As an important vertebrate model organism, zebrafish are typically studied at the embryonic stage to take advantage of their properties of transparency and rapid development. However, more and more studies require assays to be done on adults. Consequently, a good anesthetic is needed to sedate and immobilize the adult zebrafish during experimental manipulation. To date, MS-222 (tricaine methanesulfonate) is the only Food and Drug Administration approved anesthetic for aquaculture and is widely used by the zebrafish research community. Nevertheless, in adult zebrafish, MS-222 reduces heart rate and causes high mortality under long-term sedation. Consequently, adult zebrafish have limited research applications. In this study, we present a new anesthetic formula for the adult zebrafish that results in minimal side effects on its physiology under prolonged sedation. The combined use of MS-222 with isoflurane effectively extended the time of anesthesia, and the zebrafish recovered faster than when anesthetized with the traditional MS-222. Moreover, MS-222 + isoflurane did not cause reduction of heart rates, which enabled long-term electrocardiogram recording and microscopic observation on the adult zebrafish. Taken together, the new MS-222 + isoflurane formula will facilitate general applications of adult zebrafish in time-consuming experiments with minimal side effects on the model organism's overall physiology.

Findings from this study indicate the importance of work-to-family conflict to nurse turnover. While work setting has a strong, well-documented influence on job satisfaction, limiting job satisfaction efforts to work setting improvements may not yield the hoped-for results unless work-to-family conflict is also considered and addressed.

In this work, the zebrafish model organism was developed to obtain a minivertebrate host system for a Candida albicans infection study. We demonstrated that C. albicans can colonize and invade zebrafish at multiple anatomical sites and kill the fish in a dose-dependent manner. Inside zebrafish, we monitored the progression of the C. albicans yeast-to-hypha transition by tracking morphogenesis, and we monitored the corresponding gene expression of the pathogen and the early host immune response. We performed a zebrafish survival assay with different C. albicans strains (SC5314, ATCC 10231, an hgc1 mutant, and a cph1/efg1 double mutant) to determine each strain's virulence, and the results were similar to findings reported in previous mouse model studies. Finally, using zebrafish embryos, we monitored C. albicans infection and visualized the interaction between pathogen and host myelomonocytic cells in vivo. Taken together, the results of this work demonstrate that zebrafish can be a useful host model to study C. albicans pathogenesis, and they highlight the advantages of using the zebrafish model in future invasive fungal research.

Myocardial injury, such as myocardial infarction (MI), can lead to drastic heart damage. Zebrafish have the extraordinary ability to regenerate their heart after a severe injury. Upon ventricle resection, fibrin clots seal the wound and serve as a matrix for recruiting myeloid-derived phagocytes. Accumulated neutrophils and macrophages not only reduce the risk of infection but also secrete cytokines and growth factors to promote tissue repair. However, the underlying cellular and molecular mechanisms for how immune responses are regulated during the early stages of cardiac repair are still unclear. We investigated the role and programming of early immune responses during zebrafish heart regeneration. We found that zebrafish treated with an anti-inflammatory glucocorticoid had significantly reduced heart regenerative capacities, consistent with findings in other higher vertebrates. Moreover, inhibiting the inflammatory response led to excessive collagen deposition. A microarray approach was used to assess the differential expression profiles between zebrafish hearts with normal or impaired healing. Combining cytokine profiling and immune-staining, our data revealed that impaired heart regeneration could be due to reduced phagocyte recruitment, leading to diminished angiogenesis and cell proliferation post-cardiac injury. Despite their robust regenerative ability, our study revealed that glucocorticoid treatment could effectively hinder cardiac repair in adult zebrafish by interfering with the inflammatory response. Our findings may help to clarify the initiation of cardiac repair, which could be used to develop a therapeutic intervention that may enhance cardiac repair in humans to compensate for the loss of cardiomyocytes after an MI.

The 10MP model is effective at improving training outcomes and facilitating the professional development of NGNs.