gebhart/patrepeval huggingface dataset:
Multiobjective evolutionary computation for supersonic wing-shape optimization (2000)

This paper discusses the design optimization of a wing for supersonic transport (SST) using a multiple-objective genetic algorithm (MOGA). Three objective functions are used to minimize the drag for supersonic cruise, the drag for transonic cruise, and the bending moment at the wing root for supersonic cruise. The wing shape is defined by 66 design variables. A Euler flow code is used to evaluate supersonic performance, and a potential flow code is used to evaluate transonic performance. To reduce the total computational time, flow calculations are parallelized on an NEC SX-4 computer using 32 processing elements. The detailed analysis of the resulting Pareto front suggests a renewed interest in the arrow wing planform for the supersonic wing.
STAT4 Is a Critical Mediator of Early Innate Immune Responses against Pulmonary Klebsiella Infection (2004)

Bacterial pneumonia is a leading cause of morbidity and mortality in the U.S. An effective innate immune response is critical for the clearance of bacteria from the lungs. IL-12, a key T1 cytokine in innate immunity, signals through STAT4. Thus, understanding how STAT4 mediates pulmonary immune responses against bacterial pathogens will have important implications for the development of rational immunotherapy targeted at augmenting innate immunity. We intratracheally administered Klebsiella pneumoniae to wild-type BALB/c and STAT4 knockout (STAT4-/-) mice. Compared with wild-type controls, STAT4-/- mice had decreased survival following intratracheal Klebsiella administration, which was associated with a higher lung and blood bacterial burden. STAT4-/- animals also displayed impaired pulmonary IFN-gamma production and decreased levels of proinflammatory cytokines, including the ELR- CXC chemokines IFN-gamma-inducible protein-10 and monokine induced by IFN-gamma. Although total lung leukocyte populations were similar between STAT4-/- and wild-type animals following infection, alveolar macrophages isolated from infected STAT4-/- mice had decreased production of proinflammatory cytokines, including IFN-gamma, compared with infected wild-type mice. The intrapulmonary overexpression of IFN-gamma concomitant with the systemic administration of IFN-gamma partially reversed the immune deficits observed in STAT4-/- mice, resulting in improved bacterial clearance from the blood. Collectively, these studies demonstrate that STAT4 is required for the generation of an effective innate host defense against bacterial pathogens of the lung.
The Raf-1 pathway: a molecular target for treatment of select neuroendocrine tumors? (2006)

Neuroendocrine (NE) tumors such as medullary thyroid cancer, carcinoid, small cell lung cancer and pheochromocytoma are metastatic in nature, and secrete biogenic amines and hormones. In this review, we will discuss the possibility that activation of the Ras/Raf signaling pathway may be a therapeutic target for patients with select NE tumors. In-vitro activation of Raf-1 in NE tumors either by expression of the ectopic catalytic domain of Raf-1 or by a pharmacologic drug, ZM336372, resulted in growth inhibition. In addition, activation of the Ras/Raf pathway led to a significant reduction in NE markers such as serotonin, chromogranin A and calcitonin. These data support development of Raf-1-activating compounds for treatment of patients with NE tumors of selective subtypes.
Creatine Kinase Activity in Postnatal Rat Brain Development and in Cultured Neurons, Astrocytes, and Oligodendrocytes (1991)

The development and distribution of cytosolic creatine kinase (CK) activity was studied in rat brain and in cell culture. The activity of CK in whole brain increased almost fivefold during the period from birth to day 40 when adult levels of 18-19 U/mg of protein were attained. The distribution of CK activity was examined in dissected regions of the adult brain and was nonuniform; the cerebellum, the striatum, and the pyramidal tracts contained significantly higher CK activity than did whole brain. The cellular compartmentation of CK was investigated using primary cultures of purified neurons, astrocytes, and oligodendrocytes. The CK activity in neurons increased fourfold greater than that measured at the time of isolation to 4 U/mg of protein. The CK activity in astrocytes cultured for 20 days was 3.5 U/mg of protein and was 1.5-fold greater than that measured at the time of isolation. In contrast, the CK activity in cultured oligodendrocytes (day 20) was three- to fourfold higher than that determined in astrocytes and almost sevenfold higher than the activity measured at the time the cells were isolated. The high levels of CK in cultured oligodendrocytes suggest a role for this enzyme in oligodendrocyte function and/or myelinogenesis.
A powerful GABAB receptor-mediated inhibition of GABAergic neurons in arcuate nucleus (1999)

We combined histofluorescence with in situ hybridization to identify GABAergic neurons in the arcuate nucleus (ARC) following electrophysiological recordings, using GAD65 as a marker. Intracellular recordings were made in hypothalamic slices prepared from ovariectomized guinea pigs. Over 90% of ARC neurons tested with the GABA(B) receptor agonist baclofen responded with a membrane hyperpolarization or an outward current. The hyperpolarization was dose-dependent, and the GABA(B) receptor antagonist CGP 35,348 produced a rightward shift in the agonist dose-response curve. Agonist potency was lower, and the efficacy greater, in GAD-positive neurons. The use of this novel technique for identifying GABAergic neurons thus reveals differences in the pharmacodynamics of GABA(B) receptor activation GABAergic and non-GABAergic ARC neurons.
Discovery of recurrent t(6;7)(p25.3;q32.3) translocations in ALK-negative anaplastic large cell lymphomas by massively parallel genomic sequencing (2010)

The genetics of peripheral T-cell lymphomas are poorly understood. The most well-characterized abnormalities are translocations involving ALK, occurring in approximately half of anaplastic large cell lymphomas (ALCLs). To gain insight into the genetics of ALCLs lacking ALK translocations, we combined mate-pair DNA library construction, massively parallel ("Next Generation") sequencing, and a novel bioinformatic algorithm. We identified a balanced translocation disrupting the DUSP22 phosphatase gene on 6p25.3 and adjoining the FRA7H fragile site on 7q32.3 in a systemic ALK-negative ALCL. Using fluorescence in situ hybridization, we demonstrated that the t(6;7)(p25.3;q32.3) was recurrent in ALK-negative ALCLs. Furthermore, t(6;7)(p25.3;q32.3) was associated with down-regulation of DUSP22 and up-regulation of MIR29 microRNAs on 7q32.3. These findings represent the first recurrent translocation reported in ALK-negative ALCL and highlight the utility of massively parallel genomic sequencing to discover novel translocations in lymphoma and other cancers.
Protection against H5N1 Influenza Virus Induced by Matrix-M Adjuvanted Seasonal Virosomal Vaccine in Mice Requires Both Antibodies and T Cells (2015)

It remains important to develop the next generation of influenza vaccines that can provide protection against vaccine mismatched strains and to be prepared for potential pandemic outbreaks. To achieve this, the understanding of the immunological parameters that mediate such broad protection is crucial.
Myelin Basic Protein–specific T Helper 2 (Th2) Cells Cause Experimental Autoimmune Encephalomyelitis in Immunodeficient Hosts Rather than Protect Them from the Disease (1997)

Chronic inflammatory autoimmune diseases such as multiple sclerosis, diabetes, and rheumatoid arthritis are caused by CD4(+) Th1 cells. Because Th2 cells antagonize Th1 cell functions in several ways, it is believed that immune deviation towards Th2 can prevent or cure autoimmune diseases. Experimental autoimmune encephalomyelitis (EAE) is a demyelinating disease used as a model for multiple sclerosis. Using an adoptive transfer system we assessed the role of Th1 and Th2 cells in EAE. In vitro generated Th1 and Th2 cells from myelin basic protein (MBP)-specific TCR transgenic mice were transferred into normal and immunodeficient mice. Th1 cells caused EAE in all recipients after a brief preclinical phase. Surprisingly, Th2 cells also caused EAE in RAG-1 KO mice and in alphabeta T cell-deficient mice, albeit after a longer preclinical phase. Normal or gammadelta T cell-deficient mice were resistant to EAE induced by Th2 cells. The histopathological features of this disease resembled those of an allergic process. In addition, disease induction by Th1 cells was not altered by coadmininstration of Th2 cells in any of the recipients. These findings indicate that MBP-specific Th2 cells have the potential to induce EAE and that the disease induced by previously activated Th1 cells cannot be prevented by normal lymphocytes nor by previously activated Th2 cells.
Sequences containing the second-intron enhancer are essential for transcription of the human apolipoprotein B gene in the livers of transgenic mice. (1994)

To identify DNA sequence elements from the human apolipoprotein B (apoB) gene required for high-level, correct tissue-specific expression in transgenic mice, we made several constructs that included one or more of the key regulatory elements that were previously characterized with cultured liver-derived and intestine-derived cell lines. Our data show that the apoB promoter alone (-898 to +121) is not sufficient to direct transcription in transgenic mice. An enhancer located in the second intron is absolutely required to specify transcription by the homologous apoB promoter in the livers of transgenic mice; this enhancer does not direct transcription in the small intestines. Thus, the elements controlling transcriptional activation of the apoB gene in the liver and the intestine in vivo are distinct and separable. Analysis of the DNase I hypersensitivity of the integrated human transgenes in various lines of expressing and nonexpressing mice suggests that the formation of DH4, a strong hypersensitive site in intron 2, may be a prerequisite for hepatic expression of the apoB gene. Nuclear matrix association regions (MARs) of the apoB gene may play a role in transgene expression. Constructs including MAR sequences displayed higher levels of expression than those lacking them. However, these MARs did not completely insulate the associated transgenes from position effects.
Measuring absorption coefficients in small volumes of highly scattering media: source-detector separations for which path lengths do not depend on scattering properties (1997)

The noninvasive measurement of variations in absorption that are due to changes in concentrations of biochemically relevant compounds in tissue is important in many clinical settings. One problem with such measurements is that the path length traveled by the collected light through the tissue depends on the scattering properties of the tissue. We demonstrate, using both Monte Carlo simulations and experimental measurements, that for an appropriate separation between light-delivery and light-collection fibers the path length of the collected photons does not depend on scattering parameters for the range of parameters typically found in tissue. This is important for developing rapid, noninvasive, and inexpensive methods for measuring absorption changes in tissue.
Human red cell antigens (1987)

The minor red cell sialoglycoproteins--beta and gamma (also known as glycophorin C)--are believed to be important to the structural integrity of red cells. The absence of sialoglycoproteins alpha and delta, as seen in En(a-) and S-s-U- cells, respectively, results in cells with normal morphology, but the absence of sialoglycoproteins beta and gamma is associated with elliptocytosis. However, cells that lack Gerbich (Ge) antigens but have an abnormal sialoglycoprotein reactive with antibodies to beta have normal morphology. The authors used a monoclonal antibody specific for beta to explore the nature of this abnormal sialoglycoprotein and its interactions with other membrane proteins. The beta-like sialoglycoprotein of Ge-Yus- red cells appears to react poorly with some antibodies due to steric hindrance by other molecules of sites normally available to immune agglutinins. This steric hindrance is not due to a single interaction with either sialoglycoprotein alpha or delta or band 3. Furthermore, steric hindrance by other molecules does not account for the lack of Ge antigens on these cells.
Inactivation of the gbpA Gene of Streptococcus mutans Alters Structural and Functional Aspects of Plaque Biofilm Which Are Compensated by Recombination of the gtfB and gtfC Genes (1999)

Inactivation of the gbpA gene of Streptococcus mutans increases virulence in a gnotobiotic rat model and also promotes in vivo accumulation of organisms in which gtfB and gtfC have recombined to reduce virulence (K. R. O. Hazlett, S. M. Michalek, and J. A. Banas, Infect. Immun. 66:2180-2185, 1998). These changes in virulence were hypothesized to result from changes in plaque structure. We have utilized an in vitro plaque model to test the hypothesis that the absence of GbpA alters S. mutans plaque structure and that the presence of gtfBC recombinant organisms within a gbpA background restores a wild-type (wt)-like plaque structure. When grown in the presence of sucrose within hydroxyapatite-coated wells, the wt S. mutans plaque consisted primarily of large aggregates which did not completely coat the hydroxyapatite surface, whereas the gbpA mutant plaque consisted of a uniform layer of smaller aggregates which almost entirely coated the hydroxyapatite. If 25% of the gbpA mutants used as inoculum were also gtfBC recombinants (gbpA/25%gtfBC), a wt-like plaque was formed. These changes in plaque structure correlated with differences in susceptibility to ampicillin; gbpA plaque organisms were more susceptible than organisms in either the wt or gbpA/25%gtfBC plaques. These data allow the conclusion that GbpA contributes to S. mutans plaque biofilm development. Since the changes in plaque structure detailed in this report correlate well with previously observed changes in virulence, it seems likely that S. mutans biofilm structure influences virulence. A potential model for this influence, which can account for the gtfBC recombination compensating gbpA inactivation, is that the ratio of glucan to glucan-binding protein is a critical factor in plaque development.
Indexing methods for approximate string matching (2001)

Indexing for approximate text searching is a novel problem receiving much attention because of its applications in signal processing, computational biology and text retrieval, to name a few. We classify most indexing methods in a taxonomy that helps understand their essential features. We show that the existing methods, rather than completely dierent as they are regarded, form a range of solutions whose optimum is usually somewhere in between. 1
Wavelength shifting and amplification of optical pulses through cascaded second-order processes in periodically poled lithium niobate (1998)

We investigate the efficiency of wavelength shifting (generation of a pulse at the wavelength λp−Δλ from a signal at λp+Δλ under the action of a pump at λp) and parametric amplification through a cascaded second-order process in a periodically poled lithium niobate crystal. Our results show that, in a 19-mm-long sample, at λp=1.8 μm and Δλ as large as 60 nm, wavelength shifting with unit gain can be obtained with a pump intensity of 6 MW/cm2, while amplification by a factor 10 requires 18 MW/cm2.
Absence of rhodamine 123‐photochemotoxicity in human tumor xenografts (1993)

Rhodamine 123 (R123)-photochemotoxicity was assessed in BALB/c nude mice bearing a xenografted human squamous cell carcinoma at various power densities and wavelengths and a given incident fluence of 150 Joules/cm2. One hour before light delivery, 1 mg R123/kg was injected i.p. in 20 animals. Surface irradiance was performed on the tumor and an equal size hind leg area of 40 animals. Three groups of 10 animals were treated at 514.5 nm and 0.1 W/cm2, 1 W/cm2, and 30 W/cm2, and one at 488 nm and 30 W/cm2. In each group, five animals received R123. The R123 concentration was measured in the tumor (0.023 +/- 0.007 micrograms/g) and tumor-free tissue (0.023 +/- 0.008 micrograms/g) in three additional animals by high performance liquid chromatography 1 hour after R123-administration. Histologic assessment 72 hours after light delivery revealed no tissue damage at nonthermal power densities, either in the tumor or in the tumor-free tissue, irrespective of R123-administration. At 30 W/cm2, neither in the tumor nor in tumor-free tissues was there any significant difference in the depth of necrosis, irrespective of R123-administration and the wavelength applied. Our results question the validity of R123 as a photosensitizer, at least in this rodent tumor model.
Niementowski 4-Ketoquinazoline Synthesis. Part I. Modification and Mechanism (1965)

The Niementowski 4-ketoquinazoline synthesis has been modified to improve its applicability. Evidence for the course of the reaction has been provided and mechanism proposed.
Production & Characterization of a Unique Dextran from an Indigenous Leuconostoc mesenteroides CMG713 (2008)

On the basis of high enzyme activity a newly isolated strain of L. mesenteroides CMG713 was selected for dextran production. For maximum yield of dextran, effects of various parameters such as pH, temperature, sucrose concentration and incubation period were studied. L. mesenteroides CMG713 produced maximum dextran after 20 hours of incubation at 30 masculineC with 15% sucrose at pH 7.0. The molecular mass distribution of dextran produced by this strain showed that its molecular mass was about 2.0 million Da. Dextran analysis by (13)C-NMR spectrometry showed no signals corresponding to any other linkages except alpha-(1-->6) glycosidic linkage in the main chain, which has not been reported before. Physico-chemical properties of this unique dextran were also studied. These optimised conditions could be used for the commercial production of this unique high molecular weight dextran, which have significant industrial perspectives.
Three-dimensional ultrasound imaging of the prostate (1998)

Prostate cancer is the most commonly diagnosed cancer in men in North America.Since its introduction in 1971, transrectal ultrasound (TRUS) has evolved into one of the primary tools for the evaluation of prostate disease.However, with conventional TRUS, diagnosticians must mentally integrate a series of 2D images in order to develop an impression of the 30 anatomy, and the accurate and precise estimation of prostate volume is difficult.Moreover, an examination takes 10-20 minutes, often resulting in patient discomfort.We propose using 3D TRUS to overcome these problerns.In this thesis, we describe a 3D ultrasound imaging system, analyze the distortion in its images due to miscalibration, and study its performance in estimating prostate volume.Our system consists of three elements: (i) a conventional ultrasound machine and TRUS probe; (ii) a custom-built assembly for rotating the probe under microcornputer control; and, (iii) a microcomputer with an 8-bit video frame grabber.A typical scan of 200 2D B-mode images takes 13 seconds, so that the entire examination takes under 5 minutes.These images can then be rapidly reconstructed into a 3D image using an algorithm we describe, and interactively displayed using standard software.Also, we describe procedures for accurately calibrating the reconstruction parameters, so that distortions in the shape, length, area, and volume of the 3D image of an object are al1 less than 1 %.We also show that manual planimetry of 3D TRUS images can be used to estimate prostate volumes in vitro with 2.6% accuracy and 2.5% precision; and in vivo with 5.1% intra-observer variability and 11.4% inter-observer variability.By cornparison, with the height-width-length method (Volume = R 16 H WL) with conventional 2D TRUS images, in vivo estimates had 11.5% intra-observer variability and 1 3.5% inter-observer variability.Thus, 3D TRUS overcomes the limitations of 20 TRUS, and has great potential as a tool for the diagnosis, study, and management of prostate disease.
Cardiac Studies in Patients Treated with Depsipeptide, FK228, in a Phase II Trial for T-Cell Lymphoma (2006)

The data obtained in this study show that the administration of depsipeptide is not associated with myocardial damage or impaired cardiac function. The potential effect of heart rate-corrected QT interval prolongation remains under study.
AUTOMATED COLORIMETRIC IMMUNOASSAY MICROSYSTEM FOR CLINICAL DIAGNOSTICS (2010)

An automated colorimetric immunoassay microsystem has been developed for the application of clinical diagnostics. The system can perform sandwich immunoassay around 1 hour automatically. The system consists of a motorized syringe pump, a motorized valve, and a microfluidic chip. The detection method is based on colorimetric immunoassay, which utilizes gold nanoparticle indication and gold enhancement amplification. The immunoassay result can be represented by color intensity and observed by a regular camera or even the naked eye in the microfluidic chip. An example of the sandwich immunoassay has been demonstrated using this automated microsystem. The analyte concentration ranging from 0.5 to 160 ng/ml can be detected quantitatively, and the detection limit is 0.5 ng/ml. Since the detection method is simple, low cost, and can be miniaturized, the proposed system has the potential to be developed to clinical diagnostic equipment.
Contribution of sensitized P2X receptors in inflamed tissue to the mechanical hypersensitivity revealed by phosphorylated ERK in DRG neurons (2004)

The mechanism of mechanical hyperalgesia in inflammation might involve a 'mechanochemical' process whereby stretch evokes the release of adenosine 5'-triphosphate (ATP) from the damaged tissue that then excites nearby primary sensory nerve terminals. In the present study, phosphorylated extracellular signal-regulated protein kinase (pERK) immunoreactivity was used as a marker indicating functional activation of primary afferent neurons to examine the P2X receptor-mediated noxious response in DRG neurons in a rat model of peripheral inflammation. We found that very few pERK-labeled DRG neurons were detected in normal rats after alpha, beta methylene-ATP (alphabetame-ATP) intraplantar injection. However, a number of DRG neurons were labeled for pERK after alphabetame-ATP injection to the complete Freund's adjuvant (CFA) induced inflamed paw. Seventy-three percent of pERK-labeled DRG neurons co-expressed the P2X3 receptor. After mechanical noxious stimulation to the hind paw of CFA-inflamed rats, we found many more pERK-labeled neurons compared to those in the normal rats. Administration of the P2X3 receptor antagonists, pyridoxalphosphate-6-azophenyl-2',4'-disulfonic acid or 2'- (or 3')-O-(trinitrophenyl)adenosine 5'-triphosphate (TNP-ATP), significantly decreased the mechanical stimulation-evoked pERK labeling in CFA-inflamed rats, but not in normal rats. We also found the recruitment of neurons with myelinated A fibers labeled for pERK in CFA-inflamed rats, which was reversed by P2X3 receptor antagonists. Moreover, TNP-ATP dose dependently reduced the mechanical hypersensitivity of CFA rats. These data suggest that the P2X receptors in primary afferent neurons increase their activity with enhanced sensitivity of the intracellular ERK signaling pathway during inflammation and then contribute to the hypersensitivity to mechanical noxious stimulation in the inflammatory state.