gebhart/patrepeval huggingface dataset:
High-Rate Space-Time Coded Large MIMO Systems: Low-Complexity Detection and Performance (2008)

Large MIMO systems with tens of antennas in each communication terminal using full-rate non-orthogonal space- time block codes (STBC) from cyclic division algebras (CDA) can achieve the benefits of both transmit diversity as well as high spectral efficiencies. Maximum-likelihood (ML) or near-ML decoding of these large-sized STBCs at low complexities, however, has been a challenge. In this paper, we establish that near-ML decoding of these large STBCs is possible at practically affordable low complexities. We show that the likelihood ascent search (LAS) detector, reported earlier by us for V-BLAST, is able to achieve near-ML uncoded BER performance in decoding a 32 times 32 STBC from CDA, which employs 32 transmit antennas and sends 32 <sup xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink">2</sup> = 1024 complex data symbols in 32 time slots in one STBC matrix (i.e., 32 data symbols sent per channel use). In terms of coded BER, with a 16 times 16 STBC, rate-3/4 turbo code and 4-QAM (i.e., 24 bps/Hz), the LAS detector performs close to within just about 4 dB from the theoretical MIMO capacity. Our results further show that, with LAS detection, information lossless (ILL) STBCs perform almost as good as full-diversity ILL (FD-ILL) STBCs. Such low-complexity detectors can potentially enable implementation of high spectral efficiency large MIMO systems that could be considered in wireless standards.
A Gene Network Regulating Lysosomal Biogenesis and Function (2009)

Lysosomes are organelles central to degradation and recycling processes in animal cells. Whether lysosomal activity is coordinated to respond to cellular needs remains unclear. We found that most lysosomal genes exhibit coordinated transcriptional behavior and are regulated by the transcription factor EB (TFEB). Under aberrant lysosomal storage conditions, TFEB translocated from the cytoplasm to the nucleus, resulting in the activation of its target genes. TFEB overexpression in cultured cells induced lysosomal biogenesis and increased the degradation of complex molecules, such as glycosaminoglycans and the pathogenic protein that causes Huntington's disease. Thus, a genetic program controls lysosomal biogenesis and function, providing a potential therapeutic target to enhance cellular clearing in lysosomal storage disorders and neurodegenerative diseases.
Intake of Blueberry Fermented byLactobacillus plantarumAffects the Gut Microbiota of L-NAME Treated Rats (2013)

Prebiotics, probiotics, or synbiotics can be used as means to regulate the microbiota to exert preventative or beneficial effects to the host. However, not much is known about the effect of the gut microbiota on hypertension which is a major risk factor of cardiovascular disease and also a symptom of the metabolic syndrome. The N(G)-nitro-L-arginine methyl ester (L-NAME) induced hypertensive rats were used in order to test the effect of a synbiotic dietary supplement of Lactobacillus plantarum HEAL19 either together with fermented blueberry or with three phenolic compounds synthesized during fermentation. The experimental diets did not lower the blood pressure after 4 weeks. However, the fermented blueberries together with live L. plantarum showed protective effect on liver cells indicated by suppressed increase of serum alanine aminotransferase (ALAT) levels. The diversity of the caecal microbiota was neither affected by L-NAME nor the experimental diets. However, inhibition of the nitric oxide synthesis by L-NAME exerted a selection pressure that led to a shift in the bacterial composition. The mixture of fermented blueberries with the bacterial strain altered the caecal microbiota in different direction compared to L-NAME, while the three phenolic compounds together with the bacteria eliminated the selection pressure from the L-NAME.
SCLC-cluster-2 antibodies detect the pancarcinoma/epithelial glycoprotein EGP-2 (1994)

Analysis of the antibodies submitted to the 3 International Workshops on Small Cell Lung Cancer Antigens has resulted in the identification of 15 clusters of antibody reactivity. One of these clusters, named SCLC cluster 2, is characterized by reactivity against an epithelium-associated 38 kDa membrane glycoprotein. SCLC cluster 2, and a number of other antibodies with reportedly similar reactivities, were shown to recognize a protein encoded by the GA733-2 gene, whereas the newly defined SCLC cluster 13 antibodies react with the GA733-1 gene product. We propose to call the antigen detected by SCLC-cluster-2 antibodies "epithelial glycoprotein 2" (EGP-2), and the epithelium-associated glycoprotein recognized by antibodies clustered in SCLC cluster 13 (see elsewhere in this volume) "epithelial glycoprotein 1" (EGP-1). A short overview of the characteristics of both proteins and the applications of anti-EGP-2 antibodies is presented.
A precorrected-FFT method for capacitance extraction of complicated 3-D structures (1994)

In this paper we present a new approach to three-dimensional capacitance extraction based on a precorrected FFT scheme. The approach is compared to the now commonly used multipole-accelerated algorithms for a variety of structures, and the new method is shown to have substantial performance and memory advantages.
Argon Laser Irradiation Effects on Sound Root Surfaces: In Vitro Scanning Electron Microscopic Observations (1998)

Argon laser irradiated root surfaces produce surface granular to globular deposits that may provide readily mobilized tooth mineral, which may become redeposited into the underlying root surface during a cariogenic challenge and enhance resistance to caries formation. In addition, microporosities created by the argon laser may provide a means for bonding fluoride-releasing restorative and preventive materials to root surfaces and further improve the root surfaces' ability to resist cariogenic challenges.
Compressed video seamless switching using variable splicing parameters (2002)

We propose a new approach for creating splice points in compressed video streams. The resulting streams can be switched seamlessly, and therefore no decoder underflow or overflow events occur. The proposed variable splicing parameters (VSP) method eliminates major encoder buffer constraints and related video encoding issues associated with the standard approach for creating seamless splice points. These advantages are achieved at the expense of a minor increase in the splicing operation complexity. When using VSP splice points, the splicer has to wait a specific period of time (equal to the difference between the out point and in point decoding delays) before switching into the new stream (i.e. the stream with the in point).
Increased resistance to N,N',N"-triethylenethiophosphoramide (thiotepa) in cells expressing the Escherichia coli formamidopyrimidine-DNA glycosylase. (1996)

Thiotepa (N,N',N'-triethylenethiophosphoramide) is an alkylating agent used in cancer chemotherapy. A reaction pathway by which thiotepa alkylates purified DNA involves hydrolysis to aziridine, which forms N7-aminoethyl guanine and aminoethyl adenine. These lesions are repaired in Escherichia coli by the formamidopyrimidine-DNA glycosylase (Fpg) protein. To determine whether such lesions are formed by thiotepa in mammalian cells, we have overexpressed the E. coli Fpg protein in Chinese hamster ovary cells. The transfected cells were more resistant to the lethal and mutagenic effects of thiotepa than the parental cells. The number of replication-blocking lesions formed by thiotepa, measured by quantitative PCR analysis, was lower in the transfected cells. These results show that expression of the Fpg protein increases the cell resistance to thiotepa and suggest that this compound produces ring-opened guanines, which are involved in its cytotoxic action.
Histone Deacetylase Inhibitors and Neurodegenerative Disorders: Holding the Promise (2009)

Neurodegenerative disorders (NDs) such as Huntington's disease, Alzheimer's disease, Parkinson disease, amyotrophic lateral sclerosis, spinal muscular atrophy, Friedreich's ataxia, and others are multi-factorial illnesses, in which many pathways (still poorly understood) act serially and in parallel to give a determined pathologic phenotype. Thus, presently there are no effective cures for these diseases. Some phenotypic as well as mechanistic features, common to the most of NDs, can be linked to epigenetic defects, that can lead to alteration of acetylation homeostasis and impairment of the histone acetyltransferase (HAT): histone deacetylase (HDAC) balance. Here we survey most of the recent applications of HDAC inhibitors in the cited NDs, and we make the point of our (up to now) knowledge about the involvement of singular HDAC/SIRT isoform in NDs and other CNS pathologies.
Introducing mothur: Open-Source, Platform-Independent, Community-Supported Software for Describing and Comparing Microbial Communities (2009)

mothur aims to be a comprehensive software package that allows users to use a single piece of software to analyze community sequence data. It builds upon previous tools to provide a flexible and powerful software package for analyzing sequencing data. As a case study, we used mothur to trim, screen, and align sequences; calculate distances; assign sequences to operational taxonomic units; and describe the alpha and beta diversity of eight marine samples previously characterized by pyrosequencing of 16S rRNA gene fragments. This analysis of more than 222,000 sequences was completed in less than 2 h with a laptop computer.
Activation of p38 Mitogen-Activated Protein Kinase and c-Jun NH2-Terminal Kinase by Double-Stranded RNA and Encephalomyocarditis Virus: Involvement of RNase L, Protein Kinase R, and Alternative Pathways (2000)

Double-stranded RNA (dsRNA) accumulates in virus-infected mammalian cells and signals the activation of host defense pathways of the interferon system. We describe here a novel form of dsRNA-triggered signaling that leads to the stimulation of the p38 mitogen-activated protein kinase (p38 MAPK) and the c-Jun NH(2)-terminal kinase (JNK) and of their respective activators MKK3/6 and SEK1/MKK4. The dsRNA-dependent signaling to p38 MAPK was largely intact in cells lacking both RNase L and the dsRNA-activated protein kinase (PKR), i. e., the two best-characterized mediators of dsRNA-triggered antiviral responses. In contrast, activation of both MKK4 and JNK by dsRNA was greatly reduced in cells lacking RNase L (or lacking both RNase L and PKR) but was restored in these cells when introduction of dsRNA was followed by inhibition of ongoing protein synthesis or transcription. These results are consistent with the notion that the role of RNase L and PKR in the activation of MKK4 and JNK is the elimination, via inhibition of protein synthesis, of a labile negative regulator(s) of the signaling to JNK acting upstream of SEK1/MKK4. In the course of these studies, we identified a long-sought site of RNase L-mediated cleavage in the 28S rRNA, which could cause inhibition of translation, thus allowing the activation of JNK by dsRNA. We propose that p38 MAPK is a general participant in dsRNA-triggered cellular responses, whereas the activation of JNK might be restricted to cells with reduced rates of protein synthesis. Our studies demonstrate the existence of alternative (RNase L- and PKR-independent) dsRNA-triggered signaling pathways that lead to the stimulation of stress-activated MAPKs. Activation of p38 MAPK (but not of JNK) was demonstrated in mouse fibroblasts in response to infection with encephalomyocarditis virus (ECMV), a picornavirus that replicates through a dsRNA intermediate. Fibroblasts infected with EMCV (or treated with dsRNA) produced interleukin-6, an inflammatory and pyrogenic cytokine, in a p38 MAPK-dependent fashion. These findings suggest that stress-activated MAPKs participate in mediating inflammatory and febrile responses to viral infections.
Impaired Cell-Mediated Immunity in Hodgkin's Disease Mediated by Suppressor Lymphocytes and Monocytes (1978)

In Hodgkin's disease a possible mechanism for impaired cellular immunity is cell-mediated suppression, defined as the inhibitory interaction between suppressor cells and effector lymphocytes. To test for the presence of suppressor cells in peripheral blood, we have modified the standard, one-way mixed lymphocyte culture by adding mitomycin C-treated mononuclear cells from the responder. Suppression, expressed as a percent of the base-line mixed lymphocyte culture in which these extra cells are not present, results in a reduction of thymidine incorporated in the modified culture (i.e., 100% suppression = no net thymidine incorporation; 0% suppression = identical thymidine incorporation in both the modified and baseline culture). Suppression was found to be significantly increased in patients with both active Hodgkin's disease (78+/-4.6%) and remission Hodgkin's disease (58+/-9.3%) compared to normal individuals (21+/-6.9%) (mean+/-SE). The degree and frequency of suppression were not influenced by disease stage or prior therapy. Cell purification techniques revealed (in 10 patients studied) the suppressor cell to be a monocyte in 6, and a thymus-derived lymphocyte in 4. Possible genetic restriction of the suppressor cell interaction was indicated by a failure of suppressor cells to alter the response of lymphocytes from unrelated individuals, but suppression was obtained with lymphocytes from a histocompatible sibling. Although mononuclear cells from normal individuals suppress less frequently than cells from patients with Hodgkin's disease, normals may demonstrate suppression comparable to that observed in Hodgkin's patients. This finding suggests that suppression is a normal immunoregulatory mechanism which is altered in Hodgkin's disease.
1625: Neuroligin 4 ISOFORM Y: A Novel Marker for Prostate Cancer (2007)

You have accessJournal of UrologyModerated Poster 50, Tuesday, May 22, 2007, 3:30 - 5:30 pm1 Apr 20071625: Neuroligin 4 ISOFORM Y: A Novel Marker for Prostate Cancer Joseph F. Pazona, C. Shad Thaxton, Neema Navai, Brian T. Helfand, Lee C. Zhao, Brian Adley, Yi Lu, and Norm D. Smith Joseph F. PazonaJoseph F. Pazona More articles by this author , C. Shad ThaxtonC. Shad Thaxton More articles by this author , Neema NavaiNeema Navai More articles by this author , Brian T. HelfandBrian T. Helfand More articles by this author , Lee C. ZhaoLee C. Zhao More articles by this author , Brian AdleyBrian Adley More articles by this author , Yi LuYi Lu More articles by this author , and Norm D. SmithNorm D. Smith More articles by this author View All Author Informationhttps://doi.org/10.1016/S0022-5347(18)31813-5AboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissionsReprints ShareFacebookLinked InTwitterEmail "1625: Neuroligin 4 ISOFORM Y: A Novel Marker for Prostate Cancer." The Journal of Urology, 177(4S), pp. 538–539 © 2016 by American Urological AssociationFiguresReferencesRelatedDetails Volume 177Issue 4SApril 2007Page: 538-539 Advertisement Copyright & Permissions© 2016 by American Urological AssociationMetricsAuthor Information Joseph F. Pazona More articles by this author C. Shad Thaxton More articles by this author Neema Navai More articles by this author Brian T. Helfand More articles by this author Lee C. Zhao More articles by this author Brian Adley More articles by this author Yi Lu More articles by this author Norm D. Smith More articles by this author Expand All Advertisement PDF DownloadLoading ...
Combination therapy with clopidogrel and aspirin after coronary stenting (2000)

Combination antiplatelet therapy using aspirin and ticlopidine has been the standard of care for prevention of subacute thrombosis following coronary stent implantation. However, the use of ticlopidine is associated with a significant risk of adverse hematologic side effects. Clopidogrel is an inhibitor of ADP-induced platelet aggregation that has a better safety profile than ticlopidine. We examined the 30-day clinical outcome following coronary stent implantation in 253 consecutive patients treated with clopidogrel and aspirin. Follow-up was achieved in 99% of patients and four adverse events were documented. Two patients had angiographically confirmed subacute stent thrombosis (0.8%), and both of these patients underwent successful repeat angioplasty at the stent site. There were two patient deaths during follow-up (0.8%). One was sudden within 1 week of stent placement and the other occurred in a patient with multisystem organ failure after an extensive myocardial infarction that antedated the stent procedure, with no clinical evidence for stent thrombosis. The combined frequency of subacute stent thrombosis and death was 1.6%. This is comparable to prior studies using the combination of ticlopidine and aspirin following stenting. Therefore, clopidogrel in combination with aspirin appears to be a safe and effective therapy in the prevention of subacute thrombosis following coronary stent implantation. Cathet. Cardiovasc. Intervent. 50:276–279, 2000. © 2000 Wiley-Liss, Inc.
Monoclonal antibodies to murine CD3 epsilon define distinct epitopes, one of which may interact with CD4 during T cell activation. (1989)

The TCR is comprised of two variable chains that confer specificity, called alpha:beta or gamma:delta, physically associated with five different molecules that comprise the complex known as CD3. Antibodies to this complex are very useful, as they react with all T lymphocytes. A rat mAb to mouse CD3 has been prepared. It reacts with 100% of T cells in all mouse strains tested but with no other cell type. It binds to the CD3 epsilon chain. This antibody activates cloned T cell lines and normal T cells, provided suitable accessory cells and signals are present. This antibody detects a determinant similar to but not identical with those detected by two previously reported hamster anti-CD3 epsilon antibodies. This antibody fixes C efficiently, and it is thus useful for depletion of T cells from bulk populations. Activation of T cells by one of the three different anti-CD3 epsilon antibodies was inhibited by the Fab fragment of anti-CD4, similar to the effects of anti-CD4 Fab on two previously reported anti-TCR V region antibodies that bind a CD3 epsilon-associated epitope. This further defines a site involving TCR V regions and CD3 epsilon with which CD4 appears to associate during T cell activation.
Non-Acylated Ghrelin Counteracts the Metabolic But Not the Neuroendocrine Response to Acylated Ghrelin in Humans (2004)

Ghrelin possesses strong GH-releasing activity but also other endocrine activities including stimulation of PRL and ACTH secretion, modulation of insulin secretion and glucose metabolism. It is assumed that the GH secretagogue (GHS) receptor (GHS-R) 1a mediates ghrelin actins provided its acylation in Serine 3; in fact, acylated ghrelin only is able to exert endocrine activities. Acylated ghrelin (AG) is present in serum at a 2.5 fold lower concentration than unacylated ghrelin (UAG). UAG, however, is not biologically inactive; it shares with AG some non-endocrine actions like cardiovascular effects, modulation of cell proliferation and even some influence on adipogenesis. Thus, these actions are likely to be mediated by GHS-R subtypes able to bind ghrelin independently of its acylation. In order to further clarify whether UAG is really devoid of any endocrine action, we studied the interaction of the combined administration of AG and UAG (1.0 μg/kg iv) in 6 normal young volunteers (age [mean ± SE]: 25.4 ± 1.2 yr; BMI: 22.3 ± 1.0 kg/m2). As expected, AG induced marked increase (p < 0.01) in circulating GH, PRL, ACTH and cortisol levels. AG administratioin was also followed by a decrease in insulin levels (−285.4 ± 64.8 mU∗min/l; p < 0.05) and an increase in plasma glucose levels (1068.4 ± 390.4 mg*min/dl; p < 0.01). UAG alone did not induce any change in these parameters. UAG also failed to modify the GH, PRL, ACTH and cortisol responses to AG. However, when UAG was co-administered together with AG, no significant change in insulin (−0.5 ± 40.9 mU*min/l) and glucose levels (455.9 ± 88.3 mg*min/dl) was recorded anymore, indicating that the insulin and glucose response to AG has been abolished by UAG. In conclusion, non-acylated ghrelin does not affect the GH, PRL, and ACTH response to acylated ghrelin but is able to antagonize the effects of acylated ghrelin on insulin secretion and glucose levels. These findings indicate that unacylated ghrelin is metabolically active and is likely to counterbalance the influence of acylated ghrelin on insulin secretion and glucose metabolism. As GHS-R1a is not bound by unacylated ghrelin, these findings suggest that GHS receptor subtypes mediate the metabolic actions of both acylated and unacylated ghrelin.
Architecture of a Power-Gated Wireless Sensor Node (2008)

In this paper we investigate the benefits of power gating in wireless sensor nodes operating at a very low duty cycle. It is shown that the static power loss in such a node is significant portion of the total power consumption. Therefore, we have defined power-gated wireless sensor node architecture and developed a power gating mechanism to reduce the static power loss of its functional blocks. The new node architecture, its components and power gating mechanism are described in detail.
Magnetic refrigeration: Single and multimaterial active magnetic regenerator experiments (2004)

An investigation of active magnetic regenerators (AMRs) has been performed near room temperature using helium as a heat transfer fluid and a magnetic field of 2 T. To evaluate the impact of the operating conditions, the performance of two reciprocating 90 g gadolinium packed bed regenerators was mapped as a function of the fluid flux and cycle frequency. In addition, two multilayer regenerators of similar mass and dimensions, composed of a layer of gadolinium and a layer of a gadolinium–terbium alloy, were tested and compared to the performance of the Gd-only regenerators. The multilayer regenerators produced a larger temperature span and cooling power compared to the single material regenerators of equivalent mass and geometry (temperature spans of about 20 and 16 K, respectively). Theses results validate the concept of a multilayer AMR, provide useful data for magnetic refrigerator design, and provide better understanding of active magnetic refrigeration.
Beta-catenin signaling in murine liver zonation and regeneration: A Wnt-Wnt situation! (2014)

Wnt-signaling is the major upstream effector of β-catenin activity in pericentral hepatocytes and during LR. Hepatocytes, cholangiocytes, or macrophages are not the source of Wnts in regulating hepatic zonation. However, Kupffer cells are a major contributing source of Wnt secretion necessary for β-catenin activation during LR.
Pulmonary Capillary Endothelium-Bound Angiotensin-Converting Enzyme Activity in Humans (1999)

Pulmonary endothelial ACE activity can be assessed in humans at the bedside by means of indicator-dilution techniques. Our data suggest homogeneous pulmonary capillary ACE concentrations and capillary transit times (tc) in both human lungs, and similar tc within the normal range of cardiac index. Amax/Km in the right lung is 54% of total Amax/Km in both lungs, suggesting that Amax/Km is a reliable and quantifiable index of DPCSA in humans.