gebhart/patrepeval huggingface dataset:
Pattern Switchable Antenna System Using Inkjet-Printed Directional Bow-Tie for Bi-Direction Sensing Applications (2015)

In this paper, we propose a paper-based pattern switchable antenna system using inkjet-printing technology for bi-direction sensor applications. The proposed antenna system is composed of two directional bow-tie antennas and a switching network. The switching network consists of a single-pole-double-throw (SPDT) switch and a balun element. A double-sided parallel-strip line (DSPSL) is employed to convert the unbalanced microstrip mode to the balanced strip mode. Two directional bow-tie antennas have different radiation patterns because of the different orientation of the reflectors and antennas. It is demonstrated from electromagnetic (EM) simulation and measurement that the radiation patterns of the proposed antenna are successfully switched by the SPDT switch.
Inflammation, Atherosclerosis, and Coronary Artery Disease (2005)

In this review article, Göran Hansson, a pioneer in the study of the role of inflammation in atherosclerosis and coronary artery disease, summarizes new ideas on the pathogenesis of acute coronary syndromes.
The characteristics of acetabular cups worn in the human body (1978)

In laboratory tests, the ultra-high molecular weight polyethylene used for the acetabular cups of Charnley hip prostheses has a very low wear rate against steel. In the body radiographic measurements indicate that the polyethylene wears more rapidly. In order to investigate this higher wear rate, the sockets of acetabular cups removed at post-mortem have been examined using optical and electron microscopy. It has been shown that a socket wears predominantly on its superior part and that this is a direct consequence of the orientation of the cup in the body and the direction of loading of the hip. In the worn region the femoral head in effect bores out a new socket for itself, a process which is visible with the naked eye after approximately eight years. Electron microscopy shows that the predominant wear mechanism is adhesion, but after about eight years the appearance of surface cracks suggests that surface fatigue is taking place in addition to this. Laboratory wear tests have shown that pure surface fatigue is not sufficient to account for the high clinical wear rate. Other deformation processes are suggested and discussed with regard to the higher clinical wear rate.
The role of nitric oxide in proteoglycan turnover by bovine articular cartilage organ cultures (1996)

Monolayer cultures of articular chondrocytes synthesize large amounts of nitric oxide (NO) following exposure to IL-1. The latter has antianabolic and procatabolic activities on these cells, but little is known about the role, if any, of NO in the integrated metabolic pathways of the chondrocyte. In the present study, the role of endogenously produced NO in both the synthesis and degradation of proteoglycans was investigated for the first time. Bovine articular cartilage slices exposed to 20 U/ml human rIL-1 beta (hrIL-1 beta) synthesized large amounts of NO for 1 to 2 days, after which production fell to a steady state level approximately 20% of the peak value for the remainder of the 14-day incubation. The NO synthase inhibitor, N-monomethyl L-arginine (L-NMA, 1 mM), blocked NO production and enhanced the acute catabolic effects of hrIL-1 beta in cartilage derived from both cartilage derived from both calves and adult animals. However, in late cultures, release of proteoglycans was reduced in the presence of L-NMA. The proteolytic activity in conditioned medium of these cultures (measured as caseinolytic activity) was enhanced by L-NMA; however, this inhibitor did not affect the rates of synthesis of proteoglycans. Although NO is widely assumed to be a mediator of cartilage catabolism, our data suggest that it may instead have an acute protective effect. Whether this effect is maintained chronically is less clear.
Why we need Di Versity the Superjourno : editorial (2003)

While the process of putting together this edition of Review has revealed many lessons, a key lesson has been the value of taking time, and having the patience to respect that things take as long as they need. It has shown us, again, that real and true change cannot be forced. And in taking stock of the project of training and educating for media transformation, we have learnt that although we are not where we would like to be, we are not doing too badly either.
Rac Binding to p67 (1997)

Activation of the respiratory burst oxidase involves the assembly of the membrane-associated flavocytochrome b558 with the cytosolic components p47(phox), p67(phox), and the small GTPase Rac. Herein, the interaction between Rac and p67(phox) is explored using functional and physical methods. Mutually facilitated binding (EC50) of Rac1 and p67(phox) within the NADPH oxidase complex was demonstrated using steady state kinetic methods measuring NADPH-dependent superoxide generation. Direct binding of Rac1 and Rac2 to p67(phox) was shown using a fluorescent analog of GTP (methylanthraniloyl guanosine-5'-[beta,gamma-imido]triphosphate) bound to Rac as a reporter group. An increase in the methylanthraniloyl fluorescence was seen with added p67(phox) but not p47(phox), and the emission maximum shifted from 445 to 440 nm. Rac1 and Rac2 bound to p67(phox) with a 1:1 stoichiometry and with Kd values of 120 and 60 nM, respectively. Mutational studies (Freeman, J., Kreck, M., Uhlinger, D. J., and Lambeth, J. D. (1994) Biochemistry 33, 13431-13435; Freeman, J. L., Abo, A., and Lambeth, J. D. (1996) J. Biol. Chem. 271, 19794-19801) previously identified two regions in Rac1 that are important for activity: the "effector region" (residues 26-45) and the "insert region" (residues 124-135). Proteins mutated in the effector region (Rac1(N26H), Rac1(I33N), and Rac1(D38N)) showed a marked increase in both the Kd and the EC50, indicating that mutations in this region affect activity by inhibiting Rac binding to p67(phox). Insert region mutations (Rac1(K132E) and L134R), while showing markedly elevated EC50 values, bound with normal affinity to p67(phox). The structure of Rac1 determined by x-ray crystallography reveals that the effector region and the insert region are located in defined sectors on the surface of Rac1. A model is discussed in which the Rac1 effector region binds to p67(phox), the C terminus binds to the membrane, and the insert region interacts with a different protein component, possibly cytochrome b558.
Inflammasomes in cancer: a double-edged sword (2014)

Chronic inflammatory responses have long been observed to be associated with various types of cancer and play decisive roles at different stages of cancer development. Inflammasomes, which are potent inducers of interleukin (IL)-1β and IL-18 during inflammation, are large protein complexes typically consisting of a Nod-like receptor (NLR), the adapter protein ASC, and Caspase-1. During malignant transformation or cancer therapy, the inflammasomes are postulated to become activated in response to danger signals arising from the tumors or from therapy-induced damage to the tumor or healthy tissue. The activation of inflammasomes plays diverse and sometimes contrasting roles in cancer promotion and therapy depending on the specific context. Here we summarize the role of different inflammasome complexes in cancer progression and therapy. Inflammasome components and pathways may provide novel targets to treat certain types of cancer; however, using such agents should be cautiously evaluated due to the complex roles that inflammasomes and pro-inflammatory cytokines play in immunity.
One-Pot Two-Step Microwave-Assisted Reaction in Constructing 4,5-Disubstituted Pyrazolopyrimidines (2003)

[reaction: see text] A microwave-assisted reaction was developed to facilitate the construction of 4,5-disubstituted pyrazolopyrimidines. This one-pot two-step process involves a sequential S(N)Ar displacement of the C4 chloro substituent with various anilines and amines, followed by a Suzuki coupling reaction with different boronic acids. Using microwave irradiation leads to high product conversion, low side product formation, and shorter reactions.
Cloning and Characterization of a Specific Interleukin (IL)-13 Binding Protein Structurally Related to the IL-5 Receptor α Chain (1996)

Interleukin-13 (IL-13) is a cytokine secreted by activated T lymphocytes that shares many, but not all, biological activities with IL-4. These overlapping activities are probably due to the existence of common receptor components. Two proteins have been described as constituents of the IL-4 receptor, a approximately 140-kDa glycoprotein (IL-4R) and the gamma chain (gammac) of the IL-2 receptor, but neither of these proteins binds IL-13. We have cloned a cDNA encoding an IL-13 binding protein (IL-13R) from the Caki-1 human renal carcinoma cell line. The cloned cDNA encodes a 380-amino acid protein with two consensus patterns characteristic of the hematopoietic cytokine receptor family and a short cytoplasmic tail. The IL-13R shows homology with the IL-5 receptor, and to a lesser extent, with the prolactin receptor. COS-7 cells transfected with the IL-13R cDNA bind IL-13 with high affinity but do not bind IL-4. COS-7 cells co-transfected with the cloned IL-13R cDNA and IL-4R cDNA resulted in the reconstitution of a small number of receptors that recognized both IL-4 and IL-13. Reverse transcription-polymerase chain reaction analysis detected the receptor transcript only in cell lines known to bind IL-13.
Murine candidiasis: Strain dependence of host responses after immunization (1988)

Summary After recovery from acute infection with live Candida albicans , both CBA/H and BALB/c mice show increased resistance to colonization by the organism. However, the ‘susceptible’ CBA/H mice develop much stronger protective responses than do ‘resistant’ BALB/c mice. This is manifested particularly as a substantial amelioration of the severity of the lesions in the brain, and a very marked reduction in the number of fungal units therein. Analysis of granulocyte function in normal and immune mice of the two strains tended to exclude this as a basis for the different patterns of susceptibility and resistance.
Resolution doubling in fluorescence microscopy with confocal spinning-disk image scanning microscopy (2013)

We demonstrate how a conventional confocal spinning-disk (CSD) microscope can be converted into a doubly resolving image scanning microscopy (ISM) system without changing any part of its optical or mechanical elements. Making use of the intrinsic properties of a CSD microscope, we illuminate stroboscopically, generating an array of excitation foci that are moved across the sample by varying the phase between stroboscopic excitation and rotation of the spinning disk. ISM then generates an image with nearly doubled resolution. Using conventional fluorophores, we have imaged single nuclear pore complexes in the nuclear membrane and aggregates of GFP-conjugated Tau protein in three dimensions. Multicolor ISM was shown on cytoskeletal-associated structural proteins and on 3D four-color images including MitoTracker and Hoechst staining. The simple adaptation of conventional CSD equipment allows superresolution investigations of a broad variety of cell biological questions.
Molecular aspects of tumor cell invasion and metastasis (1993)

sociated with tumor-induced angiogenesis that not only allows for expansion of the primary but also permits easy access to the vascular compartment due to defects in the basement membranes of newly formed This may facilitate hematogenous spread of some tumors.To successfully establish a metastatic colony, circulating tumor cells must survive any immunologic assault, arrest at a distant vascular bed, and subsequently extravasate.Ultimately, the cells must invade and proliferate in the tissue of the secondary site.Growth of the metastatic colony beyond 1 cm3 requires that vascularization of the solid tumor take p l a ~e .~-~ Metastasis is a multistep process involving numerous tumor cell-host cell and cell-matrix as soda ti on^.'-^Interactions with the matrix, especially basement membranes, that characterize the process of invasion include the ability of tumor cells to attach, to proteolyze the matrix components, and then to migrate through the matrix defect (Fig. l).9None of these functions is unique to tumor cell behavior.Attachment, proteolysis, and migration are steps of trophoblast implantation, mammary gland involution, embryonic morphogenesis, and tissue remodeling.'0,"The difference between normal processes and the pathogenic nature of tumor cell invasion must therefore be one of regulation.Thus, an understanding of the controlling factors in the processes of cellular adhesion, matrix proteolysis, and cell migration should allow identification of new targets for therapeutic disruption of metastasis formation. Tumor Cell Adhesion: Integrin, Laminin Receptor, and Cadherin FunctionAttachment to specific glycoproteins of the extracellular matrix, such as fibronectin, collagen, and laminin, is mediated through tumor cell receptors of the inteand non-integrin variety.14,15Integrins are a large class of c@ heterodimeric receptors for adhesion molecules with broad specificity and low binding affinity.''PI6At least 14 01 and 8 p subunits have been identified, which noncovalently associate to produce at least
Neurogenic inflammation after traumatic brain injury and its potentiation of classical inflammation (2016)

As such, the neurogenic inflammatory response can exacerbate classical inflammation via a positive feedback loop, with classical inflammatory mediators such as bradykinin and prostaglandins then further stimulating TRP receptors. Accordingly, complete inhibition of neuroinflammation following TBI may require the inhibition of both classical and neurogenic inflammatory pathways.
Selective activation of FGFR4 by an FGF19 variant does not improve glucose metabolism in ob/ob mice (2009)

FGF19 is a hormone that regulates bile acid and glucose homeostasis. Progress has been made in identifying cofactors for receptor activation. However, several functions of FGF19 have not yet been fully defined, including the actions of FGF19 on target tissues, its FGF receptor specificity, and the contributions of other cofactors, such as heparin. Here, we explore the requirements for FGF19-FGFR/co-receptor interactions and signaling in detail. We show that betaKlotho was essential for FGF19 interaction with FGFRs 1c, 2c, and 3c, but FGF19 was able to interact directly with FGFR4 in the absence of betaKlotho in a heparin-dependent manner. Further, FGF19 activated FGFR4 signaling in the presence or absence of betaKlotho, but activation of FGFRs 1c, 2c, or 3c was completely betaKlotho dependent. We then generated an FGF19 molecule, FGF19dCTD, which has a deletion of the C-terminal region responsible for betaKlotho interaction. We determined that betaKlotho-dependent FGFR1c, 2c, and 3c interactions and activation were abolished, and betaKlotho-independent FGFR4 activation was preserved; therefore, FGF19dCTD is an FGFR4-specific activator. This unique FGF19 molecule specifically activated FGFR4-dependent signaling in liver and suppressed CYP7A1 expression in vivo, but was unable to activate signaling in adipose where FGFR4 expression is very low. Interestingly, unlike FGF19, treatment of ob/ob mice with FGF19dCTD failed to improve glucose levels and insulin sensitivity. These results suggest that FGF19-regulated liver bile acid metabolism could be independent of its glucose-lowering effect, and direct FGFR activation in adipose tissue may play an important role in the regulation of glucose homeostasis.
The Basic Helix-Loop-Helix Transcription Factor NEUROG3 Is Required for Development of the Human Endocrine Pancreas (2015)

Neurogenin3 (NEUROG3) is a basic helix-loop-helix transcription factor required for development of the endocrine pancreas in mice. In contrast, humans with NEUROG3 mutations are born with endocrine pancreas function, calling into question whether NEUROG3 is required for human endocrine pancreas development. To test this directly, we generated human embryonic stem cell (hESC) lines where both alleles of NEUROG3 were disrupted using CRISPR/Cas9-mediated gene targeting. NEUROG3(-/-) hESC lines efficiently formed pancreatic progenitors but lacked detectible NEUROG3 protein and did not form endocrine cells in vitro. Moreover, NEUROG3(-/-) hESC lines were unable to form mature pancreatic endocrine cells after engraftment of PDX1(+)/NKX6.1(+) pancreatic progenitors into mice. In contrast, a 75-90% knockdown of NEUROG3 caused a reduction, but not a loss, of pancreatic endocrine cell development. We conclude that NEUROG3 is essential for endocrine pancreas development in humans and that as little as 10% NEUROG3 is sufficient for formation of pancreatic endocrine cells.
Mouse models of colorectal cancer (2011)

Colorectal cancer is one of the most common malignancies in the world. Many mouse models have been developed to evaluate features of colorectal cancer in humans. These can be grouped into genetically-engineered, chemically-induced, and inoculated models. However, none recapitulates all of the characteristics of human colorectal cancer. It is critical to use a specific mouse model to address a particular research question. Here, we review commonly used mouse models for human colorectal cancer.
Identification by in vitro complementation of regions required for cell‐invasive activity of Bordetella pertussis adenylate cyclase toxin (1995)

The adenylate cyclase toxin (CyaA) of Bordetella pertussis is a 1706-residue protein composed of an amino-terminal adenylate cyclase (AC) domain linked to a 1300-residue channel-forming RTX (repeats in toxin) haemolysin. The toxin delivers its AC domain into a variety of eukaryotic cells and impairs cellular functions by catalysing unregulated synthesis of cAMP from intracellular ATP. We have examined toxin activities of a set of deletion derivatives of CyaA. The results indicate that CyaA does not have a dedicated target cell-binding domain and that structural integrity and co-operation of all domains, as well as the post-translational fatty acylation mediated by an accessory protein CyaC, are all essential for target cell association and toxin activity of CyaA. When tested individually, all toxin derivatives were inactive and impaired in the tight association with the target cell surface. However, pairs of constructs with nonoverlapping deletions complemented each other in vitro and exhibited a partially restored cytotoxic activity. This suggests that at least a part of the active toxin may act in the form of dimers or higher oligomers. The complementation analysis revealed that the last 217 residues of CyaA, containing the unprocessed secretion signal, form an autonomous domain essential for toxin activity, and that the region from residue 624 to 780 may be directly involved in delivery of the AC toxin into cells.
An architecture for network-layer routing in OSI (1987)

Work on the standardization of routing protocols for OSI is in progress. The envisioned set of routing protocols is expected to work in nearly all of the environments which constitute OSI networks. Behind these routing protocols is an architecture which outlines problems and goals, establishes a framework upon which to base the development of protocols, and provides a conceptual baseline for continued work on unsolved problems. This architecture defines routing in the OSI network layer, functionally partitions the problem into its components, defines a routing hierarchy and an address hierarchy and discusses their relationship, and discusses arms-length routing relationships between differently administered networks. This paper presents that architecture, and discusses problems which remain to be solved as work progresses towards a global OSI network.
Genetic analysis of indefinite division in human cells: identification of four complementation groups. (1988)

Hybrids obtained following fusion of normal human diploid fibroblasts with different immortal human cell lines exhibited limited division potential. This led to the conclusion that the phenotype of cellular senescence is dominant and that immortal cells arise as a result of recessive changes in the growth control mechanisms of the normal cell. We have exploited the fact that immortality is recessive and, by fusing immortal human cell lines with each other, assigned 21 cell lines to at least four complementation groups for indefinite division. A wide variety of cell lines was included in the study to determine what parameters, if any, would affect complementation group assignment. The results indicate that cell type, embryonal layer of origin, and type of tumor do not affect group assignment. There does not appear to be any correlation between expression of an activated oncogene and group assignment. However, all of the immortal simian virus 40-transformed cell lines studied (with the exception of one xerodermapigmentosum fibroblast-derived line) assign to the same group, indicating that this virus immortalizes various human cells by the same processes. The assignment of immortal human cells to distinct groups provides the basis for a focused approach to determine the genes important in normal growth regulation that have been modified in immortal cells.
Synthesis of [2H]‐labelled phase‐I‐metabolites using 1‐[2H]‐pyridinium hydrochloride (2005)

Abstract Simultaneous O ‐demethylation and hydrogen/deuterium exchange of aryl‐methyl‐ethers can be obtained using 1‐[ 2 H]‐pyridinium hydrochloride as reagent at 220°C for 6 h. This reaction was applied to dextromethorphan and various non‐steroidal anti‐inflammatory drugs. Copyright © 2005 John Wiley &amp; Sons, Ltd.
Imatinib and Nilotinib induce apoptosis of chronic myeloid leukemia cells through a Bim-dependant pathway modulated by cytokines (2007)

It is an important challenge to better understand the mechanisms of tyrosine kinase inhibitors-induced apoptosis in CML cells. Thus, we have investigated how this apoptosis can be modulated by extracellular factors. Apoptosis induced by imatinib and nilotinib was determined in BCR-ABL expressing cell lines and primary CML CD34+ cells. Both molecules induced apoptosis of BCR-ABL expressing cells. This apoptosis was inhibited by protein synthesis inhibition in both K562 and CML CD34+ cells. In K562, 80% inhibition of the BCR-ABL auto-phosphorylation by either imatinib or nilotinib induced a two fold increase in Bim-EL expression and induction of apoptosis in 48 h. Bim accumulation preceded apoptosis induction which was completely abolished by depletion in Bim using shRNA. However, the anti-proliferative effect of imatinib was preserved in Bim-depleted cells. When K562 cells were cultured in a cytokine containing medium, the pro-apoptotic effect of nilotinib was decreased by 68% and this was related to a decrease in Bim-EL dephosphorylation and accumulation. Similarly, the presence of a combination of cytokines inhibited 88% of NIL- and 39% of IMA-induced apoptosis in primary CML CD34+ cells. In conclusion, both nilotinib and imatinib induce apoptosis through Bim accumulation independently of cell cycle arrest. However, the pro-apoptotic effect of both molecules can be attenuated by the presence of cytokines and growth factors, particularly concerning nilotinib. Thus BCR-ABL inhibition restores the cytokine dependence but is not sufficient to induce apoptosis when other signaling pathways are activated.