gebhart/patrepeval huggingface dataset:
Mobile instant messaging (2003)

We describe a mobile instant messaging system, MIM, designed for mobile environments. During the design of mobile applications, several new problems and possibilities have to be considered that do not exist with applications targeted at desktop PCs. One example of an application not designed for a mobile environment is the current, very popular, instant messaging, typified by systems such as ICQ, AIM and MSN Messenger. We describe why current systems are not suitable in a mobile environment, and present our architecture for a new system, MIM, and show various implementations for different mobile devices such as PDAs, wearable computers and mobile phones.
A synthetic lethal screen identifies SLK1, a novel protein kinase homolog implicated in yeast cell morphogenesis and cell growth. (1992)

The Saccharomyces cerevisiae SPA2 protein localizes at sites involved in polarized cell growth in budding cells and mating cells. spa2 mutants have defects in projection formation during mating but are healthy during vegetative growth. A synthetic lethal screen was devised to identify mutants that require the SPA2 gene for vegetative growth. One mutant, called slk-1 (for synthetic lethal kinase), has been characterized extensively. The SLK1 gene has been cloned, and sequence analysis predicts that the SLK1 protein is 1,478 amino acid residues in length. Approximately 300 amino acids at the carboxy terminus exhibit sequence similarity with the catalytic domains of protein kinases. Disruption mutations have been constructed in the SLK1 gene. slk1 null mutants cannot grow at 37 degrees C, but many cells can grow at 30, 24, and 17 degrees C. Dead slk1 mutant cells usually have aberrant cell morphologies, and many cells are very small, approximately one-half the diameter of wild-type cells. Surviving slk1 cells also exhibit morphogenic defects; these cells are impaired in their ability to form projections upon exposure to mating pheromones. During vegetative growth, a higher fraction of slk1 cells are unbudded compared with wild-type cells, and under nutrient limiting conditions, slk1 cells exhibit defects in cell cycle arrest. The different slk1 mutant defects are partially rescued by an extra copy of the SSD1/SRK1 gene. SSD1/SRK1 has been independently isolated as a suppressor of mutations in genes involved in growth control, sit4, pde2, bcy1, and ins1 (A. Sutton, D. Immanuel, and K.T. Arnat, Mol. Cell. Biol. 11:2133-2148, 1991; R.B. Wilson, A.A. Brenner, T.B. White, M.J. Engler, J.P. Gaughran, and K. Tatchell, Mol. Cell. Biol. 11:3369-3373, 1991). These data suggest that SLK1 plays a role in both cell morphogenesis and the control of cell growth. We speculate that SLK1 may be a regulatory link for these two cellular processes.
Isolation of HLA-DR1.(staphylococcal enterotoxin A)2 trimers in solution. (1995)

Mutational studies indicate that the superantigen staphylococcal enterotoxin A (SEA) has two separate binding sites for major histocompatibility complex (MHC) class II molecules. Direct evidence is provided here for the formation of SEA-MHC class II trimers in solution. Isoelectric focusing separated SEA-HLA-DR1 complexes into both dimers and HLA-DR1.SEA2 trimers. The molar ratio of components was determined by dual isotope labeling. The SEA mutant SEA-F47S, L48S, Y92A, which is deficient in MHC class II alpha-chain binding, formed only dimers with HLA-DR1, whereas a second SEA mutant, SEA-H225A, which lacks high-affinity MHC class II beta-chain binding was incapable of forming any complexes. Thus SEA binding to its MHC receptor is a two-step process involving initial beta-chain binding followed by cooperative binding of a second SEA molecule to the class II alpha chain.
Synthesis and Physicochemical Characterization of the Impurities of Pemetrexed Disodium, an Anticancer Drug (2015)

A physicochemical characterization of the process-related impurities associated with the synthesis of pemetrexed disodium was performed. The possibility of pemetrexed impurities forming has been mentioned in literature, but no study on their structure has been published yet. This paper describes the development of the synthesis methods for these compounds and discusses their structure elucidation on the basis of two-dimensional NMR experiments and MS data. The identification of these impurities should be useful for the quality control during the production of the pemetrexed disodium salt.
Thrombospondin, a potentiator of tumor cell metastasis. (1987)

The platelet-secreted protein thrombospondin (TSP) potentiates tumor cell metastasis. Human TSP injected i.v. into mice 5 min prior to i.v. injection of T241 sarcoma cells potentiates lung tumor colony formation. Several lines of evidence suggest that the TSP-enhancing effect involves both TSP-mediated tumor cell adhesion and the host's hemostatic system: TSP potentiates the initial, rapid sequestering of tumor cells in the lung; TSP promotes the adhesion of tumor cells in vitro; the effect of TSP on tumor cell metastasis is dependent on the presence of platelets and a normal plasma clotting system, since TSP does not potentiate lung tumor colony formation in either thrombocytopenic mice or mice anticoagulated with Coumadin. Our results suggest a central role for TSP in the metastatic process.
Fixing human factor IX (fIX): correction of a cryptic RNA splice enables the production of biologically active fIX in the mammary gland of transgenic mice. (1995)

Transgenic mice and sheep secrete only low levels of human factor IX in their milk because of an aberrant splicing of the transgene RNA in the mammary gland. Removal of the cryptic 3' splice site prevents this splicing and leads to the production of relatively high levels of factor IX. The purified protein is fully active showing that the mammary gland is capable of the efficient post-translational modification of this protein and that transgenic animals are a suitable means of its production.
Online customization of teleoperation interfaces (2012)

In teleoperation, the user's input is mapped onto the robot via a motion retargetting function. This function must differ between robots because of their different kinematics, between users because of their different preferences, and even between tasks that the users perform with the robot. Our work enables users to customize this retargetting function, and achieve any of these required differences. In our approach, the robot starts with an initial function. As the user teleoperates the robot, he can pause and provide example correspondences, which instantly update the retargetting function. We select the algorithm underlying these updates by formulating the problem as an instance of online function approximation. The problem's requirements, as well as the semantics and constraints of motion retargetting, lead to an extension of Online Learning with Kernel Machines in which the width of the kernel can vary. Our central hypothesis is that this method enables users to train retargetting functions to good outcomes. We validate this hypothesis in a user study, which also reveals the importance of providing users with tools to verify their examples: much like an actor needs a mirror to verify his pose, a user needs to verify his input before providing an example. We conclude with a demonstration from an expert user that shows the potential of the method for achieving more sophisticated customization that makes particular tasks easier to complete, once users get expertise with the system.
Fantastic Voyages (2006)

This paper describes the use of nanotechnology in detection of disease at its earliest stage. Nanotechnology makes it possible to envision new devices that can deliver a 100-fold and even larger increase in sensitivity over current diagnostic techniques. Very small-scale diagnostic devices have been designed depending on the transduction mechanism—mechanical or electrical—of the biomedical stimulus. Devices that use nanocantilevers, nanowires, and nanoparticles have been built and tested, and are currently under development. The nanowire-based devices are nanometer-wide semiconductor wires coated with molecules arranged in parallel on the bottom of a microfluidic chamber where a blood sample is introduced for analysis. The binding event among the molecules on the wire and the biomarkers in the sample produces a change in the electrical conductivity of the wire that can be measured in real time and related to the amount of biomarkers in solution.
miR-192, a prognostic indicator, targets the SLC39A6/SNAIL pathway to reduce tumor metastasis in human hepatocellular carcinoma (2015)

Metastasis is one of the causes of cancer death. Functions and mechanisms of microRNAs (miRNAs) involved in hepatocellular carcinoma (HCC) metastasis are largely unknown. Here, a miRNA microarray analysis was performed in MHCC-97L, MHCC-97H and HCC-LM3 cells with gradually increasing metastatic potential to disclose crucial miRNAs involved in HCC metastasis. miR-192 expression decreased and negatively correlated with vascular invasion in HCC specimens. Gain and loss of function studies revealed that miR-192 significantly suppressed metastasis of HCC cells in vitro and in vivo. Solute carrier family 39 member 6 (SLC39A6) was identified as a direct and functional target of miR-192. In addition, SLC39A6 negatively correlated with miR-192 in HCC samples and promoted HCC cell migration and invasion. Moreover, miR-192 decreased SLC39A6 expression, subsequently downregulating SNAIL and upregulating E-cadherin expression. Suppression of migration and invasion caused by miR-192 overexpression was alleviated by exogenous Snail expression. Intriguingly, lower miR-192 expression and higher SLC39A6 expression significantly contributed to poorer outcomes in HCC patients. Multivariate analysis indicated that miR-192 was an independent and significant predictor of HCC patient overall survival. In conclusion, we newly determined that miR-192 targeted the SLC39A6/SNAIL pathway to reduce tumor metastasis in HCC cells. This axis provided insights into the mechanism underlying miRNA regulation of HCC metastasis and a novel therapeutic target for HCC treatment.
Mapping of a human T‐lymphotropic virus type I gag protein epitope that cross‐reacts with anti‐Plasmodium falciparum antibodies (1995)

Studies in Palawan, Philippines, and Irian Jaya, Indonesia, showed that indeterminate human T-lymphotropic virus type I (HTLV-I) Western blot immunoreactivity is due to cross-reacting anti-Plasmodium falciparum antibodies. To further define this immunoreactivity, mapping studies were conducted using the HTLV-I p19 protein to identify the precise epitope that reacts with these antibodies. Anti-P. falciparum antibody-positive sera from Palawan, Philippines, and Irian Jaya, Indonesia, were studied using overlapping synthetic peptides. Immunoreactivity was localized to residues 108-120 of p19. Further analysis of the sera with 5 biotinylated synthetic peptides showed that the cross-reactive epitope consists of the sequence PDSDPQI (amino acid residues 110-116), which was shown to be homologous to a 7 amino acid sequence on the Exp-1 protein of the P. falciparum blood stage parasite. This is the first study that identifies a specific HTLV-I protein epitope that cross-reacts with malaria antibodies.
SAR and B1 field distributions in a heterogeneous human head model within a birdcage coil (1998)

Calculations of radiofrequency magnetic (B1) field and specific energy absorption rate (SAR) distributions in a sphere of tissue and a multi-tissue human head model in a 12-element birdcage coil are presented. The coil model is driven in linear and quadrature modes at 63, 175, 200, and 300 MHz. Plots of B1 field magnitude and SAR distributions, average SAR, maximum local SAR, and measures of B1 field homogeneity and signal-to-noise ratio are given. SAR levels for arbitrary pulse sequences can be estimated from the calculated data. Maximum local SAR levels are lower at lower frequencies, in quadrature rather than in linear coils, and in linear fields oriented posterior-to-anterior rather than left-to-right in the head. It should be possible to perform many experiments in the head at frequencies up to 300 MHz without exceeding standard limits for local or average SAR levels.
A Method for Adjusting a Malpositioned Bifurcated Aortic Endograft (1998)

A technique is demonstrated for intra-aortic repositioning of a bifurcated stentgraft to correct insufficient deployment. If required, this technique should be attempted before conversion to an open procedure.
Variations on the fractal Sierpinski antenna flare angle (2002)

A further investigation on the fractal multiband Sierpinski antenna is introduced. It is shown that a variation on the antenna's flare angle is translated into a shift of the operating bands, as well as into a change in the impedance level and radiation patterns. The contribution of those variations to the truncation effect is outlined.
THE INFLUENCE OF ELECTROSTIMULATION ON HEXOBARBITAL INDUCED LOSS OF RIGHTING REFLEX IN RATS (1982)

Electrostimulation (ES) of slow (SF, 10 Hz) or fast (FF, 500 Hz) frequency decreases the sleeping time of rats anaesthetized by administration of acute doses of hexobarbital. When ES is applied via the ears, both SF and FF are equally efficient in reducing the loss of righting reflex (LRR), whereas if ES is applied peripherally via the paws, only FF decreases the acute narcosis time. Applied cranially, either continuous stimulation or administration of intermittent current (5 minutes on and off) were equally effective in reducing narcosis. A decreased period of 30 minutes' continuous stimulation will reduce sleeping time only if administered immediately after LRR. When restrained animals received ES for periods of up to 3 hours prior to administration of the barbiturate, the sleeping time of the stimulated and sham treated animals were not significantly different.
Nanofiber-Based Delivery of Therapeutic Peptides to the Brain (2013)

The delivery of therapeutic peptides and proteins to the central nervous system is the biggest challenge when developing effective neuropharmaceuticals. The central issue is that the blood-brain barrier is impermeable to most molecules. Here we demonstrate the concept of employing an amphiphilic derivative of a peptide to deliver the peptide into the brain. The key to success is that the amphiphilic peptide should by design self-assemble into nanofibers wherein the active peptide epitope is tightly wrapped around the nanofiber core. The nanofiber form appears to protect the amphiphilic peptide from degradation while in the plasma, and the amphiphilic nature of the peptide promotes its transport across the blood-brain barrier. Therapeutic brain levels of the amphiphilic peptide are achieved with this strategy, compared with the absence of detectable peptide in the brain and the consequent lack of a therapeutic response when the underivatized peptide is administered.
Flavonoid Apigenin Is an Inhibitor of the NAD+ase CD38 (2012)

Metabolic syndrome is a growing health problem worldwide. It is therefore imperative to develop new strategies to treat this pathology. In the past years, the manipulation of NAD(+) metabolism has emerged as a plausible strategy to ameliorate metabolic syndrome. In particular, an increase in cellular NAD(+) levels has beneficial effects, likely because of the activation of sirtuins. Previously, we reported that CD38 is the primary NAD(+)ase in mammals. Moreover, CD38 knockout mice have higher NAD(+) levels and are protected against obesity and metabolic syndrome. Here, we show that CD38 regulates global protein acetylation through changes in NAD(+) levels and sirtuin activity. In addition, we characterize two CD38 inhibitors: quercetin and apigenin. We show that pharmacological inhibition of CD38 results in higher intracellular NAD(+) levels and that treatment of cell cultures with apigenin decreases global acetylation as well as the acetylation of p53 and RelA-p65. Finally, apigenin administration to obese mice increases NAD(+) levels, decreases global protein acetylation, and improves several aspects of glucose and lipid homeostasis. Our results show that CD38 is a novel pharmacological target to treat metabolic diseases via NAD(+)-dependent pathways.
Microfilament-disrupting agents prevent the formation of apoptotic bodies in tumor cells undergoing apoptosis. (1992)

Apoptosis is a form of cell death in which the cell "participates," such that metabolic energy and often protein synthesis are required for the death to occur. Once begun, the process of apoptosis proceeds in an ordered fashion. In the earliest phase DNA fragmentation occurs, accompanied by cell shrinkage and dilation of the endoplasmic reticulum. This is followed by cell fragmentation with the formation of sealed membrane vesicles, termed apoptotic bodies. In the present study we have demonstrated that the fungal metabolite cytochalasin B inhibits cell fragmentation and the formation of apoptotic bodies, probably by its ability to interfere with actin polymerization. This effect was seen when HL-60 cells were pretreated with cytochalasin B and then exposed to one of a number of apoptosis-inducing agents, including UV irradiation, camptothecin, aphidocholin, or PMA plus ionomycin. The observed effect was not peculiar to HL-60 cells, inasmuch as it was also seen for both Molt-4 and U-937 cell lines. Cytochalasin B had no effect on DNA fragmentation occurring in the earliest stage of apoptosis, and it appeared to have no inhibitory effects on nuclear fragmentation. Staurosporin had an effect similar to that seen with cytochalasin B, probably due to its ability to inhibit protein kinase C, which is a known potentiator of microfilament assembly. These data demonstrate that microfilament assembly is necessary for the formation of apoptotic bodies in the later stages of the apoptotic process.
Changes in Tight Junctional Resistance of the Cervical Epithelium Are Associated with Modulation of Content and Phosphorylation of Occludin 65-Kilodalton and 50-Kilodalton Forms (2005)

Treatment of human cervical epithelial CaSki cells with ATP or with the diacylglyceride sn-1,2-dioctanoyl diglyceride (diC8) induced a staurosporine-sensitive transient increase, followed by a late decrease, in tight-junctional resistance (R(TJ)). CaSki cells express two immunoreactive forms of occludin, 65 and 50 kDa. Treatments with ATP and diC8 decreased the density of the 65-kDa form and increased the density of the 50-kDa form. ATP also decreased threonine phosphorylation of the 65-kDa form and increased threonine phosphorylation of the 50-kDa form and tyrosine phosphorylation of the 65- and 50-kDa forms. Staurosporine decreased acutely threonine and tyrosine phosphorylation of the two isoforms and in cells pretreated with staurosporine ATP increased acutely the density of the 65-kDa form and threonine phosphorylation of the 65-kDa form. Treatment with N-acetyl-leucinyl-leucinyl-norleucinal increased the densities of the 65- and 50-kDa forms. Pretreatment with N-acetyl-leucinyl-leucinyl-norleucinal attenuated the late decreases in R(TJ) induced by ATP and diC8 and the decrease in the 65-kDa and increase in the 50-kDa forms induced by ATP. Correlation analyses showed that high levels of R(TJ) correlated with the 65-kDa form, whereas low levels of R(TJ) correlated negatively with the 65-kDa form and positively with the 50-kDa form. The results suggest that in CaSki cells 1) occludin determines gating of the tight junctions, 2) changes in occludin phosphorylation status and composition regulate the R(TJ), 3) protein kinase-C-mediated, threonine dephosphorylation of the 65-kDa occludin form increases the resistance of assembled tight junctions, 4) the early stage of tight junction disassembly involves calpain-mediated breakdown of occludin 65-kDa form to the 50-kDa form, and 5) increased levels of the 50-kDa form interfere with occludin gating of the tight junctions.
Molecular Pathways: Sterols and Receptor Signaling in Cancer (2013)

Accelerated cholesterol and lipid metabolism are the hallmarks of cancer and contribute to malignant transformation due to the obligatory requirement for cholesterol for the function of eukaryotic membranes. To build new membranes and maintain active signaling, cancer cells depend on high intensity of endogenous cholesterol biosynthesis and uptake of lipid particles. This metabolic dependency of cancer cells on cholesterol and other lipids is tightly regulated by the cholesterol homeostasis network, including (i) sterol response element-binding proteins (SREBP), master transcriptional regulators of cholesterol and fatty acid pathway genes; (ii) nuclear sterol receptors (liver X receptors, LXR), which coordinate growth with the availability of cholesterol; and (iii) lipid particle receptors, such as low-density lipid particle (LDL) receptor, providing exogenous sterol and lipids to cancer cells. In addition, activity of oncogenic receptors, such as MUC1 or EGFR, accelerates sterol uptake and biosynthesis. Therefore, a general strategy of reducing the cholesterol pool in cancer cells is challenged by the highly efficient feedback loops compensating for a blockade at a single point in the cholesterol homeostatic network. Besides the well-established structural role of cholesterol in membranes, recent studies have uncovered potent biologic activities of certain cholesterol metabolic precursors and its oxidized derivatives, oxysterols. The former, meiosis-activating sterols, exert effects on trafficking and signaling of oncogenic EGF receptor (EGFR). Cholesterol epoxides, the highly active products of cholesterol oxidation, are being neutralized by the distal sterol pathway enzymes, emopamyl-binding protein (EBP) and dehydrocholesterol-7 reductase (DHCR7). These recently discovered "moonlighting" activities of the cholesterol pathway genes and metabolites expand our understanding of the uniquely conserved roles these sterol molecules play in the regulation of cellular proliferation and in cancer.
Structural evolution of layered Li1.2Ni0.2Mn0.6O2 upon electrochemical cycling in a Li rechargeable battery (2010)

Recently Li1.2Ni0.2Mn0.6O2, one of the most promising cathode candidates for next generation Li rechargeable batteries, has been consistently investigated especially because of its high lithium storage capacity, which exceeds beyond the theoretical capacity based on conventional chemical concepts. Yet the mechanism and the origin of the overcapacity have not been clearly understood. Previous reports on simultaneous oxygen evolution during the first delithiation may only explain the high capacity of the first charge process, and not of the subsequent cycles. In this work, we report a clarified interpretation of the structural evolution of Li1.2Ni0.2Mn0.6O2 upon the electrochemical cycling, which is the key element in understanding its anomalously high capacity, through careful study of electrochemical profiles, exsitu X-ray diffraction, HR-TEM, Raman spectroscopy, and first principles calculation. Moreover, we successfully resolved the intermediate states of structural evolution upon electrochemical cycles by intentionally synthesizing sample with large particle size. All observations made through various tools lead to the result that spinel-like cation arrangement and lithium environment are gradually created and locally embedded in layered framework during repeated electrochemical cycling. Moreover, through analyzing the intermediate states of the structural transformation, this gradual structural evolution could explain the mechanism of the continuous development of the electrochemical activity below 3.5 V and over 4.25 V.