gebhart/patrepeval huggingface dataset:
Techniques for data hiding in audio files (1995)

Data hiding is a group of techniques for embedding data in media such as images and audio signals. Ideally, the data will be directly embedded into the data stream of the host medium imperceivably, and will also be immune to the modification of the host medium, allowing the data to stay embedded. The process is constrained by the bandwidth of data to be embedded, the need for invariance of the data under conditions where the &quot;host&quot; signal is subject to distortions, and the degree to which the data must be immune to interception, modification, or removal by a third party _ Both novel and traditional techniques for data hiding are described and evaluated. This work has focused primarily on audio.
Binding of <sup>125</sup>I‐labelled human αinterferon to human lymphoid cells (1981)

To investigate the binding of interferon to human lymphoid cells, we purified human alpha interferon and radio-labelled it with iodine-125. Binding at 4 degrees C could be saturated and was inhibited by unlabelled interferon; it was specific for cells of human origin. Dissociation constants for the complex of interferon and receptor site were of the order 10(-9)-10(-11) M. All human cells tested showed such binding. Occupation of these high-affinity sites, at 37 degrees C, was compared with the inhibition of cellular growth due to interferon. The most sensitive cell line (Daudi) gave a complete biological response with only a fraction of its sites occupied. Evidence of two sites was found for a line (P3HRI) showing intermediate sensitivity. A relatively insensitive line (Raji) showed no response when all its high-affinity sites were occupied.
Non Stress Test as a Predictor of Maternal and Fetal Outcome in Patients Presenting with Reduced Fetal Movement at Term (2022)

We concluded that the Non stress test is a good predictor of maternal and fetal outcome detecting fetal hypoxia already present or likely to develop in patient presenting with reduced fetal movement in term pregnancies without complication.
Historical Perspective (2010)

Abstract Issues that have been debated throughout the history of drug metabolism are still disputed to some degree. Physiological function of drug metabolism has broadened to include endogenous compounds and endogenous regulatory pathways. The article offers insights into the history of drug metabolism studies, with special emphasis on enzymatic metabolism of drugs.
Acute Postoperative Pain (2017)

Inadequate management of acute postoperative pain increases morbidity and mortality. Poorly controlled pain results in delayed hospital discharge and may lead to the development of chronic pain. Current evidence supports the implementation of a multimodal analgesic regimen, where different pharmacologic and nonpharmacologic interventions are used. The selection of the different components of this multimodal analgesic approach should consider their potential benefits and limitations, as well as the unique patient characteristics and the surgical procedure. It is the responsibility of the perioperative health care provider to formulate an optimal pain management strategy to ultimately enhance patient satisfaction and improve short- and long-term outcomes.
Alloy Design for Fatigue and Fracture (1996)

Abstract This article reviews the basic processes of fracture and fatigue and shows how these processes occur in materials. It presents an overview of the fatigue mechanisms and some related models for appropriate classes of materials, such as carbon and alloy steels, aluminum alloys, and titanium alloys. Microstructural factors that affect the fracture toughness of these materials, are discussed. The article describes fatigue crack propagation (FCP) mechanisms and related models. It also analyzes FCP behavior in these materials, with an emphasis on general microstructural factors.
Abstract 3770: CAR-T cell harboring a camelid single domain antibody as a targeting agent to kill tumors expressing VEGFR2 (2017)

Abstract Modulation of the immune system is showing tremendous promise in the treatment of malignancies. In addition to checkpoint inhibitors that re-activate T cells present in the tumor microenvironment, exogenously transduced chimeric antigen receptor (CAR) T cells are providing excellent responses in clinical trials for the treatment of leukemias. In this study, we describe CAR-T cells that target VEGFR2-expressing tumors. Angiogenesis is the process of new blood vessel formation and is essential for a tumor to grow beyond a certain size. Tumors secrete the pro-angiogenic factor vascular endothelial growth factor (VEGF), which acts upon local endothelial cells by binding to vascular endothelial growth factor receptors (VEGFR). As VEGFR2 is also expressed by a variety of tumors, we investigated the utility of anti-VEGFR2 CAR-T cells as a method to treat VEGFR2-expressing tumors. Camelid antibodies are small (14 kD) single chain antibodies. To generate a camelid antibody targeting the extracellular domain of VEGFR2, a llama was immunized with recombinant VEGFR2/Fc. A phage display library was generated and screened to identify an antibody with high binding affinity to VEGFR2. The selected antibody was expressed in the E. coli. BL21 (DE3) pT7 system. The purified antibody was characterized by SEC, LC-MS peptide mapping and ELISA. CAR-T cells were engineered to express the camelid anti-VEGFR2 antibody in combination with the CD28 and 4-1BB costimulatory molecules and the CD3 zeta chain. Tumor cells were screened for expression of VEGFR2, and the HL-60 acute promyelocytic leukemia, ZR-75-30 breast ductal carcinoma and NCI-H23 non-small cell lung adenocarcinoma were identified. Co-incubation of anti-VEGFR2 CAR-T cells with the VEGFR-2-expressing cell lines resulted in dose-dependent target cell toxicity as measured by LDH release. In addition, T cell activity was confirmed, as high levels of IL-2 and IFN-γ were detected in the cell culture media. These results suggest that anti-VEGFR2 CAR-T may be useful in directly targeting VEGFR2-expressing tumors. We previously showed the utility of camelid antibodies in CAR-T constructs as anti-CEACAM6 CAR-T cells show both in vitro and in vitro efficacy against the pancreatic tumor Bx-PC3. The use of the a camelid V21 antibody to target VEGFR2-expressing tumors provides hope that camelid single domain antibodies can be developed for CAR-T therapies. Citation Format: Heman Chao, Baomin Tian, Marni Uger, Wah Wong. CAR-T cell harboring a camelid single domain antibody as a targeting agent to kill tumors expressing VEGFR2 [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2017; 2017 Apr 1-5; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2017;77(13 Suppl):Abstract nr 3770. doi:10.1158/1538-7445.AM2017-3770
Structure and expression of the human slow twitch skeletal muscle troponin I gene. (1994)

The contractile protein troponin I is encoded by a multigene family whose members are expressed differentially in various classes of muscle fibers. In vertebrates, the "slow" isoform of troponin I is expressed during early heart and skeletal muscle development but is restricted to slow twitch skeletal muscle in the adult. This diverse expression pattern offers an opportunity to study the regulation of a single gene within different developmental contexts. To initiate such studies, we have cloned the gene encoding the human slow twitch skeletal muscle isoform of troponin I and have identified 5'-flanking sequences required for its expression in skeletal muscle cells. The slow troponin I gene spans 12.5 kilobases and is divided into nine exons. In contrast to many muscle-specific genes, the troponin I promoter does not contain consensus CCAAT or TATA elements. Moreover, the sequence from -9 to +11 resembles an "initiator element" previously shown to direct transcription of some tissue-specific genes lacking TATA boxes (Smale, S. T., and Baltimore, D. (1989) Cell 57, 103-113; Brand, N. J., Petkovich, M., and Chambon, P. (1990) Nucleic Acids Res. 18, 6799-6806; Weis, L., and Reinberg, D. (1992) FASEB J. 6, 3300-3309). A transcriptional fusion construct, comprising 4.2 kilobases of troponin I 5'-flanking DNA linked to the bacterial chloramphenicol acetyl-transferase gene, exhibited cell type-specific and developmentally regulated expression. A muscle-specific enhancer regulated slow troponin I promoter activity.
Numerical Investigations on the Accuracy of Vortex Methods With and Without Remeshing (2003)

This article presents progress in the direction of a fully meshless formulation of the vortex method. Given that the Lagrangian formulation results in loss of blob overlap over time, a vortex method needs to incorporate some form of spatial adaption to maintain accuracy of discretization. The standard approach, motivated by the requirements of the particle strength exchange viscous scheme for an ordered particle field, has been the remeshing of vortices onto a grid. This in effect brings back the mesh to an otherwise meshless method, which has been subject of much debate. Presently, we investigate the accuracy of the vortex method with and without the standard remeshing. In addition, we formulate a new spatial adaption scheme, akin to the concept of rezoning, but based on ideas of radial basis function interpolation so that a regular mesh is not needed. Numerical experiments demonstrate the capacity of a considerable increase in accuracy. The vortex method (VM) is a Lagrangian, grid-free approach to solving the Navier-Stokes equations in vorticity formulation. It is based on spatially discretizing the vorticity field with elements (vortex blobs) that move with the local fluid velocity. The Lagrangian nature, however, implies that, due to strain, the blobs grow apart in some directions and cluster together in others. As the blobs cease to overlap they lose their ability to recover the smooth vorticity field and accuracy is lost. The widespread solution to this problem is remeshing the particle field, for which high-order interpolation kernels are used in tensor product formulations. (One should mention that some authors dislike the designation “remeshing” and instead refer to the process as “redistribution”. This may be justified as no mesh connectivity is required in the process; it does incur confusion, however, when there is a viscous scheme called vortex redistribution method.) Standard remeshing effectively controls the error due to Lagrangian distortion and long-time calculations are possible. Numerical investigations, however, demonstrate that the remeshing algorithms themselves introduce noticeable errors. In other words, these schemes bring back the mesh to an otherwise mesh-less method, and with it some numerical dissipation. Presently, experiments with a rezoning strategy based on solving the collocation problem for the blob circulation strengths have proved very encouraging. It is demonstrated that higher accuracy is possible, and in addition opportunities have been generated for providing a correction for the core spreading viscous scheme, as well as for variable resolution in the
Blood–brain barrier (2012)

Aβ=
: amyloid β; 
ABC=
: ATP-binding cassette; 
AD=
: Alzheimer disease; 
AQP4=
: aquaporin 4; 
BBB=
: blood–brain barrier; 
CAM=
: cell adhesion molecule; 
cAMP=
: cyclic adenosine monophosphate; 
EAAT=
: excitatory amino acid transporters; 
GTP=
: guanosine triphosphate; 
HIF-1=
: hypoxia-inducible factor–1; 
JAM=
: junction-associated molecules; 
LRP=
: low-density lipoprotein receptor-related protein; 
MMP=
: matrix metalloproteinase; 
MS=
: multiple sclerosis; 
NMO=
: neuromyelitis optica; 
RAGE=
: receptor for advanced glycosylation end-product; 
SLC=
: soluble carrier; 
TGF=
: transforming growth factor; 
TNF=
: tumor necrosis factor; 
VE=
: vascular endothelial; 
VEGF=
: vascular endothelial growth factor; 
ZO=
: zonula occludens

Neural survival and signaling within the CNS require a highly controlled microenvironment that depends on the normal function of a neurovascular unit, which includes several interacting structures, including capillary endothelial cells, pericytes, astrocytes, and neuronal processes (figure 1). The blood–brain barrier (BBB) is a dynamic component of this unit and is a key interface for molecular exchange between the blood and the brain interstitial fluid. The endothelial cells that form the BBB are characterized by the presence of tight junctions, the polarized expression of membrane transporters and receptors responsible for the active transport of nutrients and efflux of potentially toxic substances, and the presence of enzymes that target neurotransmitters or their precursors. All these cells participate in reciprocal interactions that are critical for local regulation of blood flow, BBB permeability, homeostasis of the neuronal microenvironment, synaptic remodeling, neurogenesis, and angiogenesis. Impaired BBB function contributes to the pathophysiology of a wide range of neurologic disorders, including traumatic, vascular, inflammatory, neoplastic, toxic-metabolic, and degenerative disorders. The pathophysiologic mechanisms include disruption of tight junctions, altered transport of molecules, inflammatory responses, impaired astrocyte function, and brain hypoperfusion. However, the normal BBB may reduce the CNS bioavailability of potentially useful therapeutic agents. Thus, the BBB constitutes an important therapeutic target. The structure and multiple functions of the BBB and their involvement in neurologic disorders have been extensively reviewed.1,–,12



Figure 1 Neurovascular unit and molecular components of the physical blood–brain barrier (BBB) 
The BBB is an integral part of the neurovascular unit, which includes brain endothelial cells, pericytes, and smooth muscle cells; astrocytes; neuronal terminals; and circulating white blood cells interacting with the vessel wall. All these different cell types express a wide variety of receptors, ion channels, and transporters and their close proximity with each other allows for effective paracrine interactions. The BBB acts as a physical barrier because of the presence of …
Antiobiotic prophylaxis to prevent surgical site infections. (2011)

Surgical site infections are the most common nosocomial infections in surgical patients, accounting for approximately 500,000 infections annually. Surgical site infections also account for nearly 4 million excess hospital days annually, and nearly $2 billion in increased health care costs. To reduce the burden of these infections, a partnership of national organizations, including the Centers for Medicare and Medicaid Services and the Centers for Disease Control and Prevention, created the Surgical Care Improvement Project and developed six infection prevention measures. Of these, three core measures contain recommendations regarding selection of prophylactic antibiotic, timing of administration, and duration of therapy. For most patients undergoing clean-contaminated surgeries (e.g., cardiothoracic, gastrointestinal, orthopedic, vascular, gynecologic), a cephalosporin is the recommended prophylactic antibiotic. Hospital compliance with infection prevention measures is publicly reported. Because primary care physicians participate in the pre- and postoperative care of patients, they should be familiar with the Surgical Care Improvement Project recommendations.
Transcriptional Regulation of the Human <i>Toll-Like Receptor 2</i> Gene in Monocytes and Macrophages (2002)

This report investigates the molecular basis for tissue-restricted and regulated expression of the pattern recognition receptor Toll-like receptor (TLR)2 in human monocytes and macrophages. To define the proximal promoter, the full 5'-sequence and transcriptional start sites of TLR2 mRNA were determined. The human TLR2 gene was found to consist of two 5' noncoding exons followed by a third coding exon. Alternative splicing of exon II was detected primarily in human blood monocytes. The proximal promoter, exon I, and part of intron I were found to be located in a CpG island. Although CpG methylation of the proximal human TLR2 promoter in cell lines correlated with TLR2 repression, the promoter was unmethylated in primary cells, indicating that CpG methylation does not contribute to the cell-type specific expression of human TLR2 in normal tissues. The promoter sequence contains putative binding sites for several transcription factors, including Sp1 and Ets family members. Reporter gene analysis revealed a minimal promoter of 220 bp that was found to be regulated by Sp1, Sp3, and possibly PU.1. Interestingly, no sequence homology was detected between human and murine TLR2 promoter regions. In contrast to murine TLR2, expression of human TLR2 in monocytes/macrophages is not induced by the proinflammatory stimuli LPS or macrophage-activating lipopeptide-2, and reporter activity of the promoter was not enhanced by stimuli-induced NF-kappaB activation in THP-1 or MonoMac-6 cells. Our findings provide an initial definition of the human TLR2 promoter and reveal profound differences in the regulation of an important pattern recognition molecule in humans and mice.
[ABO and Rh blood group factors in thyroid gland diseases]. (1980)

The blood groups of 1012 patients were investigated that underwent operations in connection with the following thyroid diseases: Basedow's disease, basedowified goiter, toxic adenoma with thyroid carcinoma. Significant discrepancies were established not to exist as compared with the distribution of the blood groups among the Bulgarian population. The percentage of the patients with blood group A is only higher in carcinoma of the thyroid gland -- 50.2 per cent and in blood group O -- lower 27.8 per cent. The comparison with a control group of 307 patients with gastric carcinoma revealed that the percentage of blood group A is considerably higher -- 54.1 per cent among them.
Extraction of Organic Pollutants from Environmental Solids with Sub- and Supercritical Water (1994)

ADVERTISEMENT RETURN TO ISSUEPREVArticleNEXTExtraction of Organic Pollutants from Environmental Solids with Sub- and Supercritical WaterSteven B. Hawthorne, Yu. Yang, and David J. MillerCite this: Anal. Chem. 1994, 66, 18, 2912–2920Publication Date (Print):September 15, 1994Publication History Published online1 May 2002Published inissue 15 September 1994https://pubs.acs.org/doi/10.1021/ac00090a019https://doi.org/10.1021/ac00090a019research-articleACS PublicationsRequest reuse permissionsArticle Views1574Altmetric-Citations394LEARN 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
Pharmacokinetics and Brain Uptake of an IgG-TNF Decoy Receptor Fusion Protein Following Intravenous, Intraperitoneal, and Subcutaneous Administration in Mice (2013)

Tumor necrosis factor (TNF)-α is a proinflammatory cytokine active in the brain. Etanercept, the TNF decoy receptor (TNFR), does not cross the blood-brain barrier (BBB). The TNFR was re-engineered for BBB penetration as a fusion protein with a chimeric monoclonal antibody (mAb) against the mouse transferrin receptor (TfR), and this fusion protein is designated cTfRMAb-TNFR. The cTfRMAb domain of the fusion protein acts as a molecular Trojan horse and mediates transport via the endogenous BBB TfR. To support future chronic treatment of mouse models of neural disease with daily administration of the cTfRMAb-TNFR fusion protein, a series of pharmacokinetics and brain uptake studies in the mouse was performed. The cTfRMAb-TNFR fusion protein was radiolabeled and injected into mice via the intravenous, intraperitoneal (IP), or subcutaneous (SQ) routes of administration at doses ranging from 0.35 to 10 mg/kg. The distribution of the fusion protein into plasma following the IP or SQ routes was enhanced by increasing the injection dose from 3 to 10 mg/kg. The fusion protein demonstrated long circulation times with high metabolic stability following the IP or SQ routes of injection. The IP or SQ routes produced concentrations of the cTfRMAb-TNFR fusion protein in the brain that exceed by 20- to 50-fold the concentration of TNFα in pathologic conditions of the brain. The SQ injection is the preferred route of administration, as the level of cTfRMAb fusion protein produced in the brain is comparable to that generated with intravenous injection, and at a much lower plasma area under the concentration curve of the fusion protein as compared to IP administration.
MODELLING 3D OBJECTS USING WEAK CSG PRIMITIVES (2004)

There have been numerous approaches to automatically extract man-made objects from images or laser scan data in the past. Many efforts have been put into the detection and measurement of object parts. However, putting those parts together in such a way that a topologically correct object representation is obtained -- which additionally meets certain regularization conditions -- has not been addressed in a satisfactory manner. In this paper, following a review of existing methods for obtaining roof topologies of buildings, an approach termed `weak constructive solid geometry (CSG) primitives&apos; is proposed. This approach is intended to fill the gap between B-rep and CSG modelling, combining advantages of both.
Compact multimode bandpass filters with wide upper stopband using dual-mode DGS resonators (2014)

A novel compact dual-mode DGS resonator (DMDGSR) is proposed, which is composed of a folded slot line resonator (FSLR) and a coplanar stepped impedance resonator (CSIR), each of them controls one resonant mode. By adding end-coupled microstrip feeding lines, a simple compact dual-mode bandpass filter (BPF) can be designed with two transmission zeros beside the passband and behaves a wide upper stopband to as far as 12 GHz with rejection better than 20 dB. As extensions, a quad-mode BPF as well as a hex-mode one is designed and fabricated by simply series connecting two or three such DGS segments. The two BPFs have a simple structure, wide upper stopband and good selectivity.