gebhart/patrepeval huggingface dataset:
Ammonium hydrogen tartronate at 240 and 20 K (2001)

The low-temperature structure determination of the title compound, alternatively called ammonium hydrogen hydroxypropanedioate, NH(4)(+) x C(3)H(3)O(5)(-), has revealed that the H atom involved in a very short asymmetric O--H...O hydrogen bond [O...O = 2.448 (2) A at 240 K and 2.4393 (10) A at 20 K] is disordered.
ChemInform Abstract: SYNTHESIS AND BIOLOGICAL EFFECTS OF ACYCLIC PYRIMIDINE NUCLEOSIDE ANALOGS (1982)

Abstract Das geschützte Cytosin (I) reagiert mit dem Chlorether (II) zum Cytosin (III), dessen Spaltung zum Alkohol (IV) führt.
The concentration of bupivacaine in fetal organs during obstetrical epidural analgesia (1986)

The concentration of bupivacaine in organs of non-viable human fetuses after obstetrical epidural analgesia in customary doses was investigated. The concentrations were determined with a gas chromatograph. The material consisted of a fetus who died following termination in the 24th week of pregnancy three minutes after birth without spontaneous respiration. The other fetus was born maturely in the 40th pregnancy week with anencephaly who lived 20 minutes following initial spontaneous respiration. Most noteworthy were the increased concentrations in the liver indicating the important metabolic function of the liver for the metabolism of bupivacaine in the fetus. Further a very high pulmonary concentration was found in the mature fetus. Even though blood gases analysis were not performed we conclude that: the lung is the best perfused organ after birth and onset of spontaneous respiration because of the closure of the ductus arteriosus; because of the increasing agonal respiratory acidosis, bupivacaine accumulates in the lung, the organ from which the acidosis originates. Also, the ionized form the bupivacaine is unable to leave the intracellular space. For the clinical use of epidural analgesia during delivery, these results constitute an important indication for avoiding fetal acidosis before and during the action of such analgesia. This mandates strict and continuous fetal monitoring. Our results in agreement with other authors show that during fetal acidosis and simultaneous administration of bupivacaine the fetal distress may be potentiated by an accelerated transfer of the anesthetic agent into the fetal placental space. Under normal conditions one may assume that this technique of analgesia has a positive effect on the fetus because of the improved placental perfusion.(ABSTRACT TRUNCATED AT 250 WORDS)
The Autonomous Data Optical Relay Experiment: first two way laser communication between an aircraft and submarine (2003)

The Autonomous Data Optical Relay Experiment (ADORE) was held at the Sea Test Range of the Pacific Missile Test Center off the coast of Southern California near San Nicolas Island during May 22-24 and May 28, 1991. The optical communication system operated with a green downlink based on a diode-pumped frequency-doubled Nd:YAG transmitter communicating with a quartz birefringent filter receiver and a blue uplink using an alexandrite laser wavelength shifted to the 455-nm doublet of cesium vapor sending information to a cesium filter receiver. Major achievements of the test included: first duplex laser communication with a submerged submarine; uplink initiated duplex laser communication from a submarine; demonstration of technologies which offer substantially higher performance at lower cost and risk compared with earlier efforts; extending the range and utility of laser communication by error correction coding and pulse summing; and establishing and experimental baseline for developing and investigating covert laser communication with submarine.< <ETX xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink">></ETX>
Ultrastructure of Canine Articular Cartilage: Comparison of Normal and Degenerative (Osteoarthritic) Hip Joints (1975)

Normal canine hip cartilage was compared with cartilage from the degenerative lesions found in young dogs with canine hip dysplasia. The upper 0.5 mm of normal cartilage was characterized. Four distinct layers or zones were found: a layer of fine fibrous material covering the surface, a layer (surface layer) of small (32 nm diameter or less) collagen fibrils tightly packed in bundles and oriented parallel to the surface, a layer (upper layer) or less tightly packed collagen fibrils oriented mostly parallel to the surface with about 33% of the fibrils 64 nm or more, and a layer (intermediate layer) of randomly oriented fibrils with more than 50% of the fibrils 64 nm or larger. Fibril density was high in the surface layer and decreased with depth into the cartilage. In a moderately advanced lesion of degenerative cartilage, there was a layer of amorphous material over the surface. The tightly packed surface layer of small fibrils was absent. The surface itself was uneven and fissued. At depths from the surface comparable to the upper and the intermediate layers in normal cartilage, the proportion of large fibrils was less than in normal cartilage. The overall density of fibrils in degenerative cartilage increased with depth into the tissue. Cells flattened parallel to the surface, with relatively large nuclei, were found in the upper layer of normal cartilage. Cells in the intermediate layers were larger and round. The oblong cells of the upper layer of normal cartilage were not found in any layer of degenerative cartilage. Differences between cells in other layers of normal and degenerative cartilages were minimal. A model for the arrangement of chondrocytes and collagen fibrils for normal and degenerative cartilage was proposed. Ultrastructural changes in degenerative cartilage were prominent in the upper 0.5 mm of cartilage. These changes were changes in the number of collagen fibrils/mum-2 and a change from a characteristic pattern of collagen fibril diameters and orientation found in normal tissue.
Human protein phosphatase 5 dissociates from heat-shock proteins and is proteolytically activated in response to arachidonic acid and the microtubule-depolymerizing drug nocodazole (2004)

Ppp5 (protein phosphatase 5) is a serine/threonine protein phosphatase that has been conserved throughout eukaryotic evolution. In mammalian cells, FLAG-tagged Ppp5 and endogenous Ppp5 are found to interact with endogenous Hsp (heat-shock protein) 70, as well as Hsp90. Incubation of cells with arachidonic acid or the microtubule-depolymerizing agent, nocodazole, causes loss of interaction of Hsp70 and Hsp90 with FLAG-tagged Ppp5 and increase of Ppp5 activity. In response to the same treatments, endogenous Ppp5 undergoes proteolytic cleavage of the N- and C-termini, with the subsequent appearance of high-molecular-mass species. The results indicate that Ppp5 is activated by proteolysis on dissociation from Hsps, and is destroyed via the proteasome after ubiquitination. Cleavage at the C-terminus removes a nuclear localization sequence, allowing these active cleaved forms of Ppp5 to translocate to the cytoplasm. The response of Ppp5 to arachidonic acid and nocodazole suggests that Ppp5 may be required for stress-related processes that can sometimes cause cell-cycle arrest, and leads to the first description for in vivo regulation of Ppp5 activity.
Influence of N interstitials on the electronic properties of GaAsN alloys (2009)

We have used rapid thermal annealing to investigate the influence of N interstitials on the electronic properties of GaAsN alloys. Nuclear reaction analysis reveals an annealing-induced decrease in the interstitial N concentration, while the total N composition remains constant. Corresponding signatures for the reduced interstitial N concentration are apparent in Raman spectra. Following annealing, both the room-T carrier concentration, n, and the mobility increase. At higher measurement-Ts, a thermally activated increase in n suggests the presence of a trap near GaAsN conduction band edge with activation energy 85±15 meV. The annealing-induced increase in n suggests the association of the trap with interstitial N.
EPI-based Multiple Video Camera Calibration for City Modeling (2002)

Diagnostic biomarkers are often measured with errors due to imperfect lab conditions or analytic variability of the assay. The ability of a diagnostic biomarker to discriminate between cases and controls is often measured by the area under the receiver operating characteristic curve (AUC), sensitivity, specificity, among others. Ignoring measurement error can cause biased estimation of a diagnostic accuracy measure, which results in misleading interpretation of the efficacy of a diagnostic biomarker. Existing assays available are either research grade or clinical grade. Research assays are cost effective, often multiplex, but they may be associated with moderate measurement errors leading to poorer diagnostic performance. In comparison, clinical assays may provide better diagnostic ability, but with higher cost since they are usually developed by industry. Correction for attenuation methods are often valid when biomarkers are from a normal distribution, but may be biased with skewed biomarkers. In this paper, we develop a flexible method based on skew-normal biomarker distributions to correct for bias in estimating diagnostic performance measures including AUC, sensitivity, and specificity. Finite sample performance of the proposed method is examined via extensive simulation studies. The methods are applied to a pancreatic cancer biomarker study.
ChemInform Abstract: Convergent Synthesis of the Amphotericin Polyol Subunit Employing Asymmetric Dienolate Addition Reactions. (1998)

Abstract ChemInform is a weekly Abstracting Service, delivering concise information at a glance that was extracted from about 100 leading journals. To access a ChemInform Abstract of an article which was published elsewhere, please select a “Full Text” option. The original article is trackable via the “References” option.
Linkage analysis of adult height with parent-of-origin effects in the Framingham Heart Study (2003)

Current linkage analysis methods for quantitative traits do not usually incorporate imprinting effects. Here, we carried out genome-wide linkage analysis for loci influencing adult height in the Framingham Heart Study subjects using variance components while allowing for imprinting effects. We used a sex-averaged map for the 22 autosomes, while chromosomes 6, 14, 18, and 19 were also analyzed using sex-specific maps. We compared results from these four analyses: 1) non-imprinted with sex-averaged maps, 2) imprinted with sex-averaged maps, 3) non-imprinted with sex-specific maps, and 4) imprinted with sex-specific maps. We found four regions on three chromosomes (14q32, 18p11-q21, 18q21-22, and 19q13) with LOD scores above 2.0, with a maximum LOD score of 3.12, allowing for imprinting and sex-specific maps, at D18S1364 on 18q21. While we obtained significant evidence of imprinting effects in both the 18p11-q21 and 19q13 regions when using sex-averaged maps, there were no significant differences between the imprinted and non-imprinted LOD scores when we used sex-specific maps. Our results illustrate the importance of allowing for gender-specific effects in linkage analyses, whether these are in the form of gender-specific recombination frequencies, or in the form of imprinting effects.
Tenascin-C promotes chronic pressure overload-induced cardiac dysfunction, hypertrophy and myocardial fibrosis (2017)

Our results are pointed toward a novel signaling mechanism that contributes to LV remodeling via MMPs upregulation, cardiomyocyte hypertrophy as well as myocardial fibrosis by TN-C under chronic pressure overload.
Low-Spin Hexacoordinate Mn(III): Synthesis and Spectroscopic Investigation of Homoleptic Tris(pyrazolyl)borate and Tris(carbene)borate Complexes (2012)

Three complexes of Mn(III) with "scorpionate" type ligands have been investigated by a variety of physical techniques. The complexes are [Tp(2)Mn]SbF(6) (1), [Tp(2)*Mn]SbF(6) (2), and [{PhB(MeIm)(3)}(2)Mn](CF(3)SO(3)) (3a), where Tp(-) = hydrotris(pyrazolyl)borate anion, Tp*(-) = hydrotris(3,5-dimethylpyrazolyl)borate anion, and PhB(MeIm)(3)(-) = phenyltris(3-methylimidazol-2-yl)borate anion. The crystal structure of 3a is reported; the structures of 1 and 2 have been previously reported, but were reconfirmed in this work. The synthesis and characterization of [{PhB(MeIm)(3)}(2)Mn]Cl (3b) are also described. These complexes are of interest in that, in contrast to many hexacoordinate (pseudo-octahedral) complexes of Mn(III), they exhibit a low-spin (triplet) ground state, rather than the high-spin (quintet) ground state. Solid-state electronic absorption spectroscopy, SQUID magnetometry, and high-frequency and -field electron paramagnetic resonance (HFEPR) spectroscopy were applied. HFEPR, in particular, was useful in characterizing the S = 1 spin Hamiltonian parameters for complex 1, D = +19.97(1), E = 0.42(2) cm(-1), and for 2, D = +15.89(2), E = 0.04(1) cm(-1). In addition, frequency domain Fourier-transform THz-EPR spectroscopy, using coherent synchrotron radiation, was applied to 1 only and gave results in good agreement with HFEPR. Variable-temperature dc magnetic susceptibility measurements of 1 and 2 were also in good agreement with the HFEPR results. This magnitude of zero-field splitting (zfs) is over 4 times larger than that in comparable hexacoordinate Mn(III) systems with S = 2 ground states. Complexes 3a and 3b (i.e., regardless of counteranion) have a yet much larger magnitude zfs, which may be the result of unquenched orbital angular momentum so that the spin Hamiltonian model is not appropriate. The triplet ground state is rationalized in each complex by ligand-field theory (LFT) and by quantum chemistry theory, both density functional theory and unrestricted Hartree-Fock methods. This analysis also shows that spin-crossover behavior is not thermally accessible for these complexes as solids. The donor properties of the three different scorpionate ligands were further characterized using the LFT model that suggests that the tris(carbene)borate is a strong σ-donor with little or no π-bonding.
Annexin A2 heterotetramer: role in tight junction assembly (2004)

The tight junction has been characterized as a domain of focal fusions of the exoplasmic leaflets of the lipid bilayers from adjacent epithelial cells. Approximating membranes to within fusion distance is a thermodynamically unfavorable process and requires the participation of membrane-bridging or -fusion proteins. No known tight junction protein exhibits such activities. Annexin A2 (A2), in particular its heterotetramer (A2t), is known to form junctions between lipid bilayer structures through molecular bridging of their external leaflets. We demonstrate abundant A2 expression in Madin-Darby canine kidney II monolayers by two-dimensional gel electrophoresis. Confocal immunofluorescence microscopic analysis suggests the bulk of A2 is located along the apical and lateral plasma membrane in its tetrameric configuration, consisting of two A2 and two p11 (an 11-kDa calmodulin-related protein, S100A10) subunits. Immunocytochemistry and ultrastructural immunogold labeling demonstrate colocalization of the A2 subunit with bona fide tight junction proteins, zonula occludens-1, occludin, and claudin-1, at cell-cell contacts. The extracellular addition of a synthetic peptide, targeted to disrupt the binding between A2 and p11, completely aborts tight junction assembly in calcium chelation studies. We propose A2t as a member of a new class of tight junction proteins responsible for the long-observed convergence of adjacent exoplasmic lipid leaflets in tight junction assembly.
MUTANT EGFR SUPPRESSION OF MICRORNA-9 INDUCES FOXP1 TO ENHANCE GLIOBLASTOMA TUMORIGENICITY (2014)

BACKGROUND: Glioblastoma (GBM) frequently displays amplification and/or mutation of the epidermal growth factor receptor (EGFR) gene. Highlighting the importance of EGFR in the pathogenesis of GBM, aberrant EGFR (ΔEGFR, also known as EGFRvIII) confers a variety of biological effects upon its expression, including resistance to radiation and chemotherapeutic agents, promotion of tumor cell motility and invasion, enhancement of tumorigenicity in vivo, and maintenance of GBM growth and heterogeneity. We hypothesized that this diverse oncogenic pathophysiology exerted by ΔEGFR is regulated, in part, through the modulation of microRNA (miR) activity, widely shown to be involved in many biological processes including cancer initiation, maintenance and progression. METHODS: To test this hypothesis, we used miR microarrays to compare miR profiles of GBM cells with activated wild type EGFR (wtEGFR) and ΔEGFR, to cells with non-activated wtEGFR or kinase-dead ΔEGFR. miRs demonstrating differential expression were validated by northern blot analysis and qRT-PCR and potential pathways regulating miR expression were interrogated by pharmacological and genetic analysis. Candidate miR targets were validated by luciferase reporter assays and western blot analysis. The role of validated miRs and targets, in modulating ΔEGFR-mediated tumorgenicity, was analyzed by overexpression and knockdown studies in engineered glioma cell lines engrafted in athymic nude mice. Validated target significance was determined by survival-association expression analysis in a patient cohort of 67 newly diagnosed and 64 recurrent GBM cases. RESULTS: We observed and validated that ΔEGFR suppresses miR-9. The repression of miR-9 was due to the negative regulation of the primary miR-9 encoding transcript, pri-miR-9-2, by ΔEGFR. Downstream of ΔEGFR, the Ras/PI3K/AKT axis was required to suppress miR-9. We identified the transcription factor, FOXP1, to be a bona-fide miR-9 target. Upregulation of miR-9 decreased expression of FOXP1 in ΔEGFR cells, suggesting that miR-9 and FOXP1 may regulate, in part, ΔEGFR-dependent GBM growth. Consistent with this, miR-9 antagonized the tumor growth advantage conferred by ΔEGFR while FOXP1 knock-down inhibited the growth of ΔEGFR-driven tumors. Upregulation of FOXP1, as a consequence of inhibiting miR-9 activity, increased the tumorigenicity of GBM cells, suggesting that miR-9 is a tumor suppressor while FOXP1 likely functions as an oncogenic factor in GBM. Finally, high FOXP1 expression was significantly associated with poor survival in GBM patients, further supporting the notion that FOXP1 is an oncogenic factor. CONCLUSIONS: Collectively, these data reveal a novel regulatory mechanism by which ΔEGFR signaling through the Ras-PI3K-Akt pathway suppresses miR-9, resulting in FOXP1 expression and increased tumorigenicity. SECONDARY CATEGORY: n/a.
Design and Performance Validation of a Conductively Heated Sealed-Vessel Reactor for Organic Synthesis (2016)

A newly designed robust and safe laboratory scale reactor for syntheses under sealed-vessel conditions at 250 °C maximum temperature and 20 bar maximum pressure is presented. The reactor employs conductive heating of a sealed glass vessel via a stainless steel heating jacket and implements both online temperature and pressure monitoring in addition to magnetic stirring. Reactions are performed in 10 mL borosilicate vials that are sealed with a silicone cap and Teflon septum and allow syntheses to be performed on a 2-6 mL scale. This conductively heated reactor is compared to a standard single-mode sealed-vessel microwave instrument with respect to heating and cooling performance, stirring efficiency, and temperature and pressure control. Importantly, comparison of the reaction outcome for a number of different synthetic transformations performed side by side in the new device and a standard microwave reactor suggest that results obtained using microwave conditions can be readily mimicked in the operationally much simpler and smaller conventionally heated device.
Transmission Secondary Emission Image Intensifiers (1962)

The tubes to be described are of the transmission secondary emission type. Electrons from a tri-alkali photo-cathode are accelerated and focused on to a series of dynodes where multiplication takes place by transmitted secondary emission. The electrons from the final dynode are then focused on to the output phosphor.
A new solar reference spectrum from 165 to 3088 nm (2017)

International audience
Glutamate signaling through the kainate receptor is critical for human B cell IgE production (91.9) (2010)

Abstract Glutamate, the major excitatory neurotransmitter, has recently been implicated in a variety of diseases. Patients with HIV, certain cancers, and autoimmune illnesses have elevated levels of glutamate in the periphery. While glutamate receptor signaling has been examined in T cells, there are currently no published observations on the effects of glutamatergic stimuli on B cells. Human B cells were first examined for the presence of glutamate receptors via RT-PCR and Western Blot. The kainate receptor (KAR), a specific subtype of ionotropic glutamate receptor was found on human B cells. We found that KAR activation increased ADAM10 mRNA which is in agreement with receptor activity in the CNS. A significant corresponding increase in CD23 released into the supernatant was seen as ADAM10 has been identified as the protease responsible for CD23’s ectodomain shedding. Remarkably, we also detect a strong increase in cellular proliferation and IgE synthesis. Thus, we report for the first time the unique presence of a neurotransmitter receptor and that activation of this receptor could serve as a novel mechanism for enhancing B cell activation. This enhancement has implications for allergic and autoimmune diseases.
Role of ephrin-A5 in the survival and connectivity of spiral ganglion neurons (2007)

In mammals, degeneration of peripheral auditory neurons constitutes one of the prime causes of the sensorineural hearing loss. We believe that studying the developing auditory portion of the inner ear can provide important insights to mechanisms that would regulate regeneration after injury. In that context, our work has focused on a family of proteins, ephrins and Eph receptors, since they have been shown to have a dynamic influence in regulating developmental functions including axonal growth and guidance, synaptic formation and functions and neurogenesis. We have shown that ephrin-A5, EphA4 and EphA7 are expressed in the cell bodies of the spiral ganglion neurons, at different stages of the cochlear development. Ephrin-A5 also seems to be present in the hair cells of the organ of Corti. On the one hand, we demonstrated that activation of the signaling pathway by complexed ephrin-A5 in spiral ganglion explants reduced neuronal survival. On the other hand, an increase of neuronal survival was observed when blocking this mechanism of transduction by monomeric ephrin-A5. Taken together, these results suggest a role for ephrin/Eph signaling in regulating neuronal population generated in the spiral ganglion, especially during the post-natal period of the cochlear innervation.