gebhart/patrepeval huggingface dataset:
Dead-Space Microdomains Hinder Extracellular Diffusion in Rat Neocortex during Ischemia (2003)

During ischemia, the transport of molecules in the extracellular space (ECS) is obstructed in comparison with healthy brain tissue, but the cause is unknown. Extracellular tortuosity (lambda), normally 1.6, increases to 1.9 in ischemic thick brain slices (1000 microm), but drops to 1.5 when 70,000 Mr dextran (dex70) is added to the tissue as a background macromolecule. We hypothesized that the ischemic increase in lambda arises from diffusion delays in newly formed dead-space microdomains of the ECS. Accordingly, lambda decreases when dead-space diffusion is eliminated by trapping dex70 in these microdomains. We tested our hypothesis by analyzing the diffusion of several molecules in neocortical slices. First we showed that diffusion of fluorescent dex70 in thick slices declined over time, indicating the entrapment of background macromolecules. Next, we measured diffusion of tetramethylammonium (TMA+) (74 Mr) to show that the reduction of lambda depended on the size of the background macromolecule. The synthetic polymer, 40,000 Mr polyvinylpyrrolidone, reduced lambda in thick slices, whereas 10,000 Mr dextran did not. The dex70 was also effective in normoxic slices (400 microm) after hypoosmotic stress altered the ECS to mimic ischemia. Finally, the dex70 effect was confirmed independently of TMA+ using fluorescent 3000 Mr dextran as a diffusion marker in thick slices: lambda decreased from 3.29 to 2.44. Taken together, these data support our hypothesis and offer a novel explanation for the origin of the large lambda observed in ischemic brain. A semiquantitative model of dead-space diffusion corroborates this new interpretation of lambda.
Predominant expression of a T cell receptor V beta gene subfamily in autoimmune encephalomyelitis. (1988)

TCR beta chain gene expression of individual T cell clones that share the same MHC class II restriction and similar fine specificity for the encephalitogenic NH2 terminus of the autoantigen myelin basic protein (MBP) has been examined. TCR V beta expression was examined by FACS analysis with mAbs specific for the V beta 8 subfamily of TCR beta chain genes. 14 of 18 (78%) NH2-terminal MBP-specific clones examined express a member of the TCR V beta 8 subfamily. Southern analysis was used to identify which member(s) of the TCR V beta 8 subfamily is expressed by these clones. Each of four clones examined uses V beta 8.2, though two different V beta 8.2-J beta 2 combinations were identified. Our findings indicate that there is restricted TCR V beta usage in the autoimmune T cell response to the dominant encephalitogenic NH2-terminal epitope of the MBP. The use of an mAb to the antigen-specific TCR in the prevention of T cell-mediated autoimmune disease has been investigated. Our results demonstrate that in vivo administration of a TCR V beta 8-specific mAb prevents induction of autoimmune encephalomyelitis.
On the Data Path Performance of Leaf-Spine Datacenter Fabrics (2013)

Modern data center networks must support a multitude of diverse and demanding workloads at low cost and even the most simple architectural choices can impact mission-critical application performance. This forces network architects to continually evaluate tradeoffs between ideal designs and pragmatic, cost effective solutions. In real commercial environments the number of parameters that the architect can control is fairly limited and typically includes only the choice of topology, link speeds, over subscription, and switch buffer sizes. In this paper we provide some guidance to the network architect about the impact these choices have on data path performance. We analyze Leaf-Spine topologies under realistic traffic workloads via high-fidelity simulations and identify what is important for performance and what is not important.
Hemojuvelin is essential for dietary iron sensing, and its mutation leads to severe iron overload (2005)

Iron homeostasis plays a critical role in many physiological processes, notably synthesis of heme proteins. Dietary iron sensing and inflammation converge in the control of iron absorption and retention by regulating the expression of hepcidin, a regulator of the iron exporter ferroportin. Human mutations in the glycosylphosphatidylinositol-anchored protein hemojuvelin (HJV; also known as RGMc and HFE2) cause juvenile hemochromatosis, a severe iron overload disease, but the way in which HJV intersects with the iron regulatory network has been unclear. Here we show that, within the liver, mouse Hjv is selectively expressed by periportal hepatocytes and also that Hjv-mutant mice exhibit iron overload as well as a dramatic decrease in hepcidin expression. Our findings define a key role for Hjv in dietary iron sensing and also reveal that cytokine-induced inflammation regulates hepcidin expression through an Hjv-independent pathway.
Long-term neurologic and cardiac correction by intrathecal gene therapy in Pompe disease (2017)

Pompe disease is a lysosomal storage disorder caused by acid-α-glucosidase (GAA) deficiency, leading to glycogen storage. The disease manifests as a fatal cardiomyopathy in infantile form. Enzyme replacement therapy (ERT) has recently prolonged the lifespan of these patients, revealing a new natural history. The neurologic phenotype and the persistence of selective muscular weakness in some patients could be attributed to the central nervous system (CNS) storage uncorrected by ERT. GAA-KO 6neo/6neo mice were treated with a single intrathecal administration of adeno-associated recombinant vector (AAV) mediated gene transfer of human GAA at 1 month and their neurologic, neuromuscular, and cardiac function was assessed for 1 year. We demonstrate a significant functional neurologic correction in treated animals from 4 months onward, a neuromuscular improvement from 9 months onward, and a correction of the hypertrophic cardiomyopathy at 12 months. The regions most affected by the disease i.e. the brainstem, spinal cord, and the left cardiac ventricular wall all show enzymatic, biochemical and histological correction. Muscle glycogen storage is not affected by the treatment, thus suggesting that the restoration of muscle functionality is directly related to the CNS correction. This unprecedented global and long-term CNS and cardiac cure offer new perspectives for the management of patients.
Powder processing of ultra‐high molecular weight polyethylene I. Powder characterization and compaction (1977)

Abstract Powders of ultra‐high molecular weight polyethylene from three suppliers were characterized for density, crystallinity, particle size, particle size distribution and particle morphology. The powders had molecular weights in the range 2‐5 million. Bulk powder behavior, compressibility, green strength and springback were evaluated and explained in terms of particle characteristics. The green densities of the powders were found to reach a plateau at pressures of about 100 MPa. These plateau density levels were found to depend upon powder, characteristics and to lie between 80 and 90 percent relative density. Green strength is shown to be a unique function of a densification parameter.
An alternative approach to deoxyoligonucleotides as hybridization probes by insertion of deoxyinosine at ambiguous codon positions. (1985)

Two deoxyoligonucleotide probes (23-mer and 26-mer) carrying deoxyinosine residues (I) at positions corresponding to ambiguous nucleotides derived from amino acid sequence have been synthesized by the phosphotriester method using a polymer support. The 23-mer and 26-mer corresponded to the mRNA for 8 amino acids from gastrin and 9 amino acids from cholecystokinin, respectively. The dIs have been used where the base in the third position of the amino acid codon is ambiguous. These deoxyoligonucleotides were used as probes for hybridization with colonies containing the corresponding cDNAs or genes. The hybrid formed between a gastrin clone and the 23-mer that harbors 5 dIs was dissociated at 50-55 degrees C, suggesting that deoxyinosine did not significantly effect the stabilization or destabilization of the DNA duplex. A similar result was obtained using the 26-mer that contains 5 dIs and a phage clone DNA of the cholecystokinin gene. Thus oligonucleotide probes with deoxyinosine residues at ambiguous points seem to be useful as hybridization probes for cloning genes for proteins containing amino acids with degenerate codons.
CD40 and B cell antigen receptor dual triggering of resting B lymphocytes turns on a partial germinal center phenotype. (1996)

Phenotypic alterations occur when resting human B lymphocytes become germinal center (GC) cells. These include the induction of surface CD38, CD95 (FAS/APO-1), and carboxy-peptidase-M (CPM), a recently described GC marker. However, the factors that govern the in vivo induction of these surface molecules on B cells remain unknown. Here, we purified resting (CD38-) human B lymphocytes from tonsils in an attempt to establish culture conditions resulting in the induction of these three GC markers. We show that interferon (IFN) alpha or IFN-gamma, as well as antibodies against the B cell antigen receptor (BCR), could induce CD38 on resting B lymphocytes, a phenomenon further enhanced by CD40 stimulation. Concomitantly, CD95 was upregulated by CD40 ligation and, to a lesser extent, by IFN-gamma. By contrast, CPM expression could be upregulated only through BCR triggering. This CPM induction was specifically enhanced by CD19 or CD40 ligation. CD40 + BCR stimulation of resting B cells with CD40 ligand-transfected fibroblastic cells in the presence of cross-linked anti-BCR monoclonal antibodies resulted in the coexpression of CD38, CD95, and CPM. As GC cells, these cells also expressed CD71, CD80 (B7.1), and CD86 (B7.2), but not CD24. However, CD10+ or CD44- B cells could not be detected in these culture conditions, suggesting that yet other signals are required for the induction of these GC markers. Consistent with a GC phenotype, CD40 + BCR-stimulated cells exhibited reduced viability when cultured for 20 h in the absence of stimulus. These results first demonstrate that cotriggering of resting B cells through BCR and CD40 induces both phenotypic and functional GC features. They also show that IFN and CD19 triggering of resting B cells specifically modulate the expression of GC markers.
Disappearing Polymorphs (1995)

ADVERTISEMENT RETURN TO ISSUEPREVArticleDisappearing PolymorphsJack D. Dunitz and Joel BernsteinCite this: Acc. Chem. Res. 1995, 28, 4, 193–200Publication Date (Print):April 1, 1995Publication History Published online1 May 2002Published inissue 1 April 1995https://pubs.acs.org/doi/10.1021/ar00052a005https://doi.org/10.1021/ar00052a005research-articleACS PublicationsRequest reuse permissionsArticle Views4657Altmetric-Citations767LEARN 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 optionsGet e-Alertsclose Get e-Alerts
Interleukin-11 induces Th2 polarization of human CD4+ T cells (2001)

Exploration of the immunomodulatory activities of the multifunctional cytokine interleukin-11 (IL-11) has prompted several therapeutic applications. The immunomodulatory effects of IL-11 on human antigen-presenting cells and on T cells were investigated. IL-11 inhibited IL-12 production by activated CD14(+) monocytes, but not by mature dendritic cells (DCs) stimulated via CD40 ligation. Moreover, IL-11 did not affect either DC maturation, as demonstrated by phenotypic analysis and evaluation of cytokine production, or DC generation from progenitor cells in the presence of specific growth factors. Molecular analysis demonstrated the expression of IL-11 receptor messenger RNA in highly purified CD14(+) monocytes, CD19(+) B cells, CD8(+), and CD4(+) T cells, and CD4(+)CD45RA(+) naive T lymphocytes. In keeping with this finding, IL-11 directly prevented Th1 polarization of highly purified CD4(+)CD45RA(+) naive T cells stimulated with anti-CD3/CD28 antibodies, as demonstrated by significant increases of IL-4 and IL-5, by significantly decreased interferon-gamma production and by flow cytometry intracellular staining of cytokines. Coincubation of naive T cells with DCs, the most potent stimulators of Th1 differentiation, did not revert IL-11-mediated Th2 polarization. Furthermore, parallel experiments demonstrated that the activity of IL-11 was comparable with that induced by IL-4, the most effective Th2-polarizing cytokine. Taken together, these findings show that IL-11 inhibits Th1 polarization by exerting a direct effect on human T lymphocytes and by reducing IL-12 production by macrophages. Conversely, IL-11 does not exert any activity on DCs. This suggests that IL-11 could have therapeutic potential for diseases where Th1 responses play a dominant pathogenic role.
A survey of stent designs (2002)

Over 100 different stent designs are currently being marketed or are in evaluation for vascular and non-vascular indications. This paper attempts to differentiate stent designs by engineering aspects. A stent design pyramid is presented, which breaks the differentiating aspects into materials, raw material forms, fabrication methods, geometrical features, and additions. The primary distinguishing factor in all groups is balloon-expansion versus self-expandability. Typical examples for each category of the pyramid are shown.
Intelligent vehicle applications worldwide (2000)

Intelligent vehicles are an application in which the words "intelligent autonomous systems" represent not only an important research topic but also a strategic solution to the mobility problems that may arise in the coming years. Vehicles that can move autonomously and navigate in everyday traffic, on highways, and in urban and unstructured scenarios will become a reality in the next few decades. Besides the obvious advantages of increasing road safety and improving the quality and efficiency of moving people and goods around, the integration of intelligent features and autonomous functionalities in vehicles will lead to major economic benefits, including reduced fuel consumption, efficient exploitation of the road network and reduced personnel. Furthermore, it is not only the automotive field (public transportation, trucks and automobiles) that is interested in these new technologies, but also other sectors, each with its own target (industrial vehicles, military systems, mission-critical systems and unmanned rescue robots). In this article, the author surveys the major intelligent vehicle projects and activities worldwide, covering not only automotive applications but also special vehicles.
Rituximab (Anti-CD20 Monoclonal Antibody) Administration in a Young Patient with Resistant B-Prolymphocytic Leukemia (1999)

Following the administration of the human anti-CD20 monoclonal antibody IDEC-C2B8 (rituximab), a 31-year-old woman with B-prolymphocytic leukemia, who had been resistant to CHOP, fludarabine, pentostatin and 2-CdA, achieved complete remission. Rituximab was administered intravenously once a week for 4 weeks. The patient only had mild but tolerable side effects during the first cycle of therapy. She remains in complete remission 8 months following the discontinuation of treatment.
Dual coding in an auto-associative network model of the hippocampus (2009)

Introduction The activity of pyramidal cells in the hippocampus has been empirically demonstrated to encode both spatial and non-spatial cues by means of a dual code [1]. The phase of place cell firing with respect to the theta oscillation encodes spatial information: primarily the position of an animal and its current heading [2]. Conversely, firing rate has been demonstrated to encode a variety of non-spatial cues, including running speed, complex visual stimuli and concepts [3-5]. Here we present a novel spiking neural network model which is, to our knowledge, the first to use a dual coding system in order to learn and recall associations between both temporally coded (spatial) and rate-coded (non-spatial) activity patterns.
Differential display using one-base anchored oligo-dT primers (1994)

Journal Article Differential display using one-base anchored oligo-dT primers Get access Peng Liang, Peng Liang * 1Division of Cell Growth and Regulation, Dana-Farber Cancer InstituteBoston, MA 021152GenHunter CorporationBrookline, MA 02146, USA *To whom correspondence should be addressed at: Division of Cell Growth and Regulation, Dana-Farber Cancer Institute, Boston, MA 02115, USA. Search for other works by this author on: Oxford Academic PubMed Google Scholar Weimin Zhu, Weimin Zhu 1Division of Cell Growth and Regulation, Dana-Farber Cancer InstituteBoston, MA 02115 Search for other works by this author on: Oxford Academic PubMed Google Scholar Xiaoying Zhang, Xiaoying Zhang 2GenHunter CorporationBrookline, MA 02146, USA Search for other works by this author on: Oxford Academic PubMed Google Scholar Zhen Guo, Zhen Guo 2GenHunter CorporationBrookline, MA 02146, USA Search for other works by this author on: Oxford Academic PubMed Google Scholar Robert P.O. O'Connell, Robert P.O. O'Connell 2GenHunter CorporationBrookline, MA 02146, USA Search for other works by this author on: Oxford Academic PubMed Google Scholar Lidia Averboukh, Lidia Averboukh 1Division of Cell Growth and Regulation, Dana-Farber Cancer InstituteBoston, MA 02115 Search for other works by this author on: Oxford Academic PubMed Google Scholar Feilan Wang, Feilan Wang 1Division of Cell Growth and Regulation, Dana-Farber Cancer InstituteBoston, MA 02115 Search for other works by this author on: Oxford Academic PubMed Google Scholar Arthur B. Pardee Arthur B. Pardee 1Division of Cell Growth and Regulation, Dana-Farber Cancer InstituteBoston, MA 02115 Search for other works by this author on: Oxford Academic PubMed Google Scholar Nucleic Acids Research, Volume 22, Issue 25, 25 December 1994, Pages 5763–5764, https://doi.org/10.1093/nar/22.25.5763 Published: 01 January 1994 Article history Published: 01 January 1994 Received: 18 October 1994 Accepted: 14 November 1994
Responses of the Cardiovascular System to Carotid Sinus Nerve Stimulation (1976)

The changes in blood pressure, heart rate, cardiac output and blood flow in the femoral and common carotid arteries on carotid sinus nerve stimulation (CSNS) were studied in chloralose anaesthetized dogs, both with spontaneous heart rhythm and during atrial pacing. Stimulation of the sinus nerves with impulse trains and with impulses of constant frequency had almost equal effects on the blood pressure. The former had a greater effect on the heart rate; these findings verified earlier observations. The reductions in cardiac output followed those in heart rate. During atrial pacing the stroke volume was reduced on CSNS. The total peripheral resistance, regional peripheral resistances and input impedance of the vascular bed of the femoral artery were calculated. The initial effects of CSNS varied in relation to the prestimulation total peripheral resistance and to stimulation frequency. Differences between stimulation with a constant frequency and the intermittent types, with the same number of impulses per cardiac cycle, were negligible as regards effects on stroke volume, blood flow and regional vascular resistances. CSNS caused changes in input impedance of the vascular bed of the femoral artery which were very similar to those observed earlier on intraarterial injection of vasodilator drugs. The different effects of intermittent and constant frequency CSNS on the heart rate in dogs with intact vagal nerves and no clamping of the common carotid arteries might be caused by asymmetries in the autonomic effects on the S.A. node. The neurophysiological mechanisms are discussed. It is deduced that greater reductions in blood pressure with intermittent stimulation are only obtained in the pre-existence of a high sympathetic tone.
The Myc/Max/Mad Network and the Transcriptional Control of Cell Behavior (2000)

The Myc/Max/Mad network comprises a group of transcription factors whose distinct interactions result in gene-specific transcriptional activation or repression. A great deal of research indicates that the functions of the network play roles in cell proliferation, differentiation, and death. In this review we focus on the Myc and Mad protein families and attempt to relate their biological functions to their transcriptional activities and gene targets. Both Myc and Mad, as well as the more recently described Mnt and Mga proteins, form heterodimers with Max, permitting binding to specific DNA sequences. These DNA-bound heterodimers recruit coactivator or corepressor complexes that generate alterations in chromatin structure, which in turn modulate transcription. Initial identification of target genes suggests that the network regulates genes involved in the cell cycle, growth, life span, and morphology. Because Myc and Mad proteins are expressed in response to diverse signaling pathways, the network can be viewed as a functional module which acts to convert environmental signals into specific gene-regulatory programs.
Physical association and functional antagonism between the p65 subunit of transcription factor NF-kappa B and the glucocorticoid receptor. (1994)

Glucocorticoids, which are widely used as antiinflammatory agents, downregulate the expression of the interleukin 6 gene and of additional cytokine genes involved in inflammatory responses. Conversely, the transcription factor NF-kappa B, a member of the Rel family of transcription factors, has been implicated in the induction of multiple genes involved in the early processes of immune and inflammatory responses. This prompted us to investigate whether one of the mechanisms by which glucocorticoids exert their antiinflammatory activities is through inhibition of gene activation mediated by NF-kappa B. We report that, in intact cells, activation of the interleukin 6 promoter by a combination of the factor NF-IL6 and the p65 subunit of NF-kappa B is inhibited by dexamethasone (ligand)-activated glucocorticoid receptor. Conversely, activation of the mouse mammary tumor virus promoter by a combination of dexamethasone and glucocorticoid receptor is inhibited by overexpression of p65. Furthermore, we provide evidence for physical association between glucocorticoid receptor and p65 in protein crosslinking and coimmunoprecipitation experiments, using either in vitro translated proteins or those present in cell extracts. These studies suggest that direct interactions between NF-kappa B and glucocorticoid receptor may partly account for the antiinflammatory properties of glucocorticoids in vivo.