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S Kol

Publications and source records attributed to S Kol.

At least 37 records · Page 2Linked to original sources

Glucocorticoids suppress basal (but not interleukin-1-supported) ovarian phospholipase A2 activity: evidence for glucocorticoid receptor-mediated regulation.

Ovulation may constitute a cyclic, inflammatory-like process, wherein the increased expression of interleukin (IL)-1 and the biosynthesis of prostaglandins may be established corollaries. In this communication we hypothesize that glucocorticoids, potent anti-inflammatory principles, may exert an antiovulatory effect by interfering with ovarian IL-1-driven prostaglandin biosynthesis. To test this hypothesis, we examined the effect of treatment with dexamethasone on the activity of ovarian phospholipase A2 (PLA2), the event-limiting enzyme in prostaglandin biosynthesis, and on the gene expression pattern of secretory and cytosolic PLA2 (sPLA2 and cPLA2, respectively). Whole ovarian dispersates from immature rats were cultured under serum-free conditions for 48 h in the absence or presence of dexamethasone. At the conclusion of this culture period, PLA2 activity was determined in cell sonicates and conditioned media. Parallel probing for sPLA2 and cPLA2 transcripts was also undertaken using a solution hybridization/RNAse protection assay. Treatment of whole ovarian dispersates with dexamethasone produced a significant (P < 0.005) decrease in basal cellular and extracellular PLA2 activity to 27 and 40% of controls, respectively. A 5-fold decrease in the basal steady state levels of sPLA2 (but not cPLA2) transcripts was also noted. Co-treatment with dexamethasone produced complete inhibition of IL-1-stimulated cPLA2 transcripts but not of IL-1-supported cellular and extracellular PLA2 activity or sPLA2 transcripts. A glucocorticoid receptor antagonist (RU486), blocked the ability of dexamethasone to inhibit basal sPLA2 transcripts and extracellular PLA2 activity. The inhibitory effect of dexamethasone proved glucocorticoid-specific in that aldosterone and 17beta-estradiol were without effect. Taken together, these observations suggest that dexamethasone is capable of inhibiting basal (but not IL-1-supported) ovarian PLA2 activity, a glucocorticoid receptor-mediated effect due, in part, to a decrease in sPLA2 gene expression. Our findings further suggest that sPLA2 and cPLA2 are differentially regulated and that they may well differ in their relative contribution to ovarian prostaglandin biosynthesis in general and to PLA2 activity in particular. To the extent that IL-1 plays a central role in the ovulatory process, these findings argue against the view that the chronic anovulatory state induced by glucocorticoid excess is due, if only in part, to suppression of ovarian IL-1-dependent PLA2 activity.

Animals↗

First established pregnancy after controlled ovarian hyperstimulation with recombinant follicle stimulating hormone and the gonadotrophin-releasing hormone antagonist ganirelix (Org 37462).

This case report describes the first established pregnancy after the use of gonadotrophin-releasing hormone (GnRH) antagonist, ganirelix (Org 37462; Organon), to prevent a premature luteinizing hormone surge during ovarian hyperstimulation with recombinant human follicle stimulating hormone (rhFSH). The pregnancy progressed normally and ended with the birth of a healthy boy and a girl after an elective Caesarean section at gestational age of 37 weeks. This case illustrates, for the first time, the use of a GnRH antagonist in combination with a pure FSH preparation for ovarian stimulation.

Adult↗

Rat ovarian prostaglandin endoperoxide synthase-1 and -2: periovulatory expression of granulosa cell-based interleukin-1-dependent enzymes.

This laboratory has previously shown that interleukin-1 (IL-1), a putative intermediary in the ovulatory process, is capable of up-regulating PG biosynthesis by cultured whole ovarian dispersates from immature rats. In part, this phenomenon was attributable to the stimulation of ovarian phospholipase A2 activity. In this communication we examine the possibility that the PG-promoting property of IL-1 is also due to the up-regulation of PG endoperoxide synthase (PGS), the rate-limiting step in prostanoid biosynthesis. The in vivo expression of ovarian PGS-2 transcripts in the course of a simulated estrous cycle rose abruptly to a peak (35-fold increase over the control value; P < 0.05) 8-12 h after hCG administration (i.e. before or during projected ovulation). PGS-1 transcripts, in turn, were not significantly altered during the periovulatory period. Treatment of cultured whole ovarian dispersates with IL-1beta resulted in dose- and time-dependent up-regulation of PGS-2 transcripts (as well as of immunoreactive PGS-2 protein and PGE2 accumulation), characterized by an ED50 of 2 ng/ml and a maximal (72-fold) increase at 10 ng/ml. Although treatment with IL-1beta also led to an increase in PGS-1 transcripts and immunoreactive PGS-1 protein, the relative magnitude of the effect was markedly reduced compared with that of PGS-2. Cotreatment with an IL-1 receptor antagonist completely reversed the IL-1 effects, thereby suggesting mediation via the IL-1 receptor. The ability of IL-1 to up-regulate PGS-2 transcripts proved relatively specific, in that other cellular regulators (insulin-like growth factor I, activin A, endothelin-1, transforming growth factor-alpha, tumor necrosis factor-alpha, vascular endothelial growth factor, leukemia inhibitor factor, hepatocyte growth factor, or keratinocyte growth factor) were not effective. The optimal IL-1 effect required heterologous contact-dependent coculturing of granulosa and thecal-interstitial cells. Taken together, these observations 1) reaffirm (by molecular probing) the granulosa cell as the primary site of ovarian PGS-1 and PGS-2 expression, 2) document an increase in ovarian PGS-2 transcripts before ovulation, and 3) reveal a marked dependence of ovarian PGS (2 >> 1) transcripts, proteins, and activity on IL-1. The effects of IL-1 proved relatively specific, contingent upon somatic cell-cell cooperation, dose and time dependent, and IL-1 receptor mediated. These results are compatible with the proposition that the PG-promoting property of IL-1 is due, in large measure, to the activation of ovarian PGS transcription and translation. The ability of IL-1 to up-regulate ovarian PGS, an obligatory component of ovulation, is in keeping with the idea that IL-1 may constitute an intermediary in the ovulatory process.

Animals↗

The midcycle increase in ovarian glucose uptake is associated with enhanced expression of glucose transporter 3. Possible role for interleukin-1, a putative intermediary in the ovulatory process.

This study characterizes the rat ovary as a site of hormonally dependent glucose transporter (Glut) expression, and explores the potential role of interleukin (IL)-1, a putative intermediary in the ovulatory process, in this regard. Molecular probing throughout a simulated estrous cycle revealed a significant surge in ovarian Glut3 (but not Glut1) expression at the time of ovulation. Treatment of cultured whole ovarian dispersates from immature rats with IL-1beta resulted in upregulation of the relative abundance of the Glut1 (4.5-fold) and Glut3 (3.5-fold) proteins as determined by Western blot analysis. Other members of the Glut family (i.e., Gluts 2, 4, and 5) remained undetectable. The ability of IL-1 to upregulate Glut1 and Glut3 transcripts proved time-, dose-, nitric oxide-, and protein biosynthesis-dependent but glucose independent. Other ovarian agonists (i.e., TNF alpha, IGF-I, interferon-gamma, and insulin) were without effect. Taken together, our findings establish the mammalian ovary as a site of cyclically determined Glut1 and Glut3 expression, and disclose the ability of IL-1 to induce the ovarian expression as well as translation of Glut1 and Glut3 (but not of Gluts 2, 4, or 5). Our observations also establish IL-1 as the first known regulator of Glut3, the most efficient Glut known to date. In so doing, IL-1, a putative component of the ovulatory process, may be acting to meet the increased metabolic demands imposed on the growing follicle and the ovulated cumulus-enclosed oocyte.

Animals↗

Helium and oxygen treatment of severe air-diving-induced neurologic decompression sickness.

BACKGROUND: The use of helium and oxygen recompression treatment of neurologic decompression sickness (DCS) has several theoretical advantages over the traditionally used air and oxygen recompression tables that have been confirmed by findings from recent animal experiments. OBJECTIVES: To evaluate the outcome of patients with neurologic DCS who had been treated with a helium-oxygen protocol and to compare it with that of a retrospective control group that was treated with air-oxygen tables. DESIGN: The study and control groups included 16 and 17 diving casualties, respectively. The severity of neurologic DCS was estimated according to a 9-point scale weighting motor, sensory, and sphincter control functions. The study group was treated with a helium-oxygen decompression protocol, and the control group was treated with the US Navy air-oxygen Table 6 or 6A. Persistent residual dysfunction was treated in both groups with daily hyperbaric oxygen sessions, at 2.5 absolute atmospheres for 90 minutes, until no further clinical improvement was noted. SETTING: The Israel Naval Medical Institute (Israel's national hyperbaric referral center), Haifa. RESULTS: Significant clinical score increments were found for both the helium-oxygen- and air-oxygen-treated groups: 2.8 +/- 2.4 (mean +/- SD) and 7.4 +/- 1.1 at presentation vs 7.6 +/- 2.1 and 8.1 +/- 1.5 at discharge, respectively (P < .001 and P = .005, respectively). Although the score at presentation was significantly lower for the helium-oxygen-treated group (P < .001), no difference was found between the groups' average outcome scores. While most of the improvement in the patients in the study group could be attributed to the helium-oxygen treatment and not to the supplemental hyperbaric oxygen, in the control group, no significant difference could be demonstrated between the scores at presentation and at completion of the air-oxygen recompression table. In 5 patients who were treated with the use of the air-oxygen tables, deterioration was observed after recompression. No deterioration or neurologic DCS relapse occurred in the helium-oxygen-treated group. CONCLUSION: The results suggest an advantage of helium-oxygen recompression therapy over air-oxygen tables in the treatment of neurologic DCS.

Decompression Sickness↗

The presence of a sponsoring embryo in a batch of poor quality thawed embryos significantly increases pregnancy and implantation rate.

OBJECTIVE: To evaluate quantitatively the effect of one good-quality (sponsoring) embryo in a batch of low-quality thawed embryos on the implantation and pregnancy rates (PR). DESIGN: Retrospective analysis of data. SETTING: Tertiary care center IVF clinic affiliated with a university medical school. PATIENT(S): Between March 1988 and April 1995, 392 IVF patients underwent a total of 440 thawing and ET cycles of 1,436 multicellular embryos. MAIN OUTCOME MEASURE(S): Implantation, clinical pregnancy, and multiple pregnancy rates. RESULT(S): In the absence of sponsoring embryos in the thawed batch of embryos, a PR of 9.8% with an implantation rate of 3.1% was achieved. In the presence of a single sponsoring embryo, the PR nearly doubled (18.2%), with a significantly higher implantation rate of 7.0%. Only singleton pregnancies were achieved in the absence of sponsoring embryos compared with 21.7% multiple pregnancies in the single sponsoring embryo group. CONCLUSION(S): The presence of a sponsoring embryo in a batch of poor quality thawed embryos is an important factor that significantly increased pregnancy and implantation rates. The optimal strategy for planning batches of multicellular frozen embryos is to include at least one sponsoring embryo in each batch when possible. We speculate that the sponsoring embryo may favorably influence the chances of low-quality embryos to undergo successful implantation.

Adult↗

Insulin-like growth factor I affects the intraovarian interleukin-1 system: evidence for suppression of type I interleukin-1 receptor expression and enhancement of secretory phospholipase A2 expression and activity.

This study assessed the possibility that the intraovarian insulin-like growth factor I (IGF-I) system interacts with the intraovarian interleukin-1 (IL-1) system, the central role of which has been the subject of increasing attention. To this end, whole ovarian dispersates from immature rats were cultured for 48 h in the absence or presence of IGF-I or IGF-binding protein-3 (IGFBP-3), with or without IL-1beta. Cellular RNA content was subjected to a solution hybridization, RNase protection assay with gel-purified [32P]-UTP-labelled antisense riboprobes for rat IL-1beta, type I IL-1 receptor (IL-1R) and secretory phospholipase A2 (sPLA2). PLA2 activity in conditioned media was assayed by measuring the release of [3H]-labelled palmitic acid from the sn-2 position of [3H]-labelled phosphatidylcholine dipalmitoyl (PCDP) substrate. Treatment with IGF-I resulted in a significant (P< 0.01) decrease in type I IL-1R transcripts (an effect which was reversed by co-treatment with IL-1beta), was without effect on IL-1beta transcripts, and significantly (P < 0.05) increased sPLA2 gene expression (an effect which was further enhanced by co-treatment with IL-1beta). Treatment with IGF-I resulted in a significant increase in extracellular PLA2 activity over untreated control. These observations suggest that IGF-I may down-regulate ovarian IL-1 action by decreasing type I IL-1R gene expression, while up-regulating sPLA2 gene expression and activity. These findings are consistent with a role for IGF-I in suppressing IL-1 actions while promoting the generation of prostaglandins. It is tempting to speculate that IGF-I, an intraovarian regulator concerned with promoting folliculogenesis, may be also entwined with priming the prostaglandin-producing potential in anticipation of subsequent ovulation.

Animals↗

Ovarian expression, cellular localization, and hormonal regulation of rat secretory phospholipase A2: increased expression by interleukin-1 and by gonadotropins.

It has been suggested that ovulation may constitute a cyclic inflammatory-like process and that gonadotropin-inducible intraovarian interleukin (IL)-1, an established mediator of inflammation, may play a central role in this regard. In support of this hypothesis, our group has been able to document the ability of IL-1 to potently stimulate prostaglandin biosynthesis by cultured rat ovarian cells. Herein we explore the possibility that the prostaglandin-stimulating action of IL-1 is due, in part, to the enhanced expression of ovarian secretory phospholipase-A2 (sPLA2). A single sPLA2 transcript of 1.4 kilobases was noted in all extraovarian tissues of immature rat origin subjected to Northern blot analysis. However, only a barely detectable signal was apparent in ovarian tissue. In contrast, the more sensitive RNase protection assay revealed the unequivocal presence of ovarian sPLA2 transcripts. Cellular localization studies by way of in situ hybridization documented sPLA2 transcripts primarily in the granulosa cell of the periovulatory ovary. Molecular probing of untreated cultured whole ovarian dispersates disclosed spontaneous elaboration of sPLA2 transcripts as early as 20 h after the introduction of cells into culture. Treatment of cultured whole ovarian dispersates with IL-1beta for 48 h produced a 1.7-fold increase (over the value in untreated controls) in the relative expression of sPLA2 transcripts (p < 0.01) along with a 1.7-fold increase in media PLA2 activity (p < 0.01). A more marked increase was documented for IL-1beta-treated cultured isolated granulosa cells (12.5-fold increase, p < 0.001). Treatment of whole ovarian dispersates with an IL-1 receptor antagonist (IL-1RA) produced a reduction in the basal expression of sPLA2 transcripts (55% at the 5 microg/ml dose level; p < 0.01) and PLA2 activity (40%; p < 0.01), thereby suggesting basal endogenous IL-1-like bioactivity. Treatment of cultured whole ovarian dispersates with either hCG or FSH led to 2.6-fold (p = 0.056) and 3-fold (p = 0.029) increases in the abundance of sPLA2 transcripts, respectively, effects blocked by the concurrent presence of IL-1RA. These observations 1) document the immature rat ovary as a site of sPLA2 gene expression, 2) localize the relevant transcripts to the postovulatory granulosa cell, 3) confirm the presence of functional secreted ovarian PLA2 activity, 4) reveal PLA2 expression to be IL-1- and gonadotropin-dependent, and 5) suggest the existence of endogenous PLA2-stimulating IL-1-like activity. These findings also suggest that the ability of hCG or FSH to up-regulate ovarian sPLA2 transcripts may be due, in part, to the endogenous elaboration of IL-like activity.

Animals↗

Assisted implantation: direct intraendometrial embryo transfer.

We report herein a technique for direct intraendometrial transfer (DIET) of human embryos. In this study we evaluated whether 2-day embryos injected into the endometrial stroma can develop normally into viable pregnancies. After in vitro fertilization the embryos were injected into the endometrium of 14 women under direct visualization using a CO2-pulsed flexible hysteroscope. A total of 44 embryos were transferred, resulting in 2 clinical (14.3% per cycle) and 2 chemical pregnancies. In 1 patient, amniocentesis revealed monosomy X and the pregnancy was terminated at 18 weeks. The 2nd patient had an uneventful pregnancy and delivered a healthy baby. The results from the present study, demonstrating a low implantation rate after DIET of 2-day embryos, suggest that the endometrial stroma does not provide an optimal environment for early embryonic development. The acidifying effect of CO2 used for insufflation may also explain the low pregnancy rate after DIET. We conclude that it is possible to achieve pregnancy by DIET in humans, but presently this procedure can be considered only in cases where the implantation site needs to be precisely determined.

Adult↗

The rat ovarian phospholipase A2 system: gene expression, cellular localization, activity characterization, and interleukin-1 dependence.

We have previously demonstrated that interleukin-1 beta (IL-1 beta), a putative intermediary in the ovulatory process, is a potent stimulator of ovarian PG biosynthesis. In this communication, we examine the possibility that this IL-1 effect reflects in part the induction of arachidonic acid mobilization by phospholipase A2 (PLA2). Molecular probing of whole ovarian material revealed the immature rat ovary to be a site of modest secretory PLA2 (sPLA2) gene expression. However, no change in ovarian sPLA2 gene expression was noted during the periovulatory period. Comparable probing for cytosolic PLA2 (cPLA2) failed to disclose a quantifiable signal. However, in situ hybridization localized both sPLA2 and cPLA2 (sPLA2 > cPLA2) transcripts to the granulosa cell layer of the ovarian follicle. Treatment of cultured whole ovarian dispersates with IL-1 beta produced significant (P < 0.01) increments in the steady state levels of transcripts corresponding to both sPLA2 (1.7-fold increase) and cPLA2 (5-fold increase), an effect reversed by an IL-1 receptor antagonist, suggesting mediation via a specific IL-1 receptor. Treatment with cycloheximide, a protein synthesis inhibitor, resulted in significant attenuation of the ability of IL-1 beta to up-regulate sPLA2 and cPLA2 gene expression as well as medium PLA2 activity. Treatment with aminoguanidine, an inhibitor of inducible nitric oxide synthase, led to augmentation of the ability of IL-1 beta to up-regulate sPLA2 and cPLA2 gene expression as well as medium PLA2 activity. Total cellular PLA2 activity proved time, cell density, and calcium dependent, with an optimal pH of 8.0-9.0 and K(m) values in the low micromolar range (2-5 microM). Our observations 1) establish the rat ovary as a site of sPLA2 and cPLA2 gene expression, 2) localize the corresponding transcripts to the granulosa cell layer, and 3) establish IL-1 beta as an up-regulatory agent for ovarian sPLA2 and cPLA2 gene expression as well as for ovarian PLA2 activity. These findings also indicate that the IL-1 effect is 1) receptor mediated, 2) contingent in part upon de novo protein biosynthesis, and 3) inhibited by nitric oxide. These observations support the proposition that PLA2 may be a key component in the IL-1-stimulated biosynthesis of ovarian PGs.

Animals↗

Interleukin-1 beta stimulates ovarian phosphoipase A2 (PLA2) expression and activity: up-regulation of both secretory and cytosolic PLA2.

Interleukin (IL)-1 beta has been shown to stimulate ovarian prostaglandin biosynthesis. We hypothesized that this effect entails the induction of phospholipase A2 (PLA2). Treatment of cultured whole ovarian dispersates of immature rat origin with IL-1 beta produced significant increases in [3H]arachidonic acid (AA) release and [3H]prostanoid accumulation as well as increases in cellular PLA2 activity and in secretory PLA2 and cytosolic PLA2 transcripts. Cotreatment with IL-1 receptor antagonist reversed IL-mediated (and basal) release of [3H]labeled AA and prostaglandin products, as well as cellular PLA2 activity. Treatment with IL-1 beta also promoted a significant decrease in the cellular content of [3H]phospholipids (apparently phosphatidylethanolamine but not phosphatidylcholine). These observations establish the ovary as a site of IL-1-dependent sPLA2 and cPLA2 gene expression, document the presence of a possible phosphatidylethanolamine-dependent PLA2 activity in cultured whole ovarian dispersates, reveal the up-regulatory, receptor-mediated action of IL-1 beta in this regard and suggest the existence of endogenous PLA2-stimulating/ IL-1-like bioactivity.

Animals↗

Interleukin (IL)-1beta increases glucose uptake and induces glycolysis in aerobically cultured rat ovarian cells: evidence that IL-1beta may mediate the gonadotropin-induced midcycle metabolic shift.

This communication explores the possibility that interleukin (IL)-1beta, a putative intermediary in the ovulatory process, may take part in the gonadotropin-driven midcycle diversion of ovarian carbohydrate metabolism toward glycolysis. We examined the effect of treatment with IL-1beta on glucose metabolism in aerobically cultured whole ovarian dispersates from immature rats. Treatment with IL-1beta increased cellular glucose consumption/uptake, stimulated extracellular lactate accumulation and media acidification, and decreased extracellular pyruvate accumulation in a receptor-mediated, time-, dose- and cell density-dependent manner. Endogenous IL-1beta-like bioactivity was shown to mediate the ability of gonadotropins to exert these same metabolic effects. The IL-1beta effect was also (1) apparent over a broad range of glucose concentrations, inclusive of the putative physiological window; (2) relatively specific, because tumor necrosis factor-alpha and insulin were inactive; (3) contingent upon cell-cell cooperation (4) and reliant on de novo protein synthesis. Comparison of the molar ratios of lactate accumulation to glucose consumption in IL-1beta-replete vs. IL-1beta-deplete cultures suggests that IL-beta promotes the conversion of all available glucose to lactate but that other substrates for lactate production may also exist. However, no lactate was generated by cells grown under glucose-free conditions. Taken together, our data suggest that IL-1beta may act as a metabolic hormone in the ovary. Subject to the limitations of the in vitro paradigm, our data also suggest that IL-1beta may mediate the gonadotropin-associated midcycle shift in ovarian carbohydrate metabolism. By converting the somatic ovarian cells into a glucose-consuming glycolytic machinery, IL-1beta may establish glycolysis as the main energy source of the relatively hypoxic preovulatory follicle and the resultant cumulus-oocyte complex. The consequent oxygen sparing may conserve the limited supply of oxygen needed for vital biosynthetic processes such as steroidogenesis. This adaptational response may also provide the glycolytically incompetent oocyte with the obligatory tricarboxylic cycle precursors it depends on to meet the increased energy demands imposed upon it by the resumption of meiosis.

Aerobiosis↗

Ovarian origin of plasma and peritoneal fluid prorenin in early pregnancy and in patients with ovarian hyperstimulation syndrome.

Prorenin is the major product of renin gene expression in the ovary. Plasma levels of prorenin are elevated in ovarian-stimulated patients and during early pregnancy. To further elucidate the source of the elevated plasma levels of prorenin, we measured prorenin, renin activity, angiotensinogen, and steroid hormone levels in the plasma, luteal fluids (luteal cysts), ascitic fluid, and in ovarian venous samples collected from a patient with severe ovarian hyperstimulation syndrome (OHSS) and ectopic pregnancy. Prorenin/renin was also measured in plasma and in peritoneal fluid obtained during, therapeutic paracentesis from four patients with OHSS. Several corpora luteal fluids were obtained that were rich in estradiol (E2) and progesterone (P). Ovarian venous E2 and P were 20-fold higher than in arterial blood and as high or higher than the levels detected in the luteal fluids. The ratios of the hormonal levels in ascitic fluid and plasma were 1.9 for P and 1.4 for E2. A wide range of prorenin concentrations [1279 +/- 918 SD ng/mL/hr, n = 6] were found in corpora luteal fluids, but in each the prorenin concentration was higher than in plasma (494 ng/mL/hr). Prorenin but not renin was higher (+23%) in ovarian venous than arterial blood. Prorenin in the 7 liters of ascitic fluid aspirated (2686 ng/mL/hr) was 5-fold higher than in plasma and similar to the levels measured in the corpora lutea with the highest prorenin concentrations. Renin in luteal cysts and ascitic fluid constituted 3% and 6% of the total renin (renin+prorenin), respectively. Total renin was also higher in peritoneal fluid (1538 +/- 925 ng/mL/hr) than in plasma (375 +/- 237 ng/mL/hr) of the 4 additional patients with severe OHSS. These findings indicate that the ovary secretes prorenin during early pregnancy and that its secretion is directed preferentially from the luteal cysts into the peritoneal cavity. In light of recent evidence of an effect of prorenin on the vascular system, the presence of a huge reservoir of prorenin in the peritoneal cavity of patients with OHSS suggests a potential role for prorenin in the pathogenesis of this syndrome.

Adult↗

Simplified riboprobe purification using translucent straws as gel tubes.

Gel purification of radioactive riboprobes enhances the quality of the ribonuclease protection assay. A simple and effective method for riboprobe purification is described. The method uses acrylamide gels in plastic tubes to achieve electrophoretic separation of the RNA polymerase products.

Animals↗

does intravenous administration of human albumin prevent severe ovarian hyperstimulation syndrome?

OBJECTIVE: To report our experience with i.v. albumin as a means to prevent ovarian hyperstimulation syndrome (OHSS) in high-risk patients. DESIGN: Retrospective case-series. SETTING: University hospital-based IVF program. PATIENTS: Five women undergoing controlled ovarian stimulation for IVF-Based on previous history and/or E2 measurements and number of ovarian follicles, these patients were considered to be at high risk for developing OHSS. INTERVENTIONS: Intravenous albumin was given at the time of oocyte retrieval. Additional doses were given 12 and 24 hours later. MAIN OUTCOME MEASURE: Development of OHSS. RESULTS: Four patients developed OHSS; two of them had the severe form of the syndrome. CONCLUSIONS: Severe OHSS may develop in high-risk patients despite the prophylactic administration of i.v. albumin.

Female↗