gebhart/patrepeval huggingface dataset:
Expected loss analysis of thresholded authentication protocols in noisy\n conditions (2010)

A number of authentication protocols have been proposed recently, where at\nleast some part of the authentication is performed during a phase, lasting $n$\nrounds, with no error correction. This requires assigning an acceptable\nthreshold for the number of detected errors. This paper describes a framework\nenabling an expected loss analysis for all the protocols in this family.\nFurthermore, computationally simple methods to obtain nearly optimal value of\nthe threshold, as well as for the number of rounds is suggested. Finally, a\nmethod to adaptively select both the number of rounds and the threshold is\nproposed.\n
CNTF Mediates Neurotrophic Factor Secretion and Fluid Absorption in Human Retinal Pigment Epithelium (2011)

Ciliary neurotrophic factor (CNTF) protects photoreceptors and regulates their phototransduction machinery, but little is known about CNTF's effects on retinal pigment epithelial (RPE) physiology. Therefore, we determined the expression and localization of CNTF receptors and the physiological consequence of their activation in primary cultures of human fetal RPE (hfRPE). Cultured hfRPE express CNTF, CT1, and OsM and their receptors, including CNTFRα, LIFRβ, gp130, and OsMRβ, all localized mainly at the apical membrane. Exogenous CNTF, CT1, or OsM induces STAT3 phosphorylation, and OsM also induces the phosphorylation of ERK1/2 (p44/42 MAP kinase). CNTF increases RPE survivability, but not rates of phagocytosis. CNTF increases secretion of NT3 to the apical bath and decreases that of VEGF, IL8, and TGFβ2. It also significantly increases fluid absorption (J(V)) across intact monolayers of hfRPE by activating CFTR chloride channels at the basolateral membrane. CNTF induces profound changes in RPE cell biology, biochemistry, and physiology, including the increase in cell survival, polarized secretion of cytokines/neurotrophic factors, and the increase in steady-state fluid absorption mediated by JAK/STAT3 signaling. In vivo, these changes, taken together, could serve to regulate the microenvironment around the distal retinal/RPE/Bruch's membrane complex and provide protection against neurodegenerative disease.
Phosphorylation by PKA and Cdk5 Mediates the Early Effects of Synapsin III in Neuronal Morphological Maturation (2015)

Synapsin III (SynIII) is a neuron-specific phosphoprotein that plays a unique role in neuronal development. SynIII is phosphorylated by cAMP-dependent protein kinase (PKA) at a highly conserved phosphorylation site and by cyclin-dependent kinase-5 (Cdk5) at a newly described site. Although SynIII is known to be involved in axon elongation in vitro, the role of its phosphorylation by PKA and Cdk5 in the modulation of this process is unknown. We expressed either wild-type (WT) or phosphorylation-site mutants of SynIII in primary SynIII knock-out (KO) mouse neurons at early stages of in vitro development. Whereas the neurite elongation phenotype of SynIII KO neurons was fully rescued by the expression of WT SynIII, the expression of nonphosphorylatable and pseudo-phosphorylated PKA mutants was ineffective. Also, the nonphosphorylatable Cdk5 mutant was unable to rescue the neurite elongation phenotype of SynIII KO neurons. By contrast, the pseudo-phosphorylated mutant rescued the delay in neuronal maturation and axonal elongation, revealing a Cdk5-dependent regulation of SynIII function. Interestingly, SynIII KO neurons also exhibited decreased survival that was fully rescued by the expression of WT SynIII, but not by its phosphorylation mutants, and was associated with increased activated caspase3 and altered tropomyosin receptor kinase B isoform expression. These results indicate that PKA and Cdk5 phosphorylation is required for the physiological action of SynIII on axon specification and neurite outgrowth and that the expression of a functional SynIII is crucial for cell survival. Significance statement: Synapsin III is an atypical member of the synapsin family of synaptic vesicle-associated phosphoproteins that is precociously expressed in neurons and is downregulated afterward. Although experimental evidence suggests a specific role for Synapsin III in neuronal development, the molecular mechanisms are still largely unknown. We found that Synapsin III plays a central role in early stages of neuronal development involving neuronal survival, polarization, and neuritic growth and that these effects are dependent on phosphorylation by cAMP-dependent protein kinase and cyclin-dependent protein kinase-5. These results explain the recently described neurodevelopmental defects in the migration and orientation of Synapsin III-depleted cortical neurons and support the potential association of Synapsin III with neurodevelopmental disorders such as schizophrenia.
Are You Experienced? The Copyright Implications of Web Site Modification Technology (2001)

Recently, several new Internet technologies that modify, or allow users to modify, the way Web sites are experienced have emerged.In many cases, these technologies give end users or third parties a greater degree of control over Web sites than the owners of the sites intended.Web site owners often object to the use of expeience-modifying technologies, and have advanced a number of legal theories to support their claims.Among these theories is the contention that employing technologies to modify how a user experiences a Web site constitutes copyright infringement.This Comment examines five types of Web site modification technology-linking and framing, comparison shopping applications, commentary Web sites and software, Web site customization tools, and ad stripping softwareand argues that their use does not infringe Web site owners' exclusive rights under existing
How cyclosporine modifies histological and molecular events in the vascular wall during chronic rejection of rat cardiac allografts. (1995)

Accelerated allograft arteriosclerosis (chronic rejection) has emerged as a major factor affecting long-term survival of human cardiac allografts. The underlying mechanism of this disorder remains unclear. The purpose of this study was to investigate the effect of cyclosporine on the development of cardiac allograft arteriosclerosis at the cellular and molecular level. Heterotopic rat cardiac allografts from DA donors to WF recipients, with a strong genetic disparity in major histocompatibility complex and non-major histocompatibility complex loci, were used. The allograft recipients received triple-drug immunosuppression consisting of methylprednisolone (0.5 mg/kg/day), azathioprine (2 mg/kg/day), and three different doses of cyclosporine A (CsA; 5, 10, and 20 mg/kg/day). The grafts were removed 3 months after transplantation and processed for histology and immunohistochemistry. Low dose CsA (5 mg/kg/day) was associated with a severe form of intimal cell accumulation and intimal thickening in epicardial arteries and in smaller intramyocardial arterioles with nearly occluded vessel lumens 3 months after transplantation. The intermediate dose CsA (10 mg/kg/day) significantly inhibited arterial intimal thickening but was not efficient in reducing intimal cell accumulation. Instead, high dose CsA (20 mg/kg/day) significantly inhibited all arteriosclerotic vascular wall changes in the allografts. Immunohistochemistry revealed that the occluded epicardial arteries of cardiac allografts with low dose CsA expressed VCAM-1 on the endothelium. Higher CsA doses significantly reduced the expression of endothelial VCAM-1. Neither ICAM-1 nor major histocompatibility complex class II were expressed. Perivascular arterial infiltrates consisting of T helper cells and monocytes/macrophages were a characteristic finding in the allograft with low dose CsA. In the allografts treated with higher doses of CsA, arterial perivascular infiltrates were seldom seen. Our results conclusively demonstrate that sufficient immunosuppression with CsA inhibits intimal thickening and intimal cell accumulation of long-surviving rat cardiac allografts in a dose-dependent fashion. Arteriosclerotic alterations associated with increased expression of arterial endothelial VCAM-1 were totally down-regulated by high doses of CsA.
Repeated Intraportal Injections of Subtherapeutic Islet Cell Isografts Restore Normoglycemia in Streptozotocin-Diabetic Rats (1997)

Poor engraftment and consequent loss of β-cell mass could be one of the factors that are responsible for function loss after intraportal islet transplantation (Tx). Streptozotocin-diabetic rats were transplanted with syngeneic islets, which were injected into the portal vein via an indwelling catheter connected to a subcutaneous port. In Group I (n = 6), 1,000 islets were injected in a single dose into the liver. In Group II (n = 6), five doses of 200 islets were repeatedly injected over a period of 14 days, for a total of 1,000 islets. In Group III (n = 4), five decreasing doses of islets were injected over a period of 14 days, for a total of 750 islets. Nonfasting blood glucose (n-FBG) and body weight (b.wt.) were determined twice a week and an intravenous glucose tolerance test (IVGTT) was performed at 30 and 90 days. In Group I, n-FBG decreased in 2 wk from the time of first islet injection, averaging 110 ± 21.9 mg/dL at 1 mo (p &lt; 0.05 vs. normal controls); this value was maintained throughout the 3-mo duration of the study. In Group II, n-FBG was normalized in 2 wk averaging 90.2 ± 25 mg/dL on day 12 (p = NS vs. normal controls) and 75.8 ± 14.6 mg/dL at 1 month (p = NS vs. normal controls); this value was maintained throughout the 3-mo duration of the study. In Group III, n-FBG decreased to normal values in 2 wk, averaging 77 ± 15.7 mg/dL at 1 mo (p = NS vs. normal controls), but normoglycemia was maintained for 40 days and then followed by a progressive increase. Only in Group II, K G (percent/min decline in glucose level) was not significantly different from that of normal controls (1.702 ± 0.531 at 1 mo and 1.676 ± 0.891 at 3 mo), while it was significantly lower than normal controls in both Group I and III animals. Body weight increase after Tx correlated with the number of transplanted islets and at 90 days, Group III rats showed less increase than Groups I and II (p &lt; 0.05), while no significant differences in b.wt. were recorded between Group I and II. The findings indicate that intraportal islet Tx, injected repeatedly and in small doses, produced better metabolic effects than injection of the same total number of islets in a single dose. Copyright © 1997 Elsevier Science Inc.
Sequential combination of high dose methotrexate andl-asparaginase followed by allogeneic transplant: a first-line strategy for CD4+/CD56+ hematodermic neoplasm (2012)

Described for the first time by Adachi et al. in 1994 [1], CD4+/CD56+ hematodermic neoplasm was thought to be of natural killer (NK) lineage due to expression of the NK-cell marker CD56 by the tumo...
Engineered peptide PLG0206 overcomes limitations of a challenging antimicrobial drug class (2022)

The absence of novel antibiotics for drug-resistant and biofilm-associated infections is a global public health crisis. Antimicrobial peptides explored to address this need have encountered significant development challenges associated with size, toxicity, safety profile, and pharmacokinetics. We designed PLG0206, an engineered antimicrobial peptide, to address these limitations. PLG0206 has broad-spectrum activity against >1,200 multidrug-resistant (MDR) ESKAPEE clinical isolates, is rapidly bactericidal, and displays potent anti-biofilm activity against diverse MDR pathogens. PLG0206 displays activity in diverse animal infection models following both systemic (urinary tract infection) and local (prosthetic joint infection) administration. These findings support continuing clinical development of PLG0206 and validate use of rational design for peptide therapeutics to overcome limitations associated with difficult-to-drug pharmaceutical targets.
Retinoid receptor-dependent and -independent effects of N-(4-hydroxyphenyl)retinamide in F9 embryonal carcinoma cells. (1999)

Fenretinide (N-[4-hydroxyphenyl]retinamide (4HPR)) is a retinoid analogue with antitumor and chemopreventive activities. The mechanism of action of 4HPR is not fully understood, but it is hypothesized that this compound acts independently of the nuclear retinoid receptor pathway. To test this hypothesis directly, we have analyzed the activity of 4HPR on a panel of F9 embryonal carcinoma cell lines, which includes wild-type and mutant lines that lack expression of retinoic acid receptor gamma, retinoid X receptor alpha, or both. 4HPR (10 microM) treatment resulted in a rapid induction of cell death in F9 cells, which was responsible for their near elimination by 48 h. This effect occurred in the receptor-null cell lines as well. Treatment of the wild-type cells for 4 days with 1 microM 4HPR also resulted in a primitive endodermal differentiated phenotype that is normally seen upon all-trans-retinoic acid treatment and is characterized by the up-regulation of laminin B1 and type IV collagen. This differentiation response did not occur in the receptor-null cells. Therefore, two distinct effects of 4HPR were identified in this system: a rapid induction of cell death and a slower induction of differentiation, which are likely to be receptor independent and dependent, respectively.
Interaction between asymmetric solutes and solvents. N-Lauroyl-L-valyl-t-butylamide as stationary phase in gas liquid partition chromatography (1971)

B. Feibush, J. Chem. Soc. D, 1971, 544 DOI: 10.1039/C29710000544
Power Electronics Thermal Management R&D; NREL (National Renewable Energy Laboratory) (2017)

Presentation containing an update for the Power Electronics Thermal Management project in the Electric Drive Train task funded by the Vehicle Technology Office of DOE. This presentation outlines the purpose, plan, and results of research thus far for cooling and material selection strategies to manage heat in power electronic assemblies such as inverters, converters, and chargers.
Nano-Media: A Novel Multi-Channel Color Image Display with Embedded Covert Information (2014)

In this paper, a novel color image display with concurrent data storage is presented. We use a Nano-Media concept that consists of a nano-fabric based on sub-wavelength pixelated structures and an intensity control layer (ICL) deposited on top of a fabric. The ICL is used to tune the brightness of individual RGB sub-pixels and to obtain the desired pattern, data or image. Using this technology, any information can be stored and displayed as optical machine and/or human readable. The experimental work is presented to show the Nano-Media used for the multispectral layers of information storage and display. The fabrication results are discussed together with the practical examples for various applications.
Sipuleucel-T in metastatic castration-resistant prostate cancer (mCRPC) patients ≥80 years-old: Data from PROCEED. (2014)

64 Background: Sipuleucel-T is an autologous cellular immunotherapy indicated for asymptomatic or minimally symptomatic mCRPC based on data from the pivotal phase 3 IMPACT trial that demonstrated a 22% reduction in the risk of death. Given the high prevalence of older men in the mCRPC patient (pt) population, we sought to understand disease characteristics and sipuleucel-T product parameters in pts ≥80 years (yrs). Methods: PROCEED is an ongoing phase 4 registry enrolling pts treated with sipuleucel-T within ≤6 months. Baseline pt demographics and disease characteristics were collected. Sipuleucel-T product parameters that were assessed included: total nucleated cell (TNC) count, antigen presenting cell (APC) count (large CD54 + cells), and APC activation (upregulation of CD54; a measure of product potency). Results: As of May 2013, 1254 subjects were enrolled and have completed treatment. Of these, 278 (20%) pts were ≥80 yrs-old. Disease and infused product characteristics in pts ≥80 yrs vs. &lt;80 yrs are detailed in the table below. Product parameters appear similar between groups. Conclusions: In this large cohort of elderly pts ≥80 yrs treated prospectively with sipuleucel-T immunotherapy, we demonstrate that product parameters were similar to their younger counterparts (&lt;80 years). This implies adequate immune up-regulation in elderly pts. Additional follow-up is needed to explore correlations between OS and various immune parameters in both groups. Clinical trial information: NCT01306890. [Table: see text]
Characterization of the baboon erythrocyte C3b-binding protein. (1989)

E from primates demonstrate type 1 CR (CR1) with binding specificities for C3b and C4b. In the present study we characterized the E C3b-binding protein of baboons. We showed that three out of four mouse mAb and one polyclonal antiserum, raised against human E CR1, cross-reacted with baboon E. In addition, one anti-human CR1 mAb (1B4) and a polyclonal anti-human CR1 inhibited the binding of C3b opsonized immune complexes to baboon E. Finally, a mAb to human CR1 (E11) recognized epitopes on E of a variety of nonhuman primates, including baboons. SDS-PAGE analysis of biochemically purified baboon E membrane fractions reactive with E11 demonstrated a 65-kDa protein as a major component. Affinity absorption and elution experiments verified this protein to be E11 reactive as well as a C3b binding protein. E surface radiolabeling, followed by C3i affinity purification, confirmed that this 65-kDa protein is the only C3b-binding protein present on the baboon E membrane. We postulate that the baboon E 65-kDa protein is the equivalent of the human E CR1. In addition, there appear to be antigenic similarities between the baboon E 65-kDa protein and the human E CR1.
THE SUITABILITY OF SPANGLER'S IOWA FORMULA FOR PREDICTING DEFLECTION IN ALL FLEXIBLE PIPES (1998)

This project assessed the impact of a school-based AIDS prevention program on student participation in sexual risk and protective behaviors such as use of condoms and use of condoms with foam and intention to participate in such behaviors. The paper focuses on students who became sexually active for the first time between the seventh and eighth grade ("changers," n = 312). The school-based intervention was developed using social cognitive theory and the social influences model of behavior change. Using an experimental, longitudinal design, 15 high-risk school districts were divided randomly into two treatment (10 districts) and one control (five districts) conditions. Students in both treatment conditions received a 10-lesson classroom program in the seventh grade with a five-lesson booster in the eighth grade, while control students received basic AIDS education (current practice in their districts) in compliance with state mandates. Results indicated classroom programs had an impact on certain protective behaviors and on frequency of sexual activity the past month. Post-intervention measures also indicated the program affected students' intentions to perform specific protective behaviors.
Ultrasonic Analysis of Peptide- and Antibody-Targeted Microbubble Contrast Agents for Molecular Imaging of α<SUB>v</SUB>β<SUB>3</SUB>-Expressing Cells (2004)

The goal of targeted ultrasound contrast agents is to significantly and selectively enhance the detection of a targeted vascular site. In this manuscript, three distinct contrast agents targeted to the alphavbeta3 integrin are examined. The alphavbeta3 integrin has been shown to be highly expressed on metastatic tumors and endothelial cells during neovascularization, and its expression has been shown to correlate with tumor grade. Specific adhesion of these contrast agents to alphavbeta3-expressing cell monolayers is demonstrated in vitro, and compared with that of nontargeted agents. Acoustic studies illustrate a backscatter amplitude increase from monolayers exposed to the targeted contrast agents of up to 13-fold (22 dB) relative to enhancement due to control bubbles. A linear dependence between the echo amplitude and bubble concentration was observed for bound agents. The decorrelation of the echo from adherent targeted agents is observed over successive pulses as a function of acoustic pressure and bubble density. Frequency-domain analysis demonstrates that adherent targeted bubbles exhibit high-amplitude narrowband echo components, in contrast to the primarily wideband response from free microbubbles. Results suggest that adherent targeted contrast agents are differentiable from free-floating microbubbles, that targeted contrast agents provide higher sensitivity in the detection of angiogenesis, and that conventional ultrasound imaging techniques such as signal subtraction or decorrelation detection can be used to detect integrin-expressing vasculature with sufficient signal-to-noise.
DSA Are Associated With More Graft Injury, More Fibrosis, and Upregulation of Rejection-associated Transcripts in Subclinical Rejection (2019)

T cell-mediated rejection seems to form a continuum of alloimmune activation. Although subTCMR exhibited less expression of TCMR-associated transcript, DSA positivity in subTCMR was associated with an upregulation of rejection-associated transcripts. The identification of DSA positive subclinical rejection might help to define patients with more inflammation in the graft and development of fibrosis.
A Novel Inhibitor of STAT5 Signaling Overcomes Chemotherapy Resistance in Myeloid Leukemia Cells (2019)

Signal transducers and activators of transcription 5A and 5B (STAT5A and STAT5B) are crucial downstream effectors of tyrosine kinase oncogenes (TKO) such as BCR-ABL in chronic myeloid leukemia (CML) and FLT3-ITD in acute myeloid leukemia (AML). Both proteins have been shown to promote the resistance of CML cells to tyrosine kinase inhibitors (TKI) such as imatinib mesylate (IM). We recently synthesized and discovered a new inhibitor (17f) with promising antileukemic activity. 17f selectively inhibits STAT5 signaling in CML and AML cells by interfering with the phosphorylation and transcriptional activity of these proteins. In this study, the effects of 17f were evaluated on CML and AML cell lines that respectively acquired resistance to IM and cytarabine (Ara-C), a conventional therapeutic agent used in AML treatment. We showed that 17f strongly inhibits the growth and survival of resistant CML and AML cells when associated with IM or Ara-C. We also obtained evidence that 17f inhibits STAT5B but not STAT5A protein expression in resistant CML and AML cells. Furthermore, we demonstrated that 17f also targets oncogenic STAT5B N642H mutant in transformed hematopoietic cells.