gebhart/patrepeval huggingface dataset:
Production of an Acellular Amniotic Membrane Matrix for Use in Tissue Engineering (2006)

A clinical need exists for an immunologically compatible surgical patch with a wide range of uses including soft tissue replacement, body wall repair, cardiovascular applications, and as a wound dressing. This study aimed to produce an acellular matrix from human amniotic membrane for future assessment as a surgical patch and a delivery system for epithelial cells. A novel detergent-based protocol was modified to remove all cellular components from amnion to render it non-immunogenic. Amnion was harvested within 24 h after elective caesarean section (n = 12). One sample group remained fresh, whereas the other was treated with 0.03% (w/v) sodium dodecyl sulphate, with hypotonic buffer and protease inhibitors, nuclease treatment, and terminal sterilization, using peracetic acid (0.1% v/v). Fresh and treated amnion was analyzed histologically for the presence of cells, deoxyribonucleic acid (DNA), collagen, glycosaminoglycans (GAGs), and elastin. Quantitative analysis was performed to determine levels of GAGs, elastin, hydroxyproline, denatured collagen, and DNA. The biomechanical properties of the membrane were determined using uniaxial tensile testing to failure. Histological analysis of treated human amnion showed complete removal of cellular components from the tissue; the histoarchitecture remained intact. All major structural components of the matrix were retained, including collagen type IV and I, laminin, and fibronectin. Differences were observed between fresh and decellularized amnion in matrix hydroxyproline (34.7 microg/mg vs 49.7 microg/mg), GAG (42.5 microg/mg vs 85.4 microg/mg), denatured collagen (2.2 microg/mg vs 1.7 microg/mg), and elastin (359.2 microg/mg vs 490.8 microg/mg) content. DNA content was diminished after treatment. Acellular matrices were biocompatible, cells grew in contact, and there was no decrease in cell viability after incubation with soluble tissue extracts. In addition, no significant reduction in ultimate tensile strength, extensibility, or elasticity was found after decellularization. Removal of the cellular components should eliminate immunological rejection. The resulting matrix was biocompatible in vitro and exhibited no adverse effects on cell morphology or viability.
BH4 peptide derivative from Bcl-xL attenuates ischemia/reperfusion injury thorough anti-apoptotic mechanism in rat hearts (2004)

These results demonstrated that TAT-BH4 attenuates myocardial ischemia/reperfusion injury through preventing myocardial apoptosis. Thus, TAT-BH4 may be a novel therapeutic agent for myocardial protection in cardiac surgery.
Cell-surface receptors for gibbon ape leukemia virus and amphotropic murine retrovirus are inducible sodium-dependent phosphate symporters. (1994)

Cell surface receptors for gibbon ape leukemia virus (Glvr-1) and murine amphotropic retrovirus (Ram-1) are distinct but related proteins having multiple membrane-spanning regions. Distant homology with a putative phosphate permease of Neurospora crassa suggested that these receptors might serve transport functions. By expression in Xenopus laevis oocytes and in mammalian cells, we have identified Glvr-1 and Ram-1 as sodium-dependent phosphate symporters. Two-electrode voltage-clamp analysis indicates net cation influx, suggesting that phosphate is transported with excess sodium ions. Phosphate uptake was reduced by > 50% in mouse fibroblasts expressing amphotropic envelope glycoprotein, which binds to Ram-1, indicating that Ram-1 is a major phosphate transporter in these cells. RNA analysis shows wide but distinct tissue distributions, with Glvr-1 expression being highest in bone marrow and Ram-1 in heart. Overexpression of Ram-1 severely repressed Glvr-1 synthesis in fibroblasts, suggesting that transporter expression may be controlled by net phosphate accumulation. Accordingly, depletion of extracellular phosphate increased Ram-1 and Glvr-1 expression 3- to 5-fold. These results suggest simple methods to modulate retroviral receptor expression, with possible applications to human gene therapy.
<title>H-bus: a media acquisition bus optimized for multiple streams</title> (1997)

The H-Bus is a dedicated input bus designed for transmitting digital media streams from multiple sources to one acquiring host device. Unlike previous solutions to this problem which utilized a star topology to connect each source to a bank of analog-to-digital converters in the host device, the H-Bus places the A/D converters at each of the sources and uses a linear topology to connect the devices together in one contiguous chain. In this paper we explain the engineering requirements which motivated our design, describe the electrical and physical characteristics of, and applications for, the H-Bus.
Diethanolamine (DEA) degradation under gas-treating conditions (1985)

ADVERTISEMENT RETURN TO ISSUEPREVArticleNEXTDiethanolamine (DEA) degradation under gas-treating conditionsChang S. Hsu and C. J. KimCite this: Ind. Eng. Chem. Prod. Res. Dev. 1985, 24, 4, 630–635Publication Date (Print):December 1, 1985Publication History Published online1 May 2002Published inissue 1 December 1985https://pubs.acs.org/doi/10.1021/i300020a025https://doi.org/10.1021/i300020a025research-articleACS PublicationsRequest reuse permissionsArticle Views464Altmetric-Citations29LEARN ABOUT THESE METRICSArticle Views are the COUNTER-compliant sum of full text article downloads since November 2008 (both PDF and HTML) across all institutions and individuals. These metrics are regularly updated to reflect usage leading up to the last few days.Citations are the number of other articles citing this article, calculated by Crossref and updated daily. Find more information about Crossref citation counts.The Altmetric Attention Score is a quantitative measure of the attention that a research article has received online. Clicking on the donut icon will load a page at altmetric.com with additional details about the score and the social media presence for the given article. Find more information on the Altmetric Attention Score and how the score is calculated. Share Add toView InAdd Full Text with ReferenceAdd Description ExportRISCitationCitation and abstractCitation and referencesMore Options Share onFacebookTwitterWechatLinked InRedditEmail Other access options Get e-Alerts
Cutting Edge: Regulatory T Cells from Lung Cancer Patients Directly Inhibit Autologous T Cell Proliferation (2002)

Active suppression by T regulatory cells plays an important role in the down-regulation of T cell responses to foreign and self-Ags. Thus far, the potential role of CD4(+)CD25(+) T cells in human tumors has not been reported. In this work we show that lung tumors contain large numbers of these cells and that they have constitutive high-level expression of CD152 (CTLA-4). Furthermore, the CD4(+)CD25(+) T cells mediate potent inhibition of autologous T cell proliferation. Finally, regulatory T cells from patient tumors failed to inhibit the proliferation of allogeneic T cells. Together these results suggest that the CD4(+)CD25(+) T cells found in lung tumors selectively inhibit the host immune response and therefore could contribute to the progression of lung cancer.
Reassociation of ankyrin with band 3 in erythrocyte membranes and in lipid vesicles. (1980)

The binding of human erythrocyte ankyrin (band 2.1) to the erythrocyte membrane has been characterized by reassociating purified ankyrin with ankyrin-depleted inside-out vesicles. Ankyrin reassociates at high affinity with a limited number of protease-sensitive sites located only on the cytoplasmic side of the erythrocyte membrane. Depleting the vesicles of band 4.2 does not affect their binding capacity. A 45,000-dalton polypeptide derived from the cytoplasmic portion of band 3 competitively inhibits the binding of ankyrin to inside-out vesicles. Although the bulk of band 3 molecules appear to have the potential for binding ankyrin, nly a fraction of the band 3 molecules in native membranes or in reconstituted liposomes actually provides accessible high affinity ankyrin binding sites.
VLA-4-Mediated Interactions Between Normal Human Hematopoietic Progenitors and Stromal Cells (1997)

The alpha 4 beta 1 integrin very late activation antigen-4 (VLA-4) has been implicated to play a role in the adhesive interactions between hematopoietic progenitor cells (HPC) and bone marrow stromal cells which express the vascular cell adhesion molecule-1 (VCAM-1) or produce fibronectin (FN). Here, we summarize some of the recent advances made in the elucidation of the role of these particular adhesive interactions for the regulation of normal hematopoiesis. HPC bind to stroma mainly through VLA-4/VCAM-1 interactions. There is evidence which suggests that more primitive HPC constitutively express VLA-4 in a high-affinity state. In vitro studies in the mouse have shown that monoclonal antibodies (mAb) against VLA-4 partly block the development of lymphocytes, myelopoietic cells, and erythropoiesis, whereas in the human system outgrowth of TdT+ B cells is severely retarded by such mAb. In vivo studies revealed that VLA-4 is involved in erythropoietic development, and is particularly important for homing and lodgement of HPC in the bone marrow. Hematopoiesis in mice with deficient expression of alpha 4 integrin or VLA-4's ligand VCAM-1 appears to develop normally. However, chimeras developed from wild-type blastocysts and beta 1 -/- embryonic stem cells do not contain beta 1 -/- hematopoietic cells, although these are present as blood islands in the yolk sac. These beta 1 -/- hematopoietic cells are capable of forming colonies, indicating that beta 1-integrin is not involved in hematopoietic differentiation, but is primarily important for migration of hematopoietic cells into the fetal hematopoietic organs. In addition to the role of VLA-4 in migration, it may also have other regulatory functions. It has been demonstrated that ligation of VLA-4 induces phosphorylation of the protein tyrosine kinase (PTK) pp125FAK as well as other proteins which may be involved in the regulation of ligand affinity. Indeed, it has been shown that tyrosine kinase-dependent stimulation of CD34+ hematopoietic cell lines with c-kit ligand (KL), IL-3 or GM-CSF transiently activates the ability of VLA-4 to bind to VCAM-1 or FN. These events are most probably involved in the induction of quiescence in HPC which adhere to stromal cells. This claim was recently substantiated: when HPC were treated with Fab fragments of an anti-VLA-4 mAb, entry into S-phase of the cell cycle was prevented. Taken together, the present data point to a role for VLA-4 in HPC migration, cell cycle regulation, erythropoiesis and B-lymphopoiesis. Moreover, these insights may explain how defects in adhesive behavior of leukemic HPC through VLA-4 contribute to their dysregulated growth and provide a rationale for therapeutically correcting those defects.
Robust rate adaptation for 802.11 wireless networks (2006)

Rate adaptation is a mechanism unspecified by the 802.11 standards, yet critical to the system performance by exploiting the multi-rate capability at the physical layer.I n this paper, we conduct a systematic and experimental study on rate adaptation over 802.11 wireless networks. Our main contributions are two-fold. First, we critique five design guidelines adopted by most existing algorithms. Our study reveals that these seemingly correct guidelines can be misleading in practice, thus incur significant performance penalty in certain scenarios. The fundamental challenge is that rate adaptation must accurately estimate the channel condition despite the presence of various dynamics caused by fading, mobility and hidden terminals. Second, we design and implement a new Robust Rate Adaptation Algorithm (RRAA)that addresses the above challenge. RRAA uses short-term loss ratio to opportunistically guide its rate change decisions, and an adaptive RTS filter to prevent collision losses from triggering rate decrease. Our extensive experiments have shown that RRAA outperforms three well-known rate adaptation solutions (ARF, AARF, and SampleRate) in all tested scenarios, with throughput improvement up to 143%.
Caveolin-1 Expression is Variably Displayed in Astroglial-derived Tumors and Absent in Oligodendrogliomas: Concrete Premises for a New Reliable Diagnostic Marker in Gliomas (2007)

Caveolins are basic constituents of flask-shaped cell membrane microdomains (caveolae), which are involved in many cell functions, including signalling, trafficking, and cellular growth control. The distribution of caveolae within the normal brain and in brain tumors is controversial. In the present study, we describe the expression of caveolin-1 (cav-1) in 64 brain tumors of different grade, of either astroglial or oligodendroglial origin. All studied astrocitomas of any grade (from II to IV) were cav-1 positive, displaying staining patterns and intensity specifically associated to the different tumor grades. In all glioblastomas and gliosarcomas, cav-1 staining was extremely intense, typically localized at the cell membrane and recognized a variable percentage of cells, including the majority of spindle cells and palisade-oriented perinecrotic cells. In anaplastic astrocytomas, a less intense membrane staining or a cytoplasmic dotlike immunoreactivity were present, the latter being almost the exclusive pattern observed in diffuse astrocitomas grade II. In contrast to astroglial tumors, the striking totality of grade II oligodendrogliomas and the large majority of grade III were lacking cav-1 expression. Interestingly, a cav-1 distribution overlapping the pattern described in tissues was observed also in primary cell cultures of human glioblastomas and astrocytomas, and also in one established glioblastoma cell line (U251 MG), analyzed by means of confocal microscopy and flow cytometry. In conclusion, among astroglial tumors cav-1 expression varies in distribution, pattern, and intensity specifically according to tumor types and grades. The association between tumor progression and a more structured membranous pattern of cav-1 expression could suggest the hypothesis of a neoplastic shift towards a mesenchymal phenotype, whose behavioral and biologic significance worth further studies. Finally, the lack of cav-1 immunoreactivity in oligodendrogliomas suggests its concrete application as a useful diagnostic marker.
The relative orientation of the Arg and Asp side chains defined by a pseudodihedral angle as a key criterion for evaluating the structure–activity relationship of RGD peptides (2004)

The ability of an integrin to distinguish between the RGD-containing extracellular matrix proteins is thought to be due partially to the variety of RGD conformations. Three criteria have been proposed for the evaluation of the structure-activity relationship of RGD-containing peptides. These include: (i) the distance between the charged centres, (ii) the distance between the Arg Cbeta and Asp Cbeta atoms, and (iii) the pseudo-dihedral angle defining the Arg and Asp side-chain orientation formed by the Arg Czeta, Arg Calpha, Asp Calpha and Asp Cgamma atoms. A comparative conformation-activity study was performed between linear RGD peptides and strongly constrained cyclic (S,S) -CDC- bearing compounds, which cover a wide range of inhibition potency of platelet aggregation. It is concluded that the fulfilment of the -45 degrees < or = pseudo-dihedral angle < or = +45 degrees criterion is a prerequisite for an RGD compound to exhibit inhibitory activity. Once this criterion is accomplished, the longer the distance between the charged centres and/or between the Arg and Asp Cbeta atoms, the higher is the biological activity. In addition, the stronger the ionic interaction between Arg and Asp charged side chains, the lower the anti-aggregatory activity.
Immunomodulatory effects of plasminogen activators on hepatic fibrogenesis (2008)

Tissue-type plasminogen activators (tPA) and urokinase-type plasminogen activators (uPA) are involved in liver repair. We examined the potential immunomodulatory actions of uPA, tPA and uPA-receptor (uPAR) in carbon-tetrachloride-induced hepatic fibrosis in wild-type (WT), tPA-/-, uPA-/- and uPAR-/- mice. Carbon-tetrachloride treatment increased fibrosis in four groups but significantly less in three knock-out models. Serum cytokines and intrahepatic T cells elevated significantly following fibrosis process in WT animals but not in the knock-out groups. In culture, uPA increased lymphocyte proliferation significantly in WT and uPA-/- but not uPAR-/- animals. Following uPA exposure in vivo, there was CD8 predominance. To isolate uPA's effect on lymphocytes, WT mice were irradiated sublethally and then reconstituted with WT or uPA-/- lymphocytes. In these animals fibrosis was decreased and T cells were reduced in the uPA-/- recipients. Based on these data we postulate that plasminogen activators affect fibrosis in part by liver-specific activation of CD8 subsets that govern the fibrogenic activity of hepatic stellate cells.
Uptake, Metabolism and Excretion of Orally and Intravenously Administered, Double‐Labeled N‐GIycoloylneuraminic Acid and Single‐Labeled 2‐Deoxy‐2,3–dehydro‐N‐acetylneuraminic Acid in Mouse and Rat (1982)

N ‐Glycoloyl‐ d ‐[2‐ 14 C,9‐ 3 H]neuraminic acid enzymically prepared from sodium [2‐ 14 C]pyruvate and N ‐glycoloyl‐ d ‐[6‐ 3 H]mannosamine by N ‐acetylneuraminate lyase in 52% yield was orally administered to 20‐day‐old fasted mice. In the course of 6 h 98% of the total radioactivity belonging to the originally administered N ‐glycoloyl‐neuraminic acid was resorbed from the intestine and appeared in the urine. 6 h after application total 0.7% of the 3 H and 0.5% of the 14 C radioactivity were recovered in blood, liver, spleen, kidney and brain. The difference between the 14 C and the 3 H quantities was detected as exhaled 14 CO 2 . After intravenous injection of N ‐glycoloylneuraminic acid into rats, 90% of the radioactivity was excreted in the urine within 10 min corresponding to the originally applied substance. After 6 h, 1.3% of the 3 H and 1% of the 14 C radioactivity were left in blood and in liver, spleen, kidney and brain. An efficient preparation of 2‐deoxy‐2,3‐dehydro‐ N ‐acetylneuraminic acid and 2‐deoxy‐2,3‐dehydroneuraminic acid from N ‐acetylneuraminic acid is described, as well as the synthesis of a tritium‐labelled 2‐deoxy‐2,3‐dehydro‐ N ‐acetylneuraminic acid. The unsaturated neuraminic acid derivative behaved similarly to N ‐glycoloylneuraminic acid after oral and intravenous application. 99% of the radioactivity orally administered was resorbed from the intestine and excreted in the urine without chemical alteration in the course of 6 h. About 1% of the radioactivity administered orally to mice and 1.7% of the same compound administered intravenously to rats were still found in blood, liver, spleen, kidney and brain after this time. The results suggest that the small amount of N ‐glycoloylneuraminic acid retained in the organism was at least partially cleaved by N ‐acetylneuraminate lyase. The high excretion rate of unchanged 2‐deoxy‐2,3‐dehydro‐ N ‐acetylneuraminic acid and the fact that it does not act as a substrate for the lyase supposes that there is no further metabolism of this sialic acid under the conditions described. It may be concluded from these observations that N ‐glycoloylneuraminic acid occurring in food cannot be used directly for the biosynthesis of glycoconjugates, which is important from an immunological point of view. The results presented here are compared with those obtained after application of double‐labeled N ‐acetylneuraminic acid in former studies [U. Nöhle and R. Schauer (1981) Hoppe‐Seyler's Z. Physiol. Chem. 362 , 1495–1506].
The high mobility group A1 molecular switch: turning on cancer – can we turn it off? (2014)

Given the widespread overexpression of HMGA1 in diverse, aggressive tumors, further research to develop technology to target HMGA1 holds immense promise as potent anticancer therapy. Previous work in preclinical models indicates that delivery of short hairpin RNA or interfering RNA molecules to 'switch off' HMGA1 expression dramatically impairs cancer cell growth and tumor progression. The advent of nanoparticle technology to systemically deliver DNA or RNA molecules to tumors brings this approach even closer to clinical applications, although further efforts are needed to translate these advances into therapies for cancer patients.
Fabrication of self-aligned silicon field emission devices and effects of surface passivation on emission current (1998)

Arrays of uniform gated Si field emitters with small gate-tip spacing and sharp tips were fabricated using a newly developed self-aligned process. Emitter tips with 80 nm gate-tip spacing were fabricated and low temperature plasma oxidation was used to sharpen the emitter tips. The enhancement factor of the field emitters increased by a factor of 2.6 after the emitter tips radius was reduced from 67 to 8 nm by plasma oxidation. Effects of surface passivation on the emission current of gated Si field emitters were investigated by exposing emitter tips to Cl2 and H2 plasmas prior to testing. Considerable improvements in the emission characteristics were observed after plasma passivation. The emission current was enhanced and the turn-on voltage was reduced after Cl2 and H2 plasma passivation, which corresponds to a work function reduction of 0.5 and 0.9 eV, respectively.