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R R dos Santos

Publications and source records attributed to R R dos Santos.

10 recordsLinked to original sources
PubMed1997

A support system for content-based medical image retrieval in object oriented databases.

This work describes both the concepts used in an Object Manager for storage of medical images as one more data type associated to objects, and a support system developed to offer this kind of tool to medical application developers. The purpose of this work is to support the retrieval of images through queries based on the graphical contents of the stored images. The usual approach uses icons and textual attributes stored with the images to specify the queries. This work uses a novel modeling technique to define the "image data type," by means of which it is possible to decide, before the query itself, the key data of each image that must be extracted from the image when it is stored in the database, so the search can be accelerated when queries are issued. This approach enables building of expansible systems, where new image processing algorithms can be added easily, using its syntactic representation stored through an Image Meta-schema into the application database schema. This work shows how such a system has been implemented, and also provides a query language used to refer and execute these algorithms from inside the database management system.

Algorithms↗
PubMed1994

Requirement for lymphocytes and resident macrophages in LPS-induced pleural eosinophil accumulation.

In this study we investigated the involvement of inflammatory cells in the pleural accumulation of eosinophils induced by lipopolysaccharide (LPS). Intrathoracic (i.t.) injection of LPS (250 ng/cavity) into rats induced a significant eosinophil accumulation that developed within 24 h, was maximal at 48 h, and returned to control values within 120 h. This eosinophil influx was preceded by a huge neutrophil influx within 4 h and accompanied by a mononuclear cell accumulation between 24 and 48 h. Pretreatment with an antineutrophil monoclonal antibody (RP-3, 2 ml per animal) selectively reduced the number of circulating neutrophils within 8 h but failed to alter the LPS-induced eosinophilia. Similarly, platelet depletion with an anti-rat platelet antiserum did not alter the LPS-induced eosinophil accumulation. Cyclosporine (50 mg/kg, 12 and 2 h before) partially inhibited (51%) the LPS-induced pleural eosinophilia, whereas the eosinophilia was not changed by prior degranulation of pleural mast cells with polymyxin B (10 micrograms/cavity, 24 h before). Moreover, selective depletion of T lymphocytes using an anti-Thy 1.0 monoclonal antibody significantly inhibited the eosinophilia triggered by LPS. The i.t. injection of liposomes containing dichloromethylene diphosphonate significantly reduced (65%) the number of resident macrophages after 5 days. Under this condition, the eosinophil infiltration induced by LPS was completely inhibited. Accordingly, the i.t. injection of supernatant from macrophage monolayers, obtained from the pleural cavities of LPS-injected rats, into naive recipient animals led to a twofold increase in the number of pleural eosinophils. In conclusion, our data suggest an important role for resident macrophages and T lymphocytes in the eosinophil accumulation induced by LPS.

Animals↗
PubMed1992

Anti-CD4 abrogates rejection and reestablishes long-term tolerance to syngeneic newborn hearts grafted in mice chronically infected with Trypanosoma cruzi.

The contribution of autoimmunity in the genesis of chronic Chagas' heart pathology is not clear. In the present study, we show that: (a) BALB/c mice chronically infected with Trypanosoma cruzi reject syngeneic newborn hearts; (b) in vivo treatment with anti-CD4 but not anti-CD8 monoclonal antibodies (mAbs) abrogates rejection; (c) CD4+ T cells from chronically infected mice proliferate in vitro to syngeneic myocardium antigens and induce heart graft destruction when injected in situ; (d) anti-CD4 treatment of chronically infected mice establishes long-term tolerance to syngeneic heart grafts; and (e) the state of tolerance is related to in vitro and in vivo unresponsiveness of the CD4+ T cells. These findings allow us to suggest that autoimmunity is the major mechanism implicated in the rejection of syngeneic heart tissues grafted into the pinna of the ear of mice chronically infected with T. cruzi. The similarity of the lesions to those found in humans suggests that autoimmunity is involved in the pathogenesis of chagasic cardiomyopathy in humans. Moreover, this could imply therapeutic strategies by reestablishing long-term tissue-specific tolerance with anti-CD4 mAb treatment, mediating anergy, or deleting the responder CD4+ T cells to heart tissue antigens.

Animals↗
PubMedDate not supplied

[Reactivation of Trypanosoma cruzi infection in patients with acquired immunodeficiency syndrome].

A patient with AIDS and asymptomatic Chagas's disease and positive xenodiagnosis was taking ketoconazole in order to suppress parasitemia and prevent reactivation of Chagas's disease. Ketoconazole was unplanned suspended after 6 months, and the patient was admitted with fever, headache, vomiting, tachycardia, postural hypotension, hepatosplenomegaly, and positive xenodiagnosis one month later. Treatment with benzonidazole was begun leading to suppression of parasitemia. The patient had probability a neurotoxoplasmosis associated and progressed to coma and death with sepsis. No parasite was found in autopsy.

AIDS-Related Opportunistic Infections↗
PubMedDate not supplied

[Experimental dilatation of the cecum and colon in rats. IV. Evaluation of a model produced by the use of lactose in the food of animals in the chronic phase of infection by the Colombia strain of T. cruzi].

Female Wistar albino rats (30 day of age) were inoculated three times in intervals of 7 days with 1 x 10(7) epimastigote forms of T. cruzi and challenged 30 days after the last inoculation with 1 x 10(5) trypomastigote forms of the Colombia strain of T. cruzi. Rats of the same sex and age were used as controls. One-hundred-fifty days after inoculation the animals were allocated into 4 groups: Group I (control), divided into subgroup L (fed lactose for 4 weeks) and subgroup S (fed saccharose for 4 weeks); Group II (inoculated), divided into subgroup L (fed lactose for 4 weeks) and subgroup S (fed saccharose for 4 weeks); Group III (control), divided into subgroup L-S (fed lactose for 4 weeks and saccharose for the following 4 weeks) and subgroup S (fed saccharose for 8 weeks); and Group IV (inoculated), divided into subgroup L-S (fed lactose for 4 weeks and saccharose for the following 4 weeks) and subgroup S (fed saccharose for 8 weeks). The disaccharide (lactose or saccharose) was added to a standard laboratory diet, 25 g/100 g of the final weight of the diet. At the end of the experimental periods the animals were sacrificed in light ether anesthesia. The volume of the large intestine was measured, and the weights of the cecum and colon were recorded.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗