gebhart/patrepeval huggingface dataset:
High mobility group protein-1 (HMG-1) is a unique activator of p53 (1998)

The binding of p53 protein to DNA is stimulated by its interaction with covalent as well as noncovalent modifiers. We report the identification of a factor from HeLa nuclear extracts that activates p53 DNA binding. This factor was purified to homogeneity and identified as the high mobility group protein, HMG-1. HMG-1 belongs to a family of highly conserved chromatin-associated nucleoproteins that bend DNA and facilitate the binding of various transcription factors to their cognate DNA sequences. We demonstrate that recombinant His-tagged HMG-1 enhances p53 DNA binding in vitro and also that HMG-1 and p53 can interact directly in vitro. Unexpectedly, HMG-1 also stimulates DNA binding by p53Delta30, a carboxy-terminally deleted form of the protein that is considered to be constitutively active, suggesting that HMG-1 stimulates p53 by a mechanism that is distinct from other known activators of p53. Finally, using transient transfection assays we show that HMG-1 can increase p53 and p53Delta30-mediated transactivation in vivo. HMG-1 promotes the assembly of higher order p53 nucleoprotein structures, and these data, along with the fact that HMG-1 is capable of bending DNA, suggest that HMG-1 may activate p53 DNA binding by a novel mechanism involving a structural change in the target DNA.
InLoc: Indoor Visual Localization with Dense Matching and View Synthesis (2018)

We seek to predict the 6 degree-of-freedom (6DoF) pose of a query photograph with respect to a large indoor 3D map. The contributions of this work are three-fold. First, we develop a new large-scale visual localization method targeted for indoor environments. The method proceeds along three steps: (i) efficient retrieval of candidate poses that ensures scalability to large-scale environments, (ii) pose estimation using dense matching rather than local features to deal with textureless indoor scenes, and (iii) pose verification by virtual view synthesis to cope with significant changes in viewpoint, scene layout, and occluders. Second, we collect a new dataset with reference 6DoF poses for large-scale indoor localization. Query photographs are captured by mobile phones at a different time than the reference 3D map, thus presenting a realistic indoor localization scenario. Third, we demonstrate that our method significantly outperforms current state-of-the-art indoor localization approaches on this new challenging data.
Time-stretched ADC arrays (2002)

This brief analyzes the performance of a new type of analog-to-digital converters (ADCs) architecture. The approach contemplates stretching the analog signal in time prior to digitization. Its benefits include an increase in the effective sampling rate and the input bandwidth, and a reduction in the sampling-jitter noise of the digitizer. It builds on the recent demonstration of high-speed analog-to-digital (A/D) conversion where a photonic preprocessor was used to successfully stretch an analog electrical signal before electronic digitization. The brief considers parallel time stretch ADC arrays capable of processing continuous time signals. In particular the effects of interchannel offset and gain mismatch, and clock skew are described and are contrasted with those in a conventional time-interleaved system. A mode of operation unique to this system is outlined wherein interchannel mismatch errors are entirely avoided at the expense of resolution bandwidth.
Cellular and molecular derangements in acute tubular necrosis (2005)

The cellular and molecular tools of modern science have provided critical new insights into the roles of apoptosis, oxidant and iron-mediated injury, endothelial changes, regeneration, and the inflammatory response in the pathogenesis of acute tubular necrosis. Novel strategies that modulate these pathways hold tremendous promise for the proactive treatment of human acute renal failure.
Tyrosine phosphorylation of paxillin and pp125FAK accompanies cell adhesion to extracellular matrix: a role in cytoskeletal assembly. (1992)

Cells in culture reveal high levels of protein tyrosine phosphorylation in their focal adhesions, the regions where cells adhere to the underlying substratum. We have examined the tyrosine phosphorylation of proteins in response to plating cells on extracellular matrix substrata. Rat embryo fibroblasts, mouse Balb/c 3T3, and NIH 3T3 cells plated on fibronectin-coated surfaces revealed elevated phosphotyrosine levels in a cluster of proteins between 115 and 130 kD. This increase in tyrosine phosphorylation was also seen when rat embryo fibroblasts were plated on laminin or vitronectin, but not on polylysine or on uncoated plastic. Integrin mediation of this effect was suggested by finding the same pattern of elevated tyrosine phosphorylation in cells plated on the cell-binding fragment of fibronectin and in cells plated on a synthetic polymer containing multiple RGD sequences. We have identified one of the proteins of the 115-130-kD cluster as pp125FAK, a tyrosine kinase recently localized in focal adhesions (Schaller, M. D., C. A. Borgman, B. S. Cobb, R. R. Vines, A. B. Reynolds, and J. T. Parsons. 1992. Proc. Natl. Acad. Sci. USA. 89:5192). A second protein that becomes tyrosine phosphorylated in response to extracellular matrix adhesion is identified as paxillin, a 70-kD protein previously localized to focal adhesions. Treatment of cells with the tyrosine kinase inhibitor herbimycin A diminished the adhesion-induced tyrosine phosphorylation of these proteins and inhibited the formation of focal adhesions and stress fibers. These results suggest a role for integrin-mediated tyrosine phosphorylation in the organization of the cytoskeleton as cells adhere to the extracellular matrix.
Canine Model of Esophageal Injury and Atrial-Esophageal Fistula After Applications of Forward-Firing High-Intensity Focused Ultrasound and Side-Firing Unfocused Ultrasound in the Left Atrium and Inside the Pulmonary Vein (2008)

This model produces esophageal ulcer when Eso-temp is >or=50 degrees C. Eso-temp is higher with HIFU/SFU applications closer to the esophagus and with HIFU/SFU applications inside the PV. Ulcer progression and left atrial-esophageal fistula were associated with reflux esophagitis.
Perispinal TNF-alpha inhibition for discogenic pain (2003)

TNF inhibition by etanercept delivered by perispinal administration may offer clinical benefit for patients with chronic, treatment-resistant discogenic pain. Further study of this new treatment modality is warranted.
Dual action of cyclin-dependent kinase inhibitors: induction of cell cycle arrest and apoptosis. A comparison of the effects exerted by roscovitine and cisplatin. (2004)

Cyclin-dependent kinases (CDKs) have recently raised considerable interest in view of their key role in the regulation of the cell cycle progression. In proliferating cells, distinct CDKs associated with specific cyclins coordinate in an orchestrated way the appropriate transition between different phases of the cell cycle. Mutations and/or aberrant expression of distinct CDKs and their regulatory components lead to uncontrolled proliferation and finally to carcinogenesis. However, in post-mitotic neurons, all CDKs with the exception of CDK5 are silent. CDK5, a proline-directed serine/threonine kinase exhibiting a close structural homology to the mitotic CDKs, binds to p35, the neuron-specific regulatory subunit of CDK5. CDK5 is very abundant in mature neurons and seems to regulate neurotransmitter release through phosphorylation and down-regulation of calcium channel activity. Therefore, the inhibition of CDKs in neurons after oxidative stress and in neurodegenerative disorders has a protective action. Selective CDKs inhibitors were developed as promising drugs for cancer therapy due to their ability to arrest cell cycle progression. The aim of this study was to compare the anti-proliferative effect of roscovitine (ROSC), a potent CDKs inhibitor, with that of cisplatin (CP) on human breast cancer MCF-7 cells. ROSC exerted stronger inhibitory effect on proliferation and cell cycle progression of MCF-7 than CP. Accumulation of G(2)/M arrested cells starting 6 h after onset of ROSC treatment coincided with a strong up-regulation of the p53. Reconstitution with caspase-3 sensitized MCF-7 cells to CP action. It implicates that ROSC inhibits more selectively and efficaciously the proliferation of human breast carcinoma cells.
The anorectic hormone amylin contributes to feeding-related changes of neuronal activity in key structures of the gut-brain axis (2004)

Amylin is a peptide hormone that is cosecreted with insulin from the pancreas during and after food intake. Peripherally injected amylin potently inhibits feeding by acting on the area postrema (AP), a circumventricular organ lacking a functional blood-brain barrier. We recently demonstrated that AP neurons are excited by a near physiological concentration of amylin. However, the subsequent neuronal mechanisms and the relevance of endogenously released amylin for the regulation of food intake are poorly understood. Therefore, we investigated 1) amylin's contribution to feeding-induced c-Fos expression in the rat AP and its ascending projection sites, and 2) amylin's ability to reverse fasting-induced c-Fos expression in the lateral hypothalamic area (LHA). Similar to amylin (20 microg/kg sc), refeeding of 24-h food-deprived rats induced c-Fos expression in the AP, the nucleus of the solitary tract, the lateral parabrachial nucleus, and the central nucleus of the amygdala. In AP-lesioned rats, the amylin-induced c-Fos expression in each of these sites was blunted, indicating an AP-mediated activation of these structures. Pretreatment with the amylin antagonist AC-187 (1 mg/kg sc) inhibited feeding-induced c-Fos expression in the AP. Food deprivation activated LHA neurons, a response known to be associated with hunger. This effect was reversed within 2 h after refeeding and also in nonrefed animals that received amylin. In summary, our data provide the first evidence that feeding-induced amylin release activates AP neurons projecting to subsequent relay stations known to transmit meal-related signals to the forebrain. Activation of this pathway seems to coincide with an inhibition of LHA neurons.
Study of patients diagnosed with advanced HIV in the HAART era – OMEGA Cohort (2005)

Our objective is to analyse patients diagnosed with late-stage HIV infection in the highly active antiretroviral therapy (HAART) area. A prospective, observational study of all patients with an initial CD4 < 50 x 10(6)/L was carried out. Epidemiological, clinical and HAART-associated data were analysed. Survival rates were estimated and pairs of survival curves were compared. The statistical program used was SPSS (version 10). In all, 349 HIV-infected patients were diagnosed, 117 (33.5%) had late-stage disease, mean CD4 23.9 x 10(6)/L and mean viral load (VL) 5.38 log10. In 98 men, mean age 39.5 years, percentage of AIDS cases at their first attendance was 83.8%. The median follow-up period was 28 months and 27 died. Pneumocystis carinii was the most frequent cause of AIDS (24.4%) and death (18.5%). Survival rates at 12, 24 and 36 months were 95.6%, 85.8% and 72.4%. HAART was started in 82.1%. VLs < 50 copies/mL at one, two and three years of treatment were 55.2%, 55.7% and 58.0%. Resource utilization included 0.58 hospitalization/patient/year and 0.07 events/patient/year. HAART-related complications were as follows: 50% lipodystrophy, 9.7% hypertension, 22.2% hyperglycaemia, 26.4% hypercholesterolaemia, 31.9% hypertrygliceridaemia and 18.1% mixed hyperlipaemia. Over one-third of our patients have advanced HIV infection at diagnosis. However, the outcome is favourable, with a good immunovirological response and few new opportunistic events. HAART-related complications were frequent.
Nanosecond, high‐intensity pulsed electric fields induce apoptosis in human cells (2003)

Electroporation by using pulsed electric fields with long durations compared with the charging time of the plasma membrane can induce cell fusion or introduce xenomolecules into cells. Nanosecond pulse power technology generates pulses with high-intensity electric fields, but with such short durations that the charging time of the plasma membrane is not reached, but intracellular membranes are affected. To determine more specifically their effects on cell structure and function, human cells were exposed to high intensity (up to 300 kV/cm) nanosecond (10-300 ns) pulsed electric fields (nsPEF) and were analyzed at the cellular and molecular levels. As the pulse duration decreased, plasma membrane electroporation decreased and appearances of apoptosis markers were delayed. NsPEF induced apoptosis within tens of minutes, depending on the pulse duration. Annexin-V binding, caspase activation, decreased forward light scatter, and cytochrome c release into the cytoplasm were coincident. Apoptosis was caspase- and mitochondria-dependent but independent of plasma membrane electroporation and thermal changes. The results suggest that with decreasing pulse durations, nsPEF modulate cell signaling from the plasma membrane to intracellular structures and functions. NsPEF technology provides a unique, high-power, energy-independent tool to recruit plasma membrane and/or intracellular signaling mechanisms that can delete aberrant cells by apoptosis.
STRUCTURE AND PHYSIOLOGIC FUNCTION OF THE LOW-DENSITY LIPOPROTEIN RECEPTOR (2005)

The low-density lipoprotein receptor (LDLR) is responsible for uptake of cholesterol-carrying lipoprotein particles into cells. The receptor binds lipoprotein particles at the cell surface and releases them in the low-pH environment of the endosome. The focus of the current review is on biochemical and structural studies of the LDLR and its ligands, emphasizing how structural features of the receptor dictate the binding of low-density lipoprotein (LDL) and beta-migrating forms of very low-density lipoprotein (beta-VLDL) particles, how the receptor releases bound ligands at low pH, and how the cytoplasmic tail of the LDLR interfaces with the endocytic machinery.
CD43 (Sialophorin, Leukosialin) Shedding is an Initial Event During Neutrophil Migration, which Could be Closely Related to the Spreading of Adherent Cells (1998)

Leukosialin is a negatively-charged mucin-like membrane protein of leukocytes. This anti-adhesive molecule prevents uncontrolled cellular interactions and is proteolytically cleaved during neutrophil activation. CD43 is shed in vivo during neutrophil migration to the inflammatory site. We have analysed the decrease in CD43 expression during in vitro adherence of TNF-alpha activated PMN. CD43 was quantitated by flow cytometry on TNF-alpha-activated PMN either maintained in suspension or allowed to adhere then detached with EDTA. Although TNF did not induce significant modification of CD43 expression on suspended cells, we showed that 40% of membrane CD43 is released during neutrophil TNF-induced adhesion to serum-coated plates or endothelial cells, and that migration through the endothelial monolayer did not result in further shedding. Adhesion-blocking anti-beta 2 integrin mAbs prevented CD43 shedding. beta 2 integrin "activation" by anti-CD 18 mAbs or Mn ions did not decrease CD43 expression if adhesion was prevented by stirring. Inhibitors of signal transduction or of cytoskeleton association, which allowed cells to adhere but not to spread, inhibited the shedding of CD43 during adhesion. We conclude that CD43 shedding is not promoted by beta 2 integrins engagement or adhesion but is concomitant with spreading of adherent cells.
Mixotrophy among Dinoflagellates1 (1999)

Mixotrophy, used herein for the combination of phototrophy and phagotrophy, is widespread among dinoflagellates. It occurs among most, perhaps all, of the extant orders, including the Prorocentrales, Dinophysiales. Gymnodiniales, Noctilucales, Gonyaulacales, Peridiniales, Blastodiniales. Phytodiniales, and Dinamoebales. Many cases of mixotrophy among dinoflagellates are probably undocumented. Primarily photosynthetic dinoflagellates with their “own” plastids can often supplement their nutrition by preying on other cells. Some primarily phagotrophic species are photosynthetic due to the presence of kleptochloroplasts or algal endosymbionts. Some parasitic dinoflagellates have plastids and are probably mixotrophic. For most mixotrophic dinoflagellates, the relative importance of photosynthesis, uptake of dissolved inorganic nutrients, and feeding are unknown. However, it is apparent that mixotrophy has different functions in different physiological types of dinoflagellates. Data on the simultaneous regulation of photosynthesis, assimilation of dissolved inorganic and organic nutrients, and phagotophy by environmental parameters (irradiance. availablity of dissolved nutrients, availability of prey) and by life history events are needed in order to understand the diverse roles of mixotrophy in dinoflagellates.
Ectopic Production of MDA-7/IL-24 Inhibits Invasion and Migration of Human Lung Cancer Cells (2004)

We have previously observed the suppression of lung tumor growth in response to overexpression of melanoma differentiation-associated gene-7 (MDA-7)/interleukin-24 (IL-24; approved gene symbol IL24) in vitro and in vivo. MDA-7/IL-24 exerts its tumor-suppressive effects by multiple mechanisms, including the activation of the caspase cascade and the inhibition of angiogenesis. In this study, we used an adenoviral vector (Ad-mda7) to examine the effect of the ectopic production of MDA-7/IL-24 on cell migration and invasion by human non-small-cell lung carcinoma cells. Lung tumor cells (H1299 and A549) treated in vitro with Ad-mda7 migrated and invaded less than cells treated with phosphate-buffered saline (PBS) or Ad-Luc (vector control). MDA-7/IL-24 inhibited migration and invasion by down-regulating the production of phosphatidylinositol 3-kinase/protein kinase B, focal adhesion kinase, and matrix metalloproteinase-2 and -9 relative to PBS and Ad-Luc. Furthermore, tumor cells treated with Ad-mda7 ex vivo or with DOTAP:Chol-mda7 complex in vivo formed significantly fewer tumors in an experimental lung metastasis model. These results show that MDA-7/IL-24 inhibits invasion and migration by lung cancer cells by down-regulating proteins associated with these processes, resulting in reduced metastasis. Thus, Ad-mda7 should be considered a therapeutic agent that can inhibit primary tumor growth and prevent metastasis.
Effect of Heat Treatment upon the Electrical Properties of Silicon Crystals (1957)

Studies have been made of the process in which donors are introduced into silicon by heating in the temperature range 300°–500°C and are caused to disappear on heating at higher temperature. This phenomena is shown to depend on the conditions of growth and the heat-treatment history of the crystal. Evidence is summarized which shows that oxygen is the impurity from which the donors are formed. The characteristics of the processes involved are described and possible mechanisms are discussed.
Cloning and Characterization of a Novel Protein Kinase That Impairs Osteoblast Differentiation in Vitro (2001)

The bone morphogenic proteins (BMPs) play a key role in skeletal development and patterning. Using the technique of differential display polymerase chain reaction (ddPCR), we have identified a novel gene whose expression is increased during BMP-2-induced differentiation of the prechondroblastic cell line, MLB13MYC clone 17, to an osteoblastic phenotype. The 6.5-kilobase mRNA recognized by this ddPCR product is increased 10-fold by BMP-2 treatment of the MLB13MYC clone 17 cells. The mRNA recognized by this ddPCR product is also increased as MC3T3-E1 cells recapitulate the program of osteoblast differentiation during prolonged culture. The full-length transcript corresponding to this ddPCR product was cloned from a MLB13MYC clone 17 cell cDNA library. Analysis of the deduced amino acid sequence demonstrated that this gene encodes a novel 126-kDa putative serine/threonine protein kinase containing a nuclear localization signal. The kinase domain, expressed in Escherichia coli, is capable of autophosphorylation as well as phosphorylation of myelin basic protein. The gene was, therefore, named BIKe (BMP-2-Inducible Kinase). The BIKe nuclear localization signal is able to direct green fluorescent protein to the nucleus in transfected COS-7 cells. When stably expressed in MC3T3-E1 cells, BIKe significantly decreases alkaline phosphatase activity and osteocalcin mRNA levels and retards mineral deposition relative to vector control. This novel kinase, therefore, is likely to play an important regulatory role in attenuating the program of osteoblast differentiation.
MACI - a new era? (2011)

Full thickness articular cartilage defects have limited regenerative potential and are a significant source of pain and loss of knee function. Numerous treatment options exist, each with their own advantages and drawbacks. The goal of this review is to provide an overview of the problem of cartilage injury, a brief description of current treatment options and outcomes, and a discussion of the current principles and technique of Matrix-induced Autologous Chondrocyte Implantation (MACI). While early results of MACI have been promising, there is currently insufficient comparative and long-term outcome data to demonstrate superiority of this technique over other methods for cartilage repair.
Fibroblast Growth Factor 21 Analogs for Treating Metabolic Disorders (2015)

Fibroblast growth factor (FGF) 21 is a member of the endocrine FGF subfamily. FGF21 expression is induced under different disease conditions, such as type 2 diabetes, obesity, chronic kidney diseases, and cardiovascular diseases, and it has a broad spectrum of functions in regulating various metabolic parameters. Many different approaches have been pursued targeting FGF21 and its receptors to develop therapeutics for treating type 2 diabetes and other aspects of metabolic conditions. In this article, we summarize some of these key approaches and highlight the potential challenges in the development of these agents.
Synthesis and Mechanistic Study of Palladium Nanobars and Nanorods (2007)

This paper describes a simple and versatile method for growing highly anisotropic nanostructures of Pd, single-crystal nanobars bounded by {100} facets and single-crystal nanorods with their side surfaces enclosed by {100} and {110} facets. According to thermodynamic arguments, Pd atoms should nucleate and grow in a solution phase to form cuboctahedrons of spherical shape with their surfaces bounded by a mix of {111} and {100} facets. Anisotropic nanostructures can only form under kinetically controlled conditions, while the cubic symmetry is broken. In the present system, we found that one-dimensional growth could be induced and maintained through an interplay of the following processes: (i) speedy reduction of the precursor to ensure prompt addition of atoms to the seed; (ii) chemisorption of bromide on the seed to promote the formation of {100} and {110} facets; and (iii) localized oxidative etching on one specific face of the seed to initiate preferential growth on this face. Experimentally, the anisotropic growth can be achieved by varying the type and concentration of reducing agent, as well as by adjusting the reaction temperature. This methodology developed for Pd has also been extended to both Au and Pt. As expected for a kinetically controlled product, the anisotropic nanostructure evolved into the thermodynamically favored shape during an aging process.