WordNet

street name for lysergic acid diethylamide (同)back breaker, battery-acid, dose, dot, Elvis, loony toons, Lucy in the sky with diamonds, pane, superman, window pane, Zen
any of various water-soluble compounds having a sour taste and capable of turning litmus red and reacting with a base to form a salt
having the characteristics of an acid; "an acid reaction"

PrepTutorEJDIC

酸性の / 酸味のある,すっぱい(sour) / (言葉・態度などが)厳しい,しんらつな / 酸 / すっぱいもの / 《俗》=LSD

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1. 尿酸のバランス uric acid balance
2. 出産時の臍帯血酸塩基分析 umbilical cord blood acid base analysis at delivery
3. 妊娠中の葉酸補充 folic acid supplementation in pregnancy
4. ポルフィリン症：概要 porphyrias an overview
5. Vitamin supplementation in disease prevention

English Journal

Stability of hepatoprotecting agent IFC-305 encapsulated into sol-gel titania nanoparticles and drug release evaluation: water and drug concentration effect.

Albarran L, López T, Quintana P, Chagoya V.Author information Universidad Autónoma Metropolitana-Xochimilco, Calzada del Hueso 1100, Col. Villa Quietud, Coyoacán, C.P 04960, D.F. México.AbstractIFC-305 was encapsulated into nanostructured titania and functionalized with OH groups by the sol-gel process using titanium n-butoxide, to be used in a drug delivery system for the treatment of liver cancer. Synthesis was carried out at different molar hydrolysis ratios: 4, 8, 16 and 24 mol of water; and drug concentration of 10, 20 and 30%. Characterization of IFC-titania reservoirs was carried out by Fourier transformed infrared spectroscopy (FTIR), X-ray diffraction (XRD), thermal analysis (DTA-TGA), scanning electron microscopy (SEM), and N2 adsorption-desorption isotherms (BET), confirms that IFC-305 is entrapped and stabilized in the TiO2-OH matrix. Drug liberation in vitro was determined by UV spectrometry over a period of 1000 h. This study demonstrated that the higher water content and the higher amount of loaded IFC, favored hydrogen bonding between titania-OH surface and IFC-NH groups, increasing the rate of drug release.
Journal of nanoscience and nanotechnology.J Nanosci Nanotechnol.2012 Mar;12(3):2199-205.
IFC-305 was encapsulated into nanostructured titania and functionalized with OH groups by the sol-gel process using titanium n-butoxide, to be used in a drug delivery system for the treatment of liver cancer. Synthesis was carried out at different molar hydrolysis ratios: 4, 8, 16 and 24 mol of wate
PMID 22755038

Prevention of in vitro hepatic stellate cells activation by the adenosine derivative compound IFC305.

Velasco-Loyden G, Pérez-Carreón JI, Agüero JF, Romero PC, Vidrio-Gómez S, Martínez-Pérez L, Yáñez-Maldonado L, Hernández-Muñoz R, Macías-Silva M, de Sánchez VC.Author information Departamento de Biología Celular y Desarrollo, Instituto de Fisiología Celular, Universidad Nacional Autónoma de México (UNAM), México 04510, D.F., Apdo. postal 70-243, Mexico.AbstractWe have previously shown that adenosine and the aspartate salt of adenosine (IFC305) reverse pre-established CCl(4)-induced cirrhosis in rats. However, their molecular mechanism of action is not clearly understood. Hepatic stellate cells (HSC) play a pivotal role in liver fibrogenesis leading to cirrhosis, mainly through their activation, changing from a quiescent adipogenic state to a proliferative myofibrogenic condition. Therefore, we decided to investigate the effect of IFC305 on primary cultured rat HSC. Our results reveal that this compound suppressed the activation of HSC, as demonstrated by the maintenance of a quiescent cell morphology, including lipid droplets content, inhibition of α-smooth muscle actin (α-SMA) and collagen α1(I) expression, and up-regulation of MMP-13, Smad7, and PPARγ expression, three key antifibrogenic genes. Furthermore, IFC305 was able to repress the platelet-derived growth factor (PDGF)-induced proliferation of HSC. This inhibition was independent of adenosine receptors stimulation; instead, IFC305 was incorporated into cells by adenosine transporters and converted to AMP by adenosine kinase. On the other hand, addition of pyrimidine ribonucleoside as uridine reversed the suppressive effect of IFC305 on the proliferation and activation of HSC, suggesting that intracellular pyrimidine starvation would be involved in the molecular mechanism of action of IFC305. In conclusion, IFC305 inhibits HSC activation and maintains their quiescence in vitro; these results could explain in part the antifibrotic liver beneficial effect previously described for this compound on the animal model.
Biochemical pharmacology.Biochem Pharmacol.2010 Dec 1;80(11):1690-9. doi: 10.1016/j.bcp.2010.08.017. Epub 2010 Sep 9.
We have previously shown that adenosine and the aspartate salt of adenosine (IFC305) reverse pre-established CCl(4)-induced cirrhosis in rats. However, their molecular mechanism of action is not clearly understood. Hepatic stellate cells (HSC) play a pivotal role in liver fibrogenesis leading to cir
PMID 20813095

An adenosine derivative compound, IFC305, reverses fibrosis and alters gene expression in a pre-established CCl(4)-induced rat cirrhosis.

Pérez-Carreón JI, Martínez-Pérez L, Loredo ML, Yañez-Maldonado L, Velasco-Loyden G, Vidrio-Gómez S, Ramírez-Salcedo J, Hernández-Luis F, Velázquez-Martínez I, Suárez-Cuenca JA, Hernández-Muñoz R, de Sánchez VC.Author information Departamento de Biología Celular, Instituto de Fisiología Celular, Universidad Nacional Autónoma de México (UNAM), Mexico 04510, D.F., Mexico; Instituto Nacional de Medicina Genómica (INMEGEN), Periférico sur 4214, Mexico, D.F., Mexico.AbstractCirrhosis is a complex process that involves a dynamic modification of liver cell phenotype associated to gene expression changes. This study investigates the reversing capacity of an adenosine derivative compound (IFC305) on a rat model of liver cirrhosis and gene expression changes associated with it. Rats were treated with IFC305 or saline for 5 or 10 weeks after cirrhosis induction (CCl(4) treatment for 10 weeks). Fibrosis score, collagenase activity and amount of hepatic stellate cells (HSC, activated and with a lipid-storing phenotype) were measured in livers. In addition, gene expression analysis was performed using 5K DNA microarrays and quantitative RT-PCR. Treatment of cirrhotic rats with IFC305 for 5 or 10 weeks compared to saline control, induced: (1) reduction of fibrosis (50-70%) and of collagen, of alpha-SMA and desmin proteins, as well as of activated HSCs in liver, (2) increased collagenase activity and cell number of lipid-storing HSC, (3) improved serum parameters of liver function, such as reduced activity of aminotransferases and bilirubin. Expression of 413 differential genes, deregulated in cirrhotic samples, tended to be normalized by IFC305 treatment. Some genes modulated at transcript level by IFC305 were Tgfb1, Fn1, Col1a1, C9, Apoa1, Ass1, Cps1, and Pparg. The present study shows that IFC305 reverses liver fibrosis through modulation of adipogenic and fibrosis-related genes and by ameliorating hepatic function. Thus, understanding of the anti-cirrhotic effect of IFC305 might have therapeutical potential in patients with cirrhosis.
The international journal of biochemistry & cell biology.Int J Biochem Cell Biol.2010 Feb;42(2):287-96. doi: 10.1016/j.biocel.2009.11.005. Epub 2009 Nov 13.
Cirrhosis is a complex process that involves a dynamic modification of liver cell phenotype associated to gene expression changes. This study investigates the reversing capacity of an adenosine derivative compound (IFC305) on a rat model of liver cirrhosis and gene expression changes associated with
PMID 19914391

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