Peak bone mass is an important determinant of future bone mass and of the risk of osteoporosis and subsequent fractures. Although some information concerning bone mineral density (BMD) in adults affected with systemic lupus erythematosus (SLE) is available, few data on children and adolescents have been reported. Many variables, such as duration and activity of the disease, reduced sun exposure, and steroid therapy have been suggested as risk factors in the pathogenesis of osteoporosis in SLE. In this study, we longitudinally evaluated, by dual energy X-ray absorptiometry (DEXA), the BMD of 20 young patients affected with juvenile SLE (JSLE), in order to establish the degree of osteoporosis and the influence of steroid treatment, among other clinical variables. At baseline, the mean BMD in JSLE patients was 0.978 g/cm2 and in controls 1.038 g/cm2 (P = 0.31). At 1 year (time 2), this value became 0.947 g/cm2 in JSLE children; the mean individual difference was 0.28 g/cm2 (3.4%). Only in those patients aged 19-25 years BMD was significantly lower than in controls, both at baseline and at time 2. Considering the steroid treatment, no significant difference between the two groups was found either at baseline or at time 2; however, the mean yearly BMD loss in the steroid patients was 0.031 g/cm2 (3.5%) vs. 0.005 g/cm2 (0.5%) in those who had not taken steroids. A significantly inverse correlation between BMD and the cumulative dosage of corticosteroids has been detected. BMD produced a significantly inverse correlation to the cumulative dosage of corticosteroids; no significant correlation has been found between BMD and disease activity or duration.

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The pivotal role of the periaqueductal grey (PAG) in fear learning is reinforced by the identification of neurons in male rat ventrolateral PAG (vlPAG) that encode fear memory through signalling the onset and offset of an auditory-conditioned stimulus during presentation of the unreinforced conditioned tone (CS+) during retrieval. Some units only display CS+ onset or offset responses, and the two signals differ in extinction sensitivity, suggesting that they are independent of each other. In addition, understanding cerebellar contributions to survival circuits is advanced by the discovery that (i) reversible inactivation of the medial cerebellar nucleus (MCN) during fear consolidation leads in subsequent retrieval to (a) disruption of the temporal precision of vlPAG offset, but not onset responses to CS+, and (b) an increase in duration of freezing behaviour. And (ii) chemogenetic manipulation of the MCN-vlPAG projection during fear acquisition (a) reduces the occurrence of fear-related ultrasonic vocalisations, and (b) during subsequent retrieval, slows the extinction rate of fear-related freezing. These findings show that the cerebellum is part of the survival network that regulates fear memory processes at multiple timescales and in multiple ways, raising the possibility that dysfunctional interactions in the cerebellar-survival network may underlie fear-related disorders and comorbidities.

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