This study describes the expression of insulin-like growth factor-I (IGF-I) and IGF-I receptor (IGF-IR) genes in the mouse uterus during the peri-implantation period (Days 1-6 of pregnancy), as well as effects of estradiol (E) and progesterone (P) on cell-specific IGF-I gene expression in the uterus of the ovariectomized adult mouse. Northern blot analysis showed that IGF-I mRNA levels were low but readily detectable in the uterus on Day 1 of pregnancy and steadily increased, reaching high levels just before (Day 4) and after initiation of implantation (Days 5 and 6). In general, IGF-IR transcripts were present in low abundance in uterine RNA throughout the peri-implantation period. However, six sizes of uterine IGF-IR transcripts were detected, and the relative abundance of two of these transcripts varied significantly during the peri-implantation period. Cell-specific expression of the IGF-I gene was examined by in situ hybridization to mRNA and immunohistochemical detection of protein. The results indicated that the synthesis of IGF-I on Days 1 and 2 was most predominant in glandular and luminal epithelial cells. However, on Days 3 and 4, stromal cells, and on Days 5 and 6, decidual cells appeared to be the predominant sites of synthesis of this growth factor. Uterine IGF-I gene expression was stimulated by ovarian steroids. Northern blot analysis showed that IGF-I transcripts were rare in the ovariectomized adult mouse uterus, but an injection of P and/or E caused a rapid accumulation of these transcripts. Analysis of the cell-specific expression of uterine IGF-I showed that E induced IGF-I gene expression primarily in epithelial cells, whereas P did so in the stroma. Superimposition of E on the P-primed uterus further stimulated IGF-I expression in the stroma. The results of these studies are consistent with an autocrine/paracrine function of uterine IGF-I, and indicate that ovarian steroids regulate the cell-specific and temporal patterns of expression of this gene in the peri-implantation mouse uterus.

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The level of TSOD, Cu/Zn-SOD, and Mn SOD isoenzyme activity decreased with age in LECs of patients with age-related cataract. A significant difference in the level of TSOD and Cu/Zn-SOD isoenzyme activity between different types of cataract was observed. The activity of all 3 SOD isoenzymes was highest in cortical cataracts.

We have investigated the expression of mRNA for interleukin 6 (IL-6) in cells infiltrating 12 epiretinal membranes, and the presence of biologically active IL-6 in vitreous humour available from five corresponding eyes. The results showed that nine of the 12 membranes (75%) contained cells expressing mRNA for this cytokine. Although in two of the specimens pigmented cells were identified as some of the cells expressing mRNA for IL-6, we did not identify the nature of IL-6 mRNA-producing cells infiltrating the membranes. Interestingly, two vitreous samples from eyes whose membranes did not contain cells with mRNA for IL-6 exhibited significant concentrations of IL-6 (315 and 28 micrograms/ml). Parallel study of mRNA for IL-6 in PVR biopsies and of IL-6 levels in corresponding vitreous may indicate how cytokine-mediated pathways of inflammation are involved in the pathogenesis of epiretinal membrane formation.

Over the last three decades the mortality rate for prostatic carcinoma has steadily increased. Carcinoma of prostate (CaP), the most common malignancy in men, is also the second most common cause of cancer deaths in men. However, few epidemiologic studies have been done, and there are scant clues to the etiology/pathogenesis of CaP. As treatment failures for advanced carcinoma continue to frustrate clinicians, more emphasis has recently been focused on strategies to prevent invasive CaP. Prostatic hyperplasia is a universal phenomenon in aging men. Mechanism and signals causing this growth are not understood. Thus, prostatic diseases affect men over the age of 45 and increase in frequency with age so that by the eighth decade more than 90% of men have benign prostatic hyperplasia, of which some progress to CaP. Data from several studies support that higher levels of active metabolite of vitamin D, 1,25-(OH)2-D, reduce the risk of prostatic hyperplasia and CaP. Men with high serum levels of 1,25-(OH)2-D have a reduced risk of poorly differentiated and clinically advanced CaP. Receptor for vitamin D has been reported in both normal and cancer prostate cells. 1,25-(OH)2-D inhibits proliferation and induces differentiation of normal and neoplastic cells. Hypercalcemic activity of 1,25-(OH)2-D or its analogues, however, thwart their use for therapy in humans. 1,25-(OH)2-D also has an established role in phosphorus homeostasis. Low dietary intake of phosphorus leads to an increase in serum concentration of 1,25-(OH)2-D. In addition, dietary fructose reduces plasma phosphate levels by 30 to 50% for more than 3 hr due to a rapid shift of phosphate from extracellular to intracellular compartment. Fruit intake has been shown to be associated with reduced risk of CaP, particularly the advanced type. Put together, these observations support that dietary determinants of hypophosphatemia, leading to increased plasma levels of 1,25-(OH)2-D, could reduce the risk of aging men to develop prostatic diseases, both benign prostatic hyperplasia and CaP.