Controlled Synthesis of Layered Sn3O4 Nanobelts by Carbothermal Reduction Method and Their Gas Sensor Properties

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

EVALUATION OF EUCALYPTUS KRAFT PULP LIGNIN THROUGH THE NITROBENZENE OXIDATION, COPPER OXIDE REDUCTION AND ACIDOLYSIS TECHNIQUES

This study aimed to evaluate the sensitiveness of the information obtained for the residual lignin from Eucalyptus grandis kraft pulps analyzed through the nitrobenzene oxidation, copper oxide (CuO) reduction and acidolysis techniques. The chips were cooked, resulting pulps of kappa number 14,5 and 16,9, respectively. Both lignins' pulps were evaluated through three methods (nitrobenzene oxidation, copper oxide oxidation and acidolysis). Then, they were subjected to an oxygen delignification stage. The 16,9 kappa number pulp resulted in higher levels of non-condensed lignin structures by the acidolysis method, higher syringyl/vanillin ratios (S/V) by the nitrobenzene and copper oxide methods and better performance in the oxygen delignification stage. The different methods allowed to differ the residual lignin pulps with kappa number 14,5 and 16,9, and the nitrobenzene oxidation method showed the highest sensitiveness in this study results.

Analysis of the effect of wash water reduction on bleached pulp characteristics

Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)

Effectiveness of hyperbaric oxygen for experimental treatment of schistosomiasis mansoni using praziquantel-free and encapsulated into liposomes: Assay in adult worms and oviposition

The treatment of schistosomiasis depends on a single drug: praziquantel (PZQ). However, this treatment presents limitations such as low and/or erratic bioavailability that can contribute to cases of tolerance. Improvements to the available drug are urgently needed and studies with a controlled system of drug release, like liposomes, have been gaining prominence. The present study evaluated the activity and synergy between liposomal-praziquantel (lip.PZQ) and hyperbaric oxygen therapy (HBO). Mice received doses of 60 or 100mg/kg PZQ or lip.PZQ, 50 days post-infection, and after the treatment, were exposed to HBO (3 atmosphere absolute - ATA) for 1h. The viability of adult worms and oviposition were analyzed, by necropsy and Kato-Katz examination performed after 15 days of treatment. A concentration of 100mg/kg of lip.PZQ+HBO was more effective (48.0% reduction of worms, 83.3% reduction of eggs/gram of feces) and 100% of the mice had altered of oograms (indicating interruption of oviposition) compared to other treatments and to the Control group (infected and untreated). It is known that PZQ requires participation of the host immune system to complete its antischistosomal activity and that HBO is able to stimulate the immune system. The drug became more available in the body when incorporated into liposomes and, used with HBO, the HBO worked as an adjuvant. This explains the decreases of oviposition and worms recovered form hepatic portal system.

Biogeochemistry of a deep-sea whale fall: sulfate reduction, sulfide efflux and methanogenesis

Deep-sea whale falls create sulfidic habits Supporting chemoautotrophic communities, but microbial processes underlying the formation Of Such habitats remain poorly evaluated. Microbial degradation processes (sulfate reduction, methanogenesis) and biogeochemical gradients were studied in a whale-fall habitat created by a 30 t whale carcass deployed at 1675 m depth for 6 to 7 yr on the California margin. A variety of measurements were conducted including photomosaicking, microsensor measurements, radio-tracer incubations and geochemical analyses. Sediments were Studied at different distances (0 to 9 in) from the whale fall. Highest microbial activities and steepest vertical geochemical gradients were found within 0.5 m of the whale fall, revealing ex situ sulfate reduction and in vitro methanogenesis rates of up to 717 and 99 mmol m(-2) d(-1), respectively. In sediments containing whale biomass, methanogenesis was equivalent to 20 to 30%, of sulfate reduction. During in vitro sediment studies, sulfide and methane were produced within days to weeks after addition of whale biomass, indicating that chemosynthesis is promoted at early stages of the whale fall. Total sulfide production from sediments within 0.5 m of the whale fall was 2.1 +/- 3 and 1.5 +/- 2.1 mol d(-1) in Years 6 and 7, respectively, of which similar to 200 mmol d(-1) were available as free sulfide. Sulfate reduction in bones was much lower, accounting for a total availability of similar to 10 mmol sulfide d(-1). Over periods of at least 7 yr, whale falls can create sulfidic conditions similar to other chemosynthetic habitats Such as cold seeps and hydrothermal vents.

Inhibition of Macrophage Oxidative Stress Prevents the Reduction of ABCA-1 Transporter Induced by Advanced Glycated Albumin

We investigated the role of aminoguanidine and benfotiamine on the inhibition of reactive oxygen species (ROS) generation in macrophages induced by advanced glycated albumin (AGE-albumin) and its relationship with cell cholesterol homeostasis, emphasizing the expression of the ATP binding cassette transporter A-1 (ABCA-1). AGE-albumin was made by incubating fatty acid-free albumin with 10 mM glycolaldehyde. ROS production and ABCA-1 protein level were determined by flow cytometry in J774 macrophages treated along time with control (C) or AGE-albumin alone or in the presence of aminoguanidine or benfotiamine. Mitochondrial function was evaluated by oxygraphy. Compared to C-albumin, AGE-albumin increased ROS production in macrophages, which was ascribed to the activities of NADPH oxidase and of the mitochondrial system. Mitochondrial respiratory chain activity was reduced in cells incubated with AGE-albumin. ROS generation along time was associated with the reduction in macrophage ABCA-1 protein level. Aminoguanidine prevented ROS elevation and restored the ABCA-1 content in macrophages; on the other hand, benfotiamine that promoted a lesser reduction in ROS generation was not able to restore ABCA-1 levels. Inhibition of oxidative stress induced by AGE-albumin prevents disturbances in reverse cholesterol transport by curbing the reduction of ABCA-1 elicited by advanced glycation in macrophages and therefore may contribute to the prevention of atherosclerosis in diabetes mellitus.

Maximal exercise and muscle oxygen extraction in acclimatizing lowlanders and high altitude natives

[EN] The tight relation between arterial oxygen content and maximum oxygen uptake (Vv(o2max)within a given person at sea level is diminished with altitude acclimatization. An explanation often suggested for this mismatch is impairment of the muscle O(2) extraction capacity with chronic hypoxia, and is the focus of the present study. We have studied six lowlanders during maximal exercise at sea level (SL) and with acute (AH) exposure to 4,100 m altitude, and again after 2 (W2) and 8 weeks (W8) of altitude sojourn, where also eight high altitude native (Nat) Aymaras were studied. Fractional arterial muscle O(2) extraction at maximal exercise was 90.0+/-1.0% in the Danish lowlanders at sea level, and remained close to this value in all situations. In contrast to this, fractional arterial O(2) extraction was 83.2+/-2.8% in the high altitude natives, and did not change with the induction of normoxia. The capillary oxygen conductance of the lower extremity, a measure of oxygen diffusing capacity, was decreased in the Danish lowlanders after 8 weeks of acclimatization, but was still higher than the value obtained from the high altitude natives. The values were (in ml min(-1) mmHg(-1)) 55.2+/-3.7 (SL), 48.0+/-1.7 (W2), 37.8+/-0.4 (W8) and 27.7+/-1.5 (Nat). However, when correcting oxygen conductance for the observed reduction in maximal leg blood flow with acclimatization the effect diminished. When calculating a hypothetical leg V(o2max)at altitude using either the leg blood flow or the O(2) conductance values obtained at sea level, the former values were almost completely restored to sea level values. This would suggest that the major determinant V(o2max)for not to increase with acclimatization is the observed reduction in maximal leg blood flow and O(2) conductance.

Convective oxygen transport and fatigue

[EN] During exercise, fatigue is defined as a reversible reduction in force- or power-generating capacity and can be elicited by "central" and/or "peripheral" mechanisms. During skeletal muscle contractions, both aspects of fatigue may develop independent of alterations in convective O(2) delivery; however, reductions in O(2) supply exacerbate and increases attenuate the rate of accumulation. In this regard, peripheral fatigue development is mediated via the O(2)-dependent rate of accumulation of metabolic by-products (e.g., inorganic phosphate) and their interference with excitation-contraction coupling within the myocyte. In contrast, the development of O(2)-dependent central fatigue is elicited 1) by interference with the development of central command and/or 2) via inhibitory feedback on central motor drive secondary to the peripheral effects of low convective O(2) transport. Changes in convective O(2) delivery in the healthy human can result from modifications in arterial O(2) content, blood flow, or a combination of both, and they can be induced via heavy exercise even at sea level; these changes are exacerbated during acute and chronic exposure to altitude. This review focuses on the effects of changes in convective O(2) delivery on the development of central and peripheral fatigue.

On the mechanisms that limit oxygen uptake during exercise in acute and chronic hypoxia: role of muscle mass

[EN] Peak aerobic power in humans (VO2,peak) is markedly affected by inspired O2 tension (FIO2). The question to be answered in this study is what factor plays a major role in the limitation of muscle peak VO2 in hypoxia: arterial O2 partial pressure (Pa,O2) or O2 content (Ca,O2)? Thus, cardiac output (dye dilution with Cardio-green), leg blood flow (thermodilution), intra-arterial blood pressure and femoral arterial-to-venous differences in blood gases were determined in nine lowlanders studied during incremental exercise using a large (two-legged cycle ergometer exercise: Bike) and a small (one-legged knee extension exercise: Knee)muscle mass in normoxia, acute hypoxia (AH) (FIO2 = 0.105) and after 9 weeks of residence at 5260 m (CH). Reducing the size of the active muscle mass blunted by 62% the effect of hypoxia on VO2,peak in AH and abolished completely the effect of hypoxia on VO2,peak after altitude acclimatization. Acclimatization improved Bike peak exercise Pa,O2 from 34 +/- 1 in AH to 45 +/- 1 mmHg in CH(P <0.05) and Knee Pa,O2 from 38 +/- 1 to 55 +/- 2 mmHg(P <0.05). Peak cardiac output and leg blood flow were reduced in hypoxia only during Bike. Acute hypoxia resulted in reduction of systemic O2 delivery (46 and 21%) and leg O2 delivery (47 and 26%) during Bike and Knee, respectively, almost matching the corresponding reduction in VO2,peak. Altitude acclimatization restored fully peak systemic and leg O(2) delivery in CH (2.69 +/- 0.27 and 1.28 +/- 0.11 l min(-1), respectively) to sea level values (2.65 +/- 0.15 and 1.16 +/- 0.11 l min(-1), respectively) during Knee, but not during Bike. During Knee in CH, leg oxygen delivery was similar to normoxia and, therefore, also VO2,peak in spite of a Pa,O2 of 55 mmHg. Reducing the size of the active mass improves pulmonary gas exchange during hypoxic exercise, attenuates the Bohr effect on oxygen uploading at the lungs and preserves sea level convective O2 transport to the active muscles. Thus, the altitude-acclimatized human has potentially a similar exercising capacity as at sea level when the exercise model allows for an adequate oxygen delivery (blood flow x Ca,O2), with only a minor role of Pa,O2 per se, when Pa,O2 is more than 55 mmHg.

Determinants of maximal oxygen uptake in severe acute hypoxia

[EN] To unravel the mechanisms by which maximal oxygen uptake (VO2 max) is reduced with severe acute hypoxia in humans, nine Danish lowlanders performed incremental cycle ergometer exercise to exhaustion, while breathing room air (normoxia) or 10.5% O2 in N2 (hypoxia, approximately 5,300 m above sea level). With hypoxia, exercise PaO2 dropped to 31-34 mmHg and arterial O2 content (CaO2) was reduced by 35% (P < 0.001). Forty-one percent of the reduction in CaO2 was explained by the lower inspired O2 pressure (PiO2) in hypoxia, whereas the rest was due to the impairment of the pulmonary gas exchange, as reflected by the higher alveolar-arterial O2 difference in hypoxia (P < 0.05). Hypoxia caused a 47% decrease in VO2 max (a greater fall than accountable by reduced CaO2). Peak cardiac output decreased by 17% (P < 0.01), due to equal reductions in both peak heart rate and stroke VOlume (P < 0.05). Peak leg blood flow was also lower (by 22%, P < 0.01). Consequently, systemic and leg O2 delivery were reduced by 43 and 47%, respectively, with hypoxia (P < 0.001) correlating closely with VO2 max (r = 0.98, P < 0.001). Therefore, three main mechanisms account for the reduction of VO2 max in severe acute hypoxia: 1) reduction of PiO2, 2) impairment of pulmonary gas exchange, and 3) reduction of maximal cardiac output and peak leg blood flow, each explaining about one-third of the loss in VO2 max.

Role of reactive oxygen and nitrogen species in the response of Prunus spp. to bicarbonate

In calcareous soils, which are a large share of agricultural soils worldwide, iron availability is limited. Consequently, the whole plant physiology is affected, because of the key role of iron in redox metabolism, resulting in reduced crop yield and quality. Peach cultivation is economically important in northern Italy, and is easily subjected to iron chlorosis. The management of iron nutrition in peach includes grafting on bicarbonate-tolerant rootstocks; other forms of management may be expensive and environmentally impacting. Four genotypes, used as rootstocks for peach and characterized by different degrees of tolerance to chlorosis, were tested in vitro on optimal and bicarbonate-enriched medium. Their redox status and antioxidant responses were assayed; the production and possible roles of nitric oxide (NO) and related compounds were also studied. The most sensitive genotypes show a stronger reduction of the antioxidant enzymatic activities and an increased oxidative stress. A high production of NO was found to be associated to resistant genotypes, whereas sensitive genotypes reacted to stress by downregulating nitrosoglutathione reductase activity. Therefore, NO is proposed to improve the internal iron availability, or to stimulate iron intake.

Lactate, not glucose, up-regulates mitochondrial oxygen consumption both in sham and lateral fluid percussed rat brains

OBJECTIVE: Failure of energy metabolism after traumatic brain injury may be a major factor limiting outcome. Although glucose is the primary metabolic substrate in the healthy brain, the well documented surge in tissue lactate after traumatic brain injury suggests that lactate may provide an energy need that cannot be met by glucose. We hypothesized, therefore, that administration of lactate or the combination of lactate and supraphysiological oxygen may improve mitochondrial oxidative respiration in the brain after rat fluid percussion injury. We measured oxygen consumption (VO2) to determine what effects glucose, lactate, oxygen, and the combination of lactate and oxygen have on mitochondrial respiration in both injured and uninjured rat brain tissue. METHODS: Anesthetized Sprague-Dawley rats were intubated and ventilated with either 0.21 or 1.0 fraction of inspired oxygen (FIO2). Brain tissue from acute sham animals was subjected in vitro to 1.1 mM, 12 mM and 100 mM concentrations of glucose and L-lactate. In another group, injury (fluid percussion injury of 2.5 +/- 0.02 atmospheres) was induced over the left hemisphere. The VO2 of mug amounts of brain tissues were measured in a microrespirometry system (Cartesian diver). RESULTS: The VO2 was found to be independent of glucose concentrations, but dose-dependent for lactate. Moreover, the lactate dependent VO2s were all significantly higher than those generated by glucose. Injured rats on FIO2 0.21 had brain tissue VO2 rates that were significantly lower than those of shams or preinjury levels. In injured rats treated with FIO2 1.0, the reduction in VO2 levels was prevented. Injured rats that received an intravenous infusion of 100 mM lactate had VO2 rates that were significantly higher than those obtained with FIO2 1.0. Combined treatment further boosted the lactate generated VO2 rates by approximately 15%. CONCLUSION: Glucose sustains mitochondrial respiration at a low level "fixed" rate because, despite increasing its concentration nearly 100-fold, it cannot up-regulate VO2 after fluid percussion injury. Lactate produces a dose-dependent VO2 response, possibly enabling mitochondria to meet the increased energy needs of the injured brain.

Lowered microvascular vessel wall oxygen consumption augments tissue pO2 during PgE1-induced vasodilation

Continuous infusion of intravenous prostaglandin E1 (PgE1, 2.5 mug/kg/min) was used to determine how vasodilation affects oxygen consumption of the microvascular wall and tissue pO(2) in the hamster window chamber model. While systemic measurements (mean arterial pressure and heart rate) and central blood gas measurements were not affected, PgE1 treatment caused arteriolar (64.6 +/- 25.1 microm) and venular diameter (71.9 +/- 29.5 microm) to rise to 1.15 +/- 0.21 and 1.06 +/- 0.19, respectively, relative to baseline. Arteriolar (3.2 x 10(-2) +/- 4.3 x 10(-2) nl/s) and venular flow (7.8 x 10(-3) +/- 1.1 x 10(-2)/s) increased to 1.65 +/- 0.93 and 1.32 +/- 0.72 relative to baseline. Interstitial tissue pO(2) was increased significantly from baseline (21 +/- 8 to 28 +/- 7 mmHg; P < 0.001). The arteriolar vessel wall gradient, a measure of oxygen consumption by the microvascular wall decreased from 20 +/- 6 to 16 +/- 3 mmHg (P < 0.001). The arteriolar vessel wall gradient, a measure of oxygen consumption by the vascular wall, decreased from 20 +/- 6 to 16 +/- 3 mmHg (P < 0.001). This reduction reflects a 20% decrease in oxygen consumption by the vessel wall and up to 50% when cylindrical geometry is considered. The venular vessel wall gradient decreased from 12 +/- 4 to 9 +/- 4 mmHg (P < 0.001). Thus PgE1-mediated vasodilation has a positive microvascular effect: enhancement of tissue perfusion by increasing flow and then augmentation of tissue oxygenation by reducing oxygen consumption by the microvascular wall.

[Bilateral surgical lung volume reduction in severe emphysema]

OBJECTIVE: To report preliminary results with a new surgical method of treating terminal emphysema by bilateral reduction of lung volume. PATIENTS AND METHODS: In a prospective study, the results obtained with the first 20 consecutive patients (mean FEV1: 590 +/- 180 ml) who underwent operative reduction of lung volume were recorded. 19 of the 20 patients had required continuous oxygen supply. RESULTS: The patients were extubated 8.5 +/- 6 h postoperatively; thoracic drainage was removed after 9 +/- 6 days. The degree of dyspnoea was decreased in all patients (3.5 +/- 0.5 vs 0.5 +/- 0.1). Significant reduction of overinflation occurred soon after the operation (residual volume 273 +/- 125 to 201 +/- 107% of normal; total capacity from 142 +/- 18 to 109 +/- 22% of normal), as well as reduction in the degree of obstruction (FEV1 from 18 +/- 6 to 24 +/- 7% of normal; for each, P < 0.05). One patient died 3 weeks post-operatively of Candida infection. CONCLUSION: The method looks promising for the treatment of selected patients and may thus provide an alternative to lung transplantation.

Element contents, sulfur and oxygen isotopes, and molecular biomarkers of phosphatic crust samples from the Chimbote Platform of the shelf off Peru

Authigenic phosphatic laminites enclosed in phosphorite crusts from the shelf off Peru (10°01' S and 10°24' S) consist of carbonate fluorapatite layers, which contain abundant sulfide minerals including pyrite (FeS2) and sphalerite (ZnS). Low d34Spyrite values (average -28.8 per mill) agree with bacterial sulfate reduction and subsequent pyrite formation. Stable sulfur isotopic compositions of sulfate bound in carbonate fluorapatite are lower than that of sulfate from ambient sea water, suggesting bacterial reoxidation of sulfide by sulfide-oxidizing bacteria. The release of phosphorus and subsequent formation of the autochthonous phosphatic laminites are apparently caused by the activity of sulfate-reducing bacteria and associated sulfide-oxidizing bacteria. Following an extraction-phosphorite dissolution-extraction procedure, molecular fossils of sulfate-reducing bacteria (mono-O-alkyl glycerol ethers, di-O-alkyl glycerol ethers, as well as the short-chain branched fatty acids i/ai-C15:0, i/ai-C17:0 and 10MeC16:0) are found to be among the most abundant compounds. The fact that these molecular fossils of sulfate-reducing bacteria are distinctly more abundant after dissolution of the phosphatic laminite reveals that the lipids are tightly bound to the mineral lattice of carbonate fluorapatite. Moreover, compared with the autochthonous laminite, molecular fossils of sulfate-reducing bacteria are: (1) significantly less abundant and (2) not as tightly bound to the mineral lattice in the other, allochthonous facies of the Peruvian crusts consisting of phosphatic coated grains. These observations confirm the importance of sulfate-reducing bacteria in the formation of the phosphatic laminite. Model calculations highlight that organic matter degradation by sulfate-reducing bacteria has the potential to liberate sufficient phosphorus for phosphogenesis.