Avaliação de características de ácidos húmicos de resíduos de origem urbana: I. métodos espectroscópicos (UV-Vis, IV, RMN 13C-CP/MAS) e microscopia eletrônica de varredura

Foram caracterizados fisico-quimicamente ácidos húmicos, obtidos de composto de resíduos sólidos urbanos (AH-CRSU) e de lodo de estação de tratamento de esgoto (AH-LETE), ambos produzidos na cidade do Rio de Janeiro, por meio da análise da composição elementar, acidez total, de dados espectroscópicos (UV-Vis; IV, RMN de 13C-CP/MAS) e microscopia eletrônica de varredura (MEV). A análise das características estruturais revelou diferenças entre os AHs estudados. A presença de sistemas aromáticos foi observada por meio da espectroscopia de UV-Vis, indicando sistemas mais substituídos nos AH-LETE. A espectroscopia na região do infravermelho (IV) mostrou a presença de estruturas alifáticas nos AHs e maior complexidade nos sinais de absorção devida a polissacarídeos nos AH-CRSU. Além disso, foram observados grupos OH, COOH, COO-, CO2NH2, e confirmada a presença de sistemas aromáticos. Com a análise de RMN de 13C-CP/MAS, foi possível verificar as diferenças quantitativas nos diferentes tipos de carbono. Os AH-LETE apresentaram maior quantidade de grupos aromáticos e de COOH. A análise de RMN de 13C-CP/MAS também mostrou presença de polissacarídeos, N em aminoácidos e grupamentos OCH3. O conjunto de propriedades avaliadas permitiu indicar que a fração ácidos húmicos dos resíduos é "do tipo" ou "análoga" aos ácidos húmicos de origem pedogênica.

Nitric oxide reduces Cl- absorption in the mouse cortical collecting duct through an ENaC-dependent mechanism.

Since nitric oxide (NO) participates in the renal regulation of blood pressure, in part, by modulating transport of Na(+) and Cl(-) in the kidney, we asked whether NO regulates net Cl(-) flux (JCl) in the cortical collecting duct (CCD) and determined the transporter(s) that mediate NO-sensitive Cl(-) absorption. Cl(-) absorption was measured in CCDs perfused in vitro that were taken from aldosterone-treated mice. Administration of an NO donor (10 μM MAHMA NONOate) reduced JCl and transepithelial voltage (VT) both in the presence or absence of angiotensin II. However, reducing endogenous NO production by inhibiting NO synthase (100 μM N(G)-nitro-l-arginine methyl ester) increased JCl only in the presence of angiotensin II, suggesting that angiotensin II stimulates NO synthase activity. To determine the transport process that mediates NO-sensitive changes in JCl, we examined the effect of NO on JCl following either genetic ablation or chemical inhibition of transporters in the CCD. Since the application of hydrochlorothiazide (100 μM) or bafilomycin (5 nM) to the perfusate or ablation of the gene encoding pendrin did not alter NO-sensitive JCl, NO modulates JCl independent of the Na(+)-dependent Cl(-)/HCO3(-) exchanger (NDCBE, Slc4a8), the A cell apical plasma membrane H(+)-ATPase and pendrin. In contrast, both total and NO-sensitive JCl and VT were abolished with application of an epithelial Na(+) channel (ENaC) inhibitor (3 μM benzamil) to the perfusate. We conclude that NO reduces Cl(-) absorption in the CCD through a mechanism that is ENaC-dependent.

Subconjunctival Injection of XG-102, a c-Jun N-Terminal Kinase Inhibitor Peptide, in the Treatment of Endotoxin-Induced Uveitis in Rats.

Abstract Purpose: XG-102, a TAT-coupled dextrogyre peptide inhibiting the c-Jun N-terminal kinase, was shown efficient in the treatment of experimental uveitis. Preclinical studies are now performed to determine optimal XG-102 dose and route of administration in endotoxin-induced uveitis (EIU) in rats with the purpose of clinical study design. METHODS: EIU was induced in Lewis rats by lipopolysaccharides (LPS) injection. XG-102 was administered at the time of LPS challenge by intravenous (IV; 3.2, 35 or 355 μg/injection), intravitreal (IVT; 0.08, 0.2 or 2.2 μg/eye), or subconjunctival (SCJ; 0.2, 1.8 or 22 μg/eye) routes. Controls received either the vehicle (saline) or dexamethasone phosphate injections. Efficacy was assessed by clinical scoring, infiltrating cells count, and expression of inflammatory mediators [inducible nitric oxide synthase (iNOS), cytokine-induced neutrophil chemoattractant-1 (CINC-1)]. The effect of XG-102 on phosphorylation of c-Jun was evaluated by Western blot. RESULTS: XG-102 demonstrated a dose-dependent anti-inflammatory effect in EIU after IV and SCJ administrations. Respective doses of 35 and 1.8 μg were efficient as compared with the vehicle-injected controls, but only the highest doses, respectively 355 and 22 μg, were as efficient as dexamethasone phosphate. After IVT injections, the anti-inflammatory effect of XG-102 was clinically evaluated similar to the corticoid's effect with all the tested doses. Regardless of the administration route, the lowest efficient doses of XG-102 significantly decreased the ration of phospho c-Jun/total c-Jun, reduced cells infiltration in the treated eyes, and significantly downregulated iNOS and CINC-1 expression in the retina. CONCLUSION: These results confirm that XG-102 peptide has potential for treating intraocular inflammation. SCJ injection appears as a good compromise to provide a therapeutic effect while limiting side effects.

Pièces relatives à l'histoire de la ville de TULLE. IV

Contient : Extrait de l'inventaire des archives de l'église de Tulle ; Extrait du cartulaire de l'église de Tulle ; Extrait du cartulaire de Saint-Martin de Tulle ; « Libellus apologetico-supplex » pour les Recollets de Tulle, par le P. Victorin Tarneau ; Extrait d'un cartulaire de Saint-Martin de Tulle ; Accord entre les chanoines de Tulle et ceux de Notre-Dame de Rocamadour, pour le règlement des droits de ces derniers (15 mars 1423) ; Extrait des statuts de l'église de Tulle ; Extraits de l'obituaire de l'église de Tulle (Molinier, Obituaires, n° 503 bis) ; Note sur diverses pièces conservées aux archives de l'évêché de Tulle ; Extrait des Decisiones Burdegalenses, de Nicolas Bohier (Lyon, 1579, in-fol.) ; Extrait des registres du Parlement de Bordeaux concernant la ville de Tulle (1555-1581) ; Rôle des noms des présidents et conseillers du Parlement de Bordeaux (décembre 1564) ; original ; Extrait des registres du Parlement de Bordeaux (1555-1563) ; Procès-verbal d'une assemblée du chapitre de Tulle, autorisant l'engagement d'une cloche pour le soulagement des pauvres (23 mai 1691) ; Mandement de Humbert [Ancelin], évêque de Tulle, pour l'usage de la viande et des oeufs durant le carême (16 février 1691) ; Autobiographie de Mascaron ; Lettres de provision de l'évêché de Tulle en faveur de Jules Mascaron (5 janvier 1671) ; Billet mortuaire du même (5 décembre 1703) ; Deux lettres du même, évêque d'Agen (19 février et 10 mars, s. d.) ; Lettre anonyme écrite de Tulle, le 19 avril 1666 ; Lettre de Louis de Guron, évêque de Comminges (8 juin 1688) à A. de Fes ; Lettre de M. de Fes à Baluze (Daux, 16 juin 1688) ; Deux lettres de [Louis de] Guron, évêque-nommé de Tulle, à Mazarin (10 décembre et 23 septembre 1652) ; Lettre de M. de Fes à Baluze (Toulouse, 5 novembre 1681) ; Notes sur les familles Guron et de Rechignevoisin ; Lettre de M. de Fes à Baluze (Toulouse, 18 mars 1688) ; Lettres de Louis de Guron, évêque de Tulle, puis de Comminges ; « Bref de N. S. Père le pape Innocent X, » envoyé à l'évêque de Tulle touchant la question du Jansénisme (21 mars 1654) ; imprimé ; Lettre de Richelieu au cardinal Antoine Barberini (25 juin 1634) ; Liste des événements notables de l'histoire de Tulle de 1545 à 1685 ; « Catalogus abbatum et episcoporum Tutellensium, » par Baluze ; placard imprimé avec nombreuses corrections de la main de l'auteur ; Diplômes de Raoul et de Louis IV pour le monastère de Tulle ; Fragments d'un traité, en latin, sur la vision en Dieu ; Lettres d'Harduin [de Péréfixe], archevêque de Paris, authentiquant des reliques rapportées par Baluze (s. d.) ; Certificat d'authenticité de ces mêmes reliques, délivré par Gaspard, cardinal prêtre du titre de San Silvestro in capite (8 novembre 1681) ; placard imprimé ; Lettres adressées à Baluze ; Copies par Baluze de diverses pièces relatives aux reliques rapportées par lui de Rome (1683-1685) ; Extrait d'un rouleau des morts du monastère d'Obazine ; « Ex epigrammatis Joannis Vulteii Remensis » (Lyon, 1537, in-8°), et extraits divers concernant Pierre du Chastel, évêque de Tulle ; Notes relatives aux Privilegia regularium, du P. Bruno Chassaing (Paris, 1648, in-fol.)

Pièces diverses, manuscrites et imprimées, concernant les affaires ecclésiastiques en Lorraine (VIIIe-XVIIIe siècle). XVI — 752-1729. — Abbayes et prieurés (IV).

Contient : Épinal (1303-1661) ; Etival (1554-1719) ; Flabémont, mss. et impr., in-4° (1526-1675) ; Flavigny : comptes des revenus du prieuré (1657) ; Freistroff (1644-1712) ; Gorze : copies et factums, impr., in-4° (752-XVIIe siècle) ; Grafenthal (1554-1556) ; Grimaucourt-près-Sampigny (1639-1720) ; Hauteseille (1585) ; Herbitzheim ; originaux et copies (1284-XVIe siècle) ; Hornbach (1513)

Decreased intraocular pressure induced by nitric oxide donors is correlated to nitrite production in the rabbit eye.

PURPOSE: To evaluate the effect of intraocular administration of nitric oxide (NO) donors in the rabbit eye on intraocular pressure (IOP), inflammation, and toxicity. METHODS: Intravitreal and intracameral injections of two NO donors, SIN-1 and SNAP, and SIN-1C and BSS were performed. Clinical examination, IOP measurements, protein evaluation in aqueous humor, and histologic analysis of the ocular globes were realized. Nitric oxide release was demonstrated by nitrite production in the aqueous humor and in the vitreous using the Griess reaction. RESULTS: The drastic decrease of IOP, observed after a single NO donor injection, was correlated directly with nitrite production and, thus, to NO release. Injection of inactive metabolite of SIN-1, SIN-1C, which is not able to release NO, did not modulate IOP. When administered in the aqueous humor or in the vitreous, NO did not diffuse from one segment of the eye to another. No inflammation or histologic damage was observed as a result of a single NO donor administration. CONCLUSIONS: Nitric oxide is implicated directly in the regulation of IOP and its acute, and massive release into the rabbit eye did not induce inflammation or other growth toxic effects on the ocular tissues.

Dipeptidyl-peptidase-IV by cleaving neuropeptide Y induces lipid accumulation and PPAR-γ expression.

We evaluated the effects of dipeptidyl peptidase-IV (DPPIV), and its inhibitor, vildagliptin, on adipogenesis and lipolysis in a pre-adipocyte murine cell line (3T3-L1). The exogenous rDPPIV increased lipid accumulation and PPAR-γ expression, whereas an inhibitor of DPPIV, the anti-diabetic drug vildagliptin, suppresses the stimulatory role of DPPIV on adipogenesis and lipid accumulation, but had no effect on lipolysis. NPY immunoneutralization or NPY Y(2) receptor blockage inhibited DPPIV stimulatory effects on lipid accumulation, collectively, indicating that DPPIV has an adipogenic effect through NPY cleavage and subsequent NPY Y(2) activation. Vildagliptin inhibits PPAR-γ expression and lipid accumulation without changing lipolysis, suggesting that this does not impair the ability of adipose tissue to store triglycerides inside lipid droplets. These data indicate that DPPIV and NPY interact on lipid metabolism to promote adipose tissue depot.

Nitric oxide activity through guanylate cyclase and phosphodiesterase modulation is impaired in fetal lambs with congenital diaphragmatic hernia.

BACKGROUND: Congenital diaphragmatic hernia (CDH) is associated with pulmonary hypertension and death. Administration of nitric oxide (NO) alone remains ineffective in CDH cases. We investigated in near full-term lambs with and without CDH the role of guanylate cyclase (GC), the enzyme activated by NO in increasing cyclic 3'-5'-guanylosine monophosphate, and the role of phosphodiesterase (PDE) 5, the enzyme-degrading cyclic 3'-5'-guanylosine monophosphate. METHODS: Congenital diaphragmatic hernia was surgically created in fetal lambs at 85 days of gestation. Pulmonary hemodynamics were assessed by means of pressure and blood flow catheters (135 days). In vitro, we tested drugs on rings of isolated pulmonary vessels. RESULTS: In vivo, sodium nitroprusside, a direct NO donor, and methyl-2(4-aminophenyl)-1,2-dihydro-1-oxo-7-(2-pyridinylmethoxy)-4-(3,4,5 trimethoxyphenyl)-3-isoquinoline carboxylate sulfate (T-1032) and Zaprinast, both PDE 5 blockers, reduced pulmonary vascular resistance in CDH and non-CDH animals. The activation of GC by sodium nitroprusside and the inhibition of PDE 5 by T-1032 were less effective in CDH animals. In vitro, the stimulation of GC by 3(5'hydroxymethyl-2'furyl)-1-benzyl indazole (YC-1) (a benzyl indazole derivative) and the inhibition of PDE 5 by T-1032 were less effective in pulmonary vascular rings from CDH animals. The YC-1-induced vasodilation in rings from CDH animals was higher when associated with the PDE 5 inhibitor T-1032. CONCLUSIONS: Guanylate cyclase and PDE 5 play a role in controlling pulmonary vascular tone in fetal lambs with or without CDH. Both enzymes seem to be impaired in fetal lambs with CDH.