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Academic literature on the topic 'Renin'

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Published: 4 June 2021
Last updated: 1 August 2024

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Journal articles on the topic "Renin"

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Kruszelnicki, Karl. "Renin or rennin?" Latest Word: The Bimonthly Newsletter for Medical Transcriptionists, The 14, no. 2 (April 2006): 11. http://dx.doi.org/10.1016/j.latestword.2006.03.006.

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2

Hosoi, Masayuki, Shokei Kim, and Kenjiro Yamamoto. "Evidence for heterogeneity of glycosylation of human renin obtained by using lectins." Clinical Science 81, no. 3 (September 1, 1991): 393–99. http://dx.doi.org/10.1042/cs0810393.

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1. In this study, the carbohydrate structure of pure human renin was examined by using various lectins. 2. Pure renin could be separated into three forms by concanavalin A chromatography, a concanavalin A-unbound form, a loosely bound form and a tightly bound form, termed renins A, B and C, respectively. Renins A, B and C accounted for 3, 13 and 84%, respectively, of the purified renin. These forms were all present in individual human plasma and the relative proportions in plasma were 27 ± 3, 33 ± 4 and 39 ± 5% (means ± sem) for renins A, B and C, respectively (n = 5). 3. Each form, electroblotted on to the nitrocellulose sheet after gel electrophoresis, was incubated with five peroxidase-labelled lectins, lentil lectin, erythroagglutinating phytohaemagglutinin, wheat-germ agglutinin, Ricinus communis agglutinin and peanut agglutinin. The protein was stained with 4-chloro-l-naphthol. 4. The staining pattern obtained with these lectins was significantly different among the three forms of human renin, confirming that they have different carbohydrate structures. Furthermore, the positive staining of human renin with erythroagglutinating phytohaemagglutinin, wheat-germ agglutinin and Ricinus communis agglutinin was in contrast with the lack of binding of rat renin to these lectins. 5. These results indicate the renal secretion of differently glycosylated multiple forms of human renin. The carbohydrate structure of human renin appears to differ from that of rat renin.
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Glorioso, N., C. Troffa, J. H. Laragh, S. A. Atlas, D. Marion, and J. E. Sealey. "The cat: an animal model for studies of inactive renin." American Journal of Physiology-Endocrinology and Metabolism 252, no. 4 (April 1, 1987): E509—E518. http://dx.doi.org/10.1152/ajpendo.1987.252.4.e509.

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Inactive renin, prorenin, is found in high concentrations in human plasma. We report herein the characteristics of trypsin-activated inactive renin from cat kidney and plasma. Cat and human plasma inactive renin were activated by similar concentrations of trypsin. As in humans, there was more inactive than active renin in cat plasma; also, inactive renin was low but detectable after nephrectomy. Trypsin-activated renal inactive renin, purified on Cibacron blue agarose and pepstatin-amino-hexyl-Sepharose chromatography, was inhibited by pepstatin and by a renin inhibitor similarly to cat and human active renins. The pH optimum of cat renin was biphasic: the higher peak of active renin was at pH 5.7, whereas that of activated inactive renin was at pH 7.5. As in humans, active and inactive plasma renin increased during sodium depletion and inactive renin increased during beta-adrenergic blockade, while active renin decreased. These results demonstrate that cat inactive renin is similar to human prorenin. Therefore, the cat may be a useful model for the study of prorenin.
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Kim, S., M. Hiruma, F. Ikemoto, and K. Yamamoto. "Importance of glycosylation for hepatic clearance of renal renin." American Journal of Physiology-Endocrinology and Metabolism 255, no. 5 (November 1, 1988): E642—E651. http://dx.doi.org/10.1152/ajpendo.1988.255.5.e642.

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Three differently glycosylated forms of renin (renin A, B-1, and B-2) were highly purified from rat kidneys by pepstatin-aminohexyl-Sepharose affinity chromatography and by serial lectin affinity chromatography on concanavalin A (con A) and lentil lectin-Sepharose, and the role of glycosylation of renin was investigated. Renin A and renin B-1 were loosely and tightly bound to con A, respectively, but did not bind to lentil lectin. Renin B-2 bound to both con A and lentil lectin. These three forms of renin were all similar in their physicochemical characteristics, including molecular weight, isoelectric point, specific activity, Km, optimum pH, and antigenicity. Each form of renin, labeled with 125I and given intravenously to anesthetized rats, disappeared from the circulation at different rates (metabolic clearance rates of 5.05 +/- 1.02, 17.1 +/- 2.5, and 36.0 +/- 4.1 ml.min-1.kg-1 for renins A, B-1, and B-2, respectively). Labeled renin A distributed to a similar extent in the liver and kidney (21.2 +/- 0.2 and 15.2 +/- 0.8% of the injected dose, respectively), whereas renins B-1 and B-2 were distributed predominantly in the liver (56.3 +/- 1.2 and 72.3 +/- 3.7% of the injected dose, respectively) and to a lesser extent in the kidney (4.3 +/- 0.3 and 2.1 +/- 0.2%, respectively). Deglycosylation of renin B-1 with endoglycosidase F resulted in no loss of its enzymatic activity or antigenicity but greatly reduced the metabolic clearance rate to 18% (from 17.1 +/- 2.5 to 3.09 +/- 0.17 ml.min-1.kg-1). Deglycosylation of renin B-1 greatly decreased its uptake by the liver (from 56.3 +/- 1.2 to 3.3 +/- 0.2%) and increased its uptake by the kidney (from 4.3 +/- 0.3 to 23.9 +/- 0.9%). These studies indicate the importance of glycosylation of renin for its hepatic uptake and metabolic clearance rate.
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Liang, Ping, Craig A. Jones, Brent W. Bisgrove, Lei Song, Sean T. Glenn, H. Joseph Yost, and Kenneth W. Gross. "Genomic characterization and expression analysis of the first nonmammalian renin genes from zebrafish and pufferfish." Physiological Genomics 16, no. 3 (February 13, 2004): 314–22. http://dx.doi.org/10.1152/physiolgenomics.00012.2003.

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Liang, Ping, Craig A. Jones, Brent W. Bisgrove, Lei Song, Sean T. Glenn, H. Joseph Yost, and Kenneth W. Gross. Genomic characterization and expression analysis of the first nonmammalian renin genes from zebrafish and pufferfish. Physiol Genomics 16: 314–322, 2004. First published November 25, 2003; 10.1152/physiol-genomics. 00012.2003.—Renin is a key enzyme in the renin-angiotensin system (RAS), a pathway which plays an important physiological role in blood pressure and electrolyte homeostasis. The origin of the RAS is believed to have accompanied early evolution of vertebrates. However, renin genes have so far only been unequivocally identified in mammals. Whether or not a bona fide renin gene exists in nonmammalian vertebrates has been an intriguing question of physiological and evolutionary interest. Using a genomic analytical approach, we identified renin genes in two nonmammalian vertebrates, zebrafish ( Danio rerio) and pufferfish ( Takifugu rubripes). Phylogenetic analysis demonstrates that the predicted fish renins cluster together with mammalian renins to form a distinct subclass of vertebrate aspartyl proteases. RT-PCR results confirm generation of the predicted zebrafish mRNA and its expression in association with the opisthonephric kidney of adult zebrafish. Comparative in situ hybridization analysis of wild-type and developmental mutants indicates that renin expression is first detected bilaterally in cells of the interrenal primordia at 24 h postfertilization, which subsequently migrate to lie adjacent to, but distinct from, the glomerulus of the developing pronephric kidney. Our report provides the first molecular evidence for the existence of renin genes in lower vertebrates. The observation that the earliest renin-expressing cells, arising during ontogeny of this teleost vertebrate, are of adrenocortical lineage raises an interesting hypothesis as regards the origin of renin-expressing cells in the metanephric kidney of higher vertebrates.
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Evans, DB, JC Cornette, TK Sawyer, DJ Staples, AE de Vaux, and SK Sharma. "Substrate specificity and inhibitor structure‐activity relationships of recombinant human renin: implications in the in vivo evaluation of renin inhibitors." Biotechnology and Applied Biochemistry 12, no. 2 (April 1990): 161–75. http://dx.doi.org/10.1111/j.1470-8744.1990.tb00089.x.

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Homogeneous, active recombinant human renin obtained from Chinese hamster ovary (CHO) cells was characterized in vitro by (i) determination of its relative rates of hydrolysis of plasma angiotensinogens (ANGs) from human, monkey, baboon, rat, pig, rabbit, hamster, and dog and (ii) analysis of several synthetic ANG‐based, inhibitors ranging in IC50 from 10(‐10) to 10(‐6) M. Comparison of the recombinant human renin with human kidney renin showed that these enzymes were indistinguishable from each other in terms of their plasma ANG specificities and inhibition by synthetic renin inhibitors. Porcine kidney renin was also characterized and shown to display plasma ANG hydrolysis profiles and inhibitor potencies that were markedly different from those of human renins. Finally, the results using the above plasma ANGs extend previous studies showing that the substrate specificity of human renin may be influenced by the amino acid residues at P2 (i.e., Ile, Val, or Tyr) and P3 (i.e., His or Tyr) sites. The relevance of these data to in vivo evaluation of renin inhibitors in animal models is discussed.
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Duan, J., J. Jaramillo, G. L. Jung, A. L. McLeod, B. H. Fernandas, and D. Mathis. "Comparative studies on differential inhibition of the rennin–angiotensin system in the anesthetized guinea pig." Canadian Journal of Physiology and Pharmacology 73, no. 10 (October 1, 1995): 1512–18. http://dx.doi.org/10.1139/y95-209.

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The present study compares the hemodynamic effects and mechanisms of action of angiotensin II (AngII) antagonists, angiotensin converting enzyme (ACE) inhibitors, and renin inhibitors in the guinea pig, an animal with high similarity to primates in terms of in vitro and in vivo responses to several human renin inhibitors. Animals were anesthetized with urethane and ketamine. The carotid artery was catheterized for monitoring blood pressure and heart rate. After 30 min stabilization, drug (or vehicle) effects were monitored for 1 h following each increasing dose (i.v. bolus injection). Drugs tested include losartan, an AngII receptor antagonist; two renin inhibitors, BILA 2157 BS and PD-134672; and captopril, an ACE inhibitor. All drugs dose dependency decreased blood pressure. Diastolic blood pressure was reduced more than systolic blood pressure, suggestive of vasodilation. The maximum decrease (32 ± 6%, p < 0.05 vs. vehicle) in mean arterial blood pressure (MABP) by losartan was achieved with a dose of 1 mg/kg. A similar decrease in MABP was observed with renin inhibitors at a dose of 3 mg/kg, without affecting heart rate. A further increase in the dose of renin inhibitors (6 mg/kg) decreased not only blood pressure but also heart rate. Captopril decreased MABP with a maximum of 48 ± 3% (p < 0.05 vs. vehicle, losartan, and PD-134672). In the presence of HOE-140, a bradykinin antagonist, the MABP decrease by captopril was only 35 ± 4%, (p < 0.05 vs. captopril alone). Bilateral nephrectomy reduced the peak MABP effect of PD-134672 by 67%, while the effects of captopril on MABP were affected to a lesser degree (57%). Therefore, captopril remains more effective in reducing MABP (p < 0.05 vs. that of PD-134672). These results suggest that renin inhibitors and AngII antagonists act more specifically on the rennin–angiotensin system cascade, while captopril acts partially by a bradykinin-dependent mechanism. The small animal model described provides a novel tool for the comparative pharmacologic assessment of different rennin–angiotensin system inhibitors.Key words: blood pressure, guinea pig, rennin–angiotensin system, rennin–angiotensin system inhibition.
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Widimský, Jiří. "The new renin inhibitor aliskiren. The new drug blocking renin-angiotensin system. Will it meet the expectations?" Cor et Vasa 49, no. 11 (November 1, 2007): 408–14. http://dx.doi.org/10.33678/cor.2007.143.

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Ioannou, P., A. Y. Loh, and D. H. Osmond. "Activation and measurement of plasma prorenin in the rat." Canadian Journal of Physiology and Pharmacology 69, no. 9 (September 1, 1991): 1331–40. http://dx.doi.org/10.1139/y91-197.

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Prorenin determination in rat plasma has been problematic from the outset. Consequently, its existence is questioned by some and its quantity by others, making it difficult for knowledge to advance as to its function relative to the renin system. The present study examines major variables in the determination of rat plasma prorenin and renin, notably different prorenin activation protocols involving blood samples obtained under various conditions from animals under different anesthetics. We found that a trypsin activation step with 5 mg/mL plasma, 60 min at 23 °C, followed by a PRA step of 10 min at 37 °C, resulted in the highest prorenin estimates, up to approximately 400 ng∙mL−1∙h−1 in terms of angiotensin I, as compared with published values of 0–190, based on other protocols. These estimates were obtained despite considerable destruction of angiotensinogen (renin substrate) by trypsin. Cryoactivation of prorenin was much less effective than in human plasma but, when followed by trypsin, it facilitated greater activation than with trypsin alone. Comparable fresh and fresh-frozen plasmas had similar prorenin–renin values, but lower values were observed in plasmas that had been repeatedly frozen and thawed. Conscious rats and those anesthetized with Inactin or ether had higher renins and prorenins than those anesthetized with methoxyflurane or halothane. Rats with kidneys in place during blood collection had higher renins (but not prorenins) than those whose kidneys were clamped off, suggesting that last-minute renin release during blood collection had occurred. We conclude that (i) trypsin generates increased renin, or renin-like, activity in plasma, suggesting activation of a precursor; (ii) on this basis, high prorenin levels exist in normal rat plasma; (iii) renin and prorenin levels are variously influenced by different anesthetics and blood handling procedures; (iv) variation in prorenin levels suggests that it is a dynamic (functional?) component of the renin system; (v) prorenin measurements are heavily influenced by methodological variations during the trypsin step or the subsequent PRA step; (vi) using standardized methodology, the rat can serve as a model for investigating the function of prorenin in normotension and hypertension.Key words: tryptic activation, angiotensinogen, adrenalectomy, anesthesia.
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Sessler, F. M., J. A. Jacquez, and R. L. Malvin. "Different production and decay rates of six renin forms isolated from rat plasma." American Journal of Physiology-Endocrinology and Metabolism 250, no. 5 (May 1, 1986): E551—E557. http://dx.doi.org/10.1152/ajpendo.1986.250.5.e551.

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Rat kidney contains six forms of renin, which are in different proportion from those found in plasma. We tested the hypothesis that differential removal and production of the forms might explain the differences between stored and circulating renins. In one group of rats, the six forms of renin were measured in plasma, 10 min after hemorrhage, or after aortic constriction. Plasma was run on an isoelectric focusing gel, and the six peaks of renin activity were expressed either as angiotensin I per hour per milliliter or as a percentage of the total plasma renin concentration. After hemorrhage or aortic constriction, the concentration of each form was significantly increased; the profile of circulating renin was significantly modified, showing an increase in proportion of form 2 and a decrease of forms 4, 5, and 6. In a second group, the disappearance of each form was measured 0 to 100 min after nephrectomy and fitted a two-exponential decay curve. Interpreted as a two-pool system with degradation from pool 1, the degradation rate decreased progressively, going from form 1 to 6. In a third group, arterial and renal venous blood were collected. The profile of secreted renin was calculated from the arterial venous difference. This profile fitted the prediction of the two-compartment model. Our data support the hypothesis that the proportion of each circulating renin form is the result of a balance between the rate of production of renin of constant composition and the degradation of the six forms at different rates.
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Dissertations / Theses on the topic "Renin"

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Pryor, Wanda G. "Tissue renin: extrarenal sources of renin and their probable functions in relation to the renin-angiotensin system." DigitalCommons@Robert W. Woodruff Library, Atlanta University Center, 1987. http://digitalcommons.auctr.edu/dissertations/2770.

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During the past thirty years, investigators of the renin-angiotensin system have found renin-like substances in a number of non-traditional locations throughout mammalian systems. These renin-like substances have been found in virtually every component of the brain, as well as the salivary glands, adrenal glands, blood vessels, genital tracts of both males and females, tumor cell lines, and even the eyeball and retina. This thesis is a literary review which will focus on extrarenal renin sources located in the uterus and the testis. These two locations are of particular interest because of the probable function in the regulation of the reproductive cycle. In addition, information on submaxillary gland renin and brain renin will also be discussed but to a lesser extent than uterine and Leydig Cell renin. Extrarenal renin sources have been tagged as renin-like enzymes, or more popularly as isorenins, because immunologically they react as true renin does. The immunoreactivity of these isorenins has been detected by a number of methods which include immunohistochemistry, specific staining characteristics of immunolabelling, native gel electrophoresis, sodium dodecyl sulfate gel electrophoresis, isoelectric focusing, double immunodiffusion, and symmetric chromatographic elution patterns. Extensive research in this area is still underway. Numerous modes of detection are being used to evaluate the specific sites of synthesis for these extrarenal renin sources, as well as their release mechanisms and physiological roles. Undoubtedly, the data resulting from these investigations will reveal significant information regarding these non-traditional renin sources and their clinical relevance in the treatment of hypertension.
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Esch, Joep Hendrikus Maria van. "Unraveling the complexities of the renin-angiotensin system: from ACE to renin inhibition." [S.l.] : Rotterdam : [The Author] ; Erasmus University [Host], 2008. http://hdl.handle.net/1765/13132.

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Brameld, John M. "The ovarian renin angiotensin system." Thesis, University of Nottingham, 1990. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.293049.

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Oldham, A. A. "Species selectivity of renin inhibitors." Thesis, Open University, 1988. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.383703.

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Skipworth, J. R. A. "Hepatic mitochondrial renin-angiotensin systems." Thesis, University College London (University of London), 2015. http://discovery.ucl.ac.uk/1462711/.

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Introduction: The circulating renin-angiotensin system (RAS) was originally described as a key endocrine regulator of intravascular homeostasis; however, the existence of a local (tissue) RAS has become increasingly reported in a variety of tissues including liver. RAS components have now also been detected in rat heart, brain and smooth muscle cell mitochondria as well as within intramitochondrial dense bodies of rat adrenal tissue. Further, reduced RAS levels have been associated with improved endurance performance and fatigue resistance in human skeletal muscle, suggesting that low RAS activity is associated with metabolic efficiency, potentially via RAS action upon, or within, mitochondria. However, such investigation has often relied heavily upon qualitative techniques (e.g. Western blotting, immunofluorescence and electron microscopy), which contain inherent limitations in that they completely rely upon the limited specificity of antibodies to demonstrate the existence of intra-mitochondrial RAS components. Methods: The presence of RAS components within the mitochondria of rat hepatic tissue and liver cell-lines was investigated via sub-fractionation of rat liver tissue and cell-lines, followed by Western blotting, as well as via immunofluorescence and confocal microscopy, and electron microscopy. The mitochondrial effects of stimulating or antagonizing hepatic RAS were assessed via functional fluorescence microscopy (for assessment of NADH, calcium and mitochondrial membrane potential) and measurement of oxygen consumption within live cells of a liver cell-line. Results: Western blotting, immunofluorescence and electron microscopy suggested the presence of RAS components within mitochondria; however, there was a lack of results consistency between techniques and the staining patterns were largely non-specific. Western blotting further demonstrated the presence of a prominent 55 kDa band, when immunostaining a mitochondrial fraction with (angiotensin-converting enzyme) ACE Cterminal antibody (usual size 180 kDa). This was further explored via isolation of the 55 kDa molecule and mass spectrometry to yield results consistent with non-specific staining only. Addition of RAS agonists or antagonists to live liver cell-lines demonstrated no consistent results, except at supra-physiological levels, where RAS antagonists improved oxygen consumption. Conclusions: Such data suggest that the previous descriptions of RAS components within mitochondria are likely to be secondary to methodological flaws, particularly the reliance upon single antibodies, which have subsequently been shown to have poor specificity. Thus, the effect of ang II on liver mitochondria is unlikely to be direct and any such action is likely to occur via one of several intracellular pathways, regulation of gene expression or mitochondrial biogenesis.
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Xiao, Fang. "The vascular renin-angiotensin-aldosterone system." Thesis, Queen Mary, University of London, 2001. http://qmro.qmul.ac.uk/xmlui/handle/123456789/1788.

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The renin-angiotensin-aldosterone system (RAAS) is one of the major regulators of blood pressure. The actions and generation of RAAS components at the tissue level are less well appreciated. This work was designed to investigate the vascular wall not only as a target of the RAAS, but also as one of its sources. Immunocytochemical and immunoblotting analysis revealed positive renin immunoreactivity in the cytoplasm of cultured bovine aortic endothelial cells. Two immunoreactive bands of molecular mass approximately 37,000 and 40,000 dalton were identified. In situ hybridization confirmed that renin mRNA was localized in the same cells. Reverse transcriptase-polymerase chain reaction (RT-PCR) using primers specific for human renin gave a clear single band with the predicted size for (pro)renin. These findings suggest that these vascular endothelial cells are a source of local synthesised renin. Conditioned medium from cultured bovine aortic endothelial cells (BAECCM) and rat aortic smooth muscle cells (RASMCCM) were shown to contain immunoreactive angiotensin II (Ang II) equivalent to 15.05 ± 4.67 pg/106 cells and 1 1.16 ± 1.8 pg/ 106 cells, respectively. Tritiated thymidine incorporation into aortic smooth muscle cells (ASMC) was increased by Ang II and by BAECCM. In both cases, this stimulated proliferation was inhibited by the Ang II type I (AT, ) receptor selective antagonist, losartan. Although tritiated thymidine uptake by rat aortic smooth muscle cells (RASMC) was not significantly enhanced by RASMCCM, it was significantly decreased by losartan in the presence of RASMCCM or of serum-free medium. Assay of RASMC proliferation by cell counting showed that the number of I cells in the presence of Ang II (10'6M) were nearly twice that in control cultures after r 2 days. These findings suggest that Ang II produced by ASMC locally may regulate ASMC growth in an autocrine or/and paracrine fashion, via the AT, receptor. RASMC was also shown to produce immunoreactive aldosterone. Ang II significantly enhanced aldosterone formation by RASMC. but not in the presence of losartan. Ang II stimulated 3H-thymidine uptake into RASMC was further enhanced by aldosterone, but inhibited by the aldosterone antagonist. spironolactone. and the 3ß-hydroxysteroid-dehydogenase inhibitor trilostane. These results suggest that the presence of locally generated aldosterone is essential for the stimulatory effects of Ang II, acting via the AT, receptor. on RASMC proliferation. Amplified products corresponding to transcripts of the CYP 11 BI gene were obtained by RT-PCR on RNA extracted from RASMC, using primers chosen from homologous parts of the exon I and exon 2 regions of CYP IIBI and CYP II B2 genes. Sequencing showed the presence of CYP 11 B1 transcript, but gave no evidence for CYP 11 B2 gene transcription. RT-PCR also gave a band corresponding to the 770 bp fragment from bases - 486 (upstream) to + 284 (exon 2) bp of the CYP 1lB1 gene. Furthermore, the present experiments demonstrated the transcription of the sequences 183-480 bp upstream from the CYP 11 B1 gene, and the use of competitive RT-PCR showed this was regulated by Ang 11. Thus. cultured RASMC may be the site of Ang 11 regulated transcription of a longer fragment of the CYP 11 B1 gene than generally expected. Finally, use of immunofluorescence and immunoblotting demonstrated the presence of an apparent binding carrier for 18-OH-DOC in cultured RASMC similar to that found in the rat adrenal.
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Xu, Di. "Expression and functions of renin isoforms." Diss., University of Iowa, 2010. https://ir.uiowa.edu/etd/3015.

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Renin is an enzyme that catalyzes the rate-limiting step in the production of angiotensin peptides, and is thus a key regulator of processes controlled by angiotensin such as blood pressure, hydromineral balance, and metabolism. Our laboratory and others have previously identified a novel isoform of renin (icRen) which, as a result of the utilization of an alternate first exon, lacks the signal peptide and first third of the pro-segment of classical secreted renin (sRen). This alternate icRen isoform thus remains within the cytoplasm of the cell, but is constitutively active. Here, we report that while sRen is the predominant form of renin expressed in most tissues during development, icRen is the predominant form of renin within the adult brain. Thus, we hypothesized that sRen and icRen play distinct physiological roles in adult mice. To examine this hypothesis, we have utilized the Cre-LoxP system to selectively delete either isoform globally or within selected cell types such as neurons and glia. We have successfully developed a "sRen-flox" model, in which endogenous mouse sRen isoform can be selectively deleted, while not affecting endogenous icRen production. Breeding these mice against the E2A-Cre, Nestin-Cre, and GFAP-Cre mouse lines resulted in global-, neuronal-, and glial-specific knockouts of sRen, respectively. Physiological characterization of resulting mice has uncovered postnatal lethality, hypotension, renal atrophy, vascular dysfunction and decreased body weight and white adipose in the global knockouts. Depletion of sRen from only neuronal or glial cells does not appear to alter any of these phenotypes at baseline. From these data, we conclude that while peripheral sRen is of primary importance to blood pressure regulation, hydromineral balance, and metabolism, central expression of this isoform is unimportant. Further, comparison of our results to published findings from global total renin knockout models indirectly supports a role for icRen in the brain. We are currently in the process of generating icRen-flox and subsequent knockout mice, which will be useful models to directly analyze the physiological role(s) of icRen.
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Weatherford, Eric Thomas. "Regulation of renin gene expression by CTCF, Nr2f2, Nr2f6, Nr4a1 and maintenance of the renin expressing cell." Diss., University of Iowa, 2011. https://ir.uiowa.edu/etd/1104.

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The renin angiotensin system (RAS) is critical for the regulation of blood pressure, electrolyte/fluid, and metabolic homeostasis. Regulation of the RAS is important in the development and treatment of hypertension. As part of the rate-limiting step in a cascade of events ending in the production of angiotensin II, renin is a major regulator of the RAS. Its expression is localized to the juxtaglomerular (JG) cells of the JG apparatus where it is exquisitely located to respond to various physiological cues. Understanding the regulation of renin expression and development of the juxtaglomerular cells is critical. Two regulatory elements, the enhancer and proximal promoter, have been found to be important in controlling cell- and tissue- specific baseline expression of the renin gene. Within the enhancer is a hormone response element (HRE) which confers a high level of activity to the enhancer. Nuclear receptors that bind this element have been found to bind the HRE and regulate renin promoter transcriptional activity. We have previously characterized the role of the orphan nuclear receptor Nr2f6 as a negative regulator of renin expression that mediates its effects through the HRE. However, gel shift assays indicate that there are other transcription factors binding this element. We have identified other orphan nuclear receptors that regulate renin expression. The first, Nr2f2 acts as a negative regulator of renin promoter activity but does not appear to affect baseline expression of the endogenous renin gene. The other, Nr4a1, is a positive regulator of renin expression, but it does not appear to mediate its effects through the HRE. The transcriptional regulation of gene expression is controlled by regulatory elements separated by large distances from promoters. We and others have found that short transgenes of the human renin (hREN) locus are not sufficient to protect them from positional effects that can be exerted upon them by neighboring regulatory elements. We discovered a random truncation in a large genomic construct of the hREN gene that resulted in ubiquitous expression of renin not seen with the intact form. By locating the genomic insertion site of that transgene in the Zbtb20 gene, we found that the hREN promoter had come under control of that gene's regulatory elements. The gene downstream of renin however maintained its tissue-specific expression. We found that CCCTC-binding factor (CTCF) bound to chromatin in and around the renin locus. The presence of CTCF suggests that insulator elements are present in the renin locus, and their loss likely explains the results above. Finally, we assessed the role of microRNAs in the development of renin expressing cells in the mouse kidneys by cell-specific deletion of the processing enzyme Dicer. This resulted in reduction of renin expression and a decrease in the number of renin expressing cells in the kidney. Mice were hypotensive and had several kidney abnormalities including a hypertrophied vasculature and striped fibrosis. These results indicate that Dicer and the miRNAs it processes are critical for the development and maintenance of renin expressing cells that contribute to normal kidney development.
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Benson, Victoria Louise St Vincent's Clinical School UNSW. "The role of calcineurin in high-renin and low-renin animal models of pressure overload left ventricular hypertrophy." Awarded by:University of New South Wales. St Vincent's Clinical School, 2005. http://handle.unsw.edu.au/1959.4/20843.

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Left ventricular hypertrophy (LVH) in response to pressure overload is associated with increased cardiovascular morbidity and mortality, making its prevention an important therapeutic goal. The role of a calcineurin-dependent molecular pathway in the induction of pressure-overload LVH is controversial. The present study tested the hypothesis that, in the setting of LV pressure overload, activation of the systemic renin-angiotensin system was necessary for activation of this calcineurin pathway. Mild LV pressure overload was induced in male Wistar rats by abdominal aortic constriction (AAC) or transverse aortic arch constriction (TAC), producing well-matched pressure gradients of 37 ?? 8 and 35 ?? 15 mmHg, respectively. Tight transverse aortic arch constriction (TTAC) in additional animals produced a pressure gradient of 75 ?? 15 mmHg. Only AAC increased plasma renin concentration and activated the calcineurin pathway, indicated by increased nuclear NFAT3 content. Plasma renin concentration and nuclear NFAT3 content were unchanged in TAC and TTAC animals. AAC animals developed more LVH 21 days post-banding than TAC and TTAC animals: the slope of the relationship between LV/body weight ratio and systolic blood pressure was much steeper in AAC animals than the combined TAC and TTAC animals (20x10-6 versus 5x10-6, p<0.001). Treatment with the calcineurin inhibitor FK506 did not significantly alter the slope of this relationship in the combined TAC and TTAC animals (8x10-6), but FK506 abolished this relationship in AAC animals (-5x10-6, R =0.0003). These data indicate that activation of the calcineurin pathway occurs only in high-renin hypertension, providing an additional stimulus to LVH induction. Calcineurin plays no role in the induction of LVH in low-renin hypertension, which is much more common clinically.
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Broderson, Claudius [Verfasser]. "Laborbeurteilung des Renin-Angiotensin-Aldosteron-Systems : Evaluation im Praxisalltag und Vergleich verschiedener Methoden zur Renin-Bestimmung / Claudius Broderson." Berlin : Medizinische Fakultät Charité - Universitätsmedizin Berlin, 2021. http://d-nb.info/1234984261/34.

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Books on the topic "Renin"

1

K, Raizada Mohan, Phillips M. Ian, and Sumners Colin, eds. Cellular and molecular biology of the renin-angiotensin system. Boca Raton, Fla: CRC, 1993.

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S, Robertson J. I., Nicholls M. G, and August Phyllis, eds. The Renin-angiotensin system. London: Gower Medical Pub., 1993.

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Kobayashi, Hideshi, and Yoshio Takei. The Renin-Angiotensin System. Berlin, Heidelberg: Springer Berlin Heidelberg, 1996. http://dx.doi.org/10.1007/978-3-642-61164-3.

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Mukhopadhyay, Amal K., and Mohan K. Raizada, eds. Tissue Renin-Angiotensin Systems. Boston, MA: Springer US, 1995. http://dx.doi.org/10.1007/978-1-4899-0952-7.

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Kobayashi, Hideshi. The renin-angiotensin system: Comparative aspects. Berlin: Springer, 1996.

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Thatcher, Sean E., ed. The Renin-Angiotensin-Aldosterone System. New York, NY: Springer New York, 2017. http://dx.doi.org/10.1007/978-1-4939-7030-8.

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Klaus, Lindpaintner, and Ganten D. 1941-, eds. The Cardiac renin-angiotensin sytem. Armonk, NY: Futura Pub. Co., 1994.

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Kim, Min-ha. Renin ŭl sarang han ot'ak'u. Sŏul-si: T'eksŭt'ŭ, 2009.

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1934-, Aurell Mattias, Tigerstedt Robert 1853-1923, and Ulfendahl H. R, eds. Renin-angiotensin: Proceedings from a symposium held at the Wenner-Gren Research Institute, Stockholm, in September 1997, honouring Robert Tigerstedt and his discovery of the renin-angiotensin system. London: Portland Press, 1998.

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De Mello, Walmor C., ed. Renin Angiotensin System and the Heart. Chichester, UK: John Wiley & Sons, Ltd, 2004. http://dx.doi.org/10.1002/0470032103.

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Book chapters on the topic "Renin"

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Trachte, George J. "Renin." In Encyclopedia of Behavioral Medicine, 1884–85. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-39903-0_277.

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Molina, Kristine M., Kristine M. Molina, Heather Honoré Goltz, Marc A. Kowalkouski, Stacey L. Hart, David Latini, J. Rick Turner, et al. "Renin." In Encyclopedia of Behavioral Medicine, 1657–58. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4419-1005-9_277.

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Hubl, W. "Renin." In Lexikon der Medizinischen Laboratoriumsdiagnostik, 1–2. Berlin, Heidelberg: Springer Berlin Heidelberg, 2017. http://dx.doi.org/10.1007/978-3-662-49054-9_2674-1.

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Hubl, W. "Renin." In Springer Reference Medizin, 2054–55. Berlin, Heidelberg: Springer Berlin Heidelberg, 2019. http://dx.doi.org/10.1007/978-3-662-48986-4_2674.

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Trachte, George J. "Renin." In Encyclopedia of Behavioral Medicine, 1–2. New York, NY: Springer New York, 2017. http://dx.doi.org/10.1007/978-1-4614-6439-6_277-2.

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Tauler Riera, Pedro, Maurizio Volterrani, Ferdinando Iellamo, Francesco Fallo, Andrea Ermolao, William J. Kraemer, Nicholas A. Ratamess, Avery Faigenbaum, Andrew Philp, and Keith Baar. "Renin." In Encyclopedia of Exercise Medicine in Health and Disease, 758. Berlin, Heidelberg: Springer Berlin Heidelberg, 2012. http://dx.doi.org/10.1007/978-3-540-29807-6_2961.

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Henning, R., A. Wagner, and B. A. Schölkens. "Renin Inhibitors." In Pharmacology of Antihypertensive Therapeutics, 483–505. Berlin, Heidelberg: Springer Berlin Heidelberg, 1990. http://dx.doi.org/10.1007/978-3-642-74209-5_11.

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Schomburg, Dietmar, and Dörte Stephan. "gamma-Renin." In Enzyme Handbook 15, 559–61. Berlin, Heidelberg: Springer Berlin Heidelberg, 1998. http://dx.doi.org/10.1007/978-3-642-58948-5_119.

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Thaisrivongs, S., D. T. Pals, and S. R. Turner. "Renin Inhibitors." In ACS Symposium Series, 163–74. Washington, DC: American Chemical Society, 1991. http://dx.doi.org/10.1021/bk-1991-0456.ch011.

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Nguyen, Genevieve, and Aurelie Contrepas. "Renin, Prorenin, and the (Pro)Renin Receptor." In Renin Angiotensin System and Cardiovascular Disease, 15–24. Totowa, NJ: Humana Press, 2009. http://dx.doi.org/10.1007/978-1-60761-186-8_3.

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Conference papers on the topic "Renin"

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Takeda, Yoshinori, Asako Itaya-Hironaka, Akiyo Yamauchi, Mai Makino, Sumiyo Sakuramoto-Tsuchida, Hiroyo Ota, Ryuji Kawaguchi, and Shin Takasawa. "Intermittent hypoxia up-regulates Renin and Cd38 mRNAs in renin-producing cells via miR-203." In ERS International Congress 2021 abstracts. European Respiratory Society, 2021. http://dx.doi.org/10.1183/13993003.congress-2021.pa2393.

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Mei, D. "Modulating Renin-Angiotensin System for the Treatment of COPD." In American Thoracic Society 2020 International Conference, May 15-20, 2020 - Philadelphia, PA. American Thoracic Society, 2020. http://dx.doi.org/10.1164/ajrccm-conference.2020.201.1_meetingabstracts.a2538.

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MATTOS, ARTHUR FIOROTTO DE, NATHALIA SILVEIRA BARSOTTI, and RAFAEL RIBEIRO ALMEIDA. "RENIN-ANGIOTENSIN-ALDOSTERONE SYSTEM INHIBITORS AND COVID-19 COMPLICATIONS." In II Brazilian Congress of Health. HEALTH2021, 2021. http://dx.doi.org/10.51162/health2021-0001.

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The world faces today a pandemic of unquestionable importance, caused by an infection with a new enveloped RNA virus that belongs to the Coronaviridae family. The new coronavirus (SARS-CoV 2) uses a glycoprotein present on its surface to bind to and infect host cells that express the angiotensin converting enzyme II (ACE-2). Although different tissues may be targeted by the virus, respiratory complications remain as the main cause of death. It has been demonstrated that Renin-Angiotensin-Aldosterone System (RAAS) inhibitors increase ACE-2 expression in animal models, raising the concern that patients under treatment with these drugs could become more susceptible to COVID-19 complications. Here, we discuss the impact of RAAS inhibitors on COVID-19 outcomes and show that no evidence so far supports that the use of these drugs could pose a risk to SARS-CoV 2-infected patients. In fact, clinical data suggest that RAAS inhibitors may even act in a protective way against COVID-19 complications and should not be discontinued.,
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Yan, Zhang. "Pathological effects of the renin-angiotensin system on cardiovascular disease." In 2015 International Conference on Social Science and Technology Education. Paris, France: Atlantis Press, 2015. http://dx.doi.org/10.2991/icsste-15.2015.19.

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Tybitanclová, Katarína, Ľudmila Szabová, and Štefan Zorad. "AT1 receptor blockade by losartan activates plasma and kidney renin." In VIIIth Conference Biologically Active Peptides. Prague: Institute of Organic Chemistry and Biochemistry, Academy of Sciences of the Czech Republic, 2003. http://dx.doi.org/10.1135/css200306112.

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Lykouras, Dimosthenis, Kleanthis Theodoropoulos, Olga Lagiou, Fotios Sampsonas, Michail Lykouras, Agathi Spiropoulou, Apostolos Voulgaridis, et al. "Renin and aldosterone levels in obstructive sleep apnea syndrome patients." In Annual Congress 2015. European Respiratory Society, 2015. http://dx.doi.org/10.1183/13993003.congress-2015.pa2335.

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Annaeva, E. R., and L. F. Kelesheva. "CORRELATION BETWEEN PERIPHERAL RENIN-ANGIOTENSIN SYSTEMS’ ACTIVITY AND TOLERANCE TO ALCOHOL." In MODERN PROBLEMS IN SYSTEMIC REGULATION OF PHYSIOLOGICAL FUNCTIONS. NPG Publishing, 2019. http://dx.doi.org/10.24108/5-2019-confnf-11.

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Doerschug, K., A. Delsing, G. Schmidt, and A. Ashare. "Renin-Angiotensin System Activation Correlates with Microvascular Dysfunction in Human Sepsis." In American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a1139.

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Nicholl, David D. M., Patrick Hanly, George Handley, Brenda Hemmelgarn, Marc Poulin, Darlene Sola, and Sofia B. Ahmed. "Obstructive Sleep Apnea And The Vascular Renin Angiotensin System In Humans." In American Thoracic Society 2012 International Conference, May 18-23, 2012 • San Francisco, California. American Thoracic Society, 2012. http://dx.doi.org/10.1164/ajrccm-conference.2012.185.1_meetingabstracts.a2185.

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Barbu, Roxana Mihaela, Bogdan Stana, Cristian Cojocaru, Manuela Stefan, Raducu Popescu, Dragos Munteanu, Alexandru Vlase, Elena Cojocaru, and Cristina Maria Gavrilescu. "Influence of SARS-CoV-2 Infection on the Renin Angiotensin System." In 2021 International Conference on e-Health and Bioengineering (EHB). IEEE, 2021. http://dx.doi.org/10.1109/ehb52898.2021.9657625.

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Reports on the topic "Renin"

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Tibi, Sedra, Garbel Zeynalvand, and Hina Mohsin. Role of the renin angiotensin aldosterone system in the pathogenesis of sepsis-induced acute kidney injury: a systematic review. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, June 2023. http://dx.doi.org/10.37766/inplasy2023.6.0098.

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Thompson, MIchele. Age Related Changes in the Activity and the Responsiveness of the Renin-angiotensin System in the 15 Month Old Rat. Portland State University Library, January 2000. http://dx.doi.org/10.15760/etd.7281.

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Yuan, Shizhu, Yueming Liu, and Qiang He. Association between early worsening of renal function and poor outcomes in patients treated with renin angiotensin system inhibitors: A meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, July 2020. http://dx.doi.org/10.37766/inplasy2020.7.0064.

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Zhang, Guoyue, and Yue Wu. The use of Renin-Angiotensin-Aldosterone-System (RAAS)-Inhibitor on severity or mortality in patients with COVID-19: A Meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, September 2020. http://dx.doi.org/10.37766/inplasy2020.9.0067.

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Xue, Xue, Xin-yan Jin, Ke-ying Li, Jia-Xuan Li, Xing-Lan Ye, Qiang Liu, Xue-han Liu, et al. Ophiocordyceps sinensis preparation combined with renin-angiotensin system inhibitor for diabetic kidney disease: an umbrella review of systematic reviews and network meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, May 2023. http://dx.doi.org/10.37766/inplasy2023.5.0066.

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Shen, Jinhai, Bowen Liang, Yun Wang, and Yong Yang. Effect of renin-angiotensin-aldosterone system inhibitors on survival outcomes in cancer patients treated with immune checkpoint inhibitors: a systematic review and meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, November 2022. http://dx.doi.org/10.37766/inplasy2022.11.0136.

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Melnyk, Iurii. Китайська газета Женьмінь Жибао про російсько-українську війну (2022). Ivan Franko National University of Lviv, March 2023. http://dx.doi.org/10.30970/vjo.2023.52-53.11733.

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The objective of the study is to outline the vision of the Russian-Ukrainian war in Renmin Ribao, the main newspaper of the People’s Republic of China. The source base of the research is the content of the Renmin Ribao website during 2022 in English, Spanish, French, Russian, German, Italian, and Portuguese languages. The material was selected using the keywords «Ukraine», «Russia» (and other derivatives), analyzed using induction, vocabulary analysis, classification analysis, and content analysis. Renmin Ribao rarely uses the term “war” to refer to events in Ukraine, resorting to streamlined formulations such as “situation”, “issue”, “crisis”, “conflict” and even “Russian military operation”. The newspaper sees the United States, not Russia, as responsible for the events in Ukraine. Rather, Moscow is a victim of many years of intrigues on the part of the United States, which manifested itself in efforts to restrain and weaken Russia, in particular with the help of Ukraine. The newspaper often reproduces Russian narratives and Russian fakes, disseminates messages typical of Russian propaganda (for example, about biological laboratories in Ukraine), reports on referendums in the occupied Ukrainian territories from the evidence of the Russian RT television channel, about the annexation of four Ukrainian regions from the testimony of Chairman State Duma Vyacheslav Volodin, about the attack on the Crimean bridge from the evidence of the FSB. Renmin Ribao is inclined to the opinion of the harmfulness of anti-Russian sanctions and the impracticality of supplying weapons to Ukraine, sees a priority way out of the Russian-Ukrainian war in an abstract “peace”, and not the victory of Ukraine. The issue in which Renmin Ribao sharply diverges from the position of official Moscow is the identification of the situation in Ukraine and the situation in Taiwan. Drawing parallels between Taiwan and Ukraine is popular in both the Russian and the Western press. However, when the war began to look less and less victorious for Russia, these parallels became unacceptable to both Renmin Ribao and official Beijing. Keywords: Russian-Ukrainian war, media of China, Renmin Ribao, anti-Russian sanctions, arms supply to Ukraine, Taiwan.
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Abdul Rahim, Nor Azura, Noor Syazril Jafri, and Muna'amirah Mohamad. DEVELOPMENT OF OIL ABSORBENT MAT FROM WASTE NBR GLOVES. Penerbit Universiti Malaysia Perlis, 2023. http://dx.doi.org/10.58915/techrpt2023.003.

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Waste NBR rubber gloves have become an environmental burden because the chemically cross-linked NBR gloves can’t be recycled. In this particular research, an initiative was made to turn the NBR waste glove into an oil absorbent mat by using the amount of chemical cross-linking inside the NBR waste glove triggered by solvents and with the help of epoxy resin as a binding agent. The absorption test used two types of oil: cooking oil and engine oil. To justify the relationship between the developed oil absorbent mat and its absorption behaviour, various tests, namely the Fourier transform infrared radiation (FTIR), scanning electron microscopy (SEM), and absorbency test, were conducted. Epoxy resin was used as a binding agent in the production of oil-absorbing mats made from waste NBR gloves. The NBR gloves mixed with binding agents of epoxy resin mats have proven to be an effective medium for oil absorbance purposes.
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Dynes, Paul J. Emerging Resin Characterization. Fort Belvoir, VA: Defense Technical Information Center, April 1989. http://dx.doi.org/10.21236/ada208173.

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Powell, K. R. Resin Longevity Studies. Office of Scientific and Technical Information (OSTI), May 2002. http://dx.doi.org/10.2172/799356.

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