Surfactant-coated microbubbles are utilized in a wide variety of applications, from wastewater purification to contrast agents in medical ultrasound imaging. In many of these applications, the stability of the microbubbles is crucial to their effectiveness. Controlling this, however, represents a considerable challenge. In this study, the potential for stabilizing microbubbles using solid nanoparticles adsorbed onto their surfaces was explored. A new theoretical model has been developed to describe the influence of interfacially adsorbed solid particles upon the dissolution of a gas bubble in a liquid. The aim of this work was to test experimentally the prediction of the model that the presence of the nanoparticles would inhibit gas diffusion and coalescence/disproportionation, thus increasing the life span of the bubbles. Near-monodisperse microbubbles (~100 μm diameter) were prepared using a microfluidic device and coated with a surfactant, with and without the addition of a suspension of spherical gold nanoparticles (~15 nm diameter). The experimental results confirmed the theoretical predictions that as the surface concentration of gold nanoparticles increased the bubbles underwent negligible changes in their size and size distribution over a period of 30 days at the ambient temperature and pressure. Under the same conditions, bubbles coated with the same surfactant but no nanoparticles survived only a matter of hours.
Temperature-dependent sex determination (TSD) was first reported in 1966 in an African lizard. It has since been shown that TSD occurs in some fish, several lizards, tuataras, numerous turtles, and all crocodilians. Extreme temperatures can also cause sex reversal in several amphibians and lizards with genotypic sex determination. Research in TSD species indicates that estrogen signaling is important for ovary development and that orthologs of mammalian genes play a role in gonad differentiation. Nevertheless, the mechanism that actually transduces temperature into a biological signal for ovary versus testis development is not known in any species. Classical genetics could be used to identify the loci underlying TSD, but only if there is segregating variation for TSD. Here, we employ the “animal model” to analyze inheritance of sexual phenotype in a 13-generation pedigree of captive leopard geckos, Eublepharis macularius, a TSD reptile. We directly demonstrate genetic variance and genotype-by-temperature interactions for sex determination. Additive genetic variation was significant at a temperature that produces a female-biased sex ratio (30°C) but not at a temperature that produces a male-biased sex ratio (32.5°C). Conversely, dominance variance was significant at the male-biased temperature (32.5°C), but not at the female-biased temperature (30°C). Non-genetic maternal effects on sex determination were negligible in comparison to additive genetic variance, dominance variance, and the primary effect of temperature. These data show for the first time that there is segregating variation for TSD in a reptile and consequently that a QTL analysis would be practicable for identifying the genes underlying TSD.
Negative glucocorticoid feedback is essential for preventing the deleterious effects of excessive hypothalamic pituitary adrenal axis axis activation, with an important target being CRH transcription in the hypothalamic paraventricular nucleus. The aim of these studies was to determine whether glucocorticoids repress CRH transcription directly in CRH neurons, by examining glucocorticoid effects on glucocorticoid receptor (GR)-CRH promoter interaction and the activation of proteins required for CRH transcription. Immunoprecipitation of hypothalamic chromatin from intact or adrenalectomized rats subjected to either stress or corticosterone injections showed minor association of the proximal CRH promoter with the GR compared with that with phospho-CREB (pCREB). In contrast, the Period-1 (Per1, a glucocorticoid-responsive gene) promoter markedly recruited GR. Stress increased pCREB recruitment by the CRH but not the Per1 promoter, irrespective of circulating glucocorticoids. In vitro, corticosterone pretreatment (30 minutes or 18 hours) only slightly inhibited basal and forskolin-stimulated CRH heteronuclear RNA in primary hypothalamic neuronal cultures and CRH promoter activity in hypothalamic 4B cells. In 4B cells, 30 minutes or 18 hours of corticosterone exposure had no effect on forskolin-induced nuclear accumulation of the recognized CRH transcriptional regulators, pCREB and transducer of regulated CREB activity 2. The data show that inhibition of CRH transcription by physiological glucocorticoids in vitro is minor and that direct interaction of GR with DNA in the proximal CRH promoter may not be a major mechanism of CRH gene repression. Although GR interaction with distal promoter elements may have a role, the data suggest that transcriptional repression of CRH by glucocorticoids involves protein-protein interactions and/or modulation of afferent inputs to the hypothalamic paraventricular nucleus.
Circadian and ultradian variations of basal glucocorticoid secretion and transient elevations during stress are essential for homeostasis. Using intronic qRT-PCR to measure changes in primary transcript (hnRNA) we have shown that secretory events induced by stress or ACTH injection are followed by episodic increases in transcription of rate limiting steroidogenic proteins, such as steroidogenic acute regulatory protein (StAR), cytochrome P450 side chain cleavage and melanocortin receptor associated protein. These transcriptional episodes imply rapid turnover of steroidogenic proteins and the need of de novo synthesis following each secretory event. In addition to episodic ACTH secretion, it is likely that intracellular feedback mechanisms at the adrenal fasciculata level contribute to the generation of episodes of transcription. The time relationship between activation and translocation of the CREB co-activator, transducer of regulated CREB activity (TORC) to the nucleus preceding transcriptional episodes suggest the involvement of TORC in the transcriptional activation of StAR and other steroidogenic proteins.
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