Oxandrolone

The development of specific growth charts for Turner Syndrome (TS) promotes adequate assessment of growth and weight gain, and earlier diagnosis of comorbidities, and may help to analyze the effectiveness of treatments to promote growth and puberty. The aim of this study was to construct a growth chart with the largest possible series of patients with a cytogenetic diagnosis of TS from a Brazilian reference center.

This is a longitudinal study, with 259 cases of TS born between 1957 and 2014 and followed between 1975 and 2019, without the use of GH or oxandrolone. 3,160 height measurements and 2,918 wt measurements were used, with subsequent calculation of the Body Mass Index (BMI). For data analysis, the "GAMLSS" package of the "R" software was used.

The mean target height was 157.8 cm (standard deviation 5.2; median 160.4 cm). The mean height of patients with TS at 20 years of age was 145.6 cm (standard deviation 5.9; median 146.7 cm). Height, weight, and BMI by age graphs were developed for TS girls between 2 and 20 years.

These growth charts may be used to monitor the growth of girls with TS and to verify the effect of adjuvant treatments on promoting growth.

Spinal cord contusion injury results in Wallerian degeneration of spinal cord axonal tracts, which are necessary for locomotor function. Axonal swelling and loss of axonal density at the contusion site, characteristic of Wallerian degeneration, commence within hours of injury. Tempol, a superoxide dismutase mimetic, was previously shown to reduce the loss of spinal cord white matter and improve locomotor function in an experimental model of spinal cord contusion, suggesting that tempol treatment might inhibit Wallerian degeneration of spinal cord axons. Here, we report that tempol partially inhibits Wallerian degeneration, resulting in improved locomotor recovery. We previously reported that Wallerian degeneration is reduced by inhibitors of aldose reductase (AR), which converts glucose to sorbitol in the polyol pathway. We observed that tempol inhibited sorbitol production in the injured spinal cord to the same extent as the AR inhibitor, sorbinil. Tempol also prevented post-contusion upregulation of AR (AKR1B10) protein expression within degenerating axons, as previously observed for AR inhibitors. Additionally, we hypothesized that tempol inhibits axonal degeneration by preventing loss of the glutathione pool due to polyol pathway activity. Consistent with our hypothesis, tempol treatment resulted in greater glutathione content in the injured spinal cord, which was correlated with increased expression and activity of γ-glutamylcysteine ligase (γGCL; EC 6.3.2.2), the rate-limiting enzyme for glutathione synthesis. Administration of the γGCL inhibitor buthionine sulfoximine abolished all observed effects of tempol administration. Together, these results support a pathological role for polyol pathway activation in glutathione depletion, resulting in Wallerian degeneration after spinal cord injury. Interestingly, methylprednisolone, oxandrolone, and clenbuterol, which are known to spare axonal tracts after spinal cord injury, were equally effective in inhibiting polyol pathway activation. These results suggest that prevention of AR activation is a common target of many disparate post-SCI interventions.