gebhart/patrepeval huggingface dataset:
Extraction of spectral peak parameters using a short-time Fourier transform modeling and no sidelobe windows (2002)

A new method which improves the estimation of frequency, amplitude and phase of the partials of a sound is presented. It allows the reduction of the analysis-window size from four periods to two periods. It therefore gives better accuracy in parameter determination, and has proved to remain efficient at low signal-to-noise ratios. The basic idea consists of using a parametric modeling of the short-time Fourier transform. The method alternately estimates the complex amplitudes and the frequencies starting from the result of the classical analysis method. It uses the least-square procedure and a first-order limited expansion of the model around previous estimations. This method leads us to design new windows which do not have any sidelobes in order to help the convergence. Finally an analysis algorithm which has been built according to the observed behavior of the method for various kinds of sound is presented.
Cytokine production by mature and immature thymocytes (1991)

We have studied the ability of subpopulations of activated thymocytes to produce four cytokines (IL-2, IL-4, IFN-gamma and TNF-alpha) which are believed to play roles in T cell development. Supernatants from various thymocyte subsets activated with calcium ionophore and PMA were tested for these cytokines. All CD3hi thymocyte subsets (CD4+8-, CD4-8- and CD4-8+) produced high titers of these four cytokines except CD3+4-8+ thymocytes, which did not produce IL-4. In contrast, CD4+8+ thymocytes did not produce any detectable cytokines. CD3-4-8- thymocytes produced IL-2, IFN-gamma, and TNF-alpha (but not IL-4) when activated by calcium ionophore + PMA and IL-1. We then separated CD3-4-8- thymocytes into IL-2R+ and IL-2R-. CD3-4-8-IL-2R+ thymocytes only produced small amounts of IL-2 when activated with calcium ionophore + PMA + IL-1, whereas CD3-4-8-IL-2R- thymocytes did not require IL-1 to produce IL-2, IFN-gamma, and TNF-alpha. Finally, CD4-8+3- thymocytes (an immature population believed to be an intermediate between CD3-4-8- and CD4+8+ thymocytes) only produced marginally detectable levels of IL-2 upon stimulation with calcium ionophore, PMA, and the addition of IL-1 did not result in increased levels of cytokine production. These observations indicate discrete patterns of cytokine production by the subsets studied and suggest specific controls of cytokine gene expression during T cell development.
Rapid evolution of the human gut virome (2013)

Humans are colonized by immense populations of viruses, which metagenomic analysis shows are mostly unique to each individual. To investigate the origin and evolution of the human gut virome, we analyzed the viral community of one adult individual over 2.5 y by extremely deep metagenomic sequencing (56 billion bases of purified viral sequence from 24 longitudinal fecal samples). After assembly, 478 well-determined contigs could be identified, which are inferred to correspond mostly to previously unstudied bacteriophage genomes. Fully 80% of these types persisted throughout the duration of the 2.5-y study, indicating long-term global stability. Mechanisms of base substitution, rates of accumulation, and the amount of variation varied among viral types. Temperate phages showed relatively lower mutation rates, consistent with replication by accurate bacterial DNA polymerases in the integrated prophage state. In contrast, Microviridae, which are lytic bacteriophages with single-stranded circular DNA genomes, showed high substitution rates (>10(-5) per nucleotide each day), so that sequence divergence over the 2.5-y period studied approached values sufficient to distinguish new viral species. Longitudinal changes also were associated with diversity-generating retroelements and virus-encoded Clustered Regularly Interspaced Short Palindromic Repeats arrays. We infer that the extreme interpersonal diversity of human gut viruses derives from two sources, persistence of a small portion of the global virome within the gut of each individual and rapid evolution of some long-term virome members.
Effect of Wood Powder Diameter on the Combustion Characteristics of A-heavy Oil and Wood Powder Cofiring (2006)

A-heavy oil and wood powder are cofired to reduce the oil consumption and cut down the harmful exhaust emission. It is found that the technique can be used to decrease the CO concentration of the exhaust gas and the particulate matter produced by A-heavy oil. However, the production cost of wood powder is related to the diameter. The wood powder of small diameter consumes more production energy while the wood powder of large diameter leads to low combustion efficiency even with heavy exhaust emission. The objective of this paper is to evaluate the optimum wood powder for the cofiring technique. 3 kinds of wood powder of different diameter are investigated, and the effect of wood powder diameter on combustion characteristics of the cofiring is discussed.
Human IL-13 production is negatively influenced by CD3 engagement. Enhancement of IL-13 production by cyclosporin A (1996)

IL-13, a T cell-derived cytokine, shares many of its biologic activities with the Th2 cytokine IL-4, including induction of a class switch to IgE and anti-inflammatory properties. Its potential impact on development of Th2 responses makes it interesting to determine how the production of IL-13 is regulated and which cell types produce IL-13. In this work, we show that IL-13 is produced optimally by T cells when stimulated with a combination of anti-CD28 and PMA. Unexpectedly, additional ligation of the TCR complex with Abs to CD3 caused an approximately fivefold inhibition of IL-13 production. Moreover, this inhibition could be reversed by cyclosporin A (CsA). The effect of CsA did not depend on the presence of PMA; upon CD3 and CD28 stimulation, CsA equally enhanced IL-13 production. Both naive and memory CD4+ T cells and CD8+ T cells produced IL-13, and production in all cell types could be enhanced by CsA. In contrast to IL-13, IL-4 production was observed mainly in CD4+ memory cells, required costimulation through CD3, and was inhibited by CsA. The unusual regulation and relative abundance of IL-13 make it an important candidate to be controlled tightly by dose and type of TCR ligands. CsA is used widely to inhibit T cell function. The finding that IL-13 production is enhanced instead of diminished in the presence of CsA may explain the Th2-inducing effects of CsA in vivo.
Progress on the sector magnets for the RIKEN SRC (2001)

Significant changes have been made to the design of the sector magnet of the RIKEN SRC (superconducting ring cyclotron). The changes are: (1) the cyclotron is almost completely covered with soft-iron slabs of 0.8 m in thickness, except in the central region, to reduce stray fields, and (2) the cold-pole scheme has been replaced with a warm-pole scheme. Owing to this magnetic shield, the stray fields, magneto-motive forces, electromagnetic forces, and so on are significantly reduced. New design of the real sector magnet is described in this report.
Selective amino acid restriction targets mitochondria to induce apoptosis of androgen‐independent prostate cancer cells (2006)

Relative specific amino acid dependency is one of the metabolic abnormalities of cancer cells, and restriction of specific amino acids induces apoptosis of prostate cancer cells. This study shows that restriction of tyrosine and phenylalanine (Tyr/Phe), glutamine (Gln), or methionine (Met), modulates Raf and Akt survival pathways and affects the function of mitochondria in DU145 and PC3, in vitro. These three restrictions inhibit energy production (ATP synthesis) and induce generation of reactive oxygen species (ROS). Restriction of Tyr/Phe or Met in DU145 and Met in PC3 reduces mitochondrial membrane potential (DeltaPsim) and induces caspase-dependent and -independent apoptosis. In DU145, Tyr/Phe or Met restriction reduces activity of Akt, mitochondrial distribution of phosphorylated Raf and apoptosis inducing factor (AIF), and increases mitochondrial distribution of Bak. Mitochondrial Bcl-XL is increased in Tyr/Phe-restricted but decreased in Met-restricted cells. Under Tyr/Phe or Met restriction, reduced mitochondrial Raf does not inactivate the pro-apoptotic function of Bak. Tyr/Phe restriction also inhibits Bcl-2 and Met restriction inhibits Bcl-XL in mitochondria. These comprehensive actions damage the integrity of the mitochondria and induce apoptosis of DU145. In PC3, apoptosis induced by Met restriction was not associated with alterations in intracellular distribution of Raf, Bcl-2 family proteins, or AIF. All of the amino acid restrictions inhibited Akt activity in this cell line. We conclude that specific amino acid restriction differentially interferes with homeostasis/balance between the Raf and Akt survival pathways and with the interaction of Raf and Bcl-2 family proteins in mitochondria to induce apoptosis of DU145 and PC3 cells.
ADD1/SREBP1 promotes adipocyte differentiation and gene expression linked to fatty acid metabolism. (1996)

Adipocyte determination and differentiation-dependent factor 1 (ADD1) is a member of the basic helix-loop-helix leucine zipper (bHLH-LZ) family of transcription factors that binds to two distinct DNA sequences and has been associated with both adipocyte development and cholesterol homeostasis (where it has been termed SREBP1). To investigate the biological role of ADD1, we expressed wild-type and dominant negative forms of this protein with retroviral vectors in preadipocytes and nonadipogenic cells. A dominant-negative form of ADD1 with a point mutation in the DNA-binding domain sharply represses the differentiation of 3T3-L1 cells as observed morphologically or by the expression of adipocyte-specific mRNAs. When NIH-3T3 cells ectopically expressing ADD1 are cultured under hormonal conditions not favoring differentiation, they do not overtly differentiate but still activate expression of mRNAs for fatty acid synthase (FAS) and lipoprotein lipase (LPL), two key genes that regulate fatty acid metabolism. Under culture conditions permissive for differentiation including a PPAR activator, 15%-20% of the cells expressing ADD1 undergo adipogenesis while 2%-3% of cells containing a control vector differentiate. Simultaneous expression of ADD1 with PPARgamma increases the transcriptional activity of this adipogenic nuclear hormone receptor, suggesting involvement of ADD1 in this pathway. These data indicate that ADD1 plays an important role in fat cell gene expression and differentiation, and suggest that it may function by augmenting a step in PPARgamma-mediated transcription.
Causes and Effects of N-Terminal Codon Bias in Bacterial Genes (2013)

Most amino acids are encoded by multiple codons, and codon choice has strong effects on protein expression. Rare codons are enriched at the N terminus of genes in most organisms, although the causes and effects of this bias are unclear. Here, we measure expression from >14,000 synthetic reporters in Escherichia coli and show that using N-terminal rare codons instead of common ones increases expression by ~14-fold (median 4-fold). We quantify how individual N-terminal codons affect expression and show that these effects shape the sequence of natural genes. Finally, we demonstrate that reduced RNA structure and not codon rarity itself is responsible for expression increases. Our observations resolve controversies over the roles of N-terminal codon bias and suggest a straightforward method for optimizing heterologous gene expression in bacteria.
Patterns of dental care utilization among patients with temporomandibular disorders (2006)

TMD subjects utilized 10% to 20% more dental services than non-TMD subjects. Gender and age were important factors with increased utilization in females and older patients. TMD diagnoses did not affect dental utilization patterns, indicating that most TMD patients continue to seek routine dental care.
Biologic activities of naturally occurring human insulin receptor mutations. Evidence that metabolic effects of insulin can be mediated by a kinase-deficient insulin receptor mutant (1991)

We have studied insulin receptor-mediated signaling in Chinese hamster ovary (CHO) cell transfectants that expressed either of two naturally occurring mutant human insulin receptors: Trp1200----Ser1200 and Ala1134----Thr1134. Compared with overexpressed normal human insulin receptors, both mutant receptors displayed normal processing and normal binding affinity; however, neither was capable of detectable insulin-stimulated autophosphorylation or tyrosine kinase activity toward endogenous (pp185) or exogenous substrates. Several biologic actions of insulin were evaluated in transfected cells. Compared with neomycin-only transfected CHO cells (CHO-NEO), cells expressing normal receptors demonstrated increased insulin sensitivity for 2-deoxyglucose uptake, [14C]glucose incorporation into glycogen, [3H]thymidine incorporation into DNA, and specific gene expression (accumulation of glucose transporter GLUT-1 mRNA). Cells expressing either Ser1200 or Thr1134 receptors showed no increase in insulin-stimulated thymidine incorporation or GLUT-1 mRNA accumulation compared with CHO-NEO. Surprisingly, cells expressing Ser1200 receptors showed increased insulin stimulation of 2-deoxyglucose uptake and glucose incorporation into glycogen compared with CHO-NEO, whereas Thr1134 receptors failed to signal these metabolic responses. We conclude that 1) transfected kinase-deficient insulin receptor mutants derived from insulin-resistant patients have distinct defects in the ability to mediate insulin action in vitro; 2) divergence of insulin signaling pathways may occur at the level of the receptor; and 3) normal activation of the receptor tyrosine kinase by insulin is not necessarily required for signaling of certain important biologic actions.
Human Platelet-Derived Transforming Growth Factor-βStimulates Parameters of Bone Growth in Fetal Rat Calvariae* (1986)

Human platelet-derived transforming growth factor type beta (TGF beta) is mitogenic for fetal rat calvariae in serum-free organ culture. It enhances DNA synthesis in short (24-h) and long (48- to 96-h) term cultures, but produces no significant stimulatory effects on bone collagen synthesis or alkaline phosphatase activity (two parameters of differentiated osteoblastic cell-type function) when present continuously in culture. Transitory treatment with TGF beta, however, induces a subsequent stimulation of collagen and noncollagen protein synthesis that depends on prior cell replication, suggesting an increase in the number of newly differentiated bone cells. In addition, TGF beta increases prostaglandin release, but this effect is probably unrelated to its mitogenic function. TGF beta activity is also found in culture medium conditioned by fetal rat calvariae, and the bone-derived factor produces effects similar to those of the human platelet factor. This polypeptide, therefore, may have an important function in early stages of bone development as well as bone repair after trauma-induced platelet degranulation.
Emerging role for regulated in development and DNA damage 1 (REDD1) in the regulation of skeletal muscle metabolism (2016)

Since its discovery, the protein regulated in development and DNA damage 1 (REDD1) has been implicated in the cellular response to various stressors. Most notably, its role as a repressor of signaling through the central metabolic regulator, the mechanistic target of rapamycin in complex 1 (mTORC1) has gained considerable attention. Not surprisingly, changes in REDD1 mRNA and protein have been observed in skeletal muscle under various physiological conditions (e.g., nutrient consumption and resistance exercise) and pathological conditions (e.g., sepsis, alcoholism, diabetes, obesity) suggesting a role for REDD1 in regulating mTORC1-dependent skeletal muscle protein metabolism. Our understanding of the causative role of REDD1 in skeletal muscle metabolism is increasing mostly due to the availability of genetically modified mice in which the REDD1 gene is disrupted. Results from such studies provide support for an important role for REDD1 in the regulation of mTORC1 as well as reveal unexplored functions of this protein in relation to other aspects of skeletal muscle metabolism. The goal of this work is to provide a comprehensive review of the role of REDD1 (and its paralog REDD2) in skeletal muscle during both physiological and pathological conditions.
Influence of an Edge Height on the Diffracted EM Field Distribution (2019)

The diffraction of light from a right-angled, lossless dielectric step, illuminated by a plane wave, forms a tilted focused beam. Its deviation angle depends on the index ratio between the structure material and host medium. This paper will demonstrate the existence of a critical height of a wavelength sized edge. This edge diffracts the incident light energy inside the higher index medium, as a specific field distribution. The analysis, done for optical frequencies, identifies lobes in the resulting field distribution. The lobes repartition is driven by a critical height and its multiples. These EM patterns are evaluated in relation with the photonic nanojet phenomenon.
Multi-omics approaches to disease (2017)

High-throughput technologies have revolutionized medical research. The advent of genotyping arrays enabled large-scale genome-wide association studies and methods for examining global transcript levels, which gave rise to the field of "integrative genetics". Other omics technologies, such as proteomics and metabolomics, are now often incorporated into the everyday methodology of biological researchers. In this review, we provide an overview of such omics technologies and focus on methods for their integration across multiple omics layers. As compared to studies of a single omics type, multi-omics offers the opportunity to understand the flow of information that underlies disease.
Shigella flexneri invasion plasmid antigens B and C: epitope location and characterization with monoclonal antibodies (1988)

Invasion plasmid antigens B (IpaB) and C (IpaC) are associated with the ability of shigellae to invade cultured mammalian cells. Monoclonal antibodies against IpaB and IpaC polypeptides were produced and used in a whole-cell enzyme-linked immunosorbent assay to show that both IpaB and IpaC polypeptides were exposed on the surface of virulent shigellae. Moreover, these surface epitopes were shown to be highly conserved among different serotypes of Shigella spp. and enteroinvasive Escherichia coli. Cross-reactive epitopes were not found on noninvasive Shigella strains or on other enteric bacteria including Salmonella, Yersinia, Campylobacter, Vibrio, and Aeromonas spp. and various pathogenic strains of E. coli. The monoclonal antibodies were used in competitive binding assays to define three unique epitopes of the IpaB polypeptide and four unique epitopes of the IpaC polypeptide. Epitope locations and their corresponding DNA-encoding regions were defined by examining the IpaB and IpaC products expressed by lambda gt11 recombinants and by constructing a genetic map of the insert DNAs of these recombinants. Three IpaB epitopes (2F1, 1H4, 4C8) were found to be encoded on three contiguous DNA regions comprising a 700-base-pair (bp) segment that corresponded to the amino-terminal end of the IpaB polypeptide. Similarly, a 640-bp DNA segment that corresponded to the amino-terminal end of the IpaC polypeptide was found to encode three clustered IpaC epitopes (5H1, 9B6, 5B1). Approximately 50 bp downstream from this region a fourth IpaC epitope-encoding region (2G2) was found. The effect of the monoclonal antibodies on plaque formation by virulent Shigella flexneri on a monolayer of cultured mammalian cells (a sensitive measure of invasiveness) was determined. Only the IpaB-specific monoclonal antibody 2F1 was able to reduce the plaque-forming capacity by greater than 50%, suggesting that this epitope of the IpaB polypeptide is involved in the invasion process.
Lysis of sensitized sheep erythrocytes in human sera deficient in the second component of complement. (1989)

Analysis of C-dependent lysis of sensitized SRBC by C2-deficient sera (C2D) led to the characterization of a C2 bypass pathway. Lysis in the total hemolytic C assay by C2D sera was Ca2+-dependent and required a high concentration of hemolysin to sensitize E. Selective component depletion indicated a requirement for C1 and C4 of the classical pathway (CP) and proteins B, P, and probably D of the alternative pathway (AP). Total hemolytic C could be restored to normal in these C2D sera by utilizing heavily sensitized E or by the addition of a supranormal concentration of B. This system most closely resembles a pathway described by J. E. May and M. M. Frank which requires antibody, C1, and the AP but not C4 or C2. It differs in its requirement for C4. We hypothesize that this pathway represents vestiges of a more primitive C pathway. It becomes evident and possibly clinically important in the setting of C2 deficiency, by allowing C activation, other than the AP, and perhaps in normal individuals, by damaging microorganisms that have evolved means to inhibit early components of the CP.
An experimental 1-Mbit BiCMOS DRAM (1987)

Three developments are proposed for high-performance DRAMs: a bipolar complementary MOS (BiCMOS) DRAM device structure featuring high soft-error immunity due to a p/SUP +/ buried layer; a high-speed circuit configuration of eight NMOS subarrays combined with BiCMOS peripheral drivers and BiCMOS data output circuitry; and BiCMOS voltage and current limiters lowering power dissipation as well as peak current. A 1.3 /spl mu/m 1-Mb DRAM is designed and fabricated to verify the usefulness of these BiCMOS DRAM technologies. Features of this chip include a typical access time of 32 ns, a typical power dissipation of 450 mW at a 60-ns cycle time, and chip size of 5.0/spl times/14.9 mm/SUP 2/.
The mRNAs for the pro-alpha 1(I) and pro-alpha 2(I) chains of type I procollagen are translated at the same rate in normal human fibroblasts and in fibroblasts from two variants of osteogenesis imperfecta with altered steady state ratios of the two mRNAs. (1983)

Homologous DNA fragments were prepared from cloned cDNAs for the pro-alpha 1(I) and pro-alpha 2(I) chains of human type I procollagen. The DNA fragments were then used to develop a dot blot hybridization assay for mRNAs for pro-alpha 1(I) and pro-alpha 2(I) chains in skin fibroblasts. In normal fibroblasts, the ratio of the steady state levels of the two mRNAs was 1.94 +/- 0.34 S.D. The ratio for the rates of synthesis of the two pro-alpha chains in the same cells was 1.84 +/- 0.13 S.D. Since the two ratios were essentially the same, the results indicated that the mRNAs for the two chains are translated at about the same rates. Therefore, there is no need to invoke translational control or more complex mechanisms to explain synthesis of pro-alpha 1(I) and pro-alpha 2(I) chains in a stoichiometry of 2:1. The dot blot hybridization assay was also used to examine the levels of the mRNAs in fibroblasts from several variants of osteogenesis imperfecta. In two of the variants, the ratios of the steady state levels of mRNAs for pro-alpha 1(I) and pro-alpha 2(I) chains were 3.05 and 2.52, respectively. In the same fibroblasts, the ratios for the rates of synthesis of the two chains were 2.99 +/- 0.43 and 2.45 +/- 0.16, respectively. Therefore, even though the ratios of the levels of the two mRNAs in the fibroblasts were abnormal, the two mRNAs were still translated at the same rates, and there was no evidence of differential regulation at the translational level.