gebhart/patrepeval huggingface dataset:
Acyl-lipid desaturases and their importance in the tolerance and acclimatization to cold of cyanobacteria (1995)

Research Article| May 15 1995 Acyl-lipid desaturases and their importance in the tolerance and acclimatization to cold of cyanobacteria N Murata; N Murata *Department of Regulation Biology, National Institute for Basic Biology, Myodaiji, Okazaki 444, Japan Search for other works by this author on: This Site PubMed Google Scholar H Wada H Wada †Deparment of Biology, Faculty of Science, Kyushu University, Ropponmatsu, Fukuoka 810, Japan Search for other works by this author on: This Site PubMed Google Scholar Biochem J (1995) 308 (1): 1–8. https://doi.org/10.1042/bj3080001 Views Icon Views Article contents Figures & tables Video Audio Supplementary Data Peer Review Share Icon Share Twitter LinkedIn Cite Icon Cite Get Permissions Citation N Murata, H Wada; Acyl-lipid desaturases and their importance in the tolerance and acclimatization to cold of cyanobacteria. Biochem J 15 May 1995; 308 (1): 1–8. doi: https://doi.org/10.1042/bj3080001 Download citation file: Ris (Zotero) Reference Manager EasyBib Bookends Mendeley Papers EndNote RefWorks BibTex toolbar search Search Dropdown Menu toolbar search search input Search input auto suggest filter your search All ContentAll JournalsBiochemical Journal Search Advanced Search This content is only available as a PDF. © 1995 The Biochemical Society, London1995 Article PDF first page preview Close Modal You do not currently have access to this content.
Endogenous Hydrogen Sulfide Regulates Pulmonary Artery Collagen Remodeling in Rats with High Pulmonary Blood Flow (2009)

The mechanisms responsible for the structural remodeling of pulmonary vasculature induced by increased pulmonary blood flow are not fully understood. This study explores the effect of endogenous hydrogen sulfide (H2S), a novel gasotransmitter, on collagen remodeling of the pulmonary artery in rats with high pulmonary blood flow. Thirty-two Sprague-Dawley rats were randomly divided into sham, shunt, sham+PPG (D,L-propargylglycine, an inhibitor of cystathionine-gamma-lyase), and shunt+PPG groups. After 4 weeks of shunting, the relative medial thickness (RMT) of pulmonary arteries and H2S concentration in lung tissues were investigated. Collagen I and collagen III were evaluated by hydroxyproline assay, sirius-red staining, and immunohistochemistry. Pulmonary artery matrix metalloproteinase-13 (MMP-13), tissue inhibitor of metalloproteinase-1 (TIMP-1), and connective tissue growth factor (CTGF) were evaluated by immunohistochemistry. After 4 weeks of aortocaval shunting, resulting in an elevation of lung tissue H2S to 116.4%, rats exhibited collagen remodeling and increased CTGF expression in the pulmonary arteries. Compared with those of the shunt group, lung tissue H2S production was lowered by 23.4%, RMT of the pulmonary artery further increased by 39.5%, pulmonary artery collagen accumulation became obvious, and pulmonary artery CTGF expression elevated (P<0.01) in the shunted rats treated with PPG. However, pulmonary artery MMP-13 and TIMP-1 expressions decreased significantly in rats of shunt+PPG group (P<0.01). This study suggests that endogenous H2S exerts an important regulatory effect on pulmonary collagen remodeling induced by high pulmonary blood flow.
A novel JAK inhibitor, peficitinib, demonstrates potent efficacy in a rat adjuvant-induced arthritis model (2016)

The Janus kinase (JAK) family of tyrosine kinases is associated with various cytokine receptors. JAK1 and JAK3 play particularly important roles in the immune response, and their inhibition is expected to provide targeted immune modulation. Several oral JAK inhibitors have recently been developed for treating autoimmune diseases, including rheumatoid arthritis (RA). Here, we investigated the pharmacological effects of peficitinib (formerly known as ASP015K), a novel, chemically synthesized JAK inhibitor. We found that peficitinib inhibited JAK1 and JAK3 with 50% inhibitory concentrations of 3.9 and 0.7 nM, respectively. Peficitinib also inhibited IL-2-dependent T cell proliferation in vitro and STAT5 phosphorylation in vitro and ex vivo. Furthermore, peficitinib dose-dependently suppressed bone destruction and paw swelling in an adjuvant-induced arthritis model in rats via prophylactic or therapeutic oral dosing regimens. Peficitinib also showed efficacy in the model by continuous intraperitoneal infusion. Area under the concentration versus time curve (AUC) at 50% inhibition of paw swelling via intraperitoneal infusion was similar to exposure levels of AUC at 50% inhibition via oral administration, implying that AUC might be important for determining the therapeutic efficacy of peficitinib. These data suggest that peficitinib has therapeutic potential for the oral treatment of RA.
PLL-Based, Impedance Controlled Output Buffer (1991)

This paper describes a PLL(Phase Lock Loop)-based, impedance controlled output buffer. This output buffer has constant impedance over a wide range in supply voltage, temperature and process fluctuation.
Demonstration of a Rational Strategy for Human Prostate Cancer Gene Therapy (1994)

The potential efficacy and clinical feasibility of gene therapy for prostate cancer were tested. Efficacy was tested using the Dunning rat prostate carcinoma model. Rats with anaplastic, hormone refractory prostate cancer treated with irradiated prostate cancer cells genetically engineered to secrete human granulocyte-macrophage colony-stimulating factor (GM-CSF) showed longer disease-free survival compared to either untreated control rats or rats receiving prostate cancer cell vaccine mixed with soluble human GM-CSF. A gene modified prostate cancer cell vaccine thus provided effective therapy for anaplastic, hormone refractory prostate cancer in this animal model. An evaluation of the clinical feasibility of gene therapy for human prostate cancer based on these findings was then undertaken. Prostate cancer cells from patients with stage T2 prostate cancer undergoing radical prostatectomy were first transduced with MFG-lacZ, a retroviral vector carrying the beta-galactosidase reporter gene. Efficient gene transfer was achieved in each of 16 consecutive cases (median transduction efficiency 35%, range 12 to 65%). Cotransduction with a drug-selectable gene was not required to achieve high yield of genetically modified cells. Histopathology confirmed malignant origin of these cells and immunofluorescence analysis of cytokeratin 18 expression confirmed prostatic luminal-epithelial phenotype in each case tested. Cell yields (2.5 x 10(8) cells per gram of prostate cancer) were sufficient for potential entry into clinical trials. Autologous human prostate cancer vaccine cells were then transduced with MFG-GM-CSF, and significant human GM-CSF secretion was achieved in each of 10 consecutive cases. Sequential transductions increased GM-CSF secretion in each of 3 cases tested, demonstrating that increased gene dose can be used to escalate desired gene expression in individual patients. These studies show a preclinical basis for proceeding with clinical trials of gene therapy for human prostate cancer.
Recombinant human growth hormone (GH)-binding protein enhances the growth-promoting activity of human GH in the rat (1996)

To address the role of the GH-binding protein (GHBP) in GH physiology, two forms of recombinant human GHBP (rhGHBP) were given alone or in combination with rhGH to hypophysectomized rats or GH-deficient dwarf rats. Hypophysectomized rats were given daily sc injections of excipient, hGH, rhGHBP, or rhGH plus rhGHBP (produced in Escherichia coli) for 7 days. Injections of rhGH induced dose-related body weight gain and bone growth that were increased by the coadministration of rhGHBP with rhGH; rhGHBP alone had no effect. Serum insulin-like growth factor increased 24 h later when rhGH was given together with rhGHBP (P < 0.01), but not when rhGH was given alone. E. coli-derived rhGHBP also enhanced the bioactivity of coadministered rhGH in the GH-deficient dwarf rat. In contrast, the glycosylated rhGHBP, made in human A293 cells, inhibited the growth-promoting activity of coadministered rhGH. The opposite effects of these two forms of rhGHBP could be explained by clearance studies that showed radiolabeled rhGH bound to A293 cell-derived rhGHBP to be cleared more rapidly from the blood than free rhGH. Natural rabbit GHBP and E. coli-derived rhGHBP both prolonged the presence of rhGH in blood. It is proposed that by slowing the clearance of GH, GHBP increased the bioactivity of GH. In summary, codelivery of rhGHBP and rhGH caused a dose-dependent enhancement of the activity of rhGH in two rat models of GH deficiency. This suggests that endogenous circulating GHBP may increase the activity of blood-borne GH in a similar manner.
Source parameters of injection-induced microearthquakes at 9 km depth at the KTB Deep Drilling site, Germany (1998)

Abstract A fluid injection-induced seismicity experiment was undertaken in the KTB (German Continental Deep Drilling Program) main borehole at 9 km depth. Several hundred microearthquakes were recorded by a three-component geophone at 4 km depth in the pilot hole of the KTB about 200 m west of the main hole. More than 100 of these events were also recorded with good signal-to-noise ratio by a 73-element temporary network at the surface. Several different clusters of microearthquakes with distinct waveforms were defined. Compound fault-plane solutions for the two most prominent clusters of seismic events were determined: a strike-slip mechanism for cluster 1 at an average depth of about 8.9 km and a strike-slip/reverse mechanism for cluster 4 (with the “main” ML = 1.2 event) at an average depth of 8.6 km. For both fault-plane solutions, the P axis is subhorizontal and oriented NNW-SSE, similar to the N160°E direction of maximum horizontal stress observed in the well bore. Both clusters were analyzed using an empirical Green's function method to derive the relative source time function (RSTF). Azimuthal variations of the RSTF were used to determine rupture directions and velocities. By combining the information about rupture directions with fault-plane solutions, it was possible to identify the active fault planes (NE striking nodal planes) for both clusters. Although injection-induced events are supposed to exhibit a dilatational component due to the tensile character of the source, the moment tensor inversion for both microearthquake clusters resulted in a double-couple contribution of about 90% and P axes similar to the direction of maximum horizontal stress observed in the borehole. The isotropic components of the moment tensors are insignificant due to the size of the location uncertainties. From records of the sensor at 4 km depth, we found seismic moments of the microearthquakes ranging from 107 to 1011 N-m. The spectra were corrected for Q [Q(f) = 420 f0.5 for P, and Q(f) = 230 f0.5 for S-waves, which were determined assuming an ω2 model]. Following Brune (1970, 1971), we found source radii between 12 and 28 m and stress drops between 0.01 and 6 MPa. The average ratio of S- to P-wave energy was determined as 14.2. Our relation between seismic moment and ML is log M0 = 1.01 ML + 9.68, and between energy and seismic moment, log E = 2.0 log M0 - 15.35. These seismic scaling relations suggest that stress drop increases with seismic moment for this data set. However, it cannot be precluded that our data, covering only somewhat more than three orders of magnitude, fall in a larger trend of constant-stress-drop scaling over many orders of magnitude due to the large scatter observed over several orders of magnitude.
Abrogation of the Chk1-mediated G(2) checkpoint pathway potentiates temozolomide-induced toxicity in a p53-independent manner in human glioblastoma cells. (2001)

Temozolomide (TMZ) produces O(6)-methylguanine in DNA, which in turn mispairs with thymine, triggering futile DNA mismatch repair (MMR) and ultimately cell death. We found previously that in p53-proficient human glioma cells, TMZ-induced futile DNA MMR resulted not in apoptosis but rather in prolonged, p53- and p21-associated G(2)-M arrest and senescence. Additionally, p53-deficient cells were relatively more TMZ resistant than p53-deficient glioma cells, which underwent only transient G(2)-M arrest before death by mitotic catastrophe. These results suggested that prolonged G(2)-M arrest might protect cells from TMZ-induced cytotoxicity. In the present study, we therefore focused on the mechanism by which TMZ induces G(2)-M arrest and on whether inhibition of such G(2)-M arrest might sensitize glioma cells to TMZ-induced toxicity. U87MG glioma cells treated with TMZ underwent G(2)-M arrest associated with Chk1 activation and phosphorylation of both cdc25C and cdc2. These TMZ-induced effects were inhibited by the Chk1 kinase inhibitor UCN-01. Although not in itself toxic, UCN-01 increased the cytotoxicity of TMZ 5-fold, primarily by inhibiting cellular senescence and increasing the percentage of cells bypassing G(2)-M arrest and undergoing mitotic catastrophe. In addition to enhancing TMZ-induced cytotoxicity in p53-proficient cells, UCN-01 also blocked TMZ-induced Chk1 activation and transient G(2)-M arrest in p53-deficient U87MG-E6 cells and similarly enhanced TMZ-induced mitotic catastrophe and cell death. Taken together, these results indicate that Chk1 links TMZ-induced MMR to G(2)-M arrest. Furthermore, inhibition of the cytoprotective G(2) arrest pathway sensitizes cells to TMZ-induced cytotoxicity and may represent a novel, mechanism-based means of increasing TMZ efficacy in both p53 wild-type and p53 mutant glioma cells.
City-Scale Location Recognition (2007)

We look at the problem of location recognition in a large image dataset using a vocabulary tree. This entails finding the location of a query image in a large dataset containing 3times10 <sup xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink">4</sup> streetside images of a city. We investigate how the traditional invariant feature matching approach falls down as the size of the database grows. In particular we show that by carefully selecting the vocabulary using the most informative features, retrieval performance is significantly improved, allowing us to increase the number of database images by a factor of 10. We also introduce a generalization of the traditional vocabulary tree search algorithm which improves performance by effectively increasing the branching factor of a fixed vocabulary tree.
Activated Expression of anArabidopsisHD-START Protein Confers Drought Tolerance with Improved Root System and Reduced Stomatal Density (2008)

Drought is one of the most important environmental constraints limiting plant growth and agricultural productivity. To understand the underlying mechanism of drought tolerance and to identify genes for improving this important trait, we conducted a gain-of-function genetic screen for improved drought tolerance in Arabidopsis thaliana. One mutant with improved drought tolerance was isolated and designated as enhanced drought tolerance1. The mutant has a more extensive root system than the wild type, with deeper roots and more lateral roots, and shows a reduced leaf stomatal density. The mutant had higher levels of abscisic acid and Pro than the wild type and demonstrated an increased resistance to oxidative stress and high levels of superoxide dismutase. Molecular genetic analysis and recapitulation experiments showed that the enhanced drought tolerance is caused by the activated expression of a T-DNA tagged gene that encodes a putative homeodomain-START transcription factor. Moreover, overexpressing the cDNA of the transcription factor in transgenic tobacco also conferred drought tolerance associated with improved root architecture and reduced leaf stomatal density. Therefore, we have revealed functions of the homeodomain-START factor that were gained upon altering its expression pattern by activation tagging and provide a key regulator that may be used to improve drought tolerance in plants.
Total synthesis of all (−)-agelastatin alkaloids (2010)

The pyrrole-imidazole family of marine alkaloids, derived from linear clathrodin-like precursors, constitutes a diverse array of structurally complex natural products. The bioactive agelastatins are members of this family that possess a tetracyclic molecular framework incorporating C4-C8 and C7-N12 bond connectivities. We provide a hypothesis for the formation of the unique agelastatin architecture that maximally exploits the intrinsic chemistry of plausible biosynthetic precursors. We report the concise enantioselective total syntheses of all known agelastatin alkaloids including the first total syntheses of agelastatins C, D, E, and F. Our gram-scale chemical synthesis of agelastatin A was inspired by our hypothesis for the biogenesis of the cyclopentane C-ring and required the development of new transformations including an imidazolone-forming annulation reaction and a carbohydroxylative trapping of imidazolones.
Durable antitumor responses to CD47 blockade require adaptive immune stimulation (2016)

Therapeutic antitumor antibodies treat cancer by mobilizing both innate and adaptive immunity. CD47 is an antiphagocytic ligand exploited by tumor cells to blunt antibody effector functions by transmitting an inhibitory signal through its receptor signal regulatory protein alpha (SIRPα). Interference with the CD47-SIRPα interaction synergizes with tumor-specific monoclonal antibodies to eliminate human tumor xenografts by enhancing macrophage-mediated antibody-dependent cellular phagocytosis (ADCP), but synergy between CD47 blockade and ADCP has yet to be demonstrated in immunocompetent hosts. Here, we show that CD47 blockade alone or in combination with a tumor-specific antibody fails to generate antitumor immunity against syngeneic B16F10 tumors in mice. Durable tumor immunity required programmed death-ligand 1 (PD-L1) blockade in combination with an antitumor antibody, with incorporation of CD47 antagonism substantially improving response rates. Our results highlight an underappreciated contribution of the adaptive immune system to anti-CD47 adjuvant therapy and suggest that targeting both innate and adaptive immune checkpoints can potentiate the vaccinal effect of antitumor antibody therapy.
Smart aortic arch catheter: Moving suspended animation from the laboratory to the field (2004)

From Alion Science and Technology, McLean, VA. Supported, in part, by the U.S. Army Telemedicine and Advanced Technology Research Center, U.S. Army Medical Research and Materiel Command, Fort Detrick, MD (award DAMD17-01-C-0069). Moving suspended animation from the laboratory to the field is now fully feasible and achievable in the near future.
Spatial learning with a minislab in the dorsal hippocampus. (1995)

We have determined the volume and location of hippocampal tissue required for normal acquisition of a spatial memory task. Ibotenic acid was used to make bilateral symmetric lesions of 20-100% of hippocampal volume. Even a small transverse block (minislab) of the hippocampus (down to 26% of the total) could support spatial learning in a water maze, provided it was at the septal (dorsal) pole of the hippocampus. Lesions of the septal pole, leaving 60% of the hippocampi intact, caused a learning deficit, although normal electrophysiological responses, synaptic plasticity, and preserved acetylcholinesterase staining argue for adequate function of the remaining tissue. Thus, with an otherwise normal brain, hippocampal-dependent spatial learning only requires a minislab of dorsal hippocampal tissue.
Chemistry of the 3a,7a-Dihydro-1H-indole Esters. Aromatization by Bromine$^\dag$ (1986)

A series of tetramethyl 1-substituted benzyl-3a,7a-dihydro-1H-indole-2,3,3a,4-tetracarboxylates were prepared and their reactions with bromine were examined. The initial reaction seemed to be the formation of the intermediate N-bromo quaternary ammonium bromide. This intermediate underwent aromatization with loss of the 3a-methoxycarbonyl group. Bromine replaced the N-substituent of the p-methoxybenzyl compound and addition of bromine occurred across the double bond of the indole ring. Bromination of the benzyl ring and aromatization occurred for the m-methoxybenzyl compound.
Acute effects of intravenous and rectal acetate on glucagon-like peptide-1, peptide YY, ghrelin, adiponectin and tumour necrosis factor-α (2009)

In animals, colonic infusion of SCFA does not affect glucagon-like peptide-1 (GLP-1) release whereas intravenous infusion does and SCFA may directly stimulate peptide YY (PYY) release. It is unknown whether SCFA and their route of administration affect human blood concentrations of GLP-1 and PYY. Our aim was to conduct a pilot study to determine the effects of intravenous and rectal acetate on blood concentrations of GLP-1, PYY, ghrelin, adiponectin and TNF-alpha in hyperinsulinaemic human subjects. Six hyperinsulinaemic female subjects were given 20 mmol sodium acetate intravenously, 60 mmol acetate rectally, or normal saline rectally or intravenously on four separate occasions in randomised order, with blood samples collected at 0, 10, 15, 30, 45 and 60 min. Change in plasma PYY was significantly higher after acetate and rectal infusions (9.69 and 13.78 pg/ml) compared with saline and intravenous (0.60 and - 3.1 pg/ml; P < 0.01), respectively. Change in plasma GLP-1 was increased by rectal and acetate infusions (0.25 and 0.23 mmol/l) v. intravenous and saline ( - 0.26 and - 0.19 mmol/l; P < 0.01). Acetate decreased TNF-alpha v. saline ( - 0.8 and 0.15 pg/ml; P < 0.05). Rectal infusions increased TNF-alpha and ghrelin (0.2 and 98.27 pg/ml) v. intravenous ( - 0.9 and - 40 pg/ml; P < 0.01). There was no effect of treatment on plasma adiponectin. These preliminary results suggest that acetate raises plasma PYY and GLP-1, and suppresses TNF-alpha. Also, distending the rectum increases PYY, GLP-1, TNF-alpha and ghrelin in hyperinsulinaemic females. Increasing colonic fermentation products, particularly acetate, could yield a new mechanism for modifying weight gain.
Applicability of Next Generation Sequencing Technology in Microsatellite Instability Testing (2015)

Microsatellite instability (MSI) is a useful marker for risk assessment, prediction of chemotherapy responsiveness and prognosis in patients with colorectal cancer. Here, we describe a next generation sequencing approach for MSI testing using the MiSeq platform. Different from other MSI capturing strategies that are based on targeted gene capture, we utilize "deep resequencing", where we focus the sequencing on only the microsatellite regions of interest. We sequenced a series of 44 colorectal tumours with normal controls for five MSI loci (BAT25, BAT26, BAT34c4, D18S55, D5S346) and a second series of six colorectal tumours (no control) with two mononucleotide loci (BAT25, BAT26). In the first series, we were able to determine 17 MSI-High, 1 MSI-Low and 26 microsatellite stable (MSS) tumours. In the second series, there were three MSI-High and three MSS tumours. Although there was some variation within individual markers, this NGS method produced the same overall MSI status for each tumour, as obtained with the traditional multiplex PCR-based method.