The Program for the Prevention of Childhood Asthma: a specialized care program for children with wheezing or asthma in Brazil

Objective

: To present the Programa Infantil de Prevenção de Asma (PIPA, Program for the Prevention of Childhood Asthma) and the characteristics of the patients followed in this program.

Methods

: Implemented in the city of Uruguaiana, Brazil, PIPA has as its target population children and adolescents (< 18 years of age) with asthma or suspected asthma. Patients either enroll in PIPA spontaneously or are referred by pediatricians or primary care physicians. In this retrospective study, we use a standardized protocol to assess PIPA patients.

Results

: By the end of the study period, 646 patients were being followed. Of those, 298 (46.1%) were ≤ 3 years of age. In this group of patients, recurrent wheezing was identified in 60.7%, and the first episode of wheezing occurred in the first six months of life in 86.0%. Severe wheezing was identified in 29.5% and 45.4% in the children ≤ 3 and > 3 years of age, respectively. Physician-diagnosed asthma was reported in 26.5% and 82.2%, respectively. In the sample as a whole, the prevalence of passive smoking was high (> 36%), occurring during pregnancy in > 15%; > 40% of the patients had been born by cesarean section; and 30% had a mother who had had < 8 years of schooling.

Conclusions

: A prevention program for children with asthma is an effective strategy for controlling the disease. Knowledge of local epidemiological and environmental characteristics is essential to reducing the prevalence of the severe forms of asthma, to improving the use of health resources, and to preventing pulmonary changes that could lead to COPD in adulthood.     

The role of behavioral impulsivity in the development of alcohol dependence: a 4-year follow-up study

Background:  Although many studies have established a close relation between impulsivity and alcohol use disorders, little is known about the role of behavioral impulsivity in the development of these disorders.
Objectives:  To determine the role of 2 laboratory paradigms of impulsivity in the development of alcohol use disorders.
Methods:  Follow-up study carried out with 471 participants diagnosed as heavy drinkers (HD) and followed-up for 4 years. Initially, they were compared with a healthy control group. Assessment of behavioral impulsivity was carried out with the Continuous Performance Test (CPT), and the Stop-Signal Task (SST) assessed behavioral inhibitory control. Differential reinforcement for low-rate responding (DRLR) was used to evaluate the delay reward dimension. The Structured Clinical Interview (SCID-DSM-IV) was used to diagnose alcohol dependence.
Results:  The HD performed worse than the control group in all the behavioral tests of impulsivity. Performance in DRLR was the only behavioral impulsivity test that classified the HD correctly compared to controls. Logistic regression analysis indicated that performance on SST was a significant predictor [odds = 1.52(CI = 1.08–2.31)] of developing alcohol dependence.
Conclusions:  Our results support the relation between behavioral impulsivity and alcohol use disorders. The paradigm related to delay of reward may be a factor associated with the use of alcohol and the incapacity to control inhibition as dependence develops.     

The interaction between a Na+-channel toxin and brain microtubule proteins in vitro

The aim of this work was to characterize the interaction of the Na+-channel toxin, purified from venom of the scorpion Leiurus quinquestriatus, with microtubule proteins in vitro. The toxin enhanced microtubule assembly, causing the formation of microtubule 'bundles'. It interacted with the Na+-channel 270 kDa subunit and was subsequently found to be unrelated to high molecular weight microtubule-associated protein with respect to apparent molecular weight and toxin binding. However, the radiolabelled toxin bound to tubulin, although with a much lower affinity than that published for the reconstituted Na+-channel. This binding appears to occur in the carboxy terminal 4 kDa region of tubulin. These results may reflect a secondary action of the toxin involved in binding to its receptors in the neural plasma membrane.     

Elimination of mycobacterium leprae subsequent to local in vivo activation of macrophages in lepromatous leprosy by other mycobacteria

This investigation studied the possibility of activating lepromatous macrophages by a local `in vivo' test.     

A carcinoembryonic antigen-directed immunotoxin built by linking a monoclonal antibody to a hemolytic toxin

Hybrid molecules prepared by linking toxins to monoclonal antibodies (MAbs) are cytotoxic to cells bearing the target antigen. The toxin most widely used has been the plant toxin ricin as the toxic component, which inhibits protein synthesis at the ribosome level. Immunotoxins based on membrane-active, hemolytic toxins can be a useful alternative when directed towards antigens which do not mediate internalization, as is the case for most carcinoma antigens. We present an alternative for toxic components using a hemolytic toxin acting at the membrane level, due to its phospholipase activity. The hemolytic toxin (HT), isolated from the sea anemone Stoichactis helianthus, has been conjugated to a MAb directed against carcinoembryonic antigen (CEA), by means of an artificial disulphide bridge. The hybrid alpha CEA-HT exhibits no hemolytic activity unless it is reduced. It is toxic for cells (MDA-MB-134) expressing CEA and not toxic for cells (MDA-MB-231) not bearing CEA. An excess of free antibody reverses toxicity.     

Heparin-induced thrombocytopenia: laboratory studies

This report describes studies into the pathophysiology of heparin- induced thrombocytopenia. The IgG fraction from each of nine patients with heparin-induced thrombocytopenia caused heparin-dependent platelet release of radiolabeled serotonin. Both the Fc and the Fab portions of the IgG molecule were required for the platelet reactivity. The platelet release reaction could be inhibited by the Fc portion of normal human or goat IgG, and patient F(ab')2, but not F(ab')2 from healthy controls. These results suggested that the Fab portion of IgG binds to heparin forming an immune complex and the immune complexes initiate the platelet release reaction by binding to the platelet Fc receptors. To directly challenge this hypothesis, we preincubated the serotonin-labeled platelets with the monoclonal antibody against the platelet Fc receptor (IV.3). This monoclonal antibody completely inhibited the release reaction caused by heparin and patient sera, as well as heat aggregated IgG, but did not block collagen or thrombin- induced platelet release. Heparin-dependent platelet release also could be inhibited in vitro by the addition of monocytes and neutrophils, but not by red cells, presumably because the Fc receptors on the phagocytic cells have a higher binding affinity for IgG complexes than do platelets. Platelets from patients with congenital deficiencies of specific glycoproteins Ib and IX (Bernard-Soulier syndrome) and IIb and IIIa (Glanzmann's thrombasthenia) displayed normal heparin-dependent release indicating that the release reaction did not require the participation of these glycoproteins. These studies indicate that heparin-induced thrombocytopenia is an IgG-heparin immune complex disorder involving both the Fab and Fc portion of the IgG molecule.