gebhart/patrepeval huggingface dataset:
Characterization of Recombinant Amino-terminal NC4 Domain of Human Collagen IX (2004)

The N-terminal NC4 domain of collagen IX is a globular structure projecting away from the surface of the cartilage collagen fibril. Several interactions have been suggested for this domain, reflecting its location and its characteristic high isoelectric point. In an attempt to characterize the NC4 domain in more detail, we set up a prokaryotic expression system to produce the domain. The purified 27.5-kDa product was analyzed for its glycosaminoglycan-binding potential by surface plasmon resonance and solid-state assays. The results show that the NC4 domain of collagen IX specifically binds heparin with a K(d) of 0.6 microm, and the full-length recombinant collagen IX has an even stronger interaction with heparin, with an apparent K(d) of 3.6 nm. The heparin-binding site of the NC4 domain was located in the extreme N terminus, containing a heparin-binding consensus sequence, whereas electron microscopy suggested the presence of at least three additional heparin-binding sites on full-length collagen IX. The NC4 domain was also shown to bind cartilage oligomeric matrix protein. This interaction and the association of cartilage oligomeric matrix protein with other regions of collagen IX were found to be heparin-competitive. Circular dichroism analyses of the NC4 domain indicated the presence of stabilizing disulfide bonds and a thermal denaturation point of about 80 degrees C. The pattern of disulfide bond formation within the NC4 domain was identified by tryptic peptide mass mapping of the NC4 in native and reduced states. A similar pattern was demonstrated for the NC4 domain of full-length recombinant collagen IX.
Split selectable markers (2019)

Selectable markers are widely used in transgenesis and genome editing for selecting engineered cells with a desired genotype but the variety of markers is limited. Here we present split selectable markers that each allow for selection of multiple "unlinked" transgenes in the context of lentivirus-mediated transgenesis as well as CRISPR-Cas-mediated knock-ins. Split marker gene segments fused to protein splicing elements called "inteins" can be separately co-segregated with different transgenic vectors, and rejoin via protein trans-splicing to reconstitute a full-length marker protein in host cells receiving all intended vectors. Using a lentiviral system, we create and validate 2-split Hygromycin, Puromycin, Neomycin and Blasticidin resistance genes as well as mScarlet fluorescent proteins. By combining split points, we create 3- and 6-split Hygromycin resistance genes, demonstrating that higher-degree split markers can be generated by a "chaining" design. We adapt the split marker system for selecting biallelically engineered cells after CRISPR gene editing. Future engineering of split markers may allow selection of a higher number of genetic modifications in target cells.
Molecular Basis of Reduced Potency of Underacylated Endotoxins (2005)

Potent TLR4-dependent cell activation by gram-negative bacterial endotoxins depends on sequential endotoxin-protein and protein-protein interactions with LPS-binding protein, CD14, myeloid differentiation protein 2 (MD-2), and TLR4. Previous studies have suggested that reduced agonist potency of underacylated endotoxins (i.e., tetra- or penta- vs hexa-acylated) is determined by post-CD14 interactions. To better define the molecular basis of the differences in agonist potency of endotoxins differing in fatty acid acylation, we compared endotoxins (lipooligosaccharides (LOS)) from hexa-acylated wild-type (wt), penta-acylated mutant msbB meningococcal strains as well as tetra-acylated LOS generated by treatment of wt LOS with the deacylating enzyme, acyloxyacylhydrolase. To facilitate assay of endotoxin:protein and endotoxin:cell interactions, the endotoxins were purified after metabolic labeling with [3H]- or [14C]acetate. All LOS species tested formed monomeric complexes with MD-2 in an LPS-binding protein- and CD14-dependent manner with similar efficiency. However, msbB LOS:MD-2 and acyloxyacylhydrolase-treated LOS:MD-2 were at least 10-fold less potent in inducing TLR4-dependent cell activation than wt LOS:MD-2 and partially antagonized the action of wt LOS:MD-2. These findings suggest that underacylated endotoxins produce decreased TLR4-dependent cell activation by altering the interaction of the endotoxin:MD-2 complex with TLR4 in a way that reduces receptor activation. Differences in potency among these endotoxin species is determined not by different aggregate properties, but by different properties of monomeric endotoxin:MD-2 complexes.
Magnetic iron microbeads coupled with HEA-125 monoclonal antibody against epithelial cell adhesion molecule (2011)

Magnetic iron microbeads coupled with HEA-125 monoclonal antibody against the epithelial cell adhesion molecule (EpCAM), abbreviated as EpCAM microbeads, have been developed primarily for the positive selection or depletion of EpCAM-positive cells (1, 2). McClelland et al. have demonstrated the feasibility of cell tracking with magnetic resonance imaging (MRI) after the hepatic progenitor cells are labeled with EpCAM microbeads (1).Superparamagnetic iron oxide (SPIO)-based agents have been intensively tested for use in cell tracking with MRI in both preclinical and clinical situations (3, 4). SPIO particles provide a strong change in signal per unit of metal in T2-weighted images without a significant effect on labeled cells and host (3, 5). For efficient cell labeling, SPIO particles are generally coated with low-molecular-weight polymers or dendrimers leading to clusters of electron-dense crystal cores covered with the polymer or dendrimer. Surface coating increases the stability of SPIO particles and allows further chemical modification of the particles with targeting ligands. Cell tracking studies have shown that the migration and homing capabilities of SPIO-labeled cells can be monitored in vivo over days to months (3, 4, 6).Nevertheless, there are still many challenges to overcome before MRI cell tracking can be considered a robust technique in preclinical settings or in clinical applications (3, 7). MRI detects the presence of SPIO contrast agents, regardless of whether SPIO particles remain in the relevant cells, are lost to the extracellular matrix, or are transferred to other cells. It is still not possible to use MRI to discriminate live cells from dead cells or relevant cells from phagocytes. Detection sensitivity also becomes an issue when cells actively divide and migrate, in which case the SPIO labels are quickly divided among daughter cells to levels that are undetectable with MRI. In vivo quantification of the cell number is more challenging because of the contrast agent dilution during cell division, contrast agent transfer to others cells, other sources of iron in tissue, and technical limitations (4, 7).McClelland et al. addressed the problem of contrast agent dilution in MRI cell tracking by using EpCAM microbeads as the label (1). The human EpCAM, also known as CD326 or epithelial-specific antigen, is a cell-surface antigen and is found on hepatic progenitor cells, including human hepatic stem cells (hHpSCs) and hepatoblasts (hHBs), on liver cancer stem cells, and on proliferating epithelial cells in other tissues (8-10). The human EpCAM is not expressed in animal cells. McClelland et al. studied the labeling of hHpSCs with EpCAM microbeads in vitro, ex vivo, and in vivo and imaged the labeled cells with MRI (1). The investigators demonstrated that the hHpSCs could be labeled with EpCAM microbeads before or after transplantation, and the transplanted hHpSCs could be monitored and counted repeatedly in the same host by injection of the label just prior to MRI (1).
Heat-induced structural changes of proteins (2000)

Conference Abstract| October 01 2000 Heat-induced structural changes of proteins Thomas D Kim; Thomas D Kim 1151–742 Department of Chemistry, College of Natural Sciences, Seoul National University, Seoul Korea2Department of Microbiology, College of Medicine, Yonsei University, Seoul, Korea Search for other works by this author on: This Site PubMed Google Scholar Chul-hak Yang; Chul-hak Yang 1151–742 Department of Chemistry, College of Natural Sciences, Seoul National University, Seoul Korea2Department of Microbiology, College of Medicine, Yonsei University, Seoul, Korea Search for other works by this author on: This Site PubMed Google Scholar Jongsun Kim Jongsun Kim 1151–742 Department of Chemistry, College of Natural Sciences, Seoul National University, Seoul Korea2Department of Microbiology, College of Medicine, Yonsei University, Seoul, Korea Search for other works by this author on: This Site PubMed Google Scholar Biochem Soc Trans (2000) 28 (5): A411. https://doi.org/10.1042/bst028a411b Views Icon Views Article contents Figures & tables Video Audio Supplementary Data Peer Review Share Icon Share Twitter LinkedIn Cite Icon Cite Get Permissions Citation Thomas D Kim, Chul-hak Yang, Jongsun Kim; Heat-induced structural changes of proteins. Biochem Soc Trans 1 October 2000; 28 (5): A411. doi: https://doi.org/10.1042/bst028a411b Download citation file: Ris (Zotero) Reference Manager EasyBib Bookends Mendeley Papers EndNote RefWorks BibTex toolbar search Search Dropdown Menu toolbar search search input Search input auto suggest filter your search All ContentAll JournalsBiochemical Society Transactions Search Advanced Search This content is only available as a PDF. © 2000 Biochemical Society2000 Article PDF first page preview Close Modal You do not currently have access to this content.
Crystallization and preliminary diffraction analysis of a truncated homodimer of human phenylalanine hydroxylase (1997)

A recombinant truncated form (delta1-102/delta428-452) of the non-heme iron-dependent metalloenzyme human phenylalanine hydroxylase (hPAH, phenylalanine 4-monooxygenase; EC 1.14.16.1) was expressed in E. coli, purified to homogeneity as a homodimer (70 kDa) and crystallized using the hanging drop vapour diffusion method. The crystals are orthorhombic, space group C222 with cell dimensions of a = 66.6 A, b = 108.4 A, c = 125.7 A. The calculated packing parameter (Vm) is 3.24 A3/Da with four 2-fold symmetric dimers (or eight momomers) in the unit cell. Data have been collected to 2.0 A resolution.
Characterizing and mitigating the impact of process variations on phase change based memory systems (2009)

Dynamic Random Access Memory (DRAM) has been used in main memory design for decades. However, DRAM consumes an increasing power budget and faces difficulties in scaling down for small feature size CMOS processing technologies. Compared to conventional DRAM, emerging phase change random access memory (PRAM) demonstrates superior power efficiency and processing scalability as VLSI technologies and integration density continue to advance. Nevertheless, using nano-scale fabrication technologies will unavoidably introduce design parameter variability in the manufacturing stage. In the past, the impact of process variation (PV) on conventional transistor-based storage cells and combinational logic has been studied extensively. However, the implication of PV on non-volatile memory design using emerging phase change techniques has not been well understood. In this paper, we take the first step toward characterizing the effect of process variation on PRAM and explore PV-aware design techniques. We show that process variation increases the PRAM programming power by 96% and degrades PRAM endurance by 50X. Our proposed circuit and two microarchtiecture techniques with system-level support reduce PRAM power by 44%, 59% and 57% and improve PRAM endurance by 27X, 277X and 268X, relative to PV-affected PRAM design. Moreover, we show that the synergy of the proposed cross-layer approaches, which achieve an average 63% power savings and 13050X endurance improvement over the conventional case, provide an attractive design solution to mitigate the deleterious impact of PV for non-volatile memory in the upcoming nano-scale processing technology era.
Use of Statistics to Assess the Global Burden of Breast Cancer (2006)

A variety of statistics are used to quantify the burden (occurrence and outcome) of cancer generally and of breast cancer specifically. When undertaking any cancer control program, understanding these statistics, their source, and their quality is important for assessing the current situation, allocating resources to different control strategies, and evaluating progress. Two core statistics are the cancer incidence rate and the cancer mortality rate, which provide estimates of the average risk of acquiring and of dying from the disease, respectively. About 16% of the world's population is covered by registration systems that produce cancer incidence statistics, while mortality data are available for about 29%. Breast cancer incidence and mortality vary considerably by world region. In general, the incidence is high (greater than 80 per 100,000) in developed regions of the world and low (less than 30 per 100,000), though increasing, in developing regions; the range of mortality rates is much less (approximately 6-23 per 100,000) because of the more favorable survival of breast cancer in (high-incidence) developed regions. The incidence of breast cancer is increasing almost everywhere. This unfavorable trend is due in part to increases in risk factors (decreased childbearing and breast-feeding, increased exogenous hormone exposure, and detrimental dietary and lifestyle changes, including obesity and less physical activity). On the other hand, mortality is now decreasing in many high-risk countries due to a combination of intensified early detection efforts and the introduction of mammographic screening, resulting in the diagnosis of more small, early stage tumors, and advances in treatment.
Adjuvant antiplatelet therapy with aspirin in colo-rectal cancer. (1982)

Sixty-six patients with Duke's B2 or C colon or rectal cancer were randomized for treatment with aspirin (ASA), 600 mg, p.o., twice daily x 2 years or placebo (P). Compliance was checked in both groups by random measurement of blood salicylate levels. Fifty-seven patients are currently evaluable. No difference in disease-free (p = .66) or overall survival (p = .90) is present between ASA and P groups. The time at which ASA therapy is started (within 2 or within 4 weeks) following surgery does not affect these results. Aspirin at conventional dosage is ineffective in preventing the appearance of metastases in patients with colo-rectal cancer.
Interleukin‐6 in peripheral blood and inflammatory sites in Behçet′s disease (1992)

Interleukin-6, a potent pro-inflammatory cytokine, might be involved in Behçet's disease (BD) pathological pathways. We investigated IL-6 levels in sera and synovial fluids collected from BD patients. The IL-6 production was also studied in vivo, by measuring its activity in culture supernatants of PBMC and alveolar macrophages, stimulated or not with LPS. The patients with BD were compared to RA patients and healthy controls. High IL-6 levels were observed in sera, synovial fluid and LPS stimulated PBMC supernatants, from active BD patients, similar to those of RA patients. Alveolar macrophages production of IL-6 was significantly elevated in two active BD patients with an interstitial pneumonia, when compared to controls. These elevated levels of IL-6 suggest its involvement in the inflammatory sites of BD, which may be related to the progression of the acute lesions, at least in the joints and in the lungs.
Treatment of Advanced Non-Small-Cell Lung Cancer: A Review of Current Randomized Clinical Trials and an Examination of Emerging Therapies (2001)

Despite progress with newer agents for the treatment of advanced NSCLC, only 14% of patients with the disease are alive at 5 years after initial diagnosis. New therapies are needed.
From BRCA1 to RAP1: a widespread BRCT module closely associated with DNA repair (1997)

Inherited mutations in BRCA1 predispose to breast and ovarian cancer, but the biological function of the BRCA1 protein has remained largely elusive. The recent correspondence of Koonin et al. [Koonin, E.V., Altschul, S.F. and Bork, P. (1996) Nature Genet. 13, 266-267] has emphasized the potential importance of the BRCA1 C-terminal region for BRCA1-mediated breast cancer suppression, as this domain shows similarities with the C-terminal regions of a p53-binding protein (53BP1), the yeast RAD9 protein involved in DNA repair, and two uncharacterized, hypothetical proteins (KIAA0170 and SPAC19G10.7). The highlighted domain has been suggested to be the result of an internal duplication, each of the tandem domains being designated as a 'BRCT domain' (for BRCA1 C-terminus). Sequence analysis using hydrophobic cluster analysis reveals here the presence of 50 copies of the BRCT domain in 23 different proteins, including, in addition to BRCA1, 53BP1 and RAD9, XRCC1, RAD4, Ect2, REV1, Crb2, RAP1, terminal deoxynucleotidyltransferases (TdT) and three eukaryotic DNA ligases. Most of these proteins are known to be involved in DNA repair. The BRCT domain is not limited to the C-termini of protein sequences and can be found in multiple copies or in a single copy as in RAP1 and TdT, suggesting that it could well constitute an autonomous folding unit of approx. 90-100 amino acids.
Regeneration of adenosine triphosphate from glycolytic intermediates for cell‐free protein synthesis (2001)

A new approach for adenosine triphosphate (ATP) regeneration in a cell-free protein synthesis system is described. We first show that pyruvate can be used as a secondary energy source to replace or supplement the conventional secondary energy source, phosphoenol pyruvate (PEP). We also report that glucose-6-phosphate, an earlier intermediate of the glycolytic pathway, can be used for ATP regeneration. These new methods provide more stable maintenance of ATP concentration during protein synthesis. Because pyruvate and glucose-6-phosphate are the first and last intermediates of the glycolytic pathway, respectively, the results also suggest the possibility of using any glycolytic intermediate, or even glucose, for ATP regeneration in a cell-free protein synthesis system. As a result, the methods described provide cell-free protein synthesis with greater flexibility and cost efficiency. © 2001 John Wiley & Sons, Inc. Biotechnol Bioeng 74: 309–316, 2001.
Naked Sendai virus vector lacking all of the envelope‐related genes: reduced cytopathogenicity and immunogenicity (2006)

The deletion of genes from the SeV genome and the additional mutation are very effective for reducing both the immunogenic and cytopathic reactions to the SeV vector. These modifications are expected to improve the safety and broaden the range of clinical applications of this new class of cytoplasmic RNA vector.
Optical Imaging With the Use of a Scattering Lens (2013)

“Turbidity” caused by multiple light scattering distorts the propagation of waves, and thus undermines optical imaging. For example, translucent biological tissues exhibiting optical turbidity have posed limitations on the imaging depth and energy transmission. Here, we introduce a novel method called turbid lens imaging (TLI) that records a transmission matrix of a scattering medium charactering the input-output response of the medium. The knowledge of this transmission matrix allows one to find an incident wave out of the distorted transmitted wave. Therefore, it converts the highly complex medium into a useful imaging optics. We demonstrate that the image distortion by a scattering medium can be eliminated by the use of the transmission matrix and a clean object image can be retrieved as a result. We extend TLI for imaging through a multimode optical fiber, which is also a scattering medium, and demonstrate an endoscopic imaging by using a single multimode optical fiber itself as a lens. In addition, we show that TLI removes the pixelation artifact in using an image fiber bundle and improve spatial resolution. Our method of making use of multiple light scattering will lay a foundation for advance optical bioimaging methods.
Cyber-physical systems: A security perspective (2015)

A cyber-physical system (CPS) is a composition of independently interacting components, including computational elements, communications and control systems. Applications of CPS institute at different levels of integration, ranging from nation-wide power grids, to medium scale, such as the smart home, and small scale, e.g. ubiquitous health care systems including implantable medical devices. Cyber-physical systems primarily transmute how we interact with the physical world, with each system requiring different levels of security based on the sensitivity of the control system and the information it carries. Considering the remarkable progress in CPS technologies during recent years, advancement in security and trust measures is much needed to counter the security violations and privacy leakage of integration elements. This paper focuses on security and privacy concerns at different levels of the composition and presents system level solutions for ensuring the security and trust of modern cyber-physical systems.
Sleep-Walking a Rarest Side Effect of Zolpidem (2015)

A 46-years-old male, with past history of road traffic accident and with no current/past history of substance abuse and no family history of sleep-walking, took zolpidem 10 mg without any prescription and after few days, the patient's son noticed the patient waking up in the middle of night and walking into their room with a staring expression and some incoherent speech. The patient had no memory of this event in the morning. This sleep-walking episode was attributed to zolpidem, as no medication change was made besides new start of zolpidem and the patient had no history of such episodes in the past. Zolpidem treatment was stopped, and since then, no further complaints of sleep-walking were reported.
CSF-1 signals directly to renal tubular epithelial cells to mediate repair in mice (2009)

Tubular damage following ischemic renal injury is often reversible, and tubular epithelial cell (TEC) proliferation is a hallmark of tubular repair. Macrophages have been implicated in tissue repair, and CSF-1, the principal macrophage growth factor, is expressed by TECs. We therefore tested the hypothesis that CSF-1 is central to tubular repair using an acute renal injury and repair model, ischemia/reperfusion (I/R). Mice injected with CSF-1 following I/R exhibited hastened healing, as evidenced by decreased tubular pathology, reduced fibrosis, and improved renal function. Notably, CSF-1 treatment increased TEC proliferation and reduced TEC apoptosis. Moreover, administration of a CSF-1 receptor-specific (CSF-1R-specific) antibody after I/R increased tubular pathology and fibrosis, suppressed TEC proliferation, and heightened TEC apoptosis. To determine the contribution of macrophages to CSF-1-dependent renal repair, we assessed the effect of CSF-1 on I/R in mice in which CD11b+ cells were genetically ablated and determined that macrophages only partially accounted for CSF-1-dependent tubular repair. We found that TECs expressed the CSF-1R and that this receptor was upregulated and coexpressed with CSF-1 in TECs following renal injury in mice and humans. Furthermore, signaling via the CSF-1R stimulated proliferation and reduced apoptosis in human and mouse TECs. Taken together, these data suggest that CSF-1 mediates renal repair by both a macrophage-dependent mechanism and direct autocrine/paracrine action on TECs.
Electrochemical Properties of  B 2 S 3 ‐ Li2 S  ‐ LiI Vitreous Electrolytes (1984)

The electrochemical properties of new Li+ ion conducting glasses belonging to the system have been investigated. The electronic conductivity is at least 106 times lower than the ionic one ( and at 25°C for the best ionic conductors); the electrochemical stability range determined by cyclic voltammetry is about 4.5V from lithium metal.