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10篇 您的检索式:作者名="Jaime Navas"
    题名 作者 年代 出处 被引量
1Hepatic lipid metabolism changes in short-and long-term prehepatic portal hypertensive rats显示文摘AIM: To verify the impairment of the hepatic lipid metabolism in prehepatic portal hypertension. METHODS: The concentrations of free fatty acids, diacylglycerol, triglycerides, and phospholipids were assayed by using D-[U-14C] glucose incorporation in the different lipid fractions and thin-layer chromatography and cholesterol was measured by spectrophotometry, in liver samples of Wistar rats with partial portal vein ligation at short- (1 mo) and long-term (1 year) (i.e. portal hypertensive rats) and the control rats. RESULTS: In the portal hypertensive rats, liver phospholipid synthesis significantly decreased (7.42 ± 0.50 vs 4.70 ± 0.44 nCi/g protein; P < 0.01) and was associated with an increased synthesis of free fatty acids (2.08 ± 0.14 vs 3.36 ± 0.33 nCi/g protein; P < 0.05), diacylglycerol (1.93 ± 0.2 vs 2.26 ± 0.28 nCi/g protein), triglycerides (2.40 ± 0.30 vs 4.49 ± 0.15 nCi/g protein) and cholesterol (24.28 ± 2.12 vs 57.66 ± 3.26 mg/g protein; P < 0.01). CONCLUSION: Prehepatic portal hypertension in rats impairs the liver lipid metabolism. This impairment consists in an increase in lipid deposits (triglycerides,diacylglycerol and cholesterol) in the liver, accompanied by a decrease in phospholipid synthesis.Maria-Angeles Aller Elena Vara Cruz García Maria-Paz Nava Alejandra Angulo Fernando Sánchez-Patán Ana Calderón Patri Vergara Jaime Arias 2006World Journal of Gastroenterology2006,12,42:2
2Partial hepatectomy, partial portal vein stenosis and mesenteric lymphadenectomy increase splanchnic mast cell infiltration in the rat显示文摘Luis M. Moquillaza María-Angeles Aller Maria-Paz Nava Luis Santamaría Patri Vergara Jaime Arias 2009Acta Histochemica2009,,4:1
3Cerebral dopamine neurotrophic factor transfection in dopamine neurons using neurotensin-polyplex nanoparticles reverses 6-hydroxydopamine-induced nigrostriatal neurodegeneration显示文摘Overexpression of neurotrophic factors in nigral dopamine neurons is a promising approach to reverse neurodegeneration of the nigrostriatal dopamine system,a hallmark in Parkinson's disease.The human cerebral dopamine neurotrophic factor(h CDNF)has recently emerged as a strong candidate for Parkinson's disease therapy.This study shows that h CDNF expression in dopamine neurons using the neurotensinpolyplex nanoparticle system reverses 6-hydroxydopamine-induced morphological,biochemical,and behavioral alterations.Three independent electron microscopy techniques showed that the neurotensin-polyplex nanoparticles containing the h CDNF gene,ranging in size from 20 to 150 nm,enabled the expression of a secretable h CDNF in vitro.Their injection in the substantia nigra compacta on day 21 after the 6-hydroxydopamine lesion resulted in detectable h CDNF in dopamine neurons,whose levels remained constant throughout the study in the substantia nigra compacta and striatum.Compared with the lesioned group,tyrosine hydroxylase-positive(TH^(+))nigral cell population and TH+fiber density rose in the substantia nigra compacta and striatum after h CDNF transfection.An increase inβIII-tubulin and growth-associated protein 43 phospho-S41(GAP43 p)followed TH^(+)cell recovery,as well as dopamine and its catabolite levels.Partial reversal(80%)of drugactivated circling behavior and full recovery of spontaneous motor and non-motor behavior were achieved.Brain-derived neurotrophic factor recovery in dopamine neurons that also occurred suggests its participation in the neurotrophic effects.These findings support the potential of nanoparticle-mediated h CDNF gene delivery to develop a disease-modifying treatment against Parkinson's disease.The Institutional Animal Care and Use Committee of Centro de Investigación y de Estudios Avanzados approved our experimental procedures for animal use(authorization No.162-15)on June 9,2019.Manuel A.Fernandez-Parrilla David Reyes-Corona Yazmin M.Flores-Martinez Rasajna Nadella Michael J.Bannon Lourdes Escobedo Minerva Maldonado-Berny Jaime Santoyo-Salazar Luis O.Soto-Rojas Claudia Luna-Herrera Jose Ayala-Davila Juan A.Gonzalez-Barrios Gonzalo Flores Maria E.Gutierrez-Castillo Armando JEspadas-Alvarez Irma A.Martínez-Dávila Porfirio Nava Daniel Martinez-Fong 2022Neural Regeneration Research2022,17,4:1
4Evaluation of effects of primary and secondary enrichment for the detection of listeria monocytogenes by real-time PCR in retail ground chicken meat显示文摘Jaime Navas Sagrario Ortiz Pilar Lopez 2004Food Borne Pathogens and Disease2004,3,4:1
5Keratoconus therapeutics advances显示文摘Keratoconus is a progressive, usually bilateral disease of the cornea that significantly diminishes visual acuity, secondary to a progressive corneal deformity which is characterized by corneal thinning, variable degrees of irregular astigmatism and specific abnormal topographic patterns. Normally it initiates during puberty and is progressive until the third or fourth decade of life, when normally the progression rate is diminished or waned. There are multiple scales to clinically classify keratoconus. One of the most commonly used is Amsler-Krumeich and recently with the development of morphometric and aberrometric techniques, additional scales have been created that allow keratoconus to be classified according to its severity. Despite certain etiology of keratoconus remains unknown, current treatment options are available in patients with ectatic corneas and they vary depending on the severity of the disease and they include spectacles, contact lenses, intrastromal rings, keratoplasty both penetrant or lamellar, cross-linking, refractive lens exchange withintraocular lens implant, phakic intraocular lenses and the combination of these alternatives. Some authors have been using excimer laser in patients with keratoconus but the safety of the procedure is controversial. Currently, the techniques for the management of keratoconus can be classified in 3 types: corneal strengthening techniques, optical optimization techniques and combined techniques.Martha Jaimes Arturo Ramirez-Miranda Enrique O Graue-Hernández Alejandro Navas 2013World Journal of Ophthalmology2013,3,3:1
6Portal hypertension produces an evolutive hepato-intestinal pro- and anti-inflammatory response in the rat显示文摘Maria Dolores Palma Maria Angeles Aller Elena Vara Maria Paz Nava Cruz Garcia Javier Arias-Diaz Jose Luis Balibrea Jaime Arias 2005Cytokine2005,,3:1
7Bacterial Translocation to Mesenteric Lymph Nodes Increases in Chronic Portal Hypertensive Rats显示文摘Miguel-ángel Llamas María-ángeles Aller Domingo Marquina María-Paz Nava Jaime Arias 2010Digestive Diseases and Sciences2010,,8:1
8Splanchnic-aortic inflammatory axis in experimental portal hypertension显示文摘Splanchnic and systemic low-grade inflammation has been proposed to be a consequence of long-term prehepatic portal hypertension.This experimental model causes minimal alternations in the liver,thus making a more selective study possible for the pathological changes characteristic of prehepatic portal hypertension.Low-grade splanchnic inflammation after longterm triple partial portal vein ligation could be associated with liver steatosis and portal hypertensive intestinal vasculopathy.In fact,we have previously shown that prehepatic portal hypertension in the rat induces liver steatosis and changes in lipid and carbohydrate metabolism similar to those produced in chronic inflammatory conditions described in metabolic syndrome in humans.Dysbiosis and bacterial translocation in this experimental model suggest the existence of a portal hypertensive intestinal microbiome implicated in both the splanchnic and systemic alterations related to prehepatic portal hypertension.Among the systemic impairments,aortopathy characterized by oxidative stress,increased levels of proinflammatory cytokines and profibrogenic mediators stand out.In this experimental model of long-term triple portal vein ligated-rats,the abdominal aortic proinflammatory response could be attributed to oxidative stress.Thus,the increased aortic reduced-nicotinamide-adenine dinucleotide phosphate[NAD(P)H]oxidase activity could be associated with reactive oxygen species production and promote aortic inflammation.Also,oxidative stress mediated by NAD(P)H oxidase has been associated with risk factors for inflammation and atherosclerosis.The splanchnic and systemic pathology that is produced in the long term after triple partial portal vein ligation in the rat reinforces the validity of this experimental model to study the chronic low-grade inflammatory response induced by prehepatic portal hypertension.Maria-Angeles Aller Natalia de las Heras Maria-Paz Nava Javier Regadera Jaime Arias Vicente Lahera 2013World Journal of Gastroenterology2013,19,44:1
9Bacterial Translocation to Mesenteric Lymph Nodes Increases in Chronic Portal Hypertensive Rats显示文摘Miguel-ángel Llamas María-ángeles Aller Domingo Marquina María-Paz Nava Jaime Arias 2010Digestive Diseases and Sciences2010,,8:1
10Tumor Necrosis Factor-α, Interleukin-1β and Nitric Oxide: Induction of Liver Megamitochondria in Prehepatic Portal Hypertensive Rats显示文摘Isabel Prieto Ph.D. Fulgencio Jiménez M.D. Maria-Angeles Aller Ph.D. Maria-Paz Nava Ph.D. Elena Vara PhD. Cruz Garcia Ph.D. Jaime Arias Ph.D 2005World Journal of Surgery2005,,7:1
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