Biomedical subjects

U Raju

Publications and source records attributed to U Raju.

58 records · Page 4Linked to original sources

PubMedDate not supplied

Quantification of the sulfates of 16 alpha-hydroxy androgens that are possible precursors of estriol-3-sulfate in human breast cyst fluid.

The concentration of 16 alpha-hydroxydehydroepiandrosterone-3-sulfate (16 alpha-OHDHAS) was determined in 29 samples of human breast cyst fluid (BCF) and in 15 of these, androst-5-ene-3 beta,16 alpha,17 beta-triol-3-sulfate (A-TriolS) was also assayed. The median value of both was about 100 ng/mL and the ranges were from 1.4 to about 1800 ng/mL. There was a significant association in the values for the two sulfates (p less than 0.05). These concentrations are consistent with a role for 16 alpha-hydroxy androgens as possible precursors for estriol-3-sulfate. The latter is highly elevated relative to other body fluids in BCF. The androgens also correlated directly with the concentrations of K+, an indicator of apocrine proliferation of breast cysts.

Androstenols↗

PubMedDate not supplied

Release of oncofetal fibronectin from human placenta.

Oncofetal fibronectin (onfFN) is an extracellular matrix (ECM) protein synthesized by tumours and fetal tissue including placenta. The appearance of onfFN and other cellular FNs in cervico-vaginal secretions and maternal blood is associated with adverse pregnancy outcomes. In the current study, we used dual (maternal and fetal) perfusion of human term placentae and primary cultures of syncytiotrophoblasts (SCTs) to determine whether the human placenta releases onfFN. ELISA and Western blotting revealed that onfFN is preferentially released to the maternal perfusate in a time-dependent manner. Immunodetection with FDC-6, extra domain A (EDA) and cell binding domain-specific antibodies revealed onfFN in maternal perfusate to be a high molecular weight (>450 kDa) protein dimer, similar to that found in amniotic fluid. This suggested that onfFN was released intact from placenta and not cleaved from an ECM. In addition, a similar high molecular weight dimeric onfFN species was noted in conditioned media from cultures of SCTs. Since SCTs directly release proteins to the intervillous space, this suggests that SCTs may be a source of onfFN detected in maternal perfusate. These results indicate that onfFN is released from human placenta and thus levels in maternal sera may provide insight into placental pathophysiology.

Blotting, Western↗

PubMedDate not supplied

Serum estradiol-binding profiles in postmenopausal women undergoing three common estrogen replacement therapies: associations with sex hormone-binding globulin, estradiol, and estrone levels.

OBJECTIVE: To compare the effects of three commonly prescribed estrogen replacement therapies-oral conjugated equine estrogens (CEE; n = 37), oral micronized estradiol (ME; n = 25), and transdermal estradiol (TE; n = 24)-on the binding characteristics of plasma estradiol as related to the concentrations of blood sex hormone-binding globulin (SHBG), estradiol, and estrone. DESIGN: Menopausal volunteers, opting for estrogen replacement therapy, gave blood at 0, 2, and 4 months. SHBG was assayed by automated immunoabsorbent technology. Estradiol and estrone were determined by quantitative gas chromatography/mass spectrometry. After tritiated estradiol was added to serum, the percentage of estradiol not bound to protein was determined by ultrafiltration and the percentage of estradiol bound to SHBG was measured by a method exploiting that this protein, even when bound to estradiol, binds avidly to Concanavalin A-Agarose. RESULTS: In each study, 2- and 4-month data were similar. Increases in SHBG concentrations were 100% (p < 0.001), 45% (p < 0.001), and 12% (nonsignificant) for subjects who were receiving CEE, ME, and TE regimens, respectively. Decreases in the percentage of estradiol not bound to protein and increases in the percentage of estradiol bound to SHBG correlated with changes in the concentrations of this protein mediated by the therapies. The order for increases in estradiol was ME-TE >> CEE, whereas for estrone, the order was ME > CEE >> TE, divergent from the SHBG responses. CONCLUSIONS: The diverse responses observed can be explained by differences in the estrogen load delivered to target tissues as controlled by the intermediary circulation and metabolism of the hormones introduced in these regimens.

Adult↗

PubMedDate not supplied

Maternal smoking and the risk of congenital birth defects: a cohort study.

BACKGROUND: The literature linking gestational smoking to congenital defects has been very inconsistent. The purpose of this study was to reinvestigate the relation between gestational smoking and congenital malformations. METHODS: This study was a retrospective cohort (N = 18,016) of live births in the TriHealth Hospital system from 1 January 1998 to 31 December 1999. The cohort included 1,943 mothers who were smokers. Congenital defects were grouped into 22 different categories. Multifactorial logistic regression was used to find any association between exposure and the possible outcomes. RESULTS: Mothers who smoked were significantly younger and had babies of lower birth weight and shorter gestational age (P < .05). Of the 22 categories of congenital defects, only cardiovascular system abnormalities showed a significant difference (P < .01) between the two groups. The remaining 21 categories of congenital defects showed no statistical difference. CONCLUSION: Women who smoke during pregnancy have infants that are significantly smaller and of shorter gestational age compared with mothers who do not smoke. Based on these data and findings from most of the available literature, however, gestational smoking is unlikely to cause a large increase in congenital birth defects.

Adult↗