Biomedical subjects

M P Trolice

Publications and source records attributed to M P Trolice.

4 recordsLinked to original sources

PubMed2000

Anesthetic efficacy of intrauterine lidocaine for endometrial biopsy: a randomized double-masked trial.

OBJECTIVE: To determine the efficacy of intrauterine lidocaine for decreasing pain associated with endometrial biopsy using the Pipelle instrument (Unimar; Wilton, CT). METHODS: Forty-one premenopausal and postmenopausal women had 5 mL of either 2% lidocaine or saline instilled in their uteri before endometrial biopsies. Subsequently, each woman completed a 20-cm visual analogue scale for subjective pain experience. We compared histologic findings in endometrial specimens. RESULTS: Before the study, analysis of specimens (n = 6) found no histologic effect on ability to interpret endometrial biopsies by pathologists who were masked to lidocaine or saline. There was no statistically significant difference in age, parity, race, history of chronic pelvic pain, menopausal status, use of tenaculum, or prior endometrial biopsy. The procedure was easy, with no clinically significant side effects. On the visual pain scale, the median (range) score for the lidocaine group (4.7, 0-19.7) compared with the placebo group (9.9, 1.6-20) showed significant reduction in pain corresponding with a decrease from moderate to mild (P < .01). CONCLUSION: Intrauterine lidocaine is simple and effective for decreasing pain associated with the Pipelle endometrial biopsy.

Administration, Intravaginal↗

PubMed1997

Basic fibroblast growth factor and N-cadherin maintain rat granulosa cell and ovarian surface epithelial cell viability by stimulating the tyrosine phosphorylation of the fibroblast growth factor receptors.

Both granulosa cells (GCs) and ovarian surface epithelial cells undergo apoptosis in vivo. Although basic fibroblast growth factor (bFGF) and N-cadherin-mediated cell contact inhibit GC apoptosis, little is known about the factors that influence rat ovarian surface epithelial (ROSE) cell apoptosis. The present studies were designed to determine whether bFGF and N-cadherin maintain the viability of both GC and ROSE cells by stimulating separate signaling pathways. For the GC studies, large GCs were collected from immature rat ovaries after Percoll gradient centrifugation and placed in serum-free culture for 24 h. These studies confirmed that about 10% of the aggregated GCs and more than 50% of single GCs were apoptotic after culture. bFGF reduced the percentage of apoptotic single GCs, but did not influence aggregated GCs. A neutralizing antibody to bFGF blocked bFGF's antiapoptotic action, but did not alter the percentage of apoptotic aggregated GCs. The antibody to N-cadherin not only increased the percentage of aggregated apoptotic GCs, but also blocked bFGF's ability to maintain the viability of single GCs. The effect of the FGF receptor antibody was similar to that of the N-cadherin antibody. Like GCs, ROSE cells also undergo apoptosis in serum-free medium. Exposure to either the N-cadherin or FGF receptor antibody, even in the presence of serum, increased the percentage of apoptotic aggregated ROSE cells. As tyrosine kinase activity is involved in maintaining cell viability, the pattern of tyrosine-phosphorylated proteins was examined after culture in control (ascites) or N-cadherin antibody-supplemented medium. Exposure to the N-cadherin antibody altered the pattern of tyrosine-phosphorylated proteins, decreasing the tyrosine phosphorylation of proteins in the 130- to 180-kDa range and increasing the tyrosine phosphorylation of one or more proteins of about 50 kDa. The identity of the 50-kDa protein is unknown. However, immunoprecipitation studies demonstrated that the N-cadherin antibody reduced the amount of tyrosine-phosphorylated FGF receptor in both GCs and ROSE cells by 50%. This decrease corresponds to an increase in apoptosis among aggregated cells. Taken together, these data suggest that homophilic N-cadherin binding and bFGF-FGF receptor binding activate signal transduction pathways that converge at the level of the FGF receptor and subsequently promote the viability of both GC and ROSE cells.

Animals↗

PubMed1996

N-cadherin-mediated cell contact inhibits granulosa cell apoptosis in a progesterone-independent manner.

Previous studies have shown that both progesterone and cell contact inhibit granulosa cell (GC) apoptosis in vitro. Since the progesterone concentration associated with aggregated GCs may be higher than that of single GCs, experiments were conducted to differentiate progesterone's action from that of cell contact. For these studies, GCs were isolated from immature rats. Large GCs were collected after Percoll gradient centrifugation and placed in serum-free culture for 24 h. These studies confirmed that the rate of apoptosis was 2-3 times higher for single GCs than for aggregated GCs. This relationship was observed in the presence of aminoglutethimide, where progesterone concentrations were 3 ng/ml or less. A dose-response studied revealed that a minimum of 100 ng/ml progesterone were required to suppress apoptosis of single GCs. In addition, a single cell contact was shown to be sufficient to suppress apoptosis, with a small nonsteroidogenic GC being as effective as a large steroidogenic GC. Taken together, these data support the concept that cell contact blocks apoptosis in a progesterone-independent manner. GC contact is due to the presence of gap and adhesion-type junctions. To assess which, if either, of these junctions is involved in mediating the antiapoptotic action of cell contact, cocultures were set-up between GCs and R2C cells. Contact with R2C cells inhibits GC apoptosis, but does not result in the formation of functional gap junctions. This demonstrates that gap junctions are not essential to maintain GC viability. Adhesion-type junctions result from a homophilic binding of N-cadherin, which is expressed by both GCs and R2C cells. When this binding is inhibited by treatment with either an antibody to N-cadherin or a synthetic N-cadherin peptide, cell aggregation is attenuated. For those cells that form cell contacts in the presence of these N-cadherin-binding inhibitors, the percentage of apoptotic cells is increased compared to that in controls. These observations suggest that homophilic binding of N-cadherin molecules on the surface membranes of adjacent GCs initiates a signal transduction cascade that ultimately inhibits apoptosis.

Animals↗

PubMed1994

Compliance problems with hormone replacement therapy.

Because menopause and its consequences constitute an endocrinopathy, long-term administration of HRT is often necessary to achieve optimal results. Compliance is therefore an important consideration in the clinical use of HRT. A number of factors appear to influence physicians in their prescribing of HRT, including estimates of benefits and risks that may not be supported by scientific data. In addition, some physicians appear to use patterns of administration of HRT that may diminish the chance of appropriate patient compliance, or of maximizing benefits while minimizing risks. Patients may elect to avoid HRT or stop HRT prematurely because of incorrect impressions about the benefits and risks, or because of bothersome side effects. Although the side effects are more prevent some appropriate candidates from using HRT. Fortunately, a range of possible options is available for prescribing HRT, and modifications may be used for patients who are experiencing problems. In order for patients to receive maximum benefit from HRT, clinicians must be willing to educate and reassure patients, and to adjust therapy when problems occur.

Drug Administration Schedule↗