gebhart/patrepeval huggingface dataset:
IRAK-M Is a Novel Member of the Pelle/Interleukin-1 Receptor-associated Kinase (IRAK) Family (1999)

The interleukin-1 receptor-associated kinase (IRAK) was first described as a signal transducer for interleukin-1 (IL-1) and has later been implicated in signal transduction of other members of the Toll/IL-1 receptor family. We now report the identification and characterization of a novel IRAK-like molecule. In contrast to the ubiquitously expressed IRAK and IRAK-2, this new IRAK-like molecule is found mainly in cells of monomyeloic origin and is, therefore, designated IRAK-M. Although IRAK-M and IRAK-2 exhibit only a negligible autophosphorylation activity, they can reconstitute the IL-1 response in a 293 mutant cell line lacking IRAK. In addition, we show for the first time that members of the IRAK family are indispensable elements of lipopolysaccharide signal transduction. The discovery of IRAK-M adds another level of complexity to our understanding of signaling by members of the Toll/IL-1 receptor family.
The biology of SPARC, a protein that modulates cell‐matrix interactions (1994)

An extracellular matrix-associated glycoprotein expressed in a variety of tissues during embryogenesis and repair, SPARC contains modular domains that can function independently to bind cells and matrix components. Because SPARC can selectively disrupt cellular contacts with matrix and thereby effect changes in cell shape, it has been referred to as an antiadhesin. Inhibition of the expression of SPARC altered axial development in frogs, and deregulated expression in nematode worms resulted in a derangement of muscle attachment and embryonic lethality. SPARC also inhibits cell cycle progression in vitro, in part through a cationic, disulfide-bonded region that is homologous to a repeated domain in the cytokine inhibitor, follistatin. Moreover, SPARC binds specifically to the B chain of platelet-derived growth factor and alters the response of cells to several cytokines. Although information concerning the expression, biochemical properties, and cellular activities of SPARC has increased significantly over the last decade, the precise function of the protein has not been resolved. Goals of future studies include characterization of cell-surface receptors for SPARC and the interactions with morphogens and growth factors that regulate specific activities during animal development.
Passive temperature-compensating package for optical fiber gratings (1995)

We demonstrate a compact, passive temperature-compensating package for fiber gratings. The grating is mounted under tension in a package comprising two materials with different thermal-expansion coefficients. As the temperature rises the strain is progressively released, compensating the temperature dependence of the Bragg wavelength. A fiber grating mounted in a package 50 mm long and 5 mm in diameter exhibited a total variation in Bragg wavelength of 0.07 nm over a 100 °C temperature range, compared with 0.92 nm for an uncompensated grating.
Contribution by synaptic zinc to the gender-disparate plaque formation in human Swedish mutant APP transgenic mice (2002)

Endogenous metals may contribute to the accumulation of amyloid plaques in Alzheimer's disease. To specifically examine the role of synaptic zinc in the plaque accumulation, Tg2576 (also called APP2576) transgenic mice (hAPP(+)) expressing cerebral amyloid plaque pathology were crossed with mice lacking zinc transporter 3 (ZnT3(-/-)), which is required for zinc transport into synaptic vesicles. With aging, female hAPP(+):ZnT3(+/+) mice manifested higher levels of synaptic zinc, insoluble amyloid beta, and plaques than males; these sex differences disappeared in hAPP(+):ZnT3(-/-) mice. Both sexes of hAPP(+):ZnT3(-/-) mice had markedly reduced plaque load and less insoluble amyloid beta compared with hAPP(+):ZnT3(+/+) mice. Hence, of endogenous metals, synaptic zinc contributes predominantly to amyloid deposition in hAPP(+) mice.
Control of surface modes in low loss hollow-core photonic bandgap fibers (2008)

We report on the fabrication and characterization of hollow-core photonic bandgap fibers that do not suffer from surface mode coupling within the photonic bandgap of the cladding. This enables low attenuation over the full spectral width of the bandgap--we measured a minimum loss of 15 dB/km and less than 50 dB/km over 300 nm for a fiber operating at 1550 nm. As a result of the increased bandwidth, the fiber has reduced dispersion and dispersion slope--by a factor of almost 2 compared to previous fibers. These features are important for several applications in high-power ultrashort pulse compression and delivery. Realizing these advances has been possible due to development of a modified fabrication process which makes the production of low-loss hollow-core fibers both simpler and quicker than previously.
Acidic fibroblast growth factor (aFGF) injection stimulates cartilage enlargement and inhibits cartilage gene expression in rat fracture healing (1990)

The effect of the administration of acidic fibroblast growth factor (aFGF) on normal fracture healing was examined in a rat fracture model. One microgram of aFGF was injected into the fracture site between the first and the ninth day after fracture either every other day or every day. aFGF-injected calluses were significantly larger than control calluses, although this does not imply an increased mechanical strength of the callus. Histology showed a marked increase in the size of the cartilaginous soft callus. Total DNA and collagen content in the cartilaginous portion of the aFGF-injected calluses were greater than those of controls, although the collagen content/DNA content ratio was not different between the aFGF-injected and control calluses. Fracture calluses injected with aFGF remained larger than controls until 4 weeks after fracture. The enlarged cartilaginous portion of the aFGF-injected calluses seen at 10 days after fracture was replaced by trabecular bone at 3 and 4 weeks. Northern blot analysis of total cellular RNA extracted separately from the cartilaginous soft callus and the bony hard callus showed decreased expression of type II procollagen and proteoglycan core protein mRNA in the aFGF-injected calluses when compared with controls. A slight decrease in types I and III procollagen mRNA expression was also observed. We concluded that aFGF injections induced cartilage enlargement and decreased mRNA expression for type II procollagen and proteoglycan core protein.
Endocannabinoids protect the rat isolated heart against ischaemia (2003)

1 The purpose of this study was to determine whether endocannabinoids can protect the heart against ischaemia and reperfusion. 2 Rat isolated hearts were exposed to low-flow ischaemia (0.5-0.6 ml min(-1)) and reperfusion. Functional recovery as well as CK and LDH overflow into the coronary effluent were monitored. Infarct size was determined at the end of the experiments. Phosphorylation levels of p38, ERK1/2, and JNK/SAPK kinases were measured by Western blots. 3 None of the untreated hearts recovered from ischaemia during the reperfusion period. Perfusion with either 300 nM palmitoylethanolamide (PEA) or 300 nM 2-arachidonoylglycerol (2-AG), but not anandamide (up to 1 micro M), 15 min before and throughout the ischaemic period, improved myocardial recovery and decreased the levels of coronary CK and LDH. PEA and 2-AG also reduced infarct size. 4 The CB(2)-receptor antagonist, SR144528, blocked completely the cardioprotective effect of both PEA and 2-AG, whereas the CB(1)-receptor antagonist, SR141716A, blocked partially the effect of 2-AG only. In contrast, both ACEA and JWH015, two selective agonists for CB(1)- and CB(2)- receptors, respectively, reduced infarct size at a concentration of 50 nM. 5 PEA enhanced the phosphorylation level of p38 MAP kinase during ischaemia. PEA perfusion doubled the baseline phosphorylation level of ERK1/2, and enhanced its increase upon reperfusion. The cardioprotective effect of PEA was completely blocked by the p38 MAP kinase inhibitor, SB203580, and significantly reduced by the ERK1/2 inhibitor, PD98059, and the PKC inhibitor, chelerythrine. 6 In conclusion, endocannabinoids exert a strong cardioprotective effect in a rat model of ischaemia-reperfusion that is mediated mainly through CB(2)-receptors, and involves p38, ERK1/2, as well as PKC activation.
Doppelgänger--a user modeling system (1991)

Thesis (B.S.)--Massachusetts Institute of Technology, Dept. of Electrical Engineering and Computer Science, 1991.
Survival and Neurologic Outcomes in a Randomized Trial of Motexafin Gadolinium and Whole-Brain Radiation Therapy in Brain Metastases (2003)

The overall results did not demonstrate significant differences by treatment arm for survival and ERC time to neurologic progression. Investigator neurologic assessments demonstrated an MGd treatment benefit in all patients. In lung cancer patients, ERC- and investigator-determined time to neurologic progression demonstrated an MGd treatment benefit. MGd may improve time to neurologic and neurocognitive progression in lung cancer.
Prostaglandin E2 promotes the cell growth and invasive ability of hepatocellular carcinoma cells by upregulating c-Myc expression via EP4 receptor and the PKA signaling pathway (2014)

Hepatocellular carcinoma (HCC) represents a major health problem worldwide. Prostaglandin E2 (PGE2), the predominant product of cyclooxygenase-2, has been implicated in hepatocarcinogenesis. However, the underlying molecular mechanisms remain to be further elucidated. c-myc, a cellular proto-oncogene, is activated or overexpressed in many types of human cancer, including HCC. The present study was designed to investigate the internal relationship and molecular mechanisms between PGE2 and c-Myc in HCC, and to define its role in HCC cell growth and invasion. Our results showed that PGE2 significantly upregulated c-Myc expression at both the mRNA and protein levels, and knockdown of c-Myc blocked PGE2-induced HCC cell growth and invasive ability in human HCC Huh-7 cells. The effect of PGE2 on c-Myc expression was mainly through the EP4 receptor, and EP4 receptor-mediated c-Myc protein upregulation largely depended on de novo biosynthesis of c-Myc mRNA and its protein. EP4 receptor signaling activated GS/AC and increased the intracellular cAMP level in Huh-7 cells. The adenylate cyclase (AC) activator forskolin mimicked the effects of the EP4 receptor agonist on c-Myc expression, while the AC inhibitor SQ22536 reduced EP4 receptor-mediated c-Myc upregulation. These data confirm the involvement of the GS/AC/cAMP pathway in EP4 receptor-mediated c-Myc upregulation. Moreover, the phosphorylation levels of CREB protein were markedly elevated by EP4 receptor signaling, and by using specific inhibitor and siRNA interference, we demonstrated that PKA/CREB was also involved in the EP4 receptor-mediated c-Myc upregulation. In summary, the present study revealed that PGE2 significantly upregulates c-Myc expression at both mRNA and protein levels through the EP4R/GS/AC/cAMP/PKA/CREB signaling pathway, thus promoting cell growth and invasion in HCC cells. Targeting of the PGE2/EP4R/c-Myc pathway may be a new therapeutic strategy to prevent and cure human HCC.
SUMO-1 conjugation to topoisomerase I: A possible repair response to topoisomerase-mediated DNA damage (2000)

Ubiquitin/26S proteasome-dependent degradation of topoisomerase I (TOP1) has been suggested to be a unique repair response to TOP1-mediated DNA damage. In the current study, we show that treatment of mammalian cells or yeast cells expressing human DNA TOP1 with camptothecin (CPT) induces covalent modification of the TOP1 by SUMO-1/Smt3p, a ubiquitin-like protein. This conclusion is based on the following observations: (i) Mammalian DNA TOP1 conjugates induced by CPT were cross-reactive with SUMO-1/Smt3p-specific antibodies both in yeast expressing human DNA TOP1 as well as mammalian cells. (ii) The formation of TOP1 conjugates was shown to be dependent on UBC9, the E2 enzyme for SUMO-1/Smt3p. (iii) TOP1 physically interacts with UBC9. (iv) Ubc9 mutant yeast cells expressing human DNA TOP1 was hypersensitive to CPT, suggesting that UBC9/SUMO-1 may be involved in the repair of TOP1-mediated DNA damage.
Compounds containing sulphur chromophores. Part I. The action of bases on heterocyclic sulphide quarternary salts (1955)

The first page of this article is displayed as the abstract.
Clinical Trials of the CytoRich Specimen-Preparation Device for Cervical Cytology (1997)

The CytoRich method may improve the overall sensitivity and specificity of the cervical cytology procedure. Clinical trials to verify these preliminary data are ongoing.
A Fluorescence In situ Hybridization Screen for E26 Transformation–Specific Aberrations: Identification of DDX5-ETV4 Fusion Protein in Prostate Cancer (2008)

Recurrent gene fusions involving E26 transformation-specific (ETS) transcription factors ERG, ETV1, ETV4, or ETV5 have been identified in 40% to 70% of prostate cancers. Here, we used a comprehensive fluorescence in situ hybridization (FISH) split probe strategy interrogating all 27 ETS family members and their five known 5' fusion partners in a cohort of 110 clinically localized prostate cancer patients. Gene rearrangements were only identified in ETS genes that were previously implicated in prostate cancer gene fusions including ERG, ETV1, and ETV4 (43%, 5%, and 5%, respectively), suggesting that a substantial fraction of prostate cancers (estimated at 30-60%) cannot be attributed to an ETS gene fusion. Among the known 5' gene fusion partners, TMPRSS2 was rearranged in 47% of cases followed by SLC45A3, HNRPA2B1, and C15ORF21 in 2%, 1%, and 1% of cases, respectively. Based on this comprehensive FISH screen, we have made four noteworthy observations. First, by screening the entire ETS transcription factor family for rearrangements, we found that a large fraction of prostate cancers (44%) cannot be ascribed to an ETS gene fusion, an observation which will stimulate research into identifying recurrent non-ETS aberrations in prostate cancers. Second, we identified SLC45A3 as a novel 5' fusion partner of ERG; previously, TMPRSS2 was the only described 5' partner of ERG. Third, we identified two prostate-specific, androgen-induced genes, FLJ35294 and CANT1, as 5' partners to ETV1 and ETV4. Fourth, we identified a ubiquitously expressed, androgen-insensitive gene, DDX5, fused in frame with ETV4, leading to the expression of a DDX5-ETV4 fusion protein.
Expanded Genetic Alphabets in the Polymerase Chain Reaction (2009)

Cleaning up polymerase chain reactions: DNA polymerases are found that copy two additional nucleotide letters (Z and P) in an expanded DNA alphabet to support six-letter polymerase chain reactions (PCR). Incorporated into external primers in a threefold multiplexed PCR, primers containing Z and P gave much cleaner results than standard multiplexed PCR. Detailed facts of importance to specialist readers are published as ”Supporting Information”. Such documents are peer-reviewed, but not copy-edited or typeset. They are made available as submitted by the authors. 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.
Graphical program development with PECAN program development systems (1984)

This paper describes the user's view of the PECAN family of program development systems. PECAN is a program development system generator for algebraic programming languages. The program development systems it produces support multiple views of the user's program, its semantics, and its execution. The program views include a syntax-directed editor, a declaration editor, and a structured flow graph editor. The semantic views include expression trees, data type diagrams, flow graphs, and the symbol table. Execution views show the program in action and the stack contents as the program executes. PECAN is designed to make effective use of powerful personal machines with high-resolution graphics displays and is currently implemented on APOLLO workstations.
Molecularly imprinted monodisperse microspheres for competitive radioassay (1999)

In the present study, molecularly imprinted affinity sorbents against theophylline and 17β-estradiol are synthesised via precipitation polymerisation, a synthetic method that yields monodisperse, spherical polymer particles in the micron-scale range, quickly, cleanly and in good yield. The specific binding sites that are created during the imprinting process are analysed via radioligand binding analysis. The molecularly imprinted microspheres are highly specific and have higher load capacities compared to the ‘classical’ particles obtained by grinding the imprinted monolith. The successful imprinting against model compounds with very different hydrophobicities demonstrates the generality of the current simple approach.
A naturally occurring isoform of the human macrophage scavenger receptor (SR-A) gene generated by alternative splicing blocks modified LDL uptake (1998)

The class A macrophage scavenger receptors (SR-A) are macrophage-specific trimeric integral membrane glycoproteins that have been implicated in many macrophage-associated physiological and pathological processes including atherosclerosis, Alzheimer's disease, and host defense. There are two forms of the receptor that have been previously cloned, and both are generated by alternative splicing of a single gene. Here we report the cloning of a third, alternatively spliced isoform of the human SR-A gene (type III hSR-A). The novel isoform is expressed in the human monocytic leukemia cell line THP-1 and also in primary human monocyte derived macrophages. When expressed in CHO-K1 cells, type III hSR-A does not internalize AcLDL despite having the domain shown to mediate this function in type I and II hSR-A. We show that type III protein has altered intracellular processing and is trapped within the endoplasmic reticulum, making it unable to perform endocytosis. Type III protein acts as a dominant negative isoform by reducing modified LDL uptake in CHO cells stably expressing either type I or type II SR-A. The demonstration that a naturally occurring splice variant of SR-A mRNA can act as a dominant negative isoform suggests a novel mechanism for regulation of scavenger receptor activity in macrophages.
The systemic administration of lethal toxin achieves a growth delay of human melanoma and neuroblastoma xenografts: Assessment of receptor contribution (2008)

Two of the three components of anthrax toxin, protective antigen (PA) and lethal factor (LF), together known as lethal toxin (LeTx), reportedly show anti-tumor activity in melanoma in vitro and in vivo. The growth inhibitory activity of LeTx in culture was determined in nine human cancer cell lines, including melanoma, neuroblastoma and adenocarcinoma cells, as well as in human umbilical vein endothelial cells (HUVEC). The contribution of the two known PA receptor proteins, ANTXR1/TEM8 and ANTXR2/CMG2, to the sensitivity of the cells was assessed. The efficacy of LeTx was evaluated in vivo in the SK-N-AS neuroblastoma and SK-MEL-28 melanoma tumor xenograft models. Sensitivity to LeTx in vitro was observed in the neuroblastoma and colorectal adenocarcinoma cells and HUVEC, as well as melanoma cells. ANTXR1/TEM8 and ANTXR2/CMG2 protein expression studies suggested that a certain threshold of the PA receptor protein level must be met for sensitivity to LeTx to be observed. However, although the SK-N-AS neuroblastoma cells expressed the highest levels of receptor proteins and achieved the lowest IC50 in vitro (0.1 ng/ml), we observed no correlation between either the ANTXR1/TEM8 or ANTXR2/CMG2 protein levels and sensitivity to LeTx in vitro. In vivo, LeTx was an active anti-tumor agent when administered intravenously to mice bearing the human SK-N-AS or SK-MEL-28 tumor xenografts. The tumor growth delays were 6-8 days with a lower dose regimen and 14-16 days with a higher dose regimen for the two tumor models. These in vitro data suggest that LeTx may have broad therapeutic indications in cancer and the in vivo studies demonstrate that LeTx has systemic efficacy in neuroblastoma as well as melanoma. The therapeutic potential of LeTx needs to be further investigated in non-melanoma tumor models expressing the ANTXR1/TEM8 and/or ANTXR2/CMG2 protein.
A Review of Osteocyte Function and the Emerging Importance of Sclerostin (2014)

➤ Osteocytes, derived from osteoblasts, reside within bone and communicate extensively with other bone cell populations to regulate bone metabolism. The mature osteocyte expresses the protein sclerostin, a negative regulator of bone mass.➤ In normal physiologic states, the protein sclerostin acts on osteoblasts at the surface of bone and is differentially expressed in response to mechanical loading, inflammatory molecules such as prostaglandin E2, and hormones such as parathyroid hormone and estrogen.➤ Pathologically, sclerostin dysregulation has been observed in osteoporosis-related fractures, failure of implant osseous integration, metastatic bone disease, and select genetic diseases of bone mass.➤ An antibody that targets sclerostin, decreasing endogenous levels of sclerostin while increasing bone mineral density, is currently in phase-III clinical trials.➤ The osteocyte has emerged as a versatile, indispensable bone cell. Its location within bone, extensive dendritic network, and close communication with systemic circulation and other bone cells produce many opportunities to treat a variety of orthopaedic conditions.
Semimetal–semiconductor transition in Bi1−xSbx alloy nanowires and their thermoelectric properties (2002)

The resistivity of Bi1−xSbx nanowire arrays exhibits complex variations as a function of Sb content x and temperature T due to the unique semimetal-to-semiconductor (SM–SC) transition experienced by the nanowires. Seebeck coefficient measurements show enhanced thermopower due to Sb alloying and the reduction in wire diameter. The theoretical model not only explains these transport measurements, but also suggests a useful technique to experimentally determine (i) whether the wire is semimetallic or semiconducting, (ii) the carrier concentration, and (iii) the conditions for the SM–SC transition.
Inverse planning for intensity-modulated arc therapy using direct aperture optimization (2003)

Intensity-modulated arc therapy (IMAT) is a radiation therapy delivery technique that combines gantry rotation with dynamic multi-leaf collimation (MLC). With IMAT, the benefits of rotational IMRT can be realized using a conventional linear accelerator and a conventional MLC. Thus far, the advantages of IMAT have gone largely unrealized due to the lack of robust automated planning tools capable of producing efficient IMAT treatment plans. This work describes an inverse treatment planning algorithm, called 'direct aperture optimization' (DAO) that can be used to generate inverse treatment plans for IMAT. In contrast to traditional inverse planning techniques where the relative weights of a series of pencil beams are optimized, DAO optimizes the leaf positions and weights of the apertures in the plan. This technique allows any delivery constraints to be enforced during the optimization, eliminating the need for a leaf-sequencing step. It is this feature that enables DAO to easily create inverse plans for IMAT. To illustrate the feasibility of DAO applied to IMAT, several cases are presented, including a cylindrical phantom, a head and neck patient and a prostate patient.