gebhart/patrepeval huggingface dataset:
Pola Spektra Ft-I Dan 13 (Cp/Mas)-Nmr Bahan Osteokonduktip (2004)

1.\t, \tABSTRAK\nSemen ionomer kaca (SIK)rnerupakan balian restorasi kedokteran gigi yang digunakan secara\nSIK jugs telan banyak ditelilisebagai atiernalif semen tu1ang. Walaupun dipandrakan dapaidigunakEili LintuK alternatif semen tulang, narnun karena kandungan asam poliakrilatnya yang tinggi SIK gagal menjadi alternatif bahan osteokonduktir karena hambatan asam poliakriiat ternadap bieaktivitas. Penelitian bertujuan mertgkaji efek penambahan kaca bibaktff ternadap karakteristik seiwng bahan koinersial semen ionomer kaca modifikasi resin (siKrviR). Specimen S!KMR yang mengandung 50% beral empat jenis kaca bionklif yang berbeda dikaji perubahan karakteristik setingnya dengan FT-1R (Fourie tra-furtn Infrared) dan MAS-NMR. (Magic Angle Spinning-Nuclear Magnetic Resonance}. Spektra FT-1R maupun CPiMAS-NMR rnenunjukkan adanya perluasan reaksi asam-basa yang lebiti kuat pada ballad osteokonduktif berbasis SIKMR dibandingkan pada StKMR karena sifat basa kaca bioaktif.\nKata kunci: bahan osteckonduktif, kaca bioaktif, semen ionomer kaca moditikasi resin, karaktenstik sating
Response to influenza infection in mice with a targeted disruption in the interferon gamma gene. (1993)

Interferon gamma (IFN-gamma) is a pleiotropic cytokine secreted by T lymphocytes and natural killer (NK) cells and has been noted to be a first line of host defense in the control of viral infections. To examine further the role of this cytokine in the control of viral infections, mice with a targeted mutation in the IFN-gamma gene were infected with influenza virus, and the in vivo antibody and cell-mediated immune response to viral infection were examined. In addition, cell lines and clones were derived from the immunized animals and the in vitro cytokine production and cytotoxic T lymphocyte (CTL) response were analyzed. The absence of IFN-gamma led to increased production of influenza-specific IgG1, IL-4, and IL-5 as compared to wild-type littermate control animals. In contrast, there was no difference noted in the development of an effective CTL response between IFN-gamma-deficient and wild-type animals. In this model of experimental influenza infection, IFN-gamma is not necessary for the development of an effective humoral or cellular immune response to challenge with this respiratory virus.
Immunization of mice with purified U1 small nuclear ribonucleoprotein (RNP) induces a pattern of antibody specificities characteristic of the anti-Sm and anti-RNP autoimmune response of patients with lupus erythematosus, as measured by monoclonal antibodies. (1986)

Sera of patients with systemic lupus erythematosus and related autoimmune diseases often possess anti-Sm and anti-ribonucleoprotein (RNP) autoantibodies that recognize antigenic sites on small nuclear (sn) RNPs containing the snRNAs U1, U2, U4, U5, and U6. Although the major immunoreactive Sm polypeptides B', B, and D are present in snRNPs U1-U6, the RNP-antigenic proteins termed 70 kDa, A, and C are found only in U1 snRNP particles. We have immunized genetically nonautoimmune C57BL/6 mice with isolated human U1 snRNP particles and found that the major RNP and Sm antigenic polypeptides are also primarily immunogenic in the experimental immune response. Monoclonal antibodies (mAbs) derived from the mice thus immunized reacted specifically with polypeptides 70 kDa or A or recognized the Sm polypeptides B', B, and D simultaneously. One mAb reacted with an epitope shared by the U1 RNP polypeptide A and the U2 RNP polypeptide B". Competitive binding studies with the mAbs and anti-RNP/Sm patient sera indicated that the mAbs recognize the same regions on the antigenic snRNP polypeptides as the autoantibodies. This shows that B cells capable of producing autoantibodies against snRNPs are in principle present in the normal immune system. The striking similarity that we observed between the antibody pattern produced by the mice against exogenous U1 snRNP particles and that of systemic lupus erythematosus patients suggests the possibility that the anti-Sm and anti-RNP autoimmune response may be triggered by the endogenous U snRNPs rather than by a crossreacting viral or bacterial neoantigen. The possibility of eliciting anti-RNP and -Sm-type autoantibodies against exogenous snRNPs in normal mice should also allow potential pathogenic effects of such circulating antibodies to be investigated.
Tcl1 Expression in Chronic Lymphocytic Leukemia Is Regulated by miR-29 and miR-181 (2006)

B-cell chronic lymphocytic leukemia (B-CLL) is the most common human leukemia in the world. Deregulation of the TCL1 oncogene is a causal event in the pathogenesis of the aggressive form of this disease as was verified by using animal models. To study the mechanism of Tcl1 regulation in CLL, we carried out microRNA expression profiling of three types of CLL: indolent CLL, aggressive CLL, and aggressive CLL showing 11q deletion. We identified distinct microRNA signatures corresponding to each group of CLL. We further determined that Tcl1 expression is regulated by miR-29 and miR-181, two microRNAs differentially expressed in CLL. Expression levels of miR-29 and miR-181 generally inversely correlated with Tcl1 expression in the CLL samples we examined. Our results suggest that Tcl1 expression in CLL is, at least in part, regulated by miR-29 and miR-181 and that these microRNAs may be candidates for therapeutic agents in CLLs overexpressing Tcl1.
Plasmin in pericellular proteolysis and cellular invasion. (1995)

Invasive tumor growth or severe inflammation is accompanied by the extravasation of fibrinogen from leaky or damaged blood vessels and the formation of a fibrin clot. The clot provides a matrix for the inward migration ('invasion,' 'infiltration') of tumor cells as well as inflammatory cells. The factors that govern the cell/fibrin interaction are not known. We have explored in vitro the possible role of the cell-surface-associated pathway of plasminogen activation in the adhesion of keratinocytes to fibrin and in the invasion of melanoma cells into fibrin gels. Our experiments provided evidence that generation of plasmin at the cell surface destabilizes the adhesive interaction between keratinocytes and fibrin, most likely by cleaving fibrin into fibrinopeptides and destroying its adhesive capacity. Moreover, we found that plasmin generated at the melanoma cell surface promotes the inward migration of these cells into three-dimensional fibrin matrices. In conclusion, the generation of plasmin at the cellular surface may be an important factor in pericellular proteolysis and the dynamic interaction between cells and fibrin-containing pericellular matrix under conditions of tumor invasion and inflammation.
A revised structure of sibiromycin (1988)

ADVERTISEMENT RETURN TO ISSUEPREVArticleNEXTA revised structure of sibiromycinJack D. Leber, John R. E. Hoover, Kenneth G. Holden, Randall K. Johnson, and Sidney M. HechtCite this: J. Am. Chem. Soc. 1988, 110, 9, 2992–2993Publication Date (Print):April 27, 1988Publication History Published online1 May 2002Published inissue 27 April 1988https://pubs.acs.org/doi/10.1021/ja00217a061https://doi.org/10.1021/ja00217a061research-articleACS PublicationsRequest reuse permissionsArticle Views288Altmetric-Citations37LEARN 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-AlertscloseSupporting Info (1)»Supporting Information Supporting Information Get e-Alerts
Differential expression and activation of a family of murine peroxisome proliferator-activated receptors. (1994)

To gain insight into the function of peroxisome proliferator-activated receptor (PPAR) isoforms in mammals, we have cloned and characterized two PPAR alpha-related cDNAs (designated PPAR gamma and -delta, respectively) from mouse. The three PPAR isoforms display widely divergent patterns of expression during embryogenesis and in the adult. Surprisingly, PPAR gamma and -delta are not activated by pirinixic acid (Wy 14,643), a potent peroxisome proliferator and activator of PPAR alpha. However, PPAR gamma and -delta are activated by the structurally distinct peroxisome proliferator LY-171883 and linoleic acid, respectively, indicating that each of the isoforms can act as a regulated activator of transcription. These data suggest that tissue-specific responsiveness to peroxisome proliferators, including certain fatty acids, is in part a consequence of differential expression of multiple, pharmacologically distinct PPAR isoforms.
Inhibition of JNK by a Peptide Inhibitor Reduces Traumatic Brain Injury–Induced Tauopathy in Transgenic Mice (2012)

Traumatic brain injury (TBI) is a major environmental risk factor for subsequent development of Alzheimer disease (AD). Pathological features that are common to AD and many tauopathies are neurofibrillary tangles (NFTs) and neuropil threads composed of hyperphosphorylated tau. Axonal accumulations of total and phospho-tau have been observed within hours to weeks, and intracytoplasmic NFTs have been documented years after severe TBI in humans. We previously reported that controlled cortical impact TBI accelerated tau pathology in young 3xTg-AD mice. Here, we used this TBI mouse model to investigate mechanisms responsible for increased tau phosphorylation and accumulation after brain trauma. We found that TBI resulted in abnormal axonal accumulation of several kinases that phosphorylate tau. Notably, c-Jun N-terminal kinase (JNK) was markedly activated in injured axons and colocalized with phospho-tau. We found that moderate reduction of JNK activity (40%) by a peptide inhibitor, D-JNKi1, was sufficient to reduce total and phospho-tau accumulations in axons of these mice with TBI. Longer-term studies will be required to determine whether reducing acute tau pathology proves beneficial in brain trauma.
Cervical nitric oxide release and persistence of high‐risk human papillomavirus in women (2010)

Nitric oxide may serve as one cofactor for human papillomavirus (HPV)-induced development of cervical cancer. Therefore, we first assessed the levels of cervical fluid nitric oxide metabolite (NOx) in 283 women with and without high-risk (hr) HPV. The NOx level in women with hr HPV (48.4 μmol/L [95% CI: 39.4-56.6], n = 199) was higher (p < 0.001) than that in women without hr HPV (24.6 μmol/L [95% CI: 19.1-38.7], n = 84). Second, we evaluated if cervical fluid NOx levels could predict the persistence of hr HPV. Therefore, we followed up 113 women with detectable hr HPV without any treatment for 12 mo and repeated hr HPV test. High-risk HPV persisted in 72 women (64%) and disappeared in 41 women (36%). The median basal levels of NOx were higher (p = 0.02) in women with persistent hr HPV (56.9 μmol/L [95% CI: 48.7-81.0]) compared to those with eradicated hr HPV (37.7 μmol/L [95% CI: 27.0-58.0]). The NOx level higher than the 75th percentile (>87.0 μmol/L) predicted hr HPV persistence (OR = 4.1 [95% CI: 1.3-13.1]). This cutoff level of NOx showed 33% sensitivity and 90% specificity in predicting the persistence of hr HPV, but it failed to predict cytological progression or regression in 12 mo. In conclusion, high cervical fluid NOx appears to be connected to the persistence of hr HPV, but the low predictive capacity of NOx prevents its clinical use at this phase.
The Eukaryotic Initiation Factor 5A Is Involved in the Regulation of Proliferation and Apoptosis Induced by Interferon- and EGF in Human Cancer Cells (2003)

Interferon-alpha (IFNalpha) can induce apoptosis, a process regulated by a complex network of cell factors. Among these, eukaryotic initiation factor-5A (eIF-5A) is peculiar because its activity is modulated by the post-translational formation of the amino acid hypusine. Here we report the effects of IFNalpha and epidermal growth factor (EGF) on apoptosis and eIF-5A activity in human epidermoid oropharyngeal KB and lung H1355 cancer cells. We found that 48-h exposure to 1000 and 2000 IU/ml IFNalpha induced about 50% growth inhibition and apoptosis in H1355 and KB cells, respectively, and the addition of EGF completely antagonized this effect. When IFNalpha induced apoptosis, a hyperactivation of MEK-1 and ERK signalling and a decrease of the hypusine-containing form and, thus, of eIF-5A activity were recorded. The latter effect was again antagonized by the addition of EGF to IFNalpha-pretreated cells, probably through the activation of the EGF-->ERK-dependent pathway, since the addition of the specific MEK-1 inhibitor PD098059 abrogated the recovery of intracellular hypusine content induced by EGF in IFNalpha-pretreated cancer cells. Subsequently, we evaluated if the hypusine synthesis inhibitor (and eIF-5A inactivator) N1-guanyl-1,7-diaminoheptane (GC7) synergized with IFNalpha in the induction of cell growth inhibition and apoptosis. The analysis of the isobologram of IFNalpha and GC7 demonstrated a strong synergism between the two drugs in inducing cell growth inhibition. We also found that GC7 and IFNalpha had a synergistic effect on apoptosis. These data suggest that the apoptosis induced by IFNalpha could be regulated by eIF-5A that, therefore, could represent a useful target for the potentiation of IFNalpha antitumor activity.
Carbon Miscibility in the Boron Layers of the MgB2 Superconductor (2002)

A detailed structural analysis of the MgB2-xCx series at low doping levels (0 ≤ x ≤ 0.1) is presented. High-resolution synchrotron X-ray powder diffraction experiments show an extremely small miscibility of carbon within the boron sheets despite the structural analogy between MgB2 and graphite. Multiphase behavior is detected for x ≥ 0.04. The coexisting phases, isostructural with the parent MgB2 compound, differ mainly in their in-plane lattice constants, as evidenced by the splitting of the (hk0) Bragg reflections. All phases contain carbon in substitution for boron but in different concentrations.
Multiple GO-SELEX for efficient screening of flexible aptamers (2014)

We describe a simple, high-speed, high-throughput aptamer screening for a group of small molecules using graphene oxide (simple Multi-GO-SELEX) without immobilizing targets. The affinities of ten different ssDNA aptamers successfully obtained for three pesticides were in the range of 10-100 nM. Besides a specific aptamer for each target, we found a couple of flexible multi-target aptamers, which can bind with 2 or 3 different molecules. These flexible aptamers developed for binding with a mixture of targets are not only significant for the rapid screening of a group of small molecules but also offer great promise for aptamer-based biosensor applications.
Identification of Hydrophobic Tags for the Degradation of Stabilized Proteins (2012)

New HyTs are a knockout: we previously reported that labeling HaloTag proteins with low molecular weight hydrophobic tags (HyTs) leads to targeted degradation of HaloTag fusion proteins. In this report, we employed a chemical approach to extend this hydrophobic tagging methodology to highly stabilized proteins by synthesizing and evaluating a library of HyTs, which led to the identification of HyT36.
Four distinct and unusual linker proteins in a mitotically dividing nucleus are derived from a 71-kilodalton polyprotein, lack p34cdc2 sites, and contain protein kinase A sites. (1994)

Tetrahymena thermophila micronuclei contain four linker-associated proteins, alpha, beta, gamma, and delta. Synthetic oligonucleotides based on N-terminal protein sequences of beta and gamma were used to clone the micronuclear linker histone (MLH) gene. The MLH gene is single copy and is transcribed into a 2.4-kb message encoding all four linker-associated proteins. The message is translated into a polypeptide (Mic LH) that is processed at the sequence decreases RTK to give proteins whose amino acid sequences differ markedly from each other, from the sequence of macronuclear H1, and from sequences of typical H1s of other organisms. This represents the first example of multiple chromatin proteins derived from a single polyprotein. The delta protein consists largely of two high-mobility-group (HMG) boxes. An evolutionary analysis of HMG boxes indicates that the delta HMG boxes are similar to the HMG boxes of tsHMG, a protein that appears in elongating mouse spermatids when they condense and cease transcription, suggesting that delta could play a similar role in the micronucleus. The micronucleus divides mitotically, while the macronucleus divides amitotically. Surprisingly, macronuclear H1 but not Mic LH contains sequences resembling p34cdc2 kinase phosphorylation sites, while each of the Mic LH-derived proteins contains a typical protein kinase A phosphorylation site in its carboxy terminus.
Regulation of the human AP-endonuclease (APE1/Ref-1) expression by the tumor suppressor p53 in response to DNA damage (2008)

The human AP-endonuclease (APE1/Ref-1), an essential multifunctional protein, plays a central role in the repair of oxidative base damage via the DNA base excision repair (BER) pathway. The mammalian AP-endonuclease (APE1) overexpression is often observed in tumor cells, and confers resistance to various anticancer drugs; its downregulation sensitizes tumor cells to those agents via induction of apoptosis. Here we show that wild type (WT) but not mutant p53 negatively regulates APE1 expression. Time-dependent decrease was observed in APE1 mRNA and protein levels in the human colorectal cancer line HCT116 p53(+/+), but not in the isogenic p53 null mutant after treatment with camptothecin, a DNA topoisomerase I inhibitor. Furthermore, ectopic expression of WTp53 in the p53 null cells significantly reduced both endogenous APE1 and APE1 promoter-dependent luciferase expression in a dose-dependent fashion. Chromatin immunoprecipitation assays revealed that endogenous p53 is bound to the APE1 promoter region that includes a Sp1 site. We show here that WTp53 interferes with Sp1 binding to the APE1 promoter, which provides a mechanism for the downregulation of APE1. Taken together, our results demonstrate that WTp53 is a negative regulator of APE1 expression, so that repression of APE1 by p53 could provide an additional pathway for p53-dependent induction of apoptosis in response to DNA damage.
DryadInc: reusing work in large-scale computations (2009)

Many large-scale (cloud) computations operate on append-only, partitioned datasets. We present two incremental computation frameworks to reuse prior work in these circumstances: (1) reusing identical computations already performed on data partitions, and (2) computing just on the newly appended data and merging the new and previous results. 1
MicroRNA profiling of clear cell renal cell cancer identifies a robust signature to define renal malignancy (2009)

MicroRNAs are short single-stranded RNAs that are associated with gene regulation at the transcriptional and translational level. Changes in their expression were found in a variety of human cancers. Only few data are available on microRNAs in clear cell renal cell carcinoma (ccRCC). We performed genome-wide expression profiling of microRNAs using microarray analysis and quantification of specific microRNAs by TaqMan real-time RT-PCR. Matched malignant and non-malignant tissue samples from two independent sets of 12 and 72 ccRCC were profiled. The microarray-based experiments identified 13 over-expressed and 20 down-regulated microRNAs in malignant samples. Expression in ccRCC tissue samples compared with matched non-malignant samples measured by RT-PCR was increased on average by 2.7- to 23-fold for the hsa-miR-16, -452*, -224, -155 and -210, but decreased by 4.8- to 138-fold for hsa-miR-200b, -363, -429, -200c, -514 and -141. No significant associations between these differentially expressed microRNAs and the clinico-pathological factors tumour stage, tumour grade and survival rate were found. Nevertheless, malignant and non-malignant tissue could clearly be differentiated by their microRNA profile. A combination of miR-141 and miR-155 resulted in a 97% overall correct classification of samples. The presented differential microRNA pattern provides a solid basis for further validation, including functional studies.
Statin Pleiotropy: Fact or Fiction? (2004)

Accumulating evidence from clinical trials and basic research indicates that statin therapy favorably influences a number of diverse clinical events through both effects related to lowering of LDL cholesterol levels and effects independent of the lowering of LDL cholesterol levels. The latter effects are referred to as pleiotropic. The full potential of this exciting class of drugs in vascular and nonvascular protection is only just being realized. The pleiotropic effects of the statins improve vascular relaxation, promote new vessel formation, and stabilize unstable plaques. Statins reduce glomerular injury, renal disease progression, insulin resistance, and bone resorption. Ezetimibe, a recently approved medication, enhances the lipid-lowering effects of the statins by lowering LDL and increasing HDL levels through its property of inhibiting absorption of cholesterol in the small intestine. These salutary effects of ezetimibe on statin levels presumably enhance the beneficial effects attributed to statin pleiotropy. It is noteworthy that the pleiotropic properties of the statins have been beneficial in a variety of diseases that involve a number of organs and organ systems. No other therapeutic agent can claim equally stellar results in such a wide variety of diseases. The common denominator in all of the diseases that have been shown to improve with statin pleiotropy could be arteriolar pathology due to hyperlipidemia, which improves in response to statins by a return of arteriolar function to normal rather than through statin pleiotropy. Recent reports indicate that higher doses of statins reverse atheromatous changes in the coronary artery when the LDL cholesterol level is lowered to well below 2.59 mmol/L (100 mg/dL). These results lend additional support to the probability that similar pathological changes that may be present in the small arteries and arterioles also can respond to adequate statin therapy. Statin pleiotropy: fact or fiction?