gebhart/patrepeval huggingface dataset:
Correlation of Kennedy pathway efficiency with seed oil content of canola (Brassica napus L.) lines (2011)

Chen, J. M., Qi, W. C., Wang, S. Y., Guan, R. Z. and Zhang, H. S. 2011. Correlation of Kennedy pathway efficiency with seed oil content of canola (Brassica napus L.) lines. Can. J. Plant Sci. 91: 251–259. The Kennedy pathway (KP) has been demonstrated to be crucial for seed oil accumulation. To answer whether the KP enzyme activities can explain seed oil content variation of conventional canola lines, six lines with three different levels of oil (high, middle and low) were tested for seed KP enzyme activities and hexose (2 sucrose+glucose+fructose) concentrations at 18, 25, 32, 39 and 46 d after pollination (DAP). The results showed that lines with high and middle seed oil content levels (HO and MO) had higher phosphatidate phosphatase (PAP) and diacylglycerol acyltransferase (DGAT) activities and higher sugar contents than the lines with low oil levels (LO). The lowest KP enzyme activity (LEA) for each combination of line and DAP can be regarded as indicator to the bioassembly efficiency. In most of the combinations, DGAT was the enzyme with LEA, and glycerol-3-phosphate acyltransferase (GPAT) or PAP acted as the enzyme with LEA in a few cases. Correlation analyses showed that peak values and averages of LEA in the lines were significantly correlated with seed oil content, indicating that KP enzyme efficiency is tightly associated with seed oil content.
Apoptosis and the kidney. (1994)

Apoptosis is a programmed form of cell death mediating the precisely controlled deletion of "unwanted" cells. This review discusses the key features of this cell death program, emphasizing that apoptosis is regulated by factors extrinsic and intrinsic to the dying cell. Furthermore, because apoptosis leads to the swift phagocytic clearance of intact cells, tissues are protected against the noxious effect of cell contents. Apoptosis occurs in the developing and adult kidney, and nephrologists now need to consider whether abnormalities of this program may contribute to renal disease. Evidence suggests that such defects could contribute to developmental abnormalities including polycystic disease, induce autoimmunity to renal tissue, and exacerbate renal inflammation and scarring. Finally, apoptosis may offer new avenues for therapy.
Effects of the TREM-1 pathway modulation during mesenteric ischemia-reperfusion in rats (2008)

The modulation of the TREM-1 pathway by the means of a synthetic peptide may be useful during acute mesenteric ischemia.
Cooking Flavor and Texture of Rice Stored under Different Conditions (1983)

Journal Article Cooking Flavor and Texture of Rice Stored under Different Conditions Get access Takashi Tsugita, Takashi Tsugita Department of Agricultural Chemistry, Faculty of Agriculture, The University of Tokyo, Bunkyo-ku, Tokyo 113, Japan Search for other works by this author on: Oxford Academic Google Scholar Takeo Ohta, Takeo Ohta Department of Agricultural Chemistry, Faculty of Agriculture, The University of Tokyo, Bunkyo-ku, Tokyo 113, Japan Search for other works by this author on: Oxford Academic Google Scholar Hiromichi Kato Hiromichi Kato Department of Agricultural Chemistry, Faculty of Agriculture, The University of Tokyo, Bunkyo-ku, Tokyo 113, Japan Search for other works by this author on: Oxford Academic Google Scholar Agricultural and Biological Chemistry, Volume 47, Issue 3, 1 March 1983, Pages 543–549, https://doi.org/10.1080/00021369.1983.10865684 Published: 01 March 1983 Article history Received: 20 August 1982 Published: 01 March 1983
1,25-Dihydroxy-24-OXO-16ene-vitamin D3, a renal metabolite of the vitamin D analog 1,25-dihydroxy-16ene-vitamin D3, exerts immunosuppressive activity equal to its parent without causing hypercalcemia in vivo (1994)

The hormone, 1,25-(OH)2D3, is metabolized into 1,25-(OH)2-24-OXO-D3, in kidney prior to conversion to its final inactive product, calcitroic acid. Similarly, 1,25-(OH)2-24OXO-16eneD3, is produced in the kidney from the Vitamin D analog, 1,25-(OH)2-16eneD3, but resists further hydroxylation. The analog's metabolite was synthesized and its biologic activity compared to the parent compound. Naive SJL/J mice, 4 weeks old, were immunized with neuroantigen in adjuvant to induce experimental autoimmune encephalomyelitis [EAE]. Treatment with 1,25-(OH)2-24OXO-16eneD3 was given at 0.05, 0.15 and 0.3 microgram I.P., on alternate days, starting 3 days prior and for up to 5 days post immunization and compared to a similar treatment with 0.1 microgram 1,25-(OH)2D3 or 1,25-(OH)2-16eneD3. Suppression of EAE was observed with 0.15 microgram 1,25-(OH)2-24OXO-16eneD3, comparable to the suppression induced with the parent compound and more potent than 1,25-(OH)2D3. However, no hypercalcemia was seen in mice treated with 0.15 microgram of OXO-metabolite (9.7 +/- 0.6 vs 9.3 +/- 1.1 mg/dl, treated vs controls), in contrast to 1,25-(OH)2D3 and 1,25-(OH)2-16eneD3 (11.2 +/- 1.0 and 11.0 +/- 0.9 mg/dl respectively; p < 0.001). In summary, our results suggest that 1,25-(OH)2-24OXO-16eneD3, a stable intermediary metabolite of the vitamin D analog, 1,25-(OH)2-16eneD3 exerts immunosuppressive activity equal to its parent without causing hypercalcemia in vivo.
Mechanisms and experimental models of seizure generation (1998)

Over the past year evidence has accumulated against the idea that seizures require re-entrant activity between spatially separate structures. Seizures in vivo typically do involve interconnected, spatially separate brain regions, but they often show no net phase lag around the putative circuit. In many cases seizure-like events can arise from localized regions such as the entorhinal cortex or hippocampus proper, through mechanisms that are starting to be identified.
Combining a CD20 Chimeric Antigen Receptor and an Inducible Caspase 9 Suicide Switch to Improve the Efficacy and Safety of T Cell Adoptive Immunotherapy for Lymphoma (2013)

Modification of T cells with chimeric antigen receptors (CAR) has emerged as a promising treatment modality for human malignancies. Integration of co-stimulatory domains into CARs can augment the activation and function of genetically targeted T cells against tumors. However, the potential for insertional mutagenesis and toxicities due to the infused cells have made development of safe methods for removing transferred cells an important consideration. We have genetically modified human T cells with a lentiviral vector to express a CD20-CAR containing both CD28 and CD137 co-stimulatory domains, a "suicide gene" relying on inducible activation of caspase 9 (iC9), and a truncated CD19 selectable marker. Rapid expansion (2000 fold) of the transduced T cells was achieved in 28 days after stimulation with artificial antigen presenting cells. Transduced T cells exhibited effective CD20-specific cytotoxic activity in vitro and in a mouse xenograft tumor model. Activation of the iC9 suicide switch resulted in efficient removal of transduced T cells both in vitro and in vivo. Our work demonstrates the feasibility and promise of this approach for treating CD20(+) malignancies in a safe and more efficient manner. A phase I clinical trial using this approach in patients with relapsed indolent B-NHL is planned.
A single immunization with a minute dose of a lentiviral vector‐based vaccine is highly effective at eliciting protective humoral immunity against West Nile virus (2005)

This study broadens the applicability of lentiviral vectors as efficient non-replicating vaccines against pathogens for which a neutralizing humoral response is one active arm of the protective immunity. The TRIP/sE(WNV) lentiviral vector appears to be a promising tool for veterinary vaccination against zoonotic WNV.
Orthogonal least squares learning algorithm for radial basis function networks (1991)

The radial basis function network offers a viable alternative to the two-layer neural network in many applications of signal processing. A common learning algorithm for radial basis function networks is based on first choosing randomly some data points as radial basis function centers and then using singular-value decomposition to solve for the weights of the network. Such a procedure has several drawbacks, and, in particular, an arbitrary selection of centers is clearly unsatisfactory. The authors propose an alternative learning procedure based on the orthogonal least-squares method. The procedure chooses radial basis function centers one by one in a rational way until an adequate network has been constructed. In the algorithm, each selected center maximizes the increment to the explained variance or energy of the desired output and does not suffer numerical ill-conditioning problems. The orthogonal least-squares learning strategy provides a simple and efficient means for fitting radial basis function networks. This is illustrated using examples taken from two different signal processing applications.
The scavenger cell pathway for lipoprotein degradation: Specificity of the binding site that mediates the uptake of negatively‐charged LDL by macrophages (1980)

Macrophages isolated from a variety of organs in several animal species exhibit high affinity binding sites that recognize chemically modified proteins. One of these binding sites recognizes human plasma low density lipoprotein (LDL) in which the positive charges on the epsilon-amino groups of lysine have been removed or neutralized by chemical modification, thus giving the protein an enhanced negative charge. Effective treatments include reaction of LDL with organic acid anhydrides (acetylation or maleylation) and reaction with aldehydes, such as treatment with malondialdehyde. After the negatively-charged LDL binds to the surface receptor sites, it is rapidly internalized by the macrophages by endocytosis and hydrolyzed in lysosomes. The liberated cholesterol is reesterified in the cytoplasm, producing massive cholesteryl ester deposition. The binding sites for negatively-charged LDL has been demonstrated so far only on macrophages and other scavenger cells. It is not expressed in cultured fibroblasts, smooth muscle cells, lymphocytes, or adrenal cells. In addition to its affinity for acetylated LDL and malondialdehyde-treated LDL, the macrophage site binds a variety of polyanions. It exhibits a particularly high affinity for certain sulfated polysaccharides (dextran sulfate and fucoidin), certain polynucleotides (polyinosinic acid and polyguanylic acid), polyvinyl sulfate, and maleylated albumin. It is possible that the site that binds negatively-charged LDL may be responsible for the massive accumulation of cholesteryl esters that occurs in vivo in macrophages and other scavenger cells in patients with high levels of circulating plasma LDL.
Mechanisms of Microglia-Mediated Neurotoxicity in a New Model of the Stroke Penumbra (2008)

After an ischemic stroke, neurons in the core are rapidly committed to die, whereas neuron death in the slowly developing penumbra is more amenable to therapeutic intervention. Microglia activation contributes to delayed inflammation, but because neurotoxic mechanisms in the penumbra are not well understood, we developed an in vitro model of microglia activation and propagated neuron killing. To recapitulate inflammatory triggers in the core, microglia were exposed to oxygen glucose-deprived neurons and astrocytes. To model the developing penumbra, the microglia were washed and allowed to interact with healthy naive neurons and astrocytes. We found that oxygen-glucose deprivation (OGD)-stressed neurons released glutamate, which activated microglia through their group II metabotropic glutamate receptors (mGluRs). Microglia activation involved nuclear factor kappaB (NF-kappaB), a transcription factor that promotes their proinflammatory functions. The activated microglia became neurotoxic, killing naive neurons through an apoptotic mechanism that was mediated by tumor necrosis factor-alpha (TNF-alpha), and involved activation of both caspase-8 and caspase-3. In contrast to some earlier models (e.g., microglia activation by lipopolysaccharide), neurotoxicity was not decreased by an inducible nitric oxide synthase (iNOS) inhibitor (S-methylisothiourea) or a peroxynitrite scavenger [5,10,15,20-tetrakis(N-methyl-4'-pyridyl)porphinato iron (III) chloride], and did not require p38 mitogen-activated protein kinase (MAPK) activation. The same microglia neurotoxic behavior was evoked without exposure to OGD-stressed neurons, by directly activating microglial group II mGluRs with (2S,2'R,3'R)-2-(2'3'-dicarboxycyclopropyl) glycine or glutamate, which stimulated production of TNF-alpha (not nitric oxide) and mediated TNF-alpha-dependent neurotoxicity through activation of NF-kappaB (not p38 MAPK). Together, these results support potential therapeutic strategies that target microglial group II mGluRs, TNFalpha overproduction, and NF-kappaB activation to reduce neuron death in the ischemic penumbra.
Isolation and characterization of the mouse ornithine decarboxylase gene. (1988)

Mouse ornithine decarboxylase (ODC) genomic clones were isolated from a bacteriophage lambda genomic library representing mouse myeloma 653-1 cells which over-produce ODC due to amplification of an active ODC gene. Sequence analysis of the amplified ODC gene revealed that ODC mRNA is encoded by 12 exons, 10 of which (exons 3 to 12) code for the ODC protein. Exon 12 also corresponds to the 3' noncoding region of the two species of ODC mRNA which are formed by alternative utilization of two polyadenylation signals separated from each other by 422 nucleotides. The transcription initiation site was mapped by S1 nuclease protection and by primer extension analysis. The 5' flanking region is extremely rich in G + C and contains typical promoter motifs such as the TATA box and SP1 transcription factor binding sites. Joining the 5' flanking region to the Escherichia coli chloramphenicol acetyltransferase structural gene and its introduction into mouse cells resulted in the expression of a high level of chloramphenicol acetyltransferase activity. Comparing the sequence of the ODC gene to our previously published sequence of ODC cDNA revealed a disagreement between the sequences located 5' to the AvaI site and demonstrated that this region of our previously reported cDNA represents a cloning artifact. The portion of the correct 5' noncoding region encoded by exon 1 is extremely rich in G + C and includes potential secondary structures which may be involved in translational regulation of ODC mRNA.
Shape-Memory Polymers and Multifunctional Composites (2010)

Overview of Shape-Memory Polymers, M. Behl and A. Lendlein The Structural Variety of Shape-Memory Polymers, H.-Y. Jiang and A.M. Schmidt Thermomechanical Behavior and Modeling Approaches, H.J. Qi and M.L. Dunn Thermomechanical Characterizations of Shape-Memory Polymers (Dual/Triple-Shape) and Modeling Approaches, K. Kratz, W. Wagermaier, M. Heuchel, and A. Lendlein Electrical, Thermomechanical and Shape-Memory Properties of the PU Shape-Memory Polymer, W.M. Huang and B. Yang Multifunctional Shape Memory Polymers and Actuation Methods, J. Leng, H. Lu and S. Du Shape Memory Polymer Composites, J. Leng, X. Lan and S. Du Applications of Shape Memory Polymers in Aerospace, Y. Liu and J. Leng Shape Memory Polymer Foam and Applications, W.M. Sokolowski Shape Memory Polymer Textile, J. Hu Applications of Shape Memory Polymers in Biomedicine, W.M. Sokolowski and J. Leng Novel Applications and Future of Shape Memory Polymers, W.M. Huang Index
Gamma Interferon (IFN-γ) Receptor Restricts Systemic Dengue Virus Replication and Prevents Paralysis in IFN-α/β Receptor-Deficient Mice (2012)

We previously reported that mice lacking alpha/beta and gamma interferon receptors (IFN-α/βR and -γR) uniformly exhibit paralysis following infection with the dengue virus (DENV) clinical isolate PL046, while only a subset of mice lacking the IFN-γR alone and virtually no mice lacking the IFN-α/βR alone develop paralysis. Here, using a mouse-passaged variant of PL046, strain S221, we show that in the absence of the IFN-α/βR, signaling through the IFN-γR confers approximately 140-fold greater resistance against systemic vascular leakage-associated dengue disease and virtually complete protection from dengue-induced paralysis. Viral replication in the spleen was assessed by immunohistochemistry and flow cytometry, which revealed a reduction in the number of infected cells due to IFN-γR signaling by 2 days after infection, coincident with elevated levels of IFN-γ in the spleen and serum. By 4 days after infection, IFN-γR signaling was found to restrict DENV replication systemically. Clearance of DENV, on the other hand, occurred in the absence of IFN-γR, except in the central nervous system (CNS) (brain and spinal cord), where clearance relied on IFN-γ from CD8(+) T cells. These results demonstrate the roles of IFN-γR signaling in protection from initial systemic and subsequent CNS disease following DENV infection and demonstrate the importance of CD8(+) T cells in preventing DENV-induced CNS disease.
Augmentation of allergic inflammation in prostanoid IP receptor deficient mice (2002)

1 To evaluate the role of prostaglandin I(2) (PGI(2)) in allergic inflammation, allergic responses in the airway, skin and T cells were studied in mice lacking the receptor for PGI(2) (the prostanoid IP receptor) through gene disruption. 2 Three inhalations of antigen caused an increase in plasma extravasation, leukocyte accumulation and cytokine (interleukin (IL)-4 and IL-5) production in the airway of sensitized mice. These airway inflammatory responses were significantly greater in IP receptor deficient mice than in wild-type mice. 3 The vascular leakage caused by passive cutaneous anaphylaxis, substance P and 5-hydroxytryptamine was markedly increased in the skin of IP receptor deficient mice, compared with comparably treated wild-type mice. 4 The inhalation of antigen in sensitized mice resulted in increased serum antigen specific IgE, total IgE and IgG levels. The magnitude of the elevations of each immunoglobulin level in IP receptor deficient mice is notably higher than that in wild-type mice. To elucidate the mechanism of an enhancement of immunoglobulin production, the activity of T cells in sensitized and non-sensitized mice was studied by means of the production of cytokines. The antigen-induced IL-4 production by spleen cells from sensitized IP receptor deficient mice was almost three times greater than that in wild-type mice. On the contrary, the anti-CD3 antibody-induced interferon-gamma production by CD4(+) T cells from non-sensitized IP receptor deficient mice was significantly lower than that in wild-type mice. 5 The present data indicate that IP receptor deficiency reinforced an allergic airway and skin inflammation by augmentation of vascular permeability increase and the T helper 2 cell function. These findings suggest a regulatory role of PGI(2) in allergic inflammation.
Electrical alternans and cardiac electrical instability. (1988)

We investigated the relationship between electrical alternans and cardiac electrical stability in a series of 20 dog experiments and in a pilot clinical study. Electrical alternans was detected in both the QRS complex and the ST-T wave by use of a novel multidimensional spectral technique. The magnitude of the alteration was expressed as the alternating electrocardiographic morphology index (AEMI), expressed as parts per million of waveform energy. Electrical stability in the dog preparations was assessed via the ventricular fibrillation threshold measurement, and in the clinical studies via programmed stimulation. In 10 dog experiments, systemic hypothermia resulted in a 60% decrease in ventricular fibrillation threshold (VFT) (p less than .0001) and a significant increase in both AEMI(QRS) form 3.7 +/- 3.0 to 1448 +/- 548 (p less than .0001) and AEMI(ST-T) from 43.9 +/- 18.4 to 19,178 +/- 5579 (p less than .0001). In 10 dog experiments, transient coronary artery ligation also resulted in a 60% decrease in VFT (p less than .0001), an increase from 76.3 +/- 46.5 to 245 +/- 11 in AEMI(QRS) (p less than .05), and an increase from 842 +/- 505 to 1365 +/- 392 in AEMI(ST-T) (p less than .002). In 119 observations in 20 animal experiments, the rank correlation between VFT and AEMI(QRS) was -.30 (p less than .001), with that between VFT and AEMI(ST-T) being -.55 (p less than .0001). In a double-blind pilot clinical trial consisting of 23 studies in 19 patients, the result of electrophysiologic testing was used as an independent measure of cardiac electrical stability. Alternation in waveform morphology identified the inducible patient population with a sensitivity of 92%, a positive predictivity of 70%, and a specificity of 50% (p less than .05). We conclude that analysis of subtle beat-to-beat variability in electrocardiographic morphology may provide a noninvasive measure of cardiac electrical stability.
Fluoroalkylated Silicon-Containing Surfaces−Estimation of Solid-Surface Energy (2010)

The design of robust omniphobic surfaces, which are not wetted by low-surface-tension liquids such as octane (γlv=21.6 mN/m) and methanol (γlv=22.7 mN/m), requires an appropriately chosen surface micro/nanotexture in addition to a low solid-surface energy (γsv). 1H,1H,2H,2H-Heptadecafluorodecyl polyhedral oligomeric silsesquioxane (fluorodecyl POSS) offers one of the lowest solid-surface energy values ever reported (γsv≈10 mN/m) and has become the molecule of choice for coating textured surfaces. In this work, we synthesize and evaluate a series of related molecules that either retain the POSS cage and differ in fluoroalkyl chain length or that retain the fluorodecyl chains surrounding a linear or cyclic molecular structure. The solid-surface energy (γsv) of these molecules was estimated using contact angle measurements on flat spin-coated silicon wafer surfaces. Zisman analysis was performed using a homologous series of n-alkanes (15.5≤γlv≤27.5 mN/m), whereas Girifalco-Good analysis was performed using a set of polar and nonpolar liquids with a wider range of liquid surface tension (15.5≤γlv≤72.1 mN/m). The hydrogen-bond-donating, hydrogen-bond-accepting, polar, and nonpolar (dispersion) contributions to the solid-surface energy of each compound were determined by probing the surfaces using a set of three liquid droplets of either acetone, chloroform, and dodecane or diiodomethane, dimethyl sulfoxide, and water.
Intrinsic chemoresistance to gemcitabine is associated with constitutive and laminin-induced phosphorylation of FAK in pancreatic cancer cell lines (2009)

In conclusion, our research demonstrates for the first time that both constitutive and LN-induced FAK phosphorylation contribute to increased intrinsic chemoresistance to Gem in pancreatic cancer cell lines and these effects are partly due to the regulation of Akt and Bad phosphorylation and survivin expression. Development of selective FAK phosphorylation inhibitors may be a promising way to enhance chemosensitivity in pancreatic cancer.