gebhart/patrepeval huggingface dataset:
Peptidergic Innervation of the Human Male Genital Tract (1983)

Four peptides--vasoactive intestinal polypeptide, substance P, somatostatin and a peptide-like avian pancreatic polypeptide--have been found in nerves of the human male genitalia using highly sensitive and specific methods of immunocytochemistry and radioimmunoassay. Five other peptides (met-enkephalin, leu-enkephalin, neurotensin, bombesin and cholecystokinin-8) were absent. Vasoactive intestinal polypeptide was the most abundant peptide, its highest concentration being in the proximal corpus cavernosum. Immunoelectron microscopy localized this peptide to large (97 +/- 20 nm), round, electron-dense granules of p-type nerve terminals. Vasoactive intestinal polypeptide-immunoreactive neuronal cell bodies were found in the prostate gland and the root of the corpus cavernosum. Substance P immunoreactive material was present in smaller concentration and was mainly localized in nerves around the corpuscular receptors of the glans penis. Somatostatin immunoreactive nerves were associated mainly with the smooth muscle of the seminal vesicle and the vas deferens. When antiserum to avian pancreatic polypeptide was applied, certain nerves were stained, particularly in the vas deferens, the prostate gland and the seminal vesicle. However, chromatography detected no pure avian pancreatic polypeptide suggesting the presence of a structurally related substance, possibly neuropeptide Y, which cross-reacts with the avian pancreatic polypeptide antiserum. Similar distributions between vasoactive intestinal polypeptide-immunoreactive and acetylcholinesterase-positive nerves and between avian pancreatic polypeptide-immunoreactive and adrenergic nerves were observed. A general neuronal marker, neuron-specific enolase, was used to investigate the general pattern of the organ's innervation. The abundance and distribution patterns of these peptide-immunoreactive nerves indicate that they may play important roles in the male sexual physiology.
Data security approach for online social network (2014)

Social Networks are very much helpful in finding and communicating with the known and unknown ones. Online social networking sites (OSNs) offer a new, easy and inexpensive way to maintain already existing relationships. It enables users to share data and digital content with friends. A wide range of OSN platforms exist (e.g., Facebook, Twitter, LinkedIn). Social networking sites come under few of the most frequently browsed categories websites in the world and mainstream communication technology. A fully flexible privacy and security management should exist to protect private data against attackers and unauthorized users. Nevertheless Social Networking sites are also vulnerable to various problems threats and attacks such as disclosure of information. Facebook is one such most popular and widely used Social Networking sites which have its own robust set of Privacy policies. They are also prone to various privacy issues and attacks. In this work new policies introduced that enhance and strengthen the existing privacy policies of Facebook since 2013. We conclude with a discussion of how these edicts may be integrated into the design of Facebook like Social Networking sites systems to facilitate interaction while enhancing the individual privacy.
Interaction of Human Complement with Sbi, a Staphylococcal Immunoglobulin-binding Protein (2008)

Staphylococcal immunoglobulin-binding protein, Sbi, is a 436-residue protein produced by many strains of Staphylococcus aureus. It was previously characterized as being cell surface-associated and having binding capacity for human IgG and beta(2)-glycoprotein I. Here we show using small angle x-ray scattering that the proposed extracellular region of Sbi (Sbi-E) is an elongated molecule consisting of four globular domains, two immunoglobulin-binding domains (I and II) and two novel domains (III and IV). We further show that together domains III and IV (Sbi-III-IV), as well as domain IV on its own (Sbi-IV), bind complement component C3 via contacts involving both the C3dg fragment and the C3a anaphylatoxin domain. Preincubation of human serum with either Sbi-E or Sbi-III-IV is inhibitory to all complement pathways, whereas domain IV specifically inhibits the alternative pathway. Monitoring C3 activation in serum incubated with Sbi fragments reveals that Sbi-E and Sbi-III-IV both activate the alternative pathway, leading to consumption of C3. By contrast, inhibition of this pathway by Sbi-IV does not involve C3 consumption. The observation that Sbi-E activates the alternative pathway is counterintuitive to intact Sbi being cell wall-associated, as recruiting complement to the surface of S. aureus would be deleterious to the bacterium. Upon re-examination of this issue, we found that Sbi was not associated with the cell wall fraction, but rather was found in the growth medium, consistent with it being an excreted protein. As such, our data suggest that Sbi helps mediate bacterial evasion of complement via a novel mechanism, namely futile fluid-phase consumption.
Flux-driven Josephson parametric amplifier (2008)

We have developed a Josephson parametric amplifier comprising a superconducting coplanar-waveguide resonator terminated by a dc superconducting quantum interference device (SQUID). An external field (the pump, ∼20 GHz) modulates the flux threading of the dc SQUID and, therefore, the resonant frequency of the cavity field (the signal, ∼10 GHz), which leads to the parametric signal amplification. We operated the amplifier at different band centers and observed amplification (17 dB at maximum) and deamplification depending on the relative phase between the pump and the signal. The noise temperature is estimated to be less than 0.87 K.
Substrate Specificity of the Escherichia coli 4-Aminobutyrate Carrier Encoded by gabP (1996)

Transport of 4-aminobutyrate into Escherichia coli is catalyzed by gab permease (GabP). Although published studies show that GabP is relatively specific, recognizing the common alpha-amino acids with low affinity, recent work from this laboratory indicates that a number of synthetic compounds are high affinity transport inhibitors (50% inhibition at 5-100 microM). Here we present evidence that many of these structurally heterogeneous compounds not only inhibit transport but also function as alternative GabP substrates (i.e. a set of observations inconsistent with the idea that the core of the GabP transport channel exhibits rigid structural specificity for the native substrate, 4-aminobutyrate.
True Atomic Resolution by Atomic Force Microscopy Through Repulsive and Attractive Forces (1993)

The (1014) cleavage plane of calcite has been investigated by atomic force microscopy in water at room temperature. True lateral atomic-scale resolution was achieved; the atomic-scale periodicities as well as the expected relative positions of the atoms within each unit cell were obtained. Along monoatomic step lines, atomic-scale kinks, representing point-like defects, were resolved. Attractive forces on the order of 10(-11) newton acting between single atomic sites on the sample and the front atoms of the tip were directly measured and provided the highest, most reliable resolution on a flat, well-ordered surface.
The Role of Norepinephrine in the Behavioral and Psychological Symptoms of Dementia (2004)

The behavioral and psychological symptoms of dementia (BPSD) are common serious problems that are a major contributor to caregiver burden. Despite their significance, the underlying neurobiology of these disturbances is still unclear. This review examines the role of norepinephrine (NE) on BPSD, including depression, aggression, agitation and psychosis. A number of lines of evidence suggest that NE dysfunction leading to BPSD may result from increased NE activity and/or hypersensitive adrenoreceptors compensating for loss of NE neurons with progression of Alzheimer's disease (AD). With greater appreciation of the underlying neurobiology of behavioral and psychological symptoms of dementia (BPSD) more effective, rational, targeted pharmacotherapy will hopefully emerge.
Ion Selective Folding of Loop Domains in a Potent Anti-HIV Oligonucleotide (1997)

Previously, we have described inhibition of HIV-1 infection by T30177, 5'-(GTGGTGGGTGGGTGGGT)-3', an oligonucleotide that is a potent inhibitor of HIV-1 integrase in vitro (Mazumder et al. (1996) Biochemistry 35, 13762). Here a family of oligonucleotides, analogs of T30177, has been studied. On the basis of thermal denaturation, we show that a folded structure of T30177 is much more stable than that of the thrombin binding aptamer, which only differs with T30177 in the loop sequence. Sequence changes reveal that loop interactions are solely responsible for this observed stability difference. In the presence of K+ ion, the fold of T30695, a designed 16mer derivative, is indeed more stable than T30177. Loop folding within T30695 is very ion selective. Quantitative analysis of thermal denaturation suggests that the loops of T30695, 5'-(GGGTGGGTGGGTGGGT)-3', and T30177 confer the ability to coordinate three equivalents of K+ ion (one bound to the core octet and two bound to the loops); however, the thrombin binding aptamer is shown to bind only one K+ equivalent. Folding kinetics and CD titration demonstrate that K+-induced folding of T30695 and T30177 is a two-step process, consistent with a sequential model in which a first equivalent of K+ binds to the octet core, followed by slow K+-induced rearrangement of the loop domains. Comparing structural stability with the capacity of the folded oligomers to inhibit the HIV-1 integrase enzyme in vitro or HIV-1 infection in cell culture, we have found that the folding and activity data are highly correlated, suggesting that formation of an orderly, ion-coordinated loop structure similar to that in T30177 or T30695 may be a prerequisite for both integrase inhibition and anti-HIV-1 activity.
Direct Associations or Internal Transformations? Exploring the Mechanisms Underlying Sequential Learning Behavior (2010)

We evaluate two broad classes of cognitive mechanisms that might support the learning of sequential patterns. According to the first, learning is based on the gradual accumulation of direct associations between events based on simple conditioning principles. The other view describes learning as the process of inducing the transformational structure that defines the material. Each of these learning mechanisms predict differences in the rate of acquisition for differently organized sequences. Across a set of empirical studies, we compare the predictions of each class of model with the behavior of human subjects. We find that learning mechanisms based on transformations of an internal state, such as recurrent network architectures (e.g., Elman, 1990), have difficulty accounting for the pattern of human results relative to a simpler (but more limited) learning mechanism based on learning direct associations. Our results suggest new constraints on the cognitive mechanisms supporting sequential learning behavior.
Expression of the mucosal vascular addressin, MAdCAM-1, on sinus-lining cells in the spleen. (1995)

The MAdCAM-1 adhesion molecule is involved in lymphocyte homing into mucosal sites and is expressed on high endothelial venules of Peyer's patches and mesenteric lymph nodes. In the spleen, where high endothelial venules are absent, expression can be found on cells in the marginal zone between red and white pulp. By immunohistochemistry and electron microscopy it was demonstrated that in the spleen cells expressing MAdCAM-1 belong to the population of sinus-lining cells and that the expression is restricted to the sinus-lining cells closest to the lymphoid white pulp. Lymphocytes that migrate from the blood into this white pulp area will have to pass through the rim of cells expressing MAdCAM-1. A functional role for MAdCAM-1 or its lymphocyte ligand, the alpha 4 beta 7 integrin complex, was investigated by in vivo short-term homing experiments with anti-MAdCAM-1 and anti-alpha 4 beta 7 antibodies, but no direct role for this receptor-ligand interaction could be demonstrated.
Gln3p Nuclear Localization and Interaction with Ure2p inSaccharomyces cerevisiae (2001)

Gln3p is one of two well characterized GATA family transcriptional activation factors whose function is regulated by the nitrogen supply of the cell. When nitrogen is limiting, Gln3p and Gat1p are concentrated in the nucleus where they bind GATA sequences upstream of nitrogen catabolite repression (NCR)-sensitive genes and activate their transcription. Conversely, in excess nitrogen, these GATA sequences are unoccupied by Gln3p and Gat1p because these transcription activators are excluded from the nucleus. Ure2p binds to Gln3p and Gat1p and is required for NCR-sensitive transcription to be repressed and for nuclear exclusion of these transcription factors. Here we show the following. (i) Gln3p residues 344-365 are required for nuclear localization. (ii) Replacing Ser-344, Ser-347, and Ser-355 with alanines has minimal effects on GFP-Gln3p localization. However, replacing Gln3p Ser-344, Ser-347, and Ser-355 with aspartates results in significant loss of its ability to be concentrated in the nucleus. (iii) N and C termini of the Gln3p region required for it to complex with Ure2p and be excluded from the nucleus are between residues 1-103 and 301-365, respectively. (iv) N and C termini of the Ure2p region required for it to interact with Gln3p are situated between residues 101-151 and 330-346, respectively. (v) Loss of Ure2p residues participating in either dimer or prion formation diminishes its ability to carry out NCR-sensitive regulation of Gln3p activity.
Leakage Power Minimization of Nanoscale CMOS Circuits via Non-Critical Path Transistor Sizing (2006)

A leakage power minimization method in nanoscale CMOS circuits by transistor sizing in non-critical paths is presented. It is shown that a small increase in delay by transistor downsizing of non-critical paths can provide a significant reduction in leakage power. Moreover, nonlinear dependence of leakage current on width (due to inverse narrow width effects) can be exploited to minimize leakage power at non-minimum widths. A 64-bit carry-lookahead adder, with carry blocks optimized for speed and sum blocks minimized for leakage power, achieves a reduction in leakage power by about 25%.
Prevention of diabetic nephropathy in db/db mice with glycated albumin antagonists. A novel treatment strategy. (1995)

Accelerated protein glycation in diabetes has been mechanistically linked to the pathogenesis of diabetic nephropathy. Because glycated albumin induces abnormalities in cultured mesangial cells that resemble those characterizing the glomerular mesangium in diabetes, and monoclonal antibodies (A717) specific for Amadori-modified glycated albumin prevent these abnormalities, we postulated that in vivo administration of A717 could retard the progression of diabetic nephropathy. To test this hypothesis, diabetic db/db mice and their nondiabetic db/m littermates were treated with eight consecutive weekly injections of 150 micrograms of A717 (Fab fragments) to reduce the elevated plasma glycated albumin concentration, or with irrelevant murine IgG (MIg). Relative to nondiabetics, diabetic mice (MIg treated) manifested proteinuria (3.35 +/- 0.15 vs 0.87 +/- 0.1 mg albumin/mg creatinine), 3.8-fold increase in mesangial matrix fraction, and renal cortical overexpression of mRNAs encoding alpha 1(IV) collagen (2.6-fold increase) and fibronectin (3.8-fold increase). Treatment of db/db mice with A717 significantly reduced the proteinuria (1.52 +/- 0.3 mg/mg creatinine), inhibited mesangial matrix expansion, and attenuated overexpression of matrix mRNAs. The nephropathic protective effects of A717 were independent of any change in blood glucose concentrations. Antibodies unreactive with glycated albumin did not duplicate the beneficial effects of A717. Thus, abrogating the biologic effects of increased glycated albumin with A717 has a salutary influence on the pathogenesis of diabetic nephropathy and has novel therapeutic potential in its management.
A case study of a system-level approach to power-aware computing (2003)

This paper introduces a systematic approach to power awareness in mobile, handheld computers. It describes experimental evaluations of several techniques for improving the energy efficiency of a system, ranging from the network level down to the physical level of the battery. At the network level, a new routing method based upon the power consumed by the network subsystem is shown to improve power consumption by 15% on average and to reduce latency by 75% over methods that consider only the transmitted power. At the boundary between the network and the processor levels, the paper presents the problem of local versus remote processing and derives a figure of merit for determining whether a computation should be completed locally or remotely, one that involves the relative performance of the local and remote system, the transmission bandwidth and power consumption, and the network congestion. At the processor level, the main memory bandwidth is shown to have a significant effect on the relationship between performance and CPU frequency, which in turn determines the energy savings of dynamic CPU speed-setting. The results show that accounting for the main memory bandwidth using Amdahl's law permits the performance speed-up and peak power versus the CPU frequency to be estimated to within 5%. The paper concludes with a technique for mitigating the loss of battery energy capacity with large peak currents, showing an improvement of up to 10% in battery life, albeit at some cost to the size and weight of the system.
Chronic Suppression of Bioelectric Activity and Cell Survival in Primary Cultures of Rat Cerebral Cortex: Biochemical Observations (1991)

Chronic suppression of spontaneously occurring bioelectric activity (BEA) has been shown to increase neuronal cell death in tissue culture, but may also affect astrocytes. We investigated this process in primary cultures of rat cerebral cortex by measuring the levels of NSE (neuron-specific enolase) and GFAP (glial fibrillary acidic protein) in relation to general tissue markers, including measurements for cell death and proliferation. In electrically active (control) cultures, the content of DNA, protein, and NSE became maximal between 21 and 28 days in vitro (DIV) and thereafter decreased, whereas the content of GFAP rose continuously up to 43 DIV. Chronic suppression of BEA by tetrodotoxin (TTX; from 6 DIV) decreased the content of DNA, total protein, and especially NSE. The content of GFAP was decreased in all culture series investigated, but with great temporal variations among culture series. Chronic TTX treatment (started at 6 DIV) increased the efflux of lactate dehydrogenase, a marker for cell lysis, between 12 and 21 DIV, but this efflux was mainly derived from the supporting glial cells with which the cerebral cortex cultures were cocultured. Chronic, but not acute (7 h) TTX treatment decreased total [3H]thymidine incorporation into DNA from 14 DIV; this appeared to be due to a reduced number of astrocytes. Chronic suppression of BEA with xylocaine from 6 DIV had similar effects on DNA-, protein-, and NSE-content as TTX, but led to an increased content of GFAP at 21 DIV. Chronic suppression of synaptic transmission with 10 mM Mg2+ and 0.2 mM Ca2+, starting at 6 DIV, increased the content of DNA, protein, and GFAP at 21 DIV, but NSE was still decreased. We conclude that chronic suppression of BEA in cerebral cortex cultures enhances neuronal cell death, whereas astrocytes are differentially affected, depending on the suppressing agent. As astrocytes may have a modulating effect on neuronal survival, their involvement should be regarded when studying the effects of chronic suppression of BEA on neuronal development.
A cytokine-mediated link between innate immunity, inflammation, and cancer (2007)

It has been established that cancer can be promoted and/or exacerbated by inflammation and infections. Indeed, chronic inflammation orchestrates a tumor-supporting microenvironment that is an indispensable participant in the neoplastic process. The mechanisms that link infection, innate immunity, inflammation, and cancer are being unraveled at a fast pace. Important components in this linkage are the cytokines produced by activated innate immune cells that stimulate tumor growth and progression. In addition, soluble mediators produced by cancer cells recruit and activate inflammatory cells, which further stimulate tumor progression. However, inflammatory cells also produce cytokines that can limit tumor growth. Here we provide an overview of the current understanding of the role of inflammation-induced cytokines in tumor initiation, promotion, and progression.
Mutation and Recombination in the Upstream Homology Box-Flanked ospE -Related Genes of the Lyme Disease Spirochetes Result in the Development of New Antigenic Variants during Infection (2000)

The ospE gene family of the Lyme disease spirochetes encodes a polymorphic group of immunogenic lipoproteins. The ospE genes are one of several gene families that are flanked by a highly conserved upstream sequence called the upstream homology box, or UHB, element. Earlier analyses in our lab demonstrated that ospE-related genes are characterized by defined hypervariable domains (domains 1 and 2) that are predicted to be hydrophilic, surface exposed, and antigenic. The flanking of hypervariable domain 1 by DNA repeats may indicate that recombination contributes to ospE diversity and thus ultimately to antigenic variation. Using an isogeneic clone of Borrelia burgdorferi B31G (designated B31Gc1), we demonstrate that the ospE-related genes undergo mutation and rearrangement during infection in mice. The mutations that develop during infection resulted in the generation of OspE proteins with altered antigenic characteristics. The data support the hypothesized role of OspE-related proteins in immune system evasion.
Large scale nanolithography using nanoimprint lithography (1999)

Nanoimprint lithography is a promising technique for fabrication of nanometer-sized structures with an eventual throughput capacity similar to UV-lithography based production of integrated circuits. In this article we address the possibility for wafer scale nanoimprint lithography, and the results presented here are all obtained from 2 in. sized substrate and stamp wafers. Our nanoimprint lithography equipment is described and some of its characteristics are discussed. These include ultrafast imprint cycle times of less than 2 min, good temperature monitoring, and control possibility of the substrate temperature. We show complete results after imprint, removal of remaining resist, and liftoff for 2 in. wafers. Furthermore, in this article the relation between polymer sticking to the stamp applied pressure, stamp depth, etc. is studied in detail.
A topical azithromycin preparation for the treatment of acne vulgaris and rosacea (2004)

A 2% azithromycin in 60% ethanol/water solution can be prepared and is stable for at least 6 months at room temperature. The methodology and power of the study were adequate to identify improvement in acne vulgaris and rosacea. Though it appears the formulation of topical azithromycin was at least comparable with topical erythromycin, larger studies would be needed to determine whether topical azithromycin has any significant advantage over topical erythromycin.