Survival, Body Condition, and Immune System of Apis mellifera liguistica Fed Avocado, Maize, and Polyfloral Pollen Diet.

Nutritional stress is the major factor contributing to decline in the honey bee (Apis mellifera L.) populations given the high degree of dependence on floral resources, and due to the habitat loss. In this sense, monocultures of maize and avocado have great extensions in Mexico, but their impact on the physiology and morphology of A. mellifera is unknown. This research evaluated the effect of total protein content in monofloral (maize or avocado pollen diets) and polyfloral (using five types of pollen: Persea americana Mill., Zea mays L., Melampodium perfoliatum Cav., Drymaria villosa Cham Schltdl., and Lopezia racemosa Cav.) on their survival, body condition (controlled density, head mass, and development of hypopharyngeal glands; protein content in hemolymph), and immune response [lytic activity and activity of prophenoloxidase in the hemolymph (proPO)]. Corbicular pollen of P. americana had the highest protein content, followed by the corbicular pollen of Z. mays, M. perfoliatum, D. villosa, and L. racemosa. Polyfloral diet seems to be better for A. mellifera than the monofloral maize and avocado. Bees fed polyfloral pollen diet showed a high content of protein in the hemolymph in comparison with that fed maize or avocado pollen diets. Bees fed polyfloral and avocado pollen diet had the highest lytic activity but showed a decrease in proPO activity. In conclusion, polyfloral diets seem to be better for A. mellifera than the monofloral maize and avocado.

Study of the surface chemistry of modified carbon nanofibers by oxidation treatments in liquid phase.

Carbon nanofibers (CNF) were grown by thermocatalytic decomposition of methane. Their texture and surface chemistry were modified by different oxidation treatments with HNO3 at different concentrations or a mixture of HNO3-H2SO4 to optimise their ability of dispersing active metal particles, because this material will be used as electrocatalytic support for polymeric electrolyte fuel cells. The effect of liquid phase oxidation on the surface chemistry and the textural properties of the CNF was studied by temperature programmed desorption (TPD), scanning electron microscopy (SEM) and N2-physisorption. Moreover, their thermal stability was studied by temperature programmed oxidation (TPO). During oxidation treatments functional groups were created and their number was function of the oxidation treatment conditions. Results indicated that an increase in severity of the oxidation treatment produces an increase in the number of surface oxygen groups and in the thermal stability. However, a very severe treatment can destroy partially the structure of carbon nanofibers.

AMnO3 (A = Sr, La, Ca, Y) Perovskite Oxides as Oxygen Reduction Electrocatalysts.

A series of perovskite-type manganites AMnO3 (A = Sr, La, Ca and Y) particles were investigated as electrocatalysts for the oxygen reduction reaction. AMnO3 materials were synthesized by means of an ionic-liquid method, yielding phase pure particles at different temperatures. Depending on the calcination temperature, particles with mean diameter between 20 and 150 nm were obtained. Bulk versus surface composition and structure are probed by X-ray photoelectron spectroscopy and extended X-ray absorption fine structure. Electrochemical studies were performed on composite carbon-oxide electrodes in alkaline environment. The electrocatalytic activity is discussed in terms of the effective Mn oxidation state, A:Mn particle surface ratio and the Mn-O distances.

Cardiac protection by pharmacological modulation of inflammation.

Inflammation is a reaction to primary injury of various kinds, such as infection and trauma, which has both beneficial and detrimental effects. Inflammation has been associated with major diseases of the heart and vessels. Research has focused not only on ischaemia but also on post-ischaemic reperfusion, which is known to activate and amplify the inflammatory response. Although reperfusion should always be attempted in the clinical environment, it has been shown experimentally that it can cause some cardiac damage, in addition to that caused by ischaemia. Therefore, it is reasonable to attempt to increase the benefit obtainable with reperfusion by modulating inflammatory processes triggered by reperfusion itself. In this field, different potential therapeutic targets have been identified and interventions have been tested over the last 30 years. With the exception of adenosine, which probably does not act merely through inhibition of the inflammatory response, no other compounds have yet proven successful in clinical trials. Active research is ongoing. Broadening the approach from the heart to the cardiovascular system, promising data is emerging on cardiovascular protection conferred by statins in patients with coronary heart disease (CHD) and high levels of C-reactive protein (CRP), a systemic marker of inflammation. Similarly, results of trials aimed at preventing cardiovascular events by eradicating chronic infections will be among the first to directly test whether such therapies will decrease risks of cardiovascular disease.

Left ventricular response to beta-adrenergic stimulation in aging rats.

The incidence of heart failure in the population increases steeply among older people. Overactivation of the sympathetic nervous system is associated to and responsible for worsening of heart failure. This study describes the influence of aging on short-term left ventricular (LV) adaptation to b-adrenergic stimulation in Wistar rats. In controls at 18 mo, interstitial fibrosis was increased with respect to 3-mo-old rats, whereas myocytes dimension and the messenger RNA (mRNA) abundance of atrial natriuretic peptide (ANP), a2(I) procollagen, transforming growth factor (TGF-b1, TGF-b3), and secreted protein, acidic and rich in cysteine (SPARC) were not different. To determine how aging affects LV adaptation to adrenergic stimulation, two groups of animals received isoproterenol (ISO, 1 mg/kg/d) for 3 days. There was no significant difference between young and older rats with respect to increase in LV weight, myocytes dimension, and mRNA abundance of all the genes considered, except a1(III) procollagen. These findings indicate that despite limited compensatory hypertrophy and higher fibrosis, LV from aged nonsenescent rats preserves the capacity to adapt to b-adrenergic stimulation through the upregulation of several genes encoding extracellular matrix-related proteins.

Influence of inhalational, neuroleptic and local anaesthesia on lymphocyte subset distribution.

We previously demonstrated that anaesthetics affect leukocyte response by inhibiting lymphocyte capping and metabolism and the phagocytic activity of neutrophils in some experimental models. In the present study, we investigated the effects of the clinical use of three different types of anaesthesia on lymphocyte subset distribution and activity: inhalational anaesthesia (isoflurane), a neuroleptoanalgesia, or local anaesthesia was used in patients submitted to the same operation (hysterectomy). At time 0 (before administering the anaesthesia) and at 10 min and 48 h from the start of the operation, heparinized blood was obtained from each of the 30 patients studied; three lymphocyte subpopulations were isolated (CD4+, CD8+ and CD19+). Cell number was identified for each lymphocyte subset, and (as an indication of cellular function) the intracellular contents of ATP and cAMP were evaluated by luminescence methods. The relevant results for each of the 3 anaesthetic methods were as follows: i) treatment with isoflurane induced a significant reduction in the number and function of CD4+ cells at 10 min, which was reversed at 48 h; a functional but not reversible decrease of CD19+ cells was obtained, ii) treatment with neuroleptic drugs induced a significant progressive functional impairment of CD4+ and CD19+ cells, and iii) local anaesthesia caused a significant functional impairment of CD8+ cells at 48 h and a significant functional impairment of CD19+ cells at 10 min and 48 h.

[Trans fatty acids: consumption effect on human health and regulation challenges]. / Ácidos grasos trans: un análisis del efecto de su consumo en la salud humana, regulación del contenido en alimentos y alternativas para disminuirlos.

Trans fatty acids (TFA) are stable to oxidative rancidity which allows them to have a long shelf-life: also they have an intermediate melting point between saturated and unsaturated fats. For these reasons they have been widely used by the food industry. However, in recent years a large number of epidemiological and clinical evidence has indicated that trans fats are a significant risk factor to suffer a cardiovascular event and appear to be involved in the process of inflammation, diabetes and cancer. The increase of 2% of the daily energy by TFA is associated with a 23% increase cardiovascular risk. Therefore, international organizations like WHO and PAHO recommend virtually eliminate them or make their consumption as low as possible, less than 1%. Considering this recommendation and the risk involved in its consumption, some countries in Europe and America have legislated to achieve a gradual reduction of these fats. Denmark is a country that has shown a reduced prevalence of cardiovascular disease by reducing sources of trans fats in the diet. Despite the evidence of their impact on health in many countries still do not take any action and significant amounts of TFA remain in their foods and therefore in the diet of its population.

Carbon monoxide and methanol oxidation at platinum catalysts supported on ordered mesoporous carbon: the influence of functionalization of the support.

The influence of different functionalization treatments of the support on the electrocatalytic activity towards CO and methanol oxidation at platinum nanoparticles deposited on ordered mesoporous carbons (OMC) has been studied for the first time. Before deposition of the metal, the carbon support was functionalized applying several procedures, with the purpose to generate oxygenated groups for anchoring the Pt nanoparticles by the formic acid (FM) and borohydride (BM) reduction methods. Good dispersion of the catalyst was obtained in all cases. It has been shown that particle size, and consequently the lattice parameter and metal surface area, depends on the functionalization treatment employed. CO and methanol electrooxidation was studied at all prepared catalysts applying cyclic voltammetry. It was observed that CO stripping occurs at more negative potentials (around 0.10-0.15 V) with these supports with respect to Vulcan XC-72 supported catalysts, and the best results for both methods were achieved with OMC functionalized with concentrated nitric acid for 0.5 h. This carbon support presents a higher amount of oxygenated groups without the loss of the ordered structure. In situ infrared studies have been performed for the first time with this type of catalyst, showing that the effect of the carbon support on the CO oxidation potential is similar to the presence of a second metal as Ru under the same experimental conditions. Methanol electrooxidation is also dependent on the nature of the support, as proved from both cyclic voltammetry and chronoamperometry. In this case, results depend on the method of nanoparticles preparation and seem to be better for BM.

Comparative efficacy of a DA2/alpha2 agonist and a beta-blocker in reducing adrenergic drive and cardiac fibrosis in an experimental model of left ventricular dysfunction after coronary artery occlusion.

Attenuation of neuroendocrine activation may be beneficial in congestive heart failure. Sympathetic nervous system overactivity can be reduced by receptors blockade or by reducing norepinephrine (NE) spillover. This study evaluated and compared the effects of a DA2-dopaminergic receptor/alpha2-adrenoceptor agonist (CHF-1024) and a beta1-adrenoreceptor antagonist in terms of hemodynamics, ventricular remodeling, beta-adrenergic drive, and cardiac fibrosis after myocardial infarction (MI) in rats. MI was induced by left coronary artery ligation in 213 rats, whereas 12 were left unoperated on. After 2 months, the operated-on animals were treated for 1 more month with CHF-1024 at either 0.33 mg/kg/day (low dose) or 1 mg/kg/day (high dose) or with metoprolol (10 mg/kg/day), delivered through implanted osmotic minipumps. Plasma concentration and urinary excretion of NE were measured before the rats were killed. Hemodynamic variables were measured and morphometric analysis was done on the diastole-arrested hearts to quantify left ventricular remodeling and interstitial collagen density. Metoprolol treatment tended to normalize LV end-diastolic pressure (LVEDP). CHF-1024 at either dose, and metoprolol, significantly reduced collagen deposition in LV of infarcted animals (from 8.8 +/- 0.5% LV area in vehicle-treated rats to 6.6 +/- 0.2% or 6.4 +/- 0.2% after the low or high dose of CHF-1024, respectively; p < 0.05). Similarly, CHF-1024 at either dose reduced the plasma concentration of NE (from 224 +/- 53 pg/ml to 60 +/- 7 pg/ml or 87 +/- 13 pg/ml; p < 0.05) and urinary excretion of NE in rats with MI, whereas beta-blockade did not affect these variables. In conclusion, CHF-1024 infused for 1 month to rats with LV dysfunction reduced heart rate, NE spillover, and collagen deposition, without unwanted effects, only appearing at the higher dose. Effective beta-blockade with metoprotol reduced LVEDP with no effects on heart function. Neither DA2/alpha2 stimulation nor beta-blockade altered LV remodeling after coronary artery ligation.

Effects of a DA2/alpha2 agonist and a beta1-blocker in combination with an ACE inhibitor on adrenergic activity and left ventricular remodeling in an experimental model of left ventricular dysfunction after coronary artery occlusion.

Renin-angiotensin-aldosterone and sympathetic nervous systems overactivity play a major role in worsening the extent of heart failure. Attenuation of neurohumoral activation with angiotensin-converting enzyme (ACE) inhibitors and beta-blockers has proven beneficial in congestive heart failure. Because ACE inhibition is a recommended treatment for heart failure, this study was designed to test the effects on neurohumoral activation, hemodynamics, and left ventricular (LV) volume of the combination of an ACE inhibitor (delapril) with a DA2-dopaminergic receptor/alpha2-adrenoceptor agonist (CHF-1024) or a beta1-adrenoceptor antagonist (metoprolol) after a moderate to large myocardial infarction (MI) in rats. MI was induced by left coronary artery ligation in 134 rats, and six were not operated on. After 2 months, the animals with ECG evidence of MI were treated for 1 more month with CHF- 1024, 0.33 mg/kg/day or with metoprolol (10 mg/kg/day), delivered through implanted osmotic minipumps, in addition to delapril (6 mg/kg/day) in the drinking water. Daily urinary excretion of norepinephrine (NE) and circulating concentration were measured. Hemodynamic variables were measured, and three-dimensional morphometric analysis was done on the diastole-arrested hearts to quantify infarct size and LV geometry. In conscious animals, delapril alone or with CHF-1024 or metropolol did not modify heart rate or systolic blood pressure. Both combination treatments, however, significantly reduced heart rate in anesthetized animals compared with the group receiving vehicle. Infarct size was not different between treatments, averaging 20-22% of LV volume. The threefold increase of LV chamber volume in infarcted rats was significantly attenuated by delapril alone or with CHF-1024 or metoprolol (-37 to -44%, p<0.05). Treatment with a combination of the ACEi and CHF-1024 tended to normalize the shape of the LV cavity. Urinary NE excretion was unaffected by delapril alone but was reduced by the addition of CHF-1024 or metoprolol. In conclusion, 1 month of treatment with doses of delapril having no hemodynamic effect, reduced LV volume in a model of chronic heart failure. When CHF-1024 or metoprolol was given with delapril, sympathetic activation decreased with no unwanted effects, such as excessive hypotension.

CHF-1024, a DA2/alpha2 agonist, blunts norepinephrine excretion and cardiac fibrosis in pressure overload.

We compared the effects of an ACE inhibitor, captopril, with those of a DA2-dopaminergic/alpha2-adrenergic receptor agonist (CHF-1024) on neuroendocrine activation and cardiac fibrosis in a model of pressure-overload hypertrophy. Interrenal aortic stenosis was performed in 89 rats, treated with CHF-1024 (0.33, 2 or 6 mg kg(-1) day(-1)), or captopril (1 g/L). Hemodynamic variables were recorded. Cardiac and renal weights, plasma aldosterone, renin activity and urinary catecholamine excretion were measured, as well as cardiac collagen. Blood pressure was lower in stenotic animals treated with CHF-1024 compared to vehicle (161 +/- 10 vs 219 +/- 10 mmHg, p < 0.01), but LV weight was similar. CHF-1024 elicited a marked dose-dependent attenuation of urinary norepinephrine excretion (1.80 +/- 0.18 in controls compared to 0.40 +/- 0.14 microg/24 h at the highest dose, p < 0.01) and of LV perivascular fibrosis. Captopril provoked a marked hypotension, reduced cardiac and body weights, plasma aldosterone concentration, dopamine excretion and perivascular collagen. The DA2/alpha2 agonist CHF-1024 effectively blunts adrenergic drive and cardiac fibrosis in a rat model of pressure overload.

Aspirin does not interact with ACE inhibitors when both are given early after acute myocardial infarction: results of the GISSI-3 Trial.

Aspirin (ASA) and angiotensin-converting enzyme inhibitor (ACEi) therapy reduce mortality when administered early after the onset of myocardial infarction. ASA can antagonize some effects of ACEi therapy by inhibiting the synthesis of vasodilating prostaglandins; however, the evidence for this effect from large controlled trials is contradictory. The authors analyzed a database of 18,895 patients of the Gruppo Italiano per lo Studio della Sopravvivenza nell'Infarto Miocardio-3 (GISSI-3) Trial in which patients were allocated either to receive lisinopril or not to receive lisinopril within 24 hours of the onset of symptoms of myocardial infarction. The aim of the study was to verify the possible negative interaction between ASA and the ACEi lisinopril in the postacute phase of acute myocardial infarction. Of 18,895 analyzable patients, 15,841 received ASA at entry. Overall lisinopril reduced 42-day mortality from 7.1% to 6.3%. In patients receiving ASA, mortality was reduced by lisinopril from 6.0% to 5.4%, and from 13.0% to 10.8% in patients not receiving ASA. The difference in proportional reductions of mortality corresponds to the fact that a more marked lisinopril effect is seen in patients at higher baseline risk across all study subgroups, one of which coincides with the no-ASA group. The analysis of the inhospital incidence of major clinical events did not reveal a potentially negative interaction between ASA and lisinopril. The same findings were obtained from the analysis of reinfarction at 42 days. The interaction between ASA and lisinopril was also tested by multivariate analysis adjusted for confounding variables at entry, and the interaction tests were not statistically significant. Serum creatinine levels at 42 days were significantly higher in lisinopril group than in the control group. Systolic and diastolic blood pressures in lisinopril group were significantly lower than controls at 42 days. The effect of lisinopril on creatinine and blood pressure did not differ between the ASA and no-ASA groups. ASA does not decrease the mortality benefit of early lisinopril after myocardial infarction, nor does it increase the risk of major adverse events. Lisinopril is safe and effective when given early after the onset of myocardial infarction, regardless of a concomitant administration of ASA started early and continued over a 6-week period.