gebhart/patrepeval huggingface dataset:
Differential modulation and demodulation of multi-frequency digital communications signals (2002)

Multiple-frequency modulation (MFM) is a bandwidth-efficient digital communication signaling technique that may be used effectively in mobile satellite communications links. Algorithms for generating and demodulating differentially encoded multifrequency quadrature phase shift keyed (MFQPSK) signals using discrete Fourier transform (DFT) techniques are discussed. The theory and a prototype system for differentially encoding and decoding MFQPSK in the frequency domain are developed. By using long baud intervals and corresponding small spacing of the carrier tones, problems associated with channel fading are greatly relieved with respect to the previous method of differentially encoding the multiple carrier tones from baud to baud. An MFM system has been configured to transmit MFQPSK over a 4-kHz bandpass channel. Tone spacings, or baud rates, of 15, 30, 60, 120, and 240 Hz were tested. Output signal-to-noise ratios were estimated by computing sample means and variances of the real and imaginary parts of X/sub a/. Experimental results are presented showing good agreement with the theory.< <ETX xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink">&gt;</ETX>
Molecular Size Distribution in Ethylene Oxide Polymers (1940)

ADVERTISEMENT RETURN TO ISSUEPREVArticleNEXTMolecular Size Distribution in Ethylene Oxide PolymersPaul J. FloryCite this: J. Am. Chem. Soc. 1940, 62, 6, 1561–1565Publication Date (Print):June 1, 1940Publication History Published online1 May 2002Published inissue 1 June 1940https://pubs.acs.org/doi/10.1021/ja01863a066https://doi.org/10.1021/ja01863a066research-articleACS PublicationsRequest reuse permissionsArticle Views2871Altmetric-Citations516LEARN ABOUT THESE METRICSArticle Views are the COUNTER-compliant sum of full text article downloads since November 2008 (both PDF and HTML) across all institutions and individuals. These metrics are regularly updated to reflect usage leading up to the last few days.Citations are the number of other articles citing this article, calculated by Crossref and updated daily. Find more information about Crossref citation counts.The Altmetric Attention Score is a quantitative measure of the attention that a research article has received online. Clicking on the donut icon will load a page at altmetric.com with additional details about the score and the social media presence for the given article. Find more information on the Altmetric Attention Score and how the score is calculated. Share Add toView InAdd Full Text with ReferenceAdd Description ExportRISCitationCitation and abstractCitation and referencesMore Options Share onFacebookTwitterWechatLinked InRedditEmail Other access optionsGet e-Alertsclose Get e-Alerts
Prognostic Significance of Bcl-2 Protein Expression and Bcl-2 Gene Rearrangement in Diffuse Aggressive Non-Hodgkin's Lymphoma (1997)

The prognostic significance of Bcl-2 protein expression and bcl-2 gene rearrangement in diffuse large cell lymphomas (DLCL) is controversial. Bcl-2 protein expression prevents apoptosis and may have an important role in clinical drug resistance. The presence of a bcl-2 gene rearrangement in de novo DLCL suggests a possible follicle center cell origin and perhaps a distinct clinical behavior more akin to low-grade non-Hodgkin's lymphoma (NHL). The purpose of this study was to determine the impact of Bcl-2 protein expression and bcl-2 gene rearrangement (mbr and mcr) on survival of a cohort of patients with DLCL who were uniformly evaluated and treated with effective chemotherapy. Patients included the original MACOP-B cohort (n = 121) and the initial 18 patients treated with the VACOP-B regimen (total = 139). All patients had advanced-stage disease, were 16 to 70 years old, and corresponded to Working Formulation categories F, G, or H. No patients had prior treatment, discordant lymphoma, or human immunodeficiency virus seropositivity. Paraffin sections from diagnostic biopsies were analyzed for bcl-2 gene rearrangement including mbr and mcr breakpoints by polymerase chain reaction and Bcl-2 protein expression by immunohistochemistry. With a median follow-up of 81 months, overall (OS), disease-free (DFS), and relapse-free survival (RFS) were measured to determine the prognostic significance of these parameters. Analyzable DNA was present in 118 of 139 (85%) cases, with 14 demonstrating a bcl-2 rearrangement (11 mbr, 3 mcr). All 14 of these bcl-2 gene rearrangement-positive cases were found in the 102 patients with a B-cell immunophenotype, but the presence of this rearrangement had no significant influence on survival. Bcl-2 protein expression was interpretable in 116 of 139 (83%) cases, with immunopositivity detected in 54 of 116 (47%). Using a cut-off of greater than 10% Bcl-2 immunopositive tumor cells for analysis, positive Bcl-2 protein expression was seen in 28 of 116 (24%) patients and the presence of this expression correlated with decreased 8-year OS (34% v 60%, P &lt; .01), DFS (32% v 66%, P &lt; .001), and RFS (25% v 59%, P &lt; .001). Bcl-2 protein expression remained significant in multivariate analysis that included the clinical international prognostic index factors and immunophenotype (P &lt; .02). In conclusion, although bcl-2 gene rearrangement status could not be shown to have an impact on outcome, Bcl-2 protein expression is a strong significant predictor of OS, DFS, and RFS in DLCLs.
Immune markers and differential signaling networks in ulcerative colitis and Crohnʼs disease (2012)

This comprehensive approach to quantifying gene expression provides insights into the pathogenesis of IBD by elucidating distinct immune signaling networks in CD and UC. Furthermore, this is the first study demonstrating that gene expression profiling in FFPE colon biopsies might be a practical and effective tool in the diagnosis and prognosis of IBD and may help identify molecular markers that can predict and monitor response to individualized therapeutic treatments.
Regiocontrolled Hydrosilation of .alpha.,.beta.-Unsaturated Carbonyl Compounds Catalyzed by Hydridotetrakis(triphenylphosphine)rhodium(I) (1995)

ADVERTISEMENT RETURN TO ISSUEPREVArticleNEXTRegiocontrolled Hydrosilation of .alpha.,.beta.-Unsaturated Carbonyl Compounds Catalyzed by Hydridotetrakis(triphenylphosphine)rhodium(I)G. Z. Zheng and T. H. ChanCite this: Organometallics 1995, 14, 1, 70–79Publication Date (Print):January 1, 1995Publication History Published online1 May 2002Published inissue 1 January 1995https://pubs.acs.org/doi/10.1021/om00001a015https://doi.org/10.1021/om00001a015research-articleACS PublicationsRequest reuse permissionsArticle Views1189Altmetric-Citations114LEARN ABOUT THESE METRICSArticle Views are the COUNTER-compliant sum of full text article downloads since November 2008 (both PDF and HTML) across all institutions and individuals. These metrics are regularly updated to reflect usage leading up to the last few days.Citations are the number of other articles citing this article, calculated by Crossref and updated daily. Find more information about Crossref citation counts.The Altmetric Attention Score is a quantitative measure of the attention that a research article has received online. Clicking on the donut icon will load a page at altmetric.com with additional details about the score and the social media presence for the given article. Find more information on the Altmetric Attention Score and how the score is calculated. Share Add toView InAdd Full Text with ReferenceAdd Description ExportRISCitationCitation and abstractCitation and referencesMore Options Share onFacebookTwitterWechatLinked InRedditEmail Other access optionsGet e-AlertscloseSupporting Info (3)»Supporting Information Supporting Information Get e-Alerts
Reliability of thyristor-based memory cells (2009)

This is the first published study of the reliability of thyristor-based high-speed memories. The T-RAM (thyristor-based random access memory) was characterized using test structures and multi-megabit product die fabricated in a 130 nm SOI logic technology. The reliability lifetime of a nominal bit was investigated by subjecting TCCT devices (thin capacitively coupled thyristor) to a DC current stress. The resulting acceleration model yields a lifetime of 1.0E+40 yrs for the data-1 state and 1.0E+5 yrs for the data-0 state. These long lifetimes are consistent with the 26 FIT long-term failure rate found for 9 Mb arrays, from dynamic lifetest on 9 Mb & 18 Mb T-RAM product die having full SRAM functionality. The susceptibility of T-RAM arrays to soft errors was assessed by accelerated neutron testing, and accelerated alpha testing, of 9 Mb T-RAM product die as well as 9 Mb SRAM product die from three suppliers. n-SER for the T-RAM is 610 FIT/Mb, better than the average of 700 FIT/Mb for 6T SRAM technology. Exposure of the T-RAM product die to X-rays showed that they tolerate doses of 450 rad or more (3-4x the dose for X-ray inspections) without degradation of nominal TCCT retention times, and without functional failure of memory cells. Taken together, the results of this study shows that T-RAM is a reliable memory technology.
Fatty-acid-binding protein as a plasma marker for the estimation of myocardial infarct size in humans. (1994)

The data indicate that FABP released from the heart after AMI is quantitatively recovered in plasma and that FABP is a useful biochemical plasma marker for the estimation of myocardial infarct size in humans.
Infliximab for refractory ulcerative colitis or indeterminate colitis: an open‐label multicentre study (2003)

Infliximab was able to induce a rapid response in some patients with UC or indeterminate colitis refractory to conventional treatment. Long-term results were less favourable, with frequent relapses, and about one-third of the patients required a colectomy.
Brain-derived neurotrophic factor promotes the survival of neurons arising from the adult rat forebrain subependymal zone. (1995)

Neuronal precursor cells persist in the adult forebrain ependymal/subependymal zone (SZ) and have been found to produce neurons in cultures derived from birds, rodents, and humans. We postulated that the survival of neurons generated from these cells might be constrained in adulthood by the local absence of trophic support. To test this hypothesis, we established explant cultures of adult rat forebrain SZ and assessed the effect of defined neurotrophins on the survival of new neurons arising from these explants. We found that microtubule-associated protein 2+ neurons arose from explants derived from a wide area of the SZ, spanning the rostral 6 mm of the ventricular system. In cultures exposed to brain-derived neurotrophic factor (BDNF), > 35% of new neurons survived at 22 days in vitro (DIV), and > 25% survived at 42 DIV, concurrent with the virtually complete loss of neurons in unsupplemented controls. The surviving cells expressed trkB, the high-affinity receptor for BDNF. In contrast, neither nerve growth factor nor neurotrophic factor 3 enhanced neuronal survival. Thus, BDNF supports the survival of neurons produced by the adult rat forebrain and may act as a permissive factor for neuronal recruitment in adulthood.
Identification of staphylococcal enterotoxin B sequences important for induction of lymphocyte proliferation by using synthetic peptide fragments of the toxin (1994)

A series of 13 synthetic peptides, approximately 30 amino acids each, which spanned the entire sequence of staphylococcal enterotoxin B (SEB) were tested to evaluate their effects on T-cell proliferation in a culture system containing elutriated human peripheral blood lymphocytes incubated with a specific ratio of mononuclear cells. Four peptide regions were found to inhibit SEB-induced proliferation; they included sequences 1 to 30 (previously thought to be involved in major histocompatibility complex class II binding), 61 to 92 (sequences which relate to the T-cell receptor site), 93 to 112 (a linear sequence corresponding to the cysteine loop), and 130 to 160 (containing a highly conserved sequence, KKKVTAQEL). Antisera raised to this last peptide were capable of neutralizing SEB-induced proliferation. Antisera raised against the peptides which overlapped this sequence also were somewhat inhibitory. Neutralizing antisera were not produced from any other peptide sequence tested. To determine if any of these effects were nonspecific with regard to SEB-induced proliferation, the peptides were tested for inhibition of phorbol dibutyryl ester-induced proliferation, and only the sequence 93 to 112 (corresponding to the cysteinyl loop region) was consistently inhibitory (40%). Of the regions which displayed inhibition of SEB-induced proliferation, the peptide 130 to 160 inhibited binding of 125I-SEB to lymphocytes. These data suggest that the residues containing and surrounding the sequence KKKVTAQEL may be critical in the SEB-induced proliferation and may be useful for developing neutralizing antisera to SEB.
The Two Major Structural Phosphoproteins (pp65 and pp150) of Human Cytomegalovirus and Their Antigenic Properties (1987)

Human cytomegalovirus (HCMV) purified from cell culture contains two dominant structural phosphoproteins with apparent molecular weights of 65,000 and 150,000, designated as pp65 and pp150 respectively. The humoral immune response of infected individuals against pp65 is relatively weak and is not always detectable by Western blot analyses. This report shows that recent clinical isolates of HCMV do not necessarily have pp65 as a prominent constituent, suggesting that the low immune reaction is due to variable expression of the pp65 in natural infections. However, the HCMV strains tested in this study produced the large structural phosphoprotein (pp150) in about equal amounts. The pp150 is remarkably immunogenic, if compared with all other virion constituents; serum pools and individual sera from HCMV-infected patients recognized this particular protein intensively in immunoblot assays. Thus, phosphoprotein pp150 seems to be the primary polypeptide candidate for expression cloning in order to develop reagents for novel ways of HCMV diagnosis.
Treatment of nonallergic perennial rhinitis (2004)

Nonallergic perennial rhinitis (also commonly referred to as vasomotor rhinitis) is a chronic non-IgE-mediated condition that is characterized by symptoms which are similar to those seen in allergic rhinitis, but which persist for over nine months each year. Although treatment of vasomotor rhinitis involves the use of either intranasal corticosteroids or antihistamines, the corticosteroids are generally not effective in treatment of all the symptoms of vasomotor rhinitis and have generally been shown to be effective in patients with eosinophilia. With the exception of azelastine, the only topical antihistamine to be approved by the FDA for the treatment of nonallergic rhinitis, the antihistamines have also produced inconsistent results. While clinical studies of azelastine have demonstrated that this drug is highly efficacious in the treatment of all the symptoms of vasomotor rhinitis, mechanistic studies have demonstrated that azelastine has potent anti-inflammatory effects (in particular attenuation of the expression and synthesis of pro-inflammatory cytokines, leukotrienes, and cell adhesion molecules), which are likely to contribute to its clinical efficacy. Furthermore, pharamacokinetic studies have suggested that since azelastine has a more rapid onset of action, compared to most other antihistamines and intranasal corticosteroids, then azelastine nasal spray may be considered as primary therapy for patients with symptoms of both allergic and/or vasomotor (nonallergic perennial) rhinitis.
Impaired Adaptive Cellular Responses to Oxidative Stress and the Pathogenesis of Alzheimer's Disease (2010)

As is generally true with other age-related diseases, Alzheimer's disease (AD) involves oxidative damage to cellular components in the affected tissue, in this case the brain. The causes and consequences of oxidative stress in neurons in AD are not fully understood, but considerable evidence points to important roles for accumulation of amyloid β-peptide upstream of oxidative stress and perturbed cellular Ca(2+) homeostasis and energy metabolism downstream of oxidative stress. The identification of mutations in the β-amyloid precursor protein and presenilin-1 as causes of some cases of early onset inherited AD, and the development of cell culture and animal models based on these mutations has greatly enhanced our understanding of the AD process, and has greatly expanded opportunities for preclinical testing of potential therapeutic interventions. In this regard, and of particular interest to us, is the elucidation of adaptive cellular stress response pathways (ACSRP) that can counteract multiple steps in the AD neurodegenerative cascades, thereby limiting oxidative damage and preserving cognitive function. ACSRP can be activated by factors ranging from exercise and dietary energy restriction, to drugs and phytochemicals. In this article we provide an overview of oxidative stress and AD, with a focus on ACSRP and their potential for preventing and treating AD.
Circadian and sleep-dependent regulation of hormone release in humans. (1999)

Daily oscillations characterize the release of nearly every hormone. The circadian pacemaker, located in the suprachiasmatic nucleus of the hypothalamus, generates circadian, approximately 24-hour rhythms in many physiologic functions. However, the observed hormonal oscillations do not simply reflect the output of this internal clock. Instead, daily hormonal profiles are the product of a complex interaction between the output of the circadian pacemaker, periodic changes in behavior, light exposure, neuroendocrine feedback mechanisms, gender, age, and the timing of sleep and wakefulness. The interaction of these factors can affect hormonal secretory pulse frequency and amplitude, with each endocrine system differentially affected by these factors. This chapter examines recent advances in understanding the effects on endocrine rhythms of a number of these factors. Sleep exerts a profound effect on endocrine secretion. Sleep is a dynamic process that is characterized by periodic changes in electrophysiologic activity. These electrophysiologic changes, which are used to mark the state and depth of sleep, are associated with periodic, short-term variations in hormonal levels. The secretion of hormones such as renin and human growth hormone are strongly influenced by sleep or wake state, while melatonin and cortisol levels are relatively unaffected by sleep or wake state. In addition, sleep is associated with changes in posture, behavior, and light exposure, each of which is known to affect endocrine secretion. Furthermore, the tight concordance of habitual sleep and wake times with certain circadian phases has made it difficult to distinguish sleep and circadian effects on these hormones. Specific protocols, designed to extract circadian and sleep information semi-independently, have been developed and have yielded important insights into the effects of these regulatory processes. These results may help to account for changes in endocrine rhythms observed in circadian rhythm sleep disorders, including the dyssomnia of shift work and visual impairment. Yet to be fully investigated are the interactions of these factors with age and gender. Characterization of the factors governing hormone secretion is critical to understanding the temporal regulation of endocrine systems and presents many exciting areas for future research.
The Oncoprotein E2A-Pbx1a Collaborates with Hoxa9 To Acutely Transform Primary Bone Marrow Cells (1999)

A recurrent translocation between chromosome 1 (Pbx1) and 19 (E2A) leading to the expression of the E2A-Pbx1 fusion oncoprotein occurs in approximately 5 to 10% of acute leukemias in humans. It has been proposed that some of the oncogenic potential of E2A-Pbx1 could be mediated through heterocomplex formation with Hox proteins, which are also involved in human and mouse leukemias. To directly test this possibility, mouse bone marrow cells were engineered by retroviral gene transfer to overexpress E2A-Pbx1a together with Hoxa9. The results obtained demonstrated a strong synergistic interaction between E2A-Pbx1a and Hoxa9 in inducing growth factor-independent proliferation of transduced bone marrow cells in vitro and leukemic growth in vivo in only 39 +/- 2 days. The leukemic blasts which coexpress E2A-Pbx1a and Hoxa9 showed little differentiation and produced cytokines such as interleukin-3, granulocyte colony-stimulating factor, and Steel. Together, these studies demonstrate that the Hoxa9 and E2A-Pbx1a gene products collaborate to produce a highly aggressive acute leukemic disease.
The Propeptide of the Transforming Growth Factor-β Superfamily Member, Macrophage Inhibitory Cytokine-1 (MIC-1), Is a Multifunctional Domain That Can Facilitate Protein Folding and Secretion (2001)

Macrophage inhibitory cytokine-1 (MIC-1) is a divergent member of the transforming growth factor-beta (TGF-beta) superfamily. While it is synthesized in a pre-pro form, it is unique among superfamily members because it does not require its propeptide for correct folding or secretion of the mature peptide. To investigate factors that enable these propeptide independent events to occur, we constructed MIC-1/TGF-beta1 chimeras, both with and without a propeptide. All chimeras without a propeptide secreted less efficiently compared with the corresponding constructs with propeptide. Folding and secretion were most affected after replacement of the predicted major alpha-helix in the mature protein, residues 56-68. Exchanging the human propeptide in this chimera with either the murine MIC-1 or TGF-beta1 propeptide resulted in secretion of the unprocessed, monomeric chimera, suggesting a specific interaction between the human MIC-1 propeptide and mature peptide. Propeptide deletion mutants enabled identification of a region between residues 56 and 78, which is important for the interaction between the propeptide and the mature peptide. Cotransfection experiments demonstrated that the propeptide must be in cis with the mature peptide for this phenomenon to occur. These results suggest a model for TGF-beta superfamily protein folding.
Conformational Switching and the Synthesis of Spiro[2H-indol]-3(1H)-ones by Radical Cyclization (1999)

Radical cyclization of 1-(2-bromophenylamino)cyclohexanecarbonitriles (3, X = CH) and 4-(2-bromophenylamino)-4-piperidinecarbonitriles (3, X = N) provide spiro[2H-indole-2-cyclohexan]-3(1H)-imines (5, X = CH) and spiro[2H-indole-2,4'-piperidin]-3(1H)-imines (5, X = N), respectively, in 33-57% yields. This contradicts a recent report that 1-(2-bromophenylamino)cyclohexanecarbonitrile (3, X-R(2) = CH(2)), treated under apparently identical conditions, led only to nitrile transfer product 6 (X-R(2) = CH(2)). Acidic hydrolyses of the imines provide the corresponding ketones 2 in quantitative yields. Single-crystal X-ray analyses of ketone 2e and nitrile 3e indicate that the relative configuration of the aromatic nitrogen has been inverted during the cyclization. In addition, NOE NMR analyses of spiroindolepiperidine 2c and its aniline-nitrogen-methylated analogue 10a show that the relative conformation of the piperidine ring has inverted. Thus, methylation of 2c acts as a conformational "switch" for the spiroindolepiperidine ring system.