Background: Plasma and urine levels of the potent vasodilator Ang-(1-7) are elevated in mid and late pregnancy and are correlated with elevated placental angiogenesis, fetal blood flow, and rapid fetal growth. We hypothesized that Ang-(1-7), its receptor (Mas1) and the enzymes involved in Ang-(1-7) production (ACE2 and Membrane metallo-endopeptidase; MME) are down regulated in response to glucocorticoid administration contributing to IUGR. Methods: Pregnant female Sprague-Dawley rats were injected with dexamethasone (DEX; 0.4 mg/kg/day) starting from 14 day gestation (dg) till sacrifice at 19 or 21 dg while control groups were injected with saline (n = 6/group). The gene and protein expression of ACE2, MME, Ang-(1-7) and Mas1 receptor in the placental labyrinth (LZ) and basal zones (BZ) were studied.

Abstract. in the present study, the expression of estrogen receptor (Er)α and Erβ isoforms in Er-positive (mcF7, t-47d and Zr-75-1) and Er-negative (mda-mB-231, SK-Br-3, mda-mB-453 and hcc1954) breast cancer cell lines was investigated. Erα mrna was expressed in Er-positive and some Er-negative cell lines. Erα ∆3, ∆5 and ∆7 spliced variants were present in mcF7 and t-47d cells; Erα ∆5 and ∆7 spliced variants were detected in ZR-75-1 cells. mda-mB-231 and hcc1954 cells expressed Erα ∆5 and ∆7 spliced variants. the Erβ1 variant was expressed in all of the cell lines and the Erβ2 variant in all of the Er-positive and some Er-negative cell lines (mda-mB-231, mda-mB-453 and SK-Br-3). mcF7, Zr-75-1, mda-mB-453, hcc1954 and t-47d cells expressed Erβ5. all cell lines expressed an Erα 66-kda protein band, and some expressed the truncated 42-kda variant. Erβ1 was detected in all of the cell lines in addition to a 38-44 kda variant. the results indicate that breast cancer cell lines widely used in research and reported as being Er-negative express Erα and/or Erβ mrna and protein.

Abstract. To establish a model of endocrine resistant breast cancer that is associated with loss of estrogen receptor (ER), MCF7 cells were transfected with several plasmid constructs intended to produce intracellular double stranded hairpin RNA to be processed into siRNA directed against different regions of the ER· mRNA. Stably transformed cells were propagated in long-term culture. One of these lines, designated pII, was selected for further analysis. pII cells exhibited reduced levels of ER· mRNA and protein as well as several estrogen-regulated genes assessed by real-time PCR and were unresponsive to addition of estradiol and tamoxifen.

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Infertility is one of the major public health problems, affecting 15% of couples who attempt pregnancy; in 50% of these, the male partner is responsible. Chromosomal abnormalities and Y microdeletions in the azoospermia factor (AZF) region are known to be associated with spermatogenetic failure. In the present study, 289 patients with primary male infertility because of spermatogenetic failure were studied in order to highlight the molecular background of male infertility in Kuwait, and to avoid the possibility of transmission of any microdeletions/chromosomal aberrations to offspring via intracytoplasmic sperm injection (ICSI). Of the 289 infertile men, 23 patients (8%) had chromosomal aberration in the form of Klinefelter syndrome/variant (16/23; 69.6%), XYY syndrome (3/23; 13%), XX male syndrome (2/23; 8.7%), 45,X/46X, i(Yp)(1/23; 4.4%) and 45,XY, t(9;22) (1/23;4.4%). Y-chromosome microdeletion in the AZFb and AZFc regions were detected in 7/266 cases (2.6%). Testicular biopsy was carried out in 31 azoospermic patients, of whom five men had Sertoli-cell only syndrome, while 26 patients had spermatogenic arrest. In conclusion, this study showed that the frequency of both chromosomal anomalies and Y microdeletions were found in 10.4% of the infertile men. The potential risk of transmitting these genetic disorders to offspring provides a rationale for screening infertile men prior to ICSI.