Although much progress has been made in our understanding of the nature of social support, the majority of this research has involved older women and has been studied cross-sectionally. The present study comes from a lifespan developmental perspective on stability and change over time that examines sex differences in the social support networks of widows (170) and widowers (25) that are compared across 12 months post-bereavement. Most levels of positive support increased from B to W1 in what appears to be a response to spousal bereavement. Sex differences generally demonstrate that widowers receive less support using various measures and across different times of measurement. These findings point to change over time, sex differences, and heterogeneity as important issues when discussing bereavement and social support.

A patient with nephrotic syndrome developed pseudotumor cerebri following glucocorticoid therapy. Diagnosis of pseudotumor cerebri was based on satisfaction of four criteria proposed by Ahlskog and O'Neill. The symptomsof pseudotumor cerebri disappeared within 10 days. After a three-week interval of remission, relapse occurred. Glycerol and urokinase produced rapid resolution of the symptomsand warfarin prevented further recurrence of pseudotumor cerebri for one year. These results suggest that the pathogenesis of pseudotumor cerebri might be associated with the hypercoagulable state which was induced by glucocorticoid therapy and nephrotic syndrome.

The distribution of heparan sulfate proteoglycan (HS‐PG) was examined electron microscopically by the high iron diamine (HID) method in puromycin aminonucleoside (PAN) nephrosis, accelerated Masugi nephritis (NTN), and serum sickness nephritis induced by bovine serum albumin (BSA nephritis) in the rat. In PAN nephrosis rats, no change was observed in the distribution of HS‐PG in the lamina rara externa (LRE) of the glomerular basement membrane (GBM) throughout the experiment. In NTN rats, however, the loss of HS‐PG was observed, and it was associated with subepithelial electron dense deposits formed possibly by serum sickness mechanism, but not with inflammatory cell infiltration. In BAS nephritis, immune deposits were seen in mesangial, subendothelial, intramembranous and subepithelial areas. The deposits in the former three areas seemed to have little reciprocity with the loss of HS‐PG and proteinuria. Urinary protein increased in accordance with the development of subepithelial deposits and the loss of HS‐PG in the area of the deposits in the LRE. These results indicate that HS‐PG could be preserved even in marked proteinuric states in morphologically Intact basement membrane, but altered and lost distribution of HS‐PG associated with subepithelial immune deposits could in turn result in the development of proteinuria.

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