gebhart/patrepeval huggingface dataset:
Alterations in cardiac gene expression during the transition from stable hypertrophy to heart failure. Marked upregulation of genes encoding extracellular matrix components. (1994)

The failing heart is characterized by impaired cardiac muscle function and increased interstitial fibrosis. Our purpose was to determine whether the functional impairment of the failing heart is associated with changes in levels of mRNA encoding proteins that modulate parameters of contraction and relaxation and whether the increased fibrosis observed in the failing heart is related to elevated expression of genes encoding extracellular matrix components. We studied hearts of 18- to 24-month-old spontaneously hypertensive rats with signs and symptoms of heart failure (SHR-F) or without evidence of failure (SHR-NF) and of age-matched normotensive Wistar-Kyoto (WKY) rats. Compared with WKY rats, SHR-NF exhibited left ventricular (LV) hypertrophy (2.2-fold) and right ventricular (RV) hypertrophy (1.5-fold), whereas SHR-F were characterized by comparable LV hypertrophy (2.1-fold) and augmented RV hypertrophy (2.4-fold; all P &lt; .01). Total RNA was isolated from ventricles and subjected to Northern blot analysis. In SHR-F hearts, the level of alpha-myosin heavy chain mRNA was decreased in both ventricles to 1/3 and 1/5 of the SHR-NF and WKY values, respectively (both P &lt; .01). Levels of beta-myosin heavy chain, alpha-cardiac actin, and myosin light chain-2 mRNAs were not significantly altered in hearts of SHR-NF or SHR-F. Levels of alpha-skeletal actin were twofold greater in SHR-NF hearts compared with WKY hearts and were intermediate in SHR-F hearts. Levels of atrial natriuretic factor (ANF) mRNA were elevated threefold in the LV of SHR-NF (P &lt; .05) but were not significantly increased in the RV of SHR-NF compared with WKY rats. During the transition to failure (SHR-F versus SHR-NF), ANF mRNA levels increased an additional 1.6-fold in the LV and were elevated 4.7-fold in the RV (both P &lt; .05). Levels of sarcoplasmic reticulum Ca(2+)-ATPase (SRCA) mRNA were maintained in the LV of hypertensive and failing hearts at levels not significantly different from WKY values. In contrast, the level of RV SRCA mRNA was 24% less in SHR-NF compared with WKY rats, and during the transition to failure, this difference was not significantly exacerbated (29% less than the WKY value). The levels of fibronectin and pro-alpha 1(I) and pro-alpha 1(III) collagen mRNAs were not significantly elevated in either ventricle of the SHR-NF group but were fourfold to fivefold higher in both ventricles of SHR-F (all P &lt; .05).(ABSTRACT TRUNCATED AT 400 WORDS)
Histopathology and ultrastructure of meiotic arrest in human spermatogenesis. (1980)

Testicular biopsy specimens with meiotic arrest during spermatogenesis were studied with light and electron microscopy. The meiotic arrest occurred constantly at the end of meiotic prophase. The first degenerative changes were seen in the nucleus as a condensation of the chromatin along the synaptionemal complexes in the late pachytene spermatocytes. Later degenerative changes could also be seen in the cytoplasm. These results seem to indicate that the meiotic arrest primarily affects the nucleus of the pachytene spermatocytes.
The P2X7 Receptor: A Key Player in IL-1 Processing and Release (2006)

Human IL-1 family proteins are key mediators of the host response to infections, injury, and immunologic challenges. The mechanism by which IL-1 activates proinflammatory responses in target cells, and the plasma membrane receptors involved, is fairly well known. This has led to the development of innovative drugs that block IL-1 downstream to its synthesis and secretion. On the contrary, the mechanism of IL-1 and other IL-1 family members (e.g., IL-18) maturation and release is incompletely understood. Accruing evidence points to a plasma membrane receptor for extracellular ATP, the P2X(7) receptor, as a key player in both processes. A deeper understanding of the mechanism by which the P2X(7) receptor triggers IL-1 maturation and exteriorization may suggest novel avenues for the treatment of inflammatory diseases and provide a deeper insight in the fundamental mechanism of protease activation and cellular export of proteins lacking a leader sequence.
Oligodeoxynucleotide Synthesis: H-Phosphonate Approach (2003)

Ribonucleoside H-phosphonates were introduced by Todd in 1957 to prepare diribonucleotide phosphate diesters (1). The H-phosphonates were activated for condensation with diphenyl chlorophosphate, and this activator was later extended to the synthesis of deoxyribonucleotide dimers (2). Activation of deoxynucleoside H-phosphonates with acyl chlorides allows for the synthesis of oligodeoxynucleotides greater than 100 bases in length (3,4). Since these initial results, a number of laboratories have used acyl chlorides and nucleoside H-phosphonates in the synthesis of oligodeoxynucleotides (5–9). This chemistry has also been extended to the synthesis of phosphate analogs of oligodeoxynucleotides (10–16).
Electroluminescence in Organic Films with Three-Layer Structure (1988)

We have succeeded in the fabrication of a stable organic electroluminescent (EL) device with a three-layer structure; hole transport layer/emitting layer/electron transport layer. The EL device was prepared by vacuum evaporation. Efficient carrier double injection into the emitting layer was realized by the use of separate hole and electron transport layers. Bright EL emission was observed in a darkened room at the dc bias voltage of 50 V. Stable emission lasted for more than five hours at this condition. The emission spectrum could be changed with variation of the organic material for the emitting layer.
Expression of Exogenous Genes Under the Control of Endogenous HSP70 and CAB Promoters in the Closterium peracerosum–strigosum–littorale complex (2008)

A unicellular charophyte alga, Closterium peracerosum-strigosum-littorale complex (C. psl. complex), has been studied in order to obtain basic information regarding sexual reproduction in plants. Systems for gene introduction and transient expression were developed for endogenous genes using phleomycin resistance (ble) and Chlamydomonas green fluorescent protein (cgfp) genes as selection markers. These genes have codon usage similar to that of genes in the C. psl. complex. To drive these genes strongly into C. psl. complex cells, two native promoters of the C. psl. complex genome-CpHSP70 and CpCAB1-were linked to a ble::cgfp fusion gene and introduced into the cells by particle bombardment. Following 2 d of incubation, we found 500 cells expressing GFP under the control of the CpHSP70 promoter, which were identified following heat shock treatment at 42 degrees C, and 100 cells expressing GFP under the control of the CpCAB1 promoter, which were observed in lit conditions. In contrast, the GFP signal was only detected in two cells when ble::cgfp under control of the cauliflower mosaic virus 35S promoter was introduced. The ble::cgfp fusion protein was detected in the nucleus, whereas the single cgfp protein was detected in the cytoplasm. Our results indicate that the newly isolated native promoters of CpHSP70 and CpCAB1 are useful tools for inducing exogenous gene expression under heat shock and lit conditions, respectively. In addition, this strategy can be used for transient assays, such as the intracellular localization of unknown gene products in the C. psl. complex.
The effect of differentiated emission taxes: does an emission tax favor industry? (2005)

Extending a standard 2x2 Heckscher−Ohlin model to incorporate emissions, this paper investigates the effect of differentiated emission taxes on output and emissions in a small open economy. The following results are derived. First, raising the emission tax imposed on one industry may increase the output of that industry. This result is quite surprising in the sense that such a paradoxical result can occur in a simple and standard model under fairly plausible values of parameters. By numerical examples and using a graphical method, it is also shown that the mechanism behind the result is the factor market adjustment effects which work through two different channels. Second, while strengthening emission taxes uniformly across industries always reduces the volume of emissions, strengthening emission tax unevenly may increase it. I would like to thank Makoto Ikema, Jota Ishikawa, Kazuharu Kiyono, Yasuhiro Takarada, Makoto Tawada, Morihiro Yomogida and seminar participants at Hitotsubashi university for their helpful comments and suggestions. All remaining errors are the author&amp;apos;s.
Getting the Most Out of a Vaccine Program (2005)

Magnesium-sensitive microelectrodes were used to measure the intracellular concentration of free Mg2+, [Mg2+]f, in rat extensor digitorum longus muscles in vitro at 30 degrees C. The intracellular activities of Na+ and K+ were also determined so that allowance could be made for the interference from these ions with the Mg2+ electrode response. The mean value for [Mg2+]f based on twenty-six measurements in twelve muscles was 0.47 mM.
Integrated Polishing Steps for Monoclonal Antibody Purification (2008)

This chapter contains sections titled: Introduction Polishing Steps in Antibody Purification Integration of Polishing Steps Conclusions Acknowledgments References
Regulation of pulmonary fibrosis by chemokine receptor CXCR3 (2004)

CXC chemokine receptor 3 (CXCR3) is the receptor for the IFN-gamma-inducible C-X-C chemokines MIG/CXCL9, IP-10/CXCL10, and I-TAC/CXCL11. CXCR3 is expressed on activated immune cells and proliferating endothelial cells. The role of CXCR3 in fibroproliferation has not been investigated. We examined the role of CXCR3 in pulmonary injury and repair in vivo. CXCR3-deficient mice demonstrated increased mortality with progressive interstitial fibrosis relative to WT mice. Increased fibrosis occurred without increased inflammatory cell recruitment. CXCR3 deficiency resulted in both a reduced early burst of IFN-gamma production and decreased expression of CXCL10 after lung injury. We identified a relative deficiency in lung NK cells in the unchallenged CXCR3-deficient lung and demonstrated production of IFN-gamma by WT lung NK cells in vivo following lung injury. The fibrotic phenotype in the CXCR3-deficient mice was significantly reversed following administration of exogenous IFN-gamma or restoration of endogenous IFN-gamma production by adoptive transfer of WT lymph node and spleen cells. Finally, pretreatment of WT mice with IFN-gamma-neutralizing Ab's enhanced fibrosis following lung injury. These data demonstrate a nonredundant role for CXCR3 in limiting tissue fibroproliferation and suggest that this effect may be mediated, in part, by the innate production of IFN-gamma following lung injury.
Direct regulation of rhodopsin 1 by Pax-6/eyeless in Drosophila: evidence for a conserved function in photoreceptors. (1997)

Pax-6 is a transcription factor containing both a homeodomain (HD) and a Paired domain (PD). It functions as an essential regulator of eye development in both Drosophila and vertebrates, suggesting an evolutionarily conserved origin for different types of metazoan eyes. Classical morphological and phylogenetic studies, however, have concluded that metazoan eyes have evolved many times independently. These apparently contradictory findings may be reconciled if the evolutionarily ancient role of Pax-6 was to regulate structural genes (e.g., rhodopsin) in primitive photoreceptors, and only later did it expand its function to regulate the morphogenesis of divergent and complex eye structures. In support of this, we present evidence that eyeless (ey), which encodes the Drosophila homolog of Pax-6, directly regulates rhodopsin 1 (rh1) expression in the photoreceptor cells. We detect ey expression in both larval and adult terminally differentiated photoreceptor cells. We show that the HD of Ey binds to a palindromic HD binding site P3/RCS1 in the rh1 promoter, which is essential for rh1 expression. We further demonstrate that, in vivo, P3/RCS1 can be replaced by binding sites specific for the PD of Ey. P3/RCS1 is conserved in the promoters of all Drosophila rhodopsin genes as well as in many opsin genes in vertebrates. Mutimerized P3 sites in front of a basal promoter are able to drive the expression of a reporter gene in all photoreceptors. These results suggest that Pax-6/Ey directly regulates rhodopsin 1 gene expression by binding to the conserved P3/RCS1 element in the promoter.
Behavior of Ar plasmas formed in a mirror field electron cyclotron resonance microwave ion source (1990)

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 S. M. Gorbatkin, L. A. Berry, J. B. Roberto; Behavior of Ar plasmas formed in a mirror field electron cyclotron resonance microwave ion source. Journal of Vacuum Science & Technology A 1 May 1990; 8 (3): 2893–2899. https://doi.org/10.1116/1.576645 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 ContentAVS: Science & Technology of Materials Interfaces and ProcessingJournal of Vacuum Science & Technology A Search Advanced Search |Citation Search
An intravitreal device providing sustained release of cyclosporine and dexamethasone (1996)

We conclude that the device maintains potentially therapeutic levels of both cyclosporine and dexamethasone in the vitreous. Reversible electroretinographic abnormalities are attributable to cyclosporine. A sustained-release device containing cyclosporine and dexamethasone may be useful for reducing inflammation in diseases such as proliferative vitreoretinopathy and uveitis.
Latexin, a carboxypeptidase A inhibitor, is expressed in rat peritoneal mast cells and is associated with granular structures distinct from secretory granules and lysosomes (2000)

Latexin, a protein possessing inhibitory activity against rat carboxypeptidase A1 (CPA1) and CPA2, is expressed in a neuronal subset in the cerebral cortex and cells in other neural and non-neural tissues of rat. Although latexin also inhibits mast-cell CPA (MCCPA), the expression of latexin in rat mast cells has not previously been confirmed. In the present study we examined the expression and subcellular localization of latexin in rat peritoneal mast cells. Western blot and reverse-transcriptase-mediated PCR analyses showed that latexin was contained and expressed in the rat peritoneal mast cells. Immunocytochemically, latexin immunofluorescence was localized on granular structures distinct from MCCPA-, histamine- or cathepsin D-immunopositive granules. Immunoelectron microscopy revealed that latexin was associated with a minority population of granules. The latexin-associated granules were separated from MCCPA- or histamine-containing granules on a self-generating density gradient of polyvinylpyrrolidone-coated silica-gel particles (Percoll). Treatments with high ionic strength and heparinase released latexin from the granules, suggesting that latexin is non-covalently associated with a heparin-like component of the granules. MCCPA and histamine were released from the mast cells after non-immunological and immunological stimulation with compound 48/80, A23187 and anti-IgE antibody, whereas latexin was not released. These results show that latexin is synthesized in rat peritoneal mast cells and suggest that it is associated with a unique type of intracellular granules distinct from MCCPA- and histamine-containing secretory granules and lysosomes.
PCA-PMC: a novel use of a priori knowledge for fast parallel model combination (2002)

This paper describes an algorithm to reduce computational complexity of the parallel model combination (PMC) method for robust speech recognition while retaining the same level of performance. Although, PMC is effective in composing a noise corrupted acoustic model from clean speech and noise models, the intense computational complexity limits its use in real-time use. The novel approach here is to encode the clean models using principal component analysis (PCA) and pre-compute the prototype vectors and matrices for the means and covariances in the linear spectral-domain using rectangular DCT and inverse DCT matrices. Therefore, transformation into the linear spectral domain is reduced to finding the projection of each vector in the eigen space of means and covariances followed by a linear combination of vectors and matrices obtained from the projections. Furthermore, the eigen space allows a better trade-off for reducing computational complexity versus accuracy. The computational savings are demonstrated both analytically and through experimental evaluations. Experiments using context independent phone recognition with TIMIT data shows that the new PMC framework can outperforms the baseline method by a factor of 1.9 with the same level of accuracy.
Biochemistry of Pro-B-Type Natriuretic Peptide-Derived Peptides: The Endocrine Heart Revisited (2004)

It is necessary to focus more on the biology of the proBNP-derived peptides. In turn, new insight into the biochemistry could pave the way for more sensitive and disease-specific assays in the clinical setting.
Macrophages and atherosclerotic plaque stability (1996)

Physical disruption of atheroma frequently causes coronary thrombosis. Ruptured plaques usually have thin fibrous caps overlying a large thrombogenic lipid core rich in lipid-laden macrophages. The biology of plaque monocyte-derived macrophages thus assumes critical importance in understanding plaque instability. Monocyte recruitment involves binding to leukocyte adhesion receptors on the endothelial surface such as intercellular adhesion molecule-1 and vascular cell adhesion molecule-1. Once adherent to the endothelial surface, monocytes enter the intima at sites of lesion predilection. This process probably requires directed migration of the mononuclear cells. A number of chemoattractant molecules, such as the monocyte chemoattractant molecule-1, may participate in signaling this entry of adherent monocytes into the artery wall. Once resident in the arterial intima, monocytes accumulate lipid, via increasingly well characterized receptor-mediated uptake, and transform into macrophage foam cells. These lesional macrophages also acquire other functional properties including production of the potent procoagulant, tissue factor, apolipoprotein E, and an increasing list of cytokines (protein mediators of information and immunity) that may participate importantly in autocrine and paracrine signaling among leukocytes and vascular endothelial and smooth muscle cells. Fatty streaks seldom cause clinical events but may evolve into complicated atheromatous plaques characterized by an accumulation of smooth muscle cells and extracellular matrix and formation of a central core containing extracellular lipid. Death of macrophages, including programmed cell death or apoptosis, probably promotes formation of this thrombogenic lipid pool whose size correlates with plaque instability. Lesion complication often culminates in rupture of the fibrous cap overlying this lipid core. The integrity of the fibrous cap, and thus its resistance to rupture, depends critically on the collagenous extracellular matrix of the plaque's fibrous cap. This aspect of plaque structure in turn depends upon the balance between synthesis and degradation of the macromolecules that comprise the extracellular matrix of the cap, principally interstitial forms of collagen derived from arterial smooth muscle cells. Collagen breakdown, however, appears to depend critically on macrophages. Plaque macrophages express a variety of matrix-degrading enzymes that can contribute to the weakening of the fibrous cap. In this way, macrophages can critically influence aspects of the biology of human atheroma related to lesion stability. We hypothesize that lipid-lowering reduces clinical events, as shown in recent trials, by stabilizing lesions in part by reversing some of the maladaptive functions of macrophages described above.
Transcriptome sequencing identifies ETV6–NTRK3 as a gene fusion involved in GIST (2015)

Gastrointestinal stromal tumours (GISTs) are the most common mesenchymal neoplasms of the gastrointestinal tract. The vast majority of GISTs are driven by oncogenic activation of KIT, PDGFRA or, less commonly, BRAF. Loss of succinate dehydrogenase complex activity has been identified in subsets of KIT/PDGFRA/BRAF-mutation negative tumours, yet a significant fraction of GISTs are devoid of any of such alterations. To address the pathobiology of these 'quadruple-negative' GISTs, we sought to explore the possible involvement of fusion genes. To this end we performed transcriptome sequencing on five KIT/PDGFRA/BRAF-mutation negative, SDH-proficient tumours. Intriguingly, the analysis unveiled the presence of an ETV6-NTRK3 gene fusion. The screening by FISH of 26 additional cases, including KIT/PDGFRA-mutated GISTs, failed to detect other ETV6 rearrangements beside the index case. This was a 'quadruple-negative' GIST located in the rectum, an uncommon primary site for GIST development (∼4% of all GISTs). The fusion transcript identified encompasses exon 4 of ETV6 and exon 14 of NTRK3 and therefore differs from the canonical ETV6-NTRK3 chimera of infantile fibrosarcomas. However, it retains the ability to induce IRS1 phosphorylation, activate the IGF1R downstream signalling pathway and to be targeted by IGF1R and ALK inhibitors. Thus, the ETV6-NTRK3 fusion might identify a subset of GISTs with peculiar clinicopathological characteristics which could be eligible for such therapies. Copyright © 2015 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.
Rethinking Digital Design: Why Design Must Change (2010)

Because of technology scaling, power dissipation is today's major performance limiter. Moreover, the traditional way to achieve power efficiency, application-specific designs, is prohibitively expensive. These power and cost issues necessitate rethinking digital design. To reduce design costs, we need to stop building chip instances, and start making chip generators instead. Domain-specific chip generators are templates that codify designer knowledge and design trade-offs to create different application-optimized chips.
Unique multipotent cells in adult human mesenchymal cell populations (2010)

We found adult human stem cells that can generate, from a single cell, cells with the characteristics of the three germ layers. The cells are stress-tolerant and can be isolated from cultured skin fibroblasts or bone marrow stromal cells, or directly from bone marrow aspirates. These cells can self-renew; form characteristic cell clusters in suspension culture that express a set of genes associated with pluripotency; and can differentiate into endodermal, ectodermal, and mesodermal cells both in vitro and in vivo. When transplanted into immunodeficient mice by local or i.v. injection, the cells integrated into damaged skin, muscle, or liver and differentiated into cytokeratin 14-, dystrophin-, or albumin-positive cells in the respective tissues. Furthermore, they can be efficiently isolated as SSEA-3(+) cells. Unlike authentic ES cells, their proliferation activity is not very high and they do not form teratomas in immunodeficient mouse testes. Thus, nontumorigenic stem cells with the ability to generate the multiple cell types of the three germ layers can be obtained through easily accessible adult human mesenchymal cells without introducing exogenous genes. These unique cells will be beneficial for cell-based therapy and biomedical research.