gebhart/patrepeval huggingface dataset:
Short-Term and Long-Term Effects of Orthopedic Biodegradable Implants (2011)

Presently, orthopedic and oral/maxillofacial implants represent a combined $2.8 billion market, a figure expected to experience significant and continued growth. Although traditional permanent implants have been proved clinically efficacious, they are also associated with several drawbacks, including secondary revision and removal surgeries. Non-permanent, biodegradable implants offer a promising alternative for patients, as they provide temporary support and degrade at a rate matching tissue formation, and thus, eliminate the need for secondary surgeries. These implants have been in clinical use for nearly 25 years, competing directly with, or maybe even exceeding, the performance of permanent implants. The initial implantation of biodegradable materials, as with permanent materials, mounts an acute host inflammatory response. Over time, the implant degradation profile and possible degradation product toxicity mediate long-term biodegradable implant-induced inflammation. However, unlike permanent implants, this inflammation is likely to cease once the material disappears. Implant-mediated inflammation is a critical determinant for implant success. Thus, for the development of a proactive biodegradable implant that has the ability to promote optimal bone regeneration and minimal detrimental inflammation, a thorough understanding of short- and long-term inflammatory events is required. Here, we discuss an array of biodegradable orthopedic implants, their associated short- and long- term inflammatory effects, and methods to mediate these inflammatory events.
Chemical fluctuation-induced nanodomains in Cu(In,Ga)Se2 films (2005)

The microstructure and chemistry of CuInSe2 single-crystals and Cu(In,Ga)Se2 thin films from high-efficiency devices are investigated by transmission electron microscopy and x-ray energy-dispersive spectroscopy. We find strong chemical fluctuations at the nanoscale, which result in a lattice comprising a mixture of relatively Cu-poor and Cu-rich nanodomains in both cases. These nanodomains are crystallographically coherent, and no structural lattice defects are found at the interfaces between them. These nanodomains may interconnect, forming three-dimensional, interpenetrating Cu-poor and Cu-rich percolation networks. Such interconnected structures may play a role in the high device performance of Cu(In,Ga)Se2 thin-film photovoltaics.
Human telomeric DNA: G-quadruplex, i-motif and Watson-Crick double helix (2002)

Human telomeric DNA composed of (TTAGGG/CCCTAA)n repeats may form a classical Watson-Crick double helix. Each individual strand is also prone to quadruplex formation: the G-rich strand may adopt a G-quadruplex conformation involving G-quartets whereas the C-rich strand may fold into an i-motif based on intercalated C*C+ base pairs. Using an equimolar mixture of the telomeric oligonucleotides d[AGGG(TTAGGG)3] and d[(CCCTAA)3CCCT], we defined which structures existed and which would be the predominant species under a variety of experimental conditions. Under near-physiological conditions of pH, temperature and salt concentration, telomeric DNA was predominantly in a double-helix form. However, at lower pH values or higher temperatures, the G-quadruplex and/or the i-motif efficiently competed with the duplex. We also present kinetic and thermodynamic data for duplex association and for G-quadruplex/i-motif unfolding.
Ultrahigh x-ray reflectivity from W∕Al2O3 multilayers fabricated using atomic layer deposition (2006)

W ∕ Al 2 O 3 multilayers were fabricated using W and Al2O3 atomic layer deposition (ALD) to produce x-ray mirrors. The x-ray reflectivity from an optimized W∕Al2O3 multilayer was 96.5%±0.5% for the first-order Bragg peak at λ=1.54Å. The ultrahigh x-ray reflectivity is attributed to the precise bilayer thicknesses and ultrasmooth interfaces obtained from ALD film growth. The self-limiting ALD surface chemistry prevents randomness during film growth and produces conformal deposition with correlated roughness that enhances the x-ray reflectivity.
Planar surface implanted diffractive grating couplers in SOI (2014)

Grating couplers are used to efficiently couple light from an optical fibre to a silicon waveguide as they allow light to be coupled into or out from any location on the device without the need for cleaving. However, using the typical surface relief grating fabrication method reduces surface planarity and hence makes further processing more difficult. The ability to manufacture high quality material layers on top of a grating coupler allows multiple active optical layers to be realized for multi-layer integrated optical circuits, and may enable monolithic integration of optical and electronic circuits on separate layers. Furthermore, the nature of the refractive index change may enable removal via rapid thermal annealing for wafer scale testing applications. We demonstrate for the first time a coupling device utilising a refractive index change introduced by lattice disorder. Simulations show 44% of the power can be extracted from the waveguide by using uniform implanted gratings, which is not dissimilar to the performance of typical uniform surface relief gratings currently used. Losses determined empirically, of 5.5 dB per coupler have been demonstrated.
The Ca2(+)-binding glycoprotein SPARC modulates cell cycle progression in bovine aortic endothelial cells. (1991)

SPARC (secreted protein, acidic and rich in cysteine) is an extracellular, Ca2(+)-binding protein associated with cellular populations undergoing migration, proliferation, and/or differentiation. Active preparations of SPARC bind to specific components of the extracellular matrix and cause mesenchymal cells to assume a rounded phenotype. In this study we show that SPARC modulates the progression of bovine aortic endothelial cells through the cell cycle. At a concentration of 20 micrograms/ml, SPARC inhibited the incorporation of [3H]thymidine into newly synthesized DNA by approximately 70%, as compared to control cultures within 24 hr after the release from G0 phase. The effect was dose-dependent and reached greater than 90% inhibition at 30 micrograms of SPARC per ml after 24 hr. A 20-residue synthetic peptide (termed 2.1) from a non-Ca2(+)-binding, disulfide-rich domain of SPARC also exhibited a dose-dependent inhibition of [3H]thymidine uptake in endothelial cells within 24 hr after release from G0 phase. An inhibition of 50% was seen with peptide 2.1 at a 0.4 mM concentration. Peptides from other regions of the SPARC protein did not produce this effect. Maximum inhibition of [3H]thymidine uptake by SPARC and peptide 2.1 occurred during the early-to-middle G1 phase of the endothelial-cell cycle. From 0-12 hr after release from G0 phase, cells exhibited delayed entry into S phase, which normally occurred at 24 +/- 2 hr. These results were further corroborated by flow cytometry. In the presence of SPARC at 20 micrograms/ml, 72% fewer cells were in S phase after a 24-hr period; a similar, but less marked, reduction was seen with peptide 2.1. Peptide 2.1 did not cause cell rounding, whereas peptide 1.1, a highly efficient inhibitor of endothelial-cell spreading, exhibited essentially no activity with respect to cell-cycle progression. It therefore appears that the transient, inhibitory effect of SPARC on the entry of endothelial cells into S phase does not depend on the overt changes in cell shape mediated through cytoskeletal rearrangement.
A systematic review of five systemic treatments for severe psoriasis (1997)

We systematically reviewed the evidence concerning the ability of five systemic treatments to induce remission in patients with severe psoriasis: ultraviolet B (UVB), photochemotherapy (PUVA), methotrexate (MTX), retinoids (RET) and cyclosporin A (CYA). An elaborate literature search was performed, the validity of studies was assessed, and data were analysed. In total, 89, 193, 101, 155 and 127 studies (n = 665) concerning UVB, PUVA, MTX, RET and CYA were found. The exclusion rate was high, mainly because of concomitant antipsoriatic therapy, outdated dosages or inadequate documentation. No study on MTX could be included. A total of 129 patient series was included in the analysis, reporting on 13,677 patients. Study size-weighted averages of the proportions of patients with clearance and good, moderate and poor response (defined, respectively, as 95-100%, 75-100%, 50-75% and < 50% reduction in the outcome measurements as compared with baseline) were calculated. PUVA therapy was associated with the highest average proportion of patients with clearance (70%), and the highest proportion of patients with good response (83%), followed by UVB (68%) and CYA (64%). Incidence of side-effects per week was highest in the RET group and lowest in the phototherapy groups. This review may provide a basis for the development of guidelines for the treatment of psoriasis. Trials comparing oral modalities applied according to currently accepted standards should also be carried out.
Concordance among Gene-Expression–Based Predictors for Breast Cancer (2006)

Even though different gene sets were used for prognostication in patients with breast cancer, four of the five tested showed significant agreement in the outcome predictions for individual patients and are probably tracking a common set of biologic phenotypes.
Cell attachment to extracellular matrices is modulated by pulsed radiation at 820 nm and chemicals that modify the activity of enzymes in the plasma membrane (2001)

The results obtained indicate that pulsed IR radiation at 820 nm increases the cell-matrix attachment. It is the modulation of the monovalent ion fluxes through the plasma membrane and not the release of arachidonic acid that is involved in the cellular signaling pathways activated by irradiation at 820 nm. Preirradiation has a protective effect against the inhibitive action of ouabain, arachidonic acid, ATP, and quinacrine on cell attachment process. It is supposed that irradiation activates those signaling pathways in cells which attenuate the inhibitive action of these chemicals.
Single-Molecule ELISA (2010)

The need for assay methods of sufficient sensitivity to determine the low concentrations of hormones present in body fluids led to the original development of immunoassays and analogous “binding” (or “ligand”) assays in the late 1950s and early 1960s. These methods depend on the use of a binding agent (also commonly referred to by other terms such as “receptor,” “binding reagent,” and “analyte-specific reagent”), a substance used to recognize and bind the target analyte. Typical binding agents include antibodies, antigens, cell receptors, and serum binding proteins. Immunoassays still constitute the most widely used class of binding assays, although microarray-based nucleic acid assays, employing oligonucleotides as binding agents, are rapidly increasing in popularity.

A principal objective in this field since the emergence of these assays has been to increase their sensitivities, especially in their application to certain analytes. Typifying such attempts, Rissin et al. (1) have recently reported a new approach to the further improvement of immunoassay sensitivities, claiming that with the use of an ELISA-type system, they were able to “detect serum proteins at subfemtomolar concentrations” and to increase the sensitivity of measurements “using a typical ELISA plate reader by a factor of about 68 000.”

But before discussing the novel features of Rissin et al.'s approach, we should briefly examine the concept of sensitivity and the meaning of the term “sensitive” to describe the performance of a binding assay—or indeed that of any measurement system. Many workers in this area, including Rissin et al., identify sensitivity with the lower limit of detection (LoD)3 of an assay. However, certain bodies, including the American Chemical Society and the International Union of Pure and Applied Chemistry, have formally defined sensitivity as the slope of the dose–response curve [or the response/dose (R/D) ratio—an intrinsically meaningless concept with which we strongly disagree (see …
Gene expression variations are predictive for stochastic noise (2010)

Fluctuations in protein abundance among single cells are primarily due to the inherent stochasticity in transcription and translation processes, such stochasticity can often confer phenotypic heterogeneity among isogenic cells. It has been proposed that expression noise can be triggered as an adaptation to environmental stresses and genetic perturbations, and as a mechanism to facilitate gene expression evolution. Thus, elucidating the relationship between expression noise, measured at the single-cell level, and expression variation, measured on population of cells, can improve our understanding on the variability and evolvability of gene expression. Here, we showed that noise levels are significantly correlated with conditional expression variations. We further demonstrated that expression variations are highly predictive for noise level, especially in TATA-box containing genes. Our results suggest that expression variabilities can serve as a proxy for noise level, suggesting that these two properties share the same underlining mechanism, e.g. chromatin regulation. Our work paves the way for the study of stochastic noise in other single-cell organisms.
Reduction in mortalin level by its antisense expression causes senescence‐like growth arrest in human immortalized cells (2004)

The data demonstrate that suppression of mortalin is sufficient to induce growth arrest in human immortalized cells that have compromised p53 and pRB functions and possess telomerase activity.
Microfluidic continuous particle/cell separation via electroosmotic-flow-tuned hydrodynamic spreading (2007)

Among the microfluidic separation methods, hydrodynamic spreading is a simple and high-throughput continuous separation technique based on the difference in size. However, it is difficult to adjust tiny pressure differences accurately in microfluidic devices. In this study, a combination of electroosmotic flow (EOF) and hydrodynamic flow spreading was employed to tune the size separation of particles. A stream with different kinds of particle suspensions was driven co-fluently with a particle-free carrier stream under both mechanical external and electroosmotic pressure in a microchannel. The EOF-tuned hydrodynamic spreading behaviour was investigated experimentally and modelled through an electric equivalent model and numerical simulation. When the magnitudes of the mechanically and electroosmotically induced pressures were similar, the EOF tuning on the pressure-driven flow became significant. Hence, the hydrodynamic spreading could be easily adjusted by a tuned power supply. The separation was studied in more detail with 1.9 and 9.9 µm fluorescent polystyrene particles. Moreover, separation of E. coli and yeast cells was accomplished. In conclusion, this technique has the advantages of good stability of mechanical-pressure-driven flow and precise tuning of the EOF, and provides a robust method for size-based separation of particles and cells.
Deep Semantic Role Labeling: What Works and What’s Next (2017)

We introduce a new deep learning model for semantic role labeling (SRL) that significantly improves the state of the art, along with detailed analyses to reveal its strengths and limitations. We use a deep highway BiLSTM architecture with constrained decoding, while observing a number of recent best practices for initialization and regularization. Our 8-layer ensemble model achieves 83.2 F1 on the CoNLL 2005 test set and 83.4 F1 on CoNLL 2012, roughly a 10% relative error reduction over the previous state of the art. Extensive empirical analysis of these gains show that (1) deep models excel at recovering long-distance dependencies but can still make surprisingly obvious errors, and (2) that there is still room for syntactic parsers to improve these results.
Increased levels of glutathione S-transferase π transcript as a mechanism of resistance to ethacrynic acid (1992)

Subpopulations of HT 29 human colon carcinoma cells (HT/M and HT/S) were selected for resistance to the glutathione S-transferase (GST) inhibitor ethacrynic acid (EA). Both clones displayed a 2-fold resistance to the selection agent and required its constant presence for the maintenance of the resistant phenotype. Purification and characterization of GST isoforms showed similar profiles in the wild-type (WT) and EA-resistant clones, with microheterogeneous forms of the pi isoenzyme detected in each case. Metabolism of EA in vitro in the presence of GSH and the isolated GST from each cell line was characterized by a biphasic disappearance of the parent drug; the initial rate at which each of these enzymes metabolized EA was similar. These enzymes also displayed similar Km values for 1-chloro-2,4-dinitrobenzene. However, the amount of GST isolated per total cellular protein was 3.0-fold in HT/M and 1.6-fold in HT/S relative to WT in the continuous presence of EA. Under these conditions GST activity was increased by 2.3-fold in HT/M and 3.2-fold in HT/S as were GSH levels (2.7- and 4.1-fold for HT/M and HT/S respectively). When EA was removed, enzyme activity and GSH concentrations decreased to values similar to those of the WT. Slot-blot and Southern analyses of the DNA gave no evidence of GST-pi-gene amplification or rearrangement. However, RNA analyses by both slot-blot and Northern studies indicate a 2.5-3.5-fold elevation in the GST pi transcript in the EA-resistant population. Results from these studies indicate that: (1) maintenance of the EA-resistant phenotype requires constant presence of the agent; (2) the 2-fold resistance to EA can be quantitatively related to a 2-3-fold increase in GST activity and amount which appears to be the result of a 2.5-3.5-fold elevation in GST transcript; (3) EA, a Michael-reaction acceptor, can induce GST at the transcriptional level.
Side chains involved in catalysis of the polymerase reaction of DNA polymerase I from Escherichia coli. (1992)

To continue our mutagenesis study of the polymerase active site of the Klenow fragment of DNA polymerase I, we have characterized new mutants with substitutions at Asp705, Glu710, and Glu883, and have investigated further the mutations in residues Arg668, Gln849, and Asp882, which showed strong Kcat effects in our previous study. To determine which step of the reaction is rate-limiting for each mutant protein, we measured the effect on the reaction rate of an alpha-thio-substituted dNTP. One group of mutants showed a substantial sulfur elemental effect, while a second group, like wild-type Klenow fragment, was unaffected by the phosphorothioate substitution. Consistent with earlier data, these results imply that, between formation of the enzyme-DNA-dNTP ternary complex and completion of phosphodiester bond formation, there are two kinetically distinct steps, only one of which is sensitive to sulfur substitution. The rather complex elemental effect data obtained with the mutant derivatives of Klenow fragment are more consistent with the elemental effect being the result of a steric clash in one of the transition states than with explanations based on electronegativity differences between sulfur and oxygen. The data suggest that the side chain of Asp882 is involved in the proposed steric clash, and that Gln849 and Glu883 participate in the sulfur-sensitive step of the reaction. Based on our results, and comparisons with other phosphoryl transfer enzymes, possible mechanisms for the polymerase reaction are discussed.
Electrical Stimulation Promotes Motoneuron Regeneration without Increasing Its Speed or Conditioning the Neuron (2002)

Motoneurons reinnervate the distal stump at variable rates after peripheral nerve transection and suture. In the rat femoral nerve model, reinnervation is already substantial 3 weeks after repair, but is not completed for an additional 7 weeks. However, this "staggered regeneration" can be temporally compressed by application of 20 Hz electrical stimulation to the nerve for 1 hr. The present experiments explore two possible mechanisms for this stimulation effect: (1) synchronization of distal stump reinnervation and (2) enhancement of regeneration speed. The first possibility was investigated by labeling all motoneurons that have crossed the repair at intervals from 4 d to 4 weeks after rat femoral nerve transection and suture. Although many axons did not cross until 3-4 weeks after routine repair, stimulation significantly increased the number crossing at 4 and 7 d, with only a few crossing after 2 weeks. Regeneration speed was studied by radioisotope labeling of transported proteins and by anterograde labeling of regenerating axons, and was not altered by stimulation. Attempts to condition the neuron by stimulating the femoral nerve 1 week before injury were also without effect. Electrical stimulation thus promotes the onset of motor axon regeneration without increasing its speed. This finding suggests a combined approach to improving the outcome of nerve repair, beginning with stimulation to recruit all motoneurons across the repair, followed by other treatments to speed and prolong axonal elongation.
Excision of the First Intron from the Gonadotropin-releasing Hormone (GnRH) Transcript Serves as a Key Regulatory Step for GnRH Biosynthesis (2003)

The mammalian gonadotropin-releasing hormone (GnRH) gene consists of four short exons (denoted as 1, 2, 3, and 4) and three intervening introns (A, B, and C). Recently, we demonstrated that excision of the first intron (intron A) from the GnRH transcript is regulated in a tissue- and developmental stage-specific fashion and is severely attenuated in hypogonadal (hpg) mouse because of its lack of exonic splicing enhancers (ESE) 3 and 4. In the present study, we examined the influence of intron A on translational efficiency, thereby establishing a post-transcriptional control over GnRH biosynthesis. First, we verified that an intron A-retained GnRH transcript is a splicing variant but not a splicing intermediate. Intron A-retained transcripts can be transported to the cytoplasm in contrast to intron B-containing transcripts, which are restricted to the nucleus. This result implicates the intron A-retained GnRH transcript as a splicing variant; it has a long 5'-untranslated region, as the GnRH prohormone open reading frame (ORF) begins on exon 2. We investigated whether an intron A-retained GnRH transcript can properly initiate translation at the appropriate start codon and found that intron A completely blocks the translation initiation of its downstream reporter ORF both in vivo and in vitro. The inhibition of translation initiation appears to be due to the presence of a tandem repeat of ATG sequences within intron A. Constructs bearing mutations of ATGs to AAGs restored translation initiation at the downstream start codon; the extent of this restoration correlated with the number of mutated ATGs. Besides the failure in the translation initiation of GnRH-coding region in the intron A-containing variant, the present study also suggests that the interference between mature GnRH mRNA and intron A-retained splicing variant could occur to lower the efficiency of GnRH biosynthesis in the GT1-1-immortalized GnRH-producing cell line. Therefore, our results indicate that the precise and efficient excision of intron A and the joining of adjacent exons may be a critical regulatory step for the post-transcriptional regulation of GnRH biosynthesis.