gebhart/patrepeval huggingface dataset:
Genomic organization of human histo-blood group ABO genes (1995)

We have isolated human genomic DNA clones encompassing 30 kbp of the histo-blood group ABO locus. The locations of the exons have been mapped and the nucleotide sequences of the exon-intron boundaries have been determined. The human ABO genes consist of at least seven exons, and the coding sequence in the seven coding exons spans over 18 kb of the genomic DNA. The exons range in size from 28 to 688 bp, with most of the coding sequence lying in exon 7.
Natural Questions: A Benchmark for Question Answering Research (2019)

We present the Natural Questions corpus, a question answering data set. Questions consist of real anonymized, aggregated queries issued to the Google search engine. An annotator is presented with a question along with a Wikipedia page from the top 5 search results, and annotates a long answer (typically a paragraph) and a short answer (one or more entities) if present on the page, or marks null if no long/short answer is present. The public release consists of 307,373 training examples with single annotations; 7,830 examples with 5-way annotations for development data; and a further 7,842 examples with 5-way annotated sequestered as test data. We present experiments validating quality of the data. We also describe analysis of 25-way annotations on 302 examples, giving insights into human variability on the annotation task. We introduce robust metrics for the purposes of evaluating question answering systems; demonstrate high human upper bounds on these metrics; and establish baseline results using competitive methods drawn from related literature.
Endogenous IFN-αβ suppresses colony-stimulating factor (CSF)-1-stimulated macrophage DNA synthesis and mediates inhibitory effects of lipopolysaccharide and TNF-α (1996)

Murine bone marrow-derived macrophages (BMM) are widely used as a suitable model to study the proliferative response to macrophage-CSF or CSF-1. We report here that the amount of DNA synthesis observed in BMM cultures in response to CSF-1 can be masked quite significantly by low levels of IFN-alpha beta produced in the cultures. It was found that Ab to IFN-alpha beta could enhance the proliferative response in CSF-treated BMM that were able to respond to endogenous IFN-alpha beta; however, BMM from mice lacking a component of the type I IFN receptor did not show any enhancement of CSF-1-dependent DNA synthesis on addition of the Ab. While DNA synthesis in CSF-1-stimulated BMM from normal mice was also very sensitive to the inhibitory actions of very low concentrations of added IFN-alpha beta, DNA synthesis in BMM from the "knockout" mice was not, indicating that the type I IFN receptor component containing the null mutation was essential for signal transduction. Previously it was shown that bacterial LPS, TNF-alpha, IFN-gamma, and cAMP could all inhibit CSF-1-stimulated BMM DNA synthesis and proliferation. Using the combined approach of blocking IFN-alpha beta Ab and the IFN receptor "knockout" mice, it was found here that the growth-inhibitory effects of LPS and TNF-alpha are due, to a significant extent, to endogenous IFN-alpha beta, whereas those of IFN-gamma and cAMP occur by a different mechanism. it is proposed that the type I IFN receptor (IFNAR 1) "knockout" mice may be useful in delineating some of the in vivo actions of CSF-1, LPS, TNF-alpha, and possibly other agents.
Insights into the Role of Follicular Helper T Cells in Autoimmunity (2014)

Follicular helper T (TFH) cells are recently highlighted as their crucial role for humoral immunity to infection as well as their abnormal control to induce autoimmune disease. During an infection, naïve T cells are differentiating into TFH cells which mediate memory B cells and long-lived plasma cells in germinal center (GC). TFH cells are characterized by their expression of master regulator, Bcl-6, and chemokine receptor, CXCR5, which are essential for the migration of T cells into the B cell follicle. Within the follicle, crosstalk occurs between B cells and TFH cells, leading to class switch recombination and affinity maturation. Various signaling molecules, including cytokines, surface molecules, and transcription factors are involved in TFH cell differentiation. IL-6 and IL-21 cytokine-mediated STAT signaling pathways, including STAT1 and STAT3, are crucial for inducing Bcl-6 expression and TFH cell differentiation. TFH cells express important surface molecules such as ICOS, PD-1, IL-21, BTLA, SAP and CD40L for mediating the interaction between T and B cells. Recently, two types of microRNA (miRNA) were found to be involved in the regulation of TFH cells. The miR-17-92 cluster induces Bcl-6 and TFH cell differentiation, whereas miR-10a negatively regulates Bcl-6 expression in T cells. In addition, follicular regulatory T (TFR) cells are studied as thymus-derived CXCR5(+)PD-1(+)Foxp3(+) Treg cells that play a significant role in limiting the GC response. Regulation of TFH cell differentiation and the GC reaction via miRNA and TFR cells could be important regulatory mechanisms for maintaining immune tolerance and preventing autoimmune diseases such as systemic lupus erythematosus (SLE) and rheumatoid arthritis (RA). Here, we review recent studies on the various factors that affect TFH cell differentiation, and the role of TFH cells in autoimmune diseases.
What are the functional consequences of neurocognitive deficits in schizophrenia? (1996)

Verbal memory and vigilance appear to be necessary for adequate functional outcome. Deficiencies in these areas may prevent patients from attaining optimal adaptation and hence act as "neurocognitive rate-limiting factors." On the basis of this review of the literature, a series of hypotheses are offered for follow-up studies.
Transcription Factor Nrf2 Plays a Pivotal Role in Protection against Elastase-Induced Pulmonary Inflammation and Emphysema (2005)

Emphysema is one of the major pathological abnormalities associated with chronic obstructive pulmonary disease. The protease/antiprotease imbalance and inflammation resulting from oxidative stress have been attributed to the pathogenesis of emphysema. Nrf2 is believed to protect against oxidative tissue damage through the transcriptional activation of a battery of antioxidant enzymes. In this study, we investigated the protective role of Nrf2 in the development of emphysema using elastase-induced emphysema as our model system. We found that elastase-provoked emphysema was markedly exacerbated in Nrf2-knockout (KO) mice compared with wild-type mice. The severity of emphysema in Nrf2-KO mice correlated intimately with the degree of lung inflammation in the initial stage of elastase treatment. The highly inducible expression of antioxidant and antiprotease genes observed in wild-type alveolar macrophages was significantly attenuated in the lungs of Nrf2-KO mice. Interestingly, transplantation of wild-type bone marrow cells into Nrf2-KO mice retarded the development of initial lung inflammation and subsequent emphysema, and this improvement correlated well with the appearance of macrophages expressing Nrf2-regulated antiprotease and antioxidant genes. Thus, Nrf2 appears to exert its protective effects through the transcriptional activation of antiprotease and antioxidant genes in alveolar macrophages.
Sox9 Expression Is Not Limited to Chondroid Neoplasms: Variable Occurrence in Other Soft Tissue and Bone Tumors With Frequent Expression by Synovial Sarcomas (2010)

The transcription factor Sox9 is known to play a crucial role in normal chondrogenesis, and antibodies against Sox9 have been proposed as a diagnostic tool for neoplasms with chondroid differentiation. However, the pattern of Sox9 immunohistochemical expression by other bone and soft tissue neoplasms, as well as its diagnostic specificity, remain unexplored. The authors have performed immunohistochemistry with antibodies against Sox9 in 106 chondroid and nonchondroid bone and soft tissue neoplasms. Moderate to intense Sox9 nuclear staining was observed in 14/20 chondrosarcomas (70%), and in 24/81 (29.6%) cases from a multitumor tissue microarray, which included 16/18 synovial sarcomas, 4/15 osteosarcomas, 2/5 peripheral primitive neuroectodermal tumor (PNET)/Ewing sarcomas, 1/1 mesenchymal chondrosarcoma, and 1/1 chondroblastoma. The results suggest that Sox9 usefulness in the diagnosis of chondroid tumors may be limited because of low sensitivity and specificity. The finding of Sox9 expression by 88.9% of synovial sarcomas represents a novel and striking observation, which deserves further investigation.
논문 : 명안어서첩(明安御書帖) 소재 언간에 대하여 (2001)

There are some relics of Princess Myeongan which are designated as National Treasure No 1220 in the City Museum located in Ojukheon, Gangreung city. These relics are quite valuable materials which are helpful to study Korean language(Hangeul), calligraphy, economy, social structure and courtly lifestyle of those times. These relics include six letters written in Korean by King Hyeonjong, Princess Myeongan`s Naming Paper written by King Hyunjong himself and two lists of Novels, the King sent to the princess. And three letters of Empress Myeongseong, King Sukjong`s Korean letters and several letters cherished by 0 Taeju(the son in law of King Hyeonjong) family are also contained in the list. In this paper, the letters of King Hyeonjong, Empress Myeongseong and King Sukjong contained in Empress Myeongseong`s Royal letter collection are examined. It has been known that of the royal letter written by in Korean language were mainly sent to the princess who had been married. But this royal letter collection of Empress Myeongseong contains letters sent to the mother of the King. Thus this letter collection shows the characteristics of courtly language.
Body fluid derived exosomes as a novel template for clinical diagnostics (2011)

Our data demonstrate that exosomes from body fluids carry esRNAs which can be analyzed and offers access to the transcriptome of the host organism. The exosomal lipid bilayer protects the genetic information from degradation. As the isolation of exosomes is a minimally invasive procedure, this technique opens new possibilities for diagnostics.
RAG-2-deficient blastocyst complementation: an assay of gene function in lymphocyte development. (1993)

We describe a system to evaluate the function of lymphocyte-specific and generally expressed genes in the differentiation and/or function of lymphocytes. RAG-2 (recombination-activating gene 2)-deficient mice have no mature B and T lymphocytes due to the inability to initiate VDJ recombination. Blastocysts from RAG-2-deficient mice generate animals with no mature B and T cells following implantation into foster mothers. However, injection of normal ES cells into RAG-2-deficient blastocysts leads to the generation of somatic chimeras with mature B and T cells all of which derive from the injected ES cells (referred to as RAG-2-deficient blastocyst complementation). Complementation of RAG-2-deficient blastocysts with mutant ES cells heterozygous for a targeted mutation that deletes all immunoglobulin heavy-chain joining (JH) gene segments (JH+/-) also leads to generation of chimeras with normal B and T cells. However, complementation with ES cells homozygous for the JH mutation (JH-/-) generates animals with normal T cells but no B cells, due to a block in B-cell development at a very early stage. Transfection of a functionally assembled mu heavy-chain gene into the JH-/- ES cells prior to blastocyst injection rescues the JH-/- mutation and allows the generation of both mature T and mature B cells. The rescued B cells express IgM but not IgD and respond normally to bacterial lipopolysaccharide stimulation by proliferating and by secreting IgM.
Immunotherapy with dendritic cells and tumor major histocompatibility complex class I-derived peptides requires a high density of antigen on tumor cells. (2000)

Immunization with dendritic cells and unfractionated MHC class I-binding peptides derived from autologous tumor cells has been shown to induce effective antitumor immunity. However, the importance of the relative abundance of tumor peptides on the surface of tumor cells is not known. We have addressed this question using peptides isolated from three tumor cell lines transfected with a minigene encoding amino acids 33-41 of the lymphocytic choriomeningitis virus glycoprotein (LCMV(33-41)). The three cell lines expressed different levels of MHC class I molecules and had different abilities to stimulate proliferation of LCMV(33-41)-specific T cells in vitro. We found that antitumor immune responses were best elicited by immunizing mice with dendritic cells and synthetic LCMV(33-41) peptide. Peptide preparations from a given tumor cell line conferred protection against challenge with the same tumor cell line. However, protective immunity to a different tumor could be induced only if the cell line used for peptide preparation presented a high relative proportion of LCMV(33-41) in association with MHC class I. Our results suggest that multiple peptide epitopes are required for the induction of an effective antitumor immune response using MHC class I-binding peptides from tumor cells. Also, the ability to induce an antitumor immune response appears to correlate with the proportion, rather than the absolute amount, of tumor-specific peptide in the mixture used for immunization.
Sequence and Regulatory Signals of the Filamentous Phage Genome (1978)

The genome of the male-specific filamentous coliphages fd, f1, and M13 is a circular single-stranded DNA of approximately 6400 bases, which codes for at least eight genes (Marvin and Hohn 1969; Ray 1977). Upon infecting a cell, a double-stranded replicative-form (RF) DNA is formed, and this RF DNA then serves as a template for mRNA synthesis as well as for progeny phage DNA production. Both reactions are catalyzed and controlled largely by host proteins. Therefore, the structure and function of the filamentous phage DNA have been studied extensively as a model system for elucidating the molecular mechanisms involved in DNA replication and gene expression. The first nucleotide sequences of filamentous phage DNA to be determined were the pyrimidine tracts obtained by the Burton and Peterson depurination procedure; tracts of up to 20 bases in length were sequenced (Petersen and Reeves 1969; Ling 1972). Oligonucleotide-primed DNA synthesis was used by Oertel and Schaller (1972) to determine the order of pyrimidine tracts in a pyrimidine-rich segment of fd DNA (positions 5539–5630, Fig. 1) and, in combination with ribosubstitution, by Sanger et al. (1973 Sanger et al. (1974) to deduce the sequence of 85 nucleotides in f1 DNA (positions 6303–6387, Fig. 1). Three ribosome-binding sites on DNA-directed mRNA were sequenced by Pieczenik et al. (1974). Ribosomes bind specifically to the start point of translation on mRNA, and the bound region can be isolated and sequenced after RNase treatment. Similar protection experiments with RNA polymerase allowed the isolation and sequencing of an RNA-polymerase-binding site from...
Bone Morphogenetic Protein-2 Inhibits Serum Deprivation-induced Apoptosis of Neonatal Cardiac Myocytes through Activation of the Smad1 Pathway (2001)

Bone morphogenetic protein (BMP)-2 has been shown to induce ectopic expression of cardiac transcription factors and beating cardiomyocytes in non-precardiac mesodermal cells, suggesting that BMP-2 is an inductive signaling molecule that participates in cardiac development. However, direct evidence of the effects of BMP-2 on cardiac myocytes has not been reported. To examine the role of BMP-2 and its receptors, we studied the ability of BMP-2 to promote survival of isolated neonatal rat cardiac myocytes. BMP receptors IA, IB, and II and activin receptor I were found to be expressed in myocytes, and BMP-2 phosphorylated Smad1 and p38 MAPK. Interestingly, BMP-2 promoted survival and inhibited apoptosis of serum-deprived myocytes, although it did not strongly induce hypertrophic growth. To explore the mechanisms for this protective effect, an adenovirus-based vector system was used. Similar to BMP-2, Smad1 promoted survival that was repressed by Smad6. Moreover, BMP-2 and Smad1 enhanced the expression of the anti-apoptotic molecule Bcl-x(L). Antisense oligonucleotides to bcl-x(L) attenuated the survival effected by BMP-2. Overall, our findings suggest that BMP-2 prevents apoptosis of myocytes by induction of Bcl-x(L) via a Smad1 pathway and might be a novel survival factor without any hypertrophic effect on myocytes.
Copolymerization of carbon dioxide and epoxide (2004)

Abstract An erratum has been published for this article in J Polym Sci Part A: Polym Chem (2005) 43(4) 916 . The alternating copolymerization of carbon dioxide and epoxide to produce polycarbonate has attracted the attention of many chemists because it is one of the most promising methodologies for the utilization of carbon dioxide as a safe, clean, and abundant raw material in synthetic chemistry. Recent development of catalysts for alternating copolymerization is based on the rational design of metal complexes, particularly complexes of transition metals with well‐defined structures. In this article, the history and recent successful examples of the alternating copolymerization of carbon dioxide and epoxide are described. © 2004 Wiley Periodicals, Inc. J Polym Sci Part A: Polym Chem 42: 5561–5573, 2004
M Phase Phosphoprotein 10 Is a Human U3 Small Nucleolar Ribonucleoprotein Component (1998)

We have previously developed a novel technique for isolation of cDNAs encoding M phase phosphoproteins (MPPs). In the work described herein, we further characterize MPP10, one of 10 novel proteins that we identified, with regard to its potential nucleolar function. We show that by cell fractionation, almost all MPP10 was found in isolated nucleoli. By immunofluorescence, MPP10 colocalized with nucleolar fibrillarin and other known nucleolar proteins in interphase cells but was not detected in the coiled bodies stained for either fibrillarin or p80 coilin, a protein found only in the coiled body. When nucleoli were separated into fibrillar and granular domains by treatment with actinomycin D, almost all the MPP10 was found in the fibrillar caps, which contain proteins involved in rRNA processing. In early to middle M phase of the cell cycle, MPP10 colocalized with fibrillarin to chromosome surfaces. At telophase, MPP10 was found in cellular structures that resembled nucleolus-derived bodies and prenucleolar bodies. Some of these bodies lacked fibrillarin, a previously described component of nucleolus-derived bodies and prenucleolar bodies, however, and the bulk of MPP10 arrived at the nucleolus later than fibrillarin. To further examine the properties of MPP10, we immunoprecipitated it from cell sonicates. The resulting precipitates contained U3 small nucleolar RNA (snoRNA) but no significant amounts of other box C/D snoRNAs. This association of MPP10 with U3 snoRNA was stable to 400 mM salt and suggested that MPP10 is a component of the human U3 small nucleolar ribonucleoprotein.
Multifocal Glasses Impair Edge‐Contrast Sensitivity and Depth Perception and Increase the Risk of Falls in Older People (2002)

The study findings indicate that multifocal glasses impair depth perception and edge-contrast sensitivity at critical distances for detecting obstacles in the environment. Older people may benefit from wearing nonmultifocal glasses when negotiating stairs and in unfamiliar settings outside the home.
The involvement of active DNA synthesis in camptothecin-induced G2 arrest: altered regulation of p34cdc2/cyclin B. (1992)

Cell cycle arrest in G2 phase is a common response to a variety of DNA-damaging agents. The coupling between DNA damage and G2 arrest was studied in synchronized HeLa cells using camptothecin, a highly specific inhibitor of topoisomerase I that damages DNA through the formation of reversible topoisomerase I-DNA cleavable complexes. Brief camptothecin treatment of early S-phase HeLa cells caused arrest at G2 phase and abolished the activation of p34cdc2 protein kinase. Both tyrosine dephosphorylation of p34cdc2 and cyclin B accumulation were altered. These cell cycle-dependent changes were not observed when DNA replication was inhibited by aphidicolin during the brief camptothecin treatment. Our results suggest that to produce G2 arrest, active DNA synthesis is required at the time of camptothecin treatment, as was previously shown for camptothecin-induced cytotoxicity. Furthermore, our results suggest that the interaction of the replication fork with DNA damage may ultimately trigger altered regulation of p34cdc2/cyclin B, leading to cell cycle arrest at the G2 phase.
Adenosine Triphosphate-Dependent Transport of Estradiol–17β(β– D –Glucuronide) in Membrane Vesicles by Mdr1 Expressed in Insect Cells (1998)

MDR1, an ABC transporter that confers multidrug resistance in tumor cells, is constitutively expressed in normal liver canalicular membrane. Human MDR1-expressing multidrug-resistant cells display increased resistance to estradiol-17beta(beta-D-glucuronide) (E217G). MDR1 substrates/modulators inhibit adenosine triphosphate (ATP)-dependent transport of E217G in the rat canalicular membrane and protect against E217G-mediated cholestasis in isolated perfused rat liver. The present studies were designed to determine if E217G is a substrate for MDR1 using a baculovirus expression system and if other estrogen glucuronides interact with MDR1. ATP-dependent transport of E217G (10 micromol/L) was linear for up to 2 minutes and yielded a rate of 45.6 pmol/min/mg protein in membrane vesicles from Sf9 cells infected with MDR1-baculovirus. This transport was saturable (Km = 62 micromol/L) and occurred into an osmotically sensitive space. ATP-dependent transport of E217G (10 micromol/L) was inhibited 63% by 10 micromol/L daunomycin, but not by 100 micromol/L S-(2,4-dinitrophenyl)glutathione (GS-DNP) (a substrate for canalicular multispecific organic anion transporter [cMOAT]). Glucuronide conjugates of the estrogen D-ring (100 micromol/L), estriol-17beta(beta-D-glucuronide) (E317G) and estriol-16(beta-D-glucuronide) (E316G), inhibited MDR1-mediated E217G transport by 58% and 35%, respectively. In contrast, noncholestatic glucuronides, estradiol-3-(beta-D-glucuronide) (E23G) or estradiol-3-sulfate-17beta(beta-D-glucuronide) (E23SO417G), had no effect. E217G neither stimulated MDR1 ATPase activity nor inhibited verapamil-stimulated ATPase activity. Infusion of 1.5 micromol/L doxorubicin or 1 micromol/L taxol protected against cholestasis induced by E316G and E317G in isolated perfused rat liver. These studies identify E217G, and probably E316G and E317G, as endogenous substrates for MDR1.
대학 영어전용 교과의 수업 방법 개선 방안 탐색과 적용: 수행공학 모형(HPT Model)을 바탕으로 (2007)

대학 교육의 국제화의 한 방안으로 일부 대학의 강의들이 영어 전용 강좌로 운영되고 있다. 그러나 원래의 목적과 취지와는 달리 영어 전용 교과가 효과적으로 운영되지 못하고 있는 경우가 빈번하다. 따라서 본 연구는 한 영어 전용 교과의 사례를 통하여 영어전용 교과의 수업 방법 개선 방안을 탐색하고 적용해보는 것을 연구의 목적으로 하였다. 이러한 연구의 목적을 위하여 ISPI의 수행공학 모형을 이용하여 크게 두 단계로 나누어진 연구를 수행하였다. 첫 번째 단계에서는 대상이 된 영어 전용 교과의 문제점 발견과 이에 대한 원인 파악, 그리고 원인을 바탕으로 한 해결방안의 모색하였다. 본 연구에서 정의된 영어 전용 강좌의 문제점은 학습자들의 학습 내용에 대한 이해 수준 저하, 제한된 수업 시간을 통한 영어 실력 향상의 부진 등이었다. 이러한 문제점에 대한 원인을 Gilbert의 BEM 모형의 틀을 사용하여 환경적인 요소와 개인적인 요소로 나누어 분석하였다. 이렇게 발견된 원인들 중 가중치를 준거로 선택된 일부 원인에 대하여 해결책을 고안하였다. 해결책은 본 수업 중에 이루어지는 것과 한정된 수업 시간 등을 보완하기 위하여 웹상의 학습 커뮤니티의 운영을 통하여 이루어지는 것으로 나뉘어 고안되었다. 두 번째 단계의 연구에서는 고안된 해결책의 적용과 이에 대한 효과성을 보고하는 것으로 연구가 진행되었다. 이와 같은 연구의 전체 절차 및 결과는 현재 영어 전용 수업을 운영하고 있는 교과전문가들에게 많은 아이디어를 제공할 것으로 사료된다.