Biomedical subjects

Yaron Hamani

Publications and source records attributed to Yaron Hamani.

9 recordsLinked to original sources

PubMed2006

Decidual NK cells regulate key developmental processes at the human fetal-maternal interface.

Human CD56(bright) NK cells accumulate in the maternal decidua during pregnancy and are found in direct contact with fetal trophoblasts. Several mechanisms have been proposed to explain the inability of NK cells to kill the semiallogeneic fetal cells. However, the actual functions of decidual NK (dNK) cells during pregnancy are mostly unknown. Here we show that dNK cells, but not peripheral blood-derived NK subsets, regulate trophoblast invasion both in vitro and in vivo by production of the interleukin-8 and interferon-inducible protein-10 chemokines. Furthermore, dNK cells are potent secretors of an array of angiogenic factors and induce vascular growth in the decidua. Notably, such functions are regulated by specific interactions between dNK-activating and dNK-inhibitory receptors and their ligands, uniquely expressed at the fetal-maternal interface. The overall results support a 'peaceful' model for reproductive immunology, in which elements of innate immunity have been incorporated in a constructive manner to support reproductive tissue development.

Angiogenesis Inducing Agents↗

PubMed2005

Modified vulvar vestibulectomy: simple and effective surgery for the treatment of vulvar vestibulitis.

OBJECTIVE: To evaluate the success of a simple modified vestibulectomy in treating vulvar vestibulitis. STUDY DESIGN: Fifty-nine patients with vulvar vestibulitis refractory to nonsurgical treatment underwent modified vestibulectomy. Response was defined as return to normal coitus and was graded as complete, partial or non-responsive. RESULTS: The postoperative follow-up period was 6 months-10 years. Thirty-nine (73.6%) patients reported complete response, 7 (13.2%) had partial response, and 7 (13.2%) were non-responsive to surgery. CONCLUSION: Surgery is an effective treatment for vulvar vestibulitis refractory to conservative treatment. Simple modified vestibulectomy is considerably less invasive, technically simpler and probably less time consuming. Postoperative results employing this surgical procedure are found to be in line with postoperative results reported by others who employ surgical methods that are more extensive.

Adult↗

PubMed2005

Fibroblast growth factor-10 and fibroblast growth factor receptors 1-4: expression and peptide localization in human decidua and placenta.

The development of the chorionic villous tree into a complex and organized ramified tubular network can be termed branching morphogenesis. Studying the molecular mechanisms involved in this process may contribute to the understanding of pregnancy complications such as preeclampsia. We hypothesized that fibroblast growth factor-10 (FGF-10) and fibroblast growth factor receptors 1-4 (FGFR 1-4) are expressed in human decidual and placental tissues. We analyzed the expression of FGF-10 and FGFRs 1-4 in 1st, 2nd and 3rd trimester placentas, as well as in decidua. RT-PCR and immunohistochemistry were employed to study mRNA and protein expression. FGF-10 was expressed by decidual cells and by cytotrophoblasts of the cytotrophoblast columns during all three trimesters. FGFR 1-4 were expressed in the placenta but not in the decidua. Placental expression of FGFRs was temporally regulated: In 1st trimester placentas, FGFR 1-4 were expressed by Hofbauer cells, FGFR-1 and FGFR-4 were expressed in cytotrophoblast columns, and the latter was also expressed by syncytiotrophoblasts. Similar expression was seen in 2nd trimester placentas with additional expression of FGFR-1 in blood vessel walls. The expression of FGFR-1 and FGFR-4 in the 3rd trimester was comparable to that seen in the 2nd trimester. The expression of FGF-10, FGFR-1 and FGFR-4 in the maternal-fetal interphase suggests their role in decidual-trophoblast interaction. The abundance of FGFR expression in Hofbauer cells implies that mesenchymal-trophoblast interaction is important for regulation of villous development.

Decidua↗

PubMed2005

Growth factor receptor-protein bound 2 (GRB2) upregulation in the placenta in preeclampsia implies a possible role for ras signalling.

OBJECTIVES: To screen for genes with altered expression in placentas from pregnancies complicated by preeclampsia. STUDY DESIGN: To corroborate gene expression profile of preeclamptic and normal placentas (ATLAS Clontech), by dot blot, Northern blot analysis and RT-PCR for growth factor receptor bound-protein 2 (GRB2), using immunohistochemistry to localize its expression in the placenta. RESULTS: Increased expression of GRB2 upregulated in the microarrays was found in preeclampsia by Dot blot and Northern blot analysis. RT-PCR performed with primers specific for GRB2 and its alternatively spliced isoform GRB3-3 showed that most of the cDNA represented in the array was GRB2. The protein was localized to the smooth muscle wall of stem vessels by immunohistochemistry. CONCLUSION: The ras signalling activated by placental receptor tyrosine kinases may play a role in the segmental thickening of the stem vascular wall in preeclamptic placentas, resulting in reduced blood flow to the developing fetus.

Adaptor Proteins, Signal Transducing↗

PubMed2005

The significance of intrauterine lesions detected by ultrasound in asymptomatic postmenopausal patients.

A retrospective study on 82 women with an incidental sonographic finding suspected to be intrauterine polyps was undertaken to assess the histopathologic characteristics of such polyps utilising operative hysteroscopy. Endometrial polyps were found in 68 patients, submucousal myomas in 7, atrophic endometrium in 6 and thickened proliferative endometrium was found in 1 patient. Simple hyperplasia was found in one polyp but neither endometrial carcinoma nor complex hyperplasia was found. The total complication rate was 3.6%. It appears that the risk of endometrial carcinoma in postmenopausal women with asymptomatic endometrial polyps is low, although a larger series is required to confirm this finding.

Aged↗

PubMed2004

Fetal inherited thrombophilias influence the severity of preeclampsia, IUGR and placental abruption.

OBJECTIVE: To determine whether common inherited thrombophilias in the fetus influence the severity of severe preeclampsia, IUGR and placental abruption. DESIGN: A case-control study among patients with complicated pregnancies. Cases were defined as fetuses with thrombophilia. SETTING: A university hospital with 3700 deliveries per year. POPULATION: Seventy cases with severe preeclampsia, IUGR or placental abruption. METHODS: Mothers and neonates were tested for mutation of factor V Leiden, prothrombin gene and methylenetetrahydrofolate reductase. MAIN OUTCOME MEASURES: Gestational age at delivery, birth weight and early neonatal complications. RESULTS: Gestational age at delivery and birth weight were significantly lower in fetuses with factor V Leiden or prothrombin gene mutation compared to control fetuses. CONCLUSIONS: Fetal factor V Leiden mutation and prothrombin gene mutation may influence the course of severe preeclampsia, IUGR and placental abruption. These thrombophilic changes may cause an earlier appearance or lead to a late pregnancy complication of a greater severity.

Abruptio Placentae↗

PubMed2004

Placental pathology in fetal thrombophilia.

The aim of this study was to test the hypothesis that placental vascular lesions of the fetal circulation are caused by fetal thrombophilic mutations. The study included 64 newborns of women with one or more of the following pregnancy complications: preeclampsia, placental abruption, and intrauterine growth restriction. The most prevalent inherited thrombophilias--factor V Leiden, factor II (prothrombin) G20210A, and homozygosity for methyltetrahydrofolate reductase C677T--were examined in maternal blood and fetal umbilical cord blood. One pathologist reviewed all of the slides for fetal vascular lesions. Associations between fetal thrombotic vasculopathy and fetal thrombophilia were tested for using Fisher's exact test; Z scores and gestational age were compared using the Student t-test. Fetal thrombophilic mutations were diagnosed in 19 of 64 newborns, 15 of whom had coexistent maternal thrombophilia. There was no statistical difference in the prevalence of thrombotic lesions of the fetal circulation between newborns with and without thrombophilia. The combination of maternal and fetal thrombophilia was also not associated with increased fetal vascular lesions. The results indicate that fetal thrombophilia alone, even in the context of maternal underperfusion, is not associated with fetal vascular lesions of the placenta, although it may represent an underlying risk factor for lesions triggered by other process(es).

Female↗

PubMed2003

[Prenatal diagnosis of developmental congenital malformations--the limitations of ultrasound scanning].

Prenatal diagnosis of congenital malformations is a major goal of obstetric sonography. Although significant progress has been made in the ability to detect fetal anomalies by ultrasound, some fetal anomalies cannot be detected during second trimester routine ultrasound scanning. Among the "undiagnosed anomalies" are many fetal anomalies that follow a developmental course in-utero and have a late-onset sonographic appearance, and hence cannot be diagnosed early in pregnancy or during the traditional mid-second trimester scan. Several mechanisms cause in-utero development of fetal malformations, and the developmental course of each fetal anomaly depends on the cause, mechanism, extent and timing of the insult. In some cases the destructive or disruptive event might occur at a relatively advanced gestational age and thus go undiagnosed. Some malformations are the result of an early insult but are manifested and detected late, while others have a "late onset". This concept of the developmental natural course of fetal anomalies in-utero, must be recognized and lead to a new nomenclature for fetal malformations. In this review we describe some developmental fetal malformations and discuss the clinical, diagnostic and medicolegal implications.

Congenital Abnormalities↗

PubMed2002

[Fallopian tube prolapse after hysterectomy].

Fallopian tube prolapse is a rare complication of hysterectomy, characterized by vaginal discharge, abdominal pain, pelvic inflammatory disease and vaginal bleeding. The diagnosis is often delayed, and is usually done after an histopathological examination identifies fallopian tube on biopsy. The advised treatment is surgical resection, which can be done through vaginal incision, abdominally or by laparoscopy. We report a case of fallopian tube prolapse after vaginal hysterectomy in 47-year-old patient in whom the prolapsed-tube was successfully resected vaginally, and review the presentation and surgical methods to correct this rare complication.

Fallopian Tube Diseases↗