gebhart/patrepeval huggingface dataset:
Heat shock protein 65 induces CD62e, CD106, and CD54 on cultured human endothelial cells and increases their adhesiveness for monocytes and granulocytes (1996)

Expression of members of the heat shock protein 60 (hsp60) family in tissues has been reported to coincide with leukocyte infiltration, but it is not known whether these proteins are directly involved in the extravasation of leukocytes. Extravasation of leukocytes requires their adhesion to endothelial cells (EC) via an interaction between adhesion molecules expressed on both cell types. The aim of the present study was to investigate the effect of recombinant mycobacterial hsp65 on the adhesive characteristics of EC for monocytes and granulocytes. Incubation of EC with hsp65 induces a concentration- and time-dependent increase in adhesiveness of these EC for monocytes and granulocytes. The effect was maximal after incubation of EC with hsp65 for 4 to 6 h. In addition, incubation of EC with hsp65 induced the expression of endothelial CD62E (E-selectin), CD106 (vascular cell adhesion molecule-1) and CD54 (intercellular adhesion molecule-1). The increased adhesion of granulocytes to hsp65-stimulated EC was inhibited completely by blocking Ab against CD62E. mAb against endothelial CD62E, CD106, or CD54 or against the monocyte adhesion molecules CD14 or CD49d (very late Ag-4) did not inhibit the increased adhesion of monocytes to hsp65-stimulated EC; however, mAb against the monocyte adhesion molecule CD18 (beta2-integrin) inhibited monocyte adhesion to hsp65-stimulated EC to the same extent as monocyte adhesion to nonstimulated EC. Hsp65 did not exert its effect in an autocrine or paracrine fashion via the endogenous production of IL-1, TNF-alpha, or other factors or via contaminating LPS. Together these results indicate that hsp65 can play an important role in the adhesion of monocytes and granulocytes to EC at sites of inflammation via modulation of the adhesive characteristics of EC and thus may facilitate extravasation of these phagocytes.
Ferrocenyl Surfactants at the Surface of Water:  Principles for Active Control of Interfacial Properties (1996)

We report the use of redox-active surfactants Fc(CH2)nN+(CH3)3·Br-, where Fc = ferrocene = [η5-C5H5]Fe[η5-C5H5] and n = 8, 11, or 15, in a study of principles for active control of interfacial properties of aqueous solutions. By comparing the surface activity of Fc(CH2)11N+(CH3)3 with that of HO(CH2)11N+(CH3)3 and CH3(CH2)11N+(CH3)3, we demonstrate that Fc(CH2)nN+(CH3)3 behave as unsymmetrical bolaform surfactants with one ionic “head” group (N+(CH3)3) and one nonionic “head” group (Fc), whereas ferrocenyl surfactants, when oxidized to Fc+(CH2)nN+(CH3)3, have properties of symmetrical bolaform surfactants such as N+(CH3)3(CH2)15N+(CH3)3. Oxidation of Fc(CH2)nN+(CH3)3 to Fc+(CH2)nN+(CH3)3 leads to changes in interfacial properties through three mechanisms, at least. First, near their critical micellar concentrations (cmc's), oxidation caused desorption of monolayers of Fc(CH2)8N+(CH3)3 and Fc(CH2)11N+(CH3)3 from the surfaces of their aqueous solutions, thereby recovering the surface tension of the aqueous electrolyte. We measured changes in surface tension as large as 23 mN/m. Second, at concentrations greater than the cmc, oxidation of Fc(CH2)11N+(CH3)3 caused little, if any, change in the excess surface concentration of surfactant. The accompanying increase in the density of charge within the monolayer did, however, cause a decrease in surface tension of 6 mN/m. Third, oxidation of Fc(CH2)15N+(CH3)3 caused its monolayers at the surface of water to change from condensed states to expanded ones at constant surface pressure. We infer the phase transition within the monolayer to be driven by changes in conformation that accompany the transfer of ferrocene, upon oxidation, from the outer region (side in contact with air) of the condensed monolayer into contact with the aqueous subphase.
IP Multiplexing by Transparent Port-Address Translator (1996)

There are certain occasions when we want to have more than one computers using a single IP address. One notable case is when we use firewalls for security reasons or when we use private IP addresses and still want to provide global IP connection. Since the computers behind the firewall or using private IP addresses do not have unique IP addresses, they can not participate in global IP network. However, we still want to provide them some means so that they can be used as if they have real IP addresses.

Another example is when we have more than one server and want to make them appear to be just one server. With the proliferation of WWW, popular WWW servers tend to be overloaded and we need a mechanism to balance the load to several servers when needed. One solution being adopted is address translation by DNS (Domain Name Service). IP reuse using network address translator (NAT) is proposed in [TE93] and standardized by RFC1631. For load balancing of the WWW servers, a round robin distribution scheme using DNS is proposed and is used at NCSA [KBM94]. However, as pointed out from the literature, these schemes are based on DNS and there are several shortcomings. We propose a novel technique to perform address translation without a DNS. Our technique is based on the idea that any internet connection is uniquely identified by the socket pair . By using a address translating bridge, we can provide computers with phony IP addresses real IP connection. The performance of our scheme is investigated using a prototype and the test results show that there is very little overhead in using our scheme.
Establishment of gene transfer systems for and construction of the genetic map of a marine Vibrio strain (1989)

Two gene transfer systems were established for a marine bacterium, Vibrio sp. strain 60. One was generalized transduction with a newly isolated bacteriophage, As3, and the other was conjugal gene transfer by the use of newly constructed transposon-facilitated recombination (Tfr) donors. As3 transduced various chromosomal markers at frequencies of 10(-4) to 10(-6). Tfr donors, which were constructed by introducing transposon Tn10 into both plasmid RP4 and the chromosome, mediated the polarized transfer of chromosomal genes from the sites of Tn10 insertion on the chromosome. By means of these gene transfer systems, a genetic map of the vibrio chromosome was constructed.
Transcriptional Activation by Wild-Type but Not Transforming Mutants of the p53 Anti-Oncogene (1990)

The protein encoded by the wild-type p53 proto-oncogene has been shown to suppress transformation, whereas certain mutations that alter p53 become transformation competent. Fusion proteins between p53 and the GAL4 DNA binding domain were made to anchor p53 to a DNA target sequence and to allow measurement of transcriptional activation of a reporter plasmid. The wild-type p53 stimulated transcription in this assay, but two transforming mutations in p53 were unable to act as transcriptional activators. Therefore, p53 can activate transcription, and transformation-activating mutations result in a loss of function of the p53 protein. The inability of the p53 mutant proteins to activate transcription may enable them to be transformation competent.
Analysis by RNA-PCR of latency and reactivation of herpes simplex virus in multiple neuronal tissues (1994)

Following intracameral inoculation with herpes simplex virus type 1 (HSV-1), BALB/c mice develop acute necrotizing chorioretinitis and infectious virus is detected in the eyes, trigeminal ganglia, brain, spinal cord and adrenal glands during acute infection. In this study, we analysed the latent phase of this experimental animal system. In mice which survived the acute infection, latent HSV-1 was recovered from the trigeminal ganglia, brain and adrenal glands by co-cultivation with Vero cells. In these tissues, both the unspliced latency-associated transcript (LAT) and the spliced LAT were detected by RNA-PCR. Following in vivo administration of cyclophosphamide and dexamethasone to induce viral reactivation, ICP0 mRNA became detectable in the multiple neural tissues, and the spliced LAT disappeared whereas the unspliced LAT remained detectable by RNA-PCR. Sequence analysis of the RNA-PCR products revealed that the GC-AG splicing signal previously reported for LATs from trigeminal ganglia was also detected in LATs from the brain and adrenal glands, suggesting that the splicing of LATs might be associated with the maintenance of and/or reactivation from latency. The generalized latent infection of HSV-1 described in this study might serve as an experimental model of possible viral reactivation from organs that do not innervate the primary port of entry.
Phosphoinositide 3-kinases and the regulation of platelet function (2004)

A clear understanding of the role of PI (phosphoinositide) 3-kinases in supporting the haemostatic function of platelets has been slow to evolve. In fact, insight into the roles of individual PI 3-kinase isoforms in platelet function remains rudimentary. However, based on in vitro studies using wortmannin and LY294002, there is evidence for an important role for PI 3-kinases in regulating a broad range of functional platelet responses, including primary platelet adhesion, cytoskeletal remodelling and platelet aggregation. One of the critical platelet responses involves affinity regulation of the major platelet integrin alphaIIbbeta3, the primary receptor mediating platelet aggregation and thrombus growth. The input signals regulating integrin alphaIIbbeta3 can be divided into three main groups: (1) G(q)-coupled receptors linked to the activation of PLCbeta (phospholipase Cbeta); (2) G(i)-coupled receptors linked to the regulation of adenylate cyclase and Rap1b; and (3) adhesion receptor signalling involving Src kinase-dependent activation of PLCgamma isoforms. PI 3-kinases have not been demonstrated to play a critical role in G(q)-dependent platelet activation; however, one or more PI 3-kinase isoforms appears to be important for G(i)-dependent activation of Rap1b and adhesion receptor activation of PLCgamma isoforms. Thus distinct co-operative PI 3-kinase signalling mechanisms appear to play an important role in regulating the adhesive function of integrin alphaIIbbeta3.
13.5nm) Light Source Employing a Dense Plasma Focus in Lithium Vapor (2000)

Initial characterization efforts ofDense Plasma Focus (DPF) technology showed that efficient conversion ofelectrical energy into in-band emitted radiation could be achieved. Results previously reported showed that 25J ofelectrical energy can be converted into O.38J ofin-band, 13.5nm radiation emitted into 2ir steradians. This prototype configuration demonstrated a 1 .5% conversion efficiency into 2ir sterdians, but exhibited several major drawbacks. The two greatest issues were
Singing voice analysis and editing based on mutually dependent F0 estimation and source separation (2015)

This paper presents a novel framework that improves both vocal fundamental frequency (F0) estimation and singing voice separation by making effective use of the mutual dependency of those two tasks. A typical approach to singing voice separation is to estimate the vocal F0 contour from a target music signal and then extract the singing voice by using a time-frequency mask that passes only the harmonic components of the vocal F0s and overtones. Vocal F0 estimation, on the contrary, is considered to become easier if only the singing voice can be extracted accurately from the target signal. Such mutual dependency has scarcely been focused on in most conventional studies. To overcome this limitation, our framework alternates those two tasks while using the results of each in the other. More specifically, we first extract the singing voice by using robust principal component analysis (RPCA). The F0 contour is then estimated from the separated singing voice by finding the optimal path over a F0-saliency spectrogram based on subharmonic summation (SHS). This enables us to improve singing voice separation by combining a time-frequency mask based on RPCA with a mask based on harmonic structures. Experimental results obtained when we used the proposed technique to directly edit vocal F0s in popular-music audio signals showed that it significantly improved both vocal F0 estimation and singing voice separation.
ESHRE PGD Consortium ‘Best practice guidelines for clinical preimplantation genetic diagnosis (PGD) and preimplantation genetic screening (PGS)’ (2004)

Among the many educational materials produced by the European Society of Human Reproduction and Embryology (ESHRE) are guidelines. ESHRE guidelines may be developed for many reasons but their intent is always to promote best quality practices in reproductive medicine. In an era in which preimplantation genetic diagnosis (PGD) has become a reality, we must strive to maintain its efficacy and credibility by offering the safest and most effective treatment available. The dominant motivators for the development of current comprehensive guidelines for best PGD practice were (i) the absence of guidelines and/or regulation for PGD in many countries and (ii) the observation that no consensus exists on many of the clinical and technical aspects of PGD. As a consequence, the ESHRE PGD Consortium undertook to draw up guidelines aimed at giving information, support and guidance to potential, fledgling and established PGD centres. The success of a PGD treatment cycle is the result of great attention to detail. We have strived to provide a similar level of detail in this document and hope that it will assist staff in achieving the best clinical outcome for their patients.
Suppression of polyclonal antibody production in Trypanosoma cruzi-infected mice by treatment with anti-L3T4 antibodies. (1987)

Acute Trypanosoma cruzi infection of mice results in a very marked polyclonal activation of B and T lymphocytes, accompanied by high numbers of Ig-secreting PFC and lectin-dependent effector CTL. Treatment of mice with monoclonal anti-L3T4 antibodies from the time of infection (days 0, 4, and 8) completely suppresses the polyclonal PFC response and CTL generation. Treatment of nude mice with antibody does not alter the lipopolysaccharide-induced polyclonal PFC response, and it only modulates the isotypic profile of the PFC response to T. cruzi infection, without reducing its magnitude. Furthermore, antibody-treated, T. cruzi-infected euthymic mice do not develop the typical B cell blastogenic response, but show high numbers of activated Lyt-2+ lymphoblasts in the spleen. These results indicate that effector cell generation in T. cruzi-infected mice is predominantly helper T cell-dependent.
Mutation of the gene encoding fibrillin-2 results in syndactyly in mice (2001)

Fibrillins are large, cysteine-rich glycoproteins that form microfibrils and play a central role in elastic fibrillogenesis. Fibrillin-1 and fibrillin-2, encoded by FBN1 on chromosome 15q21.1 and FBN2 on chromosome 5q23-q31, are highly similar proteins. The finding of mutations in FBN1 and FBN2 in the autosomal dominant microfibrillopathies Marfan syndrome (MFS) and congenital contractural arachnodactyly (CCA), respectively, has highlighted their essential role in the development and homeostasis of elastic fibres. MFS is characterized by cardiovascular, skeletal and ocular abnormalities, and CCA by long, thin, flexed digits, crumpled ears and mild joint contractures. Although mutations arise throughout FBN1, those clustering within exons 24-32 are associated with the most severe form of MFS, so-called neonatal MFS. All the mutations described in CCA occur in the "neonatal region" of FBN2. Both MFS and CCA are thought to arise via a dominant negative mechanism. The analysis of mouse mutations has demonstrated that fibrillin-1 microfibrils are mainly engaged in tissue homeostasis rather than elastic matrix assembly. In the current investigation, we have analysed the classical mouse mutant shaker-with-syndactylism using a positional candidate approach and demonstrated that loss-of-function mutations outside the "neonatal region" of Fbn2 cause syndactyly in mice. These results suggest that phenotypes distinct from CCA may result in man as a consequence of mutations outside the "neonatal region" of FBN2.
TLR2-Induced IL-10 Production Impairs Neutrophil Recruitment to Infected Tissues during Neonatal Bacterial Sepsis (2013)

Sepsis is the third most common cause of neonatal death, with Group B Streptococcus (GBS) being the leading bacterial agent. The pathogenesis of neonatal septicemia is still unsolved. We described previously that host susceptibility to GBS infection is due to early IL-10 production. In this study, we investigated whether triggering TLR2 to produce IL-10 is a risk factor for neonatal bacterial sepsis. We observed that, in contrast to wild-type (WT) pups, neonatal TLR2-deficient mice were resistant to GBS-induced sepsis. Moreover, if IL-10 signaling were blocked in WT mice, they also were resistant to sepsis. This increased survival rate was due to an efficient recruitment of neutrophils to infected tissues that leads to bacterial clearance, thus preventing the development of sepsis. To confirm that IL-10 produced through TLR2 activation prevents neutrophil recruitment, WT pups were treated with the TLR2 agonist Pam3CSK4 prior to nebulization with the neutrophil chemotactic agent LTB4. Neutrophil recruitment into the neonatal lungs was inhibited in pups treated with Pam3CSK4. However, the migration was restored in Pam3CSK4-treated pups when IL-10 signaling was blocked (either by anti-IL-10R mAb treatment or by using IL-10-deficient mice). Our findings highlight that TLR2-induced IL-10 production is a key event in neonatal susceptibility to bacterial sepsis.
WDM ring network using a centralized multiwavelength light source and add-drop multiplexing filters (1997)

We propose and experimentally demonstrate a wavelength division multiplexed (WDM) ring network employing a centralized multiwavelength light source to supply all nodes with optical carriers of precise wavelength spacing. This approach overcomes the problem of monitoring and controlling the wavelengths of optical sources dispersed throughout the network. A four-node test bed using optical lattice-type add-drop multiplexing filters and a multiwavelength light source based on resonant cavity-enhanced four wave mixing in a Fabry-Perot laser diode was constructed to demonstrate the feasibility of the proposed method. The effects of coherent crosstalk in such networks are analyzed, and methods such as phase scrambling or the use of a pulsed optical source are shown to significantly reduce the effects of coherent crosstalk. The use of four-port add-drop multiplexer (ADM) filters instead of 1:n optical wavelength multiplexer/demultiplexers to implement the wavelength add-drop function at each node is shown to lead to a broader transmission bandwidth for each channel and also easier compatibility with the coherent crosstalk suppression mechanisms described.
Activity of repellents applied to skin for protection against Amblyomma americanum and Ixodes scapularis ticks (Acari: Ixodidae). (1995)

Twenty-nine repellents were tested on human skin for duration of activity as protectants against nymphal lone star ticks (Amblyomma americanum) and against black-legged or deer ticks (Ixodes scapularis Say). Eleven of these repellents, including deet, provided > 2 h of protection against the lone star tick. One repellent, 1-(3-cyclohexenyl-ylcarbonyl) piperidine, was effective > or = 4 h. Four repellents (2 pyridines and 2 piperidines with protection lasting 2.3-3 h) showed acaricidal activity to more than half of the ticks tested after 9-12 min of exposure. Seven repellents that were most effective against A. americanum, including deet, were tested against the black-legged tick. None was effective and no knock-down was observed. These results suggest that the black-legged tick is less sensitive to repellents than the lone star tick.
A randomized comparison of nativeEscherichia coli asparaginase and polyethylene glycol conjugated asparaginase for treatment of children with newly diagnosed standard-risk acute lymphoblastic leukemia: a Children's Cancer Group study (2002)

For this study, 118 children with standard-risk acute lymphoblastic leukemia (ALL) were given randomized assignments to receive native or pegylated Escherichia coli asparaginase as part of induction and 2 delayed intensification phases. Patients treated with pegaspargase had more rapid clearance of lymphoblasts from day 7 and day 14 bone marrow aspirates and more prolonged asparaginase activity than those treated with native asparaginase. In the first delayed intensification phase, 26% of native asparaginase patients had high-titer antibodies, whereas 2% of pegaspargase patients had those levels. High-titer antibodies were associated with low asparaginase activity in the native arm, but not in the pegaspargase arm. Adverse events, infections, and hospitalization were similar between arms. Event-free survival at 3 years was 82%. A population pharmacodynamic model using the nonlinear mixed effects model (NONMEM) program was developed that closely fit the measured enzyme activity and asparagine concentrations. Half-lives of asparaginase were 5.5 days and 26 hours for pegaspargase and native asparaginase, respectively. There was correlation between asparaginase enzymatic activity and depletion of asparagine or glutamine in serum. In cerebrospinal fluid asparagine, depletion was similar with both enzyme preparations. Intensive pegaspargase for newly diagnosed ALL should be tested further in a larger population.
Recurrent Concussion and Risk of Depression in Retired Professional Football Players (2007)

Our findings suggest a possible link between recurrent sport-related concussion and increased risk of clinical depression. The findings emphasize the importance of understanding potential neurological consequences of recurrent concussion.
Suppression and promotion of tumor growth by monoclonal antibodies to ErbB-2 differentially correlate with cellular uptake. (1995)

Amplification and overexpression of the erbB-2/neu protooncogene are frequently associated with aggressive clinical course of certain human adenocarcinomas, and therefore the encoded surface glycoprotein is considered a candidate target for immunotherapy. We previously generated a series of anti-ErbB-2 monoclonal antibodies (mAbs) that either accelerate or inhibit the tumorigenic growth of erbB-2-transformed murine fibroblasts. The present study extended this observation to a human tumor cell line grown as xenografts in athymic mice and addressed the biochemical differences between the two classes of mAbs. We show that the inhibitory effect is dominant in an antibody mixture, and it depends on antibody bivalency. By using radiolabeled mAbs we found that all of three tumor-inhibitory mAbs became rapidly inaccessible to acid treatment when incubated with tumor cells. However, a tumor-stimulatory mAb remained accessible to extracellular treatments, indicating that it did not undergo endocytosis. In addition, intracellular fragments of the inhibitory mAbs, but not of the stimulatory mAb, were observed. Electron microscopy of colloidal gold-antibody conjugates confirmed the absence of endocytosis of the stimulatory mAb but detected endocytic vesicles containing an inhibitory mAb. We conclude that acceleration of cell growth by ErbB-2 correlates with cell surface localization, whereas inhibition of tumor growth is associated with an intrinsic ability of anti-ErbB-2 mAbs to induce endocytosis. These conclusions are relevant to the selection of optimal mAbs for immunotherapy and may have implications for the mechanism of cellular transformation by an overexpressed erbB-2 gene.