Rejane Cristina Schierholt

Duration of day-care attendance and acute respiratory infection

Day-care attendance accounts for an increased frequency of acute respiratory infections (ARI), in numbers of both episodes and hospitalizations. In addition to day-care exposure, risk factors include age, siblings, and crowding. The purpose of this study was to investigate a possible association between duration of day-care exposure and ARI. A cross-sectional study was carried out to compared ARI rates for children exposed to day care and children cared for at home. Children with at least one parent working in a hospital were sampled from the hospital-run day-care center and those cared for at home. An acute respiratory infection was defined as the presence of two or more signs or symptoms in the previous two weeks. Children exposed to the day-care center for 12 to 50 hours a week had a three to five times greater risk of developing ARI than those staying at home. This risk was assessed independently, taking socioeconomic status, age, and number of siblings into account. Risk of respiratory illness and day-care attendance has been described elsewhere, but this study presents original findings related to duration of exposure. With a view towards reducing risk of ARI, improvements should be made in institutional day-care centers in Brazil, where family day care is still not available.

Pre-conditioning to global cerebral ischemia changes hippocampal acetylcholinesterase in the rat.

This study shows the effect of transient global cerebral ischemia (ISC) on hippocampal acetylcholinesterase (AChE) activity. Naive adult Wistar rats received either a brief (2 min) or a long (10 min) ischemic episode by the four‐vessel occlusion method. Pre‐conditioned rats received double ischemia: a 10 min episode inflicted 24 h after a 2 min event, a condition known to confer cytoprotection to CA1 pyramidal cells of hippocampus. 2 min of ischemia caused an increase in acetylcholinesterase activity both immediately and 30 min after the episode, however enzyme activity was significantly decreased after 24 h of reperfusion. 10 min of ischemia caused an increase in activity both 60 min and 24 h after ischemia. Conversely, pre‐conditioned rats displayed lower activity both immediately and 60 min after ischemia. Our results suggest that: a) neuronal death, that follows 10 min of ischemia, is associated to a late increase in acetylcholinesterase activity; b) pre‐conditioning is related to diminished acetylcholinesterase activity. This is in agreement with previous evidence that acetylcholinesterase inhibition and maintenance of acetylcholine levels are beneficial for cell surviving after cerebral ischemia.

Effects of brain ischemia on intermediate filaments of rat hippocampus

Neurofilaments subunits (NF-H, NF-M, NF-L) and glial fibrillary acidic protein (GFAP) were investigated in the hippocampus of rats after distinct periods of reperfusion (1 to 15 days) following 20 min of transient global forebrain ischemia in the rat. In vitro [14Ca]leucine incorporation was not altered until 48 h after the ischemic insult, however concentration of intermediate filament subunits significantly decreased in this period. Three days after the insult, leucine incorporation significantly increased while the concentration NF-H, NF-M, and NF-L were still diminished after 15 days of reperfusion. In vitro incorporation of32P into NF-M and NF-L suffered immediately after ischemia, but returned to control values after two days of reperfusion. GFAP levels decreased immediately after ischemia but quickly recovered and significantly peaked from 7 to 10 days after the insult. These results suggest that transient ischemia followed by reperfusion causes proteolysis of intermediate filaments in the hippocampus, and that proteolysis could be facilitated by diminished phosphorylation levels of NF-M and NF-L.

ATP Diphosphohydrolase and 5′-Nucleotidase Activities from Hippocampal Synaptosomes after Brain Ischemia

Ischemic brain injury produced by stroke or cardiac arrest is a major cause of human neurological disability1. The molecular consequences of brain ischemia include changes in cell signalling (neurotransmitters, neuromodulators); in signal transduction (receptors, ion channels, second mesengers, phosphorylation reactions); in metabolism (carbohydrate, protein, fatty acid, free radicals); and in gene regulation and expression2. These abnormalities in cellular metabolism can produce necrosis of neurons, glia, and other supportive brain cells1, 2. Neurons differ in their intrinsic sensitivity to ischemic insults and in their ability to recover from such an impact3. The hippocampus is a classical predeliction site for ischemic injury of the selective vulnerability type3.