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A Pellicer

Publications and source records attributed to A Pellicer.

At least 19 recordsLinked to original sources
PubMed1992

A new cDNA sequence for the murine interleukin-2 gene.

We have amplified by PCR and sequenced the first exon of the interleukin 2 gene from the RF/J mouse strain DNA. When we compared the RF/J first exon sequence with the one reported previously, we found several differences. These differences are also reflected in the deduced amino acid sequence and they have been localized in the first 23 amino acids of the mature polypeptide. The finding of this new IL-2 sequence shows that there is more than one allele for the mouse IL-2 molecule and raises the possibility of functional differences between alleles.

Amino Acid Sequence↗
PubMed1992

Early neurological manifestations and brain anomalies in Marden-Walker syndrome.

We report on an infant with the Marden-Walker syndrome. In addition to the consistent neurological abnormalities described previously in this syndrome, the infant had a striking neurological constellation, absence of primitive reflexes, jerky eye movements, failure to habituate to repeated stimuli, inadequate behavior development, and absence of orientation responses to visual or auditory stimuli. Muscle biopsy showed a similar pattern to the congenital fiber-type disproportion. Ultrasonograms and magnetic resonance imaging of his brain demonstrated absence of corpus callosum, colpocephaly, hypoplastic brainstem, hypoplasia of the inferior vermis and of the cerebellar hemispheres. These findings further delineate this syndrome and suggest that prenatal central nervous system (CNS) dysfunction, mainly of the cerebellum and brainstem, may play a significant role in the pathogenesis of the Marden-Walker syndrome.

Abnormalities, Multiple↗
PubMed1992

A method to extract DNA for molecular studies from cells fixed in Carnoy.

We describe a simple method for isolation of high-molecular-weight DNA from cells fixed in Carnoy's solution for cytogenetic studies. DNA samples were extracted from NIH3T3 cells, and no apparent degradation was noticed. This method should be useful for molecular analysis of cells fixed for cytogenetic studies.

3T3 Cells↗
PubMed1992

Glucocorticoid treatment decreases sera embryotoxicity in endometriosis patients.

OBJECTIVE: To investigate the effect of short-term glucocorticoid administration on embryotoxicity of sera from infertile patients with mild to moderate endometriosis. DESIGN: Prospective longitudinal study. SETTING, PATIENTS: Eight infertile patients with mild to moderate endometriosis and a control group of eight infertile patients with tubal infertility were selected on the basis of laparoscopic examination. INTERVENTIONS: Basal (B) serum collection and day 1 (T1), day 3 (T2), day 6 (T3), and day 12 (T4) serum drawn after a 3-day glucocorticoid treatment in endometriosis patients. MAIN OUTCOME MEASURE: Embryotoxicity of endometriosis sera, before and after glucocorticoid treatment, was investigated using a bioassay performed on two-cell mouse embryos. Interleukin 1 alpha (IL-1 alpha) and antismooth muscle, antimitochondrial, and antinuclear autoantibodies were also tested in these sera. RESULTS: At 50% concentration, endometriosis serum is embryotoxic in comparison with control; 0% versus 61% of the embryos reached the blastocyst stage at 72 hours, respectively (basal versus control, P less than 0.001). However, this embryotoxicity significantly decreases 12 days after glucocorticoid treatment in comparison with untreated sera; 32.4% versus 0% of the embryos reached blastocyst stage at 72 hours, respectively (T4 versus basal, P less than 0.001), although they did not reach nontoxic levels (greater than 50%). Interleukin 1 alpha was undetectable in all samples analyzed. In endometriosis sera, antismooth muscle antibody was detected. CONCLUSIONS: At 50% concentration, serum from infertile patients with minimal to moderate endometriosis appears to be embryotoxic to the in vitro development of two-cell mouse embryos. However, this embryotoxicity significantly decreases 12 days after a 3-day treatment with glucocorticoids.

Adult↗
PubMed1992

Stroke in neonates with cardiac right-to-left shunt.

Neonatal focal cerebral arterial infarction has been rarely reported in the literature, in contrast to the watershed infarctions, which are common entities among asphyxiated infants. In neonatal postmortem series, thromboembolism was the commonest cause of cerebral arterial occlusion; the source of emboli was associated to different risk factors. Our four cases are the first alive patients reported with congenital heart disease and right-to-left shunt, who suffered a cerebral infarct with its clinical neurological correlates in the neonatal period. We assume that the most probable mechanism was paradoxical embolism, once pulmonary filter is obviated as a result of the altered hemodynamics in these patients. Our data demonstrate the value of ultrasound scanning for assessment of focal cerebral ischemic lesions. Thus, although abnormal neurological signs in this particular group of infants could be attributed to hypoxemia or specific treatments as prostaglandins, we suggest routine cerebral ultrasounds in neonates with congenital heart disease and neurological disabilities, as early complications could be not so infrequent.

Cerebrovascular Disorders↗
PubMed1992

The use of gonadotrophin releasing-hormone analogues (GnRHa), in in-vitro fertilization: some clinical and experimental investigations of a direct effect on the human ovary.

Several lines of investigation suggest a direct modulatory role for gonadotrophin-releasing hormone (GnRH) on granulosa cell functions. Also, GnRH and its analogues (GnRHa) have been implicated in the resumption of meiosis, both in vivo and in vitro. Despite the presence of specific receptors for GnRH on human granulosa and luteal cells, very little is known about the possible effects of this hormone on the ovary. The use of GnRHa for long periods of time in patients undergoing in vitro fertilization (IVF) may influence granulosa cell function and/or oocyte maturation. We describe our clinical and experimental data in which we have searched for evidence of a direct action of GnRHa on the ovary. We have found that the retrieval of higher numbers of oocytes in women treated with GnRHa is correlated with oocytes of lower quality, manifested by a decreased fertilization and implantation rate. This impairment seems to be the consequence of oocyte immaturity, as ascertained by cytogenetic analysis of unfertilized oocytes in which an increase in diploidy, as well as prematurely condensed sperm chromosomes of the G1 phase, was observed in women with an excessive response to the stimulating drugs. Follicular atresia was not increased in women treated with GnRHa. Thus, there was no evidence for a direct effect of GnRHa on the human oocyte. Rather, the observations reflect the harmful effect of pushing follicles in early stages of development using this stimulation protocol. We have also searched for possible effects of GnRHa on granulosa-luteal cells obtained at ovum collection. In vitro culture of these cells has shown that the steroidogenic pathway is affected.(ABSTRACT TRUNCATED AT 250 WORDS)

Cell Count↗
PubMed1992

Relativity of the concept 'high responder to gonadotrophins'.

Regression analysis of the proportion of unfertilized oocytes on the number of oocytes retrieved per patient was applied to three different ovarian stimulation protocols in order to establish the relativity of the concept 'high responder to gonadotrophins' for in-vitro fertilization (IVF) patients. After fitting the data to the model: probit(proportion of unfertilized oocytes) + 5 = intercept + B Log10(oocytes retrieved per patient), women with a number of oocytes retrieved greater than or equal to the value necessary to obtain 50% fertilization were defined as high responders. Exogenous gonadotrophin stimulation which was commenced after complete suppression of ovarian activity by a gonadotrophin-releasing hormone analogue (GnRHa) (long protocol) resulted in a significantly higher number of oocytes retrieved (10.15) to obtain 50% fertilization compared to a short protocol (6.84) (exogenous stimulation began 2 days after the GnRHa administration). Women stimulated without use of a GnRHa showed an intermediate response. Implantation, pregnancy and miscarriage rates showed no difference between low-moderate and high responders. These results demonstrate the relativity of the concept 'high responder to gonadotrophins' and indicate that the drawback of low fertilization in high responders could be balanced by the high number of oocytes retrieved per patient (and available embryos for transfer) and the selection of the best embryos for transfer.

Adult↗
PubMed1992

Simultaneous induction of multiple follicular development with gonadotrophins and steroid replacement for in-vitro fertilization.

Simultaneous administration of follicle stimulating hormone, oestradiol valerate and progesterone was employed in a patient with a possible enzymatic deficiency involving low production of oestradiol. The patient became pregnant after in-vitro fertilization. This case demonstrates that this treatment is useful in women with low oestradiol production and subsequent inadequate endometrial development; it also illustrates the role of oestradiol in follicular development and questions the importance of serum oestradiol measurements in the monitoring of ovulation induction.

Adult↗
PubMed1992

Expression of the genes encoding the insulin-like growth factors and their receptors in the human ovary.

Insulin-like growth factor-I (IGF-I) and IGF-II have been proposed as potential regulators of ovarian function. To gain further insight as to the possible role(s) of the IGFs in human ovarian physiology, we have characterized the expression of the genes encoding the IGFs and their corresponding receptors in the human ovary using solution hybridization/RNase protection assays. IGF-I gene expression was evident in liver, placenta, and whole premenopausal ovary, but not in luteinized granulosa cells. Use of 3'- and 5'-specific antisense RNA probes revealed the presence of IGF-I mRNAs encoding both the Ea and Eb forms of the E-peptide as well as potential 5'-untranslated region splicing variants in liver, placenta, and whole menopausal ovary. Immunohistochemical studies localized the IGF-I peptide to the thecal-interstitial compartment. IGF-II mRNA transcribed from the fetal or fetal-neonatal IGF-II promoter was found in whole premenopausal ovary, luteinized granulosa cells, and placenta. Insulin and type I and type II IGF receptor mRNAs were detected in all tissues examined. Two protected probe fragments were seen with the type I IGF receptor probe in each case, suggesting the possibility of alternate splicing. These studies provide further evidence for a role of these growth factors in human ovarian function.

DNA↗
PubMed1992

Steroidogenesis in vitro of human granulosa-luteal cells pretreated in vivo with two gonadotropin releasing hormone analogs employing different protocols.

We have previously observed impaired progesterone accumulation in vitro in response to human chorionic gonadotropin (hCG) by cells pretreated in vivo with a gonadotropin releasing hormone analog (GnRH-a). The present study was conducted in order to evaluate different protocols for GnRH-a in in vitro fertilization (IVF), employing two different available analogs. Granulosa-luteal cells were collected at ovum pick-up and stimulated with hCG. Buserelin (Bus) was employed as long (Bus-L) and short (Bus-S) protocol, and Leuprolide (Leu) was also used as long (Leu-L) and short (Leu-S) protocol. Progesterone accumulation in vitro was compared with cells treated with clomiphene citrate (CC) and gonadotropins. Maximal progesterone production was observed on culture day 6 using Bus-L in comparison to day 4 when clomiphene citrate was employed. While Leu-S showed a similar pattern of progesterone accumulation to clomiphene citrate, Leu-L and Bus-S had an intermediate pattern. The response to hCG was maximal on day 4 for the clomiphene citrate- and Leu-S-treated cells, while the rest of the protocols had a peak on day 6. In addition, hCG consistently stimulated progesterone production in all protocols except in Bus-L. These results confirm an altered progesterone accumulation in vitro when GnRH-a are used. The effect seems to be more evident in long protocols, especially when buserelin is used, suggesting a higher accumulation of the analog in follicular fluid.

Buserelin↗
PubMed1992

Oocyte maturation in human in vitro fertilisation programmes.

Oocyte immaturity represents a serious loss of efficiency in the in vitro fertilisation (IVF) treatment cycle since it is associated with a great list of detrimental effects mainly reflected in lower fertilisation and pregnancy rates. In stimulated cycles, oocyte maturation depends on stimulation protocol, ovarian response, time of human chorionic gonadotrophin (hCG) administration, hCG to oocyte retrieval interval, and/or time of in vitro culture period before insemination. The present review discusses the influence of these factors on human oocyte maturation and proposes several preventive and corrective measures. Due to the difficulty of ascertaining the grade of oocyte maturity based on morphological and physical properties of the oocyte-corona-cumulus complex (OCCC), fertilisation rate has been considered as an indirect index of nuclear and cytoplasmic maturation. The proportion of immature oocytes increases as the ovarian response to gonadotrophins increases. However, the detrimental effects of oocyte immaturity in high responders may be balanced by the higher number of oocytes retrieved per patient (and available embryos for transfer) and the selection of the best embryos for transfer. Oocyte immaturity might be prevented by delaying hCG injection and/or oocyte retrieval. Corrective strategies would involve in vitro or in vivo culture before insemination; addition of gonadotrophins or epidermal growth factor to the culture medium; and coculture with granulosa cells.

Female↗
PubMed1992

Overexpression of the N-ras proto-oncogene, not somatic mutational activation, associated with malignant tumors in transgenic mice.

We have produced transgenic mice that carry a foreign gene construct consisting of the N-ras proto-oncogene driven by the mouse mammary tumor virus (MMTV) long terminal repeat. Overexpression of the normal N-ras gene is associated with development of hyperplasias and tumors in a variety of tissues. The tumors are clearly malignant, as evidenced by the presence of metastatic lesions. Extensive analysis of the foreign ras gene in these tumors by use of polymerase chain reaction and sequencing demonstrates in all cases the absence of somatically acquired mutations at those codons normally associated with activation of the ras genes. Thus, these tumors develop from overexpression of the proto-oncogene rather than the presence of the mutated oncogene. These data demonstrate that overexpression of a protooncogene of the ras family can predispose cells in vivo to fully malignant behavior.

Animals↗
PubMed1992

ras activation in experimental carcinogenesis.

We review experimental models of carcinogenesis in which the role of ras activation has been most thoroughly studied: skin, thymus, mammary gland and liver. Qualitative changes (point mutations), as well as quantitative changes (over-expression, increased gene dosage) contribute to the transforming phenotype induced by ras genes. The activation of the three different ras family members is associated with particular tumor types, carcinogenic agents, and carcinogenic stages, suggesting the ras proteins may be involved in different biological functions. Depending on the system, ras activation has been shown to be an early and/or a late event in the multi-step process of carcinogenesis. These data underscore the possible relationship between ras activation and cell type specificity, proliferation, differentiation or cell-cell interaction.

Animals↗
PubMed1992

Multiple intragenic elements regulate the expression of the murine N-ras gene.

We have identified two separate regions within the murine N-ras transcription unit which may participate in the regulation of N-ras gene expression. One of these regions, localized to the first half of intron 1, contains a site of premature transcriptional arrest. We propose that premature transcription termination, which has been identified as an important control mechanism for several genes, may also play a role in the regulation of the N-ras gene. In addition, we have identified a positively acting region within the N-ras transcription unit. This region, localized to the end of intron 1/beginning of exon 1, was found to greatly increase expression from the N-ras promoter.

3T3 Cells↗
PubMed1991

Differential expression of the normal and mutated K-ras alleles in chemically induced thymic lymphomas.

The presence of point mutations in the K-ras gene was examined in murine thymic lymphomas induced by a single dose of N-methylnitrosourea by the RNase A mismatch cleavage method and by allelic-specific oligonucleotide hybridization of in vitro amplified DNA by polymerase chain reaction. The results show that the frequency of mutations is lower than that of tumors induced by multiple N-methylnitrosourea treatments. Four mutations identified were the aspartic acid at codon 12, a G:C to A:T transition in its second position. A G:C to T:A transversion in codon 146 was also found in one thymic lymphoma, changing the amino acid alanine to serine. The use of the RNase A assay allowed an estimation of the relative expression levels of both normal and mutant K-ras alleles. The results show that in approximately one half of the tumors the mutant allele is predominantly expressed, suggesting that the normal allele has been lost or that the mutant allele has been amplified relative to the normal. Altogether, these findings are consistent with ras mutations occurring in some instances during tumor development and with a ras effect being not strictly dominant but favoring selection for increasing levels of expression from the oncogenic allele.

Animals↗