Search

Background: Although the resident candidate interview is costly and time-consuming for both applicants and programs, it is considered critically important for resident selection. Noncognitive attributes, including communication skills and professionalism, can be assessed by the personal interview., Objective: We conducted a review of the literature on the residency interview to identify the interview characteristics used for resident selection and to ascertain to what extent the interview yields information that predicts future performance., Methods: We searched PubMed and Scopus using the following search terms: residency, internship, interview, selection, and performance. We extracted information on characteristics of the interview process, including type of interview format, measures taken to minimize bias by interviewers, and testing of other clinical/surgical skills., Results: We identified 104 studies that pertained to the resident selection interview, with highly varied interview formats and assessment tools. A positive correlation was demonstrated between a medical school academic record and the interview, especially for unblinded interview formats. A total of 34 studies attempted to correlate interview score with performance in residency, with mixed results. We also identified a number of studies that included personality testing, clinical skills testing, or surgical skills testing., Conclusions: Our review identified a wide variety of approaches to the selection interview and a range of factors that have been studied to assess its effectiveness. More research needs to be done not only to address and ascertain appropriate interview formats that predict positive performance in residency, but also to determine interview factors that can predict both residents' "success" and program attrition.

Previous studies have reported that the monotropic rise in FSH in older women is associated with decreased inhibin B and/or A levels and increased levels of activin A. Whereas most investigators have found decreased follicular-phase inhibin B, the roles of inhibin A and activin A as modulators of the FSH rise are unclear. The objectives of this study were to determine whether deficiencies in circulating levels of inhibin A, inhibin B, and/or activin A exist during the intercycle interval in ovulatory older (age, 40-45 yr; n = 16), compared with younger women (age, 20-25 yr; n = 13). Blood samples were obtained daily throughout one menstrual cycle and the follicular phase of the subsequent cycle and were analyzed for LH, FSH, estradiol, inhibin A and B, and activin A. Despite significant FSH elevation, no deficiencies in inhibin A, activin A, or estradiol were detected in older subjects. In fact, inhibin A was significantly higher in older participants during the intercycle phase (P = 0.01), whereas inhibin B was significantly lower. Thus, the monotropic rise in FSH does not appear to result from changes in inhibin A or activin A, supporting the concept that inhibin B plays a critical role in mediating the FSH rise in older women.

This study sought to determine whether the shortened follicular phase in ovulatory older women is secondary to advanced (i.e. earlier) or accelerated (i.e. more rapid) folliculogenesis. Normal ovulatory women, aged 40-45 yr (n = 15) and 20-25 yr (n = 13), underwent daily venipuncture and transvaginal ultrasonography throughout the follicular phase of a spontaneous menstrual cycle (control cycle) and after pituitary down-regulation with a GnRH agonist (study cycle). As expected, the older subjects in the control cycles demonstrated an elevated d 3 FSH and a shortened follicular phase compared with the younger subjects. After release from hypothalamic-pituitary-ovarian axis suppression, the early follicular phase FSH peak occurred earlier (6.8 vs. 9.8 d; P < 0.01) and was of a greater magnitude (12.1 vs. 6.5 mIU/ml; P < 0.01) in the older subjects. The time from release of suppression until the subsequent LH surge was also shorter (17.5 vs. 20.8 d; P < 0.01) in the older group. However, the time from FSH peak to LH surge was similar in the older and younger groups (10.7 vs. 11.0 d; P = 0.74). Compared with younger women, older subjects had normal follicular phase levels of estradiol and inhibin A and lower levels of inhibin B in both control and study cycles. We conclude that the shortened follicular phase observed in older ovulatory women is due to earlier dominant follicle selection, independent of hormonal influences from the preceding luteal phase.

Objective: To determine the effectiveness of a combined clomiphene citrate/gonadotropin protocol in a general infertility population and to evaluate factors influencing pregnancy rates obtained with this protocol., Design: A retrospective chart review. SETTING; University-based infertility clinic., Patient(s): Two hundred forty-eight patients undergoing 658 cycles of minimal stimulation (MS) protocol from 1996-2000., Intervention(s): Patients underwent treatment with clomiphene citrate and gonadotropin, often followed by intrauterine insemination., Main Outcome Measure(s): Clinical pregnancy rates., Result(s): Overall, the clinical pregnancy rate was 7.1% per cycle (n = 248 patients and 658 cycles). The age range of the patients was 24-47 years (mean +/- SD = 36.5 +/- 4.9) with 8.7% noted to have ovulatory dysfunction. Pregnancy rates varied significantly (P<.05) with patient age (9.3% in women <40 years vs. 2.4% in women > or =40), duration of infertility (9.0% in women with < or =3 years of infertility vs. 2.2% in women with >3 years of infertility) and number of follicles produced during stimulation (9.1% in women with > or =3 follicles vs. 4.6% in women with <3 follicles)., Conclusion(s): The effectiveness of the MS protocol in a general infertility population with a predominantly ovulatory status is much less than that previously reported in a younger patient population with a significant rate of ovulatory dysfunction. This protocol does not appear to lead to pregnancy rates higher than that reported for clomiphene citrate/intrauterine insemination (IUI) cycles. The clinical pregnancy rates using a minimal stimulation protocol are particularly compromised in women over 40, those with a longer duration of infertility or those who produce few follicles during stimulation.

Objective: To determine current practice patterns of obtaining informed consent for infertility treatment by reproductive endocrinologists and to assess changes in response to reports of an association between ovulation induction and ovarian cancer., Methods: Board-certified reproductive endocrinologists (n = 575) were surveyed by mail regarding how they informed patients and obtained consent for infertility treatments and how their practices had been influenced by studies suggesting a link between ovulation induction and ovarian cancer. Data were analyzed using chi2 and logistic regression analyses., Results: The return rate was 62.1% (357 of 575 surveys). Most respondents (92%) used discussions with physicians to inform their patients of risks and benefits of all infertility treatments. Additional means, such as audiovisual aids, were used significantly more often for assisted reproductive technologies (including intracytoplasmic sperm injection and use of donated eggs) than for less invasive therapies (31-43% versus 4-11%, P < .001). Most physicians (46-66%) used verbal consent alone for hysterosalpingogram, intrauterine insemination, and ovulation induction. Formal written consent was used significantly more often for the various assisted reproductive technologies than for hysterosalpingogram, intrauterine insemination, or ovulation induction (94-95% versus 26-44%). Although most physicians (70%) did not believe that ovulation induction increases the risk of ovarian cancer, 83% addressed this risk when obtaining consent and 47% reported changing their practices since an association was reported. Common changes included limiting length of treatment and addressing ovarian cancer risk., Conclusion: Current practice patterns of obtaining informed consent for various infertility treatments by board-certified reproductive endocrinologists show, as expected, that informed consent is more rigorous for assisted reproductive technologies. Although most surveyed did not believe that ovulation induction increases risk of ovarian cancer, the majority of physicians addressed that risk when obtaining consent and nearly half changed their practices on the basis of a possible association.

The current study was designed to examine the effects of prostaglandin (PG) E2 on progesterone production by primate luteal cells collected during the late luteal phase. PGE2 inhibited basal and human chorionic gonadotrophin (HCG)-stimulated progesterone production (P < 0.01) in late luteal phase corpora lutea. The ability of PGE2 to activate a second messenger system (phosphatidylinositol pathway) in corpora lutea of rhesus monkeys was also assessed. PGE2 significantly increased the accumulation of inositol phosphates (P < 0.05). This stimulation was not apparent in the early luteal phase but was manifested in the mid-late luteal phase. PGE2 also caused a rapid, yet transient, increase (P < 0.01) in intracellular free calcium ion concentrations ([Ca2+]i) in a large proportion of primate luteal cells. The proportion of luteal cells that responded to PGE2 with an increase in [Ca2+]i was smaller (P < 0.05) in corpora lutea collected during the early luteal phase (12%) in comparison with those collected during the latter half of the luteal phase (63-66%). Changes in [Ca2+]i in response to PGE2 were similar in small and large luteal cells. This study demonstrates that PGE2 activates elements of the phosphatidylinositol pathway in primate corpora lutea. This activation is augmented as the luteal phase progresses. Thus, the inhibitory effects of PGE2 on luteal progesterone production observed in the late luteal phase are associated with activation of elements of the phosphatidylinositol pathway.

The current study was designed to investigate the effects of gonadotropin on basal and prostaglandin (PG) F2 alpha-induced activity of the phosphatidylinositol pathway in corpora lutea (CL) of rhesus monkeys. Luteal progesterone production in vitro was significantly stimulated (P < 0.05) by human chorionic gonadotropin (hCG). Neither basal nor PGF2 alpha-induced phosphatidylinositol 4,5-bisphosphate hydrolysis was significantly influenced by hCG in CL of various ages (P > 0.10). Gonadotropin did induce a slight, yet sustained, increase (P < 0.05) in [Ca2+]i in approximately 70% of luteal cells. The maximal increase in [Ca2+]i in response to hCG (approximately 100 nM) was about one-tenth that induced by PGF2 alpha (approximately 1000 nM). hCG treatment did not alter (P > 0.10) the increase in [Ca2+]i induced by PGF2 alpha Treatment-induced changes in [Ca2+]i did not differ between small (17-21 microns) and large (23-28 microns) luteal cells. Therefore, luteolytic agents are more potent activators of the phosphatidylinositol pathway than luteotropins. This is consistent with the hypothesis that the phosphatidylinositol pathway is involved in primate luteal regression. The inability of hCG to acutely alter the responsiveness of this pathway to PGF2 alpha suggests that CG may rescue the CL of early pregnancy via a mechanism other than direct inhibition of the luteolytic actions of PGF2 alpha.

The current study was designed to investigate the ability of prostaglandin F2 alpha (PGF2 alpha) to activate a second messenger system (phosphatidylinositol pathway) in corpora lutea (CL) of rhesus monkeys. Activation of this pathway was assessed by monitoring the hydrolysis of phosphatidylinositol to inositol phosphates. Since inositol triphosphate mobilizes intracellular Ca2+, intracellular free calcium concentrations ([Ca2+]i) were also assessed in individual cells by fura-2 fluorescence photometry. These responses to PGF2 alpha were measured in luteal cells collected from nonpregnant rhesus monkeys. CL were collected during the early (days 4-5 after estimated LH surge; n = 4), mid (days 8-9; n = 4), and late (days 13-14; n = 5) luteal phase and 1 day after in vivo hCG treatment (15 IU/dose, morning and evening), which began during the midluteal phase (n = 5). PGF2 alpha significantly increased the accumulation of inositol phosphates in all groups (P less than 0.05), except the midluteal phase (P = 0.07). The luteal sensitivity to PGF2 alpha, judged by phosphatidylinositol hydrolysis, was low in the early to midluteal phase compared to that in the late luteal phase and after in vivo hCG treatment. PGF2 alpha also caused a rapid, yet transient, increase in [Ca2+]i in a large proportion of primate luteal cells. The proportion of luteal cells that responded to PGF2 alpha with an increase in [Ca2+]i was smaller (P less than 0.05) in CL collected during the early luteal phase than in the other groups. Luteal progesterone production was inhibited by PGF2 alpha in CL collected after in vivo hCG. CL treated in vivo with hCG also displayed in vitro the largest increases in phosphatidylinositol hydrolysis and [Ca2+]i in response to PGF2 alpha. Therefore, this study demonstrates that PGF2 alpha is a potent activator of the phosphatidylinositol pathway in the primate CL. This activation is augmented as the luteal phase progresses and is influenced by in vivo hCG treatment. This study also provides evidence that the inhibitory effects of PGF2 alpha on progesterone production are associated with the activation of the phosphatidylinositol pathway.

The role of the phosphatidylinositol second messenger system in luteal regulation has not been extensively studied, particularly in the primate. The objectives of this study were (1) to further characterize the response of the primate CL to the calcium ionophore A23187, in terms of intracellular free calcium concentrations ([Ca2+]i) and progesterone (P) production; and (2) to assess the effects of depleting, as well as elevating, available calcium on luteal P and prostaglandin (PG) production. The response to A23187, in terms of [Ca2+]i, was measured by fura-2 fluorescence microscopy of single small and large luteal cells. A23187 significantly increased [Ca2+]i in both cell types (p less than 0.01). P production (basal and hCG-stimulated) by dispersed primate luteal cells incubated for various times (1-8 h) with and without A23187 was measured. Treatment with A23187 rapidly (within 1-2 h) attenuated (p less than 0.05) the time-dependent increase in basal and hCG-stimulated P production. Luteal P and PG production following treatment with the calcium ionophore, ionomycin, alone or in combination with additional CaCl2, was also monitored. Treatment with ionomycin (p less than 0.01) and CaCl2 (p less than 0.01) inhibited luteal P production. In contrast, treatment with ionomycin stimulated (p less than 0.01) luteal PG production. To determine the effects of Ca2+ depletion on luteal function, P and PG production by cells incubated for 2 and 8 h in the absence and presence of the Ca(2+)-chelator EGTA was measured. Luteal production of both P and PG was inhibited by 8-h treatment with EGTA.(ABSTRACT TRUNCATED AT 250 WORDS)

Prostaglandin F(2alpha) (PGF(2alpha)) plays a role in the regression of the corpus luteum (CL) in a number of placental mammals. However, the mechanism of luteal regression has not been extensively studied in marsupials. The objectives of this study were to characterize changes in concentrations of PGF(2alpha) within utero-ovarian (UO) tissue/venous plasma during the luteal phase of the estrous cycle in Virginia opossums, to correlate these changes with those of plasma progesterone (P(4)), and to characterize the peripheral pattern of 13,14-dihydro-15-keto-PGF(2alpha) (PGFM) in parturient opossums. Ovaries, uteri, UO venous plasma and peripheral plasma were collected on Days 5, 9 and 12 after induced ovulation (n = 3 to 4 opossums/group). In addition, concentrations of PGFM were measured in peripheral plasma collected from two opossums during late gestation (Days 7,9,11 and 12) and at parturition (Day 13). Concentrations of P(4), PGFM and PGF(2alpha) in tissue homogenates and plasma samples were estimated by radioimmunoassay. In nonpregnant opossums, peripheral P(4) levels were highest on Day 5 (38.8 +/- 11.1 ng/ml, x +/- SEM) declined on Day 9 (22.6 +/- 7.4 ng/ml), and were at basal levels by Day 12 (2.4 +/- 0.7 ng/ml). Endometrial concentrations of PGF(2alpha) increased (P = 0.056) from Day 5 (15.7 +/- 4.1 ng/g) to Day 9 (92.1 +/- 61.0 ng/g) and were maintained to Day 12 (97.2 +/- 25.7 ng/g). Prostaglandin F(2alpha) concentrations in UO plasma increased (P < 0.01) from Day 5 (143.1 +/- 32.7 pg/ml) to Day 12 (333.0 +/- 32.4 pg/ml). Prostaglandin F(2alpha) concentrations in ovarian tissue followed a similar pattern and were correlated with UO concentrations (r = 0.708, P < 0.05). In pregnant opossums, the highest levels of peripheral PGFM were recorded in the peripartum period, when luteal regression would also be expected to occur. The negative temporal relationship between peripheral concentrations of P(4) and concentrations of PGF(2alpha) in UO tissue/venous plasma observed in this preliminary study is consistent with the notion that PGF(2alpha) from the ovary and/or uterus may play a role in CL regression in the opossum.

Prostaglandins (PG) are produced by the corpus luteum (CL) of the rhesus monkey and may be involved in luteal regulation. Intracellular calcium has also been implicated as a mediator of luteolysis in domestic and laboratory species; however, its role in primate luteal function has not been investigated. The objectives of this study were to characterize temporal changes in basal and stimulated luteal PG production by CL of rhesus monkeys, and to examine the effects of calcium ionophore (CaI) on basal and gonadotropin-stimulated progesterone (P) production by the CL. CL were collected at various times after the estimated day of the luteinizing hormone (LH) surge: 5 days (early luteal phase, n = 4), 8-10 days (mid-luteal phase, n = 8), and 12-14 days (late luteal phase, n = 5). Dispersed luteal cells were incubated in the absence and presence of CaI, or with human chorionic gonadotropin (hCG) plus CaI at 37 degrees C for 8 h. PG and P concentrations in the medium were measured by radioimmunoassay. PGE2 and 6-keto-PGF1 alpha production decreased (p less than 0.05) from early luteal phase to mid-luteal phase and remained lower (p less than 0.05) during late luteal phase for all treatment groups. PGF2 alpha production decreased (p less than 0.05) from early to mid-luteal phase and rebounded in late luteal phase to the same level (p greater than 0.05) found in early luteal phase. CaI stimulated (p less than 0.05) basal PG production. The degree of stimulation was similar throughout the luteal phase (p greater than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Stimulation of the primate corpus luteum (CL) by endogenous chorionic gonadotropin (CG) in early pregnancy, or by exogenous human (h)CG in simulated early pregnancy, results in a transient elevation of serum progesterone (P) and a persistent elevation of serum 17 beta-estradiol (E). Luteal prostaglandins (PG) may play a role in these responses. The objective of the current study was to correlate luteal PG production and steroidogenic response of CL in vitro with patterns of serum steroids during simulated early pregnancy. CL were removed from rhesus monkeys (n = 26) at 0 h, 9 h, 3 days, 6 days, and 10 days, during prolonged CG exposure of simulated early pregnancy. Dispersed cells were incubated in vitro at 37 degrees C for 8 h. Changes in basal production of P were not significantly correlated with patterns of serum steroids. Maximal stimulation of P production by hCG in vitro (stimulated minus basal) continuously declined (p less than 0.01) from 0 h (means +/- SE, 59.6 +/- 17.9 ng/ml) to 10 days (4.7 +/- 1.8 ng/ml) of simulated early pregnancy. In contrast to patterns of response to hCG, the level of enhancement in P production in response to a maximally stimulatory dose of dibutyryl (db) cyclic adenosine 3',5'-monophosphate (cAMP) declined (p less than 0.05) from 0 h (52.4 +/- 17.6 ng/ml) to 3 days (20.3 +/- 8.4 ng/ml), but was maintained through 10 days (23.7 +/- 11.6 ng/ml) of simulated early pregnancy. As such, desensitization to gonadotropin, which occurred in terms of P production, appears to involve an event subsequent to stimulation of adenylate cyclase.(ABSTRACT TRUNCATED AT 250 WORDS)