gebhart/patrepeval huggingface dataset:
[O1‐01‐06]: Correlations between cholesterol‐related genetic risk scores and lower brain‐imaging measurements of regional glucose metabolism (2005)

In a positron emission tomography (PET) study of cognitively normal, late-middle-aged persons, we demonstrated a correlation between apolipoprotein E (APOE) ϵ4 gene dose, an established contributor to the risk of late-onset Alzheimer's disease (AD), and lower measurements of the cerebral metabolic rate for glucose (CMRgl) in AD-affected brain regions. We proposed the use of PET as a quantitative, pre-symptomatic endophenotype to evaluate the individual and aggregate effects of putative genetic and non-genetic modifiers of AD risk. In a genetic study of European AD cases and controls, Papassotiropoulos recently identified a cluster of single nucleotide polymorphisms (SNPs) in 7 cholesterol-related genes (APOE, SOAT1, APOE 5’-untranslated region, OLR1, CYP46A1, LPL, LIPA, and APOA4) associated with the risk of AD. He proposed the calculation of a person's cholesterol-related genetic AD risk scores from the risk-weighted summation of his or her implicated SNPs. To test the hypothesis that the proposed cholesterol-related AD genetic risk scores in cognitively normal, late-middle persons are correlated with lower CMRgl measurements in AD-affected brain regions. A brain mapping algorithm (SPM99) was used to compute significant correlations between cholesterol-related genetic risk scores and lower PET CMRgl measurements in 118 previously studied, cognitively normal, late-middle-aged persons. They included 25 APOE ϵ4 homozygotes, 35 ϵ4 heterozygotes, and 58 ϵ4 non-carriers and were 57±5 years of age. As predicted, significant correlations between cholesterol-related genetic risk scores and lower CMRgl were observed in each of the AD-affected brain regions; several of the correlations observed in the overall group were again observed in the aggregate APOE ϵ4 carrier group and in the ϵ4 homozygotes, heterozygotes, and non-carriers; significant correlations between the risk scores and higher CMRgl were not observed in any location. Furthermore, many of the observed correlations were again noted after excluding effects of APOE ϵ4 gene dose from the genetic risk scores. This study provides further support for the role of a cluster of cholesterol-related genes in the risk of AD, and it provides further support for the role of brain imaging in the pre-symptomatic assessment of putative modifiers of AD risk.
Alteration in folding efficiency and conformation of recombinant human tumor necrosis factor-alpha by replacing cysteines 69 and 101 with aspartic acid 69 and arginine 101 (1990)

An analog of human tumor necrosis factor-alpha (TNF-alpha) was created involving the replacement of Cys69 with Asp and Cys101 with Arg. The solution structure and behavior of this analog were compared with the native protein. The analog exhibited a greatly decreased folding efficiency following dilution from urea, but essentially identical circular dichroic spectra in both the folded and unfolded states. The Stokes radius of the native and analog TNF-alpha in the folded state were identical, with the analog exhibiting a slight broadening of the eluting peak. The fluorescence emission spectrum of the native protein exhibits a plateau from 320 to 328 nm, while the spectrum of the analog consisted of a single peak with a maximum at 335 nm. The analog also had a 1.4-fold increase in the fluorescence intensity. Limited proteolysis of the analog resulted in only one of the two peptides seen following digestion of the native protein, and this product was less stable than the equivalent native protein fragment. The analog exhibited a 10-fold lower cytolytic activity than the native protein. These results demonstrated that the disulfide bond is not necessary for folding and activity, but are consistent with the analog having a looser, more flexible structure in solution than the native TNF-alpha.
A 12-Item Short-Form Health Survey (1996)

Regression methods were used to select and score 12 items from the Medical Outcomes Study 36-Item Short-Form Health Survey (SF-36) to reproduce the Physical Component Summary and Mental Component Summary scales in the general US population (n=2,333). The resulting 12-item short-form (SF-12) achieved multiple R squares of 0.911 and 0.918 in predictions of the SF-36 Physical Component Summary and SF-36 Mental Component Summary scores, respectively. Scoring algorithms from the general population used to score 12-item versions of the two components (Physical Components Summary and Mental Component Summary) achieved R squares of 0.905 with the SF-36 Physical Component Summary and 0.938 with SF-36 Mental Component Summary when cross-validated in the Medical Outcomes Study. Test-retest (2-week)correlations of 0.89 and 0.76 were observed for the 12-item Physical Component Summary and the 12-item Mental Component Summary, respectively, in the general US population (n=232). Twenty cross-sectional and longitudinal tests of empirical validity previously published for the 36-item short-form scales and summary measures were replicated for the 12-item Physical Component Summary and the 12-item Mental Component Summary, including comparisons between patient groups known to differ or to change in terms of the presence and seriousness of physical and mental conditions, acute symptoms, age and aging, self-reported 1-year changes in health, and recovery for depression. In 14 validity tests involving physical criteria, relative validity estimates for the 12-item Physical Component Summary ranged from 0.43 to 0.93 (median=0.67) in comparison with the best 36-item short-form scale. Relative validity estimates for the 12-item Mental Component Summary in 6 tests involving mental criteria ranged from 0.60 to 107 (median=0.97) in relation to the best 36-item short-form scale. Average scores for the 2 summary measures, and those for most scales in the 8-scale profile based on the 12-item short-form, closely mirrored those for the 36-item short-form, although standard errors were nearly always larger for the 12-item short-form.
Amino acid metabolism in the cases of fatty liver. (1989)

乙型肝硬変症 (以下乙型n=25) とその起因症である脂肪肝 (n=10), 肝線維症 (n=23) の血漿遊離アミノ酸の相互関連性を検討することによって脂肪肝のアミノ酸代謝から程度を知ることを目的とし, 成人 (n=566) の正常値を1として比較検討した. 総アミノ酸濃度は3群間に差はなく正常域値内の変動である. 必須アミノ酸の総和は脂肪肝は0.80, 肝線維症は0.79で, 乙型の0.90より低い. 分岐鎖アミノ酸総和はいずれの群も正常値の70%程度である. 芳香族アミノ酸は脂肪肝1.22, 肝線維症1.31, 乙型1.59であり, Gln/Gluは脂肪肝0.55, 肝線維症0.46, 乙型0.42でこれらは肝障害の悪化に比例している. したがって, アミノ酸代謝の検討から肝障害の程度を知ることが可能である.
Surface mechanical properties, corrosion resistance, and cytocompatibility of nitrogen plasma‐implanted nickel–titanium alloys: A comparative study with commonly used medical grade materials (2007)

Stainless steel and titanium alloys are the most common metallic orthopedic materials. Recently, nickel-titanium (NiTi) shape memory alloys have attracted much attention due to their shape memory effect and super-elasticity. However, this alloy consists of equal amounts of nickel and titanium, and nickel is a well known sensitizer to cause allergy or other deleterious effects in living tissues. Nickel ion leaching is correspondingly worse if the surface corrosion resistance deteriorates. We have therefore modified the NiTi surface by nitrogen plasma immersion ion implantation (PIII). The surface chemistry and corrosion resistance of the implanted samples were studied and compared with those of the untreated NiTi alloys, stainless steel, and Ti-6Al-4V alloy serving as controls. Immersion tests were carried out to investigate the extent of nickel leaching under simulated human body conditions and cytocompatibility tests were conducted using enhanced green fluorescent protein mice osteoblasts. The X-ray photoelectron spectroscopy results reveal that a thin titanium nitride (TiN) layer with higher hardness is formed on the surface after nitrogen PIII. The corrosion resistance of the implanted sample is also superior to that of the untreated NiTi and stainless steel and comparable to that of titanium alloy. The release of nickel ions is significantly reduced compared with the untreated NiTi. The sample with surface TiN exhibits the highest amount of cell proliferation whereas stainless steel fares the worst. Compared with coatings, the plasma-implanted structure does not delaminate as easily and nitrogen PIII is a viable way to improve the properties of NiTi orthopedic implants.
Reversibility of T helper 1 and 2 populations is lost after long-term stimulation. (1996)

Commitment of T helper 1 (Th1) or Th2 populations developing during an immune response to a pathogen, or an inappropriate immune response to an allergen or autoantigen, may determine the difference between health and chronic disease. We show that strongly polarized Th1 and Th2 populations assessed by immunoassay are heterogeneous using flow cytometry to detect single cells producing interferon gamma (IFN-gamma) and interleukin 4 (IL-4). Th1 populations arising after 1 wk of stimulation in IL-12 plus anti-IL-4 antibodies could convert to Th2 cells when restimulated in IL-4. Th2 populations resulting from stimulation for 1 wk in IL-4 could give rise to Th1 cells upon restimulation in IL-12 plus anti-IL-4. In contrast, the cytokine profiles of long-term Th1 and Th2 populations arising originally from repeated stimulation in IL-12 or IL-4 appeared more homogeneous and were not reversible, although IL-4 dramatically reduced the number of IFN-gamma-producing Th1 cells. This may explain previous reports that Th1 cells can be converted to Th2 cells.
Polyamidoamine cascade polymers mediate efficient transfection of cells in culture (1993)

Cascade polymers also known as Starburst dendrimers are spheroidal polycations that can be synthesized with a well-defined diameter and a precise number of terminal amines per dendrimer. We show, using luciferase and beta-galactosidase containing plasmids, that dendrimers mediate high efficiency transfection of a variety of suspension and adherent cultured mammalian cells. Dendrimer-mediated transfection is a function both of the dendrimer/DNA ratio and the diameter of the dendrimer. Maximal transfection of luciferase are obtained using a diameter of 68 A and a dendrimer to DNA charge ratio of 6/1 (terminal amine to phosphate). Expression is unaffected by lysomotrophic agents such as chloroquine and only modestly affected (2-fold decrease) by the presence of 10% serum in the medium. Cell viability, as assessed by dye reduction assays, decreases by only 30% at 150 micrograms dendrimer/mL in the absence of DNA and about 75% in the presence of DNA. Under similar conditions polylysine causes a complete loss of viability. Gene expression decreased by 3 orders of magnitude when the charge ratio is reduced to 1:1. When GALA, a water soluble, membrane-destabilizing peptide, is covalently attached to the dendrimer via a disulfide linkage, transfection efficiency of the 1:1 complex is increased by 2-3 orders of magnitude. The high transfection efficiency of the dendrimers may not only be due to their diameter and shape but may also be caused by the pKa's (3.9 and 6.9) of the amines in the polymer. The low pKa's permit the dendrimer to buffer the pH change in the endosomal compartment. The characteristics of precise control of structure, favorable pKa's, and low toxicity make the dendrimers suitable for gene-transfer vehicles.
Huge enhancement of the quadratic nonlinear optical susceptibility in push–pull chromophores based on bridged dithienylethylene spacers (2000)

Replacement of the open chain dithienylethylene π-conjugating spacer by its bridged analog in push–pull NLO-phores produces a dramatic increase of the quadratic hyperpolarisability.
Non-V600BRAF Mutations Define a Clinically Distinct Molecular Subtype of Metastatic Colorectal Cancer (2017)

Purpose Molecular diagnostic testing has become an integral part of the evaluation of patients with metastatic colorectal cancer (CRC). Expanded mutational testing, such as next-generation sequencing (NGS), often identifies mutations with unclear clinical or prognostic implications. One such example is BRAF mutations that occur outside of codon 600 (<sup>non-V600</sup> BRAF mutations). Methods We conducted this multicenter, retrospective cohort study to characterize the clinical, pathologic, and survival implications of <sup>non-V600</sup> BRAF mutations in metastatic CRC. We pooled patients in whom <sup>non-V600</sup> BRAF mutations were identified from NGS databases at three large molecular genetics reference laboratories. Results A total of 9,643 patients with metastatic CRC underwent NGS testing. We identified 208 patients with <sup>non-V600</sup> BRAF mutations, which occurred in 2.2% of all patients tested and accounted for 22% of all BRAF mutations identified. Cancers with <sup>non-V600</sup> BRAF mutations, compared with cancers with V600E BRAF (<sup>V600E</sup> BRAF) mutations, were found in patients who were significantly younger (58 v 68 years, respectively), fewer female patients (46% v 65%, respectively), and patients who had fewer high-grade tumors (13% v 64%, respectively) or right-sided primary tumors (36% v 81%, respectively). Median overall survival was significantly longer in patients with <sup>non-V600</sup> BRAF-mutant metastatic CRC compared with those with both <sup>V600E</sup> BRAF-mutant and wild-type BRAF metastatic CRC (60.7 v 11.4 v 43.0 months, respectively; P < .001). In multivariable analysis, <sup>non-V600</sup> BRAF mutation was independently associated with improved overall survival (hazard ratio, 0.18; P < .001). Conclusion <sup>Non-V600</sup> BRAF mutations occur in approximately 2.2% of patients with metastatic CRC and define a clinically distinct subtype of CRC with an excellent prognosis.
Atrial Fibrosis Helps Select the Appropriate Patient and Strategy in Catheter Ablation of Atrial Fibrillation: A DE-MRI Guided Approach (2010)

Circumferential PV antral scarring predicts ablation success in mild LA fibrosis, while posterior wall and septal scarring is needed for moderate fibrosis. This may help select the proper candidate and strategy in catheter ablation of AF.
Statisically lossless image compression for CR and DR (1999)

This paper proposes an image compression algorithm that can improve the compression efficiency for digital projection radiographs over current lossless JPEG by utilizing a quantization companding function and a new lossless image compression standard called JPEG-LS. The companding and compression processes can also be augmented by a pre- processing step to first segment the foreground portions of the image and then substitute the foreground pixel values with a uniform code value. The quantization companding function approach is based on a theory that relates the onset of distortion to changes in the second-order statistics in an image. By choosing an appropriate companding function, the properties of the second-order statistics can be retained to within an insignificant error, and the companded image can then be lossless compressed using JPEG-LS; we call the reconstructed image statistically lossless. The approach offers a theoretical basis supporting the integrity of the compressed-reconstructed data relative to the original image, while providing a modest level of compression efficiency. This intermediate level of compression could help to increase the conform level for radiologists that do not currently utilize lossy compression and may also have benefits form a medico-legal perspective.
Selective reaction with exo-isomers in ring-opening olefin metathesis polymerization (ROMP) of fluoroalkyl-substituted norbornene derivatives (1993)

ADVERTISEMENT RETURN TO ISSUEPREVArticleNEXTSelective reaction with exo-isomers in ring-opening olefin metathesis polymerization (ROMP) of fluoroalkyl-substituted norbornene derivativesNorbert Seehof, Stefan Grutke, and Wilhelm RisseCite this: Macromolecules 1993, 26, 4, 695–700Publication Date (Print):February 1, 1993Publication History Published online1 May 2002Published inissue 1 February 1993https://pubs.acs.org/doi/10.1021/ma00056a021https://doi.org/10.1021/ma00056a021research-articleACS PublicationsRequest reuse permissionsArticle Views456Altmetric-Citations31LEARN 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
1,25-Dihydroxyvitamin D3 suppresses human T helper/inducer lymphocyte activity in vitro. (1985)

The active form of vitamin D3, 1 alpha,25-dihydroxyvitamin D3 (1,25-(OH)2-D3), suppresses in vitro immunoglobulin (Ig) production by activated peripheral blood mononuclear cells (PBM) from normal human subjects by inhibiting T helper/inducer TH cell activity. Normal PBM were fractionated into B, TH and T suppressor/cytotoxic (Ts) cells by fluorescence-activated cell sorting techniques. The resultant subsets were activated with mitogens and were cultured in the presence or absence of a receptor-saturating concentration of 1,25-(OH)2-D3. The sterol reduced [3H]thymidine incorporation in TH cells by 56%, with no effect on Ts or B cells. When 1,25-(OH)2-D3-treated TH cells were co-cultured with untreated B cells and culture supernatants assayed for Ig production, 1,25-(OH)2-D3 abrogated the inducing effect of TH cells on Ig synthesis by B cells. There was no inhibitory effect of the sterol on Ts or B cell activity. In addition, 1,25-(OH)2-D3 produced a dramatic inhibition of interleukin 2 (IL 2) production by activated PBM, but did not inhibit IL 2 receptor generation by these cells. Other vitamin D metabolites tested did not produce this effect. These results suggest that the TH lymphocyte is the specific cellular target for the immunoinhibitory effects of 1,25-(OH)2-D3.
Rapid Method for the Construction of Salmonella enterica Serovar Typhimurium Vaccine Carrier Strains (2005)

Salmonella enterica serovar Typhimurium is a versatile organism for the generation of live recombinant vaccines for mucosal immunization. Various strategies have been devised for the stable and efficient expression of heterologous antigens by attenuated S. enterica strains, but these methods often require complex manipulations. Use of phage lambda Red recombinase has recently been devised for gene replacements in Escherichia coli and S. enterica after introduction of PCR products. Based on this method, we have developed an approach that allows the integration of recombinant expression cassettes for heterologous antigens in a single step. The recombinant construct is integrated into the chromosome and is devoid of any selective marker such as antibiotic resistance. We observed the stable expression of model antigens without selective pressure. In addition, the method allows the simultaneous generation of attenuating mutations by gene deletions. The novel "knock-in" approach allows the rapid and efficient construction of recombinant Salmonella strains as vaccine carriers.
C5a Receptor‐Deficient Mice Are Protected from Thrombophilia and Endothelial Cell Activation Induced by Some Antiphospholipid Antibodies (2007)

Recent findings indicate that complement activation--involving specifically C3 and C5--contributes to antiphospholipid (aPL)-mediated thrombosis. Two complement effector pathways are initiated by the cleavage of C5, C5a and C5b, which leads to the formation of the C5b-9 membrane attack complex. To delineate and distinguish the role of C5a from the C5b-9 membrane attack complex seeded by C5b, we examined the in vivo effects (thrombosis) of aPL on C5a receptor-deficient (C5aR-/-) mice. C5aR-/- and C5aR+/+ mice were injected with IgM or with IgG from two different patients with APS (IgM-APS or IgG-APS) or with control IgM or IgG (IgM-NHS or IgG-NHS) twice. Complement fixing activity of the Ig fractions and anticardiolipin activity in the sera of the mice were determined by enzyme-linked immunosorbent assay. Surgical procedures to study thrombus dynamics were performed. IgM-APS but not IgG-APS fixed C1q to cardiolipin-coated plates. IgM-APS significantly enhanced thrombus size in C5aR+/+ mice compared to C5aR+/+ mice treated with IgM-NHS (3198 +/- 2361 microm2 versus 585 +/- 460 microm2). C5aR-/- mice treated with IgM-APS showed a significant reduction in thrombi size as compared with C5aR+/+ mice (676 +/- 690 microm2 versus 3198 +/- 2361 microm2; P = 0.001). IgG-APS enhanced thrombus formation significantly in C5aR+/+ when compared to IgG-NHS-treated mice (3507 +/- 965 microm2 versus 1321 +/- 798 microm2), and these effects were not altered in C5aR-/- mice (3400 +/- 1681 microm2). The data indicate that C5aR-/- mice are protected from the thrombogenic effects of some aPL antibodies.
New tricks from an old oncogene (2010)

MYB is a leucine zipper transcription factor that is essential for hematopoesis and for renewal of colonic crypts. There is also ample evidence showing that MYB is leukemogenic in several animal species. However, it was not until recently that clear evidence was presented showing that MYB actually is an oncogene rearranged in human cancer. In a recent study, a novel mechanism of activation of MYB involving gene fusion was identified in carcinomas of the breast and head and neck. A t(6;9) translocation was shown to generate fusions between MYB and the transcription factor gene NFIB. The fusions consistently result in loss of the 3'-end of MYB, including several highly conserved target sites for microRNAs that negatively regulate MYB expression. Deletion of these target sites may disrupt the repression of MYB, leading to overexpression of MYB-NFIB transcripts and protein and to transcriptional activation of critical MYB target genes associated with apoptosis, cell cycle control, cell growth/angiogenesis and cell adhesion. This study, together with previous and recent data showing rearrangements and copy number alterations of the MYB locus in T-cell leukemia and certain solid tumors, will be the main focus of this review.
6-Aminoindole (1954)

ADVERTISEMENT RETURN TO ISSUEPREVArticleNEXT6-AminoindoleR. K. Brown and N. A. NelsonCite this: J. Am. Chem. Soc. 1954, 76, 20, 5149–5150Publication Date (Print):October 1, 1954Publication History Published online1 May 2002Published inissue 1 October 1954https://pubs.acs.org/doi/10.1021/ja01649a045https://doi.org/10.1021/ja01649a045research-articleACS PublicationsRequest reuse permissionsArticle Views228Altmetric-Citations15LEARN 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