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Background: Cardiac thyrotropin-releasing hormone (TRH) is a tripeptide with still unknown functions. We demonstrated that the left ventricle (LV) TRH system is hyperactivated in spontaneously hypertensive rats and its inhibition prevented cardiac hypertrophy and fibrosis. Therefore, we evaluated whether in vivo cardiac TRH inhibition could improve myocardial function and attenuate ventricular remodeling in a rat model of myocardial infarction (MI).Methods and Results: In Wistar rats, MI was induced by a permanent left anterior descending coronary artery ligation. A coronary injection of a specific small interfering RNA against TRH was applied simultaneously. The control group received a scrambled small interfering RNA. Cardiac remodeling variables were evaluated one week later. In MI rats, TRH inhibition decreased LV end-diastolic (1.049 ± 0.102 mL vs 1.339 ± 0.102 mL, P < .05), and end-systolic volumes (0.282 ± 0.043 mL vs 0.515 ± 0.037 mL, P < .001), and increased LV ejection fraction (71.89 ± 2.80% vs 65.69 ± 2.85%, P < .05). Although both MI groups presented similar infarct size, small interfering RNA against TRH treatment attenuated the cardiac hypertrophy index and myocardial interstitial collagen deposition in the peri-infarct myocardium. These effects were accompanied by attenuation in the rise of transforming growth factor-β, collagen I, and collagen III, as well as the fetal genes (atrial natriuretic peptide, B-type natriuretic peptide, and beta myosin heavy chain) expression in the peri-infarct region. In addition, the expression of Hif1α and vascular endothelial growth factor significantly increased compared with all groups.Conclusions: Cardiac TRH inhibition improves LV systolic function and attenuates ventricular remodeling after MI. These novel findings support the idea that TRH inhibition may serve as a new therapeutic strategy against the progression of heart failure. [ABSTRACT FROM AUTHOR]

Soy hull was evaluated as a new material for Cr(VI) removal from aqueous solutions. Cr(VI) removal was associated to a redox mechanism, in which Cr(VI) was reduced to Cr(III) by the biomass. The redox capacity of soy hull was 1.12 mmol g −1 . A kinetic model that considers the redox reaction between Cr(VI) and the biomass surface was proposed. The maximum sorption capacity was 7.286 mg g −1 at 20 °C and pH 1.5. Activation parameters and mean free energies suggest that the sorption process follows a mechanism of chemical sorption. Thermodynamic parameters show that Cr(VI) removal was spontaneous. The isosteric heat of sorption indicated that soy hull has an energetically homogeneous surface. XPS spectra showed that chromium bound on the biomass was Cr(III). These results were confirmed by XANES and EXAFS experiments. EPR spectra showed the presence of Cr(V)-soy hull at short contact time and only a signal corresponding to Cr(III)-soy hull at long contact times. Continuous sorption data were fitted to Thomas and modified dose–response models. The bed depth service time (BDST) model was used to scale-up the continuous sorption experiments. [ABSTRACT FROM AUTHOR]

Abstract: Selective oxidation of galacturonic residues of oligo and polyuronic acids by CrVI affords CO2/HCO2H, oxidized uronic acid, and CrIII as final redox products. Kinetic studies show that the redox reaction proceeds through a mechanism combining CrVI →CrIV →CrII and CrVI →CrIV →CrIII pathways. The mechanism is supported by the observation of free radicals, CrO2 2+ and CrV as reaction intermediates. The EPR spectra show that five- and six coordinated oxo-CrV intermediates are formed. Penta-coordinated oxo-CrV species are present at any [H+], whereas hexa-coordinated ones are only observed at pH <1. At low pH CrV predominating species are coordinated by carboxylate groups and Oring (g iso =1.9783/5). At pH 7.5, the predominating ones are those coordinated by alcoholate groups of the ligand (g iso =1.9800). Polygal can reduce CrVI and efficiently trap CrIII. This behaviour represents an interesting model for the study of biomaterials, which possess a high proportion of polygal, in order to remove chromium from polluted waters. [Copyright &y& Elsevier]

Abstract: Leptin, a hormone secreted by the adipose tissue, stimulates anorexigenic peptides and also inhibits orexigenic peptides in hypothalamic arcuate nuclei-located neurons. It also counteracts the starvation-induced suppression of thyroid hormones by up-regulating the expression of preproTRH gene. On the other hand, in addition to its role as a modulator of the thyroid-hypothalamic-hypophysial axis, thyrotropin-releasing hormone (TRH) acts as a modulator of the cardiovascular system. In fact, we reported that overexpression of diencephalic TRH (dTRH) induces hypertension. We have recently shown that, in rats with obesity-induced hypertension, hyperleptinemia may produce an increase of dTRH together with an elevation of arterial blood pressure (ABP) through an increase of sympathetic activity and that these alterations were reversed by antisense oligonucleotide and small interfering RNA against preproTRH treatments. Here we explore the possible role of dTRH as a mediator involved in leptin-induced hypertension in 2 obesity mouse models: agouti-yellow mice, which are hyperleptinemic and hypertensive, and ob/ob mice, which lack functional circulating leptin. These 2 models share some characteristics, but ob/ob mice show lower ABP and plasma catecholamines levels. Then, for the first time, we report that there is a clear association between ABP and dTRH levels in both mouse models, as we have found that dTRH content was elevated in agouti-yellow mice and diminished in ob/ob mice compared with their controls. We also show that, after 3 days of subcutaneous leptin injections (10 μg/12 hours), ABP and dTRH increased significantly in ob/ob mice with no alterations of thyroid hormone levels. These results add evidence to the putative molecular mechanisms for the strong association between obesity and hypertension. [Copyright &y& Elsevier]

Abstract: Thyrotropin (TSH)-releasing hormone (TRH) also known as thyroliberin was the first of a number of peptides exerting several roles as a hormone and as a neuropeptide. Its ubiquitous distribution in the hypothalamus and in the extrahypothalamic regions and its diverse pharmacological and physiological effects are all features of its dual functions. For this reason, TRH has been the subject of much research throughout the past 20 years, work that has examined the structure, function, distribution, and regulation of the tripeptide and it has been extensively reviewed elsewhere [O''Leary R., O''Connor B. Thyrotropin-releasing hormone. J Neurochem. 1995;65:953–963.; Nillni E., Sevarino K. The biology of pro-thyrotropin-releasing hormone-derived peptides. Endocrine Reviews, 1999;20:599–664.]. After a brief overview of its distribution, hypothalamic and extrahypothalamic functions, and receptors involved, this review discusses efforts devoted to support TRH role in cardiovascular regulation with a main focus on hypertension pathophysiology in experimental models and humans. [Copyright &y& Elsevier]

Water pollution by heavy metals represents a serious problem around the world. Among various treatment techniques for water remediation, adsorption is an effective and versatile method due to the low cost, effectiveness and simplicity. Chitosan is a cationic polysaccharide with an excellent adsorption capacity of heavy metal ions. Chitosan has a high molybdate adsorption capacity (265 ± 1 mg g −1 ) at 20 °C and pH 2.7. Participation of hydroxyl groups in the adsorption of molybdate anions was confirmed by FT-IR analysis. SEM images showed that morphological surface changes happen after Mo VI adsorption. Continuous adsorption data were best fitted by Modified Dose- Response model. Scale-up of continuous processes was achieved applying bed depth service time (BDST) model. Application of chitosan in molybdate removal from real groundwater samples suggest that this polysaccharide is a good option to be used for household purposes. [ABSTRACT FROM AUTHOR]