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In Reply We thank Thomas et al for their question regarding head circumference growth and postnatal cytomegalovirus infection in very low-birth-weight (VLBW) infants. It is well established that congenital cytomegalovirus (CMV) can cause congenital microcephaly, and while most infants with congenital CMV are normocephalic at birth and continue to be so at followup, a very small percentage do develop microcephaly later. 1 In our retrospective cohort study, 2 we found no differences in the head circumference at birth (prior to CMV infection) or at discharge/postmenstrual age 40 weeks between VLBW infants identified as having postnatal CMV infection (n = 273) and those without (n = 273). 2 Several other small prospective studies have reported similar findings. In a case-control study, Neuberger et al 3 found no difference in the head circumference at discharge between VLBW infants with postnatal CMV (n = 40) and those without (n = 40). 3 In addition, 3 prospective studies 4-6 from 2 cohorts of VLBW infants with and without postnatal CMV found no differences in head circumference at 12 months (n = 14 infected; n = 41 uninfected), 24 months (n = 14 infected; n = 41 uninfected), 2 to 4.5 years (n = 22 infected; n = 22 uninfected), and school age (n = 20 infected; n = 21 uninfected). [4][5][6] These 3 studies also compared neurodevelopmental outcomes of infants with and without postnatal CMV. Jim et al 4 found no differences at 12 and 24 months. The other 2 studies evaluated the same cohort of infants over time and found no differences at 2 to 4.5 years, but significantly decreased motor and cognitive function at school age in infants with postnatal CMV. 5,6 In summary, our study and others did not find an association between postnatal CMV infection and decreased head circumference in VLBW infants; however, larger studies are needed to confirm these findings and determine whether there are other neurologic sequelae of postnatal CMV infection.

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BACKGROUND: Depression is among the most prevalent mental health problems during aging. Oxidative stress is involved in its pathophysiology, while a better antioxidant defense seems to attenuate the intensity of symptoms. Lifelong training, like that of master athletes, has been associated with improved antioxidant defense. However, no studies compared depression symptoms of master athletes to untrained peers, nor verified the possible relationship between depression scores and a marker of antioxidant defense, such as catalase (CAT) activity. PURPOSE: To compare and verify possible associations between CAT and the intensity of depression symptoms in middle-aged master athletes and untrained peers. METHODS: Participants were master athletes from Sprints (MS, n=24, 50.37±6.23yr) and Endurance Running (ER, n=11, 51.30±9.21yr), besides untrained control groups of middle-aged (CO, n=13, 47.16±8.70 yr) and young individuals (YU, n=15, 23.70±4.02 yr). Blood samples were collected for CAT measures using commercial kits, and Beck Depression Inventory was applied to measure depression symptoms. ANOVA and Pearson's Correlation Coefficient were applied, with a significance level of p≤ 0.05. RESULTS:The CAT of MS and YU [768.6 U•μL -1 ±168.6 U•μL -1 and 729.9 U•μL -1 ±186.9 U•μL -1 ] were higher than CO and ER [410.3 U•μL -1 ±67.24U•μL -1 and 528.8 U•μL -1 ±103.2U•μL -1 (p< 0.0001)]. MS had lower intensity of depression symptoms compared to the YU and ER [2.86 ±2.81 vs 10.36 ±5.79 vs 7.20 ±5.20 (p=0.0002)], but there was no difference in relation to CO [5.00 ±2.25]. Negative correlation was found between CAT and intensity of depression symptoms for the entire group of master athletes [r=-0.4486 (p=0.0100)]. CONCLUSION: Master sprinters presented the lowest intensity of depression symptoms, with CAT being higher than CO and ER. CAT was negatively associated with intensity of depression symptoms, suggesting that training model of master sprinters may be an effective strategy in increasing CAT and reducing depressive symptoms.