Application of Polysaccharide Hydrogels in Adsorption and Controlled-Extended Release of Fertilizers Processes

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

Poly(hydroxybutyrate-co-hydroxyvalerate) microspheres loaded with atrazine herbicide: screening of conditions for preparation, physico-chemical characterization, and in vitro release studies

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

Dehydromonocrotaline induces cyclosporine A-insensitive mitochondrial permeability transition/cytochrome c release

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

Widespread Amazon forest tree mortality from a single cross-basin squall line event

Climate change is expected to increase the intensity of extreme precipitation events in Amazonia that in turn might produce more forest blowdowns associated with convective storms. Yet quantitative tree mortality associated with convective storms has never been reported across Amazonia, representing an important additional source of carbon to the atmosphere. Here we demonstrate that a single squall line (aligned cluster of convective storm cells) propagating across Amazonia in January, 2005, caused widespread forest tree mortality and may have contributed to the elevated mortality observed that year. Forest plot data demonstrated that the same year represented the second highest mortality rate over a 15-year annual monitoring interval. Over the Manaus region, disturbed forest patches generated by the squall followed a power-law distribution (scaling exponent alpha = 1.48) and produced a mortality of 0.3-0.5 million trees, equivalent to 30% of the observed annual deforestation reported in 2005 over the same area. Basin-wide, potential tree mortality from this one event was estimated at 542 +/- 121 million trees, equivalent to 23% of the mean annual biomass accumulation estimated for these forests. Our results highlight the vulnerability of Amazon trees to wind-driven mortality associated with convective storms. Storm intensity is expected to increase with a warming climate, which would result in additional tree mortality and carbon release to the atmosphere, with the potential to further warm the climate system. Citation: Negron-Juarez, R. I., J. Q. Chambers, G. Guimaraes, H. Zeng, C. F. M. Raupp, D. M. Marra, G. H. P. M. Ribeiro, S. S. Saatchi, B. W. Nelson, and N. Higuchi (2010), Widespread Amazon forest tree mortality from a single cross-basin squall line event, Geophys. Res. Lett., 37, L16701, doi:10.1029/2010GL043733.

13,14-Dihydro-15-Keto Prostaglandin F-2 alpha Release in Response to Oxytocin Challenge Early Post-Partum in Anoestrous Nelore Cows Submitted to Temporary Calf Removal and Progesterone Priming

The study evaluated, in early post-partum anoestrous Nelore cows, if the increase in plasma oestradiol (E2) concentrations in the pre-ovulatory period and/or progesterone priming (P4 priming) preceding ovulation, induced by hormonal treatment, reduces the endogenous release of prostaglandin PGF(2)alpha and prevents premature lysis of the corpus luteum (CL). Nelore cows were subjected to temporary calf removal for 48 h and divided into two groups: GPE/eCG group (n = 10) and GPG/eCG group (n = 10). Animals of the GPE/eCG group were treated with a GnRH agonist. Seven days later, they received 400 ID of eCG, immediately after PGF(2)alpha treatment, and on day 0, 1.0 mg of oestradiol benzoate (EB). Cows of the GPG/eCG group were similarly treated as those of the GPE/eCG group, except that EB was replaced with a second dose of GnRH. All animals were challenged with oxytocin (OT) 9, 12, 15 and 18 days after EB or GnRH administration and blood samples were collected before and 30 min after OT. Irrespective of the treatments, a decline in P4 concentration on day 18 was observed for cows without P4 priming. However, animals exposed to P4 priming, treated with EB maintained high P4 concentrations (8.8 +/- 1.2 ng/ml), whereas there was a decline in P4 on day 18 (2.1 +/- 1.0 ng/ml) for cows that received GnRH to induce ovulation (p < 0.01). Production of 13,14-dihydro-15-keto prostaglandin F-2 alpha (PGFM) in response to OT increased between days 9 and 18 (p < 0.01), and this increase tended to be more evident in animals not exposed to P4 priming (p < 0.06). In conclusion, the increase in E2 during the pre-ovulatory period was not effective in inhibiting PGFM release, which was lower in P4-primed than in non-primed animals. Treatment with EB promoted the maintenance of elevated P4 concentrations 18 days after ovulation in P4-primed animals, indicating a possible beneficial effect of hormone protocols containing EB in animals with P4 priming.

Convective storm initiation in a moist tropical environment

Radar and satellite data from the Tropical Rainfall Measuring Mission-Large-Scale Biosphere-Atmosphere (TRMM-LBA) project have been examined to determine causes for convective storm initiation in the southwest Amazon region. The locations and times of storm initiation were based on the National Center for Atmospheric Research (NCAR) S-band dual-polarization Doppler radar (S-Pol). Both the radar and the Geostationary Operational Environmental Satellite-8 (GOES-8) visible data were used to identify cold pools produced by convective precipitation. These data along with high-resolution topographic data were used to determine possible convective storm triggering mechanisms. The terrain elevation varied from 100 to 600 m. Tropical forests cover the area with numerous clear-cut areas used for cattle grazing and farming. This paper presents the results from 5 February 1999. A total of 315 storms were initiated within 130 km of the S-Pol radar. This day was classified as a weak monsoon regime where convection developed in response to the diurnal cycle of solar heating. Scattered shallow cumulus during the morning developed into deep convection by early afternoon. Storm initiation began about 1100 LST and peaked around 1500-1600 LST. The causes of storm initiation were classified into four categories. The most common initiation mechanism was caused by forced lifting by a gust front (GF; 36%). Forcing by terrain (>300 m) without any other triggering mechanism accounted for 21% of the initiations and colliding GFs accounted for 16%. For the remaining 27% a triggering mechanism was not identified. Examination of all days during TRMM-LBA showed that this one detailed study day was representative of many days. A conceptual model of storm initiation and evolution is presented. The results of this study should have implications for other locations when synoptic-scale forcing mechanisms are at a minimum. These results should also have implications for very short-period forecasting techniques in any location where terrain, GFs, and colliding boundaries influence storm evolution.

Ionotropic Glutamate Receptors in Hypothalamic Paraventricular and Supraoptic Nuclei Mediate Vasopressin and Oxytocin Release in Unanesthetized Rats

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

Effect of non-steroidal anti-inflammatory drugs (NSAID) on the histamine release induced by compound 48/80 and cardiac anaphylaxis in guinea-pig isolated heart

Histamine release from guinea pig heart treated with compound 48/80 was potentiated by the cyclooxygenase inhibitors indomethacin and piroxicam but not by aspirin or phenylbutazone. This differential effect suggests that the potentiation is not merely due to an inhibition of prostaglandin synthesis. Piroxicam potentiated the histamine release induced by cardiac anaphylaxis whereas indomethacin reduced this effect. The SRS-A antagonist FPL 55712 inhibited histamine release induced by cardiac anaphylaxis, but not that evoked by compound 48/80, and also prevented the potentiation due to indomethacin and piroxicam. In total, these data suggest that the potentiation of histamine release by piroxicam and indomethacin is probably due to a diversion of arachidonic acid metabolism from the cyclooxygenase to the lipoxygenase pathways. The resulting lipoxygenase products may then regulate histamine release, with the secretion due to antigen being more sensitive to such modulation than that evoked by compound 48/80.

Influence of temperature on the release of plasminogen activator.

Fibrinolysis is a basic defense mechanism of the organism designed to control the deposition of fibrin in the vascular system and elsewhere. Fibrinolytic activity was measured by the fibrin plate method for three groups of rats (N = 6) that were maintained at room temperature, 20-25 degrees C, 3 degrees C or 38 degrees C for 4 h before testing. Based on measurement of fibrinolytic activity, the level of plasminogen activator released from isolated aortic segments of rats maintained at room temperature (24-28 degrees C) differed significantly from that of the 38 degrees C group. The animals maintained at 3 degrees C did not release plasminogen activator, suggesting that the fibrinolytic response was impaired at low temperature.

Transient non-Darcy forced convective heat transfer from a flat plate embedded in a fluid-saturated porous medium

Transient non-Darcy forced convection on a flat plate embedded in a porous medium is investigated using the Forchheimer-extended Darcy law. A sudden uniform pressure gradient is applied along the flat plate, and at the same time, its wall temperature is suddenly raised to a high temperature. Both the momentum and energy equations are solved by retaining the unsteady terms. An exact velocity solution is obtained and substituted into the energy equation, which then is solved by means of a quasi-similarity transformation. The temperature field can be divided into the one-dimensional transient (downstream) region and the quasi-steady-state (upstream) region. Thus the transient local heat transfer coefficient can be described by connecting the quasi-steady-state solution and the one-dimensional transient solution. The non-Darcy porous inertia works to decrease the velocity level and the time required for reaching the steady-state velocity level. The porous-medium inertia delays covering of the plate by the steady-state thermal boundary layer. © 1990.

Agents that inhibit histamine release: A review

It is well known that histamine is found in high concentration in mast cell granules(1). The histamine content of these granules may be released to the extracellular space if an appropriate stimulus is provided(2). Besides histamine, other preformed active substances like enzymes, chemotatic factors and proteoglycans, as well as newly generated mediators like eicosanoids, platelet activating factor and adenosine are released during the secretion process of mast cells(3). The activation of mast cell degranulation has been associated with a number of pathologic disorders, most frequently, diseases derived from the atopic state(4). It is now evident that mast cells are the primary effector cells in the early reaction in both allergic and non-allergic asthma(5,6), although some authors doubt that the late reaction of asthma is a mast cell dependent event(6). Other studies point towards basophils as cellular elements involved in the secondary phase of inflammation in allergic diseases(7). Secretion would depend on a histamine releasing factor, and on the presence of IgE on the basophil's surface(8). There is also evidence suggesting involvement of mast cells in some non-allergic inflammatory processes like arthritis(9). The pharmacological management of these diseases basically consists in the use of methylxantines, beta 2-adrenergic agonists, glucocorticoids, sodium cromoglycate-like drugs, anticholinergic and antihistaminic H 1 antagonists(10). Their therapeutic effects include bronchodilatation, receptor and physiological antagonism, prevention of inflammatory responses induced by secondary cells, and finally, inhibition of mast cell activation(11). This review is concerned with compounds having inhibitory action on mast cell activation, and their possible importance on the pathophysiology of mast cell-related diseases.

Histamine release induced by glucose (mannose)-specific lectins isolated from Brazilian beans. Comparison with concanavalin A

The histamine releasing properties of glucose (mannose)-specific lectins isolated from Brazilian beans was examined. The Canavalia brasiliensis, Dioclea rostrata, and Dioclea virgata lectins induced histamine release in rat peritoneal mast cells similar to concanavalin A. Less potency and efficacy was observed for Canavalia maritima, Dioclea guianensis, and Dioclea violacea while very low activities were seen for the lectins from Dioclea grandiflora, Canavalia bonariensis, and Cratylia floribunda. The histamine releasing effect was quenched by higher doses of D. virgata lectin similar to what was reported for concanavalin A. This effect was abrogated by increasing the concentration of calcium in the incubating medium. As these above proteins have sites that bind calcium, higher doses of the lectins might withdraw the calcium which is essential for the mast cell secretion.