gebhart/patrepeval huggingface dataset:
Analysis and VLSI Implementation of EWA Rendering for Real-Time HD Video Applications (2012)

Nonlinear image warping or image resampling is a necessary step in many current and upcoming video applications, such as video retargeting, stereoscopic 3-D mapping, and multiview synthesis. The challenges for real-time resampling include not only image quality but also available energy and computational power of the employed device. In this paper, we employ an elliptical-weighted average (EWA) rendering approach to 2-D image resampling. We extend the classical EWA framework for increased visual quality and provide a very large scale integration architecture for efficient view rendering. The resulting architecture is able to render high-quality video sequences in real time targeted for low-power applications in end-user display devices.
Nuclear relaxation ofHe3in the presence ofO2 (1995)

We have measured the longitudinal nuclear relaxation rate ${\mathit{T}}_{1}^{\mathrm{\ensuremath{-}}1}$ for $^{3}\mathrm{He}$ in the presence of molecular oxygen in the temperature range T\ensuremath{\approxeq}200--400 K. At room temperature, ${\mathit{T}}_{1}^{\mathrm{\ensuremath{-}}1}$=0.448\ifmmode\pm\else\textpm\fi{}0.010 ${\mathrm{s}}^{\mathrm{\ensuremath{-}}1}$ per amagat ${\mathrm{O}}_{2}$, in approximate agreement with theoretical models for intermolecular dipolar relaxation. Furthermore, in this temperature range, ${\mathit{T}}_{1}^{\mathrm{\ensuremath{-}}1}$\ensuremath{\propto}${\mathit{T}}^{\mathrm{\ensuremath{-}}0.42\ifmmode\pm\else\textpm\fi{}0.04}$. Our results are of practical importance for the growing number of applications involving hyperpolarized noble gases.
Detection of aneuploidy involving chromosomes 13, 18, or 21, by fluorescence in situ hybridization (FISH) to interphase and metaphase amniocytes. (1991)

Fluorescence in situ hybridization (FISH) with chromosome-specific probes has been applied to detection of numerical aberrations involving chromosomes 13, 18, and 21 in metaphase and interphase amniocytes. High-complexity, composite probes for chromosomes 13, 18, and 21 were used as hybridization probes for this study. These probes were constructed as chromosome-specific libraries in Bluescribe plasmids and are designated pBS-13, pBS-18, and pBS-21. Elements of these probes bind at numerous sites along the target chromosome and, when detected fluorescently, stain essentially the entire long arm of the target chromosome. The target chromosome number (i.e., the number of chromosomes of the type for which the probe was specific) was correctly determined in 20 of 20 samples in which metaphase spreads were analyzed and in 43 of 43 samples in which interphase nuclei were analyzed; all of these studies were conducted in blind fashion. These results suggest the utility of FISH with composite probes for rapid detection of numerical aberrations in metaphase and interphase amniotic cells.
RETRACTED: Isolation and complete amino acid sequence of human thymopoietin and splenin. (1987)

Human thymopoietin and splenin were isolated from human thymus and spleen, respectively, by monitoring tissue fractionation with a bovine thymopoietin RIA cross-reactive with human thymopoietin and splenin. Bovine thymopoietin and splenin are 49-amino acid polypeptides that differ by only 2 amino acids at positions 34 and 43; the change at position 34 in the active-site region changes the receptor specificities and biological activities. The complete amino acid sequences of purified human thymopoietin and splenin were determined and shown to be 48-amino acid polypeptides differing at four positions. Ten amino acids, constant within each species for thymopoietin and splenin, differ between the human and bovine polypeptides. The pentapeptide active site of thymopoietin (residues 32-36) is constant between the human and bovine thymopoietins, but position 34 in the active site of splenin has changed from glutamic acid in bovine splenin to alanine in human splenin, accounting for the biological activity of the human but not the bovine splenin on the human T-cell line MOLT-4.
In Vitro Transcription of a Poly(dA){middle dot}Poly(dT)-Containing Sequence is Inhibited by Interaction between the Template and Its Transcripts (1996)

Transcription of poly(dA) x poly(dT)-containing sequences was investigated in vitro using plasmids carrying a (dA)34 x (dT)34 tract in the coding region of the lacZ gene. The efficiency of transcription of the (dT)34 sequence on the transcribing strand by Escherichia coli RNA polymerase was substantially lower (approximately 60%) than that of the (dA)34 sequence or of the control lacZ gene. Analysis of the transcription process of the (dT)34 sequence by T3 RNA polymerase showed that the transcription was frequently arrested or terminated at the middle as well as immediately proximal of the (dA)34 x (dT)34 tract, and it occurred more prominently following accumulation of transcription products. This inhibition was strongly enhanced by the addition of the oligonucleotide (dT)34 or poly(U) to the reaction mixture, while (dA)34 and the duplex (dA)34 x (dT)34 suppressed the inhibition. A similar transcriptional inhibition was also observed in transcription mediated by T7 RNA polymerase and eukaryotic RNA polymerase II. We also demonstrated RNA x DNA complex formation of the (dA)34 x (dT)34 tract with poly(U), but not with poly(A). These findings strongly suggest that poly(dT)-containing template sequences interact and form a complex with its transcription products, possibly an RNA x DNA triplex, which blocks further transcription. This would explain the instability of the plasmids transcribing mRNAs with poly(U) but not poly(A) tracts and the underrepresentation of poly(U) but not poly(A) tracts in mRNAs.
The Fastest Pedestrian Detector in the West (2010)

We demonstrate a multiscale pedestrian detector operating in near real time (∼6 fps on 640x480 images) with state-of-the-art detection performance.The computational bottleneck of many modern detectors is the construction of an image pyramid, typically sampled at 8-16 scales per octave, and associated feature computations at each scale.We propose a technique to avoid constructing such a finely sampled image pyramid without sacrificing performance: our key insight is that for a broad family of features, including gradient histograms, the feature responses computed at a single scale can be used to approximate feature responses at nearby scales.The approximation is accurate within an entire scale octave.This allows us to decouple the sampling of the image pyramid from the sampling of detection scales.Overall, our approximation yields a speedup of 10-100 times over competing methods with only a minor loss in detection accuracy of about 1-2% on the Caltech Pedestrian dataset across a wide range of evaluation settings.The results are confirmed on three additional datasets (INRIA, ETH, and TUD-Brussels) where our method always scores within a few percent of the state-of-the-art while being 1-2 orders of magnitude faster.The approach is general and should be widely applicable.
Gold-Speckled Multimodal Nanoparticles for Noninvasive Bioimaging (2008)

Multimodal Gold-speckled silica nanoparticles as contrast agents for noninvasive imaging with magnetic resonance imaging and photoacoustic tomography have been prepared in a simple one-pot synthesis using nonionic microemulsions. Magnetic resonance contrast is provided through gadolinium incorporated in the silica matrix, whereas the photoacoustic signal originates from nonuniform, discontinuous gold nanodomains speckled across the silica surface.
The ultrastructure of hepatocytes in alpha-1-antitrypsin deficiency with the genotype Pi--. (1975)

The ultrastructural appearance of the endoplasmic reticulum of the hepatocytes was found to be normal in a 5-year-old girl with alpha-1-antitrypsin deficiency with the genotype Pi--. The liver ultrastructure of this variant is therefore different from that of alpha-1-antitrypsin deficiency with the genotype PiZZ in which aggregates of an abnormal, unsecreted alpha-1-antitrypsin accumulate in the endoplasmic reticulum of the hepatocytes. The normal appearance of the endoplasmic reticulum in alpha-1-antitrypsin deficiency with the genotype Pi-- is compatible with the hypothesis, in this variant, synthesis of alpha-1-antitrypsin is completely, or nearly completely, absent; an alternative hypothesis would be that an abnormal alpha-1-antitrypsin is produced by the liver and secreted into the plasma, but disappears rapidly from the plasma.
Design strategies and application progress of therapeutic exosomes (2019)

Exosomes have great potential to be drug delivery vehicles due to their natural material transportation properties, intrinsic long-term circulatory capability, and excellent biocompatibility, which are suitable for delivering a variety of chemicals, proteins, nucleic acids, and gene therapeutic agents. However, an effective method of loading specific protein agents into exosomes for absorption by target cells is still lacking. The application potential of exosome is still limited. In this review, we discussed the methods for loading specific treating molecules (proteins, nucleic acids and small chemicals) into exosomes, the design strategies for cell and tissue targeting, and the factors for exosome formation. This review can be used as a reference for further research as well as for the development of therapeutic exosomes.
An inhibitor of collagen-induced platelet aggregation from the saliva of Triatoma pallidipennis. (1994)

The saliva of Triatoma pallidipennis, a blood-sucking triatomine bug (Hemiptera, family Reduviidae, subfamily Triatominae) was found to contain a factor that specifically inhibits collagen-induced platelet aggregation. The 19-kDa protein was purified to homogeneity and named pallidipin. Collagen-mediated aggregation of platelets in plasma and of washed platelets was inhibited with the same efficacy. No inhibition of aggregation stimulated by other effectors (ADP, thrombin, thromboxane A2 mimetic U46619, phorbol ester) was detected. Pallidipin had no effect on platelet adhesion to collagen but inhibited ATP release from platelets. It interacted reversibly with platelets and may share with collagen a common target on them. The protein exhibits a unique primary structure (predicted from cDNA clones) with no significant similarity to other previously described sequences. The protein produced in recombinant baby hamster kidney cells had antiaggregatory effects similar to those of native pallidipin. Availability of recombinant pallidipin will allow further investigation of the precise mechanism of action.
Release behaviour of 5-fluorouracil from chitosan-gel microspheres immobilizing 5-fluorouracil derivative coated with polysaccharides and their cell specific recognition (1993)

In order to provide a device releasing drugs in a controlled manner and having targetability to specific organs or cells, chitosan-gel microspheres, CMS, crosslinked with glutaraldehyde, immobilizing 1-[N-(5-aminopentyl) carbamoyl]-5-fluorouracil, 1, coated with anionic polysaccharides, such as 6-O-carboxymethyl-N-acetyl-alpha-1,4-polygalactosamine (CM-NAPGA), 6-O-carboxymethyl-chitin, alginic acid and heparin, by polyelectrolyte complex membrane formation were prepared. When chitosan was crosslinked with glutaraldehyde, 1 was simultaneously immobilized into CMS by Schiff's base formation. Average diameter of CMS obtained was estimated to be about 0.5-1.0 micron by SEM observation. In physiological saline media, only free 5-FU was released from the CMS but 1 and any 5-FU derivative was not. Release rate of 5-FU from the CMS was reduced by coating with polyelectrolyte complex membrane of cationic chitosan and anionic polysaccharides. CMS coated with CM-NAPGA showed a lectin-mediated specific aggregation phenomenon by addition of Abrus precatorius agglutinin. Moreover, the CMS immobilizing 1 coated with CM-NAPGA showed higher growth-inhibitory effect against SK-Hep-1 (human hepatoma) cells in vitro than the CMS coated with other polysaccharides.
PURINE NUCLEOTIDE METABOLISM IN THE CAT BRAIN AFTER ONE HOUR OF COMPLETE ISCHEMIA (1974)

Abstract —Complete cerebral ischemia was produced in normothermic anaesthetized cats by clamping the innominate and the left subclavian arteries combined with lowering the blood pressure. After 1 h of ischemia, ATP was no longer present in detectable amounts. Total adenine nucleotides were reduced to 34 per cent of the normal level. The breakdown of guanine nucleotides was less marked, with small amounts of GTP still being present at the end of the ischemic period. In animals with signs of functional recovery after 3–7 h of recirculation, ATP was resynthesized to 62 per cent of the control level. Total adenine nucleotides increased to 68 per cent and the adenylate energy change—[ATP + 1/2 ADP]/[AMP + ADP + ATP]—was re‐established to within 7 per cent of the pre‐ischemic value. Radiochromatography of nucleotides following intravenous injection of [ 14 C]formate indicated a marked enhancement of postischemic purine de novo synthesis. Purine nucleosides and free bases which accumulated during ischemia, were partially re‐utilized by salvage pathways: adenosine was rephosphorylated to AMP by adenosine kinase (EC 2.7.1.20); inosine and hypoxanthine were re‐used via IMP in a reaction mediated by hypoxanthine phosphoribosyltransferase (EC 2.4.2.8).
Silencing Expression of the Clusterin/Apolipoprotein J Gene in Human Cancer Cells Using Small Interfering RNA Induces Spontaneous Apoptosis, Reduced Growth Ability, and Cell Sensitization to Genotoxic and Oxidative Stress (2004)

Clusterin/Apolipoprotein J (CLU) is a heterodimeric ubiquitously expressed secreted glycoprotein that is implicated in several physiological processes and is differentially expressed in many severe physiological disturbances, including tumor formation and in vivo cancer progression. Despite extensive efforts, clarification of CLU's biological role has been exceptionally difficult and its precise function remains elusive. Short RNA duplexes, referred to as small interfering RNAs (siRNAs), provide a new approach for the elucidation of gene function in human cells. Here, we describe siRNA-mediated CLU gene silencing in osteosarcoma and prostate human cancer cells and illustrate that CLU mRNA is amenable to siRNA-mediated degradation. Our data demonstrate that CLU knockdown in human cancer cells induces significant reduction of cellular growth and higher rates of spontaneous endogenous apoptosis. Moreover, CLU knockdown cancer cells were significantly sensitized to both genotoxic and oxidative stress induced by chemotherapeutic drugs and H(2)O(2), respectively. These effects were more pronounced in cell lines that express high endogenous steady-state levels of the CLU protein and occur through hyperactivation of the cellular apoptotic machinery. Overall, our results reveal that, in the distinct cellular contexts of the osteosarcoma and prostate cancer cells assayed, CLU is a central molecule in cell homeostasis that exerts a cytoprotective function. The described CLU-specific siRNA oligonucleotides that can potently silence CLU gene expression may thus prove valuable agents during antitumor therapy or at other pathological conditions where CLU has been implicated.
Ventilator-associated lung injury in ARDS (2000)

An excellent review which presents literature from both animal experiments and human clinical trials in an attempt to form a consensus view on ventilator-induced lung injury (VILI). Animal data pertaining to alveolar overdistension, as a result of increased transpulmonary pressure during mechanical ventilation, is examined, and the difficulties in translating this evidence into the human arena are discussed. The authors highlight the fact that we can only infer that VILI occurs in humans, since a study to prove this can not be performed for obvious reasons. Nevertheless, clinical observations show that protective ventilator strategies can influence morbidity and mortality and the much publicised multicentre trial, recently completed by the NIH, is quoted here. Risk factors, incidence, monitoring, morbidity, mortality and prevention of VILI are all covered by this consensus conference. The conclusions reached, are that low tidal volumes, PEEP titrated to the PV curve, and possibly prone positioning may all protect against VILI.
Interferon-gamma inhibits interferon-alpha signalling in hepatic cells: evidence for the involvement of STAT1 induction and hyperexpression of STAT1 in chronic hepatitis C (2004)

IFN-gamma (interferon-gamma) modulates IFN-alpha therapy in chronic hepatitis C infection; however, the underlying mechanism remains unclear. Here we demonstrate that long-term (3-6 days) but not short-term (up to 1 day) IFN-gamma treatment of human hepatoma Hep3B cells attenuates IFN-alpha activation of STAT1 (signal transducers and activators of transcription factor 1), STAT2 and STAT3, but enhances IFN-gamma and interleukin 6 activation of STATs. Prolonged exposure to IFN-gamma also significantly induces STAT1 protein expression without affecting STAT2, STAT3 and ERK (extracellular-signal-regulated kinase) 1/2 protein expression. To determine the role of STAT1 protein overexpression in regulation of IFN-alpha signalling, Hep3B cells were stably transfected with wild-type STAT1. Overexpression of STAT1 via stable transfection enhances IFN-gamma activation of STAT1, but surprisingly attenuates IFN-alpha activation of STAT1, STAT2 and STAT3 without affecting Janus kinase activation. This STAT1-mediated inhibition does not require STAT1 tyrosine phosphorylation because overexpression of dominant-negative STAT1 with a mutation on tyrosine residue 701 also blocks IFN-alpha activation of STAT1, STAT2 and STAT3. Moreover, overexpression of STAT1 blocks IFN-alpha-activated STAT2 translocation from IFN-alpha receptor 2 to IFN-alpha receptor 1, a critical step in IFN-alpha signalling activation. Finally, significantly higher levels of STAT1 protein expression, which is probably induced by IFN-gamma, are detected in the majority of hepatitis C virus-infected livers compared with healthy controls. In conclusion, long-term IFN-gamma treatment inhibits IFN-alpha-activated signals most probably, at least in part, through the induction of STAT1 protein expression, which could partly contribute to IFN-alpha treatment failure in hepatitis C patients.
Poliovirus Sabin type 1 neutralization epitopes recognized by immunoglobulin A monoclonal antibodies (1997)

Immunity to poliomyelitis is largely dependent on humoral neutralizing antibodies, both after natural (wild virus or vaccine) infection and after inactivated poliovirus vaccine inoculation. Although the production of local secretory immunoglobulin A (IgA) antibody in the gut mucosa may play a major role in protection, most of information about the antigenic determinants involved in neutralization of polioviruses derives from studies conducted with humoral monoclonal antibodies (MAbs) generated from parenterally immunized mice. To investigate the specificity of the mucosal immune response to the virus, we have produced a library of IgA MAbs directed at Sabin type 1 poliovirus by oral immunization of mice with live virus in combination with cholera toxin. The epitopes recognized by 13 neutralizing MAbs were characterized by generating neutralization-escape virus mutants. Cross-neutralization analysis of viral mutants with MAbs allowed these epitopes to be divided into four groups of reactivity. To determine the epitope specificity of MAbs, virus variants were sequenced and the mutations responsible for resistance to the antibodies were located. Eight neutralizing MAbs were found to be directed at neutralization site N-AgIII in capsid protein VP3; four more MAbs recognized site N-AgII in VP1 or VP2. One IgA MAb selected a virus variant which presented a unique mutation at amino acid 138 in VP2, not previously described. This site appears to be partially related with site N-AgII and is located in a loop region facing the VP2 N-Ag-II loop around residue 164. Only 2 of 13 MAbs proved able to neutralize the wild-type Mahoney strain of poliovirus. The IgA antibodies studied were found to be produced in the dimeric form needed for recognition by the polyimmunoglobulin receptor mediating secretory antibody transport at the mucosal level.
Pathways for the Decay of Organic Dichloramines and Liberation of Antimicrobial Chloramine Gases (2008)

When neutrophils phagocytose bacteria, they generate the cytotoxic agent hypochlorous acid (HOCl). The specific role that HOCl plays in bacterial killing is unclear. In the phagosome, it should react with neutrophil proteins to form protein chloramines and dichloramines. We investigated the stability of model dichloramines that are likely to be formed on N-terminal amino acids and Lys residues of proteins contained within phagosomes. Dichloramines were much more unstable than their analogous monochloramines. The stability was affected by substituents on the alpha-carbon. Amino acid dichloramines were extremely unstable, indicating that an alpha-carboxyl group facilitated decomposition. In general, the absence of a substituent enhanced stability. The carboxyl group on N-terminal Glu residues favored break down, but this effect was not apparent with Asp residues. Unstable dichloramines that contained a substituent on their alpha-carbon were cytotoxic and killed 50% of 10(5) Staphylococcus aureus (LD50) at a dose of approximately 2.5 nmol. Their cytotoxicity declined with time. The dichloramines of N-alpha-acetyl Lys and taurine were not bactericidal up to 10 nmol per 10(5) S. aureus. None of the analogous monochloramines were cytotoxic at this dose. Dichloramines decomposed to yield chlorimines, aldehydes, and the inorganic gases ammonia monochloramine (NH2Cl) and ammonia dichloramine (NHCl2). The LD50 values were determined for NH2Cl (0.37 +/- 0.14 nmol), NHCl2 (0.08 +/- 0.02 nmol), and HOCl (0.14 +/- 0.04 nmol). Stable products formed during the breakdown of dichloramines were not bactericidal. We propose a potential antimicrobial mechanism that explains in part how HOCl can react mainly with neutrophil components but still promote killing of phagocytosed bacteria. HOCl produced in phagosomes will react with amine groups on neutrophil proteins to form unstable dichloramines that will liberate cytotoxic NH2Cl and NHCl2. These gases will contribute to killing of ingested bacteria.