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Journal articles on the topic 'Gadolinium chlorure'

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Published: 4 June 2021
Last updated: 11 February 2022

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1

&NA;. "Gadolinium chloride." Reactions Weekly &NA;, no. 1317 (September 2010): 25. http://dx.doi.org/10.2165/00128415-201013170-00081.

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2

DEAN, PETER B., PEKKA NIEMI, LEENA KIVISAARI, and MARTTI KORMANO. "Comparative Pharmacokinetics of Gadolinium DTPA and Gadolinium Chloride." Investigative Radiology 23, no. 1 (September 1988): S261. http://dx.doi.org/10.1097/00004424-198809000-00057.

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3

DEAN, PETER B., PEKKA NIEMI, LEENA KIVISAARI, and MARTTI KORMANO. "Comparative Pharmacokinetics of Gadolinium DTPA and Gadolinium Chloride." Investigative Radiology 23 (September 1988): S258—S260. http://dx.doi.org/10.1097/00004424-198809001-00055.

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4

Spencer, Andrew, Susan Wilson, and Ernest Harpur. "Gadolinium chloride toxicity in the mouse." Human & Experimental Toxicology 17, no. 11 (November 1998): 633–37. http://dx.doi.org/10.1177/096032719801701108.

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1 Groups of five male and five female CD-1 mice received a single intravenous injection of gadolinium chloride at dosages of 0 (saline control), 0.05, 0.1 and 0.2 mmol/ kg. All mice were necropsied 48 h post dose. 2 Plasma analysis showed increases in concentrations of lactate dehydrogenase (both sexes), aspartate amino-transferase and alanine aminotransferase (females only) in the 0.2 mmol/kg group. Cholesterol was elevated at all dosages in both sexes whilst globulin was raised in both sexes at 0.1 and 0.2 mmol/kg. 3 Histological lesions were present at all dosages and increased in severity in a dose-related fashion. The most common lesions were: mineral emboli in capillaries, accumulation of mineral in the mono-nuclear phagocytic system, hepatocellular necrosis, and lymphoid depletion, necrosis and mineralisation in the spleen. 4 Such observations are similar to those in rats given gadolinium chloride and should be assessed when evaluating the toxicological profile of gadolinium containing compounds being developed for nuclear magnetic resonance imaging.
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5

Klein, Andrés, Juan Oyarzún, Cristian Cortez, and Silvana Zanlungo. "Gadolinium Chloride Rescues Niemann–Pick Type C Liver Damage." International Journal of Molecular Sciences 19, no. 11 (November 14, 2018): 3599. http://dx.doi.org/10.3390/ijms19113599.

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Niemann–Pick type C (NPC) disease is a rare neurovisceral cholesterol storage disorder that arises from loss of function mutations in the NPC1 or NPC2 genes. Soon after birth, some patients present with an aggressive hepatosplenomegaly and cholestatic signs. Histopathologically, the liver presents with large numbers of foam cells; however, their role in disease pathogenesis has not been explored in depth. Here, we studied the consequences of gadolinium chloride (GdCl3) treatment, a well-known Kupffer/foam cell inhibitor, at late stages of NPC liver disease and compared it with NPC1 genetic rescue in hepatocytes in vivo. GdCl3 treatment successfully blocked the endocytic capacity of hepatic Kupffer/foam measured by India ink endocytosis, decreased the levels CD68—A marker of Kupffer cells in the liver—and normalized the transaminase levels in serum of NPC mice to a similar extent to those obtained by genetic Npc1 rescue of liver cells. Gadolinium salts are widely used as magnetic resonance imaging (MRI) contrasts. This study opens the possibility of targeting foam cells with gadolinium or by other means for improving NPC liver disease. Synopsis: Gadolinium chloride can effectively rescue some parameters of liver dysfunction in NPC mice and its potential use in patients should be carefully evaluated.
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Spencer, Andrew J., Susan A. Wilson, John Batchelor, Alexandra Reid, Jeremy Pees, and Ernest Harpur. "Gadolinium Chloride Toxicity in the Rat." Toxicologic Pathology 25, no. 3 (May 1997): 245–55. http://dx.doi.org/10.1177/019262339702500301.

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7

Spencer, A., S. Wilson, and E. Harpur. "Gadolinium chloride toxicity in the mouse." Human & Experimental Toxicology 17, no. 11 (November 1, 1998): 633–37. http://dx.doi.org/10.1191/096032798678908035.

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8

Simon, A., and T. Koehler. "A new gadolinium nitride chloride—Gd3Cl6N." Journal of the Less Common Metals 116, no. 1 (February 1986): 279–92. http://dx.doi.org/10.1016/0022-5088(86)90236-5.

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9

Khushkhov, KH B., M. K. Vindizheva, A. S. Uzdenova, and Z. A. Zhanikaeva. "Joint electroreduction of lanthanum, gadolinium and boron in halide melts." Journal of Mining and Metallurgy, Section B: Metallurgy 39, no. 1-2 (2003): 275–80. http://dx.doi.org/10.2298/jmmb0302275k.

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The joint electroreduction of La, Gd and B from chloride-fluoride melts has been studied by cyclic voltametry. Based on the analysis of voltamograms the possibility of electrosynthesis of lanthanum-gadolinium borides from chloride-fluoride melts has been shown.
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10

Lim, Jong Min, and Sang Woo Kim. "Synthesis of Nickel Coated Gadolinia Doped Ceria Nanopowder by Microwave Radiation." Materials Science Forum 569 (January 2008): 77–80. http://dx.doi.org/10.4028/www.scientific.net/msf.569.77.

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Nickel coated gadolinium doped ceria (GDC) powder was synthesized by microwave radiation and combustion. For the synthesis, the precipitates of gadolinium cerium oxycarbonate hydrate (GdxCe2-xO(CO3)2·H2O) were formed by a microwave radiated reaction between cerium nitrate (Ce(NO3)3.6H2O) and gadolinium nitrate (Gd(NO3)3.6H2O) and urea (CO(NH2)2), then nickel coatings on the gadolinium cerium oxycarbonate hydrate were performed by further microwave reaction between nickel chloride and urea. The shape and size of the gadolinium cerium oxycarbonate hydrate particles were critically dependent on aging time during microwave radiation. The irregular particles were transformed to rod shape particles with well-crystallized with increasing aging time to 40 min at 70 - 80°C because of the gradual decomposition of urea during microwave radiation. Small nickel precursor particles were homogeneously coated on the gadolinium cerium oxycarbonate hydrate particles with rod shape with aid of microwave radiation at 80 °C for 40 min. As a result, the nickel coated GDC nanopowders were sucessfully produced by the microwave radiation synthesis and further microwave combusted at 450°C for 20 min.
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11

Wang, Yanyan, Lei Qin, Guo-Jun Zhou, Xinxin Ye, Jiaqing He, and Yan-Zhen Zheng. "High-performance low-temperature magnetic refrigerants made of gadolinium-hydroxy-chloride." Journal of Materials Chemistry C 4, no. 27 (2016): 6473–77. http://dx.doi.org/10.1039/c6tc01291d.

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12

Uzdenova, A., Kh Kushkhov, M. Saleh, and L. Uzdenova. "Electrosynthesis of gadolinium borides in chloride melt." SOP Transactions on Physical Chemistry 1, no. 1 (February 28, 2014): 23–28. http://dx.doi.org/10.15764/pche.2014.01004.

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13

Sharipov, G. L., R. Kh Gainetdinov, and A. M. Abdrakhmanov. "Sonoluminescence of aqueous solution of gadolinium chloride." Russian Chemical Bulletin 54, no. 6 (June 2005): 1383–86. http://dx.doi.org/10.1007/s11172-005-0414-1.

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14

Chiang, Chen-Hua, Ying-Chi Tseng, Ai-Chi Chen, Yen-Lin Huang, David Yen-Ting Chen, Chi-Jen Chen, Yen-Kuang Lin, and Hui-Ling Hsu. "In vitro comparison of intracranial stent visibility using various concentrations of gadolinium contrast agent under 1.5 T and 3 T MR angiography." Journal of NeuroInterventional Surgery 9, no. 4 (August 10, 2016): 399–404. http://dx.doi.org/10.1136/neurintsurg-2016-012490.

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Background and purposeMR angiography (MRA) is an increasingly used evaluation method following intracranial stenting. However, the various artifacts created by the stent limit this technique. The purpose of this study was to investigate the effects of various concentrations of gadolinium contrast agent on the visibility and signal characteristics of two stents using the a contrast enhanced MRA technique.Material and methodTwo intracranial stents (Enterprise and Helistent) were placed in polyvinyl chloride tubes as vascular phantoms. They were filled with six different doses of gadolinium contrast agent (1.0, 2.0, 4.0, 6.0, 8.0, and 10.0 mmol/L dimeglumine gadopentetate, respectively) and imaged using 3 T and 1.5 T MR systems. Relative in-stent signal (RIS) was calculated and artificial luminal narrowing (ALN) was obtained using pixel by pixel analysis.ResultThe Enterprise stent, performed in both 1.5 T and 3 T MR systems, showed mean RIS values much less than those for the Helistent for all different doses of gadolinium solution. Increased gadolinium concentration resulted in a gradual reduction in RIS values in the Enterprise group. Also, ALN in the Enterprise group showed no or little change with various gadolinium doses.ConclusionsThe Enterprise stent demonstrated good luminal visibility regardless of gadolinium concentration. The relative in-stent signals were more predictable in the Enterprise stent with various doses of gadolinium. Therefore, the Enterprise stent has been shown to provide better in-stent visibility compared with the Helistent using various gadolinium doses.
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15

Piriou, Vincent, Pascal Chiari, Sandra Knezynski, Olivier Bastien, Joseph Loufoua, Jean-Jacques Lehot, Pierre Foëx, Guy Annat, and Michel Ovize. "Prevention of Isoflurane-induced Preconditioning by 5-Hydroxydecanoate and Gadolinium." Anesthesiology 93, no. 3 (September 1, 2000): 756–64. http://dx.doi.org/10.1097/00000542-200009000-00025.

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Background Both mitochondrial adenosine triphosphate-sensitive potassium (MKATP) channels (selectively blocked by 5-hydroxydecanoate) and stretch-activated channels (blocked by gadolinium) have been involved in the mechanism of ischemic preconditioning. Isoflurane can reproduce the protection afforded by ischemic preconditioning. We sought to determine whether isoflurane-induced preconditioning may involve MKATP and stretch-activated channels. Methods Anesthetized open-chest rabbits underwent 30 min of coronary occlusion followed by 3 h of reperfusion. Before this, rabbits were randomized into one of six groups and underwent a treatment period consisting of either no intervention for 40 min (control group; n = 9) or 15 min of isoflurane inhalation (1.1% end tidal) followed by a 15-min washout period (isoflurane group; n = 9). The two groups received an intravenous bolus dose of either 5-hydroxydecanoate (5 mg/kg) or gadolinium (40 micromol/kg) before coronary occlusion and reperfusion (5-hydroxydecanoate, n = 9; gadolinium, n = 7). Two additional groups received 5-hydroxydecanoate or gadolinium before isoflurane exposure (isoflurane-5-hydroxydecanoate, n = 10; isoflurane-gadolinium, n = 8). Area at risk and infarct size were assessed by blue dye injection and tetrazolium chloride staining. Results Area at risk was comparable among the six groups (29 +/- 7, 30 +/- 5, 27 +/- 6, 35 +/- 7, 31 +/- 7, and 27 +/- 4% of the left ventricle in the control, isoflurane, isoflurane-5-hydroxydecanoate, 5-hydroxydecanoate, isoflurane-gadolinium, and gadolinium groups, respectively). Infarct size averaged 60 +/- 20% (SD) in untreated controls versus 54 +/- 27 and 65 +/- 15% of the risk zone in 5-hydroxydecanoate- and gadolinium-treated controls (P = nonsignificant). In contrast, infarct size in the isoflurane group was significantly reduced to 26 +/- 11% of the risk zone (P < 0.05 vs.control). Both 5-hydroxydecanoate and gadolinium prevented this attenuation: infarct size averaged 68 +/- 23 and 56 +/- 21% of risk zone in the isoflurane-5-hydroxydecanoate and isoflurane-gadolinium groups, respectively (P = nonsignificant vs.control). Conclusion 5-Hydroxydecanoate and gadolinium inhibited pharmacologic preconditioning by isoflurane. This result suggests that MKATP channels and mechanogated channels are probably involved in this protective mechanism.
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16

Kyriakou, Loukas G., Konstantinos N. Tzirogiannis, Maria D. Demonakou, Kalliopi T. Kourentzi, Michael G. Mykoniatis, and Georgios I. Panoutsopoulos. "Gadolinium chloride pretreatment ameliorates acute cadmium-induced hepatotoxicity." Toxicology and Industrial Health 29, no. 7 (December 15, 2011): 624–32. http://dx.doi.org/10.1177/0748233711430971.

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17

Shengli, Gao, Chen Sanping, Bian Jiang, Jiao Baojuan, Zhao Fengqi, and Shi Qizhen. "Thermochemistry of gadolinium chloride hydrate with diethylammonium diethyldithiocarbamate." Journal of Chemical Thermodynamics 37, no. 3 (March 2005): 267–70. http://dx.doi.org/10.1016/j.jct.2004.04.014.

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18

Granado, M., A. I. Martín, T. Priego, M. A. Villanúa, and A. López-Calderón. "Inactivation of Kupffer cells by gadolinium administration prevents lipopolysaccharide-induced decrease in liver insulin-like growth factor-I and IGF-binding protein-3 gene expression." Journal of Endocrinology 188, no. 3 (March 2006): 503–11. http://dx.doi.org/10.1677/joe.1.06585.

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Gram-negative bacterial infection or treatment of animals with bacterial lipopolysaccharide (LPS) induces a catabolic state with proteolysis, liver injury and an inhibition of the insulin-like growth factor-I (IGF-I) system. The purpose of this work was to elucidate the role of Kupffer cells in LPS-induced inhibition of the IGF-I/IGF-binding protein-3 (IGFBP-3) system. Adult male Wistar rats were either pretreated with the Kupffer cell inhibitor gadolinium chloride (10 mg/kg, i.v., 24 h prior to LPS exposure) or saline vehicle. Rats received two i.p. injections of 1 mg/kg LPS (at 17:30 and 08:30 h the following day) and were killed 4 h after the second injection. LPS administration induced a significant decrease in body weight and in serum concentrations of IGF-I and IGFBP-3 (P < 0.01), as well as in their gene expression in the liver. LPS-injected rats had increased serum concentrations of ACTH, corticosterone (P < 0.05), tumour necrosis factor-α (TNF-α) and nitrites (P < 0.01). Pretreatment of the animals with gadolinium chloride blocked the inhibitory effect of LPS on body weight, and on serum concentrations of IGF-I, IGFBP-3 and nitrites, as well as growth hormone receptor (GHR), IGF-I and IGFBP-3 gene expression in the liver. In contrast, gadolinium chloride administration did not modify the stimulatory effect of LPS on serum concentrations of ACTH, corticosterone and TNF-α. These results suggest that Kupffer cells are important mediators in the inhibitory effect of LPS on GHR, IGF-I and IGFBP-3 gene expression in the liver, leading to a decrease in serum concentrations of IGF-I and IGFBP-3.
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19

Lázár, G., E. Husztik, G. Lázár Jr, I. Kiss, J. Oláh, and J. Szakács. "Immunomodulation by gadolinium chloride-induced Kupffer cell phagocytosis blockade." Journal of Alloys and Compounds 275-277 (July 1998): 908–10. http://dx.doi.org/10.1016/s0925-8388(98)00482-4.

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Kono, Hiroshi, Hideki Fujii, Masanori Matsuda, Masayuki Yamamoto, and Yoshiro Matsumoto. "Gadolinium Chloride Prevents Mortality in Hepatectomized Rats Given Endotoxin." Journal of Surgical Research 96, no. 2 (April 2001): 204–10. http://dx.doi.org/10.1006/jsre.2001.6099.

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21

Jeitschko, P., A. Simon, R. Ramlau, and Hj Mattausch. "Chemical Intergrowth in Gadolinium Carbide Chloride - a HRTEM Study." Zeitschrift f�r anorganische und allgemeine Chemie 623, no. 9 (September 1997): 1447–54. http://dx.doi.org/10.1002/zaac.19976230921.

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22

Bannenberg, G. "Pulmonary macrophage function in systemic gadolinium chloride-pretreated rats." Toxicology Letters 80, no. 1-3 (October 1995): 105–7. http://dx.doi.org/10.1016/0378-4274(95)03342-i.

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23

Lázár, George, Mieke van Galen, and Gerrit L. Scherphof. "Gadolinium chloride-induced shifts in intrahepatic distributions of liposomes." Biochimica et Biophysica Acta (BBA) - Molecular Cell Research 1011, no. 2-3 (May 1989): 97–101. http://dx.doi.org/10.1016/0167-4889(89)90194-8.

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Zakir'yanova, Irina D., Elena V. Nikolaeva, and Iraida V. Korzun. "The Solubility of Gd2O3 in K Cl-GdCl3 Melts." Materials Science Forum 989 (May 2020): 91–96. http://dx.doi.org/10.4028/www.scientific.net/msf.989.91.

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The differential scanning calorimetry and the method of cooling curves are used to obtain data on liquidus temperatures of oxide-chloride systems Gd2O3 – K Cl - GdCl3. The solubility of gadolinium oxide in K Cl - GdCl3 melts has been studied. This information can be used for a developing process of the reduction of solid rare-earth oxides into their metals in molten salts.
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25

Leese, Rebecca J., Atanas Ivanov, and Hari Babu-Nadendla. "The Potential to Machine Superconductors with Electrochemical Machining." Journal of Multiscale Modelling 07, no. 01 (March 2016): 1640001. http://dx.doi.org/10.1142/s1756973716400011.

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Superconductors (SCs), such as gadolinium barium copper oxide, are brittle ceramics which are very difficult to machine conventionally due to the easy propagation of cracks. The cracks formed during conventional machining destroy the superconductive properties of the material. As a result a new method to machine ceramic SCs is needed. In this paper, polarization experiments were conducted in various nonaqueous salt electrolytes to determine whether electrochemical machining (ECM) is a suitable method for machining gadolinium barium copper oxide with silver inclusions (GdBCO-Ag) for the first time. Sodium chloride in formic acid proved to be the best electrolyte for this application with higher dissolution rates and achieving a better surface finish. It was noted that GdBCO-Ag dissolved at higher rates in NaCl in formic acid than in other salt-solvent systems.
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Miller, Gordon J., Jeremy K. Burdett, Christine Schwarz, and Arndt Simon. "Molecular interstitials: an analysis of the gadolinium carbide chloride, Gd2C2Cl2." Inorganic Chemistry 25, no. 24 (November 1986): 4437–44. http://dx.doi.org/10.1021/ic00244a031.

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Xu, Jianping, Wei Liu, Xiaojuan Shi, Xiaohon Liao, Huijun Liu, Jianzhong Han, and Ziqiang Luo. "Gadolinium Chloride Attenuates Hypoxic Pulmonary Injury in the Adult Rat." Cell Biology International 34, no. 8 (August 1, 2010): S71. http://dx.doi.org/10.1042/cbi034s071d.

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Badger, D. A., R. K. Kuester, J.-M. Sauer, and I. G. Sipes. "Gadolinium chloride reduces cytochrome P450: Relevance to chemical-induced hepatotoxicity." Toxicology 121, no. 2 (August 1997): 143–53. http://dx.doi.org/10.1016/s0300-483x(97)00065-6.

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29

Pearson, Julia M., Alan P. Brown, A. Eric Schultze, Patricia E. Ganey, and Robert A. Roth. "GADOLINIUM CHLORIDE TREATMENT ATTENUATES HEPATIC PLATELET ACCUMULATION AFTER LIPOPOLYSACCHARIDE ADMINISTRATION." Shock 5, no. 6 (June 1996): 408–15. http://dx.doi.org/10.1097/00024382-199606000-00004.

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Roland, Claude R., Bashoo Naziruddin, T. Mohanakumar, and M. Wayne Flye. "Gadolinium chloride inhibits Kupffer cell nitric oxide synthase (iNOS) induction." Journal of Leukocyte Biology 60, no. 4 (October 1996): 487–92. http://dx.doi.org/10.1002/jlb.60.4.487.

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Kushkhov, H. B. "Joint Electroreduction of Lanthanum, Gadolinium and Boron in Chloride Melts." ECS Proceedings Volumes 2002-19, no. 1 (January 2002): 616–21. http://dx.doi.org/10.1149/200219.0616pv.

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32

Pagliara, P., A. Chionna, E. C. Carlà, S. Caforio, and L. Dini. "Lead nitrate and gadolinium chloride administration modify hepatocyte cell surfaces." Cell and Tissue Research 312, no. 1 (March 18, 2003): 41–48. http://dx.doi.org/10.1007/s00441-003-0708-2.

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33

Djamali, Essmaiil, and James W. Cobble. "Thermodynamic Properties of Aqueous Gadolinium Perrhenate and Gadolinium Chloride from High Dilution Calorimetry at Extreme Temperatures and Pressures." Journal of Physical Chemistry B 113, no. 8 (February 26, 2009): 2409–13. http://dx.doi.org/10.1021/jp805543j.

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Parker, James C., Claire L. Ivey, and J. Allan Tucker. "Gadolinium prevents high airway pressure-induced permeability increases in isolated rat lungs." Journal of Applied Physiology 84, no. 4 (April 1, 1998): 1113–18. http://dx.doi.org/10.1152/jappl.1998.84.4.1113.

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To determine the initial signaling event in the vascular permeability increase after high airway pressure injury, we compared groups of lungs ventilated at different peak inflation pressures (PIPs) with (gadolinium group) and without (control group) infusion of 20 μM gadolinium chloride, an inhibitor of endothelial stretch-activated cation channels. Microvascular permeability was assessed by using the capillary filtration coefficient ( K fc), a measure of capillary hydraulic conductivity. K fc was measured after ventilation for 30-min periods with 7, 20, and 30 cmH2O PIP with 3 cmH2O positive end-expiratory pressure and with 35 cmH2O PIP with 8 cmH2O positive end-expiratory pressure. In control lungs, K fc increased significantly to 1.8 and 3.7 times baseline after 30 and 35 cmH2O PIP, respectively. In the gadolinium group, K fc was unchanged from baseline (0.060 ± 0.010 ml ⋅ min−1 ⋅ cmH2O−1 ⋅ 100 g−1) after any PIP ventilation period. Pulmonary vascular resistance increased significantly from baseline in both groups before the last K fc measurement but was not different between groups. These results suggest that microvascular permeability is actively modulated by a cellular response to mechanical injury and that stretch-activated cation channels may initiate this response through increases in intracellular calcium concentration.
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van Schooten, Carina J., Shirin Shahbazi, Evelyn Groot, Beatrijs D. Oortwijn, H. Marijke van den Berg, Cécile V. Denis, and Peter J. Lenting. "Macrophages contribute to the cellular uptake of von Willebrand factor and factor VIII in vivo." Blood 112, no. 5 (September 1, 2008): 1704–12. http://dx.doi.org/10.1182/blood-2008-01-133181.

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Abstract Von Willebrand factor (VWF) and factor VIII (FVIII) circulate in a tight noncovalent complex. At present, the cells that contribute to the removal of FVIII and VWF are of unknown identity. Here, we analyzed spleen and liver tissue sections of VWF-deficient mice infused with recombinant VWF or recombinant FVIII. This analysis revealed that both proteins were targeted to cells of macrophage origin. When applied as a complex, both proteins were codirected to the same macrophages. Chemical inactivation of macrophages using gadolinium chloride resulted in doubling of endogenous FVIII levels in VWF-null mice, and of VWF levels in wild-type mice. Moreover, the survival of infused VWF was prolonged almost 2-fold in VWF-deficient mice after gadolinium chloride treatment. VWF and FVIII also bound to primary human macrophages in in vitro tests. In addition, radiolabeled VWF bound to human THP1 macrophages in a dose-dependent, specific, and saturable manner (half-maximal binding at 0.014 mg/mL). Binding to macrophages was followed by a rapid uptake and subsequent degradation of the internalized protein. This process was also visualized using a VWF–green fluorescent protein fusion protein. In conclusion, our data strongly indicate that macrophages play a prominent role in the clearance of the VWF/FVIII complex.
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Towner, Rheal A., Lester A. Reinke, Edward G. Janzen, and Shigeto Yamashiro. "In vivo magnetic resonance imaging study of Kupffer cell involvement in CCl4-induced hepatotoxicity in rats." Canadian Journal of Physiology and Pharmacology 72, no. 5 (May 1, 1994): 441–46. http://dx.doi.org/10.1139/y94-064.

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When carbon tetrachloride (CCl4) was administered to rats, a localized region of hepatic edema could be detected within 1 h by in vivo proton magnetic resonance imaging. However, if rats were pretreated with gadolinium chloride (GdCl3), an inhibitor of Kupffer cell function, the CCl4-induced edema was greatly decreased. Methyl palmitate, another Kupffer cell inhibitor, also decreased the degree of edema caused by the administration of CCl4. Electron micrographs of samples that were taken from regions of the liver where the edema was localized indicated formation of vacuoles and lipid droplets in parenchymal cells and enlargement of Kupffer cells, which exhibited numerous phagosomes and extensive pseudopod formation. These electron micrograph changes were also attenuated by pretreatment of the rats with GdCl3 and methyl palmitate. In vivo spin trapping and electron paramagnetic resonance experiments indicated that GdCl3 did not affect the metabolism of CCl4 to the trichloromethyl radical. The data in this report suggest that localized hepatic edema which occurs soon after administration of CCl4 involves activation of Kupffer cells, and that trichloromethyl radical production may be a separate but related process occurring in parenchymal cells. These observations support reports from other laboratories that Kupffer cells may be involved in CCl4-induced hepatotoxicity.Key words: carbon tetrachloride, hepatotoxicity, magnetic resonance imaging, gadolinium chloride, Kupffer cells.
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37

Wang, Yan, Da Ting Tian, and Yi Xin Yang. "Synthesis, Characterization, Room Temperature Fluorescence and Phosphorescence Properties of Complex Gd(C5H8NO3)2(C3H5N2)2Cl3•3H2O." Advanced Materials Research 399-401 (November 2011): 987–91. http://dx.doi.org/10.4028/www.scientific.net/amr.399-401.987.

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One solid coordination compound of Gadolinium chloride with N-acetyl-DL-alanine (C5H9NO3, Ac-Ala) and imidazole(C3H4N2,Im) has been prepared in absolute alcohol. The general formula Gd(C5H8NO3)2(C3H5N2)2Cl3•3H2O of these compounds was identified using the methods such as chemical and elemental analysis, FTIR spectra and UV spectra. The process of thermal decomposition was studied by TG-DTG. Room temperature fluorescence and phosphorescence measurement showed that the compound has good fluorescence and phosphorescence properties.
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Kishta, Osama A., Peter Goldberg, and Sabah N. A. Husain. "Gadolinium Chloride Attenuates Sepsis-Induced Pulmonary Apoptosis and Acute Lung Injury." ISRN Inflammation 2012 (November 1, 2012): 1–9. http://dx.doi.org/10.5402/2012/393481.

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Gadolinium chloride (GdCl3), a Kupffer cells inhibitor, attenuates acute lung injury; however, the mechanisms behind this effect are not completely elucidated. We tested the hypothesis that GdCl3 acts through the inhibition of lung parenchymal cellular apoptosis. Two groups of rats were injected intraperitoneally with saline or E. coli lipopolysaccharide. In two additional groups, rats were injected with GdCl3 24 hrs prior to saline or LPS administration. At 12 hrs, lung injury, inflammation, and apoptosis were studied. Lung water content, myeloperoxidase activity, pulmonary apoptosis and mRNA levels of interleukin-1β, -2, -5, -6, -10 and TNF-α rose significantly in LPS-injected animals. Pretreatment with GdCl3 significantly reduced LPS-induced elevation of pulmonary water content, myeloperoxidase activity, cleaved caspase-3 intensity, and attenuated pulmonary TUNEL-positive cells. GdCl3 pre-treatment upregulated IL-1β, -2 and -10 pulmonary gene expression without significantly affecting the others. These results suggest that GdCl3 attenuates acute lung injury through its effects on pulmonary parenchymal apoptosis.
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39

HIRASAWA, Fujiko, Masami KAWAGOE, Jing-Shu WANG, Szilvia ARANY, Xiao-Ping ZHOU, Ayako KUMAGAI, Yukio KOIZUMI, Souichi KOYOTA, and Toshihiro SUGIYAMA. "Gadolinium chloride suppresses styrene-induced cytochrome P450s expression in rat liver." Biomedical Research 28, no. 6 (2007): 323–30. http://dx.doi.org/10.2220/biomedres.28.323.

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40

Vollmar, Brigitte, Dominik Rüttinger, Guido A. Wanner, Rosmarie Leiderer, and Michael D. Menger. "MODULATION OF KUPFFER CELL ACTIVITY BY GADOLINIUM CHLORIDE IN ENDOTOXEMIC RATS." Shock 6, no. 6 (December 1996): 434–41. http://dx.doi.org/10.1097/00024382-199612000-00008.

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41

YONEDA, SHINJI, NOBUO EMI, YOICHIRO FUJITA, MASAYOSHI OHMICHI, SEISHIRO HIRANO, and KAZUO T. SUZUKI. "Effects of Gadolinium Chloride on the Rat Lung Following Intratracheal Instillation." Toxicological Sciences 28, no. 1 (1995): 65–70. http://dx.doi.org/10.1093/toxsci/28.1.65.

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42

Yoneda, S. "Effects of Gadolinium Chloride on the Rat Lung Following Intratracheal Instillation." Fundamental and Applied Toxicology 28, no. 1 (November 1995): 65–70. http://dx.doi.org/10.1006/faat.1995.1147.

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43

Zhang, Shuling, Suqing Kan, and Jinqing Kan. "Chemical synthesis and characterization of polyaniline nanofiber doped with gadolinium chloride." Journal of Applied Polymer Science 100, no. 2 (2006): 946–53. http://dx.doi.org/10.1002/app.23072.

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44

Lázár, George, Jr George Lázár, Joseph Kaszaki, Judit Oláh, and Elizabeth Husztik. "Protection against anaphylactic shock by gadolinium chloride-induced Kupffer cell blockade." Journal of Alloys and Compounds 225, no. 1-2 (July 1995): 619–22. http://dx.doi.org/10.1016/0925-8388(94)07075-x.

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45

Diagaradjane, Parmeswaran, Amit Deorukhkar, Juri G. Gelovani, Dipen M. Maru, and Sunil Krishnan. "Gadolinium Chloride Augments Tumor-Specific Imaging of Targeted Quantum DotsIn Vivo." ACS Nano 4, no. 7 (June 29, 2010): 4131–41. http://dx.doi.org/10.1021/nn901919w.

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46

Lázár, G., G. Lázár, J. Kaszaki, J. Oláh, I. Kiss, and E. Husztik. "Inhibition of anaphylactic shock by gadolinium chloride-induced Kupffer cell blockade." Agents and Actions 41, S1 (June 1994): C97—C98. http://dx.doi.org/10.1007/bf02007784.

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47

Lazar, G., G. Lazar, J. Kaszaki, J. Olah, I. Kiss, and E. Husztik. "Inhibition of anaphylactic shock by gadolinium chloride-induced Kupffer cell blockade." Resuscitation 29, no. 3 (June 1995): 265. http://dx.doi.org/10.1016/0300-9572(95)99661-s.

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48

Ong, Sang-Bing, Dinesh Shah, Ala Qusous, Simon M. Jarvis, and Mark J. P. Kerrigan. "Stimulation of regulatory volume increase (RVI) in avian articular chondrocytes by gadolinium chloride." Biochemistry and Cell Biology 88, no. 3 (June 2010): 505–12. http://dx.doi.org/10.1139/o09-179.

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Chondrocytes, the resident cell-type of articular cartilage, are responsible for the regulation of the extracellular matrix (ECM) in response to their physico-chemical environment. Due to the nature of cartilage loading, chondrocytes are exposed to constant changes in extracellular osmolality with a gradual increase throughout the day. As an increase in osmolality attenuates matrix synthesis, we have studied cell volume regulation (regulatory volume increase (RVI)) after hypertonic challenge and the regulation of RVI by the actin cytoskeleton. Using freshly isolated avian articular chondrocytes, changes in actin organisation were studied by confocal laser scanning microscopy following a 43% increase in extracellular osmolality. Using calcein-loading chondrocytes, the capacity for RVI was determined and the rate of volume recovery (t1/2) mathematically extrapolated. Following an increase in extracellular osmolality there was a significant increase (p < 0.05) in cortical actin, inhibited by the removal of extracellular calcium EGTA or by the addition of 100 µmol·L–1 gadolinium chloride. Most cells exhibited slow RVI (t1/2 = 55.5 ± 5.5 min), whereby inhibition of actin polymerisation by gadolinium chloride or the removal of extracellular calcium significantly increased the rate of volume recovery via a bumetanide-sensitive pathway (t1/2 of 29.6 ± 6.5 min and 13.8 ± 3.1 min, respectively). These data suggest the Na+–K+–2Cl– (NKCC) co-transporter regulated by the actin cytoskeleton is involved in avian chondrocyte RVI.
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Abe, Chikara, Chihiro Iwata, and Hironobu Morita. "Water drinking-related muscle contraction induces the pressor response via mechanoreceptors in conscious rats." Journal of Applied Physiology 114, no. 1 (January 1, 2013): 28–36. http://dx.doi.org/10.1152/japplphysiol.00923.2012.

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Water drinking is known to induce the pressor response. The efferent pathway in this response involves sympathoexcitation, because the pressor response was completely abolished by ganglionic blockade or an α1-adrenergic antagonist. However, the afferent pathway in this response has not been identified. In the present study, we hypothesized that water itself stimulates the upper digestive tract to induce the pressor response, and/or drinking-related muscle contraction induces the pressor response via mechanoreceptors. To examine this hypothesis, we evaluated the pressor response induced by spontaneous or passive water drinking in conscious rats. Since the baroreflex modulates and obscures the pressor response, the experiments were conducted using rats with sinoaortic denervation. The pressor response was not suppressed by 1) transient oral surface anesthesia using lidocaine, 2) bilateral denervation of the glossopharyngeal nerve and sensory branch of the superior laryngeal nerve, or 3) denervation of the tunica adventitia in the esophagus. However, the pressor response was significantly suppressed (by −52%) by intravenous gadolinium chloride administration. Electrical stimulation of the hypoglossal nerve induced the pressor response, which was significantly suppressed (by −57%) by intravenous gadolinium chloride administration and completely abolished by severing the distal end of this nerve. These results indicate that afferent signals from mechanoreceptors in drinking-related muscles are involved in the water drinking-induced pressor response.
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Weng, Te-I., Huang Jen Chen, Chen-Wen Lu, Yu-Chin Ho, Jia-Lun Wu, Shing-Hwa Liu, and Jong-Kai Hsiao. "Exposure of Macrophages to Low-Dose Gadolinium-Based Contrast Medium: Impact on Oxidative Stress and Cytokines Production." Contrast Media & Molecular Imaging 2018 (December 2, 2018): 1–10. http://dx.doi.org/10.1155/2018/3535769.

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The toxicity of gadolinium-based contrast agents (GBCAs) has drawn a lot of attention. Nephrogenic systemic fibrosis (NSF), a lethal disease related to the use of GBCAs, is still not understood. Recently, gadolinium retention is found in brain tissues after repeated use of GBCAs in magnetic resonance imaging (MRI). However, most of the works investigating the toxicity of GBCAs are focusing on its high-concentration (0.5–10 mM) part, which is not reflective of the physiological conditions in human beings. Macrophages play a regulatory role in immune responses and are responsible for the fibrosis process. Their role in gadolinium retention and the pathogenesis of NSF, however, has seldom been investigated. This study aimed to evaluate the immune response generated by macrophages (RAW 264.7) exposing to low levels of GBCAs. The incubation concentration of GBCAs, including Omniscan®, Primovist®, Magnevist®, and Gadovist®, is proportional to the level of gadolinium uptake when detected via inductively coupled plasma mass spectrometry (ICP-MS) and imaged by MRI, whereas Primovist® treatment groups have highest gadolinium uptake among all of the tested concentrations. Low-concentration (2.5 μmol/L) Gd chloride or GBCAs exposure promoted the reactive production of oxygen species (ROS), nitrate/nitrite, prostaglandin E2 (PGE2), and suppressed the potential of mitochondrial membrane. There was higher ROS, nitrate/nitrite, and PGE2 production in the Primovist®, Omniscan®, and Magnevist® groups compared to the Gadovist® group. In face of lipopolysaccharide (LPS) stimulation, Primovist®, Omniscan®, and Magnevist® groups exhibited elevated nitrite/nitrate and suppressed IL-1β secretion and IL-6 and IL-10 secretion. Moreover, upon LPS stimulation, there is decreased TNF-α secretion 4 hours after Primovist® or Omiscan® exposure but the TNF-α secretion increased at 24 hours. Our data suggest that there is upregulated inflammation even in the presence of low levels of GBCAs, even similar to the physiological condition in murine macrophage. Further investigation of GBCAs on the human macrophage or in vivo animal study may clarify the role of macrophage on the pathogenesis of NSF and other GBCAs-related disease.
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