An intertemporal pricing model for CO2 allowances: The impact of the clean development mechanism

A Work Project, presented as part of the requirements for the Award of a Masters Degree in Finance from the NOVA – School of Business and Economics

Determinants of Portuguese bank’s provisioning policies: Discretionary behaviour of generic and specific allowances

In this paper we test for the impact of the regulatory environment on a bank’s discretionary provisioning practices. We develop a model that structures the dynamics of the provision policy for the two classes of provisions: generic provisions and specific provisions. The model is tested using a comprehensive database of all financial institutions operating in Portugal for 1990-2000. This unique dataset comprises banks subject to the Portuguese rules as well as bank subsidiaries subject to their home-country regulation and we were able to identify distinct behaviours between them. Our results show the importance of handling he two types of provisions separately. They support the hypothesis that banks have a discretionary behaviour in setting up their provisions, and find evidence of income smoothing and capital management. We also find that the regulatory regime impacts on discretionary provisioning policies because banks when forced to increase one type of provision react by reducing the iscretionary component of the other, a finding we designated as a substitution effect.

The Growth of Brown Adipose Tissue in Cold-acclimatized Rats after Depletion of Mast Cell Histamine by Compound 48/80

Cold acclimatization (4-5°C) is accompanied by 2-3 fold increase of brown adipose tissue (BAT). This rapid growth of interscapular BAT was studied after histamine depletion. In control rats maintained at room temperature (28 ± 2°C) the BAT histamine content was 23.4 ± 5.9 (mean ± SD) µg/g of tissue and cold acclimatization (5±1°C) produced a significant increase of BAT weight, but reduced the histamine content to 8.4 ± 1.9 µg/g. The total weight of BAT after 20 days of acclimatization was unaffected by depletion of histamine due to compound 48/80. The low level of histamine in BAT of cold acclimatized rats could be due to a fast rate of amine utilization; alternatively an altered synthesis or storage process may occur during acclimatization.

Effect of Sodium Loading/Depletion on Renal Oxygenation in Young Normo-and Hypertensive Men Measured with BOLD-MRI

Objective: To measure renal tissue oxygenation in young normo-and hypertensive volunteers under conditions of salt loading and depletion using blood oxygen level dependent magnetic resonance imaging (BOLD-MRI). Design and Methods: Ten normotensive (NT) male volunteers (age 26.5_7.4 y) and eight non-treated, hypertensive (HT) male volunteers (age 28.8_5.7 y) were studied after one week on a high salt (HS) regimen (6g of salt/day added to their normal regimen) and again after one week of a low sodium diet (LS). On the 8th day, BOLD-MRI was performed under standard hydration conditions. Four coronal slices were selected in each kidney, and combination sequence was used to acquire T2* weighted images. The mean R2* (1/T2*) was measured to determine cortical and medullar oxygenation. Results: Baseline characteristics and their changes are shown in the table. The mean cortical R2* was not different under conditions of HS or LS (17.8_1.3 vs. 18.2_0.6 respectively in NT group, p_0.27; 17.4_0.6 vs 17.8_0.9 in HT group, p_0.16). However, the mean medullary R2* was significantly lower under LS conditions in both groups (31.3_0.6 vs 28.1_0.8 in NT group, p_0.05; 30.3_0.8 vs 27.9_1.5 in HT group, p_0.05), corresponding to higher medullary oxygenation as compared to HS conditions, without significant changes in hemoglobin or hematocrit values. The salt induced changes in medullary oxygenation were comparable in the two groups (ANOVA, p_0.1). Conclusion: Dietary sodium restriction leads to increased renal medullary oxygenation compared to high sodium intake in normo-and hypertensive subjects. This observation may in part explain the potential renal benefits of a low sodium intake.

Role of glutathione in macrophage activation: effect of cellular glutathione depletion on nitrite production and leishmanicidal activity.

We have examined the effects of two agents depleting the intracellular pool of glutathione (GSH) on macrophage activation induced by IFN-gamma + LPS, as measured by nitrite production and leishmanicidal activity. Diethylmaleate (DEM), which depletes intracellular GSH by conjugation via a reaction catalyzed by the GSH-S-transferase, strongly inhibited nitrite secretion and leishmanicidal activity when added before or at the time of addition of IFN-gamma + LPS; this inhibition was progressively lost when addition of DEM was delayed up to 10 hr. A close correlation was observed between levels of intracellular soluble GSH during activation and nitrite secretion. Inhibition was partially reversed by the addition of glutathione ethyl ester (GSH-Et). Buthionine sulfoximine (BSO), a specific inhibitor of gamma-glutamylcysteine synthetase, also inhibited macrophage activation, although to a lesser extent than DEM despite a more pronounced soluble GSH depletion. This inhibition was completely reversed by the addition of GSH-Et. DEM and BSO did not alter cell viability or PMA-triggered O2- production by activated macrophages, suggesting that the inhibitory effects observed on nitrite secretion and leishmanicidal activity were not related to a general impairment of macrophage function. DEM and BSO treatment reduced iNOS specific activity and iNOS protein in cytosolic extracts. DEM also decreased iNOS mRNA expression while BSO had no effect. Although commonly used as a GSH-depleting agent, DEM may have additional effects because it can also act as a sulhydryl reagent; BSO, on the other hand, which depletes GSH by enzymatic inhibition, has no effect on protein-bound GSH. Our results suggest that both soluble and protein-bound GSH may be important for the induction of NO synthase in IFN-gamma + LPS-activated macrophages.

Lack of Correlation between Seminal and Plasma HIV-1 Viral Loads is Associated with CD4T Cell Depletion in Therapy-naïve HIV-1+ Patients

The present study was conducted to investigate a possible correlation between plasma (PVL) and seminal viral load (SVL) on treatment-naïve HIV-1-infected patients in Vitória, ES, Brazil. We also evaluated whether the progressive immunosuppression associated with HIV disease (as evidenced by declining CD4 T cell counts) has any impact on the correlation between PVL and SVL HIV-1. Viral load on paired blood and semen samples from 56 consecutive treatment-naïve patients were evaluated and compared to CD4 cell counts. Viral load and T cell counts (cells/µl) were determined by NASBA and by flow cytometry, respectively. Overall, a strong positive correlation between PVL and SVL (rho = 0.438, p = 0.001) was observed. However, when patients were grouped according to their CD4 counts, this correlation was only significant among patients with CD4 counts > 200 cells/µl. Results presented here demonstrate the existence of a strong correlation between PVL and SVL on patients with CD4 cell counts > 200 cells/µl, suggesting that this association may correlate with disease progression.

Plasmodium berghei ANKA infection induces thymocyte apoptosis and thymocyte depletion in CBA mice

Immune responses to malaria infections are characterized by strong T and B cell activation, which, in addition of potentially causing immunopathology, are of poor efficacy against the infection. It is possible that the thymus is involved in the origin of immunopathological reactions and a target during malaria infections. This work was developed in an attempt to further clarify these points. We studied the sequential changes in the thymus of CBA mice infected with Plasmodium berghei ANKA, a model in which 60-90% of the infected animals develop cerebral malaria. During the acute phase of infection, different degrees of thymocyte apoptosis were recorded: (1) starry-sky pattern of diffuse apoptosis with maintenance of cortical-medullary structure; (2) intense apoptosis with cortical atrophy, with absence of large cells; (3) severe cortical thymocyte depletion, resulting in cortical-medullary inversion. In the latter, only residual clusters of small thymocytes were observed within the framework of epithelial cells. The intensity of thymus alterations could not be associated with the degree of parasitemia, the expression of clinical signs of cerebral malaria or intensity of brain lesions. The implications of these events for malaria immunity and pathology are discussed.

Effect of sodium loading/depletion on renal oxygenation in young normotensive and hypertensive men

Rapport de synthèse:Le but de cette étude était d'investiguer pour la première fois chez l'homme l'effet du sodium alimentaire et de l'hypertension artérielle sur l'oxygénation tissulaire par une technique spéciale d'imagerie à résonance magnétique nommée 'BOLD-IRM' (Blood Oxygen Level Dependent-IRM). Le BOLD-IRM est une technique nouvelle qui permet de mesurer la bio disponibilité tissulaire d'oxygène de façon non-invasive chez l'homme, en utilisant le déoxyhémoglobine comme produit de contraste endogène.Le rational de cette étude était double. Premièrement, des changements dans l'apport sodique alimentaire devraient théoriquement influencer l'oxygénation tissulaire rénale, étant donné que la réabsorption tubulaire du sodium est un transport actif nécessitant de l'énergie et de l'oxygène. Deuxièmement, des études chez l'animal suggèrent une rôle possible de l'hypoxie tissulaire dans le développement de la néphropathie hypertensive.Nous avons déterminé l'oxygénation rénale avec le BOLD-IRM chez dix hommes normo tendus (âgés de 26.5±7.4 ans) et huit hommes hypertendus non-traités (âgés de 28.8±5.7 ans) une semaine après un régime riche en sel (>200 mmol/jour), et de nouveau une semaine après un régime pauvre en sel (<100 mmol/jour). En parallèle, nous avons mesuré la clearance de l'inuline, du p- aminohippurate (PAH) et du lithium endogène, afin de déterminer respectivement la filtration glomérulaire, le flux sanguin rénal et le 'renal sodium handling', tous des paramètres ayant la capacité d'influencer la consommation et/ou la disponibilité d'oxygène tissulaire. Nous nous attendions d'une côté à une oxygénation rénale diminuée chez les sujets hypertendus par rapport aux sujets normo tendus, et d'une autre côté à une augmentation de l'oxygénation tissulaire rénale après une semaine de régime pauvre en sel par rapport à la phase d'un régime riche en sel.Nous retenons comme résultat principal une augmentation de l'oxygénation rénale médullaire suite à une restriction sodique par rapport à un régime riche en sel chez tous les participants (normo-et hypertendus). Chez les participants normotendus ces changements correlaient avec des changements dans le transport actif du sodium, et ceci indépendamment du flux sanguin rénal. Contrairement à ce qu'on attendait, l'oxygénation rénale médullaire était plus élevé chez les sujets hypertendus par rapport aux sujets normotendus.En résumé, ces observations offrent possiblement une explication pour les bénéfices rénaux liés à un régime pauvre en sel. En plus, la combinaison d'études de clearance et le BOLD- IRM comme utilisé dans cette étude se sont révélés un outil performant et prometteur qui peut stimuler la recherche dans ce domaine.

Analysis of teichoic acid biosynthesis regulation reveals that the extracytoplasmic function sigma factor sigmaM is induced by phosphate depletion in Bacillus subtilis W23.

The expression of the Bacillus subtilis W23 tar genes specifying the biosynthesis of the major wall teichoic acid, the poly(ribitol phosphate), was studied under phosphate limitation using lacZ reporter fusions. Three different regulation patterns can be deduced from these beta-galactosidase activity data: (i) tarD and tarL gene expression is downregulated under phosphate starvation; (ii) tarA and, to a minor extent, tarB expression after an initial decrease unexpectedly increases; and (iii) tarO is not influenced by phosphate concentration. To dissect the tarA regulatory pattern, its two promoters were analysed under phosphate limitation: The P(tarA)-ext promoter is repressed under phosphate starvation by the PhoPR two-component system, whereas, under the same conditions, the P(tarA)-int promoter is upregulated by the action of an extracytoplasmic function (ECF) sigma factor, sigma(M). In contrast to strain 168, sigma(M) is activated in strain W23 in phosphate-depleted conditions, a phenomenon indirectly dependent on PhoPR, the two-component regulatory system responsible for the adaptation to phosphate starvation. These results provide further evidence for the role of sigma(M) in cell-wall stress response, and suggest that impairment of cell-wall structure is the signal activating this ECF sigma factor.

Depletion of CD25+ cells during acute toxoplasmosis does not significantly increase mortality in Swiss OF1 mice

The interleukin (IL)-2R alpha chain (CD25) is expressed on regulatory T cells (Treg), which constitute more than 85% of the CD25+ T cell population in a naïve mouse. CD25 is also expressed on effector T cells in mice suffering from an acute infection by the obligate intracellular protozoan parasite, Toxoplasma gondii. Lethal toxoplasmosis is accompanied by a significant loss of Treg in mice naturally susceptible to toxoplasmosis. The present study was done to explore the role of Treg cells using an anti-CD25 antibody-mediated depletion in mice naturally resistant to toxoplasmosis. Although a significant decrease in the percentage of Treg cells was observed following anti-CD25 monoclonal antibody injections, the depletion of CD25+ cells during acute toxoplasmosis did not significantly increase the mortality of Swiss OF1 mice and no significant difference was observed in the brain parasitic load between the mice in the depleted-infected and isotype-infected groups. We found no significant difference between the titres of total IgG in the sera of the mice from the two groups in the chronic phase. However, CD25+ cells depletion was followed by significantly higher levels of IL-12 in the serum of depleted mice than in that of mice injected with the isotype control antibody.