gebhart/patrepeval huggingface dataset:
Demonstration of the interaction of native C1 with monomeric immunoglobulins and C1 inhibitor. (1985)

The association of native C1 with physiologically relevant proteins was studied by ultracentrifugation. 125I-C1 was centrifuged through numerous sucrose density gradients, each of which contained a different concentration of monomeric (19S) IgM throughout the gradient. The s-rate of C1 (16S) increased with increasing IgM input to a maximum of 32S. In the absence of C1q, the C1r2s2 subunit did not bind to the Ig. In gradients containing physiologic concentrations of IgM (1.3 mg/ml) at 0.14 M ionic strength, the observed s-rate of C1 was 21S. In the presence of 13 mg/ml IgG, C1 sedimented with an s-rate of 19S. Thus, under physiologic conditions, a significant fraction of native C1 is reversibly bound to monomeric Ig. SDS-PAGE analyses show that this interaction does not lead to C1 activation. The interaction of native C1 with C1 inhibitor (C1-In) was studied by ultracentrifugation at physiologic ionic strength. Purified 125I-C1-In alone sedimented with an s-rate of 4S. However in the presence of excess native C1, one-third of the C1-In co-sedimented with C1 at a 16S position. For these studies, 100 microM nitrophenylguanidinobenzoate (NPGB) was present throughout the sucrose density gradient to prevent C1 activation during centrifugation. As the concentration of NPGB was increased, the percent of 125I-C1-In at 16S decreased, indicating that C1-In was binding (reversibly) to the C1 active site region(s), which is at least partially accessible in uncleaved C1. In controls, when NPGB was omitted or activated C1 was used, the s-rate of 125I-C1-In was only 12S due to the release of C1rC1s(C1-In)2 from activated C1. Thus, under physiologic conditions native C1 is reversibly bound to C1-In.
Load-Line Regulation With Estimated Load-Current Feedforward: Application to Microprocessor Voltage Regulators (2006)

A consistent framework for load-line regulation design is presented, applicable to microprocessor voltage regulators (VRs) using either electrolytic or ceramic output capacitors. With conventional feedback control, the loop bandwidth is limited by stability constraints linked to the switching frequency. The output capacitor has to be chosen sufficiently large to meet the stability requirement. Load-current feedforward can extend the useful bandwidth beyond that imposed by feedback stability constraints. With load-current feedforward, the size of the output capacitor can be reduced, since it is determined solely by large-signal and switching-ripple considerations which are shown to be less constraining than the feedback stability requirement. This work points to the feasibility of microprocessor VR implementations using only a small number of ceramic output capacitors, while running at sub-megahertz switching frequencies
Los medios como componentes pedagógicos en el nuevo panorama tecnocultural (2001)

En este artículo analizamos la influencia de las actuales tecnologías de la información y la comunicación en la sociedad, al establecer nuevas formas de comprender, de sentir, de percibir y de aprender. Tratamos de la posibilidad de transformar la fascinación que producen los nuevos medios en virtudes pedagógicas y, también, del papel de la educación ante el vertiginoso mundo de las comunicaciones. Presentamos la red Internet como una fuente alternativa de información e investigación, y abordamos la alfabetización en la era de la electrónica, examinando las nuevas competencias que deben tener los profesionales de la educación.
SALMONELLOSIS: Host Immune Responses and Bacterial Virulence Determinants<sup>1</sup> (1996)

The lifestyle of bacterial pathogens requires them to establish infection in the face of host immunity. Upon entering a potential host, a variety of interactions are initiated, the outcome of which depends upon a myriad of attributes of each of the participants. In this review we discuss the interactions that occur between pathogenic Salmonella species and the host immune systems, but when appropriate to broaden perspective, we have provided a general overview of the interactions between bacterial pathogens and animal hosts. Pathogenic Salmonella species possess an array of invasion genes that produce proteins secreted by a specialized type III secretion apparatus. These proteins are used by the bacteria to penetrate the intestinal mucosa by invading and destroying specialized epithelial M cells of the Peyer's patches. This maneuver deposits the bacteria directly within the confines of the reticuloendothelial system. The host responds to these actions with nonspecific phagocytic cells and an inflammatory response as well as by activating specific cellular and humoral immune responses. Salmonella responds to this show of force directly. It appears that the bacteria invade and establish a niche within the very cells that have been sent to destroy them. Efforts are underway to characterize the factors that allow these intracellular bacteria to customize intracellular vacuoles for their own purposes. It is the constant play between these interactions that determines the outcome of the host infection, and clearly they will also shape the evolution of new survival strategies for both the bacterium and the host.
Nanofiber-hydrogel composite–mediated angiogenesis for soft tissue reconstruction (2019)

Soft tissue losses from tumor removal, trauma, aging, and congenital malformation affect millions of people each year. Existing options for soft tissue restoration have several drawbacks: Surgical options such as the use of autologous tissue flaps lead to donor site defects, prosthetic implants are prone to foreign body response leading to fibrosis, and fat grafting and dermal fillers are limited to small-volume defects and only provide transient volume restoration. In addition, large-volume fat grafting and other tissue-engineering attempts are hampered by poor vascular ingrowth. Currently, there are no off-the-shelf materials that can fill the volume lost in soft tissue defects while promoting early angiogenesis. Here, we report a nanofiber-hydrogel composite that addresses these issues. By incorporating interfacial bonding between electrospun poly(ε-caprolactone) fibers and a hyaluronic acid hydrogel network, we generated a composite that mimics the microarchitecture and mechanical properties of soft tissue extracellular matrix. Upon subcutaneous injection in a rat model, this composite permitted infiltration of host macrophages and conditioned them into the pro-regenerative phenotype. By secreting pro-angiogenic cytokines and growth factors, these polarized macrophages enabled gradual remodeling and replacement of the composite with vascularized soft tissue. Such host cell infiltration and angiogenesis were also observed in a rabbit model for repairing a soft tissue defect filled with the composite. This injectable nanofiber-hydrogel composite augments native tissue regenerative responses, thus enabling durable soft tissue restoration outcomes.
High Resolution Structure of the N-terminal Domain of Tissue Inhibitor of Metalloproteinases-2 and Characterization of Its Interaction Site with Matrix Metalloproteinase-3 (1998)

The high resolution structure of the N-terminal domain of tissue inhibitor of metalloproteinases-2 (N-TIMP-2) in solution has been determined using multidimensional heteronuclear NMR spectroscopy, with the structural calculations based on an extensive set of constraints, including 3132 nuclear Overhauser effect-based distance constraints, 56 hydrogen bond constraints, and 220 torsion angle constraints (an average of 26.9 constraints/residue). The core of the protein consists of a five-stranded beta-barrel that is homologous to the beta-barrel found in the oligosaccharide/oligonucleotide binding protein fold. The binding site for the catalytic domain of matrix metalloproteinases-3 (N-MMP-3) on N-TIMP-2 has been mapped by determining the changes in chemical shifts on complex formation for signals from the protein backbone (15N, 13C, and 1H). This approach identified a discrete N-MMP-3 binding site on N-TIMP-2 composed of the N terminus of the protein and the loops between beta-strands AB, CD, and EF. The beta-hairpin formed from strands A and B in N-TIMP-2 is significantly longer than the equivalent structure in TIMP-1, allowing it to make more extensive binding interactions with the MMP catalytic domain. A detailed comparison of the N-TIMP-2 structure with that of TIMP-1 bound to N-MMP-3 (Gomis-Ruth, F.-X., Maskos, K., Betz, M., Bergner, A., Huber, R., Suzuki, K., Yoshida, N., Nagase, H. , Brew, K., Bourne, G. P., Bartunik, H. & Bode, W. (1997) Nature 389, 77-80) revealed that the core beta-barrels are very similar in topology but that the loop connecting beta-strands CD (P67-C72) would need to undergo a large conformational change for TIMP-2 to bind in a similar manner to TIMP-1.
Clinical Usefulness of Serum Carboxyterminal Propeptide of Type I Procollagen and Pyridinoline Cross-linked Carboxyterminal Telopeptide of Type I Collagen in Patients with Prostate Cancer (1996)

A study was undertaken to evaluate the clinical usefulness of measurements of serum concentrations of the carboxyterminal propeptide of type I procollagen (PICP) and the pyridinoline cross-linked carboxyterminal telopeptide of type I collagen (ICTP) as parameters of bone metastasis in patients with prostate cancer. Serum PICP, ICTP, prostate-specific antigen (PSA), and alkaline phosphatase (ALP) were evaluated in 82 patients with prostate cancer and 26 patients with benign prostatic hyperplasia (BPH). These markers were measured serially in 16 prostate cancer patients during treatment. The serum levels of PICP, ICTP, ALP, and PSA were significantly higher in prostate cancer patients with bone metastasis than in patients with either BPH or prostate cancer without bone metastasis. Although the rate of detection of bone metastasis with PICP and ICTP was slightly lower than that with PSA determined by the receiver operating characteristic curve, the correlation between both PICP and ICTP and the extent of disease was much higher than that of PSA. PICP and ICTP levels varied with ALP and PSA levels, the patient's clinical course after the start of endocrine therapy and the progression of bone metastasis. The levels of PICP and ICTP did not change substantially in patients who developed local regrowth or lymph node metastasis, and decreased as bone metastases responded to radiotherapy. PICP and ICTP thus reflect the metastatic burden in bone and are useful for monitoring the response of bone metastasis to therapy.
Specifying operational profiles for modules (1993)

We describe a technique for specifying operational profiles for modules. The technique is more general than those of the current literature and allows more accurate specification of module usage. We also outline an algorithm for automatically generating random test cases from any such operational profile specification for a module, such that the test cases correspond to a random sampling of the module's input in actual operation. Operational-based statistical estimations, such as operational reliability, may be more meaningful when our specification method and generation algorithm are used, because our method permits more precise specifications than do other methods in the current literature.
Measurement of phagocytosis of 32P-labeled Staphylococcus aureus by bovine leukocytes: lysostaphin digestion and inhibitory effect of cream. (1975)

A procedure to measure phagocytosis by blood and milk neutrophils was developed. One milliliter of heat-killed 32P-labeled Staphylococcus aureus ([32P]SA) (180-200 X 10(6) CFU), 1 ml of phosphate-buffered saline solution (PBSS), and 2 ml of serum, whole milk, skimmed milk, whey, or PBSS were incubated in duplicate for 60 minutes at 37 C. Isolated blood or milk nuetrophils (polymorphonuclear leukocytes (PMN), 25 X 10(6) cells/ml; 1 ml) were added and incubated at 37 C for 30 minutes. Unphagocytosed [32P]SA organisms were lysed by incubation with 5 ml of lysostaphin (10 U) at 37 C for 30 minutes, and the PMN and phagocytosed T2P]SA were removed by centrifugation. Radioactivity of the supernatant was determined in a scintillation spectrometer and was used in estimate the percentage of [32P]SA phogocytosed. With this procedure, 25 assays in duplicate could be conducted each day with an expected coefficient of variation between duplicates of 5.6%. Blood PMN phagocytosed 80, 44, 74, 72, and 11% of the [32P]SA when incubated in serum, whole milk, skimmed milk, whey, and PBSS, respectively. Mik PMN phagocytosed 78, 44, 72, 74, and 22%, respectively. The addition of cream to either skimmed milk or serum reduced phagocytosis of [32P]SA by both blood and milk PMN. The inhibitory effect of cream was verified by the microscopic observation that PMN containing large quantities of ingested fat contained fewer S aureus. Seemingly, PMN upon entering the alveoli of the mammary gland become less efficiently phagocytic for bacteria, because of the presence of milk fat globules. This phef intramammary infection by invading mastitic pathogens.
Ovarian cancer progression is controlled by phenotypic changes in dendritic cells (127.7) (2012)

Abstract We have characterized the initiation and evolution of the immune response against a new p53-dependent model of aggressive ovarian carcinoma. In these previously healthy tumor-bearing hosts, we detect measurable anti-tumor immunity from very early stages, which is driven by infiltrating dendritic cells (DCs) and prevents steady tumor growth for prolonged periods. Coinciding with a phenotypic switch in expanding DC infiltrates, tumors become noticeable and aggressively progress to terminal disease in a comparatively much shorter time. Notably, tumor cells remain immunogenic at advanced stages, but the responsiveness of anti-tumor T cells decreases during tumor progression. Most importantly, their residual protective immunity is abrogated by functionally different microenvironmental DCs massively recruited to advanced tumors. Correspondingly, depleting DCs early in the disease course accelerates tumor initiation, but DC depletion at advanced stages significantly delays aggressive malignant progression. Our results indicate that aggressive ovarian cancer progression after a comparatively much longer latency period is primarily driven by both the activity of immunosuppressive microenvironmental DCs and intrinsic T cell paralysis, rather than loss of immunogenicity.
On codes, matroids and secure multi-party computation from linear secret sharing schemes. (2004)

Abstract. Error correcting codes and matroids have been widely used in the study of ordinary secret sharing schemes. In this paper, we study the connections between codes, matroids and a special class of secret sharing schemes, namely multiplicative linear secret sharing schemes. Such schemes are known to enable multi-party computation protocols secure against general (non-threshold) adversaries. Two open problems related to the complexity of multiplicative LSSSs are considered in this paper. The first one deals with strongly multiplicative LSSSs. As opposed to the case of multiplicative LSSSs, it is not known whether there is an efficient method to transform an LSSS into a strongly multiplicative LSSS for the same access structure with a polynomial increase of the complexity. We prove a property of strongly multiplicative LSSSs that could be useful in solving this problem. Namely, using a suitable generalization of the well-known Berlekamp-Welch decoder, we show that all strongly multiplicative
Ectosomes as modulators of inflammation and immunity (2010)

Vesicles released by cells have been described using various names, including exosomes, microparticles, microvesicles and ectosomes. Here we propose to differentiate clearly between ectosomes and exosomes according to their formation and release. Whereas exosomes are formed in multi-vesicular bodies, ectosomes are vesicles budding directly from the cell surface. Depending upon the proteins expressed, exosomes activate or inhibit the immune system. One of the major properties of exosomes released by antigen-presenting cells is to induce antigen-specific T cell activation. Thus, they have been used for tumour immunotherapy. By contrast, the major characteristics of ectosomes released by various cells, including tumour cells, polymorphonuclear leucocytes and erythrocytes, are the expression of phosphatidylserine and to have anti-inflammatory/immunosuppressive activities similarly to apoptotic cells.
Inclisiran for the Treatment of Heterozygous Familial Hypercholesterolemia (2020)

Among adults with heterozygous familial hypercholesterolemia, those who received inclisiran had significantly lower levels of LDL cholesterol than those who received placebo, with an infrequent dosing regimen and an acceptable safety profile. (Funded by the Medicines Company; ORION-9 ClinicalTrials.gov number, NCT03397121.).
GUI Test Script Organization with Component Abstraction (2008)

GUI (Graphical User Interface) testing plays an important role in ensuring the correctness and reliability of software applications. To perform GUI testing, a test script must be prepared (or generated by tools) so that massive user interactions and verifications can be conducted automatically. Ideally, the actions of a test script should be organized based on the structure of the GUI so that the actions are easier to extend and maintain. Unfortunately, current methodologies and tools fall short in supporting such an organization. This paper proposes an "object-based" approach, called component abstraction, to model the structure of a GUI. A GUI testing modeling language, GTML, is defined and a systematic approach in applying component abstraction is described. We show that a test script written in GTML is more robust and easier to maintain in comparison to an ordinary test script. In addition, we implement a visual environment for the development of GTML scripts so that testers (developers) do not need to write GTML scripts in plain-text language.
Al$_{x}$Ga$_{1-x}$N Ultraviolet Avalanche Photodiodes Grown on GaN Substrates (2007)

<para xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink"> Al<emphasis><formula formulatype="inline"><tex>$_{x}$</tex></formula></emphasis>Ga<emphasis><formula formulatype="inline"><tex>$_{1 - x}$</tex></formula></emphasis>N <emphasis><formula formulatype="inline"><tex>$(x = 0.05)$</tex></formula></emphasis> ultraviolet (UV) avalanche photodiodes grown on a GaN substrate are reported. The epitaxial structure was grown by metal–organic chemical vapor deposition on a free-standing bulk GaN substrate having low dislocation density. The growth conditions for Al<emphasis><formula formulatype="inline"><tex>$_{x}$</tex> </formula></emphasis>Ga<emphasis><formula formulatype="inline"><tex>$_{1-x}$</tex> </formula></emphasis>N epitaxial layers on GaN substrates were optimized to achieve improved crystalline and structural quality. With UV illumination at <emphasis><formula formulatype="inline"><tex>$\lambda \sim 250$</tex></formula></emphasis> nm, devices with mesa diameters of <emphasis><formula><tex>$\sim$</tex></formula></emphasis>30 <emphasis><formula formulatype="inline"><tex>$\mu$</tex></formula></emphasis>m achieve stable maximum optical gains of <emphasis><formula formulatype="inline"><tex>${\sim}$</tex> </formula></emphasis>50 at a reverse bias voltage of <emphasis><formula formulatype="inline"> <tex>${\sim}$</tex></formula></emphasis>87 V. </para>
Rescue of axotomized immature rat facial motoneurons by R(-)-deprenyl: stereospecificity and independence from monoamine oxidase inhibition (1993)

The role of monoamine oxidase B (MAO-B) in R(-)-deprenyl-mediated rescue of rat facial motoneurons axotomized at postnatal day 14 (P14) was investigated using the (+)- and (-)-enantiomers of deprenyl [S(+)-deprenyl and R(-)-deprenyl]. Previously, doses of R(-)-deprenyl sufficient to inhibit MAO-B were shown to increase the survival of motoneurons following an apparent loss of target-derived trophic support caused by axotomy in P14 rats. In the present experiments, motoneuronal survival was measured 21 d after unilateral facial nerve transection at P14. The animals were treated with saline or doses of R(-)- or S(+)-deprenyl ranging from 0.001 to 10 mg/kg every 2 days (/2d). Frontal serial 10 microns sections were taken through the length of the facial nuclei ipsilaterally and contralaterally to the facial nerve transections. Every third section was immunoreacted for an antibody against ChAT to identify the motoneuron somata, while every adjacent third section was Nissl stained to assess motoneuronal survival. A second series of P14 rats was treated with similar doses of the two deprenyl enantiomers or saline and the brainstems removed for measurement of MAO-A and MAO-B activity at 4 hr after the treatments. Averages of 24% of the facial motoneurons survived axotomy with either saline treatment or 0.001 mg/kg/2d doses of R(-)-deprenyl. Doses of R(-)-deprenyl of 0.005, 0.01, and 10.0 mg/kg/2d increased the surviving facial motoneuron to 38%, 51%, and 48%, respectively, indicating an ED50 of about 0.005 mg/kg/2d. Doses of S(+)-deprenyl as high as 10 mg/kg/2d did not increase motoneuronal survival, revealing a stereospecificity for the increased survival of at least 2000-fold. The ED50 for MAO-B inhibition in the P14 brainstem was approximately 0.1 mg/kg for the (-)-enantiomer and 2.0 mg/kg for the (+)-enantiomer, revealing a 20-fold higher sensitivity of the enzyme toward the (-)-enantiomer in the P14 rat brainstem. A dose of 10 mg/kg of S(+)-deprenyl inhibited about 65% of brainstem MAO-B activity without increasing motoneuronal survival, whereas 0.005 and 0.01 mg/kg of R(-)-deprenyl increased motoneuronal survival without significant inhibition of brainstem MAO-B activity.(ABSTRACT TRUNCATED AT 400 WORDS)
Overexpression of Follicle-Stimulating Hormone Receptor Activates Oncogenic Pathways in Preneoplastic Ovarian Surface Epithelial Cells (2004)

It has been previously demonstrated that human ovarian cancer cells express FSH receptor (FSHR). However, whether FSHR plays a role in ovarian cancer development is still ambiguous. To investigate the role of FSHR in tumor progression, we overexpressed the receptor in SV40 Tag immortalized ovarian surface epithelium (OSE) cell lines (IOSE-80PC, a postcrisis line, and IOSE-398), which are preneoplastic and nontumorigenic. We compared the expression levels of several selected oncogenes in nontransfected (80PC), vector-transfected (80PCV), FSHR-transfected IOSE (80PCF) cells, and established ovarian cancer cell lines (OVCAR-3 and SKOV-3). Significantly increased protein levels of epithelial growth factor receptor, HER-2/neu, and c-Myc, but not K-Ras, were observed in FSHR-overexpressing 80PCF cells when compared with 80PCV cells. Constitutive phosphorylation of ERK1/2 was augmented in 80PCF cells, whereas phosphorylation of the other MAPK including p38 and Jun N-terminal kinase was unchanged. Considerable constitutive phosphorylation of ERK1/2 was also observed in OVCAR-3 and SKOV-3 cell lines when compared with 80PCV. More importantly, 80PCF cells grew more rapidly than 80PC and 80PCV cells. In conclusion, we have demonstrated that FSHR was highly expressed in OVCAR-3 and 80PCF cells transfected with FSHR overexpression vector. The 80PCF cell line showed increased levels of epithelial growth factor receptor, HER-2/neu, and c-myc and constitutive activation of ERK1/2. The rate of proliferation of the 80PCF cells was increased, compared with control cell lines. These results suggest that the overexpression of FSHR may be associated with enhanced levels of potential oncogenic pathways and increased proliferation in preneoplastic ovarian surface epithelial cells.