gebhart/patrepeval huggingface dataset:
Physiological and molecular insights into drought tolerance (2002)

  Water is a major limiting factor in world agriculture. In general, most crop plants are highly sensitive to even a mild dehydration stress. There are however, a few genera of plants unique to Southern Africa, called “resurrection plants” which can tolerate extreme water loss or desiccation. We have used Xerophyta viscosa, a representative of the monocotyledonous resurrection plants to isolate genes that are associated with osmotic stress tolerance. Several genes that are differentially expressed, and that confer functional sufficiency to osmotically-stressed Escherichia coli are being studied at the molecular and biochemical levels. In this review, we use this as a basis to discuss the physiological and molecular insights into drought tolerance.   Key words: Drought stress, reactive oxygen species, osmoprotectants, abscisic acid, transcription factors.
Differential Extraction of Tumor-Specific Transplantation Antigen and Embryonic Antigen From Simian Virus 40-and Adenovirus 7-Induced Sarcoma Cells of Hamsters With 1-Butanol and 3 <italic>M</italic> Potassium Chloride<xref ref-type="fn" rid="FN2">2</xref> (1984)

Simian virus 40 (SV40)-induced sarcomas and adenovirus 7-induced sarcomas (Adv-7) exhibit both specific tumor-specific transplantation antigens (TSTA) and cross-protective embryonic antigens at the cell surface in the LAK:LVG(SYR) strain of Syrian golden hamsters. Specific SV40 TSTA could be released from the surfaces of living hamster sarcoma cells in a 2.5% crude 1-butanol extract (CBE) and served as immunogen to protect syngeneic recipients against subsequent homologous but not heterologous tumor cell challenge. The CBE-extracted SV40-induced TSTA (tumor-specific) was observed to be free of detectable, cross-protective embryonic antigens (EA) by tumor transplantation assays. The induction of cytotoxic lymphocyte-mediated immunity with the CBE-released TSTA was dependent on the administration of a single sensitizing injection of 12-20 micrograms antigen protein. Higher concentrations (50-1,000 micrograms) of the CBE tumor cell extract, given in a single injection, enhanced tumor growth as did two injections of 12.5 micrograms CBE-extracted SV40-induced TSTA at 1-week intervals. A cross-protective antigen(s), not detected in the CBE tumor extracts, was retained in the intact, 1-butanol-extracted SV40 and Adv-7-induced tumor cell lines after completion of the CBE extraction procedure and in similarly extracted 10-day hamster fetal cells. Some alterations in the normal immunogenicity of EA extracted with CBE followed by KCI from SV40-induced sarcoma cells could be detected in the transplantation assays and lymphocyte transformation assays, whereas EA extracted from CBE-KCI-treated Adv-7 cells or 10-day hamster fetal cells retained normal immunogenicity in vivo and in vitro. These procedures provide a means for successful separation of immunogenic SV40- and Adv-7-induced TSTA from detectable, biologically active, cross-protective EA from the surfaces of these sarcoma cells.
Optical switch configuration and lightpath assignment in wavelength routing multihop lightwave networks (2002)

A wide-area transparent optical network can be constructed by using wavelength routers and switches, each dealing with only a small number of wavelengths. In this work we consider the problem of configuring the wavelength routers based on the observed traffic. Various policies for wavelength routing, and the corresponding assignment of wavelengths along the routes have been studied before, which are based on minimizing congestion, average hop-distance, and call blocking probability or on maximizing carried traffic, and the number of clear channels. However these approaches often lead to scenarios where a significant number of available wavelengths at the input/output ports of the routers cannot be used due to potential wavelength conflict. The wavelength routing and assignment algorithms presented in this paper focus on maximizing the wavelength-utilization at the switching devices which also improve the overall network performance.
Forkhead-associated Domains of the Tobacco NtFHA1 Transcription Activator and the Yeast Fhl1 Forkhead Transcription Factor Are Functionally Conserved (2002)

NtFHA1 encodes a novel protein containing the forkhead-associated (FHA) domain and the acidic domain in Nicotiana tabacum. NtFHA1 functions as a transactivator and is targeted to the nucleus. The sequence of the FHA domain of NtFHA1 is significantly homologous to that of the Fhl1 forkhead transcription factor of yeast. FHL1 was previously identified as a suppressor of RNA polymerase III mutations, and the fhl1 deletion mutant exhibited severe growth defects and impaired rRNA processing. Ectopic expression of the FHA domain of NtFHA1 (but not its mutant form) resulted in severe growth retardation in yeast. Similarly, expression of Fhl1, its FHA domain, or chimeric Fhl1 containing the NtFHA1 FHA domain also inhibited yeast growth. Yeast cells overexpressing the FHA domains of NtFHA1 and Fhl1 contained lower levels of mature rRNAs and exhibited rRNA-processing defects, similar to the fhl1 null mutant. Chimeric Fhl1 (but not the mutant form with a small deletion in its FHA domain) fully complemented the growth and rRNA-processing defects of the fhl1 null mutant, demonstrating that the FHA domain of NtFHA1 can functionally substitute for the FHA domain of Fhl1. These results demonstrate that the FHA domains of NtFHA1 and Fhl1 are conserved in their structure and function and that the FHA domain of Fhl1 is critically involved in regulation of rRNA processing in yeast. NtFHA1 function in plants may be analogous to Fhl1 function in yeast.
Virtual Probe Approach for Time-Dependent Arterial Travel Time Estimation (2008)

Travel time estimation on arterials is a challenging task for traffic engineers due to the interrupted nature of urban traffic flows. Many research efforts have been devoted on this topic, but their successes are limited and most of them can only be used for offline purposes due to the limited availability of traffic data from signalized intersections. With the advancement of intelligent transportation systems, high-resolution detector and signal status data are available but not fully explored. In this paper, we develop an innovative algorithm for time-dependent arterial travel time estimation by tracing a virtual probe vehicle. At each time step, the virtual probe has three possible maneuvers: acceleration, deceleration and no-speed-change. The maneuver decision is determined by its own status and its surrounding traffic conditions, which can be estimated based on the availability of traffic data at intersections. An interesting property of the proposed model is that travel time estimation errors can be self-corrected with the signal status data, because the differences between a virtual probe vehicle and a real probe can be reduced when both of them meet the red signal phase. A field study at an 11-intersections arterial corridor along France Avenue in Minneapolis, MN shows the proposed model can generate accurate time-dependent travel time under various traffic conditions.
Investigating the Interaction between Osteoprotegerin and Receptor Activator of NF-κB or Tumor Necrosis Factor-related Apoptosis-inducing Ligand (2007)

Osteoprotegerin (OPG) binds the ligand for receptor activator of nuclear factor kappaB (RANKL) to prevent association with its receptor RANK and inhibit osteoclast-mediated bone resorption. OPG has been reported, recently, to inhibit tumor necrosis factor-related apoptosis-induced ligand (TRAIL)-induced tumor cell apoptosis. This raises the possibility that OPG may play a unique role in regulating these two signaling pathways. However, there are little data on the interactions between OPG, RANKL, and TRAIL, and the relative affinity of OPG for these two ligands is unknown. In the present study we examined the ability of OPG to bind native human TRAIL and RANKL under physiological conditions. Native TRAIL was expressed in Escherichia coli, purified to homogeneity, and shown to induce human myeloma cell apoptosis. OPG inhibited native TRAIL from binding the TRAILR1 at 37 degrees C in vitro. Similarly, OPG prevented RANKL from binding to RANK. TRAIL also prevented OPG-mediated inhibition of RANKL from binding RANK. The affinity of OPG for native TRAIL and RANKL at 37 degrees C was determined by plasmon surface resonance analysis. OPG had a binding affinity for TRAIL of 45 nM, whereas the affinity of OPG for RANKL was 23 nM. These data suggest that OPG can bind both RANKL and TRAIL and that the affinity of OPG for these two ligands is of a similar order of magnitude. Furthermore, OPG prevented TRAIL-mediated reductions in cell viability, whereas TRAIL inhibited OPG-mediated inhibition of osteoclastogenesis in vitro. This highlights the pivotal role of OPG in regulating the biology of both RANKL and TRAIL.
Synthetic inorganic ion-exchange materials. Part XLIX. Adsorption and desorption behaviour of heavy metal ions on hydrated titanium dioxide (1989)

The ion-exchange selectivity of a number of divalent metal ions was studied as a function of pH in nitrate and chloride media. The order of selectivity was Pb2+ > Hg2+ > Cd2+ > Mg2+ in nitrate solution and Pb2+ > Cd2+ > Ca2+ > Mg2+ > Hg2+ in chloride solution. A good linear relationship between the logarithm of the distribution coefficient of the heavy metal ions and their effective ionic radius was found. On the basis of the Kd values, the separation of a mixture of Cd2+, Hg2+ and Pb2+ and the group separation of Hg2+ and Pb2+ from several common metal ions were achieved on an ion-exchange column containing amorphous hydrated titanium dioxide.
An element of the transforming growth factor-beta 1 5'-untranslated region represses translation and specifically binds a cytosolic factor. (1993)

In many cell types, there is a discrepancy between transforming growth factor-beta 1 (TGF-beta 1) mRNA and TGF-beta 1 protein, suggesting that expression of TGF-beta 1 is regulated posttranscriptionally. We have previously shown that a 137-nucleotide (nt) region of the TGF-beta 1 5'-untranslated region (UTR) potently inhibits the expression of a heterologous reporter gene, suggesting a role for this region in the posttranscriptional inhibition of TGF-beta 1 expression. To study the mechanism of inhibition, a chimeric plasmid containing this region of the TGF-beta 1 5'-UTR and the reading frame of the human GH gene was stably transfected into C2C12 myoblastic cells. Our results show that the TGF-beta 1 5'-UTR inhibits GH expression by inhibiting GH mRNA translation. In vitro gel retardation and cross-linking assays using a radiolabelled RNA probe transcribed from this region of the TGF-beta 1 5'-UTR demonstrate the specific binding of a cytosolic factor. Deletion of a potential stem-loop-forming region abolishes binding of this factor and partially restores GH production. These results suggest that posttranscriptional inhibition of TGF-beta 1 expression is at the level of mRNA translation and that a cytosolic factor may regulate TGF-beta 1 mRNA translation.
Mechanoenergetic Estimation of Multiple Cross-Bridge Steps per ATP in a Beating Heart (2004)

The efficiency from the ventricular O(2) consumption (VO(2)) to the total mechanical energy (TME) generated by ventricular contraction has proved relatively constant at approximately 35%, independent of the loading and contractile conditions in a canine heart. TME is the sum of the external mechanical work for ejecting a stroke volume against the afterload and of the mechanical potential energy for developing ventricular pressure in each beat. The approximately 35% VO(2)-to-TME efficiency indicates an also constant approximately 60% ATP-to-TME efficiency in a beating heart, based on the nominal approximately 60% VO(2)-to-ATP efficiency in the myocardial oxidative phosphorylation. I newly attempted to explain the load-independent approximately 60% ATP-to-TME efficiency by the recently reported approximately 7-10 nm unitary step size and approximately 0.8-1.5 pN unitary force of a cross-bridge (CB) at the molecular level in in vitro motility assays. This single CB behavior suggests that its unitary cycle could generate a mechanical energy of approximately 0.6-1.5x10(-20) J at most. From the nominal free energy of approximately 10x10(-20) J per ATP, the efficiency from one ATP to the CB unitary cycle would then be approximately 6-15%. This low efficiency is only approximately 1/10-1/4 of the approximately 60% ATP-to-TME efficiency at the heart level. This discrepancy suggests that each CB would repeat the unitary cycle at least approximately 4-10 times per ATP to achieve the high constant ATP-to-TME efficiency in a beating heart. This seems to represent a considerable mechanoenergetic advantage of the heart at the integrative heart level as compared to the molecular CB level.
Structure and molecular arrangement of proteolipid protein of central nervous system myelin. (1984)

Proteolipid protein (PLP) of central nervous system myelin is one of the most hydrophobic integral membrane proteins. It consists of a 276-residue-long polypeptide chain with five strongly hydrophobic sequences of 26, 30, 39, 12, and 36 residues, respectively, linked by highly charged hydrophilic sequences. Hyposmotically dissociated bovine myelin membranes were treated with trypsin. PLP was completely cleaved into smaller fragments, whereas basic myelin protein remained essentially unaltered. The proteins and tryptic peptides of myelin were separated after the removal of the short, water-soluble peptides into three large fragments of 11, 7.3, and 9.0 kDA, respectively. They were characterized by their molecular mass and NH2-terminal amino acid sequences, which proved that trypsin cleaved predominantly at Arg-97 yielding the 11-kDa fragment from Gly-1 through Arg-97, at Arg-126 releasing the 7.3-kDa fragment from Gly-127 through Lys-191, and at Lys-191 releasing the 9-kDa fragment from Thr-192 through Phe-276. We propose that PLP is integrated into the lipid bilayer of myelin with the NH2 terminus and three positively charged hydrophilic loops oriented toward the extracytosolic side of the membrane, whereas one strongly negative hydrophilic loop and the positively charged COOH terminus cover the cytosolic side of the lipid bilayer. Basic myelin protein remains protected against tryptic cleavage, which indicates its apposition to the cytosolic side of the membrane. These cleavage sites of trypsin support the suggested orientation of PLP in the myelin membrane and thereby extend our knowledge about the molecular arrangement of the components of this membrane. In demyelinating processes membrane desintegration could be initiated by proteolysis at the external surfaces of proteolipid protein in a similar way as described here.
P2MP MPLS-TE Fast Reroute with P2MP Bypass Tunnels (2008)

This document defines procedures for fast reroute protection of
Point-To-MultiPoint (P2MP) Traffic Engineering Label Switched Paths
(TE-LSP) in MultiProtocol Label Switching (MPLS) networks, based
upon Point-To-MultiPoint Bypass Tunnels. The motivation for using
P2MP Bypass Tunnels is to avoid potentially expensive data
duplication along the backup path that could occur if Point-To-Point
Bypass Tunnels were used, i.e., to optimize the bandwidth usage,
during fast reroute protection of a link or a node. During link or
node failure the traffic carried onto a protected P2MP TE-LSP is
tunnelled within one or several P2MP Bypass Tunnels towards a set of
Merge Points. To avoid data duplication, backup labels (i.e., inner
labels) are assigned by the Point of Local Repair (PLR) according to
the RSVP-TE upstream label assignment procedure.
Activation of Mammalian Target of Rapamycin Controls the Loss of TCRζ in Lupus T Cells through HRES-1/Rab4-Regulated Lysosomal Degradation (2009)

Persistent mitochondrial hyperpolarization (MHP) and enhanced calcium fluxing underlie aberrant T cell activation and death pathway selection in systemic lupus erythematosus. Treatment with rapamycin, which effectively controls disease activity, normalizes CD3/CD28-induced calcium fluxing but fails to influence MHP, suggesting that altered calcium fluxing is downstream or independent of mitochondrial dysfunction. In this article, we show that activity of the mammalian target of rapamycin (mTOR), which is a sensor of the mitochondrial transmembrane potential, is increased in lupus T cells. Activation of mTOR was inducible by NO, a key trigger of MHP, which in turn enhanced the expression of HRES-1/Rab4, a small GTPase that regulates recycling of surface receptors through early endosomes. Expression of HRES-1/Rab4 was increased in CD4(+) lupus T cells, and in accordance with its dominant impact on the endocytic recycling of CD4, it was inversely correlated with diminished CD4 expression. HRES-1/Rab4 overexpression was also inversely correlated with diminished TCRzeta protein levels. Pull-down studies revealed a direct interaction of HRES-1/Rab4 with CD4 and TCRzeta. Importantly, the deficiency of the TCRzeta chain and of Lck and the compensatory up-regulation of FcepsilonRIgamma and Syk, which mediate enhanced calcium fluxing in lupus T cells, were reversed in patients treated with rapamcyin in vivo. Knockdown of HRES-1/Rab4 by small interfering RNA and inhibitors of lysosomal function augmented TCRzeta protein levels in vitro. The results suggest that activation of mTOR causes the loss of TCRzeta in lupus T cells through HRES-1/Rab4-dependent lysosomal degradation.
The Golgi-Associated Protein p115 Mediates the Secretion of Macrophage Migration Inhibitory Factor (2009)

Macrophage migration inhibitory factor (MIF) is a leaderless protein that is secreted from cells by a specialized, nonclassical export pathway. The release of MIF nevertheless is regulated and its production in response to different inflammatory, mitogenic, and hormonal stimuli plays an important role in diverse physiologic and pathologic processes. We report herein the identification of the Golgi complex-associated protein p115 as an intracellular binding partner for MIF. MIF interacts with p115 in the cytoplasm and the stimulated secretion of MIF results in the accumulation of both proteins in supernatants, which is consistent with MIF release from cells in conjunction with p115. The depletion of p115 from monocytes/macrophages decreases the release of MIF but not other cytokines following inflammatory stimulation or intracellular bacterial infection. Notably, the small molecule MIF inhibitor 4-iodo-6-phenylpyrimidine inhibits MIF secretion by targeting the interaction between MIF and p115. These data reveal p115 to be a critical intermediary component in the regulated secretion of MIF from monocytes/macrophages.
Factors governing ferroelectric switching characteristics of thin VDF/TrFE copolymer films (2006)

A series of ferroelectric switching measurements are performed on the 75/25mol% vinylidene fluoride/trifluoroethylene copolymer thin films with various structures to elucidate the factors governing the switching characteristics of such films. It is shown that the spin-coated and well-annealed samples exhibit a remanent polarization P <sub xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink">r</sub> of 85 mC/m <sup xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink">2</sup> . Unlike that in previous reports, the switching time tau <sub xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink">s</sub> of these samples is independent of thickness down to 50 nm if Au electrodes are used instead of Al electrodes. Thin films with different metal electrodes exhibit anisotropic tau <sub xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink">s</sub> due to a potential difference between metal electrodes produced by their work function difference. A train of unipolar short on-off electric field pulses induce a slow but full polarization reversal whose time evolution supports the nucleation and growth mechanism. Continuous switching under bipolar on-off electric field pulses reveals an accelerated polarization reversal with decreasing pulse width. This means that tau <sub xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink">s</sub> is a function of not only applied electric field but also the preceding poling conditions. Fatigue is significantly improved using Au electrodes instead of Al electrodes. The results are discussed in relation to the microscopic features of the VDF/TrFE copolymer and the underlying nucleation-growth mechanism
Mobilization and collection of autologous hematopoietic progenitor/stem cells. (2007)

Autologous hematopoietic progenitor/stem cell (HPC) transplantation has become a standard treatment for a wide variety of malignancies. Most HPCs at present are collected from the peripheral blood via leukapheresis following chemotherapy and/or growth factor-mediated mobilization. Several commercial platforms are available to enumerate the circulating levels of CD34+ HPCs. These values can then be used to guide the timing of leukapheresis as well as to measure the success of daily collections. Most mobilization regimens consist of chemotherapy followed by one or more growth factors such as granulocyte colony-stimulating factor, granulocyte-macrophage colony-stimulating factor, erythropoietin, or AMD3100. Occasionally a subset of patients will prove unable to mobilize effectively enough to collect at least 2 x 106 CD34+ cells/kg, the number of HPCs currently considered to be appropriate for timely engraftment and recovery of hematopoiesis. In this subset of patients, repeat HPC collection or marrow harvest with or without growth factor stimulation may be tried. The importance of the stem cell niche in mobilization, in particular the relationship of osteoblasts and the sympathetic nervous system in the release of HPCs and other cells from the marrow stroma, may lead to entirely different or improved methods of mobilization in the future. Recent research has explored the benefits of using HPCs outside of the oncology arena, notably in the area of cardiac myocyte regeneration following infarction, making the subject of mobilization potentially important to physicians in many areas of medicine.
Localization of insulin-like growth factor I and inhibition of coronary smooth muscle cell growth by somatostatin analogues in human coronary smooth muscle cells. A potential treatment for restenosis? (1994)

In this study, we demonstrate, for the first time, the localization of insulin-like growth factor I (IGF-I) in de novo and restenotic human coronary atherectomy plaques by using immunocytochemical techniques. Smooth muscle cells (SMCs) exhibiting the synthetic phenotype contained a statistically significant higher concentration of IGF-I than SMCs of the contractile phenotype or SMCs from normal coronary arteries. In addition, we provide data to suggest that the long-acting somatostatin analogues octreotide and angiopeptin inhibit IGF-I- and basic fibroblast growth factor (b-FGF)- induced human coronary artery SMC proliferation. Platelet-derived growth factor (PDGF)-stimulated cultures were minimally affected by the addition of octreotide but were significantly inhibited by angiopeptin. All three growth factors stimulated SMC migration in a dose-dependent manner. The somatostatin analogues tested had no effect on growth factor-stimulated SMC migration. Our data suggest that by reducing SMC proliferation, somatostatin analogues may have clinical usefulness in reducing the high incidence of restenosis observed after percutaneous transluminal coronary artery interventions.