gebhart/patrepeval huggingface dataset:
Molecular Biophysics of Elastin Structure, Function and Pathology (2007)

Owing to the presence of the recurring sequence XPGX' (where X and X' are hydrophobic residues), the molecular structure of the sequences between cross-links in elastin is viewed primarily as a series of beta-turns which become helically ordered by hydrophobic folding into beta-spirals, which in turn assemble hydrophobically into twisted filaments. Both hydrophobic folding and assembly occur when the temperature is raised above Tt, the onset of an inverse temperature transition. Using poly[fv(VPGVG),fx(VPGXG)] (where fv and fx are mole fractions with fv + fx = 1 and X is now any of the naturally occurring amino acid residues), plots of fx versus Tt result in a new hydrophobicity scale based directly on the hydrophobic folding and assembly processes of interest. With the reference values chosen at fx = 1, the most hydrophobic residues of elastin, Tyr (Y) and Phe (F), have low values of Tt, -55 and -30 degrees C, respectively, and the most hydrophilic residues, Glu (E-), Asp (D-) and Lys (K+), have high values of 250, 170 and 120 degrees C, respectively. Raising the average value of Tt for a chain or chain segment from below to above physiological temperature drives hydrophobic unfolding and disassembly; lowering Tt does the reverse. This delta Tt mechanism has been used reversibly to interconvert many energy forms and is used here to explain initiating events of elastogenesis, pulmonary emphysema, solar elastosis and the paucity of elastic fibres in scar tissue. In general, oxidation and/or photolysis convert(s) hydrophobic residues into polar residues with the consequences of irreversibly raising Tt to above 37 degrees C, hydrophobic unfolding and disassembly (fibre swelling), and greater susceptibility to proteolysis.
Schemes to measure available bandwidth and link capacity with ternary search and compound probe for packet networks (2010)

Accurate measurement of network parameters such as available bandwidth (ABW) and link capacity are needed for analyzing network performance. Active measurement is an attractive approach as it has the advantage of controllability and flexibility for performing network measurement. However, it can affect both the data traffic and the measurement process itself, affecting the accuracy of the measurement if significant amount of probe traffic is injected into the network. Furthermore, measurement must be completed in short time to effectively monitor the network state. In this paper, we present two new measurement schemes: one for measuring ABW, and the other for measuring per-hop link capacities of an end-to-end path. The ABW measurement scheme performs measurement in short period of time and with small amount of probe traffic, and it achieves accuracy comparable to that of IGI and Pathload. The link-capacity measurement scheme provides immunity to cross traffic. We present ns-2 simulation results of the ABW and link-capacity measurement schemes to show their performance.
Anti-Tumor Immunity Elicited by a Recombinant Vaccinia Virus Expressing CD70 (CD27L) (1999)

CD70, a ligand of the T cell costimulatory receptor CD27, is expressed mainly on activated B cells and has been shown to increase cytotoxic activity and proliferation of preferentially unprimed T cells. Reported herein is the construction of a recombinant vaccinia virus encoding CD70 (designated rV-CD70) and a demonstration of its biological effect on naive T cells in vitro and in vivo. In a whole tumor cell vaccine model, the growth of CD70-negative murine colon adenocarcinoma (MC38) tumor cells infected with rV-CD70 (multiplicity of infection [MOI] of 0.1) and transplanted into syngeneic C57BL/6 mice was inhibited completely while control tumors infected with wild-type vaccinia grew rapidly and killed mice within 3-5 weeks. Tumor-free mice previously immunized with rV-CD70-infected tumors were partially protected against rechallenge with wild-type tumors, demonstrating the induction of systemic anti-tumor immunity. In addition, immunization of C57BL/6 mice with rV-CD70 admixed with vaccinia virus encoding carcinoembryonic antigen (rV-CEA) was superior to treatment with rV-CEA alone in inducing CEA-specific lymphoproliferative T cell responses and reducing growth of murine colon carcinomas transduced with CEA. These studies demonstrate for the first time the potential utility of a recombinant vaccinia virus expressing CD70 to enhance T cell responses and mediate anti-tumor immunity.
Multiple gustatory receptors required for the caffeine response in Drosophila (2009)

The ability of insects to detect and avoid ingesting naturally occurring repellents and insecticides is essential for their survival. Nevertheless, the gustatory receptors enabling them to sense toxic botanical compounds are largely unknown. The only insect gustatory receptor shown to be required for avoiding noxious compounds is the Drosophila caffeine receptor, Gr66a. However, this receptor is not sufficient for the caffeine response, suggesting that Gr66a may be a subunit of a larger receptor. Here, we report that mutations in the gene encoding the gustatory receptor, Gr93a, result in a phenotype identical to that caused by mutations in Gr66a. This includes an inability to avoid caffeine or the related methylxanthine present in tea, theophylline. Caffeine-induced action potentials were also eliminated in Gr93a-mutant animals, while the flies displayed normal responses to other aversive compounds or to sugars. The Gr93a protein was coexpressed with Gr66a in avoidance-gustatory receptor neurons (GRNs), and functioned in the same GRNs as Gr66a. However, misexpression of both receptors in GRNs that normally do not express either Gr93a or Gr66a does not confer caffeine sensitivity to these GRNs. Because Gr93a- and Gr66a-mutant animals exhibit the identical phenotypes and function in the same cells, we propose that they may be caffeine coreceptors. In contrast to mammalian and Drosophila olfactory receptors and mammalian taste receptors, which are monomeric or dimeric receptors, we propose that Drosophila taste receptors that function in avoidance of bitter compounds are more complex and require additional subunits that remain to be identified.
Targeted adriamycin delivery to MXT-B2 metastatic mammary carcinoma cells by transferrin liposomes: Effect of adriamycin ADR-to-lipid ratio (2005)

In the protein-targeted therapy for cancer, transferrin (Tf) is used to reach a selective and specific target in cancer cells. Tf is used conjugated to chemotherapeutic drugs, insulin, toxins, antibodies, polymers, nanoparticles, lipoplexes and liposomes. Using this latter approach, hydrophobically derivatized Tf was incorporated to liposomal bilayers. The biological activity of Tf-liposome was tested using MXT-B2 cells, a metastatic mammary carcinoma cell line. In Tf binding assays, the Scatchard analysis indicated 4.5x10(5) Tf receptors/cell. In cell growth assays, Tf-liposomes stimulated cell growth in a dose-dependent manner, up to a maximum of 32% of the total free Tf stimulation. Following this, we prepared Tf-liposomes encapsulating adriamycin (ADR) at two different ADR-to-lipid ratios. In vitro cytotoxicity assays against MXT-B2 cells gave IC(50) values 2.1-times lower for Tf-liposomal ADR in comparison to control liposomal ADR. However, similar IC(50) values were found for low ADR-to-lipid ratio Tf-liposomal ADR, as well as for control liposomal ADR. The free Tf added in excess increased the IC(50) value of Tf-liposomal ADR by 51%, while the IC(50) value of control liposomal ADR was unaffected, supporting a receptor-mediated mechanism of targeting by Tf. In addition, the lower IC(50) value is correlated with a higher total of ADR accumulation in the cells.
Spontaneous lifetime and quantum efficiency in light emitting diodes affected by a close metal mirror (1993)

The spontaneous lifetime and quantum efficiencies of dipoles placed close to a metal mirror are calculated. The importance of these effects is demonstrated in the recent experimental work on InGaAs-GaAs quantum-well light-emitting diodes (QW LEDs) in which the modulations rates were varied from 0.8 GHz to 1.4 GHz through the placement of a QW next to a Ag mirror (D.G. Deppe et al., 1990). Classical energy transfer theory is used to treat the spontaneous radiation of a QW in a semiconductor system. The spontaneous radiative lifetime and internal quantum efficiency are strongly affected by the location of the QW, which confines the dipoles, by the orientation of the dipole in the well, by the metal reflector material, and by the metal mirror thickness. In general, the internal quantum efficiency decreases when the dipole is closer to the metal, because of the nonradiative energy transfer from the dipole to the absorptive metal. The overall effect of closely spaced metal mirrors on the measurable external quantum efficiency, which is important for fast light emitting diode design, is presented.< <ETX xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink">&gt;</ETX>
Effects of a motilin receptor agonist (ABT-229) on upper gastrointestinal symptoms in type 1 diabetes mellitus: a randomised, double blind, placebo controlled trial (2001)

The motilin agonist ABT-229 was not efficacious in the relief of postprandial symptoms in diabetes mellitus in the presence or absence of delayed gastric emptying.
TNF-alpha/IL-1/NF-kappaB transduction pathway in human cancer prostate. (2008)

TNFalpha exerts apoptosis throughout an intracellular transduction pathway that involves the kinase proteins TRAF-2 (integration point of apoptotic and survival signals), ASK1 (pro-apoptotic protein), MEK-4 (p38 activator and metastasis suppressor gene), JNK (stress mitogen activated protein kinase) and the transcription factor AP-1. TNFalpha also exerts proliferation by p38 activation, or when TRAF-2 simultaneously induces the transcription factor NF-kappaB by NIK. NIK and p38 may also be activated by IL-1. P38 activated several transcription factors such as Elk-1, ATF-2 and NF-kappaB. NIK also may activate NF-kappaB. The aim of the present article was to evaluate the different components of this TNFalpha/IL-1 transduction pathway in human prostate carcinoma (PC) in comparison with normal human prostate. In prostate cancer, pro-apoptotic TNFalpha/AP-1 pathway is probably inactivated by different factors such as p21 (at ASK-1 level) and bcl-2 (at JNK level), or diverted towards p38 or NIK activation. IL-1alpha enhances proliferation through IL-1RI that activates either NIK or p38 transduction pathway. P38 and NIK activate different transcription factors related with cell proliferation and survival such as ATF-2, Elk-1 or NF-kappaB. In order to search a possible target to cancer prostate treatment we proposed that inhibition of several proinflamatory cytokines such as IL-1 and TNFalpha might be a possible target for PC treatment, because decrease the activity of all transduction pathway members that activate transcription factors as NF-kappaB, Elk-1 or ATF-2.
Comparative study of the wear of UHMWPE with zirconia ceramic and stainless steel femoral heads in artificial hip joints (1994)

The wear of ultra high molecular weight polyethylene (UHMWPE) when sliding against zirconia ceramic and stainless steel counterfaces has been compared in a pin-on-plate reciprocator and in a hip joint simulator. A lower wear factor was found for the UHMWPE when sliding on the zirconia ceramic counterfaces in the pin-on-plate tests. In the hip joint simulator test, the acetabular cups articulating on zirconia heads showed consistently lower volume changes than the cups articulating on stainless steel heads. The higher volume changes found with the stainless steel heads were associated with an increased roughness of the femoral heads during the tests. This roughening was caused by the adherence of a rough polymer transfer film.
Body Mass Index, Metabolic Syndrome, and Risk of Type 2 Diabetes or Cardiovascular Disease (2006)

People with normal weight and MetS or IR or with obesity but no MetS or IR were not uncommon in our sample. Risk factor clustering or IR appear to confer much of the risk for diabetes or CVD commonly associated with elevated BMI.
Designing polymer surfaces via vapor deposition (2010)

Chemical Vapor Deposition (CVD) methods significantly augment the capabilities of traditional surface modification techniques for designing polymeric surfaces. In CVD polymerization, the monomer(s) are delivered to the surface through the vapor phase and then undergo simultaneous polymerization and thin film formation. By eliminating the need to dissolve macromolecules, CVD enables insoluble polymers to be coated and prevents solvent damage to the substrate. Since de-wetting and surface tension effects are absent, CVD coatings conform to the geometry of the underlying substrate. Hence, CVD polymers can be readily applied to virtually any substrate: organic, inorganic, rigid, flexible, planar, three-dimensional, dense, or porous. CVD methods integrate readily with other vacuum processes used to fabricate patterned surfaces and devices. CVD film growth proceeds from the substrate up, allowing for interfacial engineering, real-time monitoring, thickness control, and the synthesis of films with graded composition. This article focuses on two CVD polymerization methods that closely translate solution chemistry to vapor deposition; initiated CVD and oxidative CVD. The basic concepts underlying these methods and the resultant advantages over other thin film coating techniques are described, along with selected applications where CVD polymers are an enabling technology.
Alterations in forearm vascular reactivity in patients with septic shock (2008)

Patients with septic shock are haemodynamically unstable and suffer from vasodilation. Studying the human forearm vascular bed in patients with septic shock, we tested the hypothesis that the responses to regionally infused endothelium-(in)dependent vasodilators and vasoconstrictors are uniformly impaired. Forearm blood flow (FBF, venous occlusion plethysmography) and brachial arterial pressure were determined to calculate forearm vascular resistance (FVR) in eight consecutive sedated, mechanically ventilated patients with septic shock (APACHE II Score range 21-34, SOFA Score 11-16) and 11 healthy volunteers. Despite increased baseline FBF in patients with septic shock (6.1 (SD 1.5) ml x min(-1) x (100 ml of tissue)(-1) compared to 4.7 (1.4) in volunteers) the significant decreases in FVR seen in response to exogenous nitric oxide (nitroprusside) and acetylcholine did not differ between groups. However, compared to volunteers, mitigation of endogenous nitric oxide production by a low dose of N(G)-methyl-L-arginine acetate (L-NMMA) caused a significant increase (+6.7 mmHg x min x ml(-1)) in septic patients. Regional vasoconstriction in response to phenylephrine (FVR: +9.9 vs +30.7 mmHg x min x ml(-1) in controls) and angiotensin II (FVR: +9.0 vs +67.4 mmHg x min x ml(-1)) was markedly impaired. In contrast, vasopressin, in dosages evoking no vasoconstriction in volunteers, induced a significant increase in FVR in septic patients (+10.0 mmHg x min x ml(-1)). In the forearm of patients with septic shock, vasoconstriction by alpha1- and angiotensin II receptor agonists is selectively impaired, whereas the vasoconstrictor response to vasopressin is exaggerated. These findings exclude a generalised impairment of vasomotor activity in patients with septic shock and provide a rationale for vasopressin administration.
A Soluble Form of the Triggering Receptor Expressed on Myeloid Cells-1 Modulates the Inflammatory Response in Murine Sepsis (2004)

The triggering receptor expressed on myeloid cells (TREM)-1 is a recently discovered receptor expressed on the surface of neutrophils and a subset of monocytes. Engagement of TREM-1 has been reported to trigger the synthesis of proinflammatory cytokines in the presence of microbial products. Previously, we have identified a soluble form of TREM-1 (sTREM-1) and observed significant levels in serum samples from septic shock patients but not controls. Here, we investigated its putative role in the modulation of inflammation during sepsis. We observed that sTREM-1 was secreted by monocytes activated in vitro by LPS and in the serum of animals involved in an experimental model of septic shock. Both in vitro and in vivo, a synthetic peptide mimicking a short highly conserved domain of sTREM-1 appeared to attenuate cytokine production by human monocytes and protect septic animals from hyper-responsiveness and death. This peptide seemed to be efficient not only in preventing but also in down-modulating the deleterious effects of proinflammatory cytokines. These data suggest that in vivo modulation of TREM-1 by sTREM peptide might be a suitable therapeutic tool for the treatment of sepsis.
Microregional Expression of Glucose Transporter-1 and Oxygenation Status: Lack of Correlation in Locally Advanced Cervical Cancers (2005)

The suitability of GLUT-1 as an endogenous marker of tumor hypoxia seems questionable. The association with prognosis may partially depend on confounding factors.
Pregnancy-Associated Plasma Protein-A Accounts for the Insulin-Like Growth Factor (IGF)-Binding Protein-4 (IGFBP-4) Proteolytic Activity in Human Pregnancy Serum and Enhances the Mitogenic Activity of IGF by Degrading IGFBP-4in Vitro1 (2001)

Pregnancy-associated plasma protein-A (PAPP-A) has been identified as the insulin-like growth factor (IGF)-dependent IGF-binding protein-4 (IGFBP-4) protease produced by human fibroblasts. Recently, we found that serum proteases induced during human pregnancy cleaved IGFBP-4 in both an IGF-II-dependent and an IGF-II-independent fashion. This study sought to determine whether PAPP-A is the predominant IGFBP-4 protease in human pregnancy serum (PS) and to assess the in vitro role of serum PAPP-A. Immunoprecipitation with PAPP-A antibody effectively depleted PAPP-A from the PS and completely abolished both IGF-II-dependent and IGF-II-independent IGFBP-4 proteolytic activity in PS. Direct addition of PAPP-A antibody to PS completely blocked IGFBP-4 proteolysis and partially blocked IGFBP-5 proteolysis, but had no effect on IGFBP-3 proteolysis. To evaluate the role of serum PAPP-A, we tested whether PAPP-A in PS modulated the inhibitory activity of IGFBP-4 on IGF-II-induced cell proliferation in human osteosarcoma MG63 cells. The wild-type IGFBP-4 (WTBP-4; 200 ng/mL) failed to inhibit proliferation of the cells treated with PS (0.1% or 0.3%) alone or in combination with IGF-II (40 ng/mL), whereas the inhibitory effect of WTBP-4 was observed in the cells treated with nonpregnancy serum alone or in combination with IGF-II (P < 0.05). In contrast to WTBP-4, a protease-resistant IGFBP-4 was able to inhibit proliferation of the cells treated with PS alone or in combination with IGF-II (P < 0.05). In the presence of PAPP-A neutralizing antibody, the inhibitory effect of WTBP-4 on proliferation of the cells treated with IGF-II and PS was restored. In summary, these data demonstrate 1) that PAPP-A represents the predominant IGFBP-4 protease in PS; 2) that PAPP-A may in part contribute to IGFBP-5, but not IGFBP-3, proteolytic activity in PS; and 3) that PAPP-A enhances the bioactivity of IGFs in vitro by degrading IGFBP-4.
CD39 wird in vivo und in vitro von Ovarialkarzinomzellen exprimiert und inhibiert die lytische Aktivität von NK-Zellen (2009)

Fragestellung:„Tumor immune escape“-Mechanismen sind beim Ovarialkarzinom klinisch bedeutsam (Curiel TJ et al., Nat. Med., 2004). In dieser Arbeit wird die Expression der Ectonukleotidase CD39 in Ovarialkarzinomgewebe und auf humanen Ovarialkarzinomzelllinien nachgewiesen. Zudem wird untersucht, welche Effekte die CD39-abhängige Adenosin-Generierung auf NK-Zellen ausübt. Methodik: Mittels immunhistochemischer Färbungen wurden Paraffinschnitte von Ovarialkarzinomen und benignen Ovarien auf die Expression von CD39 untersucht. Die humanen Ovarialkarzinomzelllinien SK-OV-3 und OaW42 wurden mit einem anti-CD39 Antikörper gefärbt und gegenüber einer Isotypenkontrolle mittels Durchflusszytometer vermessen. Zur Darstellung der funktionellen Relevanz von CD39 wurden Ovarialkarzinomzelllinien mit CFDA-SE gefärbt und mit einem funktionell blockierenden anti-CD39 Antikörper inkubiert. Mithilfe modifizierter 4h FATAL-assays wurde die lytische Aktivität polyklonaler NK-Zellen gegenüber SK-OV-3- oder OaW42-Zellen in An- oder Abwesenheit von funktionell blockierenden Antikörpern gegen CD39 bestimmt. Ergebnisse: 7 von 9 Ovarialkarzinomen und alle untersuchten Ovarialkarzinomlinien wiesen eine mäßige bis starke Expression von CD39 auf, wohingegen im Stroma von 0 von 3 benignen Ovarien eine Expression gezeigt werden konnte. Zudem wurde die hemmende Wirkung der CD39-abhängigen Adenosin-Produktion auf polyklonale NK-Zellen nachgewiesen. Schlussfolgerung: Die Expression von CD39 auf Ovarialkarzinomzelllinien führt zu einer Unterdrückung der Aktivität von NK-Zellen. Durch therapeutische Inhibition dieser Ectonukleotidase könnte eine Verbesserung der antitumoralen Immunantwort erreicht werden.
Expression of the mad gene during cell differentiation in vivo and its inhibition of cell growth in vitro. (1995)

Mad is a basic region helix-loop-helix leucine zipper transcription factor which can dimerize with the Max protein and antagonize transcriptional activation by the Myc-Max transcription factor heterodimer. While the expression of Myc is necessary for cell proliferation, the expression of Mad is induced upon differentiation of at least some leukemia cell lines. Here, the expression of the mad gene has been explored in developing mouse tissues. During organogenesis in mouse embryos mad mRNA was predominantly expressed in the liver and in the mantle layer of the developing brain. At later stages mad expression was detected in neuroretina, epidermis, and whisker follicles, and in adult mice mad was expressed at variable levels in most organs analyzed. Interestingly, in the skin mad was highly expressed in the differentiating epidermal keratinocytes, but not in the underlying proliferating basal keratinocyte layer. Also, in the gut mad mRNA was abundant in the intestinal villi, where cells cease proliferation and differentiate, but not in the crypts, where the intestinal epithelial cells proliferate. In the testis, mad expression was associated with the completion of meiosis and early development of haploid cells. In cell culture, Mad inhibited colony formation of a mouse keratinocyte cell line and rat embryo fibroblast transformation by Myc and Ras. The pattern of mad expression in tissues and its ability to inhibit cell growth in vitro suggests that Mad can cause the cessation of cell proliferation associated with cell differentiation in vivo.