Neonatal cerebrovascular autoregulation.

Cerebrovascular pressure autoregulation is the physiologic mechanism that holds cerebral blood flow (CBF) relatively constant across changes in cerebral perfusion pressure (CPP). Cerebral vasoreactivity refers to the vasoconstriction and vasodilation that occur during fluctuations in arterial blood pressure (ABP) to maintain autoregulation. These are vital protective mechanisms of the brain. Impairments in pressure autoregulation increase the risk of brain injury and persistent neurologic disability. Autoregulation may be impaired during various neonatal disease states including prematurity, hypoxic-ischemic encephalopathy (HIE), intraventricular hemorrhage, congenital cardiac disease, and infants requiring extracorporeal membrane oxygenation (ECMO). Because infants are exquisitely sensitive to changes in cerebral blood flow (CBF), both hypoperfusion and hyperperfusion can cause significant neurologic injury. We will review neonatal pressure autoregulation and autoregulation monitoring techniques with a focus on brain protection. Current clinical therapies have failed to fully prevent permanent brain injuries in neonates. Adjuvant treatments that support and optimize autoregulation may improve neurologic outcomes

Dissecting the Shared Genetic Architecture of Suicide Attempt, Psychiatric Disorders, and Known Risk Factors

Background Suicide is a leading cause of death worldwide, and nonfatal suicide attempts, which occur far more frequently, are a major source of disability and social and economic burden. Both have substantial genetic etiology, which is partially shared and partially distinct from that of related psychiatric disorders. Methods We conducted a genome-wide association study (GWAS) of 29,782 suicide attempt (SA) cases and 519,961 controls in the International Suicide Genetics Consortium (ISGC). The GWAS of SA was conditioned on psychiatric disorders using GWAS summary statistics via multitrait-based conditional and joint analysis, to remove genetic effects on SA mediated by psychiatric disorders. We investigated the shared and divergent genetic architectures of SA, psychiatric disorders, and other known risk factors. Results Two loci reached genome-wide significance for SA: the major histocompatibility complex and an intergenic locus on chromosome 7, the latter of which remained associated with SA after conditioning on psychiatric disorders and replicated in an independent cohort from the Million Veteran Program. This locus has been implicated in risk-taking behavior, smoking, and insomnia. SA showed strong genetic correlation with psychiatric disorders, particularly major depression, and also with smoking, pain, risk-taking behavior, sleep disturbances, lower educational attainment, reproductive traits, lower socioeconomic status, and poorer general health. After conditioning on psychiatric disorders, the genetic correlations between SA and psychiatric disorders decreased, whereas those with nonpsychiatric traits remained largely unchanged. Conclusions Our results identify a risk locus that contributes more strongly to SA than other phenotypes and suggest a shared underlying biology between SA and known risk factors that is not mediated by psychiatric disorders.Peer reviewe

EXPERIMENTS WITH DISPERSION ENGINEERED BOSE-EINSTEIN CONDENSATES: RAMAN DRESSING AND NOVEL OPTICAL LATTICES

This thesis aims at the investigation of complex condensed matter phenomena using quantum degenerate ultra-cold atomic gases as a well-controlled model system. The phenomena range from a novel spin-momentum coupling and periodic optical potentials, to mean field anti-ferromagnetic like ordering. Additionally the status of the implementation of a novel multi-dimensional optical super-lattice is reported. The first set of experiments presented in this thesis employ a Raman dressing scheme to realize spin-orbit coupling in a BEC. An understanding of the dynamic processes associated with this coupling is developed starting from the single particle level. After this, the many body ground state of the system is investigated and is found to provide an intriguing mapping to the Dicke model known from quantum optics. Next, the Raman dressing is combined with a weak moving optical lattice. This leads to a more complex band structure that is experimentally probed by exciting dynamical instabilities of the system. The combination of the Raman dressing with optical lattices has the potential to realize systems with large effective magnetic flux and novel phases. Finally, following a previous line of research in the WSU BEC group, novel dynamics due to the spatial Rabi winding of an elongated two-component BEC are presented. The experiments are conducted with an experimental apparatus built at WSU. To facilitate the studies of this thesis, a number of new tools have been installed in the setup, such as multi-dimensional optical lattices, precision magnetic field control, and a Raman laser system. Details of these technological advances will be described together with the scientific results that they have enabled

Simulations indicate that scores of lionfish (Pterois volitans) colonized the Atlantic Ocean

The invasion of the western Atlantic Ocean by the Indo-Pacific red lionfish (Pterois volitans) has had devastating consequences for marine ecosystems. Estimating the number of colonizing lionfish can be useful in identifying the introduction pathway and can inform policy decisions aimed at preventing similar invasions. It is well-established that at least ten lionfish were initially introduced. However, that estimate has not faced probabilistic scrutiny and is based solely on the number of haplotypes in the maternally-inherited mitochondrial control region. To rigorously estimate the number of lionfish that were introduced, we used a forward-time, Wright-Fisher, population genetic model in concert with a demographic, life-history model to simulate the invasion across a range of source population sizes and colonizing population fecundities. Assuming a balanced sex ratio and no Allee effects, the simulations indicate that the Atlantic population was founded by 118 (54–514, 95% HPD) lionfish from the Indo-Pacific, the Caribbean by 84 (22–328, 95% HPD) lionfish from the Atlantic, and the Gulf of Mexico by at least 114 (no upper bound on 95% HPD) lionfish from the Caribbean. Increasing the size, and therefore diversity, of the Indo-Pacific source population and fecundity of the founding population caused the number of colonists to decrease, but with rapidly diminishing returns. When the simulation was parameterized to minimize the number of colonists (high θ and relative fecundity), 96 (48–216, 95% HPD) colonists were most likely. In a more realistic scenario with Allee effects (e.g., 50% reduction in fecundity) plaguing the colonists, the most likely number of lionfish increased to 272 (106–950, 95% HPD). These results, in combination with other published data, support the hypothesis that lionfish were introduced to the Atlantic via the aquarium trade, rather than shipping. When building the model employed here, we made assumptions that minimize the number of colonists, such as the lionfish being introduced in a single event. While we conservatively modelled the introduction pathway as a single release of lionfish in one location, it is more likely that a combination of smaller and larger releases from a variety of aquarium trade stakeholders occurred near Miami, Florida, which could have led to even larger numbers of colonists than simulated here. Efforts to prevent future invasions via the aquarium trade should focus on the education of stakeholders and the prohibition of release, with adequate rewards for compliance and penalties for violations