The fate of nitrogen in agroecosystems: An illustration using Canadian estimates

Agroecosystems rely on inputs of nitrogen (N) to sustain productivity. But added N can leak into adjacent environments, affecting the health of other ecosystems and their inhabitants. Worries about global warming have cast further attention on the N cycle in farmlands because farms are a main source of N₂O, and because carbon sequestration, proposed to help reduce CO₂ loads, requires a build-up of N. Our objective was to estimate, as an illustrative example, the net N balance of Canadian agroecosystems in 1996 and then infer some hypotheses about the routes of N loss, their magnitude, and ways of reducing them. We defined agroecosystems as all agricultural lands in Canada including soil to 1 m depth and all biota, except humans. Only net flows of N across those boundaries were counted in our balance – all others represent internal cycling. Based on our estimates, about 2.35 Tg N entered Canadian agroecosystems from biological fixation, fertilizers, and atmospheric deposition (excluding re-deposited NH₃). In the same year, about 1.03 Tg N were exported in crop products and 0.19 Tg were exported in animals and animal products. Consequently, N inputs exceed exports in products by about 1.13 Tg, a surplus that is either accumulating in agroecosystems or lost to the environment. Because potential soil organic matter gains can account for only a small part of the surplus N, most is probably lost to air or groundwater. Our finding, that N losses amount to almost half of N added, concurs with field experiments that show crop recovery of added N in a given year is often not more than 60%. Better management may reduce the fraction lost somewhat but, because N in ecosystems eventually cycles back to N₂, substantive gains in efficiency may not come easily. As well as trying to reduce losses, research might also focus on steering losses directly to N₂, away from more harmful intermediates. If some of the `missing N' can be assimilated into organic matter, agricultural soils in Canada may need little added N to achieve C sequestration targets.     

Controlling nickel silicide phase formation by Si implantation damage

In the context of fabrication process of contacts in CMOS integrated circuits, we studied the effect of implantation-induced damage on the Ni silicide phase formation sequence. The device layers of Silicon-on-insulator samples were implanted with 30 or 60 keV Si ions at several fluences up to amorphization. Next, 10 or 30 nm Ni layers were deposited. The monitoring of annealing treatments was achieved with time-resolved X-ray diffraction (XRD) technique. Rutherford Backscattering Spectrometry and pole figure XRD were also used to characterize some intermediate phase formations. We show the existence of an implantation threshold (1 ions/nm²) from where the silicidation behaviour changes significantly, the formation temperature of the disilicide namely shifting abruptly from 800 to 450 °C. It is also found that the monosilicide formation onset temperature for the thinner Ni deposits increases linearly by about 30 °C with the amount of damage.     

Predicting compliance of children with and without developmental delay.

Noncompliance is a common problem exhibited by children with developmental delay (DD; Walker, 1993). The authors evaluated whether performance on the Assessment of Basic Learning Abilities (ABLA) test would predict compliance of children with and without DD to instructions alone (IA) versus instructions with modelling and/or gestures (IMG) administered by their caregivers. The ABLA test uses standard prompting and reinforcement procedures to assess the ease or difficulty with which a testee is able to learn a simple imitation and five two-choice discriminations. Twenty-one children without DD and 16 children with DD were presented with five age-appropriate educational tasks by their respective caregivers in a structured teaching session that included IA on some trials and IMG on others. The ABLA test performance reliably predicted the compliance of the children in the two conditions, and the results were consistent across both groups. The results are important for providing information to caregivers on how best to instruct their children in an effort to increase compliance. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Apoferritin Modified Magnetic Particles as Doxorubicin Carriers for Anticancer Drug Delivery

Magnetic particle mediated transport in combination with nanomaterial based drug carrier has a great potential for targeted cancer therapy. In this study, doxorubicin encapsulation into the apoferritin and its conjugation with magnetic particles was investigated by capillary electrophoresis with laser-induced fluorescence detection (CE-LIF). The quantification of encapsulated doxorubicin was performed by fluorescence spectroscopy and compared to CE-LIF. Moreover, the significant enhancement of the doxorubicin signal was observed by addition of methanol into the sample solution.     

A Novel Insight into the Cardiotoxicity of Antineoplastic Drug Doxorubicin

Doxorubicin is a commonly used antineoplastic agent in the treatment of many types of cancer. Little is known about the interactions of doxorubicin with cardiac biomolecules. Serious cardiotoxicity including dilated cardiomyopathy often resulting in a fatal congestive heart failure may occur as a consequence of chemotherapy with doxorubicin. The purpose of this study was to determine the effect of exposure to doxorubicin on the changes in major amino acids in tissue of cardiac muscle (proline, taurine, glutamic acid, arginine, aspartic acid, leucine, glycine, valine, alanine, isoleucine, threonine, lysine and serine). An in vitro interaction study was performed as a comparison of amino acid profiles in heart tissue before and after application of doxorubicin. We found that doxorubicin directly influences myocardial amino acid representation even at low concentrations. In addition, we performed an interaction study that resulted in the determination of breaking points for each of analyzed amino acids. Lysine, arginine, β-alanine, valine and serine were determined as the most sensitive amino acids. Additionally we compared amino acid profiles of myocardium before and after exposure to doxorubicin. The amount of amino acids after interaction with doxorubicin was significantly reduced (p = 0.05). This fact points at an ability of doxorubicin to induce changes in quantitative composition of amino acids in myocardium. Moreover, this confirms that the interactions between doxorubicin and amino acids may act as another factor most likely responsible for adverse effects of doxorubicin on myocardium.     

Follow-up outcome in short-term group therapy for complicated grief.

This study investigated 4 types of outcome over a 6-month follow-up period for 84 psychiatric outpatients who had been treated for complicated grief using short-term group therapy. The 4 types differed in regard to whether and when patients achieved clinically significant change on a primary grief outcome variable. Approximately half of the patients achieved clinically significant change by the end of treatment and maintained it over follow-up (maintenance). Another quarter of the patients reported clinically significant change, but only at follow-up (delayed recovery). A few patients achieved clinically significant change at the end of treatment, but not at follow-up (relapse). Finally, nearly a quarter of the patients failed to achieve clinically significant change (nonrecovery). The findings suggest that investigators look beyond the end of treatment when assessing improvement in patients treated with short-term group therapy for complicated grief. Inclusion of delayed recovery patients can substantially modify conclusions about the usefulness of short-term therapies for complicated grief. Delayed recovery patients differed from the other types of patients on greater perceived social support and greater change during the follow-up period. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

Attenuation coefficient and propagation speed estimates of rat and pig intercostal tissue as a function of temperature

Attenuation coefficient and propagation speed of intercostal tissues were estimated as functions of temperature (22, 30, and 37 degrees C) from fresh chest walls from eight 10- to 11-week-old female Sprague-Dawley (SD) rats, eight 21- to 24-week-old female Long-Evans (LE) rats, and ten 6- to 10-week-old mixed sex Yorkshire (York) pigs. The primary purpose of the study was to estimate the temperature dependence of the intercostal tissue's attenuation coefficient so that accurate estimates of the in situ (at the pleural surface) acoustic pressure levels could be made for our ultrasound-induced lung hemorrhage studies. The attenuation coefficient of intercostal tissue for both species was independent of the temperature at the discrete frequencies of 3.1 MHz (-0.0076, 0.0065, and 0.016 dB/cm/degrees C for SD rats, LE rats, and York pigs, respectively) and 6.2 MHz (-0.015, 0.014, and 0.014 dB/cm/degrees C for SD rats, LE rats, and York pigs, respectively). However, the temperature-dependent regressions yielded a significant temperature dependency of the intercostal tissue attenuation coefficients in SD and LE rats (over the 3.1 to 9.6 MHz frequency range); there was no temperature dependency in York pigs (over the 3.1 to 8.6 MHz frequency range). There was no significant temperature dependency of the intercostal tissue propagation speed in SD rats; there was a temperature dependency in LE rats and York pigs (-0.59, -1.6, and -2.9 m/s/degrees C for SD rats, LE rats, and York pigs, respectively). Even though the attenuation coefficient's temperature dependency was significant from the linear regression functions, the differences were not very great (-0.040 to -0.13, 0.011 to 0.18, and 0.055 to 0.10 dB/cm/degrees C for SD rats, LE rats, and York pigs, respectively, over the data frequency range). These findings suggest that it is not necessary to determine the attenuation coefficient of intercostal tissue at body temperature (37 degrees C), but rather it is sufficient to determine the attenuation coefficient at room temperature (22 degrees C), a much easier experimental procedure.     

The effects of vitamin E and selenium intake on oxidative stress and plasma lipids in hamsters fed fish oil

The aim of the present work was to test the effects of large-dose supplementation of vitamin E (Vit E) and selenium (Se), either singly or in combination, on fish oil (FO)-induced tissue lipid peroxidation and hyperlipidemia. The supplementation of Se has been shown to lower blood cholesterol and increase tissue concentrations of the antioxidant glutathione (GSH); however, the effects of Se supplementation, either alone or in combination with supplemental Vit E, on FO-induced oxidative stress and hyperlipidemia have not been studied. Male Syrian hamsters received FO-based diets that contained 14.3 wt% fat and 0.46 wt% cholesterol supplemented with Vit E (129 IU d-α-tocopheryl acetate/kg diet) and/or Se (3.4 ppm as sodium selenate) or that contained basal requirements of both nutrients. The cardiac tissue of hamsters fed supplemental Se showed increased concentrations of lipid hydroperoxides (LPO) but decreased oxidized glutathione (GSSG) concentrations. The higher concentrations of LPO in the hearts of Se-supplemented hamsters were not lowered with concurrent Vit E supplementation. In the liver, Se supplementation was associated with higher Se-dependent glutathione peroxidase activity and an increase in the GSH/GSSG ratio, whereas a lower hepatic non-Se-dependent glutathione peroxidase activity was seen with Vit E supplementation. Supplemental intake of Se was associated with lower plasma concentrations of total cholesterol and low density lipoprotein cholesterol plus very low density lipoprotein cholesterol. In view of the pro-oxidative effects of Se supplementation on cardiac tissue, a cautionary approach needs to be taken regarding the plasma lipid-lowering properties of supplemental Se.     

The envelope glycoprotein ectodomains determine the efficiency of CD4+ T lymphocyte depletion in simian-human immunodeficiency virus-infected macaques

CD4+ T lymphocyte depletion in human immunodeficiency virus type 1 (HIV-1)-infected humans underlies the development of acquired immune deficiency syndrome. Using a model in which rhesus macaques were infected with chimeric simian-human immunodeficiency viruses (SHIVs), we show that both the level of viremia and the structure of the HIV-1 envelope glycoprotein ectodomains individually contributed to the efficiency with which CD4(+) T lymphocytes were depleted. The envelope glycoproteins of recombinant SHIVs that efficiently caused loss of CD4(+) T lymphocytes exhibited increased chemokine receptor binding and membrane-fusing capacity compared with those of less pathogenic viruses. These studies identify the HIV-1 envelope glycoprotein ectodomains as determinants of CD4(+) T lymphocyte loss in vivo and provide a foundation for studying pathogenic mechanisms.