gebhart/patrepeval huggingface dataset:
Small-scale polymer structures enabled by thiol-ene copolymer systems (2009)

The research described herein is aimed at exploring the thermo-mechanical properties of thiol-ene polymers in bulk form, investigating the ability of thiol-ene polymers to behave desirably as photolithographic media, and providing the first characterization of the mechanical properties of two-photon stereolithography-produced polymer structures. The thiol-ene polymerization reaction itself is well-characterized and described in the literature, but the thermomechanical properties of thiol-ene and thiol-ene/acrylate polymers still require more rigorous study. Understanding the behavior of thiol-ene networks is a crucial step towards their expanded use in bulk form, and particularly in specialized applications such as shape memory devices. Additionally, the thiol-ene polymerization reaction mechanism exhibits unique properties which make these polymers well suited to photolithography, overcoming the typical dichotomy of current materials which either exhibit excellent photolithographic behavior or have controllable properties. Finally, before two-photon stereolithography can create mechanisms and devices which can serve any mechanically functional role, the mechanical properties of the polymers they produce must be quantitatively characterized, which is complicated by the extremely small scale at which these structures are produced. As such, mechanical characterization to date has been strictly qualitative.&#13;\n&#13;\nFourier transfer infrared spectroscopy revealed functional group conversion information and sol-fraction testing revealed the presence of unconverted monomer and impurities, while dynamic mechanical analysis and tensile testing revealed the thermomechanical responses of the systems. Nanoindentation was employed to characterize the mechanical properties of polymers produced by two-photon stereolithography. Optical and electron microscopy were exploited to provide quantitative and qualitative evaluations of thiol-ene/acrylate performance in small-scale polymerization regimes.&#13;\n&#13;\nThe broad objective of the research was to explore thiol-ene polymer behavior both in bulk and at the small scale in an effort to supplement the material library currently used in these fields and to expand the design envelope available to researchers. The significance of the research is the advancement of a more complete and fundamental understanding of thiol-ene polymerization from kinetics to final properties, the quantitative establishment of the mechanical properties of materials created with two-photon stereolithography, and the comprehensive characterization of a supplementary class of photopatternable polymers with greater property tunability than is possible with currently used materials.
Antineurogenic phenotypes induced by truncated Notch proteins indicate a role in signal transduction and may point to a novel function for Notch in nuclei. (1993)

Loss of any one of several neurogenic genes of Drosophila results in overproduction of embryonic neuroblasts at the expense of epidermoblasts. In this paper a variety of altered Notch proteins are expressed in transgenic flies. Dominant lethal, antineurogenic phenotypes were produced by expression of three classes of mutant proteins: (1) a protein comprised of the cytoplasmic domain of Notch and devoid of sequences permitting membrane association; (2) a transmembrane protein lacking the extracellular, lin12/Notch repeats; and (3) transmembrane proteins carrying amino acid substitutions replacing one or both extracellular cysteines thought to be involved in Notch dimerization. These Notch proteins not only suppress the neural hypertrophy observed in Notch- embryos, but also generate a phenotype in which elements of the embryonic nervous system are underproduced. Action of the intracellular cdc10 repeats appears to be essential for wild-type Notch function or for the antineurogenic activity of these proteins. The activities of the dominant, gain-of-function proteins indicate that Notch functions as a signal transducing receptor during ectoderm development. Production of antineurogenic Notch proteins in embryos deficient for the other neurogenic genes allowed functional dependencies to be established. Delta, mastermind, bigbrain, and neuralized appear to function in elaboration of a signal upstream of Notch. Genes of the Enhancer of split complex act after Notch. The cytoplasmic domain of Notch contains nuclear localization sequences that function in cultured cells, and one of the Notch antineurogenic proteins, the cytoplasmic domain, accumulates in nuclei in vivo.
HbS-Oman Heterozygote: A New Dominant Sickle Syndrome (1998)

Hemoglobin (Hb) S-Oman has two mutations in the β-chains. In addition to the classic βS mutation (β6 Glu → Val), it contains a second mutation in the same chain (β121 Glu → Lys) identical to that of HbOARAB. We have studied a pedigree of heterozygous carriers of HbS-Oman that segregates into two types of patients: those expressing about 20% HbS-Oman and concomitant −/ thalassemia and those with about 14% of HbS-Oman and concomitant −/− thalassemia. The higher expressors of S-Oman have a sickle cell anemia (SS) clinical syndrome of moderate intensity, while the lower expressors have no clinical syndrome, and are comparable to the solitary case first described in Oman. In addition, the higher expressors exhibit a unique form of irreversibly sickled cell reminiscent of a “yarn and knitting needle” shape, in addition to folded and target cells. The CSAT of S-Oman is identical to that of S-Antilles, another supersickling hemoglobin, whose carriers express the abnormal hemoglobin at 40% to 50%, with a very similar clinical picture to HbS-Oman. Because the level of expression is so different and the clinical picture so similar, and based on the hemolysates CSAT’s, we conclude that HbS-Oman produces pathology beyond its sickling tendencies. A clue for this additional pathogenesis is found in the fact that homozygous HbOARAB, which has the same second substitution as S-Oman, has a moderately severe hemolytic anemia; when HbOARAB is combined with HbS, it makes the phenotype of this double heterozygote as severe as SS. Properties of HbS-Oman red blood cells (RBCs) include reticulocytes that are much denser than normal (similar to those of SC and CC disease), a decrease in the Km for Ca2+ needed to activate the Gardos’ channel (making this transporter more sensitive to Ca2+), increased association of HbS-Oman with the RBC membrane, the presence of dense cells by isopycnic gradient, the presence of folded cells, and abundant nidus of polymerization under the membrane. Other properties include a clear increase in volume and N-ethylmaleimide–stimulated K:Cl cotransport in RBCs expressing more than 20% HbS-Oman. We conclude that the pathology of heterozygous S-Oman is the product of the sickling properties of the β6 Val mutation which are enhanced by the second mutation at β121. In addition, the syndrome is further enhanced by a hemolytic anemia induced by the mutation at β121. We speculate that this pathology results from the abnormal association of the highly positively charged HbS-Oman (3 charges different from normal hemoglobin) with the RBC membrane.
Detection with embedded known symbols: optimal symbol placement and equalization (2002)

The detection of a data sequence with embedded known symbols is considered. For a class of symbol-by-symbol decision feedback receivers, known symbol distributions optimal with respect to the criterion of average mean square error (A-MSE) are presented. Optimal design of the decision feedback receiver is also obtained. Simulation results show that, compared to the performance with conventional symbol placement strategy, considerable gain can be obtained by the joint optimization of symbol placement and equalizer.
Radar rainfall estimation from vertical reflectivity profile using neural network (2002)

An adaptive radial basis function (RBF) neural network to estimate the ground rainfall from a vertical profile of reflectivity factor (Z) is presented in this paper. This RBF network was applied to two months of WSR-88D radar data to estimate rainfall. Results show that the adaptive RBF developed here can estimate rainfall fairly well. Results were also compared with the WSR-88D, Z-R relationship and the Z-R algorithm derived from previous day observations.
Constitutive high-level production of human lymphotoxin by CHO-K1 cells transformed with the human lymphotoxin gene controlled by a human .BETA.-actin promoter. (1991)

To achieve high-level production of human lymphotoxin (hLT), a plasmid (p beta LT-ldhfr) containing the hLT genomic DNA, a mouse dihydrofolate reductase (DHFR) cDNA, and a bacterial Ecogpt gene was cotransfected with a plasmid (p beta LTML) encoding only the hLT genomic DNA into Chinese hamster ovary (CHO-K1) cells at a 1:7 molar ratio. Subsequently one of the Ecogpt-positive clones (clone A31) was grown in stepwise increasing concentrations of methotrexate (MTX). A large amount of the hLT was secreted by cells resistant to increased levels of MTX as a result of coamplification of the DHFR cDNA and the hLT gene. A cell clone (clone M-1) resistant to up to 500 nM MTX constitutively expressed the hLT at a concentration of 80 micrograms per ml at an elevated level for about 2 months. The hLT was produced in glycosylated form the molecular mass of which was 23,000 daltons and the mRNA was normally spliced, so the protein molecules were probably homogeneous.
Interactions between Naïve and Infected Macrophages Reduce Mycobacterium tuberculosis Viability (2011)

A high intracellular bacillary load of Mycobacterium tuberculosis in macrophages induces an atypical lysosomal cell death with early features of apoptosis that progress to necrosis within hours. Unlike classical apoptosis, this cell death mode does not appear to diminish M. tuberculosis viability. We previously reported that culturing heavily infected macrophages with naïve macrophages produced an antimicrobial effect, but only if naïve macrophages were added during the pre-necrotic phase of M. tuberculosis-induced cell death. In the present study we investigated the mechanism of antimicrobial activity in co-cultures, anticipating that efferocytosis of bacilli in apoptotic bodies would be required. Confocal microscopy revealed frustrated phagocytosis of M. tuberculosis-infected macrophages with no evidence that significant numbers of bacilli were transferred to the naïve macrophages. The antimicrobial effect of naïve macrophages was retained when they were separated from infected macrophages in transwells, and conditioned co-culture supernatants transferred antimicrobial activity to cultures of infected macrophages alone. Antimicrobial activity in macrophage co-cultures was abrogated when the naïve population was deficient in IL-1 receptor or when the infected population was deficient in inducible nitric oxide synthase. The participation of nitric oxide suggested a conventional antimicrobial mechanism requiring delivery of bacilli to a late endosomal compartment. Using macrophages expressing GFP-LC3 we observed the induction of autophagy specifically by a high intracellular load of M. tuberculosis. Bacilli were identified in LC3-positive compartments and LC3-positive compartments were confirmed to be acidified and LAMP1 positive. Thus, the antimicrobial effect of naïve macrophages acting on M. tuberculosis in heavily-infected macrophages is contact-independent. Interleukin-1 provides an afferent signal that induces an as yet unidentified small molecule which promotes nitric oxide-dependent antimicrobial activity against bacilli in autolysosomes of heavily infected macrophages. This cooperative, innate antimicrobial interaction may limit the maximal growth rate of M. tuberculosis prior to the expression of adaptive immunity in pulmonary tuberculosis.
Low temperature direct wafer to wafer bonding for 3D integration: Direct bonding, surface preparation, wafer-to-wafer alignment (2010)

In this paper the integration challenges related to oxide-oxide bonding for wafer-to-wafer stacking technology are discussed. Furthermore, interface defectivity, wafer-to-wafer alignment and bond strength data are presented.
Halofenate (1975)

In vitro binding studies on antiinflammatory and uricosuric acidic anions performed under "physiologic" conditions have demonstrated that these substances displace urate from its protein bond. The property of urate displacement appears to be a useful marker for potential uricosuric activity in vivo, and thereby a means to detect novel uricosuric drugs. One such drug, halofenate, was indeed a safe and effective uricosuric (comparable to probenecid) when used to treat hyperuricemia/gout over the long term; it did result in a modest and variable fall in serum lipid concentrations. However, used as a single fixed dose, halofenate did not produce a marked and consistent effect on the elevated serum triglyceride concentrations so commonly present in gouty patients.
La capacidad fiscal de los municipios como gobiernos autónomos descentralizados en Ecuador. ¿Gestión tributaria o pereza fiscal? (2012)

The municipal tax management when it is conceived as the capacity or constitutional
power to generate tax income, is achievable in our country, however in fact, this power is
incompletely performed by most municipalities, depriving themselves of more income and
therefore more public work. In simple words, failing to achieve optimum levels of financial
and performance indicators. For this reason it is necessary to have some monitoring tools
in order to evaluate public management.
Gap Junction Uncoupler Heptanol Prevents Cell-to-Cell Progression of Hypercontracture and Limits Necrosis During Myocardial Reperfusion (1997)

These results demonstrate that hypercontracture may be transmitted to adjacent myocytes through gap junctions and that heptanol may interfere with this transmission and reduce the final extent of myocardial necrosis during reoxygenation or reperfusion. These findings are consistent with the hypothesis tested and open a new approach to limitation of infarct size by pharmacological control of gap junction conductance.
Prediagnostic Serum Levels of Cytokines and Other Immune Markers and Risk of Non-Hodgkin Lymphoma (2011)

Although severe immune dysregulation is an established risk factor for non-Hodgkin lymphoma (NHL), it is unclear whether subclinical immune system function influences lymphomagenesis. To address this question, we conducted a nested case-control study within the Prostate, Lung, Colorectal, and Ovarian Cancer Screening Trial to investigate whether circulating levels of cytokines and other immune markers are associated with future risk of NHL. Selected cytokines [interleukin (IL)-4, IL-6, IL-10, and TNF-α] and other immune markers [soluble TNF receptor 1 (sTNF-R1), sTNF-R2, C-reactive protein, and sCD27] were measured in prediagnostic serum specimens from 297 incident NHL cases and 297 individually matched controls. ORs and 95% confidence intervals (CI) relating quartiles of analyte concentration to NHL risk were calculated by using conditional logistic regression. Statistically significant associations with increased NHL risk were observed for elevated serum levels of sTNF-R1 (quartile 4 vs. quartile 1: OR = 1.7, 95% CI: 1.1-2.8; P(trend) = 0.02) and sCD27 (OR = 5.3, 95% CI: 2.9-9.4; P(trend) < 0.0001). These associations remained in analyses of cases diagnosed longer than 6 years following blood collection (sTNF-R1: OR = 2.1, 95% CI: 1.0-4.0, P(trend) = 0.01; sCD27: OR = 4.1, 95% CI: 1.9-8.5, P(trend) = 0.0001). Elevated levels of IL-10, TNF-α and sTNF-R2 were also significantly associated with increased risk of NHL overall; however, these associations weakened with increasing time from blood collection to case diagnosis and were null for cases diagnosed longer than 6 years postcollection. Our findings for sTNF-R1 and sCD27, possible markers for inflammatory and B-cell stimulatory states, respectively, support a role for subclinical inflammation and chronic B-cell stimulation in lymphomagenesis.
Targeting the Inflammatory Response in Healing Myocardial Infarcts (2006)

Healing of myocardial infarcts depends on an inflammatory cascade that ultimately results in clearance of dead cells and matrix debris and formation of a scar. Myocardial necrosis activates complement, Nuclear Factor (NF)-kappaB and Toll-like Receptor (TLR)-dependent pathways, and generates free radicals, triggering an inflammatory response. Chemokines and cytokines are markedly induced in the infarct and mediate recruitment and activation of neutrophils and mononuclear cells. Extravasation of platelets and plasma proteins, such as fibrinogen and fibronectin, results in formation of a clot, consisting of platelets embedded in a mesh of crosslinked fibrin. This provisional matrix provides a scaffold for migration of cells into the infarct. Monocytes differentiate into macrophages and secrete fibrogenic and angiogenic growth factors inducing formation of granulation tissue, containing myofibroblasts and neovessels. Repression of proinflammatory cytokine and chemokine synthesis, mediated in part through Transforming Growth Factor (TGF)-beta and Interleukin (IL)-10, is critical for resolution of the inflammatory infiltrate and transition to fibrous tissue deposition. Infarct myofibroblasts deposit extracellular matrix proteins and a collagen-based scar is formed. As the wound matures, fibroblasts undergo apoptosis and neovessels regress, resulting in formation of a scar with a low cellular content containing dense, cross-linked collagen. The pathologic and structural changes associated with infarct healing directly influence ventricular remodeling and affect prognosis in patients with myocardial infarction. Understanding the mechanisms involved in the regulation of the post-infarction inflammatory response, and the spatial and temporal parameters of wound healing is necessary in order to identify specific molecular targets for therapeutic intervention.
Mapping genes for autoimmunity in humans: type 1 diabetes as a model (2002)

Type 1 diabetes (T1D) arises from autoimmune destruction of the beta cells of the pancreas leading to a complete dependence on exogenous insulin for survival. Like many autoimmune disorders, the etiology of T1D is complex, resulting from the action of multiple genes and environmental factors. Identification of genes that contribute to T1D susceptibility should improve disease prediction and contribute to the understanding of the underlying pathology of the disorder. Two regions of the human genome, the human leukocyte antigen (HLA) region and the insulin gene region are generally thought to contain susceptibility loci for T1D. Although additional putative T1D loci have been reported, the supporting evidence has often been of modest significance and findings have displayed poor reproducibility across multiple studies. This review summarizes the current state of genetic linkage and association studies in T1D and suggests future directions. We argue that much of the difficulty in mapping T1D susceptibility loci has resulted from inadequate sample sizes and we illustrate the substantial gains in power that can be achieved by pooling data across studies. These findings suggest that substantial progress toward the identification of susceptibility genes in T1D and other genetically complex disorders may be achieved through increased collaboration and consortium mapping efforts.
Synthesis of (–)-Allosamizoline, the Pseudoaminosugar Moiety of Allosamidin, a Chitinase Inhibitor (1993)

The enantioselective synthesis of (–)-allosamizoline (2a), the aminocyclitol moiety of allosamidin (1a), was achieved by starting from D-glucosamine (3). Intramolecular nitrile oxide cycloaddition was adopted as the key step to construct a functional cyclopentane ring system with proper stereochemistry.
Topiramate Inhibits the Initiation of Plateau Potentials in CA1 Neurons by Depressing R‐type Calcium Channels (2005)

We have found that TPM reduces ictal-like activity in CA1 hippocampal neurons through a novel inhibitory action of R-type calcium channels.
Phase calibration and applications of a liquid-crystal spatial light modulator (1995)

A simple phase-characterization method for spatial light modulators is proposed. The low-cost method permits high-precision measurement and provides data for the setting of the spatial-light-modulator operating point in the phase-modulation mode. The dynamic phase response is used to perform efficient kinoform recording. In order to record the kinoform, we modify the global iterative coding to compute phase holograms. Finally, modified phase-phase correlation is introduced. The phase-phase correlator permits sharper correlation peaks, better energy transmission, and higher discrimination than an amplitude-phase correlation. Optical experimental results are presented.
Matrix Metalloproteinase-26 Is Associated with Estrogen-Dependent Malignancies and Targets α1-Antitrypsin Serpin (2004)

Proteases exert control over cell behavior and affect many biological processes by making proteolytic modification of regulatory proteins. The purpose of this paper is to describe novel, important functions of matrix metalloproteinase (MMP)-26. alpha1-Antitrypsin (AAT) is a serpin, the primary function of which is to regulate the activity of neutrophil/leukocyte elastase. Insufficient antiprotease activity because of AAT deficiency in the lungs is a contributing factor to early-onset emphysema. We recently discovered that AAT is efficiently cleaved by a novel metalloproteinase, MMP-26, which exhibits an unconventional PH(81)CGVPD Cys switch motif and is autocatalytically activated in cells and tissues. An elevated expression of MMP-26 in macrophages and polymorphonuclear leukocytes supports the functional role of MMP-26 in the AAT cleavage and inflammation. We have demonstrated a direct functional link of MMP-26 expression with an estrogen dependency and confirmed the presence of the estrogen-response element in the MMP-26 promoter. Immunostaining of tumor cell lines and biopsy specimen microarrays confirmed the existence of the inverse correlations of MMP-26 and AAT in cells/tissues. An expression of MMP-26 in the estrogen-dependent neoplasms is likely to contribute to the inactivation of AAT, to the follow-up liberation of the Ser protease activity, and because of these biochemical events, to promote matrix destruction and malignant progression. In summary, we hypothesize that MMP-26, by cleaving and inactivating the AAT serpin, operates as a unique functional link that regulates a coordinated interplay between Ser and metalloproteinases in estrogen-dependent neoplasms.
The Anopheles gambiae Odorant Binding Protein 1 (AgamOBP1) Mediates Indole Recognition in the Antennae of Female Mosquitoes (2010)

Haematophagous insects are frequently carriers of parasitic diseases, including malaria. The mosquito Anopheles gambiae is the major vector of malaria in sub-Saharan Africa and is thus responsible for thousands of deaths daily. Although the role of olfaction in A. gambiae host detection has been demonstrated, little is known about the combinations of ligands and odorant binding proteins (OBPs) that can produce specific odor-related responses in vivo. We identified a ligand, indole, for an A. gambiae odorant binding protein, AgamOBP1, modeled the interaction in silico and confirmed the interaction using biochemical assays. RNAi-mediated gene silencing coupled with electrophysiological analyses confirmed that AgamOBP1 binds indole in A. gambiae and that the antennal receptor cells do not respond to indole in the absence of AgamOBP1. This case represents the first documented instance of a specific A. gambiae OBP-ligand pairing combination, demonstrates the significance of OBPs in odor recognition, and can be expanded to the identification of other ligands for OBPs of Anopheles and other medically important insects.