gebhart/patrepeval huggingface dataset:
Female sex hormones at the onset of systemic lupus erythematosus affect survival (1998)

Female sex hormones affect susceptibility to systemic lupus erythematosus (SLE). To determine the effect of female sex hormones at onset of SLE on the survival of these patients, a retrospective survey was performed. The charts of 168 female SLE patients were evaluated to study the disease course, in particular the presence and kind of SLE criteria. Patients were classified as either belonging to the 'high female sex hormone at onset (HH)' or 'low female sex hormone at onset (LH)' group according to age at diagnosis. The statistics of the Dutch population, matched for age, were used to control for differences in life expectancy in these groups. A Cox regression model revealed that the relative mortality risk of HH patients vs HH controls was 4.2 times higher than the relative mortality risk of LH patients compared to LH controls. No differences in the frequency of SLE criteria between HH and LH patients were found that could explain the observed difference in mortality risk.
Nipah Virus Encephalitis Outbreak in Malaysia (2002)

Emerging infectious diseases involving zoonosis have become important global health problems. The 1998 outbreak of severe febrile encephalitis among pig farmers in Malaysia caused by a newly emergent paramyxovirus, Nipah virus, is a good example. This disease has the potential to spread to other countries through infected animals and can cause considerable economic loss. The clinical presentation includes segmental myoclonus, areflexia, hypertension, and tachycardia, and histologic evidence includes endothelial damage and vasculitis of the brain and other major organs. Magnetic resonance imaging has demonstrated the presence of discrete high-signal-intensity lesions disseminated throughout the brain. Nipah virus causes syncytial formation in Vero cells and is antigenically related to Hendra virus. The Island flying fox (Pteropus hypomelanus; the fruit bat) is a likely reservoir of this virus. The outbreak in Malaysia was controlled through the culling of >1 million pigs.
Variable product specificity of microsomal dehydrodolichyl diphosphate synthase from rat liver (1991)

Several detergents activated microsomal dehydrodolichyl diphosphate synthase of rat liver, but the chain length of products shifted downward from C90 and C95 with increasing concentration of the detergents. Maximum activation was observed at the concentration of 2% Triton X-100, 30 mM octyl glucoside, 30 mM 3-[(3-cholamidopropyl)dimethylammonio]-1-propanesulfonate, and 10 mM deoxycholate with the product chain length being C80-C85, C65-C75, C70-C75, and C55-C65, respectively. The activity of Triton X-100 solubilized enzyme was decreased by asolectin, phosphatidylethanolamine, and phosphatidylcholine. The chain lengths of products formed in the presence of these phospholipids were C85 and C90. In the presence of both phosphatidylcholine and Mg2+ the solubilized enzyme was able to produce C90 and C95 dehydrodolichyl diphosphates like native microsomal enzyme. Microsomal enzyme preparations from rat liver, brain, and testis catalyzed the formation of dehydrodolichyl diphosphates with the same chain lengths as those of the natural dolichols occurring in individual tissues. The chain length distribution of dehydrodolichyl products by (rat liver) microsomes also depended on the concentration of substrates. Not only did increasing the concentration of isopentenyl diphosphate lead to longer chain product, but decreasing that of farnesyl diphosphate increased product chain length.
Inhibition of PRC2 Activity by a Gain-of-Function H3 Mutation Found in Pediatric Glioblastoma (2013)

Sequencing of pediatric gliomas has identified missense mutations Lys27Met (K27M) and Gly34Arg/Val (G34R/V) in genes encoding histone H3.3 (H3F3A) and H3.1 (HIST3H1B). We report that human diffuse intrinsic pontine gliomas (DIPGs) containing the K27M mutation display significantly lower overall amounts of H3 with trimethylated lysine 27 (H3K27me3) and that histone H3K27M transgenes are sufficient to reduce the amounts of H3K27me3 in vitro and in vivo. We find that H3K27M inhibits the enzymatic activity of the Polycomb repressive complex 2 through interaction with the EZH2 subunit. In addition, transgenes containing lysine-to-methionine substitutions at other known methylated lysines (H3K9 and H3K36) are sufficient to cause specific reduction in methylation through inhibition of SET-domain enzymes. We propose that K-to-M substitutions may represent a mechanism to alter epigenetic states in a variety of pathologies.
Separating Bit and Lithology Effects from Drilling Mechanics Data (1988)

Abstract Most real time drilling interpretation is performed using some sort of normalized rate of penetration to infer changes in lithology and diagnose the condition of the bit. This frequently leads to ambiguous or confusing results because it is impossible to separate all bit effects from lithology effects with only one measurement. This paper shows how a second measurement, downhole torque, can be used with rate of penetration to confidently separate the bit effects from the lithology effects when drilling with milled tooth or PDC bits. Simple drilling equations for rate of penetration and bit torque are derived and compared with well known formulae. These lead to simple "quicklook" interpretations which can be made at the wellsite with a hand calculator. A detailed analysis can be performed on a wellsite computer. Many field case studies were made to examine the effects of lithology changes on the drilling response of milled tooth and PDC bits. A few of the studies are presented. The results indicate that: changes in bit torque can be used to broadly classify the lithology into three categories, namely: porous, argillaceous (shaly), and tight, corresponding to high, medium and low torque respectively, trends in bit torque and rate of penetration (ROP) in shale type formations can be used to separate the wear of milled tooth and PDC bits from changes in shale strength, it was not possible to interpret bit wear in non-shaly type formations, surface drilling measurements can be insensitive to major formation changes (eg. sand/shale boundaries), particularly in deviated wells.
Management of primary biliary cirrhosis (2000)

Primary biliary cirrhosis (PBC) is a presumed autoimmune disease of the liver, which predominantly affects women once over the age of 20 years. Most cases are diagnosed when asymptomatic (60%). The antimitochondrial antibody is present in serum in most, but not in all, patients with PBC. The disease generally progresses slowly but survival is less than an age- and gender-matched general population. The symptomatic patient may have fatigue, generalized pruritus, portal hypertension, osteoporosis, skin xanthomata, fat soluble vitamin deficiencies, and/or recurrent asymptomatic urinary tract infections. Many nonhepatic autoimmune diseases are found in association with PBC and may prompt initial presentation. To date, immunosuppressive therapy has not been shown to prolong survival in PBC. The hydrophilic bile acid, ursodeoxycholic acid (UDCA), has been shown when given in a dose of 13 to 15 mg/kg daily for up to 4 years to delay the time to liver transplantation or death. This therapy also causes a significant improvement of all the biochemical markers of cholestasis but has no beneficial effects on any of the symptoms or associated disorders. Treatment with UDCA does not obviate the need for liver transplantation. Therapies to prevent complications arising from malabsorption, portal hypertension, and/or osteoporosis are required as well. Good control of pruritus can be achieved in most patients. PBC is diagnosed with increasing frequency, but the agent(s) responsible for this slowly progressive destruction of the interlobular bile ducts remains elusive and hence a specific therapy remains unavailable.
Design, biochemical, biophysical and biological properties of cooperative antisense oligonucleotides (1995)

Short oligonucleotides that can bind to adjacent sites on target mRNA sequences are designed and evaluated for their binding affinity and biological activity. Sequence-specific binding of short tandem oligonucleotides is compared with a full-length single oligonucleotide (21mer) that binds to the same target sequence. Two short oligonucleotides that bind without a base separation between their binding sites on the target bind cooperatively, while oligonucleotides that have a one or two base separation between the binding oligonucleotides do not. The binding affinity of the tandem oligonucleotides is improved by extending the ends of the two oligonucleotides with complementary sequences. These extended sequences form a duplex stem when both oligonucleotides bind to the target, resulting in a stable ternary complex. RNase H studies reveal that the cooperative oligonucleotides bind to the target RNA with sequence specificity. A short oligonucleotide (9mer) with one or two mismatches does not bind at the intended site, while longer oligonucleotides (21mers) with one or two mismatches still bind to the same site, as does a perfectly matched 21mer, and evoke RNase H activity. HIV-1 inhibition studies reveal an increase in activity of the cooperative oligonucleotide combinations as the length of the dimerization domain increases.
Splitting of the interband absorption edge in Au: Temperature dependence (1975)

The optical absorption spectra of bulk gold were measured polarimetrically at 90, 295, and 725 K in the 1.0-3.5-eV region. The experimental data have been fitted using a model calculation which accounts for the temperature-induced smearing of the Fermi surface. The optical gaps and the interband matrix elements for the $d$-bands to Fermi-surface transitions near $X$ and $L$ have been determined as a function of temperature. The present data show that the parabolic shape of the absorption edge, which has been reported to extend to 3.5 eV, is largely coincidental for photon energies above 2.65 eV. Rather a tentative analysis suggests that the transitions in the vicinity of $L$ lose their dominant importance in shaping the absorption edge above 2.65 eV.
High expression of the chemokine receptor CCR3 in human blood basophils. Role in activation by eotaxin, MCP-4, and other chemokines. (1997)

Eosinophil leukocytes express high numbers of the chemokine receptor CCR3 which binds eotaxin, monocyte chemotactic protein (MCP)-4, and some other CC chemokines. In this paper we show that CCR3 is also highly expressed on human blood basophils, as indicated by Northern blotting and flow cytometry, and mediates mainly chemotaxis. Eotaxin and MCP-4 elicited basophil migration in vitro with similar efficacy as regulated upon activation normal T cells expressed and secreted (RANTES) and MCP-3. They also induced the release of histamine and leukotrienes in IL-3-primed basophils, but their efficacy was lower than that of MCP-1 and MCP-3, which were the most potent stimuli of exocytosis. Pretreatment of the basophils with a CCR3-blocking antibody abrogated the migration induced by eotaxin, RANTES, and by low to optimal concentrations of MCP-4, but decreased only minimally the response to MCP-3. The CCR3-blocking antibody also affected exocytosis: it abrogated histamine and leukotriene release induced by eotaxin, and partially inhibited the response to RANTES and MCP-4. In contrast, the antibody did not affect the responses induced by MCP-1, MCP-3, and macrophage inflammatory protein-1alpha, which may depend on CCR1 and CCR2, two additional receptors detected by Northern blotting with basophil RNA. This study demonstrates that CCR3 is the major receptor for eotaxin, RANTES, and MCP-4 in human basophils, and suggests that basophils and eosinophils, which are the characteristic effector cells of allergic inflammation, depend largely on CCR3 for migration towards different chemokines into inflamed tissues.
Direct synergistic effects of interleukin-7 on in vitro myelopoiesis of human CD34+ bone marrow progenitors (1994)

Interleukin-7 (IL-7) is an important growth factor in B and T lymphopoiesis in mouse and human, whereas IL-7 has been regarded to lack proliferative effects on cells within the myeloid lineage. However, we have recently reported that IL-7 potently can enhance colony stimulating factor (CSF)-induced myelopoiesis from primitive murine hematopoietic progenitors, showing a novel role of IL-7 in early murine myelopoiesis. Using CD34+ human hematopoietic progenitor cells, we show here a similar role of IL-7 in human myelopoiesis, although interesting differences between the two species were found as well. Although purified recombinant human (rh)IL-7 alone did not induce any proliferation of CD34+ cells, IL-7 in a concentration-dependent manner enhanced the colony formation induced by all four CSFs up to threefold. Furthermore, stem cell factor (SCF)-induced granulocyte-macrophage (GM) colony formation was increased fourfold in the presence of IL-7. Single- cell cloning assays showed that these synergistic effects of IL-7 were directly mediated on the targeted progenitors, and that IL-7 increased the number, as well as the size of the colonies formed. Morphological examination showed that IL-7 affected the progeny developed from CD34+ cells stimulated by G-CSF or IL-3, increasing the number of CFU-M (colony forming unit-macrophage) and CFU-granulocyte-macrophage, whereas the number of CFU-granulocyte were unaltered.
Realization of dynamic range controllers on a digital signal processor for audio systems. (1995)

This paper describes a new design method of dynamic range controllers, such as compressor, limiter, expander and noise gate, on a DSP for digital audio systems. For the compressor, we have previously proposed an efficient implementing method on DSP by calculating the polynomial expression to approximate the power transformation. Based on the approximation algorithm, we extend the positive compression ratio to the negative compression ratio for the compressor. Then, we design an expander based on the facts that the ideal compression characteristic could be obtained by application of a polynomial expression. By defining an expansion (downward expansion) characteristic with two threshold levels, the gain for getting the expansion may be decomposed into a gain of an upward expansion with an integer expansion ratio, a gain of a compression and gain shift. By this method, the ideal input-output characteristic can be achieved by using seven-order polynomial expression for dynamic range control of 50dB. The digital signal processing on DSP is about 130 steps for the compressor, and 120 steps for the expander with a given expansion ratio equal to or smaller than 15.
Isolating highly enriched populations of circulating epithelial cells and other rare cells from blood using a magnetic sweeper device (2009)

The enumeration of rare circulating epithelial cells (CEpCs) in the peripheral blood of metastatic cancer patients has shown promise for improved cancer prognosis. Moving beyond enumeration, molecular analysis of CEpCs may provide candidate surrogate endpoints to diagnose, treat, and monitor malignancy directly from the blood samples. Thorough molecular analysis of CEpCs requires the development of new sample preparation methods that yield easily accessible and purified CEpCs for downstream biochemical assays. Here, we describe a new immunomagnetic cell separator, the MagSweeper, which gently enriches target cells and eliminates cells that are not bound to magnetic particles. The isolated cells are easily accessible and can be extracted individually based on their physical characteristics to deplete any cells nonspecifically bound to beads. We have shown that our device can process 9 mL of blood per hour and captures >50% of CEpCs as measured in spiking experiments. We have shown that the separation process does not perturb the gene expression of rare cells. To determine the efficiency of our platform in isolating CEpCs from patients, we have isolated CEpCs from all 47 tubes of 9-mL blood samples collected from 17 women with metastatic breast cancer. In contrast, we could not find any circulating epithelial cells in samples from 5 healthy donors. The isolated CEpCs are all stored individually for further molecular analysis.
Colloborative Law Introduction (2004)

Introduction to Collaborative Law Symposium.
Role of Hsp70 in Cancer Growth and Survival (2012)

Hsp70 is a highly conserved protein that refolds misfolded proteins and has numerous housekeeping functions which regulate apoptosis and other cell activities. Hsp70 consists of a nucleotide binding domain which binds ATP and a substrate binding domain that binds misfolded proteins. The substrate binding domain contains a peptide binding pocket which is covered by a helical lid. In humans, there are three major cytosolic Hsp70 isotypes, Hsp70-8, Hsp70-1 and Hsp70-2. Leukemic and numerous other cancer cells have a greater amount of Hsp70-1 and -2, which help the cancer cells inhibit apoptosis in response to stress. This review summarizes the structure and role of Hsp70 proteins in cancer survival.
Electrokinetic resolution of amino acid enantiomers with copper(II)-aspartame support electrolyte (1987)

ADVERTISEMENT RETURN TO ISSUEPREVArticleNEXTElectrokinetic resolution of amino acid enantiomers with copper(II)-aspartame support electrolytePhilippe. Gozel, Ernst. Gassmann, Hope. Michelsen, and Richard N. ZareCite this: Anal. Chem. 1987, 59, 1, 44–49Publication Date (Print):January 1, 1987Publication History Published online1 May 2002Published inissue 1 January 1987https://pubs.acs.org/doi/10.1021/ac00128a009https://doi.org/10.1021/ac00128a009research-articleACS PublicationsRequest reuse permissionsArticle Views406Altmetric-Citations305LEARN ABOUT THESE METRICSArticle Views are the COUNTER-compliant sum of full text article downloads since November 2008 (both PDF and HTML) across all institutions and individuals. These metrics are regularly updated to reflect usage leading up to the last few days.Citations are the number of other articles citing this article, calculated by Crossref and updated daily. Find more information about Crossref citation counts.The Altmetric Attention Score is a quantitative measure of the attention that a research article has received online. Clicking on the donut icon will load a page at altmetric.com with additional details about the score and the social media presence for the given article. Find more information on the Altmetric Attention Score and how the score is calculated. Share Add toView InAdd Full Text with ReferenceAdd Description ExportRISCitationCitation and abstractCitation and referencesMore Options Share onFacebookTwitterWechatLinked InRedditEmail Other access optionsGet e-Alertsclose Get e-Alerts
ETV1 Is a Novel Androgen Receptor-Regulated Gene that Mediates Prostate Cancer Cell Invasion (2007)

Androgens and the androgen receptor (AR) act in cells by modulating gene expression. Through gene microarray studies, we have identified Ets Variant Gene 1 (ETV1) as a novel androgen-regulated gene. Our data demonstrate that ETV1 mRNA and protein are up-regulated in response to ligand-activated AR in androgen-dependent LNCaP cells, but there is no detectable ETV1 expression in normal prostate cells. The ETV1 promoter is induced by androgens and recruits the AR in the context of chromatin. ETV1-regulated endogenous matrix metalloproteinase genes can be induced by ligand-activated AR. In contrast to the hormone-induced expression in androgen-dependent LNCaP cells, ETV1 expression in androgen-independent LNCaP cells is high and unresponsive to androgen. This androgen-independent ETV1 expression contrasts with the hormone-dependent expression observed for TMPRSS2 in these androgen-independent prostate cancer cells. ETV1 is overexpressed in prostate cancer independent of the TMPRSS2:ETV1 translocation. Disruption of ETV1 expression in both androgen-dependent and androgen-independent prostate cancer cells significantly compromises the invasion capacity of these cells, suggesting an important role for ETV1 in prostate cancer metastasis. Collectively, these results demonstrate that ETV1 expression transitions from androgen-induced to androgen-independent as prostate cancer cells switch from hormone-dependent to hormone-refractory and suggest that this transition may be in part responsible for the elevated levels of ETV1 observed in prostate tumors. Additionally, our data provide an indirect mechanism of AR regulation of gene expression, via the transactivation of the transcription factor ETV1.
Chronic Lymphocytic Leukemia (2005)

Our concept of the pathogenesis of chronic lymphocytic leukemia has undergone remarkable changes during the past decade. This review addresses the latest ideas concerning the origin of this common form of leukemia and discusses how molecular investigations are beginning to change the management of the disease.
Adult nutrient intake as a risk factor for Parkinson's disease (1999)

These results suggest an association of PD with high intake of total fat, saturated fats, cholesterol, lutein and iron.
Ribosomal binding and dipeptide formation by misacylated tRNAPhe's (1988)

Eight structurally modified peptidyl-tRNA(Phe),s were employed to study P-site binding and peptide bond formation in a cell-free system involving Escherichia coli ribosomes programmed with poly(uridylic acid). It was found that the two analogues (N-acetyl-D-phenylalanyl-tRNA(Phe) and N-acetyl-D-tyrosyl-tRNA(Phe] containing D-amino acids functioned poorly as donors in the peptidyltransferase reaction and that two N-acetyl-L-phenylalanyl-tRNA(Phe)'s differing from the prototype substrate in that they contained 2'- or 3'-deoxyadenosine at the 3'-terminus failed to form dipeptide at all when L-phenylalanyl-tRNA(Phe) was the acceptor tRNA. Interestingly, all four of these peptidyl-tRNA's bound to ribosomes to about the same extent as tRNA's that functioned normally as donors in the peptidyltransferase reaction, at least in the absence of competing peptidyl-tRNA species. Two peptidyl-tRNA's lacking an amino group were also tested. In comparison with N-acetyl-L-phenylalanyl-tRNA(Phe) it was found that trans-cinnamyl-tRNA(Phe) and 3-phenylpropionyl-tRNA(Phe)'s formed dipeptides to the extent of 53 and 80%, respectively, when L-phenylalanyl-tRNA(Phe)was used as the acceptor tRNA. N-Acetyl-beta-phenylalanyl-tRNA(Phe) was found to be the most efficient donor substrate studied. Both isomers transferred N-acetyl-beta-phenylalanine to L-phenylalanyl-tRNA(Phe); the nature of the dipeptides formed in each case was verified by HPLC in comparison with authentic synthetic samples. Further, the rate and extent of peptide bond formation in each case exceeded that observed with the control tRNA, N-acetyl-L-phenylalanyl-tRNA(Phe).
CLK2 inhibition ameliorates autistic features associated with SHANK3 deficiency (2016)

SH3 and multiple ankyrin repeat domains 3 (SHANK3) haploinsufficiency is causative for the neurological features of Phelan-McDermid syndrome (PMDS), including a high risk of autism spectrum disorder (ASD). We used unbiased, quantitative proteomics to identify changes in the phosphoproteome of Shank3-deficient neurons. Down-regulation of protein kinase B (PKB/Akt)-mammalian target of rapamycin complex 1 (mTORC1) signaling resulted from enhanced phosphorylation and activation of serine/threonine protein phosphatase 2A (PP2A) regulatory subunit, B56β, due to increased steady-state levels of its kinase, Cdc2-like kinase 2 (CLK2). Pharmacological and genetic activation of Akt or inhibition of CLK2 relieved synaptic deficits in Shank3-deficient and PMDS patient-derived neurons. CLK2 inhibition also restored normal sociability in a Shank3-deficient mouse model. Our study thereby provides a novel mechanistic and potentially therapeutic understanding of deregulated signaling downstream of Shank3 deficiency.