Some sex hormone profiles are consistent over time in normal menstruating women: implications for sports injury epidemiology.

PURPOSE: It is unclear whether sex hormone profiles obtained in two consecutive months are consistent within women. Month-to-month consistency in daily, nadir, peak and mean hormone concentrations during the early follicular and luteal phases in recreationally active, young eumenorrheic women was prospectively examined. METHODS: 60 healthy, non-smoking women who reported normal and consistent menstrual cycles lasting 26-32 days for the past 6 months were followed prospectively to obtain serum samples for the first 6 days of menses and for 8 days after a positive ovulation test over two consecutive months. Month-to-month consistency of daily concentrations of oestradiol (pg/ml), progesterone (ng/ml), testosterone (ng/dl), sex hormone-binding globulin (nmol/l) and free androgen index were determined using linear mixed models. Month-to-month consistency in nadir, peak and mean concentrations were then assessed using intraclass correlation coefficients and SEM to more precisely examine intraindividual consistency. RESULTS: Linear mixed models revealed stable hormone concentrations across cycles and cycles by day. Reliability estimates for nadir, peak, mean menses and mean postovulatory concentrations range from 0.56 to 0.86 for oestradiol, 0.44 to 0.91 for progesterone, 0.60 to 0.86 for testosterone, 0.88 to 0.97 for sex hormone-binding globulin and 0.78 to 0.91 for free androgen index. CONCLUSIONS: Hormone profiles were reproducible over two consecutive months. To reduce month-to-month intraindividual variations and improve measurement consistency, it is recommended that multiple samples be taken over consecutive days as opposed to a single sample.

Progressive dendritic pathology in cynomolgus macaques infected with simian immunodeficiency virus.

Neuronal pathology in acquired immunodeficiency syndrome (AIDS) is of interest in relation to cognitive impairment in AIDS patients and from the broader perspective of the pathogenesis of neurodegeneration. Cortical dendritic spine loss has been described in patients with AIDS and the aim of this study was to test the hypothesis that similar pathology is present in cynomolgus macaques infected with simian immunodeficiency virus (SIV). These animals develop an AIDS-like illness, but multinucleated giant cell encephalitis is not a feature and CNS virus load is found to be very low. Four animals infected for 2.5-3 months and four infected for 2-3 years were compared with four controls. The Golgi-Cox technique was employed to demonstrate dendritic morphology in the frontal cortex and the diameter of apical dendrites, dendritic spine density and dendritic spine lengths were measured in layer V pyramidal cells. Immunohistochemistry for microtubule-associated protein-2 (MAP-2), MHC class II and glial fibrillary acidic protein (GFAP) was also performed. In infected animals there was progressive spine loss and atrophy of remaining spines with loss of MAP-2 immunoreactivity at late time points. No parallel increase in GFAP immunostaining or MHC-class II expression in microglial cells was seen. We conclude that progressive neuronal dendritic pathology is a feature of SIVmac251 infection of cynomolgus macaques and is apparent relatively early in disease. Furthermore, dendritic abnormalities occur in the absence of either multinucleated giant cell pathology or substantial CNS virus load.

Changes in neuron size in cynomolgus macaques infected with various immunodeficiency viruses and poliovirus.

Human immunodeficiency virus (HIV) infection leads to clinically significant neuronal pathology, but the underlying mechanism remains unclear. Infection of rhesus macaques with the simian immunodeficiency virus SIVmac251 has been shown to cause atrophy of hippocampal pyramidal cells. The aim of the current investigation was to determine whether SIVmac251 and other viruses with differing abilities to cause immune suppression or encephalitis could cause neuronal atrophy in cynomolgus macaques. Animals infected with SIVmac251 (n = 22), HIV-2 (n = 6). SIVmac239 (n = 7) and poliovirus (n = 10) were investigated, together with 16 controls. Hippocampal pyramidal cell diameter, averaged across the four CA subfields, was reduced by 16.6% in the SIVmac251 group (P < 0.0001) and by 13.3% in the HIV-2 group (P < 0.001), even though the latter virus does not generally cause immunosuppression. Conversely, SIVmac239, which does cause immunosuppression, caused an average neuronal hypertrophy of 6.8% (P = 0.033). Of possible relevance to the different behaviour of the two SIVs is that SIVmac239 is lymphocyte tropic and does not infect CNS microglia in vivo whereas SIVmac251 does. Animals inoculated with poliovirus into the lumbar spinal cord for polio vaccine neurovirulence testing acted as positive controls for CNS inflammation and they also showed an increase in neuronal diameter (4.1%, P = 0.025). The atrophy seen with SIVmac251 and HIV-2 involved all CA subfields but the hypertrophy following SIVmac239 or poliovirus infection was restricted to CA1 and CA2. These observations show a dissociation between the ability of immunodeficiency viruses to cause immune suppression and neuronal pathology and demonstrate that CNS inflammation per se may cause neuronal hypertrophy.

Hippocampal neuronal atrophy occurs in rhesus macaques following infection with simian immunodeficiency virus.

There is strong evidence that patients with AIDS have loss of cortical neurons. In this study we have examined the hippocampus of rhesus monkeys infected with simian immunodeficiency virus (SIV) to determine whether neuronal damage occurs in this model of human AIDS and to investigate its time course. Twenty-eight infected monkeys (23 young [< 9 years] and five elderly [> 16 years]) were compared with 11 controls (six young and five elderly). Numbers of nucleolated neurons per unit area of section and mean pyramidal cell diameters were measured in each CA sub-field of each animal. There was neuronal atrophy in all regions examined, as early as 3 months following inoculation. An initial apparent increase in neuronal density at 3 months did not reach statistical significance. In younger animals, however, there was a later, significant association between the reduction in neuronal density and duration of infection. Elderly animals were only examined at a single, early time point. These results show that there is neuronal pathology following infection with SIV and that there is probably subsequent neuronal death.

Sentence repetition in preschoolers: effects of length, complexity, and word familiarity.

Seventy-two sentences presented to ten preschool children for repetition were designed so that three sentence construction factors varied independently. The factors were (1) length in number of words, (2) complexity of personal pronouns and main verbs as scaled by Lee (1974), and (3) word familiarity, defined as common vocabulary or the substitution of a nonsense word in place of a typical noun or verb in the model sentence. Three methods were employed for scoring the children's responses: (1) number of retained words, (2) Developmental Sentence Scoring (Lee, 1974), and (3) Stephens's Categories (Stephens, 1974). Eighteen sentences were re-presented for the assessment of reliability. The results of multiple regression analyses indicated that length was the important contributing factor in the children's responses to the model sentences and that Stephens's Category Scale of response scoring was the most sensitive method for detecting the influence of the three sentence factors on the children's responses.