gebhart/patrepeval huggingface dataset:
Inferior vena cava filters: in vitro comparison of clot trapping and flow dynamics. (1988)

Using a flow model that simulated the inferior vena cava (IVC), the authors conducted an in vitro comparison of the Mobin-Uddin (MU), Kimray-Greenfield (KG), Amplatz spider (A), Günther basket (G), Simon nitinol (SN), and bird's nest (BN) filters. The following parameters were evaluated: clot-trapping capacity and flow dynamics, which included measurements of pressure gradients across filters and assessment of flow patterns. The MU, A, G, SN, and BN filters trapped an average of 80%-100% of small clots and 100% of large clots. The KG filter, in a central position, trapped 0%-10% of small clots and 60%-100% of larger clots. In the eccentric position, the KG filter trapped only 20% of all clots. The BN and SN filters showed the least flow turbulence. Moderate turbulence was observed with the G and KG filters, while the MU and A filters showed marked turbulence. The current standard KG filter allowed the passage of small and large clots. When specific parameters were considered--such as clot-trapping capacity and flow-dynamic performance--the BN, SN, and G IVC filters were superior to the other filters that were tested.
Low-complexity Visible Light Networking with LED-to-LED communication (2012)

Visible Light Communication (VLC) is an emerging technology in which Light Emitting Diodes (LEDs) transport information wirelessly, using the visible light spectrum. While most of the research on VLC has focused on wideband white LEDs used in ambient illumination, narrowband and colored LEDs have received little attention. Short-range free-space optical communication based on narrowband LEDs as visible light transmitters and receivers enable a variety of applications, a scenario we refer as LED-to-LED communication. In this paper, we introduce the communication and networking protocols of LED-to-LED communication. Our work addresses fundamental challenges such as efficient collision detection medium access protocol and elimination of light flicker. We build a prototype and demonstrate bi-directional data exchange in a network of up to four LEDs. We further study the trade-offs in the system design and measure the achievable bit-rate and transmission distances.
Mutations associated with amyotrophic lateral sclerosis convert superoxide dismutase from an antiapoptotic gene to a proapoptotic gene: studies in yeast and neural cells. (1995)

Familial amyotrophic lateral sclerosis (FALS) is associated with mutations in SOD1, the gene encoding copper/zinc superoxide dismutase (CuZnSOD). However, the mechanism by which these mutations lead to amyotrophic lateral sclerosis is unknown. We report that FALS mutant SODs expressed in yeast lacking CuZnSOD are enzymatically active and restore the yeast to the wild-type phenotype. In mammalian neural cells, the overexpression of wild-type SOD1 inhibits apoptosis induced by serum and growth factor withdrawal or calcium ionophore. In contrast, FALS-associated SOD1 mutants promote, rather than inhibit, neural apoptosis, in a dominant fashion, despite the fact that these mutants retain enzymatic SOD activity both in yeast and in mammalian neural cells. The results dissociate the SOD activity of FALS-associated mutants from the induction of neural cell death, suggesting that FALS associated with mutations in SOD1 may not be simply the result of a decrease in the enzymatic function of CuZnSOD. Furthermore, the results provide an in vitro model that may help to define the mechanism by which FALS-associated SOD1 mutations lead to neural cell death.
Novel antiepileptic drug levetiracetam decreases dyskinesia elicited by L‐dopa and ropinirole in the MPTP‐lesioned marmoset (2003)

Long-term dopamine replacement therapy of Parkinson's disease leads to the occurrence of dyskinesias. Altered firing patterns of neurons of the internal globus pallidus, involving a pathological synchronization/desynchronization process, may contribute significantly to the genesis of dyskinesia. Levetiracetam, an antiepileptic drug that counteracts neuronal (hyper)synchronization in animal models of epilepsy, was assessed in the MPTP-lesioned marmoset model of Parkinson's disease, after coadministration with (1) levodopa (L-dopa) or (2) ropinirole/L-dopa combination. Oral administration of levetiracetam (13-60 mg/kg) in combination with either L-dopa (12 mg/kg) alone or L-dopa (8 mg/kg)/ropinirole (1.25 mg/kg) treatments was associated with significantly less dyskinesia, in comparison to L-dopa monotherapy during the first hour after administration. Thus, new nondopaminergic treatment strategies targeting normalization of abnormal firing patterns in basal ganglia structures may prove useful as an adjunct to reduce dyskinesia induced by dopamine replacement therapy without affecting its antiparkinsonian action.
Holographic television by liquid crystal device (1991)

The authors make the holographic fringe pattern for moving object on TV camera, transform the hologram pattern to electrical signal and transmit it within the TV frequency band, then display the hologram fringe pattern on the liquid crystal device (LCD) and reconstruct the 3-D image. The characteristics of this system are considered. The possibility of holographic television is examined.
Sox9 coordinates a transcriptional network in pancreatic progenitor cells (2007)

During pancreas development, both the exocrine and endocrine lineages differentiate from a common pool of progenitor cells with similarities to mature pancreatic duct cells. A small set of transcription factors, including Tcf2, Onecut1, and Foxa2, has been identified in these pancreatic progenitor cells. The Sry/HMG box transcription factor Sox9 is also expressed in the early pancreatic epithelium and is required for normal pancreatic exocrine and endocrine development in humans. In this study, we found Sox9 in mice specifically expressed with the other progenitor transcription factors in both pancreatic progenitor cells and duct cells in the adult pancreas. Sox9 directly bound to all three genes in vitro and in intact cells, and regulated their expression. In turn, both Foxa2 and Tcf2 regulated Sox9 expression, demonstrating feedback circuits between these genes. Furthermore, Sox9 activated the expression of the proendocrine factor Neurogenin3, which also depends on the other members of the progenitor transcription network. These studies indicate that Sox9 plays a dual role in pancreatic progenitor cells: both maintaining a stable transcriptional network and supporting the programs by which these cells differentiate into distinct lineages.
Planar anchoring of nematic 4-n-pentyl-4′-cyanobiphenyl on self-assembled monolayers formed from alkanethiols on gold (1996)

We report measurements of planar anchoring of nematic 4-n-pentyl-4′-cyanobiphenyl (5CB) on self-assembled monolayers (SAMs) formed from CH3(CH2)mSH (7⩽m⩽17) on films of gold (prepared without oblique deposition) by using reflection interferometry. The anchoring observed contrasts with past reports of homeotropic anchoring of 5CB by surfaces, such as monolayers formed from octadecyltrichlorosilane on silica, with energies as low as alkanethiols on gold (19 mN/m). The anisotropic dispersion force acting between 5CB and gold was calculated to favor planar anchoring of 5CB on SAMs formed from CH3(CH2)15SH by ∼0.1 mN/m, and can, therefore, override self-interactions of 5CB that lead to homeotropic anchoring. Electric field-induced Freederiksz transitions of 5CB supported on bare gold, and on SAMs formed from CH3(CH2)15SH on gold, confirm weaker (planar) anchoring of 5CB on SAMs on gold as compared to bare gold.
A prophylactic vaccine for breast cancer? Why not? (2010)

In a recent issue of Breast Cancer Research, Watson and Gusterson wrote a viewpoint article [1] about our strategy for developing a prophylactic breast cancer vaccine [2]. Th e authors base much of their view on several misconceptions and misrepresentations that we wish to clarify. We did not immunize mice with an antibody as the authors claim in their abstract. We immunized mice with a single injection of whole recombinant mouse α-lactalbumin protein, and this single immunization provided highly signifi cant protection and therapy against the growth of tumors in several widely used mouse models for breast cancer. Th e authors indicate that our ‘approach was based on the hypothesis that removal of an organ will provide protection against cancer developing in that organ’ [1]. Th e notion that excised organs have decreased risk for developing tumors is obviously simplistic and misrepresents our actual hypothesis stated in the fi rst sentence of our article: ‘a full-strength autoimmune attack suffi cient to induce organ-specifi c failure may provide protection and therapy against tumors derived from the targeted organ’ [2].
DEBS &ndash;&nbsp;a unification theory for dry eye and blepharitis (2016)

For many years, blepharitis and dry eye disease have been thought to be two distinct diseases, and evaporative dry eye distinct from aqueous insufficiency. In this treatise, we propose a new way of looking at dry eye, both evaporative and insufficiency, as the natural sequelae of decades of chronic blepharitis. Dry eye is simply the late form and late manifestation of one disease, blepharitis. We suggest the use of a new term in describing this one chronic disease, namely dry eye blepharitis syndrome (DEBS). Bacteria colonize the lid margin within a structure known as a biofilm. The biofilm allows for population densities that initiate quorum-sensing gene activation. These newly activated gene products consist of inflammatory virulence factors, such as exotoxins, cytolytic toxins, and super-antigens, which are then present for the rest of the patient's life. The biofilm never goes away; it only thickens with age, producing increasing quantities of bacterial virulence factors, and thus, increasing inflammation. These virulence factors are likely the culprits that first cause follicular inflammation, then meibomian gland dysfunction, aqueous insufficiency, and finally, after many decades, lid destruction. We suggest that there are four stages of DEBS which correlate with the clinical manifestations of folliculitis, meibomitis, lacrimalitis, and finally lid structure damage evidenced by entropion, ectropion, and floppy eyelid syndrome. When one fully understands the structure and location of the glands within the lid, it becomes easy to understand this staged disease process. The longer a gland can resist the relentless encroachment of the invading biofilm, the longer it can maintain normal function. The stages depend purely on anatomy and years of biofilm presence. Dry eye now becomes a very easy disease to understand. We feel that dry eye should be treated and prevented by early and routine biofilm removal through electromechanical lid margin debridement.
Melaleuca alternifolia(Tea Tree) Oil: a Review of Antimicrobial and Other Medicinal Properties (2006)

Complementary and alternative medicines such as tea tree (melaleuca) oil have become increasingly popular in recent decades. This essential oil has been used for almost 100 years in Australia but is now available worldwide both as neat oil and as an active component in an array of products. The primary uses of tea tree oil have historically capitalized on the antiseptic and anti-inflammatory actions of the oil. This review summarizes recent developments in our understanding of the antimicrobial and anti-inflammatory activities of the oil and its components, as well as clinical efficacy. Specific mechanisms of antimicrobial and anti-inflammatory action are reviewed, and the toxicity of the oil is briefly discussed.
Penetration of Endogenous Steroid Hormones Corticosterone, Cortisol, Aldosterone and Progesterone into the Brain is Enhanced in Mice Deficient for Both mdr1a and mdr1b P‐Glycoproteins (2002)

Numerous investigations have confirmed an important role for multidrug-resistance gene 1-type P-glycoproteins (MDR1-type P-gps) in the blood-brain barrier, protecting the brain against the accumulation of a wide range of toxic xenobiotics and drugs. Several studies have provided evidence in vitro that certain steroid hormones are transported by MDR1-type P-gps; however, the question of whether this might also apply to the situation in vivo still remained to be determined. We used mice deficient for both murine mdr1a and mdr1b P-gps [mdr1a/1b(-/-)] to determine the uptake of [3H]-cortisol, [3H]-corticosterone, [3H]-aldosterone and [3H]-progesterone into the plasma, brain, testes, liver, spleen, pituitary and adrenal glands. We provide evidence that the access of the endogenous steroid hormones corticosterone, cortisol and aldosterone is regulated by MDR1-type P-gps in vivo. As peripherally administered steroid hormones accumulate in the brain of mice deficient for MDR1-type P-gps, mdr1a/1b proteins are likely to transport these hormones out of the brain, providing a kinetic barrier to their entry. Intracerebral progesterone concentrations are influenced by MDR1-type P-gp function as well; however, the effects are only small. In addition, all four endogenous glucocorticoid hormones accumulated in the testes of mdr1a/1b(-/-) mice. Our findings underline the importance of MDR1-type P-gps as an endogenous barrier system controlling the access of endogenous steroid hormones at the blood-brain barrier to maintain homeostatic control and to protect central nervous system neurones.
Dibenzothiophene Sulfone-Based Phosphine Oxide Electron Transporters with Unique Asymmetry for High-Efficiency Blue Thermally Activated Delayed Fluorescence Diodes (2016)

Three asymmetrical electron transporters as dibenzothiophene sulfone (DBSO)-diphenylphosphine oxide (DPPO) hybrids, collectively named mnDBSODPO, were designed and prepared. All of these materials achieve the high triplet energy of ∼3.0 eV to restrain the exciton linkage from emissive layers. The dependence of inductive and steric effects for DPPO groups on the substitution position, the intermolecular interaction suppression, the encapsulations of high-polar DBSO cores, and the favorable electrical performance are successfully integrated on 36DBSODPO, which can simultaneously suppress the exciton quenching by formation of an interfacial dipole and enhancing the charge flux balance. As a result, 36DBSODPO endowed its tetralayer blue thermally activated delayed fluorescence (TADF) devices with impressive performance, including the maximum external quantum efficiency around 19%, and reduced efficiency roll-offs, which verifies the great potential of asymmetrical electron transporting materials for highly efficient TADF devices.
INDUCTION OF XENOREACTIVE CD4+ T-CELL ANERGY BY SUPPRESSOR CD8+CD28??? T CELLS1 (2000)

These data indicate that Ts induce anergy of xenoreactive human Th cells upon specific recognition of MHC class I antigens. Hence, Ts may prevent the activation of T cell-mediated immune responses against xenogeneic transplants.
Increased plasma levels of interleukin-6 in sepsis [see comments] (1989)

Interleukin-6 (IL-6) is likely to be an important mediator of the inflammatory response. We measured levels of this cytokine in plasma samples from 37 patients with sepsis or septic shock obtained at the time of admission to the intensive care unit and related these levels to hemodynamic and biochemical parameters as well as to clinical outcome. In 32 of the 37 patients, increased levels of IL-6 were found, occasionally up to 7,500 times the normal level. The highest IL-6 levels were encountered in patients who suffered from septic shock (P value of the difference between patients with and without shock less than .0001). In addition, IL-6 significantly correlated with plasma lactate (P less than .0001), heart rate (P = .05) and, inversely, with mean arterial pressure (P = .01) and platelet counts (P = .0002). Significant correlations of IL-6 with the anaphylatoxins C3a (P = .0001) and C4a (P = .0002) and with the main inhibitor of the classical pathway of complement, C1-inhibitor (inverse correlation, P = .05), were also observed. IL-6 on admission appeared to be of prognostic significance: levels were higher in septic patients who subsequently died than in those who survived (P = .0003), in particular when only patients with septic shock were considered (P less than .0001). All nine septic patients with levels of less than 40 U/mL on admission survived, whereas 89% of the nine patients with levels exceeding 7,500 U/mL died. These data provide evidence for a role of IL-6 in the pathophysiology of septic shock. Further studies are needed to reveal whether IL-6 in sepsis is directly involved in mediating lethal complications or whether it is to be considered as an "alarm hormone" that reflects endothelial cell injury probably mediated by the anaphylatoxines.
Receptor Protein-tyrosine Phosphatase RPTPμ Binds to and Dephosphorylates the Catenin p120 (2000)

RPTPmu is a prototypic receptor-like protein-tyrosine phosphatase (RPTP) that mediates homotypic cell-cell interactions. Intracellularly, RPTPmu consists of a relatively large juxtamembrane region and two phosphatase domains, but little is still known about its substrate(s). Here we show that RPTPmu associates with the catenin p120(ctn), a tyrosine kinase substrate and an interacting partner of cadherins. No interaction is detectable between RPTPmu and beta-catenin. Furthermore, we show that tyrosine-phosphorylated p120(ctn) is dephosphorylated by RPTPmu both in vitro and in intact cells. Complex formation between RPTPmu and p120(ctn) does not require tyrosine phosphorylation of p120(ctn). Mutational analysis reveals that both the juxtamembrane region and the second phosphatase domain of RPTPmu are involved in p120(ctn) binding. The RPTPmu-interacting domain of p120(ctn) maps to its unique N terminus, a region distinct from the cadherin-interacting domain. A mutant form of p120(ctn) that fails to bind cadherins can still associate with RPTPmu. Our findings indicate that RPTPmu interacts with p120(ctn) independently of cadherins, and they suggest that this interaction may serve to control the tyrosine phosphorylation state of p120(ctn) at sites of cell-cell contact.
AAV-mediated gene transfer of pigment epithelium-derived factor inhibits choroidal neovascularization. (2002)

These data suggest that intraocular expression of PEDF or other antiangiogenic proteins with AAV vectors may provide a new treatment approach for ocular neovascularization.
Peripheral but not central axotomy induces changes in Janus kinases (JAK) and signal transducers and activators of transcription (STAT) (2000)

Nerve injury leads to the release of a number of cytokines which have been shown to play an important role in cellular activation after peripheral nerve injury. The members of the signal transducer and activator of transcription (STAT) gene family are the main mediators in the signal transduction pathway of cytokines. After phosphorylation, STAT proteins are transported into the nucleus and exhibit transcriptional activity. Following axotomy in rat regenerating facial and hypoglossal neurons, a transient increase of mRNA for JAK2, JAK3, STAT1, STAT3 and STAT5 was detected using in situ hybridization and semi-quantitative polymerase chain reaction (PCR). Of the investigated STAT molecules, only STAT3 protein was significantly increased. In addition, activation of STAT3 by phosphorylation on position Tyr705 and enhanced nuclear translocation was found within 3 h in neurons and after 1 day in astrocytes. Unexpectedly, STAT3 tyrosine phosphorylation was obvious for more than 3 months. In contrast, none of these changes was found in response to axotomy of non-regenerating Clarke's nucleus neurons, although all the investigated models express c-Jun and growth-associated protein-43 (GAP-43) in response to axonal injury. Increased expression of Janus kinase (JAK) and STAT molecules after peripheral nerve transection suggests changes in the responsiveness of the neurons to signalling molecules. STAT3 as a transcription factor, which is expressed early and is activated persistently until the time of reinnervation, might be involved in the switch from the physiological gene expression to an 'alternative program' activated only after peripheral nerve injury.
Characterizing monoclonal antibodies to antigenic domains of TCblR/CD320, the receptor for cellular uptake of transcobalamin-bound cobalamin (2010)

Monoclonal antibodies (mAbs) were generated to the extracellular domain of transcobalamin receptor (TCblR) and used to identify the regions of the receptor protein involved in antibody binding. Based on the effect of transcobalamin bound cobalamin (TC-Cbl) on antibody binding, this study identified both blocking and binding antibodies. Both types of antibodies bind apo as well as holo receptors, whereas the blocking antibody when bound to the apo receptor prevents the binding and cellular uptake of TC-Cbl. Binding of these antibodies to truncated receptor constructs has identified the peptide domains of the receptor involved in antibody binding. These antibodies have potential utility in blocking cellular uptake of Cbl and delivery of drugs via TCblR, which is over-expressed in many cancers.
Humanization of an Anti-CD34 Monoclonal Antibody by Complementarity-determining Region Grafting Based on Computer-assisted Molecular Modelling (2008)

4C8 is a new mouse anti-human CD34 monoclonal antibody (mAb), which recognizes class II CD34 epitopes and can be used for clinical hematopoietic stem/progenitor cell selection. In an attempt to improve its safety profiles, we have developed a humanized antibody of 4C8 by complementarity-determining region (CDR) grafting method in this study. Using a molecular model of 4C8 built by computer-assisted homology modelling, framework region (FR) residues of potential importance to the antigen binding were identified. A humanized version of 4C8, denoted as h4C8, was generated by transferring these key murine FR residues onto a human antibody framework that was selected based on homology to the mouse antibody framework, together with the mouse CDR residues. The resultant humanized antibody was shown to possess antigen-binding affinity and specificity similar to that of the original murine antibody, suggesting that it might be an alternative to mouse anti-CD34 antibodies routinely used clinically.
LPS induces CD40 gene expression through the activation of NF-κB and STAT-1α in macrophages and microglia (2005)

CD40 is expressed on various immune cells, including macrophages and microglia. Aberrant expression of CD40 is associated with autoimmune inflammatory diseases such as multiple sclerosis and rheumatoid arthritis. Interaction of Toll-like receptor-4 (TLR4) with the Gram-negative bacteria endotoxin lipopolysaccharide (LPS) results in the induction of an array of immune response genes. In this study, we describe that LPS is a strong inducer of CD40 expression in macrophages and microglia, which occurs at the transcriptional level and involves the activation of the transcription factors nuclear factor-kappaB (NF-kappaB) and signal transducer and activator of transcription 1alpha (STAT-1alpha). LPS-induced CD40 expression involves the endogenous production of the cytokine interferon-beta (IFN-beta), which contributes to CD40 expression by the activation of STAT-1alpha. Blocking IFN-beta-induced activation of STAT-1alpha by IFN-beta-neutralizing antibody reduces LPS-induced CD40 gene expression. Furthermore, LPS induces acetylation and phosphorylation of histones H3 and H4 and the recruitment of NF-kappaB, STAT-1alpha, and RNA polymerase II on the CD40 promoter in vivo in a time-dependent manner, all events important for CD40 gene transcription. These results indicate that both LPS-induced NF-kappaB activation and endogenous production of IFN-beta that subsequently induces STAT-1alpha activation play critical roles in the transcriptional activation of the CD40 gene by LPS.