gebhart/patrepeval huggingface dataset:
Nitrogen Utilization Efficiency: Relationships with Grain Yield, Grain Protein, and Yield‐Related Traits in Rice (2006)

Rice ( Oryza sativa L.) breeders have historically not included nitrogen utilization efficiency (NUE) as a selection criterion in breeding for cultivars, even though it has economic and ecological implications. This study examined the significance and magnitude of variation in N content, NUE, N translocation ratio (NTR), and grain protein concentration among diverse rice genotypes. Fifteen rice genotypes were studied representing the combinations of low and high levels of four yield‐related traits: maximum number of tillers, grain mass, main culm panicle node number, and panicle mass. These genotypes included ‘Lemont’, ‘Teqing’, and 13 advance recombinant inbred genotypes obtained from a Lemont × Teqing cross. Field data were obtained from experiments conducted during two cropping seasons. Plant samples were analyzed for N concentration. There was significant variation in N content and NUE among genotypes. The genotype NUE means ranged from 25.3 to 63.9 kg grain kg −1 N in a square meter of plants (kg grain kg −1 N), with the top four NUE values ranging from 56.6 to 63.9 kg grain kg −1 N. Nitrogen content and NUE were not significantly correlated with each other, and they had significant positive direct effects on grain yield. Grain yield was positively correlated with NUE, N content, and NTR, whereas NTR was correlated with grain protein concentration. Plant breeders could use these significant correlations to their advantage in breeding for rice cultivars that not only produce high yield but also utilize N efficiently and produce grain with a higher protein concentration.
Mismatched and Matched dNTP Incorporation by DNA Polymerase β Proceed via Analogous Kinetic Pathways (2008)

While matched nucleotide incorporation by DNA polymerase beta (Pol beta) has been well-studied, a true understanding of polymerase fidelity requires comparison of both matched and mismatched dNTP incorporation pathways. Here we examine the mechanism of misincorporation for wild-type (WT) Pol beta and an error-prone I260Q variant using stopped-flow fluorescence assays and steady-state fluorescence spectroscopy. In stopped-flow, a biphasic fluorescence trace is observed for both enzymes during mismatched dNTP incorporation. The fluorescence transitions are in the same direction as that observed for matched dNTP, albeit with lower amplitude. Assignments of the fast and slow fluorescence phases are designated to the same mechanistic steps previously determined for matched dNTP incorporation. For both WT and I260Q mismatched dNTP incorporation, the rate of the fast phase, reflecting subdomain closing, is comparable to that induced by correct dNTP. Pre-steady-state kinetic evaluation reveals that both enzymes display similar correct dNTP insertion profiles, and the lower fidelity intrinsic to the I260Q mutant results from enhanced efficiency of mismatched incorporation. Notably, in comparison to WT, I260Q demonstrates enhanced intensity of fluorescence emission upon mismatched ternary complex formation. Both kinetic and steady-state fluorescence data suggest that relaxed discrimination against incorrect dNTP by I260Q is a consequence of a loss in ability to destabilize the mismatched ternary complex. Overall, our results provide first direct evidence that mismatched and matched dNTP incorporations proceed via analogous kinetic pathways, and support our standing hypothesis that the fidelity of Pol beta originates from destabilization of the mismatched closed ternary complex and chemical transition state.
GET WELL: an automated surveillance system for gaining new epidemiological knowledge (2011)

The application is in regular use at the Swedish Institute for Infectious Disease Control. A system based on web queries is flexible in that it can be adapted to any disease; we get information on other individuals than those who seek medical care; and the data do not suffer from reporting delays. Although Google data are based on a substantially larger search volume, search patterns obtained from the medical web site may still convey more information from an epidemiological perspective. Furthermore we can see advantages with having full access to the raw data.
Biochemical and functional consequences of dissociation of the platelet membrane glycoprotein IIb-IIIa complex (1985)

The platelet membrane glycoproteins, IIb and IIIa, form a Ca2+- dependent heterodimer complex that functions as the fibrinogen receptor in activated platelets to mediate platelet aggregation. Little is known about factors that affect the IIb-IIIa complex within the platelet membrane. It has been observed that platelets incubated with ethylene glycol tetra-acetic acid (EGTA) at 37 degrees C are unable to aggregate or to bind monoclonal antibodies specific for the IIb-IIIa complex. To determine whether this is due to a dissociation of IIb from IIIa, we developed a method for quantitating the complex on nondenaturing, polyacrylamide gradient gels. Platelets were surface-labeled with 125I and then solubilized and electrophoresed in 0.2% Triton and 10 mmol/L CHAPS. Under these conditions and in the presence of 1 mmol/L Ca2+, glycoproteins IIb and IIIa migrated on the gels as a discrete band at Rf = 0.33. Protein that was eluted from this band bound to an immunoaffinity column specific for the IIb-IIIa complex. In contrast, when the IIb-IIIa complex was solubilized and then dissociated with EGTA, the discrete band at Rf = 0.33 was no longer present, and IIb and IIIa were now found in a broad band at Rf = 0.45 to 0.50. To study IIb and IIIa within the surface membrane, the 125I-labeled platelets were first incubated with 0.5 mmol/L EGTA (1 nmol/L free Ca2+) at 22 degrees C and then solubilized in the absence of EGTA. The IIb and IIIa from these platelets migrated at Rf = 0.33, indicating the presence of the intact IIb-IIIa complex. In contrast, when the platelets were incubated at 37 degrees C for one hour with the EGTA, the discrete band at Rf = 0.33 representing the IIb-IIIa complex gradually disappeared. This phenomenon could not be reversed by adding Ca2+ back to the platelets before solubilization and electrophoresis. This loss of the IIb-IIIa complex from intact platelets was accompanied by (a) a progressive and irreversible decrease in adenosine diphosphate (ADP)-induced platelet aggregation and (b) decreased binding of a complex-dependent monoclonal antibody to the platelets. These studies demonstrate that when platelets are exposed to low Ca2+ at 37 degrees C, the IIb-IIIa heterodimer complexes in their surface membranes are irreversibly disrupted. Because intact IIb-IIIa complexes are required for platelet aggregation, the loss of these complexes may account for the failure of these platelets to aggregate in response to ADP.
A Simple Method for Improving Protein Solubility and Long-Term Stability (2004)

Increasing a protein concentration in solution to the required level, without causing aggregation and precipitation is often a challenging but important task, especially in the field of structural biology; as little as 20% of nonmembrane proteins have been found to be suitable candidates for structural studies predominantly due to poor protein solubility. We demonstrate here that simultaneous addition of charged amino acids L-Arg and L-Glu at 50 mM to the buffer can dramatically increase the maximum achievable concentration of soluble protein (up to 8.7 times). These amino acids are effective in preventing protein aggregation and precipitation, and they dramatically increase the long-term stability of the sample; additionally, they protect protein samples from proteolytic degradation. Specific protein-protein and protein-RNA interactions are not adversely affected by the presence of these amino acids. These additives are particularly suitable for situations where high protein concentration and long-term stability are required, including solution-state studies of isotopically labeled proteins by NMR.
Some physical properties of undoped amorphous silicon prepared by a new CVD process using iodosilanes (1990)

ADVERTISEMENT RETURN TO ISSUEPREVArticleNEXTSome physical properties of undoped amorphous silicon prepared by a new CVD process using iodosilanesG. Tamizhmani, Michael Cocivera, Richard T. Oakley, and Paul Del Bel BelluzCite this: Chem. Mater. 1990, 2, 4, 473–476Publication Date (Print):July 1, 1990Publication History Published online1 May 2002Published inissue 1 July 1990https://pubs.acs.org/doi/10.1021/cm00010a029https://doi.org/10.1021/cm00010a029research-articleACS PublicationsRequest reuse permissionsArticle Views239Altmetric-Citations4LEARN 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
Human Epidermal Growth Factor Receptor 2 Regulates Angiopoietin-2 Expression in Breast Cancer via AKT and Mitogen-Activated Protein Kinase Pathways (2007)

Abnormal activation of human epidermal growth factor receptor 2 (HER2; ErbB-2) in breast tumors results in increased metastasis and angiogenesis, as well as reduced survival. Here, we show that angiopoietin-2 (Ang-2) expression correlates with HER2 activity in human breast cancer cell lines. Inhibiting HER2 activity with anti-HER2 monoclonal antibody trastuzumab (Herceptin) or HER2 short interfering RNA in tumor cells down-regulates Ang-2 expression. Consistent with the important roles of AKT and mitogen-activated protein kinase in the HER2 signaling pathway, AKT and ERK mitogen-activated protein kinase (MAPK) kinase activity is necessary for Ang-2 up-regulation by HER2. Moreover, overexpression of HER2 protein up-regulates Ang-2 expression. Heregulin-beta1-induced Ang-2 up-regulation is abrogated when AKT and ERK kinase activity are blocked. Immunohistochemical analysis of HER2 and Ang-2 proteins in human breast carcinomas shows that Ang-2 expression in breast cancer correlates with HER2 expression. These studies provide evidence that the Ang-2 gene is regulated by HER2 activity in breast cancer, and propose an additional mechanism for HER2 contributing to tumor angiogenesis and metastasis.
Expression and Regulation of Cyclin Genes in Breast Cancer (1995)

Cyclins, the regulatory subunits of cyclin-dependent kinases, control passage through key check-points within the cell cycle. Since dysregulated expression and function of cyclins can lead to loss of normal growth control some of these genes are oncogenes. We have studied cyclin gene expression, regulation and function in breast cancers. Induction of cyclin D1 is an early event in mitogenic stimulation of breast cancer cells by growth factors and steroids. Furthermore, inhibition of cyclin D1 expression is an early response to growth inhibition by antioestrogens. Ectopic expression of cyclin D1 in T-47D breast cancer cells demonstrated that cyclin D1 is rate-limiting for progression through G1 phase and is sufficient for growth arrested cells to complete the cell cycle. Since this gene is frequently overexpressed in human breast cancers it may contribute to the development and progression of some breast carcinomas.
Autologous collagen: a new treatment for dermal defects. (1997)

Autologous collagen has been proven to be an effective, longer-term collagen filler for cosmetic imperfections. For those who cannot afford surgery, this is an excellent alternative therapy. Safety is not a major concern and the patient can be reassured that this autologous preparation has less chance of causing untoward effects than other biological materials used for the same procedures. Ongoing investigations of this product and new applications discovered may continue to provide safe, relatively inexpensive methods, for cosmetic improvement.
Glutamine transport in C6 glioma cells: Substrate specificity and modulation in a glutamine deprived culture medium (2001)

A previous study has shown that glutamine (Gln) uptake in C6 cells grown in a standard medium containing 2 mM Gln, is predominantly mediated by a sodium-dependent system that is inhibited by ASC system substrates alanine (Ala), serine (Ser), cysteine (Cys) and threonine (Thr), shows pH sensitivity and partial tolerance to substitution of Na+ by Li+, features compatible with system ASCT2 that is strongly expressed in cultured astrocytes. The uptake was not inhibited by the model system A substrate alpha-(methylamino)isobutyric acid (MeAiB), and glycine (Gly) or proline (Pro), indicating that the substrate-regulated system A as defined by routine criteria is relatively inactive in these cells (Dolinska et al., 2000). In this study we compared the uptake of radiolabeled Gln and a model ASC substrate -Thr in cells grown to the same density in Gln-containing and Gln-deprived media. Cells grown in the absence of Gln showed a reduced activity of system ASC-mediated Gln uptake, and the system lost tolerance for Li+ and became somewhat more resistant to lowering pH of the medium. In contrast to cultured astrocytes deprived of Gln, the overall Gln uptake activity in C6 cells adapted to grow in a medium without Gln was lower than in cells grown in a Gln containing medium, and the uptake by system A remained inactive. C6 cells cultured both in the presence and absence of Gln expressed ASCT2 mRNA, indicating that system ASCT2-mediated Gln uptake is modulated at a posttranscriptional level. In contrast to Gln uptake, Thr uptake was more active in cells cultured in the absence of Gln and showed neither pH dependence nor lithium tolerance in either medium, which is typical of an uptake mediated by the widespread ASCT1 isoform of system ASC. In C6 cells grown in the presence or absence of Gln alike, approximately 20% of the sodium-dependent Gln uptake was resistant to MeAiB+Thr, indicating contribution of system N. The N system-mediated uptake in C6 cells grown in the absence, but not in the presence of Gln was not inhibited by glutamate (Glu) that conforms to the characteristics of the glial N system variant, SN1.
Synthesis of a star‐shaped poly(ethylene‐<i>co</i>‐propylene) copolymer as a viscosity index improver for lubricants (2001)

Abstract A saturated star‐shaped poly(ethylene‐ co ‐propylene) copolymer, (EP) star , has been synthesized for use as a viscosity index improver in lubricants. Polyisoprene arms were first anionically synthesized using n ‐butyllithium as the initiator, followed by a linking reaction with divinylbenzene at the optimum temperature of 60°C. The resulting star‐shaped polyisoprene, (I) star , was then hydrogenated to eliminate the double bonds of the polyisoprene forming the poly(ethylene‐ co ‐propylene) structure. The degree of branching (number of arms on each molecule) increases with increase in the mole ratio of divinylbenzene to n ‐butyllithium. Increasing the arm length adversely affects the linking efficiency and a minimum amount of tetrahydrofuran (THF) at a THF: n ‐butyllithium molar ratio of 1.12 was needed in order to achieve a maximum linking efficiency of approximately 85%. The T g of poly(ethylene‐ co ‐propylene) is about 10°C higher than that of the original polyisoprene. Compared with (I) star , (EP) star has a thermal decomposition temperature that is 50°C higher but is independent of the arm length or the degree of branching. Viscosity measurement results for (EP) star reveal that intrinsic viscosity depends only on the arm length but not the degree of branching. Adding 1 wt % of (EP) star markedly increases the viscosity index of a LN base oil. The addition of 1 wt % of (EP) star increases the viscosity index (95 for base oil) up to a number between 111 and 145, with the exact number depending upon its arm length and degree of branching. With a fixed arm length, an (EP) star having a higher degree of branching increases the viscosity index more than one having a lower degree of branching. On the other hand, the viscosity index increases with increase in the arm length when the degree of branching is fixed. Adding 1 wt % of (EP) star also causes a change in the pour point of the lubricant with the pour point decreasing with increase in the degree of branching. © 2002 Wiley Periodicals, Inc. J Appl Polym Sci 83: 1911–1918, 2002
In Vitro Selection of Mutations in the Human Immunodeficiency Virus Type 1 Reverse Transcriptase That Decrease Susceptibility to (−)-β- <scp>d</scp> -Dioxolane-Guanosine and Suppress Resistance to 3′-Azido-3′-Deoxythymidine (2000)

Human immunodeficiency virus type 1 (HIV-1) isolates resistant to (-)-beta-D-dioxolane-guanosine (DXG), a potent and selective nucleoside analog HIV-1 reverse transcriptase (RT) inhibitor, were selected by serial passage of HIV-1(LAI) in increasing drug concentrations (maximum concentration, 30 microM). Two independent selection experiments were performed. Viral isolates for which the DXG median effective concentrations (EC(50)s) increased 7.3- and 12.2-fold were isolated after 13 and 14 passages, respectively. Cloning and DNA sequencing of the RT region from the first resistant isolate identified a K65R mutation (AAA to AGA) in 10 of 10 clones. The role of this mutation in DXG resistance was confirmed by site-specific mutagenesis of HIV-1(LAI). The K65R mutation also conferred greater than threefold cross-resistance to 2',3'-dideoxycytidine, 2', 3'-dideoxyinosine, 2',3'-dideoxy-3'-thiacytidine, 9-(2-phosphonylmethoxyethyl)adenine, 2-amino-6-chloropurine dioxolane, dioxolanyl-5-fluorocytosine, and diaminopurine dioxolane but had only marginal effects on 3'-azido-3'-deoxthymidine (AZT) susceptibility. However, when introduced into a genetic background for AZT resistance (D67N, K70R, T215Y, T219Q), the K65R mutation reversed the AZT resistance. DNA sequencing of RT clones derived from the second resistant isolate identified the L74V mutation, previously reported to cause ddI resistance. The L74V mutation also decreased the AZT resistance when the mutation was introduced into a genetic background for AZT resistance (D67N, K70R, T215Y, T219Q) but to a lesser degree than the K65R mutation did. These findings indicate that DXG and certain 2',3'-dideoxy compounds (e.g., ddI) can select for the same resistance mutations and thus may not be optimal for use in combination. However, the combination of AZT with DXG or its orally bioavailable prodrug (-)-beta-D-2, 6-diaminopurine-dioxolane should be explored because of the suppressive effects of the K65R and L74V mutations on AZT resistance.
Wound healing and fibrosis in intestinal disease (2006)

Twelve blood parameters were studied in five groups of women totalling 120 subjects--group I: 26 blood donors (average age 45.2 years, range 23-66); group II: 18 patients with various cerebral, cardiovascular, or infectious illnesses (average age 79.9 years, range 66-92); group III: 28 patients with femoral neck fractures (average age 79.4 years, range 56-95); group IV: 12 patients with hip osteoarthrosis (average age 71.7 years, range 60-87); group V: 36 patients with vertebral crush fractures associated with postmenopausal and involutional osteoporosis (average age 63.0 years, range 51-75). The parameters measured were total proteins, albumin, total, alpha 1, alpha 2, beta, and gamma globulins, total calcium, phosphates, alkaline phosphatase, bilirubin, and haemoglobin. Statistical analysis showed that each group differed from the others even with adjustment for age. Among the discriminant parameters, serum albumin had a distinctive position. Significantly high concentrations of serum albumin in the group with osteoarthrosis raise the question of the possible existence of a population prone to osteoarthrosis in whom the serum albumin level may reflect a special nutritional state associated with the well known bone density in subjects with hip osteoarthrosis. Albumin values in patients with femoral neck fractures are lower than normal but non-significantly. The difference between the group with vertebral crush fractures and that with femoral neck fractures seems to be due to age.
Cell surface-bound IL-1α is an upstream regulator of the senescence-associated IL-6/IL-8 cytokine network (2009)

Inflammation underlies most age-related diseases, including cancer, but the etiology is poorly understood. One proposed factor is the presence of senescent cells, which increase with age. The senescence response arrests the proliferation of potentially oncogenic cells, and most senescent cells secrete high levels of proinflammatory cytokines and other proteins. The complex senescence-associated secretory phenotype is likely regulated at multiple levels, most of which are unknown. We show that cell surface-bound IL-1alpha is essential for signaling the senescence-associated secretion of IL-6 and IL-8, 2 proinflammatory cytokines that also reinforce the senescence growth arrest. Senescent human fibroblasts expressed high levels of IL-1alpha mRNA, intracellular protein, and cell surface-associated protein, but secreted very little protein. An IL-1 receptor (IL1R) antagonist, neutralizing IL-1alpha antibodies, and IL-1alpha depletion by RNA interference all markedly reduced senescence-associated IL-6/IL-8 secretion. Depletion of the key IL-1R signaling component IRAK1 also suppressed this secretion, and IL-1alpha neutralizing antibodies prevented IRAK1 degradation, indicating engagement of the IL-1R signaling pathway. Furthermore, IL-1alpha depletion reduced the DNA binding activity of NF-kappaB and C/EBPbeta, which stimulate IL-6/IL-8 transcription. IL-1alpha was a general regulator of senescence-associated IL-6/IL-8 secretion because IL-1alpha blockade reduced IL-6/IL-8 secretion whether cells senesced owing to DNA damage, replicative exhaustion, oncogenic RAS, or chromatin relaxation. Furthermore, conditioned medium from IL-1alpha-depleted senescent cells markedly reduced the IL-6/IL-8-dependent invasiveness of metastatic cancer cells, indicating that IL-1alpha regulates the biological effects of these cytokines. Thus, cell surface IL-1alpha is an essential cell-autonomous regulator of the senescence-associated IL-6/IL-8 cytokine network.