gebhart/patrepeval huggingface dataset:
Augmenting the mouse with pressure sensitive input (2007)

In this paper we investigate the use of a uni-pressure and dual-pressure augmented mouse. With a pressure augmented mouse users can simultaneously control cursor positions as well as multiple levels of discrete selection modes for common desktop application tasks. Two or more independent pressure sensors can be mounted onto several locations on the body of the mouse. To highlight the design potential of a pressure augmented mouse we conducted a multi-part study. In the first part we identified the number of maximum discrete levels controllable with a uni-pressure augmented mouse, the most appropriate locations for installing pressure sensors on the mouse, and the design of new interaction techniques to support selection with pressure-based input. In a follow-up design we introduced an additional sensor and two different types of selection techniques to control a larger number of discrete levels with two pressure sensors. Our results show that users can comfortably control up to 64 modes with a dual-pressure augmented mouse. We discuss the findings of our results in the context of several desktop interaction techniques and identify several design recommendations.
Effects of Ag Doping on the Photoluminescence of ZnO Films Grown on Si Substrates (2005)

Silver (Ag) doped and undoped ZnO films were grown on Si (100) substrates by the sol-gel process. Photoluminescence (PL) of two kinds of samples as a function of the excitation intensity has been measured, and PL intensities have been fitted by a power law. It is found that Ag doping increases the intensity of free emission from ZnO and does not change the position and the full width at half-maximum of the free exciton emission. In PL spectra of two kinds of samples under various excitation powers, no visible emission bands related to the deep levels were observed. These results reveal that doped Ag in ZnO films only enhances emission efficiency from free exciton recombination, not giving rise to new emissions.
Identification of novel protein tyrosine phosphatases of hematopoietic cells by polymerase chain reaction amplification (1991)

Polymerase chain reaction (PCR) conditions were used to amplify cDNAs that encode putative protein tyrosine phosphatases (PTPs) from a murine interleukin-3-dependent myeloid cell line. Primers for the reactions were based on conserved sequences of the catalytic domain that are shared among all known PTPs. Sequencing of 100 PCR-amplified cDNA clones identified seven different cDNA sequences. Two of these sequences were identical to the murine PTP genes Ly5/CD45/LCA and LRP/R- PTP-alpha. Two of the cDNA sequences were 95% identical to human PTP epsilon (HPTP epsilon) and rat brain PTP (PTP1B), respectively, and are likely to represent their murine homologs. Three of the cDNA sequences encoded novel potential PTPs. One of the putative PTPs was ubiquitously expressed while a second was predominantly expressed in brain, kidney, and liver and at much lower levels in a variety of other cell tkpes and tissues. The third novel putative phosphatase was expressed primarily in hematopoietic cells and tissues in a pattern that was comparable with Ly5/CD45/LCA. Further characterization of these novel PTPs will provide insights into the growth regulation of hematopoietic cells.
The role of the eaeA gene in diarrhea and neurological complications in a gnotobiotic piglet model of enterohemorrhagic Escherichia coli infection (1995)

We reported previously that mutation of the chromosomal gene eaeA from enterohemorrhagic Escherichia coli (EHEC) serotype O157:H7 prevented bacterial attachment in vivo. Attachment was restored when the EHEC or enteropathogenic E. coli (EPEC) eaeA gene was introduced into the mutant on a plasmid. In this communication we have compared in gnotobiotic piglets the pathogenicities of wild-type O157:H7 strain 86-24 and its eaeA mutant UMD619 with those of the two plasmid-complemented strains expressing IntiminO157 (EHEC) and IntiminO127 (EPEC). 86-24 colonized the surface and glandular epithelium of the large intestine and induced diarrhea, while UMD619 did not colonize any intestinal site and induced little or no diarrhea. Surprisingly, strain UMD619 expressing IntiminO127 behaved in pigs more like EPEC than EHEC strains; it colonized the distal half of the small intestine and the surface of the large intestine, inducing serious diarrhea. In contrast, strain UMD619 expressing IntiminO157 colonized the colon extremely poorly, inducing little or no diarrhea. While only the two strains causing extensive attachment--86-24 and UMD619 expressing IntiminO127--induced diarrhea, neurological symptoms attributed to Shiga-like toxin II occurred equally in all four groups of animals. The intimate bacterial attachment and mucosal damage were not a prerequisite for Shiga-like toxin II translocation from the gut lumen into the circulation. IntiminO127 appears not only to facilitate intimate attachment to cells but also to influence the site of intestinal colonization and other characteristics of EPEC infection.
SGN-CD33A: a novel CD33-targeting antibody–drug conjugate using a pyrrolobenzodiazepine dimer is active in models of drug-resistant AML (2013)

Outcomes in acute myeloid leukemia (AML) remain unsatisfactory, and novel treatments are urgently needed. One strategy explores antibodies and their drug conjugates, particularly those targeting CD33. Emerging data with gemtuzumab ozogamicin (GO) demonstrate target validity and activity in some patients with AML, but efficacy is limited by heterogeneous drug conjugation, linker instability, and a high incidence of multidrug resistance. We describe here the development of SGN-CD33A, a humanized anti-CD33 antibody with engineered cysteines conjugated to a highly potent, synthetic DNA cross-linking pyrrolobenzodiazepine dimer via a protease-cleavable linker. The use of engineered cysteine residues at the sites of drug linker attachment results in a drug loading of approximately 2 pyrrolobenzodiazepine dimers per antibody. In preclinical testing, SGN-CD33A is more potent than GO against a panel of AML cell lines and primary AML cells in vitro and in xenotransplantation studies in mice. Unlike GO, antileukemic activity is observed with SGN-CD33A in AML models with the multidrug-resistant phenotype. Mechanistic studies indicate that the cytotoxic effects of SGN-CD33A involve DNA damage with ensuing cell cycle arrest and apoptotic cell death. Together, these data suggest that SGN-CD33A has CD33-directed antitumor activity and support clinical testing of this novel therapeutic in patients with AML.
Fungitoxic Activity of Essential Oil Components on Food Storage Fungi (1989)

Click to increase image sizeClick to decrease image sizeKey Words: anetholcarvacrolcinnamaldehydeeugenolsafroleRhizopusMucorAspergillus
<title>Dynamic vision for precise depth measurement and robot control</title> (1993)

Dynamic vision is a powerful and effective sensing modality for a broad variety of numerous industrial applications. Two of them will be introduced as examples. One, relates to a novel implementation of motion stereo allowing precise distance measurements by a moving robot in real time with an uncalibrated camera. The other, behavior-based navigation, allows a robot to accomplish a desired navigation task by activation of an appropriate sequence of system- immanent behavior patterns.
REGULATION OF DENDRITIC CELL RECRUITMENT BY CHEMOKINES (2002)

Dendritic cells (DC) are a heterogeneous family of cells that function as sentinels of the immune system. This article summarizes observations suggesting that inflammatory chemokines secreted at the site of pathogen invasion determine the DC subset recruited and influence the class of the immune response initiated. Langerhans cells are selectively recruited by MIP-3alpha/CCL20. In contrast, CCR7 ligands have a key role in the accumulation of antigen-loaded mature DC in T cell-rich areas of the draining lymph node. Improved understanding of the regulation of DC trafficking might offer new opportunities for therapeutic interventions to control immune responses.
Prenatal Determination of Fetal RhD Type by DNA Amplification (1993)

Determining fetal RhD type in amniotic cells without invading the fetomaternal circulation is a reliable method that will be valuable in the management of Rh alloimmunization.
Coagulase-negative staphylococci isolated from two cases of toxic shock syndrome lack superantigenic activity, but induce cytokine production (1996)

Two strains of Staphylococcus epidermidis isolated from patients with toxic shock symptoms have been reported to carry genes related to S. aureus enterotoxins B and C by dot-blot hybridisation, although the corresponding superantigenic toxins were not detected immunologically. We here show that these strains produce no superantigens capable of stimulating proliferation of human mononuclear leukocytes or rabbit splenocytes, and that no DNA homologous to the seb or sec genes can be detected by PCR. However, stimulation of human monocytes by whole killed bacteria induced dose-dependent production of the cytokines TNF alpha, IL-1 beta and IL-6, which may be responsible for the clinical symptoms in these patients.
Multiple defects in Escherichia coli mutants lacking HU protein (1989)

The HU protein isolated from Escherichia coli, composed of two partially homologous subunits, alpha and beta, shares some of the properties of eucaryotic histones and is a major constituent of the bacterial nucleoid. We report here the construction of double mutants totally lacking both subunits of HU protein. These mutants exhibited poor growth and a perturbation of cell division, resulting in the formation of anucleate cells. In the absence of HU, phage Mu was unable to grow, to lysogenize, or to carry out transposition.
Functional delivery of viral miRNAs via exosomes (2010)

Noncoding regulatory microRNAs (miRNAs) of cellular and viral origin control gene expression by repressing the translation of mRNAs into protein. Interestingly, miRNAs are secreted actively through small vesicles called “exosomes” that protect them from degradation by RNases, suggesting that these miRNAs may function outside the cell in which they were produced. Here we demonstrate that miRNAs secreted by EBV-infected cells are transferred to and act in uninfected recipient cells. Using a quantitative RT-PCR approach, we demonstrate that mature EBV-encoded miRNAs are secreted by EBV-infected B cells through exosomes. These EBV-miRNAs are functional because internalization of exosomes by MoDC results in a dose-dependent, miRNA-mediated repression of confirmed EBV target genes, including CXCL11/ITAC , an immunoregulatory gene down-regulated in primary EBV-associated lymphomas. We demonstrate that throughout coculture of EBV-infected B cells EBV-miRNAs accumulate in noninfected neighboring MoDC and show that this accumulation is mediated by transfer of exosomes. Thus, the exogenous EBV-miRNAs transferred through exosomes are delivered to subcellular sites of gene repression in recipient cells. Finally, we show in peripheral blood mononuclear cells from patients with increased EBV load that, although EBV DNA is restricted to the circulating B-cell population, EBV BART miRNAs are present in both B-cell and non-B-cell fractions, suggestive of miRNA transfer. Taken together our findings are consistent with miRNA-mediated gene silencing as a potential mechanism of intercellular communication between cells of the immune system that may be exploited by the persistent human γ-herpesvirus EBV.
Monocyte chemotactic protein 3 is a most effective basophil- and eosinophil-activating chemokine. (1994)

CC chemokines constitute a novel class of cytokines that attract and activate monocytes and lymphocytes, as well as basophil and eosinophil leukocytes, with distinct target cell profiles, and are believed to be involved in the regulation of different types of inflammation. The action of the recently identified monocyte chemotactic protein 3 (MCP-3) on human basophil and eosinophil function was studied and compared with that of other CC chemokines. In basophils, MCP-3, MCP-1, RANTES, and macrophage inflammatory protein (MIP)-1 alpha all induced cytosolic-free calcium concentration ([Ca2+]i) changes and, with different efficacies, chemotaxis (RANTES = MCP-3 >> MCP-1 > MIP-1 alpha), histamine release (MCP-1 = MCP-3 >> RANTES > MIP-1 alpha), and leukotriene C4 formation, after IL-3 pretreatment (MCP-1 = MCP-3 >> RANTES > MIP-1 alpha). Thus, MCP-3 was as effective as MCP-1 as an inducer of mediator release, and as effective as RANTES as a stimulus of basophil migration. In contrast to MCP-1, MCP-3 was also a stimulus for eosinophils, and induced [Ca2+]i changes and chemotaxis as effectively as RANTES, which is the most potent chemotactic cytokine for these cells. Desensitization of the transient changes in [Ca2+]i was used to assess receptor usage. In basophils, stimulation with MCP-3 prevented responsiveness to MCP-1 and RANTES, but not to MIP-1 alpha. No single CC chemokine (except for MCP-3 itself) affected the response to MCP-3, however, which was prevented only when the cells were prestimulated with both MCP-1 and RANTES. In eosinophils, by contrast, cross-desensitization between RANTES and MCP-3 was obtained. RANTES and to a lesser extent MCP-3 also desensitized eosinophils toward MIP-1 alpha. The desensitization data suggest the existence of three chemokine receptors: (a) a MCP-1 receptor expressed on basophils but not eosinophils that is activated by MCP-1 and MCP-3; (b) a RANTES receptor in basophils and eosinophils that is activated by RANTES and MCP-3; and (c) a MIP-1 alpha receptor that is activated by MIP-1 alpha, RANTES and, more weakly, by MCP-3. This study shows that MCP-3 combines the properties of RANTES, a powerful chemoattractant, and MCP-1, a highly effective stimulus of mediator release, and thus has a particularly broad range of activities toward both human basophil and eosinophil leukocytes.
Region-dependent effects of flibanserin and buspirone on adenylyl cyclase activity in the human brain (2002)

The mode of action of antidepressant drugs may be related to mechanisms of receptor adaptation, involving overall the serotonin 1A (5-HT1A) receptor subtype. However, so far, the clinical effectiveness of selective compounds acting at this level has proved disappointing. This could be explained by the heterogeneity of 5-HT1A receptors within the central nervous system. In animals, two 5-HT1A agonists, flibanserin and buspirone, have shown different pharmacological properties, depending on the brain region. Since no evidence supports this observation in humans, this study sought to investigate whether these two drugs exert different effects on 5-HT1A receptor activation in three different human brain areas: the prefrontal cortex, hippocampus and raphe nuclei. 5-HT1A-mediated inhibition of forskolin-stimulated adenylyl cyclase (AC) was taken as an index of 5-HT1A receptor activation. Flibanserin significantly reduced the activity of AC post-synaptically, i.e. in the prefrontal cortex [EC50 (mean +/- S.E.M.), 28 +/- 10.2 nM; Emax, 18 +/- 2.3%] and in the hippocampus (EC50, 3.5 +/- 3.1 nM; Emax, 20 +/- 4.0%), but had no effect in the raphe nuclei, i.e. at pre-synaptic level. Vice versa, buspirone was only slightly but significantly effective in the raphe (EC50, 3.0 +/- 2.8 nM; Emax, 12 +/- 1.9%). Agonist effects were sensitive to the 5-HT1A antagonists WAY-100135 and pindobind 5-HT1A in the cortex and raphe nuclei, whereas buspirone antagonized flibanserin in the hippocampus. These findings suggest a region-related action of flibanserin and buspirone on forskolin-stimulated AC activity in human brain.
Indium Metal as a Reducing Agent. Selective Reduction of the Carbon−Carbon Double Bond in Highly Activated Conjugated Alkenes (2001)

[reaction: see text] Indium metal in aqueous ethanolic ammonium chloride reduces the C=C bond in highly activated conjugated alkenes such as alpha,alpha-dicyano olefins, beta-arylenones, and enone esters.
Viscoelasticity of hyaluronic acid with different molecular weights (1994)

Storage and loss moduli of hyaluronic acid solutions with different molecular weights were observed as a function of frequency in the presence of sugars and salts. The hyaluronic acid solutions of higher molecular weight (Mw > 17 x 10(6)) fractions showed entanglement, whereas lower molecular weight fractions did not. For inducing the entanglement of molecular chains of hyaluronic acid, increasing the molecular weight of hyaluronic acid was more effective than increasing the concentration of the lower molecular weight fractions (Mw = 7. 8 x 10(5). Glucose, fructose, galactose, and sucrose increased both storage and loss moduli, while NaCl, KCl and CaCl2 decreased both moduli. It is suggested that sugars create hydrogen bonds and strengthen the transient network. Cations shield the electrostatic repulsion of hyaluronic acid molecules, and the polymer chains are shrunk into compact coils from expanded stiffened coils.
Detection of Soluble Amyloid‐β Oligomers and Insoluble High‐Molecular‐Weight Particles in CSF: Development of Methods with Potential for Diagnosis and Therapy Monitoring of Alzheimer′s Disease (2011)

The diagnosis of probable Alzheimer's disease (AD) can be established premortem based on clinical criteria like neuropsychological tests. Post mortem, specific neuropathological changes like amyloid plaques define AD. However, the standard criteria based on medical history and mental status examinations do not take into account the long preclinical features of the disease, and a biomarker for improved diagnosis of AD is urgently needed. In a large number of studies, amyloid-β (Aβ) monomer concentrations in CSF of AD patients are consistently and significantly reduced when compared to healthy controls. Therefore, monomeric Aβ in CSF was suggested to be a helpful biomarker for the diagnosis of preclinical AD. However, not the monomeric form, but Aβ oligomers have been shown to be the toxic species in AD pathology, and their quantification and characterization could facilitate AD diagnosis and therapy monitoring. Here, we review the current status of assay development to reliably and routinely detect Aβ oligomers and high-molecular-weight particles in CSF.
Two-dimensional cylindrical dielectric resonatorantenna array (1998)

A square 2 × 2 subarray and infinite phased array of aperture-coupled cylindrical dielectric resonator antennas is investigated experimentally. The return loss, radiation pattern, and antenna gain are studied and compared with those of the single element antenna, and the waveguide simulator is used to measure the return loss of the element in an infinite array environment
Metabolic syndrome and mitochondrial function: Molecular replacement and antioxidant supplements to prevent membrane peroxidation and restore mitochondrial function (2007)

Metabolic syndrome consists of a cluster of metabolic conditions, such as hypertriglyceridemia, hyper-low-density lipoproteins, hypo-high-density lipoproteins, insulin resistance, abnormal glucose tolerance and hypertension, that-in combination with genetic susceptibility and abdominal obesity-are risk factors for type 2 diabetes, vascular inflammation, atherosclerosis, and renal, liver and heart disease. One of the defects in metabolic syndrome and its associated diseases is excess cellular oxidative stress (mediated by reactive oxygen and nitrogen species, ROS/RNS) and oxidative damage to mitochondrial components, resulting in reduced efficiency of the electron transport chain. Recent evidence indicates that reduced mitochondrial function caused by ROS/RNS membrane oxidation is related to fatigue, a common complaint of MS patients. Lipid replacement therapy (LRT) administered as a nutritional supplement with antioxidants can prevent excess oxidative membrane damage, restore mitochondrial and other cellular membrane functions and reduce fatigue. Recent clinical trials have shown the benefit of LRT plus antioxidants in restoring mitochondrial electron transport function and reducing moderate to severe chronic fatigue. Thus LRT plus antioxidant supplements should be considered for metabolic syndrome patients who suffer to various degrees from fatigue.
Citrus Juice Flavonoids with Anticarcinogenic and Antitumor Properties (1993)

Citrus flavonoids have a broad spectrum of biological activity including anticarcinogenic and antitumor activities. Quercetin inhibits carcinogenesis in a number of models and is able to selectively inhibit a variety of tumor cell growth. Polymethoxylated flavonoids, such as tangeretin and nobiletin, are more potent inhibitors of tumor cell growth than hydroxylated flavonoids. They also possess potent anti-invasive and anti-metastatic activities. In this chapter the biological activity of citrus flavonoids is briefly overviewed. Emphasis is on their anticarcinogenic and antitumor activities.
Retinitis pigmentosa (2006)

Retinitis pigmentosa (RP) is an inherited retinal dystrophy caused by the loss of photoreceptors and characterized by retinal pigment deposits visible on fundus examination. Prevalence of non syndromic RP is approximately 1/4,000. The most common form of RP is a rod-cone dystrophy, in which the first symptom is night blindness, followed by the progressive loss in the peripheral visual field in daylight, and eventually leading to blindness after several decades. Some extreme cases may have a rapid evolution over two decades or a slow progression that never leads to blindness. In some cases, the clinical presentation is a cone-rod dystrophy, in which the decrease in visual acuity predominates over the visual field loss. RP is usually non syndromic but there are also many syndromic forms, the most frequent being Usher syndrome. To date, 45 causative genes/loci have been identified in non syndromic RP (for the autosomal dominant, autosomal recessive, X-linked, and digenic forms). Clinical diagnosis is based on the presence of night blindness and peripheral visual field defects, lesions in the fundus, hypovolted electroretinogram traces, and progressive worsening of these signs. Molecular diagnosis can be made for some genes, but is not usually performed due to the tremendous genetic heterogeneity of the disease. Genetic counseling is always advised. Currently, there is no therapy that stops the evolution of the disease or restores the vision, so the visual prognosis is poor. The therapeutic approach is restricted to slowing down the degenerative process by sunlight protection and vitaminotherapy, treating the complications (cataract and macular edema), and helping patients to cope with the social and psychological impact of blindness. However, new therapeutic strategies are emerging from intensive research (gene therapy, neuroprotection, retinal prosthesis).