would benefit from new and more personalized treatments. Preclinical in vivo studies are needed to consolidate the SAHA and Radicicol treatment in ultra-HR NBL patients.
Subanesthetic Effects of the Noncompetitive NMDA Antagonist, Ketamine, in Humans (1994)

These data indicate that N-methyl-D-aspartate antagonists produce a broad range of symptoms, behaviors, and cognitive deficits that resemble aspects of endogenous psychoses, particularly schizophrenia and dissociative states.
Ultrasonographic Features of Papillary Thyroid Carcinoma in Patients with Graves' Disease (2010)

Our results suggest that patients with Graves' disease more frequently have atypical PTC findings on ultrasonography.
Localization of the site of origin of cardiac activation by means of a heart-model-based electrocardiographic imaging approach (2001)

We have developed a new approach to solve the inverse problem of electrocardiography in terms of heart model parameters. The inverse solution of the electrocardiogram (ECG) inverse problem is defined, in the present study, as the parameters of the heart model, which are closely related to the physiological and pathophysiological status of the heart, and is estimated by using an optimization system of heart model parameters, instead of solving the matrix equation relating the body surface ECGs and equivalent cardiac sources. An artificial neural network based preliminary diagnosis system has been developed to limit the searching space of the optimization algorithm and to initialize the model parameters in the computer heart model. The optimal heart model parameters were obtained by minimizing the objective functions, as functions of the observed and model-generated body surface ECGs. We have tested the feasibility of the newly developed technique in localizing the site of origin of cardiac activation using a pace mapping protocol. The present computer simulation results show that, the present approach for localization of the site of origin of ventricular activation achieved an averaged localization error of about 3 mm [for 5-muV Gaussian white noise (GWN)] and 4 mm (for 10-muV GWN), with standard deviation of the localization errors of being about 1.5 mm. The present simulation study suggests that this newly developed approach provides a robust inverse solution, circumventing the difficulties of the ECG inverse problem, and may become an important alternative to other ECG inverse solutions.
Fast and robust two- and three-qubit swapping gates on multi-atomic ensembles in quantum electrodynamic cavity (2011)

Creation of quantum computer is outstanding fundamental and practical problem. The quantum computer could be used for execution of very complicated tasks which are not solvable with the classical computers. The first prototype of solid state quantum computer was created in 2009 with superconducting qubits. However, it suffers from the decoherent processes and it is desirable to find more practical encoding of qubits with long-lived coherence. It could be single impurity or vacancy centers in solids, but their interaction with electromagnetic radiation is rather weak. So, here, ensembles of atoms were proposed for the qubit encoding by using the dipole blockade mechanism in order to turn multilevel systems in two level ones. But dipole-dipole based blockade introduces an additional decoherence that limits its practical significance. Recently, the collective blockade mechanism has been proposed for the system of three-level atoms by using the different frequency shifts for the Raman transitions between the collective atomic states characterized by a different number of the excited atoms. Here, we propose two qubit gate by using another collective blockade mechanism in the system of two level atoms based on exchange interaction via the virtual photons between the multi-atomic ensembles in the resonator. Also we demonstrate the possibility of three qubit gate (Controlled SWAP gate) using a suppression of the swap-process between two multi-atomic ensembles due to dynamical shift of the atomic levels controlled by the states of photon encoded qubit.