gebhart/patrepeval huggingface dataset:
Lysophosphatidylcholine: a chemotactic factor for human monocytes and its potential role in atherogenesis. (1988)

Native low density lipoprotein (LDL) does not affect monocyte/macrophage motility. On the other hand, oxidatively modified LDL inhibits the motility of resident peritoneal macrophages yet acts as a chemotactic factor for circulating human monocytes. We now show that lysophosphatidylcholine (lyso-PtdCho), which is generated by a phospholipase A2 activity during LDL oxidation, is a potent chemotactic factor for monocytes. It is not chemotactic for neutrophils or for resident macrophages. Platelet-activating factor, after treatment with phospholipase A2, becomes chemotactic for monocytes, whereas the intact factor is not. Synthetic 1-palmitoyl-lyso-PtdCho showed chemotactic activity comparable to that of the lyso-PtdCho fraction derived from oxidized LDL. The results suggest that lyso-PtdCho in oxidized LDL may favor recruitment of monocytes into the arterial wall during the early stages of atherogenesis. Generation of lyso-PtdCho, either from LDL itself or from membrane phospholipids of damaged cells, could play a more general role in inflammatory processes throughout the body.
Adhesive RFID Sensor Patch for Monitoring of Sweat Electrolytes (2014)

Wearable digital health devices are dominantly found in rigid form factors such as bracelets and pucks. An adhesive radio-frequency identification (RFID) sensor bandage (patch) is reported, which can be made completely intimate with human skin, a distinct advantage for chronological monitoring of biomarkers in sweat. In this demonstration, a commercial RFID chip is adapted with minimum components to allow potentiometric sensing of solutes in sweat, and surface temperature, as read by an Android smartphone app with 96% accuracy at 50 mM Na(+) (in vitro tests). All circuitry is solder-reflow integrated on a standard Cu/polyimide flexible-electronic layer including an antenna, but while also allowing electroplating for simple integration of exotic metals for sensing electrodes. Optional paper microfluidics wick sweat from a sweat porous adhesive allowing flow to the sensor, or the sensor can be directly contacted to the skin. The wearability of the patch has been demonstrated for up to seven days, and includes a protective textile which provides a feel and appearance similar to a standard Band-Aid. Applications include hydration monitoring, but the basic capability is extendable to other mM ionic solutes in sweat (Cl(-), K(+), Mg(2+), NH4(+), and Zn(2+)). The design and fabrication of the patch are provided in full detail, as the basic components could be useful in the design of other wearable sensors.
호손의 『 주홍 글씨 』 : 페미니즘적 접근 (1997)

호손이 작품을 쓴 연도인 19세기 중반은 미국내에서 유토피아 건설, 노예폐지운동, 여성해방운동 등등 사회개혁운동이 활기를 띠기 시작한 시기와 맞물려 있고, 또한 유럽혁명의 격변기와도 동일선상에 있으며, 이 작품의 실제 배경이 된 17세기 중반은 영국의 찰스 1세와 의회와의 분쟁이 있던 시기와 맞물려 있는 묘한 연관관계를 맺으면서 격동과 변화 그리고 무질서의 시대상에 부합하는 획기적이고 파격적인 여주인공 헤스터의 탄생이 그 부산물로서 생겨났다. 페미니즘이 성숙되기 훨씬 이전에 쓰여진 이 작품을 현대적 시각인 페미니즘의 관점에서 살펴보며 초기 페미니즘 작품으로 분류할 수 있는지 판단해 보고자 한다. 남성지배주의의 가부장적인 퓨리탄 사회에서, 또한 남성과 여성의 이분법의 논리로 된 위계질서가 뚜렷한 사회에서, 자신의 개별성과 독립적인 개체성을 상실하고 단지 이미지나 심볼로 남는 것을 거부하는 헤스터의 자구적 노력과 그러면서도 사회와의 절연을 강요당하는 상황하에서 사회와의 타협을 꾀하는 유화적 제스쳐를 취할 수밖에 없는 어정쩡한 모습의 헤스터에게서 19세기 남성 작가인 호손의 한계성과 부담감을 엿볼 수 있다. 새로운 사회에서 자유로운 삶을 추구하고자하는 헤스터의 마음속 반역의 표출에 뒤이은 좌절의 양상과, 특히 전통적이고 순종적이며 자기희생적인 여성상으로 생을 마감하는 헤스터의 모습을 취급하는 결론 부분 때문에 이 작품을 단순히 반페미니즘적 결론으로 종지부를 찍었다고 단정짓기에는 미진한 점이 있다. 헤스터 자신의 문제를 개인의 문제가 아니라 여성전체의 문제로 확대시키고자 하는 헤스터의 분명한 의도와 작품의 말미에서 보여지는 -확실하고 세세하게 모든 것을 드러내는 것은 결코 아니지만- 헤스터의 마음속에 들끓고 있는 여성의식의 변화를 전제조건으로 하는 당시로서는 과격하고 진보적인 남녀 평등사회의 실현에 대한 소망과 야망은 페미니즘에 이끌리는 자신의 성향을 거부하지도 확증하지도 못하는 어정쩡한 호손의 모습을 덮어 줄만하며 감히 호손을 초기 페미니즘 작가로 부를 수 있게 한다.
High mesothelin correlates with chemoresistance and poor survival in epithelial ovarian carcinoma (2009)

The objective of this paper is to investigate the mesothelin expression level to the clinicopathological features, chemoresponse, and to the outcome of patients with epithelial ovarian carcinoma (EOC). Mesothelin mRNA was detected by real-time quantitative reverse-transcription PCR in 139 EOC patients. Clinical characteristics, histopathological items, responses to chemotherapy, progression-free survival (PFS), and overall survival (OS) were recorded. Tumours with advanced stages had higher mesothelin than those with early stages. The chemoresistant patients showed significantly higher mesothelin than did chemosensitive patients (2.81 vs 0.43, P<0.001), irrespective of optimal or suboptimal surgery in those with advanced stages. Highly expressed levels of mesothelin were an independent but poor prognostic factor in the PFS (2.03 (1.23-3.37) P=0.006) and OS (3.72 (1.64-8.45), P=0.002) of the 139 EOC patients in multivariate analysis. In addition, patients in advanced stages with highly expressed mesothelin also had significantly worse OS, regardless of whether they had undergone optimal (13.85 (1.76-125.60), P=0.013) or suboptimal (4.47 (1.83-10.88), P=0.001) debulking surgery in multivariate analysis. Out results provide new evidence that mesothelin expression is associated with chemoresistance and with shorter disease-free survival and worse OS of patients with EOC.
Role of complement in IgA nephropathy (2015)

Immunoglobulin A nephropathy (IgAN) is characterized by the deposition of IgA in the mesangium of glomeruli. This mesangial IgA has been found to consist mainly of polymeric IgA1 which drives the activation of the mesangial cells and results in excessive production of several inflammatory mediators. The activation of mesangial cells is amplified by the ability of IgA to activate the complement system, originally thought to occur mainly via the alternative pathway of complement. However more recent studies indicate that lectin pathway involvement has a strong association with progression of renal disease. In this review we summarize the contribution of complement to the IgA- mediated inflammatory process.
Standoff Laser-Induced Breakdown Spectroscopy (LIBS) Using a Miniature Wide Field of View Spatial Heterodyne Spectrometer with Sub-Microsteradian Collection Optics (2017)

A spatial heterodyne spectrometer (SHS) is described for standoff laser-induced breakdown spectroscopy (LIBS) measurements. The spatial heterodyne LIBS spectrometer (SHLS) is a diffraction grating based interferometer with no moving parts that offers a very large field of view, high light throughput, and high spectral resolution in a small package. The field of view of the SHLS spectrometer is shown to be ∼1° in standoff LIBS measurements. In the SHLS system described here, the collection aperture was defined by the 10 mm diffraction gratings in the SHS and standoff LIBS measurements were made up to 20 m with no additional collection optics, corresponding to a collection solid angle of 0.2 μsr, or f/2000, and also using a small telescope to increase the collection efficiency. The use of a microphone was demonstrated to rapidly optimize laser focus for 20 m standoff LIBS measurements.
Immunocytochemical localization of a neuronal nicotinic receptor: the beta 2-subunit (1993)

We have characterized in adult rat the tissue-specific expression of the nicotinic ACh receptor (AChR) beta 2-subunit using antisera raised against fusion protein constructs. Immunohistochemical localization revealed immunoreactivity distributed throughout the neuraxis. Overall, beta 2-like immunoreactivity (beta 2-LI) correlated well with in situ localization of beta 2 transcript in neuronal cell bodies. Particularly strong labeling was detected in the thalamus, and scattered other regions, whereas relatively weak staining was observed in the hypothalamus and amygdala. At the cellular level, beta 2-LI appeared to be exclusively neuronal and concentrated predominantly in perikarya, although strongly positive dendrites (cerebral cortical pyramidal neurons, cerebellar Purkinje cells) and axon terminals (e.g., striatum) were detected. At the ultrastructural level, beta 2-LI was membrane associated, with strong staining observed in endoplasmic reticulum and cytoplasmic transport vesicles. beta 2-LI was rarely detected at synapses. The widespread distribution of beta 2 suggests it may serve as a common subunit in different AChR combinations in various brain regions. Regulation of the expression of beta 2-subunit appears to be relatively unrestrained, with an apparent excess of protein synthesized in the cytoplasm relative to that which ultimately arrives at functional targets in the plasma membrane.
Pathogenic protein seeding in alzheimer disease and other neurodegenerative disorders (2011)

The misfolding and aggregation of specific proteins is a seminal occurrence in a remarkable variety of neurodegenerative disorders. In Alzheimer disease (the most prevalent cerebral proteopathy), the two principal aggregating proteins are β-amyloid (Aβ) and tau. The abnormal assemblies formed by conformational variants of these proteins range in size from small oligomers to the characteristic lesions that are visible by optical microscopy, such as senile plaques and neurofibrillary tangles. Pathologic similarities with prion disease suggest that the formation and spread of these proteinaceous lesions might involve a common molecular mechanism-corruptive protein templating. Experimentally, cerebral β-amyloidosis can be exogenously induced by exposure to dilute brain extracts containing aggregated Aβ seeds. The amyloid-inducing agent probably is Aβ itself, in a conformation generated most effectively in the living brain. Once initiated, Aβ lesions proliferate within and among brain regions. The induction process is governed by the structural and biochemical nature of the Aβ seed, as well as the attributes of the host, reminiscent of pathogenically variant prion strains. The concept of prionlike induction and spreading of pathogenic proteins recently has been expanded to include aggregates of tau, α-synuclein, huntingtin, superoxide dismutase-1, and TDP-43, which characterize such human neurodegenerative disorders as frontotemporal lobar degeneration, Parkinson/Lewy body disease, Huntington disease, and amyotrophic lateral sclerosis. Our recent finding that the most effective Aβ seeds are small and soluble intensifies the search in bodily fluids for misfolded protein seeds that are upstream in the proteopathic cascade, and thus could serve as predictive diagnostics and the targets of early, mechanism-based interventions. Establishing the clinical implications of corruptive protein templating will require further mechanistic and epidemiologic investigations. However, the theory that many chronic neurodegenerative diseases can originate and progress via the seeded corruption of misfolded proteins has the potential to unify experimental and translational approaches to these increasingly prevalent disorders.
Task adaptation using MAP estimation in N-gram language modeling (2002)

Describes a method of task adaptation in N-gram language modeling for accurately estimating the N-gram statistics from the small amount of data of the target task. Assuming a task-independent N-gram to be a-priori knowledge, the N-gram is adapted to a target task by MAP (maximum a-posteriori probability) estimation. Experimental results showed that the perplexities of the task-adapted models were 15% (trigram) and 24% (bigram) lower than those of the task-independent model, and that the perplexity reduction of the adaptation went up to a maximum of 39% when the amount of text data in the adapted task was very small.
Purification of complexes of nuclear oncogene p53 with rat and Escherichia coli heat shock proteins: in vitro dissociation of hsc70 and dnaK from murine p53 by ATP. (1988)

Oligomeric protein complexes containing the nuclear oncogene p53 and the simian virus 40 large tumor antigen (D. I. H. Linzer and A. J. Levine, Cell 17:43-51, 1979), the adenovirus E1B 55-kilodalton (kDa) tumor antigen, and the heat shock protein hsc70 (P. Hinds, C. Finlay, A. Frey, and A. J. Levine, Mol. Cell. Biol. 7:2863-2869, 1987) have all been previously described. To begin isolating, purifying, and testing these complexes for functional activities, we have developed a rapid immunoaffinity column purification. p53-protein complexes are eluted from the immunoaffinity column by using a molar excess of a peptide comprising the epitope recognized by the p53 monoclonal antibody. This mild and specific elution condition allows p53-protein interactions to be maintained. The hsc70-p53 complex from rat cells is heterogeneous in size, with some forms of this complex associated with a 110-kDa protein. The maximum apparent molecular mass of such complexes is 660,000 daltons. Incubation with micromolar levels of ATP dissociates this complex in vitro into p53 and hsc70 110-kDa components. Nonhydrolyzable substrates of ATP fail to promote this dissociation of the complex. Murine p53 synthesized in Escherichia coli has been purified 660-fold on the same antibody affinity column and was found to be associated with an E. coli protein of 70 kDa. Immunoblot analysis with specific antisera demonstrated that this E. coli protein was the heat shock protein dnaK, which has extensive sequence homology with the rat hsc70 protein. Incubation of the immunopurified p53-dnaK complex with ATP resulted in the dissociation of the p53-dnaK complex as it did with the p53-hsc70 complex. This remarkable conservation of p53-heat shock protein interactions and the specificity of dissociation reactions suggest a functionally important role for heat shock proteins in their interactions with oncogene proteins.
Heparin-associated thrombocytopenia: isolation of the antibody and characterization of a multimolecular PF4-heparin complex as the major antigen. (1994)

Sera of 34 patients with heparin-associated thrombocytopenia (HAT), giving a positive result in the serotonin release assay (SRA), were assessed in a platelet factor 4 (PF4)/heparin ELISA. Three sera revealing indeterminate results in the SRA and 10 control sera were also investigated. Both tests correlated closely (Kappa 0.742; p = 2.67 x 10(-7)), but one positive serum in the SRA was negative in the pF4/heparin ELISA. We have isolated the HAT antibodies by absorbtion and elution of HAT sera using endothelial cells (HUVEC). Eluates gave similar results as the sera in the PF4/heparin ELISA (Kappa 0.837, p = 9.26 x 10(-9)), and they also correlated very closely with the SRA (Kappa 0.888; p = 8.89 x 10(-10)). This demonstrates that HAT antibodies bind to the same epitope on platelets and on endothelial cells. High heparin concentrations released PF4 in a dose dependent manner from microtiter plates if PF4/heparin, but not if PF4 alone, was covalently linked. Concomitant to the release of PF4, binding of HAT antibodies to PF4/heparin decreased, as indicated by the median optical density (OD) values of OD 0.88 in the presence of buffer compared to OD 0.181 in the presence of 100 IU/ml heparin. The latter values were similar to those obtained when plates were coated with PF4 alone (median OD 0.203). Binding of three eluates was not inhibited by high heparin concentrations and they reacted also with PF4 alone. We conclude that multimolecular PF4/heparin complexes represent the major antigen in HAT. These multimolecular complexes might present several epitopes and form immune complexes after HAT antibody binding which activate platelets via the FcRII. In a few cases, PF4 alone can be recognized by the antibody. However, there is also evidence that other molecules might be involved in some patients.
Spectroscopic analysis of the interaction of rat liver short-chain, medium-chain, and long-chain acyl coenzyme A dehydrogenases with acyl coenzyme A substrates (1985)

We systematically studied the visual spectral changes of short-chain, medium-chain, and long-chain acyl coenzyme A (acyl-CoA) dehydrogenases, purified from rat liver mitochondria, that occur upon reaction with acyl-CoA in the absence of an electron acceptor (half-reaction). Acyl-CoA esters having various chain lengths were tested, and changes in the steady-state spectral parameters were correlated with the turnover number in the complete reaction, which represented the ability of an enzyme/substrate combination to produce an enoyl-CoA. The long-wavelength absorbance, centered around 580 nm, was observed only in the enzyme/substrate combinations in which enoyl-CoA product was produced at a significant rate in the complete reaction. There was a good correlation between the magnitudes of the long-wavelength absorbance and the turnover numbers. In contrast, the bleaching of the flavin chromophore at 450 nm was observed not only in the titration with preferred substrates but also in that with unfavorable substrates, which were shorter than favorable substrates. In the interaction with the shorter than favorable substrates, however, enoyl-CoA was not produced, nor did long-wavelength absorbance occur. When short-chain and medium-chain acyl-CoA dehydrogenases were reacted with longer than favorable substrate from which no enoyl-CoA was produced, neither the appearance of the long-wavelength absorbance nor bleaching of flavin chromophore was observed. These data suggest that the catalytic base, which abstracts alpha-proton, and flavin adenine dinucleotide are internally located, and the region containing these two sites may physically be in the form of crevice or pocket.
The impact of oxidative stress on eukaryotic iron metabolism (1996)

The processes of iron uptake and distribution are highly regulated in mammalian cells. Expression of the transferrin receptor is increased when cells are iron-depleted, while expression of the iron sequestration protein ferritin is increased in cells that are iron-replete. Regulation of expression of proteins of iron uptake (transferrin receptor) and iron sequestration (ferritin) presumably ensures that levels of reactive free iron are not high in cells. Formation of reactive oxygen species occurs when free iron reacts with oxygen, and tight regulation of iron metabolism may enable cells to avoid engaging in destructive chemical reactions. Levels of intracellular iron are directly sensed by two iron sensing proteins. Iron regulatory protein 1 (IRP1) is a bifunctional protein; in cells that are iron-replete, IRP1 contains an iron-sulfur cluster and functions as cytosolic aconitase. In cells that are iron-depleted, IRP1 binds stem-loop structures in RNA transcripts known as iron responsive elements (IREs). Iron regulatory protein 2 (IRP2) binds similar stem-loop structures, but the mode of regulation of IRP2 is different in that IRP2 is rapidly degraded in iron-replete cells. The post-transcriptional regulation of genes of iron metabolism in mammalian cells ensures that cells have an adequate supply of iron, and also ensures that cells do not generate excess reactive oxygen species through the interaction of free iron and oxygen.
Serum Pro-hepcidin Could Reflect Disease Activity in Patients with Rheumatoid Arthritis (2010)

The aim of this study was to analyze the relationship between serum pro-hepcidin concentration and the anemia profiles of rheumatoid arthritis (RA) and to estimate the pro-hepcidin could reflect the disease activity of RA. RA disease activities were measured using Disease Activity Score 28 (DAS28), tender/swollen joint counts, erythrocyte sedimentation rate (ESR), and C-reactive protein (CRP). Anemia profiles such as hemoglobin, iron, total iron binding capacity (TIBC), ferritin, and transferrin levels were measured. Serum concentration of pro-hepcidin, the prohormone of hepcidin, was measured using enzyme-linked immunosorbent assay (ELISA). Mean concentration of serum pro-hepcidin was 237.6+/-67.9 ng/mL in 40 RA patients. The pro-hepcidin concentration was correlated with rheumatoid factor, CRP, ESR, and DAS28. There was a significant correlation between pro-hepcidin with tumor necrosis factor (TNF)-alpha, interleukin (IL)-1beta, and IL-6. The pro-hepcidin concentration was significantly higher in the patients with active RA (DAS28>5.1) than those with inactive to moderate RA (DAS28< or =5.1). However, the pro-hepcidin concentration did not correlate with the anemia profiles except hemoglobin level. There was no difference of pro-hepcidin concentration between the patients with anemia of chronic disease and those without. In conclusion, serum concentration of pro-hepcidin reflects the disease activity, regardless of the anemia states in RA patients, thus it may be another potential marker for disease activity of RA.
Computational genomic analysis of PARK7 interactome reveals high BBS1 gene expression as a prognostic factor favoring survival in malignant pleural mesothelioma (2015)

The aim of our study was to assess the differential gene expression of Parkinson protein 7 (PARK7) interactome in malignant pleural mesothelioma (MPM) using data mining techniques to identify novel candidate genes that may play a role in the pathogenicity of MPM. We constructed the PARK7 interactome using the ConsensusPathDB database. We then interrogated the Oncomine Cancer Microarray database using the Gordon Mesothelioma Study, for differential gene expression of the PARK7 interactome. In ConsensusPathDB, 38 protein interactors of PARK7 were identified. In the Gordon Mesothelioma Study, 34 of them were assessed out of which SUMO1, UBC3, KIAA0101, HDAC2, DAXX, RBBP4, BBS1, NONO, RBBP7, HTRA2, and STUB1 were significantly overexpressed whereas TRAF6 and MTA2 were significantly underexpressed in MPM patients (network 2). Furthermore, Kaplan-Meier analysis revealed that MPM patients with high BBS1 expression had a median overall survival of 16.5 vs. 8.7 mo of those that had low expression. For validation purposes, we performed a meta-analysis in Oncomine database in five sarcoma datasets. Eight network 2 genes (KIAA0101, HDAC2, SUMO1, RBBP4, NONO, RBBP7, HTRA2, and MTA2) were significantly differentially expressed in an array of 18 different sarcoma types. Finally, Gene Ontology annotation enrichment analysis revealed significant roles of the PARK7 interactome in NuRD, CHD, and SWI/SNF protein complexes. In conclusion, we identified 13 novel genes differentially expressed in MPM, never reported before. Among them, BBS1 emerged as a novel predictor of overall survival in MPM. Finally, we identified that PARK7 interactome is involved in novel pathways pertinent in MPM disease.
The PowerAtlas: a power and sample size atlas for microarray experimental design and research (2006)

This resource provides a valuable tool for investigators who are planning efficient microarray studies and estimating required sample sizes.