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J L Roberts

Publications and source records attributed to J L Roberts.

273 records · Page 16Linked to original sources
PubMedDate not supplied

Gonadotropin-releasing hormone and chorionic gonadotropin gene expression in human placental development.

Control of human chorionic gonadotropin (hCG) synthesis during pregnancy is poorly understood, although in vitro data suggest a role for placental gonadotropin releasing hormone (GnRH) in its regulation. To study GnRH regulation during placental development, placental tissue of different gestational ages was analyzed for GnRH and beta hCG mRNA content. cRNA probes to exonic/intronic sequences of GnRH and beta hCG transcripts were constructed and used to perform solution hybridization/nuclease protection and in situ hybridization assays. The levels of GnRH mRNA were approximately 0.1-1% of that of beta hCG mRNA, in agreement with its suggested paracrine, rather than endocrine, role. While beta hCG mRNA content decreased significantly from first trimester to term (643 to 21.6 pg/microgram RNA), there was no significant change in GnRH mRNA (0.179 to 0.155 pg/microgram RNA). While beta hCG mRNA was localized almost exclusively in syncytiotrophoblasts, GnRH mRNA was present in all cell types of the placenta, including the stroma. In the course of performing sense-strand controls in the in situ hybridization, we noted that the placenta appeared to express more antisense GnRH than sense GnRH mRNA, again, in all cell types. Solution hybridization/nuclease protection analysis with exon 1 and exon 3 probes confirmed this observation, showing that there is two to three times more antisense GnRH RNA than sense GnRH mRNA. These studies suggest that GnRH gene expression and its role in regulating hCG production in human placenta is complex and does not fit a simple model for paracrine regulation of hCG.

Chorionic Gonadotropin↗
PubMedDate not supplied

Subepithelial electron-dense deposits in proliferative glomerulonephritis of systemic lupus erythematosus.

Subepithelial electron-dense deposits (SED) were found in the renal biopsies of 36 of 59 patients with systemic lupus erythematosus (SLE). The SED were divided into two groups based on their ultrastructural appearance and distribution within the glomeruli. Type I SED were regular in size and shape, had a homogeneous electron density and a diffuse distribution within the glomeruli, and involved all of the glomeruli in the biopsy. In contrast, the type II SED were irregular in size and shape, tended to be quite large, and had variable electron density. They were present in reduced numbers in involved capillary loops, and they were absent from other loops within the same glomerulus. Type I SED were seen in cases of membranous SLE glomerulonephritis (GN), and type II SED were associated with severe proliferative SLE GN. Although the patients with proliferative GN had more active urinary sediments at the time of biopsy than did the patients with membranous GN, the mean serum creatinine and urinary protein excretion were not significantly different in the two groups. The mean followup was almost twice as long for the membranous compared to the proliferative lesions (33.70 months +/- SE 7.96 vs. 16.78 +/- 4.21), but at the end of the study, mean renal function was better preserved in patients with proliferative GN (2.13 mg/dl +/- SE 0.49). As a group, patients with type I SED had mild serologic abnormalities compared to patients with type II SED. In contrast the abnormal serologies of the patients with type II SED were not significantly different from patients with proliferative SLE GN in general. The results suggest that the heterogeneous morphology of SED may reflect different pathogenetic mechanisms responsible for their formation. When focal and segmental SED (type II) are seen in proliferative SLE GN, they should be interpreted with caution, for they have very different clinical, prognostic, and therapeutic implications from type I SED.

Basement Membrane↗