The two-step process of ovarian follicular growth and maturation in mammals can be compared to a fruit ripening where quality depends on the second step

In human IVF, the main uncertainty factor impacting on success is oocyte quality, which largely depends on the follicular status at the time of collection. Decades of debate ensued to find the perfect stimulation protocol demonstrated the complexity of the ovarian response to exogenous gonadotropins and the dynamic nature of late folliculogenesis. Although several follicular markers, proteins, RNA from granulosa cells or microRNA and follicular fluid metabolites have been associated with outcome, the possibility to influence them during stimulation remains elusive. The heterogeneity of the follicle’s maturity following control ovarian stimulation is also an important factor to explain average poor oocyte quality still observed today. In this review, the analogy between the apple ripening on the tree and follicular development is presented to focus the attention on a biphasic process: growth and differentiation. The molecular analysis of the progressive follicular differentiation indicates 2 competing phenomena: growth and differentiation where a delicate balance must operate from one to the other to ensure proper maturity at ovulation. As long as FSH stimulates growth, follicles remain green, and it is only when FSH is replaced by LH that the ripening process begins, and “apples” become red. Both fruits, follicles and apples, depend on a perfect timing of events to generate offspring.

Catalytic conversion of fructose into 5-HMF under eco-friendly-biphasic process

One-pot conversion of fructose into valuable 5-hydroxymethyl-2-furaldehyde (5-HMF) was investigated under a deep eutectic solvent-biphasic system.

Control of seed coat rupture by ABA-INSENSITIVE 5 in Arabidopsis thaliana

In Arabidopsis, seed germination is a biphasic process involving rupture of the seed coat followed by emergence of the radicle through the micropylar endosperm. Embryo expansion results in seed coat rupture and removal of seed coat imposed dormancy with DELLA proteins blocking embryo expansion in the absence of gibberellins. Exogenous abscisic acid (ABA) treatment does not block seed coat rupture but does block radicle emergence. We used this limited effect of exogenous ABA to further investigate the mechanism by which it blocks the onset of germination marked by seed coat rupture. We show that physical nicking of the seed coat results in exogenous ABA treatment blocking both seed coat and endosperm rupture and this block requires the transcription factors ABI3 and ABI5, but not ABI4. Furthermore, we show that the repression of expression of several EXPANSIN genes (EXPA1, EXPA2, EXPA3, EXPA9 and EXPA20) by exogenous ABA requires ABI5. We conclude that ABI5 plays an important role in the ABA-mediated repression of germination through prevention of seed coat rupture and propose that this involves EXPANSIN related control of cell wall loosening.

Water-assisted selective hydrodeoxygenation of phenol to benzene over the Ru composite catalyst in the biphasic process

Schematic illustration of HDO of phenol to benzene in the biphasic catalytic process.

Time course of compensatory physiological responses to central hypovolemia in high- and low-tolerant human subjects

Lower body negative pressure (LBNP) simulates hemorrhage in human subjects. Most subjects (67%) exhibited high tolerance (HT) to hypovolemia, while the remainder (33%) had low tolerance (LT). To investigate the mechanisms for decompensation to central hypovolemia in HT and LT subjects, we characterized the time course of total peripheral resistance (TPR), heart rate (HR), and muscle sympathetic nerve activity (MSNA) during LBNP to tolerance determined by the onset of decompensation (presyncope, PS). We hypothesized that 1) maximum (Max) TPR, HR, and MSNA would coincide, and 2) PS would result from simultaneous decreases in TPR, HR, and MSNA in LT and HT subjects but occur earlier in LT than in HT subjects. Max TPR was lower and occurred earlier in LT ( n = 59) than in HT ( n = 113) subjects (LT: 24 ± 1 mmHg·min·1−1at 756 ± 31 s; HT: 28 ± 1 mmHg·min·1−1at 1,265 ± 37 s, P < 0.01). Max TPR occurred several minutes before PS. During subsequent decrease in TPR, HR and MSNA continued to increase. Max HR (LT: 111 ± 2 beat/min at 923 ± 27 s; HT: 130 ± 2 beats/min at 1489 ± 23 s, P < 0.01) occurred several seconds before PS. Higher MSNA ( P < 0.01) was attained in HT ( n = 10; 51 ± 5 bursts/min at max TPR; 54 ± 5 bursts/min at max HR) than LT subjects ( n = 4; 41 ± 8 bursts/min at max TPR; 39 ± 8 bursts/min at max HR). The onset of cardiovascular decompensation is a biphasic process in which vasodilation occurs before bradycardia and sympathetic withdrawal. This pattern was similar in LT and HT but occurred earlier in LT subjects. We conclude that sudden bradycardia plays a critical role in the determination of tolerance to central hypovolemia.