gebhart/patrepeval huggingface dataset:
Recent Advances in Camera Planning for Large Area Surveillance (2016)

With recent advances in consumer electronics and the increasingly urgent need for public security, camera networks have evolved from their early role of providing simple and static monitoring to current complex systems capable of obtaining extensive video information for intelligent processing, such as target localization, identification, and tracking. In all cases, it is of vital importance that the optimal camera configuration (i.e., optimal location, orientation, etc.) is determined before cameras are deployed as a suboptimal placement solution will adversely affect intelligent video surveillance and video analytic algorithms. The optimal configuration may also provide substantial savings on the total number of cameras required to achieve the same level of utility. In this article, we examine most, if not all, of the recent approaches (post 2000) addressing camera placement in a structured manner. We believe that our work can serve as a first point of entry for readers wishing to start researching into this area or engineers who need to design a camera system in practice. To this end, we attempt to provide a complete study of relevant formulation strategies and brief introductions to most commonly used optimization techniques by researchers in this field. We hope our work to be inspirational to spark new ideas in the field.
Endothelial Dysfunction (2006)

We tested the hypothesis that endothelial dysfunction could cause placentation-related defects, persist after the complicated pregnancy, and probably cause cardiovascular disease later in life. Brachial arterial reactivity and factors related to endothelial dysfunction, such as circulating cholesterol, uric acid, nitrites, l-arginine, asymmetrical dimethylarginine, vascular endothelial growth factor, and soluble vascular endothelial growth factor receptor-1, in women with previous healthy pregnancies (n=22), patients with severe preeclampsia (n=25), or patients with recurrent pregnancy loss (n=29), at day 10 of the luteal phase of an ovulatory cycle an average of 11 to 27 months after pregnancy were evaluated. Both groups with placentation defects had a significant decrease in endothelium-dependent dilatation, a higher rate of endothelial dysfunction, lower serum nitrites, and higher cholesterol as compared with control subjects; subjects with previous preeclampsia additionally had higher normal blood pressures and a greater parental prevalence of cardiovascular disease. Patients with recurrent pregnancy loss also demonstrated a significantly lower endothelium-independent vasodilatation. A trend to an inverse correlation was found between serum cholesterol serum and endothelial-mediated vasodilatation in the whole study population. Uric acid, l-arginine, asymmetrical dimethylarginine, vascular endothelial growth factor, and soluble vascular endothelial growth factor receptor-1 were similar in all of the groups. We postulate that endothelial dysfunction may represent a link between preeclampsia and increased cardiovascular disease latter in life and propose that women with unexplained recurrent miscarriages are also at increased cardiovascular risk. The identification and correction of endothelial dysfunction detected during the reproductive stage on obstetric outcome and on cardiovascular diseases needs to be elucidated.
Large Integrated Absorption Enhancement in Plasmonic Solar Cells by Combining Metallic Gratings and Antireflection Coatings (2010)

We describe an ultrathin solar cell architecture that combines the benefits of both plasmonic photovoltaics and traditional antireflection coatings. Spatially resolved electron generation rates are used to determine the total integrated current improvement under AM1.5G solar illumination, which can reach a factor of 1.8. The frequency-dependent absorption is found to strongly correlate with the occupation of optical modes within the structure, and the improved absorption is mainly attributed to improved coupling to guided modes rather than localized resonant modes.
Generating efficient data movement code for heterogeneous architectures with distributed-memory (2013)

Programming for parallel architectures that do not have a shared address space is extremely difficult due to the need for explicit communication between memories of different compute devices. A heterogeneous system with CPUs and multiple GPUs, or a distributed-memory cluster are examples of such systems. Past works that try to automate data movement for distributed-memory architectures can lead to excessive redundant communication. In this paper, we propose an automatic data movement scheme that minimizes the volume of communication between compute devices in heterogeneous and distributed-memory systems. We show that by partitioning data dependences in a particular non-trivial way, one can generate data movement code that results in the minimum volume for a vast majority of cases. The techniques are applicable to any sequence of affine loop nests and works on top of any choice of loop transformations, parallelization, and computation placement. The data movement code generated minimizes the volume of communication for a particular configuration of these. We use a combination of powerful static analyses relying on the polyhedral compiler framework and lightweight runtime routines they generate, to build a source-to-source transformation tool that automatically generates communication code. We demonstrate that the tool is scalable and leads to substantial gains in efficiency. On a heterogeneous system, the communication volume is reduced by a factor of 11× to 83× over state-of-the-art, translating into a mean execution time speedup of 1.53×. On a distributed-memory cluster, our scheme reduces the communication volume by a factor of 1.4× to 63.5× over state-of-the-art, resulting in a mean speedup of 1.55×. In addition, our scheme yields a mean speedup of 2.19× over hand-optimized UPC codes.
Isabelle Konstantinovic, Montaigne et Plutarque (1990)

Béné Charles. Isabelle Konstantinovic, Montaigne et Plutarque. In: Bulletin de l'Association d'étude sur l'humanisme, la réforme et la renaissance, n°31, 1990. pp. 117-120.
Meals and medicines (2006)

Food and its constituents may have a significant effect on both the rate and extent of absorption of drugs after oral administration. Understanding the effect of meals on medicines enables health professionals to advise patients about taking medicines with or without food. Co-administration of drugs with food generally delays drug absorption. However, meals may have a variable effect on the extent of absorption -depending on the characteristics of the meal, the drug and its formulation. Some drugs have strict guidelines about when they should be taken in relation to meals. Generally, patients should be advised to take their medicines consistently at the same time with respect to meals.
Effect of methenolone enanthate (NSC-64967) in advanced cancer of the breast (1968)

Methenolone enanthate, a synthetic long-acting anabolic steroid, was evaluated by a randomized study in the treatment of advanced carcinoma of the breast in postmenopausal women following the protocol established by the Cooperative Breast Cancer Group. Of 27 patients receiving methenolone enanthate, (48%) had objective improvement. There were no improvements in 13 patients receiving testosterone propionate. The median duration of therapy and the median period of survival from the onset of hormone therapy to death or present living time was greater for the responders to methenolone enanthate than the nonresponders. The unusual high incidence of regression from methenolone enanthate therapy may be due to the massive dose employed, a defect in the method of study being employed in clinical trials, a difference that could occur by chance alone or a difference in the biological nature of the disease in the two groups. Since the difference may indicate that methenolene enanthate is an effective hormone, further studies are warranted.
Color Atlas of Clinical Application of Fiberoptic Bronchoscopy (1990)

Color atlas of clinical application of fiberoptic bronchoscopy , Color atlas of clinical application of fiberoptic bronchoscopy , کتابخانه دانشگاه علوم پزشکی و خدمات درمانی بوشهر
Influence of Off-resonance in myocardial T1-mapping using SSFP based MOLLI method (2013)

Regional variations due to the inability to completely shim the B0-field variation around the heart appear as regional variation in T1, which is artifactual.
Mutations at codon 184 in simian immunodeficiency virus reverse transcriptase confer resistance to the (-) enantiomer of 2',3'-dideoxy-3'-thiacytidine (1997)

Variants of simian immunodeficiency virus (SIV) that display greater than 2,000-fold resistance to the (-) enantiomer of 2',3'-dideoxy-3'-thiacytidine (3TC) were generated through in vitro passage and drug selection. The polymerase regions of several of these resistant viruses were sequenced and were found to share either of two codon alterations at site 184 in reverse transcriptase (ATG to ATA [methionine to isoleucine] and ATG to GTA [methionine to valine]). The biological relevance of these substitutions for 3TC was confirmed by site-directed mutagenesis with the SIVmac239 infectious recombinant clone of SIV.
Interacción entre receptores de glutamato y receptores de nucleótidos en neuronas granulares de cerebelo en cultivo (2010)

ATP elicits Ca2+ transients in cultured cerebellar granule neurons acting through specific ionotropic (P2X) and metabotropic (P2Y) purinergic receptors. In these neurons, application of L-Glutamate (L-Glu) immediately before ATP induced a prolonged reduction of ATP-mediated responses that remains at least 5 minutes after L-Glu wash out. alpha-amino-3-hydro-5-methyl-4-isoxazolpropionic acid (AMPA), N-methyl-D-aspartate (NMDA) and 3,5-dihydroxyphenyl-glycine (DHPG), selective agonists of ionotropic non-NMDA, NMDA and Group I metabotropic glutamate receptors respectively, mimicked Glu-induced attenuating effects. The activity of calcium-calmodulin dependent protein kinase II (CaMKII) seems to be involved, at least at long term, because inhibitors of CaMKII, 1-[N,O-bis(5-isoquinolinesulfonyl)-N-methyl-L-tyrosyl]-4phenylpiperazine (KN-62) and N-[2-[[[3-(4'-chlorophenyl)-2-propenyl]methylamino]methyl]phenyl]-N-(2-hydroxyethyl)-4'-methoxybenzenesulfonamide (KN-93), abolished the inhibitory effect of L-Glu on ATP-mediated responses. However, it is likely that other protein kinases could be involved in the cross-talk process between both groups of receptors at short term. Therefore, these results demonstrate that the activation of glutamate receptors is able to modulate nucleotide responses in cerebellar granule neurons.
Removing the depth-degeneracy in optical frequency domain imaging with frequency shifting (2004)

A novel technique using an acousto-optic frequency shifter in optical frequency domain imaging (OFDI) is presented. The frequency shift eliminates the ambiguity between positive and negative differential delays, effectively doubling the interferometric ranging depth while avoiding image cross-talk. A signal processing algorithm is demonstrated to accommodate nonlinearity in the tuning slope of the wavelength-swept OFDI laser source.
Tissue welding with lasers. (1991)

Over the last several years, several exciting developments have occurred that may facilitate the use of the laser in reconstructive surgery. The goal of future research should be to make the procedure less operator-dependent (dye enhanced or automated welding). Another avenue of research would be to give the operator instantaneous feedback to assess parameters at the weld site to allow modification of the energy delivered. Currently, only color change of the tissue and experience provide the endpoints. With future research into these and other areas, laser welding continues to hold promise to become a useful adjunct in reconstructive surgery.
A bipartite U1 site represses U1A expression by synergizing with PIE to inhibit nuclear polyadenylation (2007)

U1A protein negatively autoregulates itself by polyadenylation inhibition of its own pre-mRNA by binding as two molecules to a 3'UTR-located Polyadenylation Inhibitory Element (PIE). The (U1A)2-PIE complex specifically blocks U1A mRNA biosynthesis by inhibiting polyA tail addition, leading to lower mRNA levels. U1 snRNP bound to a 5'ss-like sequence, which we call a U1 site, in the 3'UTRs of certain papillomaviruses leads to inhibition of viral late gene expression via a similar mechanism. Although such U1 sites can also be artificially used to potently silence reporter and endogenous genes, no naturally occurring U1 sites have been found in eukaryotic genes. Here we identify a conserved U1 site in the human U1A gene that is, unexpectedly, within a bipartite element where the other part represses the U1 site via a base-pairing mechanism. The bipartite element inhibits U1A expression via a synergistic action with the nearby PIE. Unexpectedly, synergy is not based on stabilizing binding of the inhibitory factors to the 3'UTR, but rather is a property of the larger ternary complex. Inhibition targets the biosynthetic step of polyA tail addition rather than altering mRNA stability. This is the first example of a functional U1 site in a cellular gene and of a single gene containing two dissimilar elements that inhibit nuclear polyadenylation. Parallels with other examples where U1 snRNP inhibits expression are discussed. We expect that other cellular genes will harbor functional U1 sites.
Tissue Distribution of (8<sub>-</sub><sup>14</sup>C)<sub>-</sub>Octacosanol in Liver and Muscle of Rats after Serial Administration (1995)

The present study investigates the metabolic disposition of octacosanol in liver and muscle of rats after serial doses administration. Three groups of experimental animals received various doses of (8-14C)-octacosanol (2.0 microCi/dose) orally through a stomach tube. When expressed per organ, the highest amount of radioactivity was found in the liver (9.5% of administered dose), followed by the digestive tracts (8.2%) and the muscle (3.5%) at all doses of administration. The radioactivity in all other tissues examined was insignificant (< 0.9% in each) at any time during this period. The radioactivity in liver disappeared rapidly after 2-dose administration, even when the doses were increased. In contrast, the muscle seemed to be able to store a considerable amount of octacosanol in response to doses of administration. In case of 9-dose serial administration, after 3 and 9 days the accumulation of radioactivity in muscle was higher than that of the liver, possibly due to slow elimination of radioactivity from muscle. By the time when radioactivity in liver and muscle was low (after 6 and 10 doses), the radioactivity of octacosanol in plasma reached a maximum, particularly after administration of 6 doses. The plasma concentration and the fecal excretion of the radioactivity of octacosanol reached a maximum at the third day after the oral 6 doses, which reflected not only the saturation of radioactivity uptake by liver and muscle but also the metabolism and excretion of octacosanol with time at the same period. The results are discussed in the light of the role of octacosanol in increasing muscle endurance in exercise.
New Amines for CO2 Capture. I. Mechanisms of Amine Degradation in the Presence of CO2 (2009)

Degradation of 12 different amines with CO2 was evaluated in 100 mL stainless steel batch reactors for 15 days at 140 °C using a 4 mol·kg−1 amine solution and a CO2 pressure of 2 MPa. At the end of the run, most of degradation products were identified by gas chromatography (GC)/mass spectrometry (MS); amounts of starting amine and its degradation products were determined with a quantitative GC method. This work compares the degradation of ethanolamines (including MEA) having one or two hydroxyl groups with the degradation of ethylenediamines. They were chosen to establish relationships between amine structure and stability properties: replacement of one alcohol function by one amine function, effect of amine function nature, impact of steric hindrance and cyclic structure. Significant differences were observed. The main degradation products are described, and some mechanisms are proposed to explain their formation.
Simply Connected Manifolds with no Conjugate Points Which are Flat Outside a Compact Set (1991)

In this note we improve a previous result to show that euclidean $n$-space $(n \geq 3)$ is the only simply connected manifold without conjugate points which is flat outside a compact set.
Characterization of the phosphatase activity of a baculovirus-expressed calcineurin A isoform. (1992)

Calcineurin A was purified by calmodulin-Sepharose affinity chromatography from Sf9 cells infected with recombinant baculovirus containing the cDNA of a rat calcineurin A isoform. The Sf9-expressed calcineurin A has a low basal phosphatase activity in the presence of EDTA (0.9 nmol/min/mg) which is stimulated 3-5-fold by Mn2+. Calmodulin increased the Mn2+ stimulated activity 3-5-fold. Bovine brain calcineurin B increased the A subunit activity 10-15-fold, and calmodulin further stimulated the activity of reconstituted A and B subunits 10-15-fold (644 nmol/min/mg). The Km of calcineurin A for 32P-RII pep (a peptide substrate (DLDVPIPGRFDRRVSVAAE) for CaN), was 111 microM with or without calmodulin, and calmodulin increased the Vmax about 4-fold. The Km of reconstituted calcineurin A plus B for 32P-RII pep was 20 microM, and calmodulin increased the Vmax 18-fold without affecting the Km. CaN A467-492, a synthetic autoinhibitory peptide (ITSFEEAKGLDRINERMPPRRDAMP) from calcineurin, inhibited the Mn2+/calmodulin-stimulated activities of the reconstituted enzyme and the A subunit with IC50's of 25 microM and 90 microM, respectively. The reconstitution of the phosphatase activity of an expressed isoform of calcineurin A by purified B subunit and calmodulin may facilitate comparative studies of the regulation of calcineurin A activity by the B subunit and calmodulin.
Iterating the sum-of-divisors function (1995)

Let $\\sigma^0(n) = n$ and $\\sigma^m(n) = \\sigma(\\sigma^{m-1}(n))$, where\n$m\\ge1$ and $\\sigma$ is the sum-of-divisors function. We say that $n$\nis $(m,k)$-perfect if $\\sigma^m(n) = kn$. We have tabulated all\n$(2,k)$-perfect numbers up to $10^9$ and all $(3,k)$- and\n$(4,k)$-perfect numbers up to $2\\cdot10^8$. These tables have\nsuggested several conjectures, some of which we prove here. We ask in\nparticular: For any fixed $m\\ge1$, are there infinitely many\n$(m,k)$-perfect numbers? Is every positive integer $(m,k)$-perfect,\nfor sufficiently large $m\\ge1$? In this connection, we have obtained\nthe smallest value of $m$ such that $n$ is $(m,k)$-perfect, for $1\\le\nn\\le1000$. We also address questions concerning the limiting behaviour\nof $\\sigma^{m+1}(n)/\\sigma^m(n)$ and $(\\sigma^m(n))^{1/m}$, as\n$m\\to\\infty$.
Very long-chain fatty acid accumulation causes lipotoxic response via 5-lipoxygenase in cerebral adrenoleukodystrophy (2010)

Childhood adrenoleukodystrophy (cALD) is a metabolic disorder in which very long-chain fatty acids (VLCFA) accumulate due to ALD protein gene defects, ultimately leading to lipotoxicity-induced neuroinflammatory demyelinating disease. Therefore, we examined VLCFA-mediated alterations in the metabolism of lipoxidative enzymes and inflammatory mediators in the cALD brain. 5-Lipoxygenase (5-LOX)-derived leukotrienes were significantly elevated in all the areas of white matter in the cALD brain. Unlike cyclooxygenase-2 expression, which was moderately high only in the plaque area, expression of 5-LOX and cytosolic phospholipase A2 was prominent in all the areas. This lipoxidative burden in the cALD brain was further shown by reduced levels of glutathione and enhanced expression of heat shock protein-70/manganese superoxide dismutase. These pathological observations were confirmed through in vitro mechanistic investigation. After increasing VLCFA through silencing Abcd1+Abcd2 in mouse primary astrocytes, enhanced expression of 5-LOX was observed, and this increased expression was blocked by treatment with monoenoic fatty acids. These results link the previously observed accumulation of VLCFA in cALD to the 5-LOX enzyme pathway. A similar increase in 5-LOX expression in astrocytes was also detected following treatment with exogenous VLCFA (C26:0). In sum, through 5-LOX activation, VLCFA accumulation causes a lipotoxic response consistent with cALD brain pathology.
Hepatocyte Growth Factor Gene Therapy for Pancreatic Islets in Diabetes: Reducing the Minimal Islet Transplant Mass Required in a Glucocorticoid-Free Rat Model of Allogeneic Portal Vein Islet Transplantation (2003)

Islet transplantation for diabetes is limited by the availability of human islet donors. Hepatocyte growth factor (HGF) is a potent beta-cell mitogen and survival factor and improves islet transplant outcomes in a murine model. However, the murine model employs renal subcapsular transplant and immunodeficient mice, features not representative of human islet transplantation protocols. Therefore, we have developed a more rigorous, marginal-mass rat islet transplant model that more closely resembles human islet transplantation protocols: islet donors are allogeneic Lewis islets; recipients are normal Sprague Dawley rats; islets are delivered intraportally; and immunosuppression is accomplished using the same immunosuppressants employed by the Edmonton group. We demonstrate that 1) surprisingly, the Edmonton immunosuppression regimen induces marked insulin resistance and beta-cell toxicity in rats, 2) adenovirus does not adversely affect islet transplant outcomes, 3) the Edmonton immunosuppressants may delay or block rejection of adenovirally transduced islets, and more importantly, 4) pretransplant islet adenoviral gene therapy with HGF markedly improves islet transplant outcomes, 5) this enhanced function persists for months, and 6) HGF enhances islet function and survival even in the setting of immunosuppressant-induced insulin resistance and beta-cell toxicity. This approach may enhance islet transplantation outcomes in humans.
Clinical Aspects of Gastrointestinal Food Allergy in Childhood (2003)

Gastrointestinal food allergies are a spectrum of disorders that result from adverse immune responses to dietary antigens. The named disorders include immediate gastrointestinal hypersensitivity (anaphylaxis), oral allergy syndrome, allergic eosinophilic esophagitis, gastritis, and gastroenterocolitis; dietary protein enterocolitis, proctitis, and enteropathy; and celiac disease. Additional disorders sometimes attributed to food allergy include colic, gastroesophageal reflux, and constipation. The pediatrician faces several challenges in dealing with these disorders because diagnosis requires differentiating allergic disorders from many other causes of similar symptoms, and therapy requires identification of causal foods, application of therapeutic diets and/or medications, and monitoring for resolution of these disorders. This review catalogs the spectrum of gastrointestinal food allergies that affect children and provides a framework for a rational approach to diagnosis and management.