You Don\u27t Own Me: Recommendations to Protect Human Contributors of Biological Material after \u3cem\u3eWashington University v. Catalona\u3c/em\u3e

As research using human biological materials has rapidly developed, so too has the debate over the ownership of these highly valuable materials. Most recently, the Eighth Circuit in Washington University v. Catalona held that research participants do not retain any ownership interest in the biological materials they contribute to research. This note argues that the misguided Catalona decision, in combination with unclear, outdated, and inadequate federal research regulations, has left human contributors of biological material largely unprotected and vulnerable to the goals of researchers, institutions, and biotechnology firms. Accordingly, this note proposes critical amendments to the federal research regulations that will ensure the continued advancement of biomedical research by protecting the human sources who make this research possible

Ending Terrorism with Civil Remedies: \u3cem\u3eBoim v. Holy Land Foundation\u3c/em\u3e and the Proper Framework of Liability

Counterterrorism experts agree that, because money is the lifeblood of terrorists, one of the most effective means of combating terrorism is eradicating vital sources of funding. Recognizing this, Congress passed legislation throughout the 1990s that holds individuals criminally liable for providing financial or other material support to terrorists or terrorist organizations. Additionally, Congress created a civil remedy for victims who are injured or killed by reason of an act of international terrorism. In the first case to utilize the 18 U.S.C. § 2333 civil cause of action, the parents of David Boim, a Jewish-American teenager killed in Israel by alleged Hamas terrorists, filed suit in 2000 against several individuals and nonprofit organizations that allegedly funneled money to Hamas through charitable fronts for Hamas. The Court of Appeals for the Seventh Circuit has addressed Boim v. Holy Land Foundation for Relief and Development on three occasions: on an interlocutory appeal in Boim I, on appeal from a $156 million jury verdict in Boim II, and, most recently, on rehearing en banc in Boim III, in which the Seventh Circuit held that defendants who donate or provide other material support to terrorist or terrorist-linked organizations are liable under § 2333 as long as they knew that the donee organization engages in terrorism. This Note discusses the Boim III majority opinion written by Judge Posner, as well as a dissenting opinion written by Judge Rovner. By analyzing the strengths and weaknesses of both judges\u27 frameworks, this Note concludes that neither framework provides the ideal basis for liability. Accordingly, this Note proposes an alternative structure for § 2333 liability that can guide other courts in applying this vitally important statute to complicated situations like that in Boim

Reorganisation of brain networks in frontotemporal dementia and progressive supranuclear palsy.

The disruption of large-scale brain networks is increasingly recognised as a consequence of neurodegenerative dementias. We assessed adults with behavioural variant frontotemporal dementia and progressive supranuclear palsy using magnetoencephalography during an auditory oddball paradigm. Network connectivity among bilateral temporal, frontal and parietal sources was examined using dynamic causal modelling. We found evidence for a systematic change in effective connectivity in both diseases. Compared with healthy subjects, who had focal modulation of intrahemispheric frontal-temporal connections, the patient groups showed abnormally extensive and inefficient networks. The changes in connectivity were accompanied by impaired responses of the auditory cortex to unexpected deviant tones (MMNm), despite normal responses to standard stimuli. Together, these results suggest that neurodegeneration in two distinct clinical syndromes with overlapping profiles of prefrontal atrophy, causes a similar pattern of reorganisation of large-scale networks. We discuss this network reorganisation in the context of other focal brain disorders and the specific vulnerability of functional brain networks to neurodegenerative disease

The impact of non-harmonious goals on partner support and taking on opportunities

Romantic partners often support each other to progress toward goals. However, at times partners’ goals are not in harmony and conflict with partner or relationship needs, leading to negative consequences for couple members. The present study examined whether non-harmonious opportunities were associated with support provider’s and recipient’s behavior, perceived partner support, and goal outcomes. We further examined whether these effects were moderated by attachment styles. Findings from two experimental (n1= 296, n2= 117) and one dyadic daily diary (n3= 267) showed how having non-harmonious goals lead to problematic goal pursuit. Partners are less likely to behave positively toward the support provider, provide partner support, view their partners as supportive, and report less commitment to partners, and make less goal progress when goal non-harmony is present. Importantly, we did not find moderation effects of attachment styles for these processes. The findings highlight the importance of managing goal non-harmony in couples

Perseveration and choice in Parkinson's disease: the impact of progressive frontostriatal dysfunction on action decisions.

We have previously shown that patients with Parkinson's disease (PD) perseverate in their choice of action relative to healthy controls, and that this is affected by dopaminergic medication (Hughes LE, Barker RA, Owen AM, Rowe JB. 2010. Parkinson's disease and healthy aging: Independent and interacting effects on action selection. Hum Brain Mapp. 31:1886-1899). To understand further the neural basis of these phenomena, we used a new task that manipulated the options to repeat responses. Seventeen patients with idiopathic PD were studied both "on" and "off" dopaminergic medication and 18 healthy adults were scanned twice as controls. All subjects performed a right-handed 3-choice button press task, which controlled the availability of repeatable responses. The frequency of choosing to repeat a response (a form of perseveration) in patients was related to dopamine therapy and disease severity as a "U-shaped" function. For repetitive trials, this "U-shaped" relationship was also reflected in the BOLD response in the caudate nuclei and ventrolateral prefrontal cortex. Our results support a U-shaped model of optimized cortico-striatal circuit function and clearly demonstrate that flexibility in response choice is modulated by an interaction of dopamine and disease severity

The prefrontal cortex achieves inhibitory control by facilitating subcortical motor pathway connectivity

Communication between the prefrontal cortex and subcortical nuclei underpins the control and inhibition of behavior. However, the interactions in such pathways remain controversial. Using a stop-signal response inhibition task and functional imaging with analysis of effective connectivity, we show that the lateral prefrontal cortex influences the strength of communication between regions in the frontostriatal motor system. We compared 20 generative models that represented alternative interactions between the inferior frontal gyrus, presupplementary motor area (preSMA), subthalamic nucleus (STN), and primary motor cortex during response inhibition. Bayesian model selection revealed that during successful response inhibition, the inferior frontal gyrus modulates an excitatory influence of the preSMA on the STN, thereby amplifying the downstream polysynaptic inhibition from the STN to the motor cortex. Critically, the strength of the interaction between preSMA and STN, and the degree of modulation by the inferior frontal gyrus, predicted individual differences in participants’ stopping performance (stop-signal reaction time). We then used diffusion-weighted imaging with tractography to assess white matter structure in the pathways connecting these three regions. The mean diffusivity in tracts between preSMA and the STN, and between the inferior frontal gyrus and STN, also predicted individual differences in stopping efficiency. Finally, we found that white matter structure in the tract between preSMA and STN correlated with effective connectivity of the same pathway, providing important cross-modal validation of the effective connectivity measures. Together, the results demonstrate the network dynamics and modulatory role of the prefrontal cortex that underpin individual differences in inhibitory control

The impact of neurodegeneration on network connectivity: a study of change detection in frontotemporal dementia.

The neural response to unpredictable auditory events is suggested to depend on frontotemporal interactions. We used magnetoencephalography in patients with behavioral variant frontotemporal dementia to study change detection and to examine the impact of disease on macroscopic network connectivity underlying this core cognitive function. In patients, the amplitudes of auditory cortical responses to predictable standard tones were normal but were reduced for unpredictable deviant tones. Network connectivity, in terms of coherence among frontal, temporal, and parietal sources, was also abnormal in patients. In the beta frequency range, left frontotemporal coherence was reduced. In the gamma frequency range, frontal interhemispheric coherence was reduced whereas parietal interhemispheric coherence was enhanced. These results suggest impaired change detection resulting from dysfunctional frontotemporal interactions. They also provide evidence of a rostro-caudal reorganization of brain networks in disease. The sensitivity of magnetoencephalography to cortical network changes in behavioral variant frontotemporal dementia enriches the understanding of neurocognitive systems as well as showing potential for studies of experimental therapies for neurodegenerative disease.This work has been supported by the Wellcome Trust (088324), the Medical Research Council’s Cognition and Brain Sciences Unit (MC-A060-5PQ30), and the NIHR Cambridge Comprehensive Biomedical Research Centr

Hierarchical Organization of Frontotemporal Networks for the Prediction of Stimuli across Multiple Dimensions.

Brain function can be conceived as a hierarchy of generative models that optimizes predictions of sensory inputs and minimizes "surprise." Each level of the hierarchy makes predictions of neural events at a lower level in the hierarchy, which returns a prediction error when these expectations are violated. We tested the generalization of this hypothesis to multiple sequential deviations, and we identified the most likely organization of the network that accommodates deviations in temporal structure of stimuli. Magnetoencephalography of healthy human participants during an auditory paradigm identified prediction error responses in bilateral primary auditory cortex, superior temporal gyrus, and lateral prefrontal cortex for deviation by frequency, intensity, location, duration, and silent gap. We examined the connectivity between cortical sources using a set of 21 generative models that embedded alternate hypotheses of frontotemporal network dynamics. Bayesian model selection provided evidence for two new features of functional network organization. First, an expectancy signal provided input to the prefrontal cortex bilaterally, related to the temporal structure of stimuli. Second, there are functionally significant lateral connections between superior temporal and/or prefrontal cortex. The results support a predictive coding hypothesis but go beyond previous work in demonstrating the generalization to multiple concurrent stimulus dimensions and the evidence for a temporal expectancy input at the higher level of the frontotemporal hierarchy. We propose that this framework for studying the brain's response to unexpected events is not limited to simple sensory tasks but may also apply to the neurocognitive mechanisms of higher cognitive functions and their disorders.This work was supported by the Medical Research Council (Grant MC-A060-5PQ30 and a doctoral training award to H.N.P.), the Wellcome Trust (Grants 088324 and 103838 to J.B.R. and L.E.H., Biomedical Research Fellowship WT093811MA to T.A.B.), and the James F. McDonnell Foundation 21st Century Science Initiative: Understanding Human Cognition.This is the final version of the article. It first appeared from Society for Neuroscience via http://dx.doi.org/10.1523/JNEUROSCI.5095-14.201

Neurophysiological and brain structural markers of cognitive frailty differs from Alzheimer’s disease

AbstractWith increasing life span, there is growing importance of understanding the mechanisms of successful cognitive ageing. In contrast, cognitive frailty has been proposed to be a precursor to Alzheimer’s disease. Here we test the hypothesis that cognitively frail adults represent a branch of healthy ageing, distinct from latent dementia. We used electro-magnetoencephalography and magnetic resonance imaging to investigate the structural and neurophysiological features of cognitive frailty in relation to healthy aging, and clinical presentations of mild cognitive impairment and Alzheimer’s disease. Cognitive performance of the cognitively frail group was similar to those with mild cognitive impairment. We used a novel cross-modal oddball task to induce mismatch responses to unexpected stimuli. Both controls and cognitively frail showed stronger mismatch responses and larger temporal grey matter volume, compared to people with mild cognitive impairment and Alzheimer’s disease. Our results suggest that cognitively frail represents a spectrum of normal ageing rather than incipient or undiagnosed Alzheimer’s disease. Lower cognitive reserve, hearing impairment and medical comorbidity might contribute to the aetiology of cognitive impairment.The study was supported by the Medical Research Council [SUAG/004 RG91365, SUAG/046 RG101400; SUAG/051 RG101400], the Wellcome Trust [103838], the Dementias Platform UK [MR/L023784/1 & MR/L023784/2], Alzheimer’s Research UK [ARUK-PG2017B-19], a Holt Fellowship, and NIHR Cambridge Biomedical Research Centre (BRC-1215-20014). The views expressed are those of the authors and not necessarily those of the NIHR or the Department of Health and Social Care. For the purpose of open access, the author has applied a CC BY public copyright license to any Author Accepted Manuscript version arising from this submission

Model responses to CO(2) and warming are underestimated without explicit representation of Arctic small-mammal grazing

© The Author(s), 2021. This article is distributed under the terms of the Creative Commons Attribution License. The definitive version was published in Rastetter, E. B., Griffin, K. L., Rowe, R. J., Gough, L., McLaren, J. R., & Boelman, N. T. Model responses to CO(2) and warming are underestimated without explicit representation of Arctic small-mammal grazing. Ecological Applications, (2021): e02478, https://doi.org/10.1002/eap.2478.We use a simple model of coupled carbon and nitrogen cycles in terrestrial ecosystems to examine how “explicitly representing grazers” vs. “having grazer effects implicitly aggregated in with other biogeochemical processes in the model” alters predicted responses to elevated carbon dioxide and warming. The aggregated approach can affect model predictions because grazer-mediated processes can respond differently to changes in climate compared with the processes with which they are typically aggregated. We use small-mammal grazers in a tundra as an example and find that the typical three-to-four-year cycling frequency is too fast for the effects of cycle peaks and troughs to be fully manifested in the ecosystem biogeochemistry. We conclude that implicitly aggregating the effects of small-mammal grazers with other processes results in an underestimation of ecosystem response to climate change, relative to estimations in which the grazer effects are explicitly represented. The magnitude of this underestimation increases with grazer density. We therefore recommend that grazing effects be incorporated explicitly when applying models of ecosystem response to global change.This work was supported in part by the National Science Foundation under NSF grants 1651722, 1637459, 1603560, 1556772, 1841608 to E.B.R.; 1603777 to N.T.B. and K.L.G.; 1603654 to R.J.R.; 1603760 to L.G.; and 1603677 to J.R.M