gebhart/patrepeval huggingface dataset:
Trends in megabit DRAM circuit design (1990)

The state of the art in megabit dynamic random access memory (DRAM) circuit and chip design is reviewed in terms of essential design parameters such as signal-to-noise ratio, power dissipation, and speed. The memory cell signal charge has decreased gradually with an increase in memory cell size, despite the vertically structured cell designs. To offset this decrease, multidivided data-line structures, low-power design, and transposition of folded data lines are essential. To reduce power dissipation, an increase in the maximum refresh cycle and multidivided data lines combined with shared I/O in addition to a reduced operating voltage are efficient. A BiCMOS circuit provides a high-speed access time with low cost due to the high drivability of the driver and high sensitivity of the amplifier. It is predicted that the current DRAM technology might be diversified in the future so that a large-memory-capacity-oriented technology would coexist with a high-speed-oriented technology, posing power-supply standardization as a continuing serious concern.< <ETX xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink">></ETX>
The Full-Length Isoform of Human Papillomavirus 16 E6 and Its Splice Variant E6* Bind to Different Sites on the Procaspase 8 Death Effector Domain (2009)

Human papillomavirus 16 is a causative agent of most cases of cervical cancer and has also been implicated in the development of some head and neck cancers. The early viral E6 gene codes for two alternatively spliced isoforms, E6(large) and E6*. We have previously demonstrated the differential effects of E6(large) and E6* binding on the expression and stability of procaspase 8, a key mediator of the apoptotic pathway. Additionally, we have reported that E6 binds to the FADD death effector domain (DED) at a novel E6 binding domain. Sequence similarities between the FADD and procaspase 8 DEDs suggested a specific region for E6(large)/procaspase 8 binding, which was subsequently confirmed by mutational analysis as well as by the ability of peptides capable of blocking E6/FADD binding to also block E6(large)/caspase 8 binding. However, the binding of the smaller isoform, E6*, to procaspase 8 occurs at a different region, as deletion and point mutations that disrupt E6(large)/caspase 8 DED binding do not disrupt E6*/caspase 8 DED binding. In addition, peptide inhibitors that can block E6(large)/procaspase 8 binding do not affect the binding of E6* to procaspase 8. These results demonstrate that the residues that mediate E6*/procaspase 8 DED binding localize to a different region on the protein and employ a separate binding motif. This provides a molecular explanation for our initial findings that the two E6 isoforms affect procaspase 8 stability in an opposing manner.
Impaired Fast-Spiking, Suppressed Cortical Inhibition, and Increased Susceptibility to Seizures in Mice Lacking Kv3.2 K<sup>+</sup>Channel Proteins (2000)

Voltage-gated K(+) channels of the Kv3 subfamily have unusual electrophysiological properties, including activation at very depolarized voltages (positive to -10 mV) and very fast deactivation rates, suggesting special roles in neuronal excitability. In the brain, Kv3 channels are prominently expressed in select neuronal populations, which include fast-spiking (FS) GABAergic interneurons of the neocortex, hippocampus, and caudate, as well as other high-frequency firing neurons. Although evidence points to a key role in high-frequency firing, a definitive understanding of the function of these channels has been hampered by a lack of selective pharmacological tools. We therefore generated mouse lines in which one of the Kv3 genes, Kv3.2, was disrupted by gene-targeting methods. Whole-cell electrophysiological recording showed that the ability to fire spikes at high frequencies was impaired in immunocytochemically identified FS interneurons of deep cortical layers (5-6) in which Kv3.2 proteins are normally prominent. No such impairment was found for FS neurons of superficial layers (2-4) in which Kv3.2 proteins are normally only weakly expressed. These data directly support the hypothesis that Kv3 channels are necessary for high-frequency firing. Moreover, we found that Kv3.2 -/- mice showed specific alterations in their cortical EEG patterns and an increased susceptibility to epileptic seizures consistent with an impairment of cortical inhibitory mechanisms. This implies that, rather than producing hyperexcitability of the inhibitory interneurons, Kv3.2 channel elimination suppresses their activity. These data suggest that normal cortical operations depend on the ability of inhibitory interneurons to generate high-frequency firing.
Toward a complete dataset of drug–drug interaction information from publicly available sources (2015)

Although potential drug-drug interactions (PDDIs) are a significant source of preventable drug-related harm, there is currently no single complete source of PDDI information. In the current study, all publically available sources of PDDI information that could be identified using a comprehensive and broad search were combined into a single dataset. The combined dataset merged fourteen different sources including 5 clinically-oriented information sources, 4 Natural Language Processing (NLP) Corpora, and 5 Bioinformatics/Pharmacovigilance information sources. As a comprehensive PDDI source, the merged dataset might benefit the pharmacovigilance text mining community by making it possible to compare the representativeness of NLP corpora for PDDI text extraction tasks, and specifying elements that can be useful for future PDDI extraction purposes. An analysis of the overlap between and across the data sources showed that there was little overlap. Even comprehensive PDDI lists such as DrugBank, KEGG, and the NDF-RT had less than 50% overlap with each other. Moreover, all of the comprehensive lists had incomplete coverage of two data sources that focus on PDDIs of interest in most clinical settings. Based on this information, we think that systems that provide access to the comprehensive lists, such as APIs into RxNorm, should be careful to inform users that the lists may be incomplete with respect to PDDIs that drug experts suggest clinicians be aware of. In spite of the low degree of overlap, several dozen cases were identified where PDDI information provided in drug product labeling might be augmented by the merged dataset. Moreover, the combined dataset was also shown to improve the performance of an existing PDDI NLP pipeline and a recently published PDDI pharmacovigilance protocol. Future work will focus on improvement of the methods for mapping between PDDI information sources, identifying methods to improve the use of the merged dataset in PDDI NLP algorithms, integrating high-quality PDDI information from the merged dataset into Wikidata, and making the combined dataset accessible as Semantic Web Linked Data.
Study on access permission control for the Web of Things (2015)

The Web of Things (WoT) research is exploring ways on the interoperation among the smart things, since the Web has proven its potentials as open communication environment for accommodating a variety of Web resources. The Web technologies has enabled the Web-enabled devices to publish and exchange their resource information over the Web, whereas the Web-enabled devices should cope with the security threat regarding the information exposures over the Web, particularly, access permissions for the resources about the things. Thus, in this paper we analyse access permission control mechanism considering both the WoT characteristics and the REST-compliant resource-oriented Web architecture. In contrast to existing access control logics, the proposed mechanism utilizes not only the requester information such as the typical identity and the internet addresses, but also the context of the thing itself. Based on this mechanism, we present web-resource structure for access permission control, and describe an exemplary procedure in detail. This research contributes to the flexible and decentralized access permission control for WoT.
Ferromagnetic domain structure and hysteresis of exchange bias in NiFe/NiMn bilayers (2002)

Magnetization reversal in NiFe/NiMn bilayers was studied by measuring anisotropic magnetoresistance and pseudo-Hall effect simultaneously. Since the single domain state of the ferromagnetic layer could be well traced in such measurements, we were able to distinguish hysteresis of exchange bias from inhomogeneous magnetization. The exchange bias was found to have two components during the single domain reversal process. Domain breaking in given fields took place when the biasing field became more random.
Genetic and Pharmacological Suppression of Oncogenic Mutations in <i>RAS</i> Genes of Yeast and Humans (1989)

The activity of an oncoprotein and the secretion of a pheromone can be affected by an unusual protein modification. Specifically, posttranslational modification of yeast a-factor and Ras protein requires an intermediate of the cholesterol biosynthetic pathway. This modification is apparently essential for biological activity. Studies of yeast mutants blocked in sterol biosynthesis demonstrated that the membrane association and biological activation of the yeast Ras2 protein require mevalonate, a precursor of sterols and other isoprenes such as farnesyl pyrophosphate. Furthermore, drugs that inhibit mevalonate biosynthesis blocked the in vivo action of oncogenic derivatives of human Ras protein in the Xenopus oocyte assay. The same drugs and mutations also prevented the posttranslational processing and secretion of yeast a-factor, a peptide that is farnesylated. Thus, the mevalonate requirement for Ras activation may indicate that attachment of a mevalonate-derived (isoprenoid) moiety to Ras proteins is necessary for membrane association and biological function. These observations establish a connection between the cholesterol biosynthetic pathway and transformation by the ras oncogene and offer a novel pharmacological approach to investigating, and possibly controlling, ras-mediated malignant transformations.
Developmental biology and building a tooth. (2003)

During the last 15 years, we have started to understand tooth development at the gene level. The list of genes known to regulate the position, shape, or number of teeth is lengthening rapidly. Interestingly, so far all these genes have important functions in the mediation of cell communication, which is generally considered the most important mechanism driving embryonic development. The communication is mediated by small signal molecules that are sent to nearby cells, thereby affecting their behavior and advancing differentiation. There are dozens of different signals and their receptors and target genes, which together form complicated signaling networks. The defects in several human conditions affecting tooth development have been identified recently, and these genes have turned out to be necessary components of signaling networks. Experimental studies using transgenic mice as models for human syndromes such as ectodermal and cleidocranial dysplasia have pinpointed the exact roles of the disease genes and indicated ways for possible new therapies. It is also possible that by combining the knowledge of molecular regulation of tooth development with the recent breakthroughs in stem cell research, dreams of building new teeth in dental practice may come true in the future.
“Overview of short-reach optical interconnects: From VCSELs to silicon nanophotonics” (2010)

This article consists of a collection of slides from the author's conference presentation on short-reach optical interconnection from VCSELs to silicon nanophotonics. Some of the specific topics discussed include: an introduction to the technology of optical interconnects; fibers, connectors, and module packaging; packaging processes; energy efficiency metrics and goals; silicon photonics and wavelength division multiplexing; an overview of recent optical components; and the key features and applications supported by microchips.
Chemokine (C-C Motif) Ligand 2 Mediates the Prometastatic Effect of Dysadherin in Human Breast Cancer Cells (2006)

Dysadherin, a cancer-associated membrane glycoprotein, down-regulates E-cadherin and promotes cancer metastasis. This study examined the role of dysadherin in breast cancer progression. Expression of dysadherin was found to be highest in breast cancer cell lines and tumors that lacked the estrogen receptor (ER). Knockdown of dysadherin caused increased association of E-cadherin with the actin cytoskeleton in breast cancer cell lines that expressed E-cadherin. However, knockdown of dysadherin could still suppress cell invasiveness in cells that had no functional E-cadherin, suggesting the existence of a novel mechanism of action. Global gene expression analysis identified chemokine (C-C motif) ligand 2 (CCL2) as the transcript most affected by dysadherin knockdown in MDA-MB-231 cells, and dysadherin was shown to regulate CCL2 expression in part through activation of the nuclear factor-kappaB pathway. The ability of dysadherin to promote tumor cell invasion in vitro was dependent on the establishment of a CCL2 autocrine loop, and CCL2 secreted by dysadherin-positive tumor cells also promoted endothelial cell migration in a paracrine fashion. Finally, experimental suppression of CCL2 in MDA-MB-231 cells reduced their ability to metastasize in vivo. This study shows that dysadherin has prometastatic effects that are independent of E-cadherin expression and that CCL2 could play an important role in mediating the prometastatic effect of dysadherin in ER-negative breast cancer.
The Role of Magnesium in Clinical Biochemistry: An Overview (1991)

Magnesium is the second most abundant intracellular cation. It is essential for a wide variety of metabolically important reactions, in particular those involving ATP. Hypomagnesaemia is surprisingly common in hospital populations but is sometimes either undetected or overlooked. Serum magnesium concentrations provide a guide to magnesium status but while hypomagnesaemia is a reliable indicator of magnesium deficiency, normomagnesaemia does not exclude magnesium depletion. A wide variety of conditions predispose to magnesium depletion. Clinical magnesium deficiency has potentially fatal consequences in vulnerable groups of patients and should be excluded in all such cases. Magnesium deficiency may result in hypokalaemia, hypocalcaemia or other disturbances of electrolyte homeostasis, refractory cardiac arrhythmias, or increased sensitivity to digoxin. The capacity to measure serum and urine magnesium concentrations rapidly, regularly and reliably should be part of the repertoire of all clinical chemistry laboratories involved in the care of critically ill patients.
Pressure Shift Freezing as Potential Alternative for Generation of Decellularized Scaffolds (2013)

Background. Protocols using chemical reagents for scaffold decellularization can cause changes in the properties of the matrix, depending on the type of tissue and the chemical reagent. Technologies using physical techniques may be possible alternatives for the production grafts with potential superior matrix characteristics. Material and Methods. We tested four different technologies for scaffold decellularization. Group 1: high hydrostatic pressure (HHP), 1 GPa; Group 2: pressure shift freezing (PSF); Group 3: pulsed electric fields (PEF); Group 4: control group: detergent (SDS). The degree of decellularization was assessed by histological analysis and the measurement of residual DNA. Results. Tissue treated with PSF showed a decellularization with a penetration depth (PD) of 1.5 mm and residual DNA content of 24% ± 3%. HHD treatment caused a PD of 0.2 mm with a residual DNA content of 28% ± .4%. PD in PEF was 0.5 mm, and the residual DNA content was 49% ± 7%. In the SDS group, PD was found to be 5 mm, and the DNA content was determined at 5% ± 2%. Conclusion. PSF showed promising results as a possible technique for scaffold decellularization. The penetration depth of PSF has to be optimized, and the mechanical as well as the biological characteristics of decellularized grafts have to be evaluated.
Ontogenesis of the Mite<i>Varroa Jacobsoni</i>in Worker and Drone Honeybee Brood Cells (1983)

SummaryOntogenesis of the mite Varroa jacobsoni Oudemans (1904) was observed at 4 h intervals in brood cells of the honeybee Apis mellifera cecropia. Between July and November 1981, in the region of Thessaloniki, 241 worker and 107 drone cells infested with fertile mites were examined in the post-capping period. A macroscopic distinction between the sexes was recorded photographically as early as the first mobile phase of mite ontogenesis. In cells containing either worker or drone brood, egg-laying by the mite began about 60 h after the cell was capped and one egg was laid every 30 min. Normally the offspring included only one male, which developed from an egg laid about 96 h after capping. Ontogenesis lasted 7·5 days in the female Varroa and 5·5 days in the male. The mite can lay at most 7 eggs in a drone cell and 6 in a worker cell.
Involvement of Hydrogen Peroxide in Collagen Cross-linking by High Glucose in Vitro and in Vivo (1996)

The Maillard reaction has been implicated in cross-linking and fluorescence formation of collagen exposed to high glucose in vitro. However, several pharmacologic agents, whose action seems unrelated to pathways of nonenzymatic glycation, have been demonstrated to prevent cross-linking in diabetes. To clarify this discrepancy, kinetic changes in glycation, glycoxidation (carboxymethyllysine, CML), and cross-linking (measured as tendon breaking time, TBT) were evaluated in rat tail tendons incubated in 5 and 30 mM glucose in vitro and in tendons implanted in vivo into diabetic rat peritoneal cavity. In vitro, rates were found to be both O2- and glucose-dependent. Tendon preglycation and presence of added 2 mM glycosylamine and Amadori compounds (Amadori product of glucose and propylamine) catalyzed these changes in a primarily O2-dependent manner. In the presence of Amadori compounds, kinetic changes were dramatically increased and were preventable by addition of catalase to the medium. Tendons implanted into diabetic rat peritoneum became more rapidly glycoxidized and cross-linked when implanted at day 30 from diabetes onset (high tissue glycation) compared to day 3 (low tissue glycation) in spite of similar glycation kinetics, suggesting a mechanistic dissociation between glycation, glycoxidation, and cross-linking in diabetes. Indeed, intraperitoneal injection of catalase and other antioxidants dramatically suppressed cross-linking, fluorescence formation, and, to some extent, glycoxidation, without affecting glycation. This study confirms the role of oxidative stress in protein cross-linking by the Maillard reaction in vitro and provides the first evidence for a role of H2O2 in cross-linking in diabetes. Whereas Amadori products are a potent source of H2O2 formation in vitro, their precise contribution to H2O2 generation and the actual role of Maillard reaction products in collagen cross-linking in diabetes requires further investigation.
Front-end CMOS chipset for 10 Gb/s communication (2003)

A 10 Gb/s communication chipset is realized for the first time in 0.18 /spl mu/m generic CMOS. It comprises (all fully differential): (i) a transimpedance amplifier: gain=1300 /spl Omega/, bandwidth 9 GHz; optical. (ii) a limiting amplifier: t/sub rise/, t/sub fall/<23 ps; sensitivity=5 mV at BER=10/sup -12/. (iii) a laser driver: adjustable I/sub bias/ (up to 40 mA) and I/sub mod/ (up to 35 mA), driving a laser module with Z/sub in/=50 /spl Omega/.
UNCONVENTIONALLY HIGH AND LOW FREQUENCY EDDY CURRENT METHODS FOR MATERIAL SURFACE CHARACTERIZATIONS (2010)

Views Icon Views Article contents Figures & tables Video Audio Supplementary Data Peer Review Share Icon Share Twitter Facebook Reddit LinkedIn Tools Icon Tools Reprints and Permissions Cite Icon Cite Search Site Citation N. Nakagawa, C. C. H. Lo; UNCONVENTIONALLY HIGH AND LOW FREQUENCY EDDY CURRENT METHODS FOR MATERIAL SURFACE CHARACTERIZATIONS. AIP Conf. Proc. 22 February 2010; 1211 (1): 1471–1478. https://doi.org/10.1063/1.3362242 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 ContentAIP Publishing PortfolioAIP Conference Proceedings Search Advanced Search |Citation Search
Therapeutic potential of cyclodextrins in the treatment of Niemann–Pick type C disease (2012)

Niemann-Pick type C (NPC) disease is an autosomal recessive neurovisceral lipid and storage disorder characterized by abnormal sequestration of unesterified cholesterol within the late endosomal/lysosomal compartment of all cells in the body. This disease primarily affects children and is characterized by hepatic and pulmonary dysfunction, neurodegeneration and death at an early age. Currently, there is no effective treatment for NPC disease. It was recently discovered that 2-hydroxypropyl-β-cyclodextrin (2HPBCD), when administered systemically to a murine model of either NPC1 or NPC2 disease, significantly reduced lysosomal cholesterol accumulation in almost every organ, delayed the progression of neurodegeneration and significantly prolonged lifespan by allowing trapped cholesterol within the late endosome/lysosome to be released. When 2HPBCD was administered directly into the CNS of <i>Npc1<sup>-/-</sup></i> mice, neurodegeneration was completely prevented. This review will explore the pathophysiology of NPC disease and the use of 2HPBCD as a possible therapeutic modality.
A Low-Power Wideband Transmitter Front-End Chip for 80 GHz FMCW Radar Systems With Integrated 23 GHz Downconverter VCO (2012)

A low-power FMCW 80 GHz radar transmitter front-end chip is presented, which was fabricated in a SiGe bipolar production technology ( <i xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink">f</i> <sub xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink">T</sub> =180 GHz, <i xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink">f</i> <sub xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink">max</sub> =250 GHz ). Additionally to the fundamental 80 GHz VCO, a 4:1-frequency divider (up to 100 GHz), a 23 GHz local oscillator (VCO) with a low phase noise of -112 dBc/Hz (1 MHz offset), a PLL-mixer and a static frequency divider is integrated together with several output buffers. This chip was designed for low power consumption (in total <; 0.5 W, i.e., 100 mA at 5 V supply voltage), which is dominated by the 80 GHz VCO due to the demands for high output power (≈ 12 dBm) and low phase noise (minimum -97 dBc/Hz at 1 MHz offset) within the total wide tuning range from 68 GHz to 92.5 GHz (Δ <i xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink">f</i> = 24.5 GHz). Measurements of the double-PLL system at 80 GHz showed a low phase noise of -88 dBc/Hz at 10 kHz offset frequency.