Proyecto actividad, acondicionamiento de una nave industrial para almacenamiento

Descripcion del acondicionamiento de una nave industrial, su limatizacion y calculo del plan de incendio

Role of nitric oxide in hepatic IGF-I response to inflammation

Objetivos: Estudiar la implicación del óxido nítrico (NO) en el efecto inhibidor de la inflamación, tanto aguda como crónica, sobre el factor de crecimiento similar a la insulina- I (IGF-I), ya que este gas es un mediador importante de la respuesta inflamatoria. Material y métodos: Para ello se analizó el efecto del bloqueo de la óxido nítrico sintasa inducida por las citoquinas (iNOS), mediante la administración de aminoguanidina (AG) a ratas macho, sobre la inhibición del IGF-I sérico y hepático que se produce en respuesta a la inflamación. La inflamación aguda se indujo mediante la administración de lipopolisacárido de E-coli (LPS), y la crónica, mediante la administración de adyuvante de Freund, que produce en los animales una artritis crónica. Las concentraciones séricas y hepáticas de IGF-I se midieron mediante RIA. Resultados: La administración de AG a ratas artríticas disminuyó el grado de inflamación (p < 0,01), pero no modificó el IGF-I sérico o hepático. En las ratas tratadas con LPS, la AG no alteró el IGF-I hepático, pero normalizó el IGF-I sérico. Conclusiones: 1) El NO no participa en el descenso del IGF-I hepático observado en la inflamación aguda o crónica. 2) El NO está implicado en los mecanismos responsables del descenso del IGF-I sérico en la inflamación aguda.Objective: To study the role of nitric oxide (NO) in the inhibitory effect of the acute and chronic inflammation on the insulin-like growth factor-I (IGF-I), since this gas is a mediator of inflammation. Material and methods: For this purpose, the inhibition of the enzyme NO synthase inducible by citoquines (iNOS), through aminoguanidine (AG) administration to male rats, and its effect on the decrease in serum and hepatic IGF-I observed during inflammation, was studied. Acute inflammation was induced by administration of bacterial lipopolysaccharide (LPS), and chronic inflammation by administration of Freund adjuvant, that induces chronic arthritis. Serum and hepatic IGF-I concentrations was measured by RIA. Results: AG administration to arthritic rats decreased the severity of inflammation (p < 0.01), but it did not modify serum or hepatic IGF-I. In LPS-treated rats, the AG did not change the hepatic IGF-I content, but it normalised serum IGF-I levels. Conclusions: 1) NO does not mediate the decrease in the hepatic IGF-I in acute and chronic inflammation. 2) NO is involved in the mechanisms responsible for the decrease in serum IGF-I levels in acute inflammation.FIS (00/0949)0.111 SJR (2004) Q3, 1175/1864 Medicine (miscellaneus)UE

Anti-inflammatory effect of the ghrelin agonist growth hormone-releasing peptide-2 (GHRP-2) in arthritic rats

Chronic arthritis induces hypermetabolism and cachexia. Ghrelin is a gastrointestinal hormone that has been proposed as a treatment to prevent cachexia. The aim of this work was to examine the effect of administration of the ghrelin agonist growth hormone-releasing peptide-2 (GHRP-2) to arthritic rats. Male Wistar rats were injected with Freund’s adjuvant, and 15 days later arthritic and control rats were daily injected with GHRP-2 (100 μg/kg) or with saline for 8 days. Arthritis induced an increase in serum ghrelin (P < 0.01) and a decrease in serum concentrations of leptin (P < 0.01), whereas GHRP-2 administration increased serum concentrations of leptin. GHRP-2 increased food intake in control rats but not in arthritic rats. However, in arthritic rats GHRP-2 administration ameliorated the external symptoms of arthritis, as it decreased the arthritis score (10.4 ± 0.8 vs. 13.42 ± 0.47, P < 0.01) and the paw volume. In addition, circulating IL-6 and nitrites/nitrates were increased by arthritis, and GHRP-2 treatment decreased the serum IL-6 levels (P < 0.01). To elucidate whether GHRP-2 is able to modulate IL-6 release directly on immune cells, peritoneal macrophage cultures were incubated with GHRP-2 or ghrelin, the endogenous ligand of the growth hormone (GH) secretagogue receptor. Both GHRP-2 (10−7 M) and ghrelin (10−7 M) prevented endotoxin-induced IL-6 and decreased nitrite/nitrate release from peritoneal macrophages in vitro. These data suggest that GHRP-2 administration has an anti-inflammatory effect in arthritic rats that seems to be mediated by ghrelin receptors directly on immune cells.Programa Nacional de Promoción General del Conocimiento, Plan Nacional de Investigación Científica, Ministerio de Ciencia y Tecnología (BFI-2003-02149)4.456 JCR (2005) Q1, 6/75 Physiology, 18/89 Endocrinology & metabolismUE

Ghrelin receptor agonist GHRP-2 prevents arthritis-induced increase in E3 ubiquitin-ligating enzymes MuRF1 and MAFbx gene expression in skeletal muscle

Chronic arthritis is a catabolic state associated with an inhibition of the IGF system and a decrease in body weight. Cachexia and muscular wasting is secondary to protein degradation by the ubiquitin-proteasome pathway. The aim of this work was to analyze the effect of adjuvant-induced arthritis on the muscle-specific ubiquitin ligases muscle ring finger 1 (MuRF1) and muscle atrophy F-box (MAFbx) as well as on IGF-I and IGF-binding protein-5 (IGFBP-5) gene expression in the skeletal muscle. We also studied whether the synthetic ghrelin receptor agonist, growth hormone releasing peptide-2 (GHRP-2), was able to prevent arthritis-induced changes in the skeletal muscle. Arthritis induced an increase in MuRF1, MAFbx (P < 0.01), and tumor necrosis factor (TNF)-α mRNA (P < 0.05) in the skeletal muscle. Arthritis decreased the serum IGF-I and its gene expression in the liver (P < 0.01), whereas it increased IGF-I and IGFBP-5 gene expression in the skeletal muscle (P < 0.01). Administration of GHRP-2 for 8 days prevented the arthritis-induced increase in muscular MuRF1, MAFbx, and TNF-α gene expression. GHRP-2 treatment increased the serum concentrations of IGF-I and the IGF-I mRNA in the liver and in the cardiac muscle and decreased muscular IGFBP-5 mRNA both in control and in arthritic rats (P < 0.05). GHRP-2 treatment increased muscular IGF-I mRNA in control rats (P < 0.01), but it did not modify the muscular IGF-I gene expression in arthritic rats. These data indicate that arthritis induces an increase in the activity of the ubiquitin-proteasome proteolytic pathway that is prevented by GHRP-2 administration. The parallel changes in muscular IGFBP-5 and TNF-α gene expression with the ubiquitin ligases suggest that they can participate in skeletal muscle alterations during chronic arthritisPrograma Nacional de Promoción General del Conocimiento, Plan Nacional de Investigación Científica, Ministerio de Educación Ciencia (BFI-2003–02149)4.456 JCR (2005) Q1, 6/75 Physiology, 18/89 Endocrinology & metabolismUE

Dexamethasone administration attenuates the inhibitory effect of lipopolysaccharide on IGF-I and IGF-binding protein-3 in adult rats

The aim of this study was to investigate whether glucocorticoid administration had a beneficial effect on serum concentrations of insulin-like growth factor I (IGF-I) and on IGF-binding protein 3 (IGFBP-3) in rats injected with lipopolysaccharide (LPS). Adult male rats were injected with LPS or saline and pretreated with dexamethasone or saline. Dexamethasone administration decreased growth hormone (GH) receptor and IGF-I mRNA levels in the liver of control rats. LPS decreased GH receptor and IGF-I gene expression in the liver of saline-treated rats but not in the liver of dexamethasone-pretreated rats. In the kidney, GH receptor mRNA levels were not modified by dexamethasone or LPS treatment. However, LPS decreased renal IGF-I gene expression and dexamethasone pretreatment prevented this decrease. Serum concentrations of IGF-I were decreased by LPS, and dexamethasone pretreatment attenuated this effect. The gene expression of IGFBP-3 in the liver and kidney and its circulating levels were decreased by LPS. In control rats dexamethasone increased circulating IGFBP-3 and its gene expression in the liver, and decreased the proteolysis of this protein. Dexamethasone pretreatment attenuated the LPS-induced decrease in IGFBP-3 gene expression in the liver and prevented the LPS-induced decrease in IGFBP-3 gene expression in the kidney. Moreover, dexamethasone pretreatment attenuated the LPS-induced decrease in serum concentrations of IGFBP-3 and decreased the LPS-induced IGFBP-3 proteolysis in serum. In conclusion, dexamethasone pretreatment partially attenuates the inhibitory effect of LPS on serum IGF-I by blocking the decrease of its gene expression in the kidney as well as by attenuating the decrease in serum concentrations of IGFBP-3.Comunidad Autónoma de Madrid (0.870017/2003 1)3.059 JCR (2005) Q2, 31/89 Endocrinology & metabolismUE

The inhibition of inducible nitric oxide synthase reverts arthritic-induced decrease in pituitary growth hormone mRNA but not in liver insulin-like growth factor I mRNA expression

Experimental arthritis induced by Freund-adjuvant administration is a model of chronic inflammation and rheumatoid arthritis associated with a decrease in pituitary growth hormone (GH) and hepatic insulin-like growth factor I (IGF-I) gene expression. Excessive nitric oxide (NO) synthesis by inducible NO synthase (iNOS) has been implicated in the pathogenesis of inflammatory illness. Moreover, NO participates in the regulation of GH secretion at both the hypothalamus and the pituitary. We have examined the role of iNOS activation in producing the changes in the GH-IGF-I axis in arthritic rats. Adult male Wistar rats received aminoguanidine or vehicle from day 20, after adjuvant or vehicle injection, until day 28. Two hours and 30 min after the last aminoguanidine injection, all rats were killed by decapitation. Arthritis increased hypothalamic expression of somatostatin mRNA while it decreased pituitary GH mRNA expression, and both effects were prevented by aminoguanidine administration. In arthritic rats, the parallel decrease in serum IGF-I, and in hepatic IGF-I content and mRNA expression, correlates with the decrease in circulating GH concentrations. Aminoguanidine administration to arthritic rats did not modify either serum GH or serum IGF-I concentrations, or hepatic IGF-I mRNA expression. However, aminoguanidine administration to control rats resulted in a decrease in serum GH concentrations and in a decrease in both hepatic IGF-I mRNA expression and serum IGF-I concentrations. These data suggest that NO mediates the arthritis-induced decrease in GH mRNA expression by acting at a hypothalamic level, but it is not involved in the decrease in hepatic IGF-I mRNA expression.Sin financiación3.418 JCR (2003) Q2, 24/88 Endocrinology & metabolism, 50/198 NeurosciencesUE

NO plays a role in LPS-induced decreases in circulating IGF-I and IGFBP-3 and their gene expression in the liver

In this study, we administered aminoguanidine, a relatively selective inducible nitric oxide synthase (iNOS) inhibitor, to study the role of nitric oxide (NO) in LPS-induced decrease in IGF-1 and IGFBP-3. Adult male Wistar rats were injected intraperitoneally with LPS (100 μg/kg), aminoguanidine (100 μg/kg), LPS plus aminoguanidine, or saline. Rats were injected at 1730 and 0830 the next day and killed 4 h after the last injection. LPS administration induced an increase in serum concentrations of nitrite/nitrate (P < 0.01) and a decrease in serum concentrations of growth hormone (GH; P < 0.05) and IGF-I (P < 0.01) as well as in liver IGF-I mRNA levels (P < 0.05). The LPS-induced decrease in serum concentrations of IGF-I and liver IGF-I gene expression seems to be secondary to iNOS activation, since aminoguanidine administration prevented the effect of LPS on circulating IGF-I and its gene expression in the liver. In contrast, LPS-induced decrease in serum GH was not prevented by aminoguanidine administration. LPS injection decreased IGFBP-3 circulating levels (P < 0.05) and its hepatic gene expression (P < 0.01), but endotoxin did not modify the serum IGFBP-3 proteolysis rate. Aminoguanidine administration blocked the inhibitory effect of LPS on both IGFBP-3 serum levels and its hepatic mRNA levels. When aminoguanidine was administered alone, IGFBP-3 serum levels were increased (P < 0.05), whereas its hepatic mRNA levels were decreased. This contrast can be explained by the decrease (P < 0.05) in serum proteolysis of this binding protein caused by aminoguanidine. These data suggest that iNOS plays an important role in LPS-induced decrease in circulating IGF-I and IGFBP-3 by reducing IGF-I and IGFBP-3 gene expression in the liver.Sin financiación4.431 JCR (2004) Q1, 6/74 Physiology, 16/87 Endocrinology & metabolismUE

Czechoslovak and French relations in 1948-1956

Československo-francouzské vztahy po druhé světové válce zatím zůstávaj í v české historiografii opomíjeným tématem. Monografie, která by se uceleně věnovala právě těmto vztahům neexistuje, s vy jímkou práce Karla Bartoška!), která se ale zaměřuje na speciální problematiku vzájemných vztahů a kontaktů mezi komunistickými stranami obou států. K základnímu seznámení s tématem je možné využít prací Karla Kaplana a Jindřicha Dejmka2 ), které se věnují mezinárodně-politickým vztahům Československa v období let 1945 - 1948, resp. 1918 - 1992. K vlastním dějinám Francie je dodnes použitelné souhrm1é zpracování francouzských dějin z roku 1988 Dějiny Francie,3) kvalitní je i publikace francouzského autora M. Perottina o politickém systému poválečné Francie, která u nás vyšla v českém překladu minulý rok. 4) Kromě těchto knih má český historik k dispozici dva vydané soubory dokumentů k československofrancouzským vztahům za druhé světové válki), v případě publikace P. Petrůfa s přesahem do roku 1948. Při studiu československo-francouzských vztahů může badatel narazit i na jiný problém. Je jím jazyková bariéra, zejména práce o dějinách francouzské čtvrté republiky jsou v České republice dostupné pouze ve francouzštině. Francouzsky ostatně publikují i někteří domácí badatelé, např. již zmínění Karel Kaplan a Jindřich..