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Marine diseases have caused large scale decreases in coral cover across the Caribbean and are unfortunately projected to increase as sea surface temperatures rise. Identifying the main drivers of disease transmission is essential for our understanding and response to diseases in the future. This study investigates the effects of direct-contact, waterborne, Symbiodiniaceae composition, and butterflyfish foraging on the transmission rates of stony coral tissue loss disease (SCTLD) across Montastraea cavernosa (MCAV) coral fragments. M. cavernosa fragments were placed in direct contact with diseased Orbicella and Montastraea colonies with the purpose of creating disease MCAV fragments for experimental trials with butterflyfish. Three treatments were used to investigate waterborne transmission (control), mechanically injury to a healthy coral (limited), and direct contact feeding across a diseased and healthy coral (unlimited). After the experimental trials, the composition of Symbiodiniaceae was analyzed for every MCAV fragment. Direct contact transmission took on average 3.9 days in 2019 and 11.9 days in 2020 with significantly quicker rates of transmission between donor diseased Orbicella and Montastraea than Montastraea to Montastraea. The composition of Symbiodiniaceae differed significantly between the fragments used in 2019 (dominated by Durusdinium) than in 2020 (dominated by Cladocopium spp.). The limited treatment had the quickest time to transmission compared to the unlimited and control treatments. Symbiodiniaceae differences between 2019 and 2020 might explain differences in transmission rates and overall susceptibility between the years. The species of Symbiodiniaceae may play a role in the susceptibility of corals to the transmission of SCTLD. Additionally, we also have some suggestive evidence that butterflyfish do not directly increase infection rates, but instead might be increasing infection recovery.

Aggression in juveniles is an evolutionarily adaptive behavior documented in many species, but the neural mechanisms behind these displays are poorly understood. In humans, the importance of knowing what is happening in the brain during maladaptive aggression is especially key in instances of psychiatric disorders that display as aggressive tendencies in childhood, such as autism spectrum disorders (ASD), schizophrenia, and borderline personality disorder. Mimetic poison frog (Ranitomeya imitator) tadpoles live in small pools with limited resources and have evolved offensive aggressive tendencies towards conspecific tadpoles in defense of these resources. Tadpoles will attack, kill, and cannibalize other tadpoles as a primary resource defense mechanism. I examined the neural basis of neonate aggression in these tadpoles by comparing individuals that were placed in aggressive encounters and individuals placed in an environment with a non-threatening stimulus. I first did a longitudinal study to determine that the tadpoles were most aggressive when they were around five or six weeks old. I then compared patterns of generalized neural activity using immunohistochemical detection of phosphorylated ribosomes and a candidate neuropeptide, arginine vasotocin, which has been implicated in aggression in other vertebrates. Vasotocin cells in the preoptic area of the hypothalamus were not more active in aggressive tadpoles. I then examined neural activation across several brain regions suspected to be involved in aggression, and found that the anterior amygdala had the most neural activation in aggressive tadpoles compared to controls and the other brain regions. Through molecularly profiling active neurons using phosphoTRAP, I identified proopiomelanocortin (POMC), a precursor polypeptide with multiple post-translational peptides, as enriched in active neurons during aggression. Through pharmacological manipulations with the peptides of POMC (aMSH, ACTH, and B-endorphin), I found that a B-endorphin antagonist significantly increased aggressive behavior in tadpoles. Overall, this project is advancing understanding of how aggression is regulated in the juvenile brain.

The glomerular array in the olfactory bulb of many vertebrates is segregated into molecularly and anatomically distinct clusters linked to different olfactory functions. In anurans, glomerular clustering is so far only described in Xenopus laevis. We traced olfactory projections to the bulb in tadpoles belonging to six distantly related anuran species in four families (Pipidae, Hylidae, Bufonidae, Dendrobatidae) and found that glomerular clustering is remarkably conserved. The general bauplan consists of four unequally sized glomerular clusters with minor inter-species variation. During metamorphosis, the olfactory system undergoes extensive remodeling. Tracings in metamorphotic and juvenile Dendrobates tinctorius and Xenopus tropicalis suggest a higher degree of variation in the glomerular organization after metamorphosis is complete. Our study highlights, that the anatomical organization of glomeruli in the main olfactory bulb (MOB) is highly conserved, despite an extensive ecomorphological diversification among anuran tadpoles, which suggests underlying developmental constraints.

Many high-throughput compound screens have focused on biochemical and cell-based assays, followed by phenotypic assays at the organismal level. However, these widely applied methods limit the identification of new targets. Since nervous system disease biology is complex, targeted biochemical and cell-based assays may not be effective. To address these issues we initiated the Neuroplant Project which engages experts in neuroscience, plant biology, chemistry, and engineering. Our goal is to leverage medicinal plants and animal behavior to identify new chemical and molecular entry points for the treatment of neurological and psychiatric diseases.

We report on a 59-year-old female with symptomatic cholelithiasis on a background of morbid obesity who underwent an elective LC with an uncomplicated intraoperative course; however, she experienced a refractory hypotension within one hour postoperatively with an acute haemoglobin drop requiring fluid resuscitation and blood transfusion. A triphasic computed tomography scan revealed a large intrahepatic subcapsular haematoma (ISH) measuring 21 cm×3.1 cm×17 cm surrounding the lateral surface of the right hepatic lobe without active bleeding. She was managed conservatively with serial monitoring of haemoglobin and haematoma size. A follow-up ultrasound scan after eight weeks confirmed complete resolution of the haematoma. Giant ISH is a fairly rare, but life-threatening complication following LC which merits special attention. This case demonstrates the necessity of close postoperative monitoring of patients undergoing LC and considering the possibility of ISH, although being rare event, in those who experience a refractory postoperative hypotension. It also highlights the decisive role of diagnostic imaging in securing a timely and accurate diagnosis of post LC-ISH.

Supplementary information of detailed qPCR methods, and tables of primer sequences, qPCR cycling parameters, and statistical results