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Biomedical subjects

S Yagel

Publications and source records attributed to S Yagel.

At least 73 records · Page 4Linked to original sources
PubMed1998

Superior mesenteric artery blood flow velocimetry: cross-sectional Doppler sonographic study in normal fetuses.

Our objectives were to describe the flow velocity waveform of the fetal superior mesenteric artery and to establish a nomogram for its pulsatility index. In a cross-sectional study using color Doppler ultrasonography, superior mesenteric artery flow velocimetry was investigated prospectively in 96 healthy fetuses of between 14 and 37 weeks of gestation. In normal fetuses the pulsatility index measurements showed a slight but insignificant increase over the course of gestation (r = 0.26; P > 0.5). The lowest mean +/- standard deviation for pulsatility index in the superior mesenteric artery was 1.86 +/- 0.45 (95% confidence interval 1.67-2.06), recorded between 18 and 21 weeks' gestation. Thereafter the pulsatility index increased to 1.94 +/- 6.4 (95% confidence interval 1.74-2.8) at 22 to 25 weeks, and from weeks 26 to 29 it increased to 2.18 +/- 0.52 (95% confidence interval 1.91-2.46). During the third trimester and at term, the mean pulsatility index of 2.23 +/- 0.32 (95% confidence interval 1.43-3.03) did not change significantly with gestational age. In normal fetuses, except for the early stages, a relatively stable vascular resistance of the intestinal circulation was found. The application of this nomogram in clinical practice may facilitate evaluation of intestinal perfusion in compromised fetuses with blood flow centralization.

Adult↗
PubMed1997

Interleukin-1 beta inhibits progesterone accumulation in rat corpora luteal cell cultures in a mechanism dissociated from its effects on nitric oxide and prostaglandin E accumulation.

The objective of this study was to examine the effect of interleukin-1 beta (IL-1) on progesterone (P) biosynthesis and the potential intermediary involvement of prostaglandin (PG) E and nitric oxide (NO) in P accumulation in PMSG/hCG-primed rat corpora luteal (CL) cell cultures. Exposure of primed CL cells to IL-1 (10 ng/ml) for 48 h resulted in a 65-86% reduction (P < 0.01) in P accumulation concurrent with a 2-3.4-fold increase in PGE content, a 70% increase in PGF2 alpha content and a 1.9-3.3-fold increase in nitrite generation. These effects were abolished by the IL-1 receptor antagonist, suggesting specific IL-1 receptor-mediated effects. Indomethacin, a cyclooxygenase inhibitor, abolished PGE and PGF2 alpha production and attenuated the basal (but not IL-1-stimulated) accumulation of P. N(G)-Nitro-L-arginine (NNLA), a competitive inhibitor of nitrite synthesis, slightly reduced basal P accumulation but had no effect on IL-1-induced suppression of P accumulation. NNLA reduced basal PGE accumulation and IL-1-stimulated PGE accumulation (55 and 61%, respectively). Transforming growth factor beta 1 (TGF-beta 1; 10 ng/ml) significantly attenuated the IL-1-stimulated PGE and NO production (61 and 42%, respectively), but did not affect the ability of IL-1 to suppress P accumulation. Thus, NO, PGF2 alpha and PGE are not obligatory intermediaries of IL-1-mediated suppression of P accumulation in rat CL, but are involved in basal P biosynthesis and NO seems to have a regulatory role in the biosynthesis of PGE. The present observations suggest a pleiotropic response of PMSG/hCG-primed CL cells to IL-1, characterized by an independent suppression of P accumulation and a concomitant increase in NO, PGF2 alpha and PGE generation. Since IL-1 attenuates P accumulation, these findings may imply a direct autocrine/paracrine function for IL-1 in the maintenance or the demise of rat CL.

Animals↗
PubMed1997

Congenital heart defects: natural course and in utero development.

BACKGROUND: Most congenital heart defects (CHDs) are diagnosed on targeted prenatal transvaginal (TVS) or transabdominal (TAS) ultrasonography during the early second trimester or at midgestation. Nevertheless, delayed diagnosis in some cardiac malformations still remains despite detailed echocardiographic examination. The present study was conducted to evaluate the evolution of fetal cardiac anomalies and assess their development in utero. METHODS AND RESULTS: We retrospectively reviewed 22,050 pregnant women who were divided into two groups: 6924 who had initial TVSs at 13 to 16 weeks' gestation, followed by TASs at 20 to 22 weeks, and 15,126 who had initial TASs at 20 to 22 weeks. Both groups were subsequently examined in their third trimester. All newborns were examined by certified pediatricians. CHD was diagnosed in 168 babies: 66 in group A and 102 in group B. In group A, 42 malformations (64%) were detected at the first TVS examination, and 11 (17%) were found during the subsequent TAS. Three additional anomalies (4%) were found during the third trimester, and 10 malformations (15%) were detected postnatally. In group B, 80 malformations (78%) were detected in the initial examination at midtrimester, and an additional 7 (7%) were found in the third trimester, whereas 15 (15%) were diagnosed postnatally. The 10 anomalies (group A, n=3; group B, n=7) that were detected only during the third trimester comprised aortic stenosis (n=2), cardiac rhabdomyoma (n=2), subaortic stenosis (n=1), tetralogy of Fallot (n= 1), aortic coarctation (n=1), sealed foramen ovale (n=1), ventricular septal defects (n=1), and hypertrophic cardiomyopathy (n=1). CONCLUSIONS: Although most fetal cardiac anomalies are detectable early in gestation, some may evolve in utero at different stages of pregnancy.

Adolescent↗
PubMed1997

Trisomy 2: confined placental mosaicism in a fetus with intrauterine growth retardation.

In a pregnancy that was monitored due to increased risk for Down syndrome in the triple test, a normal karyotype was found in amniocentesis. Follow-up by serial ultrasound examinations revealed intrauterine growth retardation (IUGR) at 20 weeks of gestation. The parents decided to terminate the pregnancy and the karyotype of the placental fibroblasts was 47,XX,+2. Analysis of polymorphic markers of chromosome 2 demonstrated (a) that trisomy 2 was confined to the placenta (CPM), (b) that the trisomy 2 cell line was a result of a meiotic I error of paternal origin, and (c) that the fetal tissues with a normal karyotype were biparental disomy 2.

Adult↗
PubMed1997

Cerebral lateral ventricular asymmetry: is this a normal ultrasonographic finding in the fetal brain?

OBJECTIVE: To evaluate the clinical significance of in utero detection of fetal cerebral lateral ventricular asymmetry. METHODS: We used high resolution ultrasonography to study asymmetries of the fetal lateral ventricles in the human brain. A retrospective survey was conducted on 7200 pregnant women who presented at two large district hospitals in Israel. Only fetuses with a difference of greater than 2.4 mm (two standard deviations) in the width of the lateral ventricles, with no known brain pathology, were included in the study. Index cases were evaluated regarding maternal complications, prenatal ultrasound examinations, postnatal imaging studies, and neonatal outcome up to 6 months of age. RESULTS: Lateral ventricular asymmetry was found in 21 subjects, all with available clinical data. In 15 fetuses (71%), the body or the occipital horn of the left lateral ventricle was larger than the right, whereas in six fetuses (29%), the right was larger than the left. In four cases (20%), serial scans noted resolution of asymmetry; in 15 (75%), it was persistent; and in one (5%), asymmetry increased. In one case, termination of pregnancy was performed; however, pathologic examination of the fetal brain failed to detect any structural abnormality. Underlying cerebral pathology was later found only in three fetuses (14%); one had subclinical cytomegalovirus ventriculitis, one had insidious periventricular hemorrhage, and in one fetus with increased asymmetry, trisomy 21 was verified. All the remaining 17 cases had normal neurologic development. CONCLUSIONS: Some degree of asymmetry of the lateral ventricles exists in the human fetal brain and is detectable in utero. Lateral ventricular asymmetry alone is probably not clinically significant, and it may be considered as a normal variant, rather than a pathologic finding.

Adult↗
PubMed1997

Prenatal diagnosis of fetal primary cytomegalovirus infection.

OBJECTIVE: To evaluate the validity of prenatal diagnosis work-up for congenital cytomegalovirus (CMV) in women with primary infection. METHODS: Sixty-three pregnant women with primary cytomegalovirus disease (including two with twin pregnancies), referred to three tertiary perinatal centers over 4 years, underwent evaluation for congenital cytomegalovirus. Fetal diagnosis was made after 21 weeks' gestation by amniocentesis and fetal blood sampling (40 subjects), or amniocentesis only (23 subjects). RESULTS: Twenty-two (35%) pregnancies showed evidence of vertical transmission: 13 of them underwent funipuncture, but only ten (77%) of the 13 showed positive immunoglobulin (Ig)-M results in fetal blood. No cases of positive fetal serum Ig-M with negative amniotic fluid culture or polymerase chain reaction were observed. In nine (41%) of the 22 pregnancies with evidence of vertical transmission, abnormal ultrasonographic findings were recorded. Six (27%) women with evidence of vertical transmission continued their pregnancies and in only one (with prenatal ultrasonographic abnormalities) was an infant born with neurologic sequelae. In 41 (65%) pregnancies, no evidence of vertical transmission was found, and 37 continued to term. Only one newborn from this subgroup subsequently showed mild motor disability during a median of 23 months of follow-up. CONCLUSION: Among pregnant patients with primary CMV infection, analysis of amniotic fluid detected all of the infected fetuses. Thus, this is a reliable tool for counseling pregnant women with primary infection. This may guide the patient as to whether or not pregnancy can be continued with a high level of confidence.

Amniocentesis↗
PubMed1997

Prenatal ultrasonographic diagnosis of fetal heart echogenic foci: no correlation with Down syndrome.

OBJECTIVE: To determine whether karyotype is indicated when fetal heart echogenic foci are encountered on prenatal sonogram. METHODS: Pregnant women who presented at two large district hospitals in Israel that treat 7200 gravidas per year, and in whom fetal heart echogenic foci were diagnosed, were studied prospectively. Identified cases had detailed prenatal and postnatal echocardiographic examinations, and pregnancy outcome was assessed. RESULTS: During 18 months, 2214 low-risk pregnant women were examined sonographically, and 163 (7.4%) cases of fetal heart echogenic foci were detected at the first transvaginal sonography at 13-16 weeks' gestation. On a repeat scan at 20-22 weeks' gestation, 59.5% of the foci could not be identified, leaving only 66 (3%) cases for postnatal evaluation. Left ventricle-right ventricle ratio for location of the fetal heart echogenic foci was 3:1; 4.9% of all cases had bilateral findings. The karyotypes of 16 fetuses were normal and no additional abnormalities were found. The remaining 50 cases were normal in appearance at delivery without any features that suggested trisomy 21. A review of the English language literature revealed that six of 489 cases with fetal heart echogenic foci (1.2%) had trisomy 21. However, statistical analysis of a hypothetical sample that produced these six cases revealed that the calculated risk of trisomy 21 in a fetus with fetal heart echogenic foci is about 0.002%. CONCLUSION: Karyotyping is unwarranted in the mid-trimester fetus with incidental findings of fetal heart echogenic foci.

Down Syndrome↗
PubMed1997

Limb amputation in amniotic band syndrome: serial ultrasonographic and Doppler observations.

A 28-year-old woman, gravida 7, para 6, was referred at 21 weeks' gestation to our ultrasound unit because of bilateral fetal lower limb edema diagnosed previously. Ultrasonography showed a constriction ring around both legs, and, with the aid of color Doppler, arterial flow was demonstrated in both legs beneath the constriction ring. Subsequent examinations during the 24th and 28th weeks revealed absence of flow below the constriction ring of the right leg and decreased flow in the left leg. This was followed by the gradual bending, breaking and resorption of the tibia and fibula of the right leg. Between weeks 30 and 34, gradual shrinkage of the remains of the right leg beneath the knee was recorded by serial ultrasonic observations. At the 38th week of gestation, a male infant was born by normal vaginal delivery. Examination at birth revealed amputation of the right leg below the knee, with a denuded end of the stump. There was a partial amputation of the left leg below the knee, with tissue continuity being maintained by the posterior neurovascular bundle, and a posterior strip of skin. The left foot was extremely edematous, with an area of necrosis dorsally. This case afforded us the opportunity of in utero following of natural limb amputation in the amniotic band syndrome.

Adult↗
PubMed1997

In-vitro modulation of plasminogen activator activity, prostaglandin E and nitric oxide production by interleukin-1 in pregnant mare serum gonadotrophin-primed theca-interstitial cells.

To examine the participation of the theca-interstitial (TI) compartment in cytokine modulation of ovarian function, the effects of interleukin-1beta (IL-1) on plasminogen activator (PA) activity and on prostaglandin E (PGE) and nitric oxide (NO) production were examined in cultures of pregnant mare serum gonadotrophin (PMSG)-primed rat TI cells. Exposure to IL-1 (10 ng/ml) resulted in a 25% reduction (P < 0.001) in PA activity, concurrent with a 4.6-fold increase in the ability of the corresponding conditioned media to inhibit exogenous urokinase activity. IL-1 also produced a 4.7-fold increase in PGE content and a 2.8-fold increase in NO generation. These effects of IL-1 were abolished by the IL-1 receptor antagonist, suggesting specific IL-1 receptor-mediated effects. Transforming growth factor (TGF)-beta1 (10 ng/ml) significantly attenuated the IL-1-stimulated PGE production and NO generation but did not affect the ability of IL-1 to suppress PA activity and stimulate urokinase inhibitor production. The NO synthase inhibitor N-nitro-L-arginine attenuated the IL-1-induced NO generation but had no effect on PA activity or PGE production. Thus, NO is not an obligatory mediator of IL-1 effects on plasminogen activation and PGE generation in rat ovary. The present observations attest to a pleiotropic response of PMSG-primed TI cells to IL-1, and suggest a paracrine/autocrine function for the TI compartment in ovulation and corpus luteum formation.

Animals↗
PubMed1997

Tamoxifen exerts oestrogen-agonistic effects on proliferation and plasminogen activation, but not on gelatinase activity, glycogen metabolism and p53 protein expression, in cultures of oestrogen-responsive human endometrial adenocarcinoma cells.

To elucidate potential mechanisms involved in the increased incidence of endometrial carcinomas in tamoxifen-treated patients, we examined the in-vitro effects of tamoxifen on endometrial cancer cells. The effects of tamoxifen, alone and in combination with oestradiol, on cell proliferation, plasminogen activator (PA) activity, glycogen synthase and phosphorylase activities, p53 protein concentration, and collagenase expression were assessed in two human adenocarcinoma cell lines. These lines were the oestrogen receptor-positive (Ishikawa) cells, representing a well-differentiated endometrial adenocarcinoma, and oestrogen receptor-negative (HEC-1A) cells, derived from a poorly differentiated endometrial adenocarcinoma. Tamoxifen or oestradiol alone and their combination significantly enhanced cellular proliferation of Ishikawa but not of HEC-1A cells. Both lines produced appreciable PA activity, most of which was of the urokinase type. Tamoxifen and oestradiol stimulated this activity in Ishikawa cells but not in HEC-1A cells. The effect of oestradiol was dose-dependent in a linear fashion, while tamoxifen produced a stimulation peaking at 10(-8) M and declining at higher concentrations. Tamoxifen in combination with oestradiol exhibited a synergistic effect on proliferation and on PA activity. The response of PA extended beyond the increase in proliferation, leading to higher specific activity of PA in the tamoxifen-treated cultures. In Ishikawa cells, oestradiol also increased glycogen synthase and glycogen phosphorylase activities, while tamoxifen markedly suppressed these enzymes. Oestradiol, tamoxifen, and their combination had no apparent effect on the expression of protein p53 in Ishikawa cells, or on gelatinase activity in either Ishikawa or HEC-1A cells. The present findings imply that tamoxifen produces oestrogen-agonistic effects on cell proliferation and PA activity, and oestrogen antagonistic effects on glycogen synthase and glycogen phosphorylase activities, but fails to regulate p53 and gelatinase expression. The tamoxifen-responsive systems were only observed in oestrogen-responsive adenocarcinoma cells. Thus, only certain potential oncogenic effects of tamoxifen can be simulated in vitro, and when present, these effects are enhanced in the presence of oestradiol.

Adenocarcinoma↗
PubMed1996

Thomas syndrome: potter sequence with cleft lip/palate and cardiac anomalies.

Holzgreve et al. [Am J Med Genet 18:177-184, 1984] first reported on a syndrome including renal anomalies, heart defect, polydactyly, and cleft palate with other oropharyngeal anomalies. We report here on four sibs with renal adysplasia associated in two with cardiovascular malformations and cleft lip or cleft palate in two. We propose that these patients as the two siblings reported by Thomas et al. [Am J Med Genet 45:767-769, 1993] are affected with a syndrome different of the one described by Holzgreve et al. [Am J Med Genet 18:177-184, 1984] mainly because of the absence of polydactyly. Thomas syndrome is probably inherited as an autosomal recessive trait with marked variability.

Abnormalities, Multiple↗
PubMed1996

Sonographic evaluation of the uterus in postmenopausal women receiving tamoxifen: characterization of mid-uterine abnormalities.

BACKGROUND: Tamoxifen is known to exert agonist estrogenic effects on the uterus. Its use in postmenopausal women has also been associated with various endometrial and uterine abnormalities that can be detected by endovaginal sonography. OBJECTIVE: To study postmenopausal patients receiving tamoxifen who were referred for evaluation following the detection of abnormal uterine findings by endovaginal sonography. METHODS: Fifty-two women treated with tamoxifen for breast cancer who were found to have an abnormal uterine sonogram constituted the study population. Uterine sonograms were reviewed and clinical and sonographic data were correlated with the results of the histologic examinations. RESULTS: Forty-five women demonstrated a thickened mid-uterine structure. Of these, in thirty-nine patients (87%) either no tissue of scant fragments of normal endometrium were obtained on curettage, and six women (13%) had endometrial hyperplasia. Seven women had fluid loculation lined by thin endometrium. Their subsequent histologic examination was normal. The sonograms of the women who demonstrated an appearance of a thickened endometrium but no neoplasia, characteristically demonstrated hyperechogenic cystic area with no midline echo. CONCLUSIONS: Among 52 postmenopausal patients receiving tamoxifen presented with an abnormal uterine sonogram, 39 (75%) women were found to have a thick mid-uterine structure resembling a thickened endometrium without histologic evidence of neoplasia. This phenomenon can be characterized by typical sonographic features, and may be differentiated from other uterine abnormalities.

Adult↗
PubMed1996

Prenatal ultrasonographic diagnosis of fetal hepatic hyperechogenicities: clinical significance and implications for management.

The clinical significance of sonographically detected fetal hepatic hyperechogenicities has not been fully established. The aim of this study was to assess various aspects of fetal hepatic hyperechogenicities detected in utero, including natural history, prenatal investigation and pregnancy outcome. In a retrospective survey of pregnant women presenting to the ultrasonographic unit, five fetuses with a mean gestational age of 20 weeks (range 14-24 weeks) were antenatally diagnosed as having hepatic hyperechogenicities. All cases underwent extensive investigation to establish the etiology and to determine the spectrum of ultrasonographic presentation. In three fetuses, only parenchymal lesions were found, while two had combined lesions: parenchymal and peritoneal. The earliest prenatal ultrasonographic diagnosis was made at 14 weeks' gestation in a fetus with combined hyperechogenic lesions, which, at 12 weeks' gestation, demonstrated unexplained fetal ascites. Associated abnormalities were found in only one fetus in which a solitary parenchymal lesion was associated with direct communication of the intrahepatic portion of the umbilical vein with the right atrium, and high output cardiac failure. In this case, termination of pregnancy confirmed ischemic hepatic necrosis. In the other four cases, no direct etiology could be determined, and all four pregnancies continued to term with normal neonatal follow up until 12 months of age. The present data suggest that in cases of fetal hepatic hyperechogenicities, where apparent intrauterine infection or neoplasia can be ruled out, a vascular disruption phenomenon is a putative etiology. If there are no associated morphological abnormalities or abnormal karyotypes, the prognosis may be favorable.

Adult↗
PubMed1996

Prenatal diagnosis of persistent right umbilical vein.

A persistent right umbilical vein is thought to be a rare anomaly, frequently associated with other life-threatening malformations. Eight cases of prenatal diagnosis of persistent right umbilical vein are presented. All cases were discovered on a routine second-trimester sonogram in an unselected population. Of the seven babies who were delivered, one had a dextrocardia and right-sided descending aorta, but none had other associated major malformations. The outcome was favorable in all cases and all seven infants are well and thriving with up to a year and a half of follow-up. Our findings suggest that persistent right umbilical vein might not be as rare as the paucity of reports in the literature implies. Provided that no other malformations are present, this anomaly is probably of little prognostic significance, requiring no further evaluation or follow-up.

Adult↗
PubMed1996

Late selective termination of fetal abnormalities in twin pregnancies: a multicentre report.

OBJECTIVE: To evaluate the outcome of late selective fetal termination based on combined data from eight tertiary perinatal centres. DESIGN: Israeli law requires institutional committee approval for pregnancy termination. Moreover, after 24 weeks only a district superior committee can approve the termination. A total of 36 bichorionic twin pregnancies who underwent selective fetal termination after 24 complete gestational weeks were identified in eight Israeli centres. RESULTS: In 23 women (63.9%) the indication for selective termination was structural anomaly, and in 13 (36.1%) the indication was chromosomal abnormality. The mean gestational age at the time of diagnosis was 24.1 +/- 1.9 weeks. The termination procedure was performed at a mean gestational age of 25.5 +/- 2.0 weeks (median 25, range 24-33 weeks). There was one case of immediate procedure-related complication (i.e. amnionitis) and the unaffected infant died, which was the only perinatal death in this series. No evidence of coagulopathy was reported. Only five women (13.8%) delivered before 34 completed weeks. The mean gestational age at delivery was 36.9 +/- 2.9 weeks (28-41 weeks), and the mean procedure-to-delivery interval was 11.8 +/- 3.2 weeks (median 13, range 3-17 weeks). CONCLUSIONS: Late (> 24 weeks) selective termination in twin pregnancies is associated with favourable perinatal outcome of the healthy twin. In countries where the law permits late pregnancy termination, the parents should be informed of that possibility.

Adult↗
PubMed1996

Cytokine-mediated regulation of type IV collagenase expression and production in human trophoblast cells.

The invasive property of trophoblast cells is dependent on the activity of proteolytic enzymes of the metallo- and serine proteases family. Interleukin-1 (IL-1) was found to be involved in the regulation of these proteases in various systems, serving as an important modulator in trophoblast physiology (e.g. induction of hCG beta, cytokines, and others). Therefore, consideration is given in this report to the role of IL-1 in the regulation of metalloprotease activity in human trophoblasts. Human trophoblast cells were isolated from first trimester placentas by trypsin degradation and Percoll fractionation. Primary cell cultures of first trimester trophoblasts constitutively elaborated two species of collagenase type IV (92 and 72 kDa), as assessed in gelatin matrix. Treatment with IL-1 further augmented the 92-kDa type IV collagenase secretion in a dose-dependent manner. Furthermore, IL-1 significantly (P < 0.01) increased 92-kDa collagenase gene expression by trophoblast cells, as determined by solution hybridization/ribonuclease protection assay. Both the increase in gene expression and protein biosynthesis of the 92-kDa collagenase type IV were neutralized by the soluble IL-1 receptor, indirectly suggesting a receptor-mediated response. Interestingly, transforming growth factor-beta a putative modulator of IL-1 induced effects, was shown to induce the 92-kDa collagenase type IV secretion as well. These results provide indirect evidence supporting the idea that IL-1 and transforming growth factor-beta may play an intermediary role in trophoblast invasion at the feto-maternal interface by regulating trophoblast expression of 92-kDa type IV collagenase, a protease of prime importance in trophoblast invasion.

Cells, Cultured↗
PubMed1995

Renal anomalies in Marden-Walker syndrome: a clue for prenatal diagnosis.

Marden-Walker syndrome is an autosomal-recessive disorder characterized by psychomotor retardation, blepharophimosis, joint contractures, arachnodactyly, failure to thrive, and, infrequently, renal anomalies. We report on the prenatal diagnosis of Marden-Walker syndrome in a fetus which had had a previously affected sib with this syndrome. The ultrasonic findings indicative of the diagnosis in this fetus were intrauterine growth retardation and renal cystic disease. We emphasize the importance of renal anomalies which, when present in combination with other ultrasound evidence of this syndrome, should be used as a clue for the diagnosis of Marden-Walker syndrome.

Abnormalities, Multiple↗