gebhart/patrepeval huggingface dataset:
Identification of Some DNA Damage-Inducible Genes of Mycobacterium tuberculosis : Apparent Lack of Correlation with LexA Binding (2001)

The repair of DNA damage is expected to be particularly important to intracellular pathogens such as Mycobacterium tuberculosis, and so it is of interest to examine the response of M. tuberculosis to DNA damage. The expression of recA, a key component in DNA repair and recombination, is induced by DNA damage in M. tuberculosis. In this study, we have analyzed the expression following DNA damage in M. tuberculosis of a number of other genes which are DNA damage inducible in Escherichia coli. While many of these genes were also induced by DNA damage in M. tuberculosis, some were not. In addition, one gene (ruvC) which is not induced by DNA damage in E. coli was induced in M. tuberculosis, a result likely linked to its different transcriptional arrangement in M. tuberculosis. We also searched the sequences upstream of the genes being studied for the mycobacterial SOS box (the binding site for LexA) and assessed LexA binding to potential sites identified. LexA is the repressor protein responsible for regulating expression of these SOS genes in E. coli. However, two of the genes which were DNA damage inducible in M. tuberculosis did not have identifiable sites to which LexA bound. The absence of binding sites for LexA upstream of these genes was confirmed by analysis of LexA binding to overlapping DNA fragments covering a region from 500 bp upstream of the coding sequence to 100 bp within it. Therefore, it appears most likely that an alternative mechanism of gene regulation in response to DNA damage exists in M. tuberculosis.
Phase I Study of Amrubicin Hydrochloride and Cisplatin in Patients Previously Treated for Advanced Non-small Cell Lung Cancer (2006)

The recommended dose was thus determined to be 25 mg/m(2) amrubicin with 20 mg/m(2) cisplatin for 3 consecutive days. A phase II study is currently underway.
Kinetics of Oxidation of Dextrose, Galactose and Fructose, l-Arabinose and d-Xylose by Alkaline Bivalent Copper in Presence of Tartarate (1957)

Article Kinetics of Oxidation of Dextrose, Galactose and Fructose, l-Arabinose and d-Xylose by Alkaline Bivalent Copper in Presence of Tartarate was published on July 1, 1957 in the journal Zeitschrift für Physikalische Chemie (volume 207O, issue 1).
Differential expression of five N‐methyl‐D‐aspartate receptor subunit mRNAs in the cerebellum of developing and adult rats (1994)

Five N-methyl-D-aspartate (NMDA) receptor subunits have been identified thus far: NR1, NR2A, NR2B, NR2C, and NR2D. Here, we have analyzed the expression patterns of mRNAs for the NMDA receptor subunits in the developing and adult rats by in situ hybridization. The developmental changes of the expression patterns were most salient in the cerebellum. In the external granular layer, hybridization signals of mRNAs for NR1, NR2A, NR2B, and NR2C appeared by postnatal day 3, but no NR2D mRNA was expressed at any developmental stage examined. The NR1 mRNA was expressed in all cerebellar neurons at all developmental stage examined. The NR1 mRNA was expressed in all cerebellar neurons at all developmental stages examined. The signals for the NR2A mRNA appeared in Purkinje cells and granule cells during the second postnatal week. The signals for the NR2B mRNA in granule cells were seen transiently during the first 2 weeks after birth. The signals for NR2C mRNA appeared in granule cells and glial cells during the second postnatal week. The signals for NR2D mRNA appeared transiently in Purkinje cells during the first 8 postnatal days; in adult rats, these were seen in stellate and Golgi cells. In the cerebellar nuclei, mRNAs for NR1, NR2A, NR2B, and NR2D were more or less expressed on postnatal day 0, while expression signals for the NR2C mRNA were first detected in postnatal day 14. Thus, the most conspicuous changes of expression patterns were observed in the cerebellar cortex during the first 2 weeks after birth, when development and maturation of the cerebellum proceed most rapidly.
Induction of Early–Immediate Genes by Tumor Necrosis Factor α Contribute to Liver Repair Following Chemical–Induced Hepatotoxicity (1997)

We and others have shown that tumor necrosis factor alpha (TNF-alpha) expression is increased in the livers of experimental animals following exposure to the chemical hepatotoxin, carbon tetrachloride (CCl4). Because TNF-alpha is involved in mediating inflammatory responses, its elevated expression is presumed to be associated with potentiating hepatotoxicity and/or aiding in liver repair processes. To study the role of TNF-alpha in chemical-induced hepatotoxicity, mice were administered neutralizing antibodies to TNF-alpha before administration of low, but hepatotoxic, doses of CCl4. Antibody treatment prevented CCl4-mediated increases in early-immediate gene expression associated with liver regeneration, including expression of c-jun and c-fos proto-oncogenes, as well as DNA binding of the activator protein-1 (AP-1) nuclear transcription factor. Hepatocyte proliferation following CCl4 treatment was also reduced in anti-TNF-alpha antibody-treated mice, as evidenced by a lack of proliferating cell nuclear antigen (PCNA) staining. Antibody treatment slightly delayed liver repair processes, as evidenced by extending the period in which plasma liver enzyme levels were increased and hepatocellular necrosis could be observed. Consistent with the above observations, injection of recombinant TNF-alpha into control mice induced rapid expression of c-jun and c-fos proto-oncogenes. Taken together, these results indicate that TNF-alpha positively modulates liver recovery following CCl4 exposure presumably by stimulating early-immediate genes involved in hepatic mitogenesis, a phenomenon also observed following partial hepatectomy.
Is PSA Testing Still Useful? (2004)

Our website uses cookies to enhance your experience. By continuing to use our site, or clicking "Continue," you are agreeing to our Cookie Policy | Continue JAMA HomeNew OnlineCurrent IssueFor Authors Publications JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry (1919-1959) Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More JN Learning / CMESubscribeJobsInstitutions / LibrariansReprints & Permissions Terms of Use | Privacy Policy | Accessibility Statement 2023 American Medical Association. All Rights Reserved Search All JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Forum Archive JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry Input Search Term Sign In Individual Sign In Sign inCreate an Account Access through your institution Sign In Purchase Options: Buy this article Rent this article Subscribe to the JAMA journal
Surfactant-Assisted Synthesis of SnS Nanowires Grown on Tin Foils (2006)

Crystalline SnS wires of micro- and nanometer scale have been synthesized over tin metal foils at room temperature using a simple surfactant-assisted approach. Scanning electron microscopy, transmission electron microscopy, UV−Vis−near infrared (NIR) and Fourier transform infrared (FTIR) spectroscopy were used to characterize the SnS nanowires. X-ray diffraction (XRD) analysis confirmed the formation of the pure orthorhombic phase of SnS. The optical band gap of the samples was found to be ∼1.4 eV. From the investigation, the formation of nanowires could be explained in two steps: initial cracking/splitting of the nanoflakes was followed by a top-growth mechanism to form ultralong nanowires. Effects of various experimental parameters on the growth mechanism were investigated. Present studies have shown that this facile process also can be extended for the synthesis of other low dimensional structures.
Plastidic Phosphatidic Acid Phosphatases Identified in a Distinct Subfamily of Lipid Phosphate Phosphatases with Prokaryotic Origin (2007)

Plastidic phosphatidic acid phosphatase (PAP) dephosphorylates phosphatidic acid to yield diacylglycerol, which is a precursor for galactolipids, a primary and indispensable component of photosynthetic membranes. Despite its functional importance, the molecular characteristics and phylogenetic origin of plastidic PAP were unknown because no potential homologs have been found. Here, we report the isolation and characterization of plastidic PAPs in Arabidopsis that belong to a distinct lipid phosphate phosphatase (LPP) subfamily with prokaryotic origin. Because no homolog of mammalian LPP was found in cyanobacteria, we sought an LPP ortholog in a more primitive organism, Chlorobium tepidum, and its homologs in cyanobacteria. Arabidopsis had five homologs of cyanobacterial LPP, three of which (LPP gamma, LPP epsilon 1, and LPP epsilon 2) localized to chloroplasts. Complementation of yeast Delta dpp1 Delta lpp1 Delta pah1 by plastidic LPPs rescued the relevant phenotype in vitro and in vivo, suggesting that they function as PAPs. Of the three LPPs, LPP gamma activity best resembled the native activity. The three plastidic LPPs were differentially expressed both in green and nongreen tissues, with LPP gamma expressed the highest in shoots. A knock-out mutant for LPP gamma could not be obtained, although a lpp epsilon 1 lpp epsilon 2 double knock-out showed no significant changes in lipid composition. However, lpp gamma homozygous mutant was isolated only under ectopic overexpression of LPP gamma, suggesting that loss of LPP gamma may cause lethal effect on plant viability. Thus, in Arabidopsis, there are three isoforms of plastidic PAP that belong to a distinct subfamily of LPP, and LPP gamma may be the primary plastidic PAP.
Adhesion of Monocytes to Arterial Endothelium and Initiation of Atherosclerosis Are Critically Dependent on Vascular Cell Adhesion Molecule-1 Gene Dosage (2001)

- Vascular cell adhesion molecule-1 (VCAM-1/Vcam1) is a cytokine-inducible member of the immunoglobulin gene superfamily that is expressed by arterial endothelial cells in regions predisposed to atherosclerosis and at borders of atherosclerotic plaques. To determine whether VCAM-1 expression regulates atherosclerotic lesion formation, we crossed Vcam1 domain 4-deficient (D4D) mice, which partially circumvent the embryonic lethality of Vcam1 null mice, with apolipoprotein E null (Apoe(-/-)) mice, which spontaneously develop hypercholesterolemia and atherosclerosis. In the Apoe(-/-) background, mice homozygous for the Vcam1 D4D allele had markedly reduced arterial VCAM-1 expression, monocyte adherence in the aortic root, and fatty streak formation. Heterozygous Vcam1 D4D mice revealed a Vcam1 gene-dosage effect and had intermediate, yet significant, reductions in these parameters. Our data demonstrate that VCAM-1 plays a pivotal role in the initiation of atherosclerosis in Apoe(-/-) mice.
Evaluation of oxygen uptake kinetics and oxygen kinetics of peripheral skeletal muscle during recovery from exercise in patients with chronic obstructive pulmonary disease (2003)

The biochemical features of skeletal muscle and its contribution to exercise intolerance in patients with chronic obstructive pulmonary disease (COPD) is under active investigation. Near-infrared spectroscopy (NIRS) can non-invasively provide information on the oxidative capacity of muscle. To clarify whether oxygenation of peripheral muscle is one determinant of exercise tolerance, we simultaneously examined the oxygen uptake (V O 2off) kinetics and oxygen kinetics of peripheral skeletal muscle evaluated by NIRS during recovery from exercise in COPD patients. Fifteen patients with COPD and five normal control subjects performed a symptom-limited incremental exercise test. On the following day, all patients performed a constant work rate exercise test while being monitored using NIRS continuously for changes in concentration of oxygenated haemoglobin (HbO2) and during expired gas analysis. We found that the time constant of during recovery from constant work rate exercise (V O 2off) and the time constant of V O 2off during recovery (tau V O 2off) were significantly longer in COPD patients than in normal control subjects. was inversely correlated with absolute values of forced expiratory volume in 1 s (FEV1.0) and FEV1.0 (% predicted). However, no significant correlation was found between and FVC (forced vital capacity), FEV1.0/FVC, or diffusing capacity of the lung for CO (DLCO). Moreover, was inversely correlated with maximal V O 2off and maximal work rate. In contrast, exhibited a significant positive correlation with tau V O 2off. These results indicate that V O 2off kinetics during recovery is related to re-oxygenation of peripheral skeletal muscle evaluated by NIRS in patients with COPD. Therefore, NIRS may be a useful tool to estimate the impairment of cardiopulmonary responses and re-oxygenation of peripheral skeletal muscle during the immediate recovery phase after exercise in COPD patients.
RIF1: A novel regulatory factor for DNA replication and DNA damage response signaling (2014)

DNA double strand breaks (DSBs) are highly toxic to the cells and accumulation of DSBs results in several detrimental effects in various cellular processes which can lead to neurological, immunological and developmental disorders. Failure of the repair of DSBs spurs mutagenesis and is a driver of tumorigenesis, thus underscoring the importance of the accurate repair of DSBs. Two major canonical DSB repair pathways are the non-homologous end joining (NHEJ) and homologous recombination (HR) pathways. 53BP1 and BRCA1 are the key mediator proteins which coordinate with other components of the DNA repair machinery in the NHEJ and HR pathways respectively, and their exclusive recruitment to DNA breaks/ends potentially decides the choice of repair by either NHEJ or HR. Recently, Rap1 interacting factor 1 has been identified as an important component of the DNA repair pathway which acts downstream of the ATM/53BP1 to inhibit the 5'-3' end resection of broken DNA ends, in-turn facilitating NHEJ repair and inhibiting homology directed repair. Rif1 is conserved from yeast to humans but its function has evolved from telomere length regulation in yeast to the maintenance of genome integrity in mammalian cells. Recently its role in the maintenance of genomic integrity has been expanded to include the regulation of chromatin structure, replication timing and intra-S phase checkpoint. We present a summary of these important findings highlighting the various aspects of Rif1 functions and discuss the key implications for genomic integrity.
Hydrogenation of Carbon Dioxide is Promoted by a Task‐Specific Ionic Liquid (2007)

A basic hydrogenation catalyst: The combination of a basic ionic liquid (IL) and a supported ruthenium complex catalyzes the hydrogenation of CO2 with satisfactory activity and selectivity (see scheme). The resulting formic acid is easily collected and the ionic liquid and catalyst can be reused directly after an easy separation step. Supporting information for this article is available on the WWW under http://www.wiley-vch.de/contents/jc_2002/2008/z704487_s.pdf or from the author. Please note: The publisher is not responsible for the content or functionality of any supporting information supplied by the authors. Any queries (other than missing content) should be directed to the corresponding author for the article.
Design and Performance of Circulation Control Geometries (2013)

With the pursuit of more advanced and environmentally-friendly technologies of today’s society, the airline industry has been pushed further to investigate solutions that will reduce airport noise and congestion, cut down on emissions, and improve the overall performance of aircraft. These items directly influence airport size (runway length), flight patterns in the community surrounding the airport, cruise speed, and many other aircraft design considerations which are setting the requirements for next generation aircraft. Leading the research in this movement is NASA, which has set specific goals for the next generation regional airliners and has categorized the designs that meet the criteria as Cruise Efficient Short Takeoff and Land (CESTOL) aircraft. With circulation control (CC) technology addressing most of the next generation requirements listed above, it has recently been gaining more interest, thus the basis of this research. CC is an active flow control method that uses a thin sheet of high momentum jet flow ejected over a curved trailing edge surface and in turn utilizes Coanda effect to increase the airfoil’s circulation, augmenting lift, drag, and pitching moment. The technology has been around for more than 75 years, but is now gaining more momentum for further development due to its significant payoffs in both performance and system complexity. The goal of this research was to explore the design of the CC flap shape and how it influences the local flow field of the system, in attempt to improve the performance of existing CC flap configurations and provide insight into the aerodynamic characteristics of the geometric parameters that make up the CC flap. Multiple dual radius flaps and alternative flap geometry, prescribed radius, flaps were developed by varying specific flap parameters from a baseline dual radius flap configuration that had been previously developed and researched. The aerodynamics of the various flap geometries were analyzed at three different flight conditions using two-dimensional CFD. The flight conditions examined include two low airspeed cases with blown flaps at 60° and 90° of deflection, and a transonic cruise case with no blowing and 0° of flap deflection. Results showed that the shorter flaps of both flap configurations augmented greater lift for the low airspeed cases, with the dual radius flaps producing more lift than the corresponding length prescribed radius. The large lift generation of these flaps was accompanied by significant drag and negative pitching moments. The incremental lift per drag and moment produced was best
TheStaphyloccous aureusEap Protein Activates Expression of Proinflammatory Cytokines (2008)

The extracellular adhesion protein (Eap) secreted by the major human pathogen Staphylococcus aureus is known to have several effects on human immunity. We have recently added to knowledge of these roles by demonstrating that Eap enhances interactions between major histocompatibility complex molecules and human leukocytes. Several studies have indicated that Eap can induce cytokine production by human peripheral blood mononuclear cells (PBMCs). To date, there has been no rigorous attempt to identify the breadth of cytokines produced by Eap stimulation or to identify the cell subsets that respond. Here, we demonstrate that Eap induces the secretion of the proinflammatory cytokines interleukin 6 (IL-6) and tumor necrosis factor alpha (TNF-alpha) by CD14(+) leukocytes (monocytes and macrophages) within direct ex vivo PBMC populations (note that granulocytes are also CD14(+) but are largely depleted from PBMC preparations). Anti-intercellular adhesion molecule 1 (CD54) antibodies inhibited this induction and implicated a role for this known Eap binding protein in cellular activation. IL-6 and TNF-alpha secretion by murine cells exposed to Eap was also observed. The activation of CD14(+) cells by Eap suggests that it could play a significant role in both septic shock and fever, two of the major pathological features of S. aureus infections.
Probing hydration contributions to the thermodynamics of ligand binding by proteins. Enthalpy and heat capacity changes of tacrolimus and rapamycin binding to FK506 binding protein in deuterium oxide and water (1993)

The stabilities of native proteins and protein-ligand complexes result from differential interactions among numerous polar and nonpolar atoms within the proteins and ligands and of these atoms with water. Delineation of the various energetic contributions of the stabilities of proteins or protein-ligand complexes in aqueous solution, and an evaluation of their structural basis, requires a direct account of the changes, in the interactions of the protein with the solvent, that accompany the folding or binding reactions. Two largely nonpolar, structurally related macrolide ligands, tacrolimus (also known as FK506) and rapamycin, each bind with high affinity to a common site on a small FK506 binding protein (FKBP-12) and inhibit its peptidylprolyl cis-trans-isomerase activity. In an effort to elucidate the influence of water on the thermodynamics of their binding reactions, we have measured the enthalpies of tacrolimus and rapamycin binding to FKBP-12, in buffered solutions of H2O (at pH 7.0) or D2O (at pD 7.0), by high-precision titration calorimetry in the temperature range 5-30 degrees C. For both tacrolimus and rapamycin binding, a large enthalpic destabilization of binding is observed in D2O relative to H2O, in the temperature range examined. Additionally, large negative constant pressure heat capacity changes are observed for the binding of the ligands in both H2O and D2O. A thermodynamic analysis is presented to identify the structural determinants of the differences in the energetics of binding in light and heavy water. The analysis suggests that a chief contributor to the observed enthalpic destabilization is the differential hydration, of protein and ligand atoms, by light and heavy water.
Studies on the selectivity of DNA precipitation by spermine (1981)

We have examined the selectivity of the precipitation of DNA by spermine. We have found that the intra- and intermolecular condensation of DNA induced by spermine is highly selective even in the presence of added protein or triphosphates. We have also investigated the influence of buffer components on the threshold concentration of spermine required for DNA precipitation. Representative applications exploiting the selectivity of the precipitation reaction are also described.
Axonal development in the cerebral white matter of the human fetus and infant (2005)

After completion of neuronal migration to form the cerebral cortex, axons undergo rapid elongation to their intra- and subcortical targets, from midgestation through infancy. We define axonal development in the human parietal white matter in this critical period. Immunocytochemistry and Western blot analysis were performed on 46 normative cases from 20-183 postconceptional (PC) weeks. Anti-SMI 312, a pan-marker of neurofilaments, stained axons as early as 23 weeks. Anti-SMI 32, a marker for nonphosphorylated neurofilament high molecular weight (NFH), primarily stained neuronal cell bodies (cortical, subcortical, and Cajal-Retzius). Anti-SMI 31, which stains phosphorylated NFH, was used as a marker of axonal maturity, and showed relatively low levels of staining (approximately one-fourth of adult levels) from 24-34 PC weeks. GAP-43, a marker of axonal growth and elongation, showed high levels of expression in the white matter from 21-64 PC weeks and lower, adult-like levels beyond 17 postnatal months. The onset of myelination, as seen by myelin basic protein expression, was approximately 54 weeks, with progression to "adult-like" staining by 72-92 PC weeks. This study provides major insight into axonal maturation during a critical period of growth, over an age range not previously examined and one coinciding with the peak period of periventricular leukomalacia (PVL), the major disorder underlying cerebral palsy in premature infants. These data suggest that immature axons are susceptible to damage in PVL and that the timing of axonal maturation must be considered toward establishing its pathology relative to the oligodendrocyte/myelin/axonal unit.