Accumulating evidence suggests the possible association between the concentrations of serum brain-derived neurotrophic factor (BDNF) and psychiatric disease with impaired brain development. Yet the reasons remain unclear. We therefore investigated the characteristics of serum BDNF as well as its age-related changes in healthy controls in comparison to autism cases. BDNF was gradually released from platelets at 4 degrees C, reached a maximal concentration after around 24 h, and remained stable until 42 h. At room temperature, BDNF was found to be immediately degraded. Circadian changes, but not seasonal changes, were found in serum levels of BDNF existing as the mature form with a molecular mass of 14 kDa. In healthy controls, the serum BDNF concentration increased over the first several years, then slightly decreased after reaching the adult level. There were no sex differences between males and females. In the autism cases, mean levels were significantly lower in children 0-9 years old compared to teenagers or adults, or to age-matched healthy controls, indicating a delayed BDNF increase with development. In a separate study of adult rats, a circadian change in serum BDNF was found to be similar to that in the cortex, indicating a possible association with cortical functions.

Our aim was to identify risk factors for falling and establish a method to assess risk for falls in adults with intellectual disabilities. In a cross-sectional survey of 144 Japanese adults, we found that age, presence of epilepsy, and presence of paretic conditions were independent risk factors. The Tinetti balance and gait instrument was successfully administered to this population and resulted in high diagnostic accuracy (sensitivity 88.9%, specificity 91.9%) for identifying individuals at risk when the cutoff score was set at 25. Participants whose balance and gait deteriorated showed a decrease in the Tinetti score of at least 2 points per year. Thus, the Tinetti instrument may be an effective tool to detect an increased risk of fall in this population.

We investigated the mechanisms by which corticosteroids affect atherosclerosis. Male New Zealand White rabbits were injected with 0.125 mg dexamethasone (n = 10) or vehicle (control group, n = 10). Both groups were fed a 1% cholesterol diet for 8 weeks. Although the dexamethasone-treated animals exhibited a greater degree of hvperlipidemia, they exhibited significantly less atherosclerotic plaque of the aortic surface than control animals (7.8% versus 47.2%). Immunofluorescence study of the aortic plaque specimens showed that dexamethasone administration reduced both macrophages and T lymphocytes. In vitro, dexamethasone suppressed the proliferation and differentiation of U937 cells and inhibited uptake and degradation of 0-very low density lipoproteins by mouse peritoneal macrophages. These findings suggest that dexamethasone suppresses the development of atherosclerosis in the aorta of rabbits by inhibiting recruitment and proliferation of macrophages and the formation of foam cells in plaques. {Arteriosclerosis and Thrombosis 1993;13:892-899)

A 33-year-old man with nephrotic syndrome and rapid deterioration of renal function showed curious glomerular morphological abnormalities. Ballooning of the glomerular capillaries due to a substance accumulated in the capillary lumina and mesangiolysis were prominent histological features. The deposits in the capillary lumen were positive for Sudan III staining, and also for β-lipoprotein, apoprotein B and apoprotein E by immunofluorescent technique. The staining of β-lipoprotein in a flower leaf pattern was a striking characteristic, while such staining was negative when studied in 20 patients with nephrotic syndrome who were used as controls. Based on these findings, the morphological abnormalities in this case were considered to be related to lipoprotein deposition in the glomeruli. This case is thought to be the first reported in a complete form in the literature which could be classified as a new kind of disease related to lipoprotein metabolism abnormalities.

CD59 is a molecule which is present on the host cell membranes and inhibits formation of membrane attack complex. A monoclonal antibody, 6D1, recognizes a rat analogue of human CD59. 6D1 inhibits function of rat CD59 and can enhance complement-mediated hemolysis in vitro. To assess the role of CD59 in complement-mediated glomerular injury, 6D1 was tested in a model of experimental glomerulonephritis induced by a lectin and its antibodies. The left kidney of a rat was perfused either with 200 micrograms of Lens culinaris hemagglutinin (LCH) plus 1 mg of 6D1 (IgG1 fraction) (Group I and III) or with LCH only (Group II) through a cannula placed in the left renal artery. All the perfusate was discarded from a cannula in the renal vein. The holes in the artery and vein were repaired by microsurgery and the blood circulation was re-established. Rats were injected either with 0.125 ml of rabbit anti-LCH serum (Group I and II), or with normal rabbit serum (Group III) via tail vein one minute after the recirculation. Fifteen minutes after injection, significant C9 deposition in the glomeruli was observed only in Group I, whereas C3 deposition in Group I and II were comparable. At Day 4, total glomerular cells, proliferating cells, glomerular expression of intercellular adhesion molecule-1 and fibrin deposition in Group I were all significantly increased when compared with Group II. At Day 7, number of total glomerular cells and leukocytes in the glomeruli of Group I were significantly higher than in Group II. The glomeruli in Group III appeared normal throughout experiments. These data indicate that the functional inhibition of a rat analogue of human CD59 worsens complement-mediated glomerular injury in vivo.