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Autonomous vehicles (AV) promise a reduction in the number of deadly traffic accidents. However, should accidents occur, attributions of responsibility are complicated by the fact that there is a human agent (driver) and a non-human agent (AV), and thus responsibility is likely shared between parties. In two studies, participants (n = 310 and n = 260) read a vignette modeled after an actual lethal AV accident. Across four experimental conditions, participants were told that the human driver either needed to maintain oversight of the AV; did not need to maintain oversight of the AV; did not specify whether the human needed to maintain oversight of the AV; or the artificial intelligence was turned off and the human driver was fully in control. Participants assigned responsibility to the human driver, the AV company, the pedestrian, and an act of God, and determined whether the human driver and company CEO should be held criminally responsible in court. Consistent with previous research, the human driver was held most responsible regardless of oversight condition. However, companies were not absolved of responsibility, even when they required the human driver to maintain oversight of the AV. Implications of these findings for the introduction and legal regulation of AVs are discussed., Author(s): Christopher J. Copp [sup.1] , Jean J. Cabell [sup.1] , Markus Kemmelmeier [sup.1] Author Affiliations: (1) grid.266818.3, 0000 0004 1936 914X, Interdisciplinary Social Psychology Ph.D. Program, University of Nevada, [...]

The genetic basis of human neural tube defects (NTDs), such as anencephaly and spina bifida (SB), is complex and heterogeneous. Grainyhead-like genes represent candidates for involvement in NTDs based on the presence of SB and exencephaly in mice carrying loss-of-function alleles of Grhl2 or Grhl3. We found that reinstatement of Grhl3 expression, by bacterial artificial chromosome (BAC)-mediated transgenesis, prevents SB in Grhl3-null embryos, as in the Grhl3 hypomorphic curly tail strain. Notably, however, further increase in expression of Grhl3 causes highly penetrant SB. Grhl3 overexpression recapitulates the spinal NTD phenotype of loss-of-function embryos, although the underlying mechanism differs. However, it does not phenocopy other defects of Grhl3-null embryos such as abnormal axial curvature, cranial NTDs (exencephaly) or skin barrier defects, the latter being rescued by the Grhl3-transgene. Grhl2 and Grhl3 can form homodimers and heterodimers, suggesting a possible model in which defects arising from overexpression of Grhl3 result from sequestration of Grhl2 in heterodimers, mimicking Grhl2 loss of function. This hypothesis predicts that increased abundance of Grhl2 would have an ameliorating effect in Grhl3 overexpressing embryo. Instead, we observed a striking additive genetic interaction between Grhl2 and Grhl3 gain-of-function alleles. Severe SB arose in embryos in which both genes were expressed at moderately elevated levels that individually do not cause NTDs. Furthermore, moderate Grhl3 overexpression also interacted with the Vangl2Lp allele to cause SB, demonstrating genetic interaction with the planar cell polarity signalling pathway that is implicated in mouse and human NTDs.

Failure of neural tube closure leads to neural tube defects (NTDs), common congenital abnormalities in humans. Among the genes whose loss of function causes NTDs in mice, Grainyhead-like3 (Grhl3) is essential for spinal neural tube closure, with null mutants exhibiting fully penetrant spina bifida. During spinal neurulation Grhl3 is initially expressed in the surface (non-neural) ectoderm, subsequently in the neuroepithelial component of the neural folds and at the node-streak border, and finally in the hindgut endoderm. Here, we show that endoderm-specific knockout of Grhl3 causes late-arising spinal NTDs, preceded by increased ventral curvature of the caudal region which was shown previously to suppress closure of the spinal neural folds. This finding supports the hypothesis that diminished Grhl3 expression in the hindgut is the cause of spinal NTDs in the curly tail, carrying a hypomorphic Grhl3 allele. Complete loss of Grhl3 function produces a more severe phenotype in which closure fails earlier in neurulation, before the stage of onset of expression in the hindgut of wild-type embryos. This implicates additional tissues and NTD mechanisms in Grhl3 null embryos. Conditional knockout of Grhl3 in the neural plate and node-streak border has minimal effect on closure, suggesting that abnormal function of surface ectoderm, where Grhl3 transcripts are first detected, is primarily responsible for early failure of spinal neurulation in Grhl3 null embryos.

Ventriculomegaly and hydrocephalus are associated with loss of function of glycine decarboxylase (Gldc) in mice and in humans suffering from non-ketotic hyperglycinemia (NKH), a neurometabolic disorder characterized by accumulation of excess glycine. Here, we showed that ventriculomegaly in Gldc-deficient mice is preceded by stenosis of the Sylvian aqueduct and malformation or absence of the subcommissural organ and pineal gland. Gldc functions in the glycine cleavage system, a mitochondrial component of folate metabolism, whose malfunction results in accumulation of glycine and diminished supply of glycine-derived 1-carbon units to the folate cycle. We showed that inadequate 1-carbon supply, as opposed to excess glycine, is the cause of hydrocephalus associated with loss of function of the glycine cleavage system. Maternal supplementation with formate prevented both ventriculomegaly, as assessed at prenatal stages, and postnatal development of hydrocephalus in Gldc-deficient mice. Furthermore, ventriculomegaly was rescued by genetic ablation of 5,10-methylene tetrahydrofolate reductase (Mthfr), which results in retention of 1-carbon groups in the folate cycle at the expense of transfer to the methylation cycle. In conclusion, a defect in folate metabolism can lead to prenatal aqueduct stenosis and resultant hydrocephalus. These defects are preventable by maternal supplementation with formate, which acts as a 1-carbon donor., Introduction Hydrocephalus results from abnormal cerebrospinal fluid (CSF) hydrodynamics (overproduction, diminished drainage, or impaired flow) leading to progressive enlargement of the cerebral ventricular system and subsequent pathology (1). Hydrocephalus can [...]

Drift studies are central to stream and river ecological research. However, a fundamental aspect of quantifying drift--how net clogging affects the accuracy of results--has been widely ignored. Utilizing approaches from plankton and suspended sediment studies in oceanography and hydrology, we examined the rate and dynamics of net clogging across a range of conditions. We found that nets clog nonlinearly over time and that suspended solid concentrations and net mesh size exerted a strong effect on clogging rates. Critically, net clogging introduced unpredictable biases in resultant data due to the inaccuracies in water volume estimates introduced by progressive clogging. This renders the widespread approach to linearly 'correct' for clogging inadequate. Using a meta-analysis of 77 drift studies spanning 25 years, we demonstrate that the detrimental effects of net clogging are routinely unappreciated, even though the results of most of these studies were likely affected by clogging. We close by describing an approach for avoiding net clogging, which will increase the accuracy and reproducibility of results in future freshwater, lotic drift studies. Les etudes de la derive constituent une composante centrale de la recherche sur l'ecologie des cours d'eau et rivieres. Toutefois, un aspect fondamental de la quantification de la derive, l'incidence de l'encrassement des filets sur l'exactitude des resultats, est rarement pris en consideration. En utilisant des approches tirees d'etudes du plancton et des sediments en suspension en oceanographie et en hydrologie, nous avons examine le taux et la dynamique de l'encrassement des filets dans un eventail de conditions. Nous avons constate que l'encrassement des filets n'est pas lineaire dans le temps et que les concentrations de solides en suspension et la taille des mailles du filet ont une grande incidence sur les taux d'encrassement. Fait crucial, l'encrassement des filets introduit des biais imprevisibles dans les donnees en raison de l'inexactitude des estimations du volume d'eau causee par l'encrassement graduel. Cela fait en sorte que l'approche repandue de ' correction ' lineaire pour tenir compte de l'encrassement est inadequate. En utilisant une metaanalyse de 77 etudes de la derive couvrant 25 ans, nous demontrons que les effets deleteres de l'encrassement des filets sont regulierement sous-apprecies, meme si l'encrassement a vraisemblablement une incidence sur les resultats de la plupart de ces etudes. Enfin, nous decrivons une approche permettant d'eviter l'encrassement des filets qui accroitra l'exactitude et la reproductibilite des resultats de futures etudes de la derive en milieux lotiques d'eau douce. [Traduit par la Redaction], Introduction Drift in stream and river ecosystems is essential to the maintenance, dispersal, and life histories of many freshwater invertebrate populations and also provides a key food source for drift-feeding [...]