gebhart/patrepeval huggingface dataset:
Co-expression and amplification of dihydrofolate reductase cDNA and the Escherichia coli XGPRT gene in Chinese hamster ovary cells. (1981)

We have transformed Chinese hamster ovary cells with a plasmid containing mouse dihydrofolate reductase (DHFR) cDNA and the Escherichia coli xanthine-guanine phosphoribosyl transferase (XGPRT) gene under the control of the mouse mammary tumor virus and SV40 early promoters, respectively. Selection for the expression of XGPRT using the dominant selection scheme described by Mulligan and Berg yields clones that simultaneously express DHFR. Growth of these cells in progressively increasing concentrations of methotrexate, results in selection of cells that overproduce DHFR and its messenger RNA 250-500 fold. ANalyses of the plasmid DNA sequences in these cells reveal that the increased production of DHFR is due in part to gene amplification (approximately 50-fold) and in part to a selective overproduction of DHFR RNA. Last, the methotrexate-resistant cells contain 50 times more XGPRT RNA and DNA than the initial transformant; this demonstrates the potential for using gene amplification as a means for overproducing the products of genes linked to DHFR cDNA in plasmid vectors.
Studies in experimental behavior genetics: III. Selection and hybridization analyses of individual differences in the sign of geotaxis. (1962)

Uploaded by Plazi for TaxoDros. We do not have abstracts.
Persistent Noncytopathic Infection of Normal Human T Lymphocytes with AIDS-Associated Retrovirus (1985)

Infection of normal peripheral blood T cells by the acquired immune deficiency syndrome (AIDS)-associated retrovirus (ARV) was evaluated in long-term cultures of helper-inducer T cells (T4 cells). Cells that were inoculated with ARV and maintained in medium supplemented with interleukin-2 remained productively infected with this virus for more than 4 months in culture, although they showed no cytopathic effects characteristic of acute ARV infection. The presence of replicating virus was demonstrated by reverse transcriptase activity of culture fluids and by viral antigens and budding particles detected on cells by immunofluorescence and electron microscopy. Virus produced in these cultures remained infectious and could induce cytopathic effects and viral antigens in uninfected lymphoid cells. The finding that normal lymphocytes may be productively infected by an AIDS retrovirus in the absence of cell death suggests that a range of biologic effects may occur after infection in vivo.
Superparamagnetic Iron Oxide Nanoparticles as MRI contrast agents for Non-invasive Stem Cell Labeling and Tracking (2013)

Stem cells hold great promise for the treatment of multiple human diseases and disorders. Tracking and monitoring of stem cells in vivo after transplantation can supply important information for determining the efficacy of stem cell therapy. Magnetic resonance imaging (MRI) combined with contrast agents is believed to be the most effective and safest non-invasive technique for stem cell tracking in living bodies. Commercial superparamagnetic iron oxide nanoparticles (SPIONs) in the aid of transfection agents (TAs) have been applied to labeling stem cells. However, owing to the potential toxicity of TAs, more attentions have been paid to develop novel SPIONs with specific surface coating or functional moieties which facilitate effective cell internalization in the absence of TAs. This review aims to summarize the recent progress in the design and preparation of SPIONs as cellular MRI probes, to discuss their applications and current problems facing in stem cell labeling and tracking, and to offer perspectives and solutions for the future development of SPIONs in this field.
Helicobacter pylori infection and tumour necrosis factor-α increase gastrin release from human gastric antral fragments (1997)

H. pylori infection is associated with enhanced gastrin release from human antrum and TNF-alpha produces a similar effect. Proinflammatory cytokines generated in the antrum in response to the infection are likely to play a significant role in the hypergastrinaemia of H. pylori infection.
UWIT: underwater image toolbox for optical image processing and mosaicking in MATLAB (2003)

This paper shows results from our development of an extended MATLAB image processing toolbox, which implements some useful optical image processing and mosaicking algorithms found in the literature. We surveyed and selected algorithms from the field which showed promise in application to the underwater environment. We then extended these algorithms to explicitly deal with the unique constraints of underwater imagery in the building of our toolbox. As such, the algorithms implemented include: contrast limited adaptive histogram specification (CLAHS) to deal with the inherent nonuniform lighting in underwater imagery, Fourier based methods for scale, rotation, and translation recovery which provide robustness against dissimilar image regions, local normalized correlation for image registration to handle the low-feature, unstructured environment of the seafloor, multiresolution pyramidal blending of images to form a composite seamless mosaic without blurring or loss of detail near image borders. In this paper we highlight the mathematical formulation behind each of these algorithms using consistent notation and a unified framework. We depict some of our MATLAB toolbox results with an assortment of underwater imagery.
Discovery of Potent and Selective Inhibitors of Ataxia Telangiectasia Mutated and Rad3 Related (ATR) Protein Kinase as Potential Anticancer Agents (2011)

DNA-damaging agents are among the most frequently used anticancer drugs. However, they provide only modest benefit in most cancers. This may be attributed to a genome maintenance network, the DNA damage response (DDR), that recognizes and repairs damaged DNA. ATR is a major regulator of the DDR and an attractive anticancer target. Herein, we describe the discovery of a series of aminopyrazines with potent and selective ATR inhibition. Compound 45 inhibits ATR with a K(i) of 6 nM, shows >600-fold selectivity over related kinases ATM or DNA-PK, and blocks ATR signaling in cells with an IC(50) of 0.42 μM. Using this compound, we show that ATR inhibition markedly enhances death induced by DNA-damaging agents in certain cancers but not normal cells. This differential response between cancer and normal cells highlights the great potential for ATR inhibition as a novel mechanism to dramatically increase the efficacy of many established drugs and ionizing radiation.
Human Intestinal H+/Peptide Cotransporter (1995)

In mammalian small intestine, a H(+)-coupled peptide transporter is responsible for the absorption of small peptides arising from digestion of dietary proteins. Recently a cDNA clone encoding a H+/peptide cotransporter has been isolated from a rabbit intestinal cDNA library (Fei, Y.J., Kanai, Y., Nussberger, S., Ganapathy, V., Leibach, F.H., Romero, M.F., Singh, S.K., Boron, W. F., and Hediger, M. A. (1994) Nature 368, 563-566). Screening of a human intestinal cDNA library with a probe derived from the rabbit H+/peptide cotransporter cDNA resulted in the identification of a cDNA which when expressed in HeLa cells or in Xenopus laevis oocytes induced H(+)-dependent peptide transport activity. The predicted protein consists of 708 amino acids with 12 membrane-spanning domains and two putative sites for protein kinase C-dependent phosphorylation. The cDNA-induced transport process accepts dipeptides, tripeptides, and amino beta-lactam antibiotics but not free amino acids as substrates. The human H+/peptide cotransporter exhibits a high degree of homology (81% identity and 92% similarity) to the rabbit H+/peptide cotransporter. But surprisingly these transporters show only a weak homology to the H(+)-coupled peptide transport proteins present in bacteria and yeast. Chromosomal assignment studies with somatic cell hybrid analysis and in situ hybridization have located the gene encoding the cloned human H+/peptide cotransporter to chromosome 13 q33-->q34.
Synthesis and Characterization of Long‐Chain‐Branched Polyolefins with Metallocene Catalysts: Copolymerization of Ethylene with Poly(ethylene‐co‐propylene) Macromonomer (2003)

Abstract Poly(ethylene‐ co ‐propylene) macromonomer (EPM) was synthesized in a high‐temperature continuous stirred tank reactor (CSTR) with [C 5 Me 4 (SiMe 2 N t Bu)]TiMe 2 (CGC‐Ti) as the catalyst system. PE samples with EPM long chain branching (LCB) were produced by semi‐batch copolymerization of ethylene and EPM with CGC‐Ti. The LCB frequencies were up to 21.8 EPM side chains per PE backbone. The effects of temperature and ethylene pressure on the degree of EPM grafting and catalyst activity were examined. Incorporation of EPM into a growing PE chain forming an LCB polymer. magnified image Incorporation of EPM into a growing PE chain forming an LCB polymer.
The inflammatory action of CD40 ligand (CD154) expressed on activated human platelets is temporally limited by coexpressed CD40 (2001)

Recently, we have demonstrated that human platelets carry preformed CD40 ligand (CD154) molecules, which rapidly appear on the platelet surface following stimulation by thrombin. Once on the surface, platelet CD154 induces an inflammatory reaction of CD40-bearing endothelial cells. This study shows that strong platelet agonists other than thrombin also lead to the expression of CD154 on the platelet surface. At the same time, several lines of evidence are presented that together indicate that thrombotic events in the vasculature are generally accompanied by activation of the inflammatory potential of platelet CD154. This study also reports the constitutive expression of CD40, the receptor for CD154, on platelets. The binding of CD154 to coexpressed CD40 in the platelet aggregate leads within minutes to hours to the cleavage of membrane-bound surface CD154 and the release of an 18-kd soluble form of the molecule. Soluble CD154 (sCD154), in contrast to transmembrane CD154, can no longer induce an inflammatory reaction of endothelial cells. These findings indicate that the interaction of platelet CD154 with CD40 on neighboring cells is temporally limited to prevent an uncontrolled inflammation at the site of thrombus formation. Thus, similar to the very tight regulation of the CD154-CD40 interaction in the immune system, an effective mechanism controls the inflammatory potential of platelet CD154 in the vascular system. (Blood. 2001;98:1047-1054)
Phosphatidylinositol 3-Kinase Is a Negative Regulator of Cellular Differentiation (1997)

Phosphatidylinositol 3-kinase (PI3K) has been shown to be an important mediator of intracellular signal transduction in mammalian cells. We show here, for the first time, that the blockade of PI3K activity in human fetal undifferentiated cells induced morphological and functional endocrine differentiation. This was associated with an increase in mRNA levels of insulin, glucagon, and somatostatin, as well as an increase in the insulin protein content and secretion in response to secretagogues. Blockade of PI3K also increased the proportion of pluripotent precursor cells coexpressing multiple hormones and the total number of terminally differentiated cells originating from these precursor cells. We examined whether any of the recently described modulators of endocrine differentiation could participate in regulating PI3K activity in fetal islet cells. The activity of PI3K was inversely correlated with the hepatocyte growth factor/scatter factor–induced downregulation or nicotinamideinduced upregulation of islet-specific gene expression, giving support to the role of PI3K, as a negative regulator of endocrine differentiation. In conclusion, our results provide a mechanism for the regulation of hormone-specific gene expression during human fetal neogenesis. They also suggest a novel function for PI3K, as a negative regulator of cellular differentiation.
Endotoxin-Free Purification of Monocytes for Dendritic Cell Generation via Discontinuous Density Gradient Centrifugation Based on Diluted Ficoll-Paque Plus<sup>®</sup> (2002)

Since Ficoll-Paque Plus is commercially available in an endotoxin-free form, this modified Ficoll gradient offers a simple modality for isolating large amounts of monocytes under endotoxin-free conditions without introducing further potential monocyte-activating agents or procedures.
Hydrodynamic Characterization of Surfactant Encapsulated Carbon Nanotubes Using an Analytical Ultracentrifuge (2008)

The hydrodynamic properties of surfactant encapsulated single-walled carbon nanotubes (SWNTs) have been characterized by optically measuring their spatial and temporal redistribution in situ in an analytical ultracentrifuge. The measured redistribution profiles are fit to the Lamm equation, thus determining the sedimentation, diffusion, and hydrodynamic frictional coefficients of the surfactant encapsulated SWNTs. For sodium cholate encapsulated SWNTs, we demonstrate that the technique of analytical ultracentrifugation can be utilized to determine the linear packing density of surfactant molecules along the length of the SWNTs, 3.6 +/- 0.8 nm(-1), and the anhydrous molar volume of the surfactant molecules on the SWNT surfaces, 270 +/- 20 cm(3) mol(-1). Additionally, analytical ultracentrifugation is used to measure and compare the sedimentation rates of bundled and isolated carbon nanotubes. This study should serve as a guide for designing centrifuge-based processing procedures for preparing samples of SWNTs for a wide variety of applications and studies. Additionally, the results obtained here should aid in understanding the hydrodynamic properties of SWNTs and the interactions between SWNTs and surfactants in aqueous solution.
Modulation of the dynamic instability of tubulin assembly by the microtubule-associated protein tau. (1992)

Microtubule-associated proteins (MAP), such as tau, modulate the extent and rate of microtubule assembly and play an essential role in morphogenetic processes, such as axonal growth. We have examined the mechanism by which tau affects microtubule polymerization by examining the kinetics of microtubule assembly and disassembly through direct observation of microtubules using dark-field microscopy. Tau increases the rate of polymerization, decreases the rate of transit into the shrinking phase (catastrophe), and inhibits the rate of depolymerization. Tau strongly suppresses the catastrophe rate, and its ability to do so is independent of its ability to increase the elongation rate. Thus, tau generates a partially stable but still dynamic state in microtubules. This state is perturbed by phosphorylation by MAP2 kinase, which affects all three activities by lowering the affinity of tau for the microtubule lattice.
BMPR-II deficiency elicits pro-proliferative and anti-apoptotic responses through the activation of TGFβ-TAK1-MAPK pathways in PAH (2012)

Pulmonary arterial hypertension (PAH) is a cardiovascular disorder associated with enhanced proliferation and suppressed apoptosis of pulmonary arterial smooth muscle cells (PASMCs). Heterozygous mutations in the type II receptor for bone morphogenetic protein (BMPR2) underlie the majority of the inherited and familial forms of PAH. The transforming growth factor β (TGFβ) pathway is activated in both human and experimental models of PAH. However, how these factors exert pro-proliferative and anti-apoptotic responses in PAH remains unclear. Using mouse primary PASMCs derived from knock-in mice, we demonstrated that BMPR-II dysfunction promotes the activation of small mothers against decapentaplegia-independent mitogen-activated protein kinase (MAPK) pathways via TGFβ-associated kinase 1 (TAK1), resulting in a pro-proliferative and anti-apoptotic response. Inhibition of the TAK1-MAPK axis rescues abnormal proliferation and apoptosis in these cells. In both hypoxia and monocrotaline-induced PAH rat models, which display reduced levels of bmpr2 transcripts, this study further indicates that the TGFβ-MAPK axis is activated in lungs following elevation of both expression and phosphorylation of the TAK1 protein. In ex vivo cell-based assays, TAK1 inhibits BMP-responsive reporter activity and interacts with BMPR-II receptor. In the presence of pathogenic BMPR2 mutations observed in PAH patients, this interaction is greatly reduced. Taken together, these data suggest dysfunctional BMPR-II responsiveness intensifies TGFβ-TAK1-MAPK signalling and thus alters the ratio of apoptosis to proliferation. This axis may be a potential therapeutic target in PAH.
Randomized phase II study of picoplatin in combination with 5-fluorouracil and leucovorin (FOLPI) as a neuropathy-sparing alternative to modified FOLFOX-6 as first-line therapy for colorectal cancer (CRC) (2009)

4026 Background: Picoplatin (Pico) was designed to overcome platinum resistance and has the potential for improved safety compared to other platinum agents. FOLFOX (5-FU, LV, oxaliplatin [oxali]) treatment for advanced CRC has dose-limiting oxali- related neurotoxicity. The incidence of grade (G) 3–4 neurotoxicity with single-agent Pico across studies was &lt;2%, suggesting that Pico may provide a neuropathy-sparing alternative to oxali. A Phase I trial identified the Pico MTD at 150 mg/m 2 when infused Q4W with Q2W FU/LV. The present study evaluates Pico when administered Q4W with Q2W FU and LV (FOLPI) vs. modified (m) FOLFOX-6 (FOLFOX) as 1st line treatment for patients (pts) with advanced CRC. Methods: Each pt received LV and infusional FU per mFOLFOX-6 Q2W. Pts with no prior chemotherapy for advanced CRC received Pico Q4W (150 mg/m 2 ) or oxali Q2W (85 mg/m 2 ). Tumor response was assessed by RECIST using CT scans. Adverse events (AEs) were assessed with CTCAE. Neuropathy was assessed using the FACT-Neurotoxicity questionnaire and by a neurologist blinded to treatment. Results: 101 pts were randomized (50 to FOLPI, 51 to FOLFOX). Pts have received 213 (median 4, max 11) 4-week cycles of FOLPI and 414 (median 8, max 21) 2-week cycles of FOLFOX. Median dose intensity of Pico = 28 mg/m 2 /wk (range 19–44); mean relative dose intensity = 77%. Median dose intensity of oxali = 36 mg/m 2 /wk (range 28–43); mean relative dose intensity = 86%. Neurotoxicity was observed in 65% of pts on FOLFOX (10% G 3/4) and 28% of pts on FOLPI (no G 3/4). Most frequent G 3/4 AEs on FOLPI were neutropenia (60%), thrombocytopenia (40%) and anemia (14%). In the FOLFOX arm, other than neuropathy, the most frequent G 3/4 AEs were neutropenia (20%) and thrombocytopenia (12%). Disease control (CR+PR+SD) was 76% for FOLPI and 76% for FOLFOX. In the FOLPI arm there were 1 CR (2%) and 11 PR (22%). In the FOLFOX arm there were no CRs and 13 PR (26%). Conclusions: In this ongoing trial, FOLPI with Pico Q4W shows comparable disease control as measured by RECIST compared to FOLFOX. Neurotoxicity was less frequent and less severe in the FOLPI arm compared to the FOLFOX arm. Pico therefore may be a neuropathy-sparing alternative to oxaliplatin in CRC. [Table: see text]
Epidemiology of pancreatic cancer (2016)

Cancer of the pancreas remains one of the deadliest cancer types. Based on the GLOBOCAN 2012 estimates, pancreatic cancer causes more than 331000 deaths per year, ranking as the seventh leading cause of cancer death in both sexes together. Globally, about 338000 people had pancreatic cancer in 2012, making it the 11<sup>th</sup> most common cancer. The highest incidence and mortality rates of pancreatic cancer are found in developed countries. Trends for pancreatic cancer incidence and mortality varied considerably in the world. A known cause of pancreatic cancer is tobacco smoking. This risk factor is likely to explain some of the international variations and gender differences. The overall five-year survival rate is about 6% (ranges from 2% to 9%), but this vary very small between developed and developing countries. To date, the causes of pancreatic cancer are still insufficiently known, although certain risk factors have been identified, such as smoking, obesity, genetics, diabetes, diet, inactivity. There are no current screening recommendations for pancreatic cancer, so primary prevention is of utmost importance. A better understanding of the etiology and identifying the risk factors is essential for the primary prevention of this disease.
The Roles of Placental Growth Hormone and Placental Lactogen in the Regulation of Human Fetal Growth and Development (2000)

The human growth hormone (hGH)/human placental lactogen (hPL) gene family, which consists of two GH and three PL genes, is important in the regulation of maternal and fetal metabolism and the growth and development of the fetus. During pregnancy, pituitary GH (hGH-N) expression in the mother is suppressed; and hGH-V, a GH variant expressed by the placenta, becomes the predominant GH in the mother. hPL, which is the product of the hPL-A and hPL-B genes, is secreted into both the maternal and fetal circulations after the sixth week of pregnancy. hGH-V and hPL act in concert in the mother to stimulate insulin-like growth factor (IGF) production and modulate intermediary metabolism, resulting in an increase in the availability of glucose and amino acids to the fetus. In the fetus, hPL acts via lactogenic receptors and possibly a unique PL receptor to modulate embryonic development, regulate intermediary metabolism and stimulate the production of IGFs, insulin, adrenocortical hormones and pulmonary surfactant. hGH-N, which is expressed by the fetal pituitary, has little or no physiological actions in the fetus until late in pregnancy due to the lack of functional GH receptors on fetal tissues. hGH-V, which is also a potent somatogenic hormone, is not released into the fetus. Taken together, studies of the hGH/hPL gene family during pregnancy reveal a complex interaction of the hormones with one another and with other growth factors. Additional investigations are necessary to clarify the relative roles of the family members in the regulation of fetal growth and development and the factors that modulate the expression of the genes.
How Does a Gold Nanorod Melt? (2000)

Structural transformation of gold nanorods are investigated by high-resolution transmission electron microscopy after they have been exposed to low-energy femtosecond and nanosecond laser pulses in colloidal solution. The pulse energies were below the gold nanorod melting threshold, but allowed early stage shape transformation processes. It is found that while the as-prepared nanorods are defect-free, laser-irradiation induces point and line defects. The defects are dominated by (multiple) twins and stacking faults (planar defects), which are the precursor that drives the nanorods to convert their {110} facets into the more stable {100} and {111} facets and hence minimize their surface energy. These observations suggest that short-laser pulsed photothermal melting begins with the creation of defects inside the nanorods followed by surface reconstruction and diffusion, in contrast with the thermal melting of the rods or the bulk material, where the melting starts at the surface.