Contraception knowledge and practices among students in Lebanese universities.

This study aimed to evaluate the proportion of contraception users among Lebanese youth, and the extent of knowledge and perception on birth control; and to raise awareness and sensitise young adults to sexual health, which remains taboo in Lebanon. The 30-item questionnaire was broadcasted to students in private and public universities in Lebanon, through social media and it collected information on contraception use and student knowledge. Over 30% of responders were medical students, and 41% have ever used contraceptives (mostly women); among which, 52.1% for contraception versus 47.9% for medical reasons. According to responders, the pill ranked high in terms of effectiveness (72.4% of responders perceive the pill as effective), followed by the male condom (69.1%) and the hormonal intrauterine device (29.6%). Some would not use contraception in the future, for religious reasons (30.8%) or for fear of complications (46.2%); indeed, around a third of contraceptive users (all female) have experienced adverse effects. Finally, students expressed concern about long-term complications of contraceptive use (pulmonary embolism/phlebitis, breast/endometrial/ovarian cancer, stroke, depression and myocardial infarction). Though less frequent than in the Western world, contraception use in Lebanon is non-negligible and gaps in university students' knowledge on contraception were identified; which should prompt sexual education and family planning initiatives in Lebanon.

Use of Oral Misoprostol for Cervical Priming before Hysteroscopy: A Randomized Comparison of Two Dosages.

OBJECTIVE: The study aims to compare the safety and effectiveness of 200 and 400 µg of oral misoprostol for cervical priming before hysteroscopy. METHODS: A double-blinded randomized study included 70 patients scheduled for hysteroscopy in a Lebanese University Hospital. Two dosages of oral misoprostol (200 or 400 µg) were randomly distributed to these patients 1 h before surgery under general anesthesia. Subjective assessment of the ease of dilatation, size of the first used Hegar, cervical injuries, bleeding or uterine perforation, duration of the procedure and misoprostol adverse effect were all noted and compared. RESULTS: The difficulty of dilation until a Hegar 10 was similar for both treatment groups. Operative time was not reduced with a higher misoprostol dosage. We found 2 uterine perforations within the 200 µg group (6.7%), and none within the 400 µg group. Cervical lacerations and bleeding were similar (20%) for both treatment groups. A 2-fold increase in side effects (nausea, vomiting and cramps) is reported among the 400 µg group. CONCLUSIONS: Increasing the dose of misoprostol from 200 to 400 mg doubled the rate of side effects while no clinical benefit was noted. Larger trials are needed to assess rates of uterine perforation with the 200 µg dosage.

Inhibition of prostaglandin E(2) signaling through the EP(1) receptor does not affect prostacyclin production in human endothelial cells.

Accumulating evidence suggests that cyclooxygenase-2 (COX-2) and prostaglandin E(2) (PGE(2)) may play an important role in colon carcinogenesis. Thus, blockage of this pathway may be a suitable strategy for colon cancer chemoprevention. Recent clinical studies suggest that COX-2 inhibitors cause adverse cardiovascular effects due to prostacyclin (PGI(2)) inhibition. To test our hypothesis that inhibition of PGE(2) signaling through E-prostanoid (EP) receptors may offer a safer cardiovascular profile than COX-2 inhibition, we analyzed expression of 6-keto PGF(1alpha), a hydrated form of PGI(2) and PGI(2) synthase, which was stimulated with cytokines in human umbilical vein endothelial cells (HUVECs) treated with the EP(1) receptor antagonist ONO-8711 or the COX-2 inhibitor celecoxib. ONO-8711 did not inhibit both 6-keto PGF(1alpha) production and PGIS expression, whereas celecoxib did in HUVECs. ONO-8711 also inhibited cytokine-induced tissue factor expression in HUVECs. These results suggest that ONO-8711 may be a safer chemopreventive agent with respect to cardiovascular events.

Role for sphingosine kinase 1 in colon carcinogenesis.

Sphingosine kinase 1 (SphK1) phosphorylates sphingosine to form sphingosine-1-phosphate (S1P) and is a critical regulator of sphingolipid-mediated functions. Cell-based studies suggest a tumor-promoting function for the SphK1/S1P pathway. Also, our previous studies implicated the SphK1/S1P pathway in the induction of the arachidonic acid cascade, a major inflammatory pathway involved in colon carcinogenesis. Therefore, we investigated whether the SphK1/S1P pathway is necessary for mediating carcinogenesis in vivo. Here, we report that 89% (42/47) of human colon cancer samples stained positively for SphK1, whereas normal colon mucosa had negative or weak staining. Adenomas had higher expression of SphK1 vs. normal mucosa, and colon cancers with metastasis had higher expression of SphK1 than those without metastasis. In the azoxymethane (AOM) murine model of colon cancer, SphK1 and S1P were significantly elevated in colon cancer tissues compared to normal mucosa. Moreover, blood levels of S1P were higher in mice with colon cancers than in those without cancers. Notably, SphK1(-/-) mice subjected to AOM had significantly less aberrant crypt foci (ACF) formation and significantly reduced colon cancer development. These results are the first in vivo evidence that the SphK1/S1P pathway contributes to colon carcinogenesis and that inhibition of this pathway is a potential target for chemoprevention.

Regulation of T-cell function by endogenously produced angiotensin II.

The adaptive immune response and, in particular, T cells have been shown to be important in the genesis of hypertension. In the present study, we sought to determine how the interplay between ANG II, NADPH oxidase, and reactive oxygen species modulates T cell activation and ultimately causes hypertension. We determined that T cells express angiotensinogen, the angiotensin I-converting enzyme, and renin and produce physiological levels of ANG II. AT1 receptors were primarily expressed intracellularly, and endogenously produced ANG II increased T-cell activation, expression of tissue homing markers, and production of the cytokine TNF-alpha. Inhibition of T-cell ACE reduced TNF-alpha production, indicating endogenously produced ANG II has a regulatory role in this process. Studies with specific antagonists and T cells from AT1R and AT2R-deficient mice indicated that both receptor subtypes contribute to TNF-alpha production. We found that superoxide was a critical mediator of T-cell TNF-alpha production, as this was significantly inhibited by polyethylene glycol (PEG)-SOD, but not PEG-catalase. Thus, T cells contain an endogenous renin-angiotensin system that modulates T-cell function, NADPH oxidase activity, and production of superoxide that, in turn, modulates TNF-alpha production. These findings contribute to our understanding of how ANG II and T cells enhance inflammation in cardiovascular disease.