Given an abstract of a paper, generate a title for this paper such that conveys the key focus of the paper.

Input: Consider Input: Abstract: The 2-cell murine embryo bioassay as quality control for human in vitro fertilization (IVF) was used to evaluate the effects of protein supplements, medium aging, and surgical glove coatings. Ham's F-10 medium (GIBCO, Grand Island, NY) without protein supplementation supported growth of the 2-cell embryos to blastocysts. Addition of bovine serum albumin (BSA), fetal cord serum (FCS), or maternal serum (MS) did not enhance or reduce the blastulation rates (medium alone, 89.4%; BSA, 86.4%; FCS, 90%; MS, 74.7%). Unsupplemented Ham's F-10 medium was found to contain three major peaks of approximately 50,000 daltons and several minor peaks, analyzed on high-performance liquid chromatography (HPLC) and sodium sulfate-polyacrylamide gel electrophoresis (SDS-PAGE), suggesting the presence of protein(s) in the medium itself. The storing of medium up to 425 days at 4 degrees C affected neither the HPLC profile nor its ability to support embryo growth (blastulation rates: fresh, 84%; stored 150 to 425 days, 77.7%). The coating of surgical gloves affected embryo growth. Both talc-coated (TC) and "talc-free," starch-coated (SC) surgical gloves were found to be progressively embryotoxic when they touched the medium for increasing lengths of time, compared with uncoated latex (UL) gloves and untouched control medium. Quality control of medium preparation and handling in murine embryo bioassay is reemphasized, with requirements for protein supplementation, use of fresh medium, and possible contamination with even talc-free, SC surgical gloves reevaluated.

Output: Factors influencing murine embryo bioassay: effects of proteins, aging of medium, and surgical glove coatings.

Input: Consider Input: Abstract: The dose-response curves of the central and peripheral airways to intravenously injected nicotine were studied in 55 anesthetized dogs. With intact vagi, nicotine caused a dose-dependent increase in central airway resistance (Rc) similar to the increase in peripheral airway resistance (Rp) at concentrations ranging from 4 to 64 micrograms/kg. However, the responses of both Rc and Rp fell progressively when sequential doses of nicotine greater than 256 micrograms/kg were administered. With intact vagi and the administration of propranolol, there was a greater increase in Rp than in Rc at a nicotine dose of 64 micrograms/kg (P less than 0.05). With vagotomy, the responsiveness of both central and peripheral airways to nicotine decreased with doses of nicotine less than 64 micrograms/kg, but with doses of nicotine greater than 256 micrograms/kg the suppressive effect of nicotine on both Rc and Rp was less than that seen with intact vagi. Under conditions in which the vagi were cut and atropine administered, the responsiveness of nicotine was even further depressed. Combinations either of atropine and chlorpheniramine or atropine and phenoxybenzamine also completely blocked reactions to nicotine. Additionally reactions to nicotine were completely blocked by hexamethonium. These results suggest that nicotine increases both Rc and Rp mainly through a vagal reflex and stimulation of the parasympathetic ganglia.

Output: Dose-response curves of central and peripheral airways to nicotine injections in dogs.

Input: Consider Input: Abstract: We studied the interaction between dopamine and estradiol on PRL release by cultured normal and tumorous PRL-secreting cells prepared from human pituitaries. If pituitary glands were obtained within 3 h after sudden death of previously normal individuals, the viability of isolated pituitary cells prepared by dispersion with dispase was more than 75%. After 4 days of culture, dopamine (500 nM) inhibited PRL release by cells prepared from four normal pituitaries by 24 +/- 3% (+/- SEM). Pretreatment of the cells with 100 nM estradiol did not alter dopamine-mediated inhibition of PRL release. Estradiol alone increased basal PRL release and cell PRL content. Cultured PRL-secreting pituitary tumor cells, obtained by transsphenoidal operation from four patients, were similarly sensitive to dopamine. Estradiol stimulated tumor cell PRL release and content, but significantly diminished the inhibitory effect of dopamine. The estrogen receptor blocker tamoxifen did not alter PRL release, but it did reverse the estradiol-induced insensitivity of the prolactinoma cells to the dopamine agonist bromocriptine. In conclusion, these in vitro results indicate that estrogens do not antagonize the effect of dopamine on normal human PRL-secreting pituitary cells. In human pituitary tumor cells, however, estradiol decreased the sensitivity of PRL release to dopamine (agonists), and the estrogen action can be acutely reversed by tamoxifen.
Output: Differences in the interaction between dopamine and estradiol on prolactin release by cultured normal and tumorous human pituitary cells.