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Biomedical subjects

A Arici

Publications and source records attributed to A Arici.

At least 19 recordsLinked to original sources
PubMed2006

Long-term pituitary down-regulation before in vitro fertilization (IVF) for women with endometriosis.

BACKGROUND: Women with endometriosis who are treated with in vitro fertilization (IVF) or intracytoplasmic sperm injection (ICSI) have a lower pregnancy rate compared to women with tubal factor infertility. It has been suggested that the administration of gonadotrophin releasing hormone (GnRH) agonists for a few months prior to IVF or ICSI increases the pregnancy rate. OBJECTIVES: To determine the effectiveness of administering GnRH agonists for three to six months prior to IVF or ICSI in women with endometriosis. SEARCH STRATEGY: We used computer searches of the Cochrane Central Register of Controlled Trials (CENTRAL), MEDLINE, EMBASE, the National Research Register (NRR) and the MDSG Specialised Register of controlled trials. We handsearched proceedings of annual meetings of the American Society for Reproductive Medicine (ASRM) and the European Society for Human Reproduction and Embryology (ESHRE). We reviewed lists of references in original research and review articles. We contacted experts in various countries to identify unpublished trials. SELECTION CRITERIA: We included randomised controlled trials using any GnRH agonist prior to IVF or ICSI to treat women with any degree of endometriosis diagnosed by laparoscopy or laparotomy DATA COLLECTION AND ANALYSIS: Two independent review authors abstracted data (HNS and JGV). We sent e-mails to investigators to seek additional information. We assessed the validity of each study using the methods suggested in the Cochrane Handbook. The data were checked by the third review author (SD) and any disagreement was resolved by arbitration with the fourth review author (AA). We generated 2 x 2 tables for principal outcome measures. The Peto-modified Mantel-Haenszel technique was used to calculate odds ratios (OR) and assess statistical heterogeneity between studies. MAIN RESULTS: Three randomised controlled trials (with 165 women) were included. The live birth rate per woman was significantly higher in women receiving the GnRH agonist compared to the control group (OR 9.19, 95% CI 1.08 to 78.22). However, this was based on one trial reporting "viable pregnancy" only. The clinical pregnancy rate per woman was also significantly higher (three studies: OR 4.28, 95% CI 2.00 to 9.15). The information on miscarriage rates came from two trials with high heterogeneity and, therefore, results of the meta-analysis were doubtful. The included studies provided insufficient data to investigate the effects of administration of GnRH agonists on multiple or ectopic pregnancies, fetal abnormalities or other complications. AUTHORS' CONCLUSIONS: The administration of GnRH agonists for a period of three to six months prior to IVF or ICSI in women with endometriosis increases the odds of clinical pregnancy by fourfold. Data regarding adverse effects of this therapy on the mother or fetus are not available at present.

Drug Administration Schedule↗
PubMed2005

Immunology of endometriosis.

Endometriosis is classically described as the presence of both endometrial glandular and stromal cells outside the uterine cavity, mainly in the pelvis. The pathogenesis of this enigmatic disorder still remains controversial despite extensive research. Although multiple theories have been put forth to explain the pathophysiology and pathogenesis of endometriosis, the retrograde menstruation theory of Sampson is the most widely accepted. However, since retrograde menstruation occurs in most of the reproductive age women, it is clear that there must be other factors which may contribute to the implantation of endometrial cells and their subsequent development into endometriotic disease. There is substantial evidence to support that the alterations in both cell-mediated and humoral immunity contribute to the pathogenesis of endometriosis. Increased number and activation of peritoneal macrophages, decreased T cell and natural killer (NK) cell cytotoxicities are the alterations in cellular immunity and result in inadequate removal of ectopic endometrial cells from the peritoneal cavity. Moreover, increased levels of several cytokines and growth factors which are secreted by either immune and endometrial cells seem to promote implantation and growth of ectopic endometrium by inducing proliferation and angiogenesis. In addition to the impaired capacity of the immune cells to mediate endometrial cell removal, inherent resistance of the ectopic endometrial cells against immune cells is another interesting concept in the pathogenesis of endometriosis. Endometriosis has also been considered to be an autoimmune disease, since it is often associated with the presence of autoantibodies, other autoimmune diseases, and possibly with recurrent immune-mediated abortion.

Autoantibodies↗
PubMed2004

Regulation of Fas ligand expression by vascular endothelial growth factor in endometrial stromal cells in vitro.

When Fas ligand (FasL) interacts with the Fas receptor, it induces apoptosis through autocrine and/or paracrine signalling. Vascular endothelial growth factor (VEGF) is a potent mitogenic cytokine. VEGF plays a role during remodelling of the endometrium following menstruation. We hypothesized that, by regulating FasL expression, VEGF may play a role in endometrial stromal cell survival by decreasing autocrine apoptotic signalling. We aimed to determine the expression of FasL in cultured endometrial stromal cells and its modulation by VEGF. VEGF induced a decrease in both FasL-positive cell number and FasL intensity as determined by immunocytochemistry and western blot respectively (P < 0.05). These effects of VEGF were observed in a concentration-dependent manner (10-42%; P < 0.05). Anti-VEGF neutralizing antibody alone resulted in an increase in the FasL expression. When combined with VEGF, anti-VEGF reversed the VEGF-induced decrease in FasL level up to 100% (P < 0.05). In addition, western blot analysis showed that FasL expression in endometrial stromal cells demonstrated a cyclic change every 12 h during 48 h of incubation. These results suggest that down-regulation of FasL by VEGF may affect endometrial stromal cell survival in an autocrine or paracrine manner. The decrease in FasL level may be due to a stimulation of its degradation. Our results show that FasL in endometrial stromal cells in culture has a cyclic expression model, suggesting that there may be a regulation at the translation level.

Adult↗
PubMed2004

Endocrine-immune interactions in human endometrium.

The immune system is a complex entity designed to eliminate foreign intruding antigens and is influenced by and, in turn, influences the function of the reproductive system. Despite the widespread associations between immunology and reproductive medicine, the study of system interactions remains in its infancy. Many diverse facts are accumulating, and pieces of the puzzle are becoming available to provide a clearer picture. In this review article, we focus on the interactions between endocrine and immune systems in the human endometrium. Understanding the molecular pathways in endocrine-immune interactions in the human endometrium is crucial to understand events such as menstrual bleeding, tissue repair and regeneration, inflammation, angiogenesis, blastocyst implantation, and progression of pregnancy. These events require a balanced regulation of endometrial differentiation, proliferation, cell survival, leukocyte recruitment, apoptosis, and angiogenesis by sex steroids. In this review, we first outline the role of survival factors such as phosphoinositol 3-kinase/protein kinase B, PTEN, NFkappaB, and apoptotic molecules (Fas-FasL, Bcl-2). We then discuss their regulation by estrogen and progesterone in the endometrium. We present evidence for direct and/or indirect roles of steroid hormones on the expression of chemotactic cytokines (interleukin-8 and monocyte chemotactic protein-1) and on the survival versus apoptosis of resident endometrial cells (stromal, epithelial, and endothelial cells) and nonresident cells (leukocytes).

Endocrine System↗
PubMed2003

The effect of oral versus vaginal misoprostol on cervical dilatation in first-trimester abortion: a double-blind, randomized study.

OBJECTIVES: To determine the effect of oral versus vaginal misoprostol on cervical dilatation in first-trimester intrauterine evacuation or menstrual regulation (MR). DESIGN AND METHODS: A total of 120 patients were randomly assigned to a double-blind prestudy. Four groups, each consisting of 30 cases, were administered one of four regimens: 200 microg misoprostol orally, 200 microg misoprostol intravaginally, placebo orally, or placebo intravaginally, 10 h before MR, respectively. Age, number of births and abortions, birth methods, date of last delivery and last abortion were recorded. The gestational age was determined by ultrasonography. Prior to MR, data regarding the time of the application of the drug, the presence of placenta in the cervical canal, the degree of cervical dilatation, the duration of MR and patients' complaints were recorded. The MRs were performed by the same physician. The statistical analyses were evaluated with the chi(2) test and Fisher's exact test in the Aegean University Science Faculty Department of Statistics. RESULTS: In the oral misoprostol group, four patients had cervical bleeding and one had intracervical placenta. In the intravaginal misoprostol group, cervical bleeding was observed in seven patients and intracervical placenta was recorded in four cases. Cervical bleeding was observed in one case and intracervical placenta was also observed in one case in the oral placebo group. Cervical dilatation reached 8 mm in seven patients in the oral misoprostol group and in three patients in the intravaginal group, with none in the placebo group. Symptoms such as pelvic pain, headache and nausea were observed in 11 cases in the oral and 14 cases in the vaginal misoprostol groups. CONCLUSIONS: Different methods of misoprostol administration may not be equivalent in terms of efficacy and side-effects. Therefore, we decided to extend the study to include more patients so as to achieve statistically significant results.

Abortifacient Agents, Nonsteroidal↗
PubMed2001

Diagnosis and laparoscopic management of a fallopian tube torsion following Irving tubal sterilization: a case report.

Tubal torsion is a very rare but serious clinical entity. Its occurrence has been reported following Pomeroy tubal ligation and laparoscopic tubal cauterization. The following case report will be the first one describing a tubal torsion after an Irving tubal ligation in a patient who also had a history of pelvic inflammatory disease (PID). This study includes the presentation of a case of tubal torsion that is diagnosed and managed laparoscopically and the review of the literature through a computerized search of MEDLINE for relevant cases in the English literature published between January 1966 and July 1999. The patient is a 26-year-old woman with a history of PID and Irving tubal ligation. She presented with a second episode of acute right lower quadrant pain. The patient underwent a diagnostic laparoscopy and was found to have a 6 x 5 cm hemorrhagic and necrotic fallopian tube consistent with torsion of the right tube. A right salipingectomy was done laparoscopically. Combination of PID and tubal sterilization in the medical history of a patient presenting with acute or intermittent pelvic pain may suggest tubal torsion.

Adult↗
PubMed2001

Expression of aminopeptidase N in human endometrium and regulation of its activity by estrogen.

OBJECTIVES: To determine whether aminopeptidase N (APN) regulates the cycle-dependent bioavailability of interleukin-8 (IL-8) in the endometrium. DESIGN: Prospective study. SETTING: University medical center. PATIENT(S): Women without endometrial pathology from the proliferative (n = 25) or secretory (n = 18) phase of the menstrual cycle. INTERVENTION(S): We first immunolocalized APN in the endometrium using an anti-APN antibody. We then determined the regulation of APN kinetic activity by sex steroids in endometrial stromal cell cultures. MAIN OUTCOME MEASURE(S): Expression of APN in human endometrium throughout the menstrual cycle. Regulation of APN activity by estradiol and progesterone in cultured endometrial stromal cells. RESULT(S): Immunohistochemistry of endometrial sections revealed staining of endometrial stroma throughout the menstrual cycle. There was no detectable staining in glandular cells. The expression of APN as detected by immunohistochemistry was significantly lower in the early proliferative phase. In cultured cells, estradiol inhibited APN activity in a concentration-dependent manner. Progesterone did not have a significant effect. CONCLUSION(S): Stromal localization of APN in endometrium may explain the epithelial rather than stromal presence of IL-8 in vivo. Decreased expression of APN may increase IL-8 bioavailability thus contributing to angiogenesis and polymorphonuclear leukocyte chemotaxis in early proliferative phase.

CD13 Antigens↗
PubMed2001

Effect of gonadotropin-releasing hormone agonists on monocyte chemotactic protein-1 production and macrophage infiltration in leiomyomatous uterus.

OBJECTIVE: The level of monocyte chemotactic protein-1 (MCP-1), a potent chemoattractant for monocytes, is fivefold higher in myometrium than in leiomyoma. We have previously shown that myometrium from women using GnRH agonists (GnRH-a) express the highest levels of MCP-1, which has antiproliferative effects on leiomyoma cells. We hypothesized that MCP-1 may have a direct paracrine effect in leiomyomatous uterus rather than acting by way of chemoattraction of macrophages. DESIGN: Cross-sectional study. SETTING: University medical center. PATIENT(S): Women with leiomyoma (n = 32). INTERVENTION(S): Immunohistochemical analysis performed in the myometrium and leiomyoma of women receiving (n = 11) and not receiving (n = 21) GnRH-a treatment. MAIN OUTCOME MEASURE(S): The MCP-1 levels and macrophage counts determined by immunohistochemistry in the myometrium and leiomyoma of women receiving GnRH-a were compared to the levels and counts in women not receiving GnRH-a. RESULT(S): Samples from all 11 patients using GnRH-a revealed strong MCP-1 staining, whereas staining was only weakly present in 11 and absent in 10 samples from patients not receiving GnRH-a, revealing a significant difference in MCP-1 expression between GnRH-a users versus nonusers (P=.006). The number of tissue macrophages between GnRH-a users and nonusers was not significantly different. CONCLUSION(S): We found that there is an increase in the MCP-1 protein expression in the myometrium of women receiving GnRH-a treatment. On the other hand, we have not observed a difference in the macrophage count and distribution with GnRH-a treatment, suggesting a potentially direct antiproliferative role for MCP-1 rather than acting by means of chemoattraction of macrophages.

Cell Count↗
PubMed2001

Interleukin 8 production and interleukin 8 receptor expression in human myometrium and leiomyoma.

OBJECTIVE: Interleukin 8 is a potent chemoattractant cytokine that is expressed in a variety of human tumors and is known to induce mitogenesis. We aimed to investigate the production of interleukin 8 and the expression of its receptor in myometrium and leiomyoma, in which we hypothesized that interleukin 8 may contribute to cellular proliferation. STUDY DESIGN: Myometrial and leiomyoma tissue pairs (n = 14) were obtained from human uteri after hysterectomy conducted for leiomyomatous uterus. Expression of interleukin 8 and interleukin 8 receptor type A was identified in the leiomyomatous myometrium by means of specific antibodies directed against interleukin 8 and interleukin 8 receptor type A for immunohistochemical detection. Interleukin 8 production by cultured cells was measured by enzyme-linked immunosorbent assay. The regulation of interleukin 8 messenger ribonucleic acid expression was assessed by means of the Northern blot analysis after treatment of myometrial cells with interleukin 1alpha and tumor necrosis factor alpha. Myometrial cell proliferation was determined by means of colorimetric assay after cells were treated with interleukin 8 and antihuman interleukin 8 neutralizing antibody. RESULTS: Immunostaining for both interleukin 8 and interleukin 8 receptor type A was stronger in the myometrium adjacent to leiomyoma compared with leiomyoma itself (2-fold, P <.05). Compared with samples from nonusers, samples from patients who had used gonadotropin-releasing hormone agonists revealed a trend for decreased staining for both interleukin 8 and interleukin 8 receptor type A. Interleukin 1alpha and tumor necrosis factor alpha caused a time- and dose-dependent increase in interleukin 8 production by myometrial cells (P <.001). There was a dose-dependent inhibition of cell proliferation with antihuman interleukin 8 antibody to 55% of the control (P <.001). CONCLUSION: Our demonstration of high levels of interleukin 8 and its receptor in myometrium immediately surrounding leiomyoma and the inhibition of cell proliferation when interleukin 8 is blocked by a neutralizing antibody suggest a potential role for interleukin 8 in the growth of myometrial tissue surrounding leiomyomatous tissue. This study could lead to a better understanding of potential involvement of cytokines in leiomyoma growth and in gonadatropin-releasing hormone agonist-induced regression.

Blotting, Northern↗
PubMed2001

Regulation of Fas ligand expression by estradiol and progesterone in human endometrium.

Implantation involves a complex set of events, including apoptosis in endometrial cells. Apoptosis in human endometrium coincides with the implantation window, suggesting a potential role for steroid hormones in its regulation. Fas ligand (FasL) is one of the mediators of apoptosis in differentiated cells and in embryonic development. Interaction of FasL with its receptor, Fas, induces apoptosis through autocrine and paracrine signaling. We hypothesized that FasL expression in human endometrium is cycle-dependent and that sex steroid hormones regulate FasL expression. We first studied menstrual cycle-dependent expression of FasL in human endometrium by immunohistochemistry in 24 samples. We then investigated the in vitro regulation of FasL expression by ovarian steroid hormones. Throughout the menstrual cycle immunohistochemical staining intensity was stronger in the functional layer of endometrium than it was in the basal layer. FasL immunoreactivity increased gradually through the mid- and late-proliferative phases in both endometrial stromal and glandular cells. Strong FasL expression was observed throughout the late-proliferative and secretory phases. Semiquantitative reverse transcription-polymerase chain reaction analysis in cultured endometrial glandular cells demonstrated that estradiol and progesterone stimulate FasL mRNA expression. Western blot analysis in endometrial glandular and stromal cells in culture revealed that estradiol alone and in combination with progesterone up-regulated FasL protein expression. These results suggest that estradiol and progesterone may have a role in the regulation of maternal immunotolerance for the implantation of a semiallograft embryo by inducing FasL expression. We speculate that increased FasL expression may mediate the apoptosis of endometrial cells and thus may play a role in trophoblast invasion.

Adult↗
PubMed2001

Endometriosis and assisted reproductive technologies: are outcomes affected?

The preponderance of recent data suggests that endometriosis does not adversely affect in-vitro fertilization pregnancy rates. However, many studies demonstrate impaired oocyte quality, decreased fertilization, and compromised implantation rates. Such findings give insight into the mechanisms by which endometriosis may impact on fertility, and provide clues as how to focus assisted reproductive technologies in order to overcome these deficiencies. Specifically, extended downregulation protocols, ample use of gonadotropins for ovarian stimulation, and conservative management of endometriomas have all been suggested as means to optimize in-vitro fertilization outcomes for women with endometriosis.

Endometriosis↗
PubMed2001

Interleukin-8 in the human fallopian tube.

The human fallopian tube is a dynamic structure that undergoes cyclic variation in its functional epithelium. This epithelium contains both secretory and ciliated cells. The mechanisms regulating the growth and function of the tubal epithelium are not fully understood. Interleukin-8 (IL-8) is one potential local regulatory factor. We therefore characterized the IL-8 system, which includes IL-8, its receptors A and B, and its degradative enzyme aminopeptidase N, in the human fallopian tube by immunohistochemistry. Immunohistochemistry was performed on isthmic, ampullary, and fimbrial fallopian tubal segments obtained from women undergoing gynecological surgical procedures for benign conditions (n = 52). IL-8 was found in the human fallopian tube predominantly in the epithelial cells. It was present in greater amounts in the distal compared with the proximal tube. IL-8 receptors A and B localized in the tube in similar patterns. The degradative enzyme aminopeptidase N is found in tubal stromal tissue at the epithelial stromal border and perivascularly and may limit the systemic effects of epithelial IL-8. The IL-8 system seems to be an active component of tubal physiology.

CD13 Antigens↗
PubMed2000

Transforming growth factor-beta3 is expressed at high levels in leiomyoma where it stimulates fibronectin expression and cell proliferation.

OBJECTIVE: To investigate the expression of TGF-beta3 in leiomyoma and myometrium as well as the effect of TGF-beta3 on the expression of fibronectin and on the proliferation of leiomyoma and myometrial cells. DESIGN: Observational and in vitro experimental study. SETTING: University medical center. PATIENT(S): Women with (n = 18) leiomyoma. INTERVENTION(S): First TGF-beta3 mRNA and protein levels in myometrium and leiomyoma were measured, and then myometrial and leiomyoma cells in culture were treated with TGF-beta3. MAIN OUTCOME MEASURE(S): TGF-beta3 and fibronectin mRNA were evaluated by Northern analysis. Myometrial and leiomyoma cell proliferation was assessed with use of [(3)H]thymidine incorporation. RESULT(S): The TGF-beta3 mRNA level in the leiomyoma samples was 3.5-fold higher than in the myometrial samples. The highest TGF-beta3 mRNA level was observed in leiomyoma samples from midsecretory phase and was 5-fold higher than in proliferative phase samples. Fibronectin mRNA expression also was higher in the leiomyoma than in the myometrium. TGF-beta3 induced fibronectin expression in leiomyoma cells and directly stimulated myometrial and leiomyoma cell proliferation in cultures. CONCLUSION(S): These findings suggest that TGF-beta3 may be mediating the growth-promoting effects of sex steroids on leiomyomas by playing a role in the fibrogenic process and cell proliferation that characterize these tumors.

Cell Division↗
PubMed2000

Empty follicle syndrome: evidence for recurrence.

The empty follicle syndrome (EFS) is a frustrating condition in which no oocytes are retrieved in an IVF cycle. Although this is an infrequent event in IVF patients, the economic consequences as well as the emotional frustration of a cancelled cycle due to the inability to obtain oocytes are enormous. The mechanisms responsible for EFS remain obscure, though many hypotheses have been put forward ranging from dysfunctional folliculogenesis to a drug-related problem. We found that the EFS is a rare event (1.8% of oocyte retrievals) but with profound implications for counselling the couple about their future reproductive performance. The chances of recurrence of EFS increase with the age of the patient (24% recurrence rate for the 35-39 year age group, and 57% for those over 40 years). We postulate that ovarian ageing, through altered folliculogenesis, may be implicated in the aetiology of EFS and its recurrence.

Adult↗
PubMed2000

Hyperinsulinism and its interaction with hyperandrogenism in polycystic ovary syndrome.

Polycystic ovary syndrome (PCOS) is the most common endocrine disorder in women of reproductive age. It has become increasingly evident that insulin resistance plays a significant role both as a cause and result of the syndrome. The purpose of this review is to summarize the possible mechanisms leading to insulin resistance and resultant hyperinsulinism (HI) and their interaction with hyperandrogenism (HA) in PCOS. We conducted a computerized search of MEDLINE for relevant studies in the English literature published between January 1966 and January 2000. We reviewed all studies that investigated the roles of insulin, insulin receptor, and insulin gene in insulin resistance and its interaction with hyperandrogenism in PCOS. Insulin resistance in PCOS seems to involve a postbinding defect in the insulin receptor and/or in the receptor signal transduction. Current research has focused on identifying a genetic predisposition for insulin resistance in this syndrome. The answer to the question whether HI or HA is the initiating event is still unclear inasmuch as there are clinical and molecular evidences to support both of these approaches. Our view is that whichever is the triggering insult, a vicious cycle is established where HI acts to aggravate HA and vice versa. In this model, obesity and genetic predisposition seem to be the independent factors that can give rise or contribute to HI, HA, or both simultaneously. It seems that "hyperinsulinemic hyperandrogenism" represents a significant subgroup of PCOS, which probably needs to be renamed and reclassified in the light of this new approach.

Animals↗