gebhart/patrepeval huggingface dataset:
Voluntary health workers′ knowledge, attitude and practices regarding record keeping in Akinyele LGA of Oyo State, Nigeria (2002)

Lack of basic health data for monitoring and evaluation of health services continue to affect the planning, implementation and evaluation of health services in Nigeria. This has contributed to the poor health status and inefficient health services in the country. In the primary health care management information system (PHCMIS), Voluntary Village Health Workers (VHWs) and Traditional Birth Attendants (TBAs) are responsible for collecting information at the community/village level. Trained research assistants administered a pretested semi structured questionnaire and filled an observation checklist to all the voluntary health workers in Akinyele LGA of Oyo State in a cross-sectional survey conducted to assess their record keeping practices as well as their knowledge of and attitude towards it. Results showed that almost half of the respondents had no formal education and a similar proportion had been VHWs for between over 10 years. Over eighty per cent knew the uses of record keeping for monitoring and evaluation purposes. Their attitude towards it was positive and almost all felt it was easy to keep records. Ninety six percent keep records of their health activities and most forward them. It was observed that only 11 (10.8%) respondents had the VHW/TBA record of work produced and recommended by the Federal Ministry of Health because they were reportedly not supplied to them. The factors that were associated with record keeping practices were positive attitude towards record keeping, duration of work as a VHW/TBA, prior training on record keeping and receiving feedback on records kept. Recommendations made included periodic training and retraining of the VHWs on record keeping, ensuring consistent supply of record forms and providing regular feedback on records kept to the VHWs.
High-Resolution Radon Demultiple (2001)

AbstractIt is well known that conventional Radon demultiple may fail when there is limited differential moveout between primaries and multiples or when the input data contain aliased events. These limitations can be overcome by an extension of the conventional Radon transform which uses data-derived constraints to enhance the focusing of energy in the transform domain. This leads to better separation of primaries and multiples and an improved resistance to errors due to noise and aliasing.Data examples show the benefits that result in practice from this high-resolution version of the transform: a) Better multiple removal and signal preservation when primaries and multiples have small differential moveout.b) Removal of aliased multiples without the need for pre-interpolation.c) Removal of aliased noise in the course of demultiple processing. KeywordsmultiplesRadonresolutionaliasing
Virus and Antibody Dynamics in Acute West Nile Virus Infection (2008)

IgM and IgG develop rapidly after viremia and before RNA levels become undetectable, which occurred a mean of 13.2 days after the index donation among donors in this study. WNV RNA detection by replicate TMA rarely persists for >40 days after the index donation and is accompanied by WNV-specific neutralizing antibody, consistent with an absence of WNV transmission via transfusion of seropositive blood components.
Function of the Respiratory Syncytial Virus Small Hydrophobic Protein (2007)

Respiratory syncytial virus (RSV), a member of the Paramyxoviridae family, encodes a small hydrophobic (SH) protein of unknown function. Parainfluenza virus 5 (PIV5), a prototypical paramyxovirus, also encodes an SH protein, which inhibits tumor necrosis factor alpha (TNF-alpha) signaling. In this study, recombinant PIV5 viruses without their own SH but containing RSV SH (from RSV strain A2 or B1) in its place (PIV5DeltaSH-RSV SH) and RSV lacking its own SH (RSVDeltaSH) were generated and analyzed. The results indicate that the SH protein of RSV has a function similar to that of PIV5 SH and that it can inhibit TNF-alpha signaling.
Use of the water absorption spectrum to quantify tissue chromophore concentration changes in near-infrared spectroscopy (1994)

We describe a simple method for measuring the 'differential pathlength' of photons in a scattering medium utilizing the spectral absorption features of water. Determination of this differential pathlength is a prerequisite for quantifying chromophore concentration changes measured by near-infrared spectroscopy (NIRS), and the method proposed here achieves this without the need for time- or frequency-resolved measurements. The quantification of tissue chromophore concentration measurements is a major goal in NIRS research, allowing, for example, the non-invasive measurement of blood flow and volume in the brain and other organs. We present the results of validation experiments performed on tissue phantoms comparing the differential path estimates yielded by water absorption and time-resolved measurements, finding that the weak water absorption feature at 820 nm can yield a differential path estimate in addition to the main feature at 975 nm. We also present results from in vivo studies in which we find that whilst the 820 nm feature is measured with lower accuracy for a given light flux than the 975 nm feature, it is intrinsically a more accurate differential path estimator. Studies on the adult forearm showing differences between time-resolved and water absorption differential path estimates suggest that the measurement of both could aid in quantifying NIRS signals in heterogeneous tissues.
A Classical Thermodynamic Discussion of the Effect of Composition on Glass-Transition Temperatures (1978)

ADVERTISEMENT RETURN TO ISSUEPREVArticleNEXTA Classical Thermodynamic Discussion of the Effect of Composition on Glass-Transition TemperaturesP. R. Couchman and F. E. KaraszCite this: Macromolecules 1978, 11, 1, 117–119Publication Date (Print):January 1, 1978Publication History Published online1 May 2002Published inissue 1 January 1978https://pubs.acs.org/doi/10.1021/ma60061a021https://doi.org/10.1021/ma60061a021research-articleACS PublicationsRequest reuse permissionsArticle Views2428Altmetric-Citations635LEARN 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
Abstract C270: In vitro and in vivo antitumor activity of DCBCI0901, a potent PI3K/mTORC1/mTORC2 inhibitor. (2013)

Abstract The mammalian target of rapamycin (mTOR) is a highly conserved Ser/Thr protein kinase and a central controller of cell growth, proliferation, and survival. Studies have linked the hyperactive PI3K-AKT-mTOR signaling pathway in a variety of human cancers. Drugs targeting to PI3K and mTOR are likely to be an effective treatment for human malignancies that rely on these targets for their growth. Institute of Pharmaceutics at Development Center for Biotechnology in Taiwan has developed a novel and potent small molecule DCBCI0901 as PI3K/mTORC1/mTORC2 inhibitor. DCBCI0901 attenuated cell survival and proliferation in both in vitro and in vivo models. DCBCI0901 possessed IC50 of 8.4 nM against mTOR kinase and IC50 of 78 nM against PI3Kα (p110α/p85α) while exerting high selectivity against a panel of 20 other serine/ threonine and tyrosine kinases. In addition, DCBCI0901 is highly active in cellular assays. It causes a significant reduction in phospho-p70S6K (mTORC1 substrate), phospho-AKT (S473) (mTORC2 substrate), and phospho-AKT (T308) (PI3K substrate) levels. The antitumor efficacy of DCBCI0901 was evaluated in diverse human tumor cell lines. DCBCI0901 effectively inhibits cell proliferation of five well-established cell lines (one NSCLC, A549; two prostate cancers, PC-3 and LNCap; two breast cancers, HCC1954 and BT474), with IC50 values ranging from 6 to 48 nM. Notably, DCBCI0901 is effective against a panel of nine lung cancer cell lines (one cell line is EGFR-TKI sensitive model and eight cell lines are EGFR-TKI resistant model), with IC50 in the ten of nanomolar range. DCBCI0901 showed significant antitumor efficacy in mouse xenograft models including lung cancer, prostate cancer, and leukemia with tumor growth inhibition greater than 65%. DCBCI0901 also demonstrated effective suppression of tumor growth in advanced-stage xenograft models (lung cancer (A549), mean tumor volume &amp;gt; 350mm3 at the start of treatment). Furthermore, in an EGFR-TKI resistant lung cancer H1975 xenograft model, DCBCI0901 effectively suppressed tumor growth. Based on the in vitro/in vivo pharmacology data, DCBCI0901 was selected as a drug candidate for further development as anticancer agent. This publication is dedicated to the memory of Dr. Paonien Chen. Citation Information: Mol Cancer Ther 2013;12(11 Suppl):C270. Citation Format: Ying-Shuan E. Lee, Mann-Yan Kuo, Yi-Ting Huang, Yu-Wen Tseng, Yu Jie Lin, Yen His Liu, Shian-Yi Chiou, Li Jung Chen, Y.-Y. Lu, Chih-Hsin Yang, Pan-Chyr Yang. In vitro and in vivo antitumor activity of DCBCI0901, a potent PI3K/mTORC1/mTORC2 inhibitor. [abstract]. In: Proceedings of the AACR-NCI-EORTC International Conference: Molecular Targets and Cancer Therapeutics; 2013 Oct 19-23; Boston, MA. Philadelphia (PA): AACR; Mol Cancer Ther 2013;12(11 Suppl):Abstract nr C270.
Solubilization, Partial Purification, and Affinity Labeling of the Membrane-Bound Isoprenylated Protein Endoprotease (1996)

A previously described [Ma, Y.-T., & Rando, R. R. (1992) Proc. Natl. Acad. Sci. U.S.A. 89, 6275-6279] membrane-associated isoprenylated protein endoprotease is important in the processing of isoprenylated proteins terminating with CAAX. The enzyme is of substantial interest because specific inhibitors of it block the processing and functioning of ras in vivo. The enzyme appears to be an integral membrane protein, as it can only be removed from microsomal membranes with detergent. The enzyme is effectively solubilized by the detergent CHAPSO and can be partially purified (approximately 10-fold) by anion ion exchange and size exclusion chromatography. Attempts to further purify the enzyme by other column means, including affinity chromatography, were unsuccessful. The partially purified enzyme is very sensitive to thiol reagents but insensitive to other kinds of protease inhibitors, suggesting that the enzyme is a thiol protease. Potent and specific chloroketone containing affinity labeling agents have been developed. These novel inactivators owe their potency to an S-farnesylcysteine moiety which is recognized by the enzyme. Specific inhibitors of this type should allow for the identification and cloning of this protease, which is important for signal transduction.
Molecular Genetic Analysis of Two Human Sperm Fibrous Sheath Proteins, AKAP4 and AKAP3, in Men With Dysplasia of the Fibrous Sheath (2001)

Dysplasia of the fibrous sheath (DFS) is characterized by male infertility, asthenozoospermia, and morphologically abnormal flagella that possess a severely malformed fibrous sheath. In many cases, DFS is familial, suggesting a genetic component. Human AKAP4 and AKAP3 are structural proteins of the fibrous sheath that also function to anchor protein kinase A to this structure via the regulatory subunit of the kinase. We hypothesized that defects in either AKAP4 or AKAP3 might cause DFS. No quantitative or qualitative differences between patients with DFS and normal controls were detected when sperm proteins were analyzed by either silver staining or immunoblot analysis using antibodies raised against AKAP4 and AKAP3. Additionally, AKAP4 and AKAP3 from DFS sperm retained the ability to bind the regulatory subunit of protein kinase A. Localization at the light and electron microscopic levels showed that AKAP3 and AKAP4 localized correctly to the FS of the amorphous flagellum in DFS sperm. Partial sequence analysis of the AKAP4 and AKAP3 genes in patients with DFS did not identify any significant alterations in potential AKAP4/AKAP3 binding regions, suggesting that the two proteins interact normally in DFS sperm. Our results did not find evidence to support the hypothesis that mutations in either gene are responsible for DFS in humans.
Sterols. XCIII. epi-Pseudosarsasapogenin, Pseudosarsasapogenone and Pseudochlorogenin (1940)

ADVERTISEMENT RETURN TO ISSUEPREVArticleNEXTSterols. XCIII. epi-Pseudosarsasapogenin, Pseudosarsasapogenone and PseudochlorogeninRussell E. Marker, Ewald Rohrmann, and Eldon M. JonesCite this: J. Am. Chem. Soc. 1940, 62, 3, 648–649Publication Date (Print):March 1, 1940Publication History Published online1 May 2002Published inissue 1 March 1940https://pubs.acs.org/doi/10.1021/ja01860a062https://doi.org/10.1021/ja01860a062research-articleACS PublicationsRequest reuse permissionsArticle Views45Altmetric-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
Role of T3 surface molecules in human T-cell activation: T3-dependent activation results in an increase in cytoplasmic free calcium. (1984)

The human T-cell leukemia, Jurkat, and a T3-negative mutant of Jurkat (S.5) were used to study the role of T3 in human T-cell activation. Incubation of Jurkat with phytohemagglutinin (PHA) resulted in the production of interleukin 2, which was markedly increased by the addition of phorbol 12-myristate 13-acetate (PMA). Antibodies reactive with T3 could activate Jurkat only if added together with PMA. However, S.5 cells failed to produce interleukin 2 in response to PHA and produced 1/16th the interleukin 2 activity that Jurkat produced in response to PHA and PMA. Incubation of S.5 cells with the calcium ionophore A23187 and PMA resulted in the production of interleukin 2 activity comparable to that produced by Jurkat. Like antibodies reactive with T3, A23187 demonstrated an obligate requirement for PMA in order to activate Jurkat or S.5. These observations suggested that T3 might participate in T-cell activation through mechanisms that increase intracellular Ca2+. This was examined by using the Ca2+ sensitive fluor, quin-2, to measure levels of cytoplasmic free Ca2+ [( Ca2+]i). Addition of PHA, A23187, or monoclonal antibodies reactive with T3 to Jurkat cells resulted in substantial increases of [Ca2+]i. In contrast, only A23187 could induce an increase in [Ca2+]i in S.5 cells. Three other monoclonal antibodies reactive with other membrane antigens expressed on Jurkat or S.5 did not increase [Ca2+]i. These results suggest that T3 and/or associated molecules participate in T-cell activation through mechanisms that lead to increases in [Ca2+]i and that their expression is a relative requirement for T-cell activation by PHA.
Comparison of the effects on colonic function caused by feeding rice bran and wheat bran. (1988)

A study was designed to investigate the effects of a new fibre source, rice bran, on colonic function, and to compare it with wheat bran. The diet of eight normal male volunteers was supplemented with similar amounts of indigestible residue from rice (17.1 g/d) and wheat bran (15.0 g/d) for periods of 10 d each. During the last 7 d of each of these periods, and also of a 10-d control period when no supplement was taken, the volunteers collected their stools into plastic bags. This allowed calculation of stool mass and frequency, and gastrointestinal transit time by a continuous radio-opaque marker technique. Rice bran increased the mass of faeces produced and the stool frequency by more than the wheat bran, but both had a similar accelerating effect on the transit time. The mechanism of the efficient stool bulking caused by the rice bran may be due to a high content of retrograded starch.
Structural Recognition of a Novel Fibrinogen γ Chain Sequence (117–133) by Intercellular Adhesion Molecule-1 Mediates Leukocyte-Endothelium Interaction (1995)

In addition to its role in hemostasis, fibrinogen is obligatorily required to mount competent inflammatory responses in vivo. A molecular prerequisite of fibrinogen-dependent inflammation may reside in its ability to associate with intercellular adhesion molecule-1 (ICAM-1), and enhance monocyte adhesion to endothelium by bridging the two cell types. Structure-function characterization of the novel ICAM-1 recognition of fibrinogen was carried out by synthetic peptidyl mimicry of the fibrinogen gamma chain. A novel peptide sequence, N117NQ-KIVNLKEKVAQLEA133, designated gamma 3, dose-dependently inhibited (IC50 approximately 20-40 micrograms/ml) binding of 125I-fibrinogen to endothelial cells or ICAM-1-expressing B lymphoblastoid Daudi cells. In contrast, none of the previously identified vascular cell fibrinogen interacting sequences was effective. Increasing concentrations of gamma 3 completely inhibited fibrinogen-mediated adhesion of peripheral blood mononuclear cells or vitamin D3-differentiated monocytic HL-60 cells to endothelium, but did not affect leukocyte-endothelium interaction in the absence of fibrinogen. 125I-Labeled gamma 3 bound specifically and saturably to genetically engineered ICAM-1 transfectants, but not to control non-transfected cells, and associated with ICAM-1 on cytokine-activated endothelium with a Kd of 34 microM. Consistent with functional recognition of ICAM-1, immobilized gamma 3 supported adhesion of JY lymphoblasts in a dose-dependent reaction inhibited by monoclonal antibodies to ICAM-1. We conclude that a novel fibrinogen gamma 3 sequence N117NQKIVNLKEKVAQLEA133 binds to ICAM-1 and modulates ICAM-1-dependent adhesion. These findings define the structural basis of fibrinogen:ICAM-1 recognition and provide a potential selective target for inhibiting fibrinogen-dependent inflammatory responses.
Antiproliferative effect of neomycin in glioma cells (2002)

The angiogenic growth factor (AGF) family of signaling molecules has been implicated in normal development and in physiological process as well as in human malignancy. Since blockage of nuclear translocation of AGF in endothelial cells with neomycin resulted in inhibition of the growth factor capacity to induce angiogenesis, we treated glioma cells with neomycin and assessed its effects on cell proliferation. Administration of 10mM neomycin during two days resulted in a 56% inhibition of glioma cells proliferation. This result may provide the basis for the development of a novel adjuvant therapeutic strategy forgliomas.
Pdx1inactivation restricted to the intestinal epithelium in mice alters duodenal gene expression in enterocytes and enteroendocrine cells (2009)

Null mutant mice lacking the transcription factor pancreatic and duodenal homeobox 1 (Pdx1) are apancreatic and survive only a few days after birth. The role of Pdx1 in regulating intestinal gene expression has therefore yet to be determined in viable mice with normal pancreatic development. We hypothesized that conditional inactivation of Pdx1 restricted to the intestinal epithelium would alter intestinal gene expression and cell differentiation. Pdx1(flox/flox);VilCre mice with intestine-specific Pdx1 inactivation were generated by crossing a transgenic mouse strain expressing Cre recombinase, driven by a mouse villin 1 gene promoter fragment, with a mutant mouse strain homozygous for loxP site-flanked Pdx1. Pdx1 protein is undetectable in all epithelial cells in the intestinal epithelium of Pdx1(flox/flox);VilCre mice. Goblet cell number and mRNA abundance for mucin 3 and mucin 13 genes in the proximal small intestine are comparable between Pdx1(flox/flox);VilCre and control mice. Similarly, Paneth cell number and expression of Paneth cell-related genes Defa1, Defcr-rs1, and Mmp7 in the proximal small intestine remain statistically unchanged by Pdx1 inactivation. Although the number of enteroendocrine cells expressing chromogranin A/B, gastric inhibitory polypeptide (Gip), or somatostatin (Sst) is unaffected in the Pdx1(flox/flox);VilCre mice, mRNA abundance for Gip and Sst is significantly reduced in the proximal small intestine. Conditional Pdx1 inactivation attenuates intestinal alkaline phosphatase (IAP) activity in the duodenal epithelium, consistent with an average 91% decrease in expression of the mouse enterocyte IAP gene, alkaline phosphatase 3 (a novel Pdx1 target candidate), in the proximal small intestine following Pdx1 inactivation. We conclude that Pdx1 is necessary for patterning appropriate gene expression in enterocytes and enteroendocrine cells of the proximal small intestine.
Discovery of Embelin as a Cell-Permeable, Small-Molecular Weight Inhibitor of XIAP through Structure-Based Computational Screening of a Traditional Herbal Medicine Three-Dimensional Structure Database (2004)

The X-linked inhibitor of apoptosis (XIAP) is a promising new molecular target for the design of novel anticancer drugs aiming at overcoming apoptosis-resistance of cancer cells to chemotherapeutic agents and radiation therapy. Recent studies demonstrated that the BIR3 domain of XIAP where caspase-9 and Smac proteins bind is an attractive site for designing small-molecule inhibitors of XIAP. Through computational structure-based screening of an in-house traditional herbal medicine three-dimensional structure database of 8221 individual natural products, followed by biochemical testing of selected candidate compounds, we discovered embelin from the Japanese Ardisia herb as a small-molecular weight inhibitor that binds to the XIAP BIR3 domain. We showed that embelin binds to the XIAP BIR3 protein with an affinity similar to that of the natural Smac peptide using a fluorescence polarization-based binding assay. Our NMR analysis further conclusively confirmed that embelin interacts with several crucial residues in the XIAP BIR3 domain with which Smac and caspsase-9 bind. Embelin inhibits cell growth, induces apoptosis, and activates caspase-9 in prostate cancer cells with high levels of XIAP, but has a minimal effect on normal prostate epithelial and fibroblast cells with low levels of XIAP. In stably XIAP-transfected Jurkat cells, embelin effectively overcomes the protective effect of XIAP to apoptosis and enhances the etoposide-induced apoptosis and has a minimal effect in Jurkat cells transfected with vector control. Taken together, our results showed that embelin is a fairly potent, nonpeptidic, cell-permeable, small-molecule inhibitor of XIAP and represents a promising lead compound for designing an entirely new class of anticancer agents that target the BIR3 domain of XIAP.