PubMed · 15856446
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Martha Bridge Denckla. 2005. Why assess motor functions "early and often?".. https://doi.org/10.1002/mrdd.20054
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BACKGROUND: Growth deficit has been reported as a frequent complication of the treatment of acute lymphoblastic leukemia (ALL). PROCEDURE: Longitudinal analysis of the growth of 129 children, from a total of 351 cases diagnosed between 1987 and 1994 in Brazil, was determined. Height data were converted into standard deviation Z scores. Only girls younger than 10 and boys younger than 12 years old at diagnosis were included. Patients were treated according to a German BFM-83 based protocol. Fifty-eight children received 18 Gy cranial irradiation, four 12 Gy, and two 24 Gy. Patients were aggregated into five non-excluding groups according to availability of height data at diagnosis, during the treatment, at the end of it, and several years after; 35 children reached their final height. RESULTS: Height deficit at the end of the therapeutic treatment was evident (P < 0.0001). Catch-up occurred 1 year after stopping treatment (P = 0.016). At the last follow-up, over 5 years after the end of treatment (n = 83) or at final height (n = 35), impressive height deficits were recorded (P < 0.0001 for both end points). Multivariate analysis demonstrated that growth impairment was more severe in children younger than 4 years at diagnosis and in those who received cranial irradiation. No significant effect of gender was observed. Children who were treated solely with chemotherapy also had significant height loss. CONCLUSIONS: Treatment of ALL in children is associated with growth deficit during the treatment and several years after it, affecting the final height negatively, particularly in patients younger than 4 and in those who received cranial irradiation.
AIM: To describe the expected fluctuation in the mean deviation (MD) scores on a large, long-term series of stable visual field reports for particular grades of defect in order to give clinicians an aid to the correct diagnosis of glaucomatous progression. METHOD: Visual field reports of subjects with five reliable consecutive Humphrey 24-2 visual fields, recorded over a period of at least 3 years, were scored using the Advanced Glaucoma Intervention Study (AGIS) system. The AGIS scores of the first and last visual fields were required to be identical. RESULTS: A total of 202 eyes from 202 patients were used in the study, with a total of 1010 visual fields being used in the analysis. Visual fields with no defect (AGIS score 0) had a 99% confidence interval (CI) of 0.3 dB, mild defects 0.4 dB, moderate defects 0.8 dB, severe 1 dB, and 1.3 dB for end-stage defects when considering variation of MD scores. Using a one-way ANOVA incorporating all stages showed very little fluctuation throughout the series (P=0.96). The correlation between the CI and grade of field defect showed a good positive correlation (r=0.7, P=0.0003) indicating an increase in CI as field defects worsen. CONCLUSION: When considering a series of reliable visual fields in a stable eye, one should expect only very little fluctuation in the MD, indicating that an increase in the MD beyond that of the 99% CI described may suggest progression. The reliability indices of the visual field test should be regarded as a primary consideration when assessing visual fields.
Heat shock protein 27 (Hsp27) is a stress-inducible protein in cells that functions as a molecular chaperone and also as an anti-apoptotic protein. Methylglyoxal (MGO) is a reactive dicarbonyl compound produced from cellular glycolytic intermediates that reacts non-enzymatically with proteins to form products such as argpyrimidine. We found considerable amount of Hsp27 in phosphorylated form (pHsp27) in human cataractous lenses. pHsp27 was the major argpyrimidine-modified protein in brunescent cataractous lenses. Modification by MGO enhanced the chaperone function of both pHsp27 and native Hsp27, but the effect on Hsp27 was at least three-times greater than on pHsp27. Phosphorylation of Hsp27 abolished its chaperone function. Transfer of Hsp27 using a cationic lipid inhibited staurosporine (SP)-induced apoptotic cell death by 53% in a human lens epithelial cell line (HLE B-3). MGO-modified Hsp27 had an even greater effect (62% inhibition). SP-induced reactive oxygen species in HLE-B3 cells was significantly lower in cells transferred with MGO-modified Hsp27 when compared to native Hsp27. In vitro incubation experiments showed that MGO-modified Hsp27 reduced the activity of caspase-9, and MGO-modified pHsp27 reduced activities of both caspase-9 and caspase-3. Based on these results, we propose that Hsp27 becomes a better anti-apoptotic protein after modification by MGO, which may be due to multiple mechanisms that include enhancement of chaperone function, reduction in oxidative stress, and inhibition of activity of caspases. Our results suggest that MGO modification and phosphorylation of Hsp27 may have important consequences for lens transparency and cataract development.