Problems of behaviour, reading and arithmetic: assessments of comorbidity using the Strengths and Difficulties Questionnaire.

BACKGROUND: Estimates of academic underachievement among school children vary widely, depending on the geographical location and on the criteria used to define attainment. AIM: To examine the relationship between behaviour problems and academic attainment in a large UK primary school. METHOD: A school population (364 children from Years 3 to 6 inclusive) were assessed on a range of cognitive ability tasks. These included standardised tests of reading, arithmetic and verbal and non-verbal intelligence. Under-achievement was assessed using different criteria. To assess behaviour, teachers completed the Strengths and Difficulties Questionnaire (Goodman, 1997) for each participating child. Finally, academic progress of a subset of children was assessed after one year. RESULTS: Indicated a significant relationship between behaviour and academic attainment; prosocial behaviour was positively correlated with reading and arithmetic, hyperactivity and conduct problems were negatively correlated. This association was especially strong in the children rated by the questionnaire as hyperactive, where around 1 in 5 had a specific reading deficit. However, there was no evidence to indicate that children with behaviour problems made less academic progress over a one-year period relative to their peers. CONCLUSION: The study highlights the importance of assessing both cognitive skills and behaviour, particularly when planning the educational management of children with reading difficulties.

Analysis of age-associated changes in collagen crosslinking in the skin and lung in monkeys and rats.

The present study was designed to address a specific question: can we define collagen aging in vivo in terms of alterations in collagen crosslinking? In order to assess the complete spectrum of change throughout life, tissues from rats, monkeys and (where available) humans were examined at ages ranging from fetal to old. Skin and lung were selected in order to include all of the crosslinks derived from lysyl oxidase-generated aldehydes that have been identified thus far, both reducible and nonreducible. Crosslinks analyzed included hydroxylysinonorleucine, dihydroxylysinorleucine, histidinohydroxymerodesmosine, hydroxypyridinium, lysyl pyridinium, and a deoxy analogue of hydroxypyridinium found in skin that differs structurally from lysyl pyridinium. Tissues from both a short-lived species (rats) and a long-lived species (monkeys) were analyzed to test further the hypothesis that changes in crosslinking are linked predominantly to biological age of the animal, rather than temporal aging. We found that biological aging seems to regulate certain predictable changes during the first part of the lifespan: the disappearance postnatally of dihydroxylysinonorleucine in skin, the rapid decrease in difunctional crosslink content in lung and skin during early growth and development, and the gradual rise in hydroxypyridinium and lysyl pyridinium in lung tissue. Changes in crosslinking were far less predictable during the second half of the lifespan. Although hydroxypridinium content continued to rise or reached a plateau in rat and monkey lungs, respectively, it showed a decrease in human lungs. The analogous trifunctional crosslink in skin, the so-called 'pyridinoline analogue', decreased dramatically in both rats and monkeys in later life. Our data suggest that caution must be taken in drawing inferences about human connective tissue aging from experiments performed in short-lived species such as rodents. Furthermore, the finding that there may be fewer total lysyl oxidase-derived crosslinks per collagen molecule in very old animals as compared with young animals suggests that we may need to expand our concepts of collagen crosslinking.

Long-term consequences of exposure to ozone. II. Structural alterations in lung collagen of monkeys.

The effects of chronic exposure to ozone on lung collagen crosslinking were investigated in two groups of juvenile cynomolgus monkeys exposed to 0.61 ppm of ozone 8 hrs per day for 1 year. One group was killed immediately after the exposure period; the second exposed group breathed filtered air for 6 months after the ozone exposure before being killed. Previous studies of these monkeys had revealed that lung collagen content was increased in both exposed groups (J.A. Last et al., (1984). Toxicol. Appl. Pharmacol. 72, 111-118). In the present study specific collagen crosslinks were quantified in order to determine whether the excess collagen in the lungs of these animals was structurally normal or abnormal. In the group killed immediately after exposure, the difunctional crosslink dehydrodihydroxylysinonorleucine (DHLNL) was elevated, as was the ratio of DHLNL to dehydrohydroxylysinonorleucine (HLNL). Lung content of the mature nonreducible crosslink hydroxypyridinium was also increased in this group. In the group killed after a 6-month postexposure period, lung content of the difunctional crosslinks DHLNL and HLNL was indistinguishable from control values. However, lung hydroxypyridinium content was significantly increased. The changes in collagen crosslinking observed in the group killed at the termination of exposure are characteristic of those seen in lung tissue in the acute stage of experimental pulmonary fibrosis. The changes seen in the postexposure group suggest that while the lung collagen being synthesized at the time the animals were killed was apparently normal, "abnormal" collagen synthesized during the period of ozone exposure was irreversibly deposited in the lungs. This study suggests that long-term exposure to relatively low levels of ozone may cause irreversible changes in lung collagen structure.