High Throughput Selection of Effective Serodiagnostics for Trypanosoma cruzi infection

The diagnosis of Trypanosoma cruzi infection (the cause of human Chagas disease) is difficult because the symptoms of the infection are often absent or non-specific, and because the parasites themselves are usually below the level of detection in the infected subjects. Therefore, diagnosis generally depends on the measurement of T. cruzi–specific antibodies produced in response to the infection. However, current methods to detect anti–T. cruzi antibodies are relatively poor. In this study, we have conducted a broad screen of >400 T. cruzi proteins to identify those proteins which are best able to detect anti–T. cruzi antibodies. Using a set of proteins selected by this screen, we were able to detect 100% of >100 confirmed positive human cases of T. cruzi infection, as well as suspect cases that were negative using existing tests. This protein panel was also able to detect apparent changes in infection status following drug treatment of individuals with chronic T. cruzi infection. The results of this study should allow for significant improvements in the detection of T. cruzi infection and better screening methods to avoid blood transfusion–related transmission of the infection, and offer a crucial tool for determining the success or failure of drug treatment and other intervention strategies to limit the impact of Chagas disease

Measurement of IL-10 serum levels in BALB/c mice treated with beta-1,3 polyglucose or sulfadiazine and acutely infected by Toxoplasma gondii

Acute infection by Toxoplasma gondii leads to suppression of cell-mediated immunity, facilitating chronic infection. One of the causes of immunosuppression is Interleukin-10 (IL-10) production. Glucan is used to stimulate phagocytosis. Our objective was to study IL-10 induction in male BALB/c mice with acute T. gondii BTU-2 strain infection, glucan immunostimulation, and sulfadiazine treatment. Animals were distributed into 7 groups: G1: infected with T. gondii; G2: infected with T. gondii and treated with sulfadiazine; G3: infected with T. gondii and immunostimulated with glucan; G4: infected with T. gondii, immunostimulated with glucan, and treated with sulfadiazine; G5: imunostimulated with glucan; G6: treated with saline; and G7: treated with sulfadiazine. IL-10 levels were determined by ELISA; the highest levels were found in G2, G3 and G4, and the lowest in G1 (p<0.001). Groups G1 to G5 and G7 had substantially higher levels than G6 (p<0.001). In this study, the highest IL-10 levels were found in groups treated with glucan

Pulmonary interstitial emphysema in fatal asthma: case report and histopathological review

Abstract Background Mortality related to asthma has decreased worldwide since the introduction of inhaled corticosteroid therapy in the past decades. However, there are still some asthma fatalities identified mainly in populations with less access to regular treatment. Pulmonary interstitial emphysema due to alveolar rupture has been rarely described as a complication of an acute severe asthma attack, and its identification in pathological analysis can be difficult. Previous studies reported the association of pulmonary interstitial emphysema and bronchial ductal gland ectasia in asthma. Case presentation We present the case of a 42-year- old man that died due to a fatal asthma attack. Postmortem computed tomography revealed the unusual finding of acute Pulmonary Interstitial Emphysema, confirmed by pathological analysis. We reviewed 28 cases of fatal asthma tissue and identified the presence of pulmonary interstitial emphysema in 10% of the cases. Conclusions Postmortem computed tomography is a useful complimentary diagnostic tool for autopsies. Pulmonary Interstitial Emphysema in acute exacerbations of asthma seems to be more frequent than reported. Alveolar hyperdistension and bronchial duct gland ectasia causing tissue rupture are possible mechanisms involved in the formation of Pulmonary Interstitial Emphysema. The clinical impact of Pulmonary Interstitial Emphysema in asthma is unknown

Capillary dynamics are determined by the ambulatory blood pressure profile.

This study aimed to evaluate whether experimental Chagas disease in acute phase under benznidazole therapy can cause DNA damage in peripheral blood, liver, heart, and spleen cells or induce nitric oxide synthesis in spleen cells. Twenty Balb/c mice were distributed into four groups: control (non-infected animals); Trypanosoma cruzi infected; T. cruzi infected and submitted to benznidazole therapy; and only treated with benznidazole. The results obtained with the single cell gel (comet) assay showed that T. cruzi was able induce DNA damage in heart cells of both benznidazole treated or untreated infected mice. Similarly, T. cruzi infected animals showed an increase of DNA lesions in spleen cells. Regarding nitric oxide synthesis, statistically significant differences (p < 0.05) were observed in all experimental groups compared to negative control, the strongest effect observed in the T. cruzi infected group. Taken together, these results indicate that T. cruzi may increase the level of DNA damage in mice heart and spleen cells. Probably, nitric oxide plays an important role in DNA damaging whereas benznidazole was able to minimize induced T. cruzi genotoxic effects in spleen cells. © 2006 Elsevier Inc. All rights reserved

3.55 keV line in minimal decaying dark matter scenarios

We investigate the possibility of reproducing the recently reported 3:55 keV line in some simple decaying dark matter scenarios. In all cases a keV scale decaying DM is coupled with a scalar eld charged under SM gauge interactions and thus capable of pair production at the LHC. We will investigate how the demand of a DM lifetime compatible with the observed signal, combined with the requirement of the correct DM relic density through the freeze-in mechanism, impacts the prospects of observation at the LHC of the decays of the scalar eld.peerReviewe