gebhart/patrepeval huggingface dataset:
Sizes and shapes of 10-Ma Distal fall pyroclasts in the Ogallala gGroup, Nebraska (2003)

Size distributions of distal ashfall particles from correlated 10-Ma layers in Nebraska, measured using laser diffraction methods, are lognormal with mode diameters of ∼90 mm. This ashfall is ∼100% bubble-wall shards of rhyolite glass and apparently represents a distal ashfall from an eruption 1400 km away. Measured terminal velocities of these ash particles are 0.2–18 cm/s, consistent with Stokes Law settling of spherical particles with diameters of 9–50 mm. Surface area of the ash particles, measured with gas adsorption, is 20–30 times the surface area of equivalent Stokes spheres. These results highlight the effects of shape and atmospheric drag in distal ashfalls. They also highlight atmospheric transport and fallout of distal ashfall particles, because these deposits resemble many other ashfalls preserved in the Great Plains of North America throughout the Tertiary and Quaternary. Because the ashfalls preserve major mammalian death assemblages, they demonstrate that deposits with modes of optical diameters 1100 mm are still hazardous by aerodynamic definitions of lung disease risk and include particles substantially within hazardous PM10 ranges. The aerodynamically fine particle size may lead to substantial aeolian redistribution, causing local thicknesses of 12 m. Overall, the ashfall thicknesses observed are at least several times larger than would be expected based on exponential thinning from the volcano. Shape measurements of distal ash particles may be necessary to assess risk. The possible health risks in the central United States from a future rhyolitic eruption in the western United States may be significant.
Bends in Optical Dielectric Guides (1969)

Light transmission through a curved dielectric rod of rectangular cross section embedded in different dielectrics is analyzed in closed, though approximate form. We distinguish three ranges: (i) Small cross section guides such as a thin glass ribbon surrounded by air—Making its width 1 percent of the wavelength, most of the power travels outside of the glass; the attenuation coefficient of the guide is two orders of magnitude smaller than that of glass, and the radius of curvature that doubles the straight guide loss is around 10,000Λ. (ii) Medium cross section guide for integration optics—It is only a few microns on the side and capable of guiding a single mode either in low loss bends with short radii of curvature or in a high Q closed loop useful for filters. Q's of the order of 10 <sup xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink">8</sup> are theoretically achievable in loops with radii ranging from 0.04 to 1 mm, if the percentage refractive index difference between guide and surrounding dielectric lies between 0.1 and 0.01. (iii) Large cross section guides—They are multimode and are used in fiber optics. Conversion to higher order modes are found more significant than radiation loss resulting from curvature.
Continuous culture of human lymphoblasts from peripheral blood of a child with acute leukemia (1965)

H blood buffy coat specimens derived from leukemic and non-leukemic patients have been studied extensively by various methods of cell culture with and without "feeder layers."l, 4, 6 , 1 6 , 2 1 Recent studies employing modifications of these methods of stationary or monolayer cell culture have resulted in the derivation of a line of monocytic cells from the buffy coat of an adult leukemic patient.11 In these laboratories (and ekewhere, so far as is known at this time) experience with a variety of stationary or monolayer cultures initiated with cells obtained from bone marrow and peripheral blood buffy coat of children with acute leukemia during the past 10 or more years has been unsuccessful.
Biomedical Nanomagnetics: A Spin Through Possibilities in Imaging, Diagnostics, and Therapy (2010)

Biomedical nanomagnetics is a multidisciplinary area of research in science, engineering and medicine with broad applications in imaging, diagnostics and therapy. Recent developments offer exciting possibilities in personalized medicine provided a truly integrated approach, combining chemistry, materials science, physics, engineering, biology and medicine, is implemented. Emphasizing this perspective, here we address important issues for the rapid development of the field, i.e., magnetic behavior at the nanoscale with emphasis on the relaxation dynamics, synthesis and surface functionalization of nanoparticles and core-shell structures, biocompatibility and toxicity studies, biological constraints and opportunities, and in vivo and in vitro applications. Specifically, we discuss targeted drug delivery and triggered release, novel contrast agents for magnetic resonance imaging, cancer therapy using magnetic fluid hyperthermia, in vitro diagnostics and the emerging magnetic particle imaging technique, that is quantitative and sensitive enough to compete with established imaging methods. In addition, the physics of self-assembly, which is fundamental to both biology and the future development of nanoscience, is illustrated with magnetic nanoparticles. It is shown that various competing energies associated with self-assembly converge on the nanometer length scale and different assemblies can be tailored by varying particle size and size distribution. Throughout this paper, while we discuss our recent research in the broad context of the multidisciplinary literature, we hope to bridge the gap between related work in physics/chemistry/engineering and biology/medicine and, at the same time, present the essential concepts in the individual disciplines. This approach is essential as biomedical nanomagnetics moves into the next phase of innovative translational research with emphasis on development of quantitative in vivo imaging, targeted and triggered drug release, and image guided therapy including validation of delivery and therapy response.
Flexible and Transparent Gas Molecule Sensor Integrated with Sensing and Heating Graphene Layers (2014)

Graphene leading to high surface-to-volume ratio and outstanding conductivity is applied for gas molecule sensing with fully utilizing its unique transparent and flexible functionalities which cannot be expected from solid-state gas sensors. In order to attain a fast response and rapid recovering time, the flexible sensors also require integrated flexible and transparent heaters. Here, large-scale flexible and transparent gas molecule sensor devices, integrated with a graphene sensing channel and a graphene transparent heater for fast recovering operation, are demonstrated. This combined all-graphene device structure enables an overall device optical transmittance that exceeds 90% and reliable sensing performance with a bending strain of less than 1.4%. In particular, it is possible to classify the fast (≈14 s) and slow (≈95 s) response due to sp(2) -carbon bonding and disorders on graphene and the self-integrated graphene heater leads to the rapid recovery (≈11 s) of a 2 cm × 2 cm sized sensor with reproducible sensing cycles, including full recovery steps without significant signal degradation under exposure to NO2 gas.
Regulation of Natural mRNAs by the Nonsense-Mediated mRNA Decay Pathway (2014)

The nonsense-mediated mRNA decay (NMD) pathway is a specialized mRNA degradation pathway that degrades select mRNAs. This pathway is conserved in all eukaryotes examined so far, and it triggers the degradation of mRNAs that prematurely terminate translation. Originally identified as a pathway that degrades mRNAs with premature termination codons as a result of errors during transcription, splicing, or damage to the mRNA, NMD is now also recognized as a pathway that degrades some natural mRNAs. The degradation of natural mRNAs by NMD has been identified in multiple eukaryotes, including Saccharomyces cerevisiae, Drosophila melanogaster, Arabidopsis thaliana, and humans. S. cerevisiae is used extensively as a model to study natural mRNA regulation by NMD. Inactivation of the NMD pathway in S. cerevisiae affects approximately 10% of the transcriptome. Similar percentages of natural mRNAs in the D. melanogaster and human transcriptomes are also sensitive to the pathway, indicating that NMD is important for the regulation of gene expression in multiple organisms. NMD can either directly or indirectly regulate the decay rate of natural mRNAs. Direct NMD targets possess NMD-inducing features. This minireview focuses on the regulation of natural mRNAs by the NMD pathway, as well as the features demonstrated to target these mRNAs for decay by the pathway in S. cerevisiae. We also compare NMD-targeting features identified in S. cerevisiae with known NMD-targeting features in other eukaryotic organisms.
Strong Neuroprotection by Inhibition of NF-κB After Neonatal Hypoxia-Ischemia Involves Apoptotic Mechanisms but Is Independent of Cytokines (2008)

Inhibition of NF-kappaB has strong neuroprotective effects that involve downregulation of apoptotic molecules but are independent of inhibition of cytokine production.
Alterations in nitric oxide production in various forms of circulatory shock. (1995)

The free radical nitric oxide (NO.) is synthesized from the guanidino group of L-arginine by a family of enzymes termed NO. synthase (NOS). In the earlier phases of shock, activation of the endothelial, constitutive NOS (ecNOS) occurs, which, in the case of endotoxic shock, is triggered by endotoxin-induced, acute release of platelet-activating factor (PAF) and also other potential mediators. This early overproduction of NO. results in reduced contractile responsiveness to norepinephrine and contributes to the acute decrease in blood pressure afforded by endotoxin. In the delayed phase of endotoxic shock, a distinct isoform of NOS (iNOS) is induced in various organs and in the vessel wall. The induction of iNOS is mediated by the release of endogenous tumor necrosis factor-alpha (TNF-alpha), interleukin-1 (IL-1), and PAF by endotoxin. These mediators, in turn, act in parallel, or in synergy to induce iNOS. Induction of iNOS contributes to delayed vascular hyporeactivity in vivo and ex vivo, and to the delayed decrease in blood pressure in rats with endotoxic shock. As endotoxic shock, hemorrhagic shock also leads to an early activation of ecNOS, which is responsible for the early vascular hyporeactivity, and a delayed induction of iNOS that contributes to delayed circulatory failure (vascular decompensation and hyporeactivity). The induction of iNOS in hemorrhagic shock is unlikely to be mediated by endogenous release of endotoxin, e.g., due to intestinal ischemia. Endogenous circulating glucocorticoids exert a tonic suppression of the induction of iNOS, as well as the cardiovascular failure in response to endotoxin. Endotoxin tolerance is associated with increased plasma levels of glucocorticoids, which may account for the blunted cardiovascular response and reduced induction of iNOS in these animals. A wide variety of drugs that exert protective effects in various models of circulatory shock also inhibit the induction of iNOS, and this effect is likely to contribute to their protective actions. These drugs include glucocorticoids, TNF-alpha antibodies, IL-1 receptor blockers/antibodies, PAF antagonists, dihydropyridine calcium-channel antagonists, tyrosine kinase inhibitors, and the experimental drug cloricromene. Various forms of shock can also lead to an inhibition of NO. production by the calcium-dependent ecNOS.(ABSTRACT TRUNCATED AT 400 WORDS)
A convergent liquid‐phase synthesis of salmon calcitonin (1999)

Salmon calcitonin (sCT) was prepared in good yield and high purity by the condensation of Nalpha-Boc-cyclic decapeptide, Boc-C1SNLSTC7VLG-OH (1,7-disulfide), with protected docosapeptide (Psc)LSQE(OPse)LHK(Psc)LQTYPRTNTGSGTP-NH2 x 3TFA, followed by deprotection of Boc with trifluoroacetic acid and Psc/Pse with piperidine. The 2-(phenylsulfonyl)ethoxycarbonyl (Psc) and 2-(phenylsulfonyl)ethyl (Pse) protecting groups were recently developed. The two peptides were built up by stepwise and fragment condensation using appropriate Nalpha-Boc-amino acids and subsequent deprotection in solution. The synthetic sCT exhibited hypocalcemic potency of more than 4000 IU/mg in rats.
Migration of Fibroblastoid Stromal Cells In Murine Blood (1985)

This paper describes the kinetics of fibroblastic colony forming units (CFU-f) in murine blood after phenylhydrazine-induced haemolytic anaemia and their subsequent migration into haemopoietic organs. Murine blood contained 5.3 +/- 0.8 CFU-f per 10(6) nucleated cells. Absence of particle ingestion and factor VIII-related antigen in addition to the enzyme pattern in CFU-f-derived cells confirmed that these cells did not have a macrophage-like or endothelial nature. Phenylhydrazine treatment of mice resulted in a 3-fold increase in blood CFU-f numbers which was accompanied by increases in blood cellularity and granulocyte-macrophage progenitor numbers. When both partners of CBA/N and CBA/T6T6 mice in parabiosis had been treated with phenylhydrazine, spleens and femoral bone marrow of both mice were shown to contain partner-derived CFU-f. These data suggest that circulating CFU-f represent a stromal cell population which can migrate into haemopoietic organs.
Fast, scalable generation of high‐quality protein multiple sequence alignments using Clustal Omega (2011)

Multiple sequence alignments are fundamental to many sequence analysis methods. Most alignments are computed using the progressive alignment heuristic. These methods are starting to become a bottleneck in some analysis pipelines when faced with data sets of the size of many thousands of sequences. Some methods allow computation of larger data sets while sacrificing quality, and others produce high-quality alignments, but scale badly with the number of sequences. In this paper, we describe a new program called Clustal Omega, which can align virtually any number of protein sequences quickly and that delivers accurate alignments. The accuracy of the package on smaller test cases is similar to that of the high-quality aligners. On larger data sets, Clustal Omega outperforms other packages in terms of execution time and quality. Clustal Omega also has powerful features for adding sequences to and exploiting information in existing alignments, making use of the vast amount of precomputed information in public databases like Pfam.
New Therapies for Castration-Resistant Prostate Cancer (2010)

On April 29, 2010, the Food and Drug Administration (FDA) approved a new immunotherapy, sipuleucel-T, for the treatment of patients with asymptomatic or minimally symptomatic castration-resistant prostate cancer. Traditionally, immune-based therapies have been categorized according to whether the agent has direct antitumor effects (so-called passive immunotherapy) or stimulates a host antitumor response (active immunotherapy) and whether the agent elicits a general increase in immune activation (nonspecific) or an immune response based on tumor recognition (specific). Sipuleucel-T is a form of active specific immunotherapy.The sipuleucel-T intervention involves harvesting the patient's peripheral-blood mononuclear cells (PBMCs), culturing them with a chimeric protein . . .
Investigations of the genomic region that contains the clf1 mutation, a causal gene in multifactorial cleft lip and palate in mice (2005)

The clf1 mutation is a genomic alteration present in A/WySn and absent in the ancestral chromosomal segment in CBA/J. The IAP retrotransposon insertion near Wnt9b in A/WySn fits this criterion; we predict that interference with Wnt9b function by this IAP is the clf1 mutation.
Anti-angiogenic tyrosine kinase inhibitors: what is their mechanism of action? (2009)

Tyrosine kinases are important cellular signaling proteins that have a variety of biological activities including cell proliferation and migration. Multiple kinases are involved in angiogenesis, including receptor tyrosine kinases such as the vascular endothelial growth factor receptor. Inhibition of angiogenic tyrosine kinases has been developed as a systemic treatment strategy for cancer. Three anti-angiogenic tyrosine kinase inhibitors (TKIs), sunitinib, sorafenib and pazopanib, with differential binding capacities to angiogenic kinases were recently approved for treatment of patients with advanced cancer (renal cell cancer, gastro-intestinal stromal tumors, and hepatocellular cancer). Many other anti-angiogenic TKIs are being studied in phase I-III clinical trials. In addition to their beneficial anti-tumor activity, clinical resistance and toxicities have also been observed with these agents. In this manuscript, we will give an overview of the design and development of anti-angiogenic TKIs. We describe their molecular structure and classification, their mechanism of action, and their inhibitory activity against specific kinase signaling pathways. In addition, we provide insight into what extent selective targeting of angiogenic kinases by TKIs may contribute to the clinically observed anti-tumor activity, resistance, and toxicity. We feel that it is of crucial importance to increase our understanding of the clinical mechanism of action of anti-angiogenic TKIs in order to further optimize their clinical efficacy.
CCC1 Is a Transporter That Mediates Vacuolar Iron Storage in Yeast (2001)

The budding yeast Saccharomyces cerevisiae can grow for generations in the absence of exogenous iron, indicating a capacity to store intracellular iron. As cells can accumulate iron by endocytosis we studied iron metabolism in yeast that were defective in endocytosis. We demonstrated that endocytosis-defective yeast (Delta end4) can store iron in the vacuole, indicating a transfer of iron from the cytosol to the vacuole. Using several different criteria we demonstrated that CCC1 encodes a transporter that effects the accumulation of iron and Mn(2+) in vacuoles. Overexpression of CCC1, which is localized to the vacuole, lowers cytosolic iron and increases vacuolar iron content. Conversely, deletion of CCC1 results in decreased vacuolar iron content and decreased iron stores, which affect cytosolic iron levels and cell growth. Furthermore Delta ccc1 cells show increased sensitivity to external iron. The sensitivity to iron is exacerbated by ectopic expression of the iron transporter FET4. These results indicate that yeast can store iron in the vacuole and that CCC1 is involved in the transfer of iron from the cytosol to the vacuole.
Measurement of Elastic Constants at Low Temperatures by Means of Ultrasonic Waves–Data for Silicon and Germanium Single Crystals, and for Fused Silica (1953)

Ultrasonic waves (shear or longitudinal) in the 10–30 mc range are transmitted down a fused silica rod, through a polystyrene or silicone one-quarter wavelength seal, and into the solid specimen. Measurement of reflections within the specimen yields values for velocities of propagation and elastic constants. Data obtained over a temperature range of 78° to 300°K for silicon and germanium single crystals, and 1.6° to 300°K for fused silica are listed. For the latter, a high loss is noted, with an indicated maximum near 30°K.
Sugar-nucleotide donor specificity of histo-blood group A and B transferases is based on amino acid substitutions. (1990)

Four amino acid substitutions (aa 176, 235, 266, and 268) have been found between the coding regions of cDNAs for histo-blood group A and B transferases (Yamamoto F., Clausen, H., White, T., Marken, J., and Hakomori, S. (1990) Nature 345, 229-233). Here we establish the basis of differential affinity of these glycosyltransferases to nucleotide-sugar (UDP-GalNAc or UDP-Gal). On the basis of gene reconstruction experiments and studies of expression in DNA transfected HeLa cells, the third as well as the fourth aa substitutions (leucine and glycine in A and methionine and alanine in B), which were calculated to modify flexibility of the protein, were found to be crucial in determining nucleotide-sugar specificity. The second substitution (glycine in A and serine in B) also affects the specificity. We have also created new enzymes which catalyze the transfer of both GalNAc and Gal, and may provide an explanation of the rare cis-AB phenotype.
Tolerant, Growing Cells from Nutrient Shifts Are Not Persister Cells (2017)

There is much controversy about the metabolic state of cells that are tolerant to antibiotics, known as persister cells. In this opinion piece, we offer an explanation for the discrepancy seen: some laboratories are studying metabolically active and growing cell populations (e.g., as a result of nutrient shifts) and attributing the phenotypes that they discern to persister cells while other labs are studying dormant cells. We argue here that the metabolically active cell population should more accurately be considered tolerant cells, while the dormant cells are the true persister population.
Genomic instability in Ip and human malignancies (1996)

Both cytogenetic and molecular genetic approaches have unveiled non-random genomic alterations in 1p associated with a number of human malignancies. These have been interpreted to suggest the existence of cancer-related genes in 1p. Earlier studies had employed chromosome analysis or used molecular probes mapped by in situ hybridization. Further, studies of the various tumor types often involved different molecular probes that had been mapped by different technical approaches, like linkage analysis, radioactive or fluorescence in situ hybridization, or by employing a panel of mouse x human radiation reduced somatic cell hybrids. The lack of maps fully integrating all loci has complicated the generation of a comparative and coherent picture of 1p damage in human malignancies even among different studies on the same tumor type. Only recently has the availability of genetically mapped, highly polymorphic loci at (CA)n repeats with sufficient linear density made it possible to scan genomic regions in different types of tumors readily by polymerase chain reaction (PCR) with a standard set of molecular probes. This paper aims at presenting an up-to-date picture of the association of 1p alterations with different human cancers and compiles the corresponding literature. From this it will emerge that the pattern of alterations in individual tumor types can be complex and that a stringent molecular and functional definition of the role that Ip alterations might have in tumorigenesis will require a more detailed analysis of the genomic regions involved.
Chromosomal Aberrations and Schizophrenia (1992)

Chromosomal aberrations associated with schizophrenic disorders may suggest regions in which to focus a search for genes predisposing to schizophrenia by a linkage strategy. As for other genetic illnesses, chromosomal abnormalities may also provide useful tools for subsequent physical mapping, fine localisation, and isolation of important susceptibility genes. Identification of several chromosomal aberrations may be especially important, given the unknown pathophysiology, the paucity of known brain genes, and the probable genetic heterogeneity of schizophrenia and manic-depression. However, because psychiatric disorders are common and inherited in a complex manner, researchers must use caution when drawing inferences about associations with chromosomal aberrations. Reported abnormalities involving autosomes (chromosomes 1-22) associated with psychotic disorders are reviewed. Their relevance to linkage studies localising genes for schizophrenia was estimated by standardised criteria for specificity, diagnosis, family history, and overall weight of evidence. Four 'possibly relevant' chromosomal regions were identified: 5q, 11q, 18q, and 19p. This paper outlines strategies for future studies to detect new chromosomal aberrations associated with major psychotic disorders that may be relevant to isolating the genes for schizophrenia.