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Neuroimaging research has raised ethical concerns such as the management of unexpected findings and the classification and assessment of risks. Research ethics boards (REBs) bear responsibility for the oversight of these challenges but neuroimagers struggle with the practical aspects of ethics review and report that administrative load and inconsistency contribute to eroding confidence and trust in ethics review. Our goal was to discuss and propose strategies for institutional and educational change to improve ethics review. We used an iterative and deliberative workshop-based writing process involving multiple disciplines. We propose recommendations in three tension areas: (1) communication between researchers and REBs; (2) collaboration and sharing of expertise between REBs; and (3) practical considerations and the needs of neuroimagers engaged in the ethics review process. Our recommendations are intended as openings rather than endpoints. Researchers and research ethics governance communities should decide on the future uptake of these recommendations.
Thalamic glutamine loss and grey matter reduction suggest
neurodegeneration in first-episode schizophrenia, but the duration is
To observe glutamine and glutamate levels, grey matter volumes and social
functioning in patients with schizophrenia followed to 80 months after
Grey matter volumes and proton magnetic resonance spectroscopy
metabolites in left anterior cingulate and left thalamus were measured in
17 patients with schizophrenia before medication and 10 and 80 months
after diagnosis. Social functioning was assessed with the Life Skills
Profile Rating Scale (LSPRS) at 80 months.
The sum of thalamic glutamate and glutamine levels decreased over 80
months, and correlated inversely with the LSPRS. Thalamic glutamine and
grey matter loss were significantly correlated in frontal, parietal,
temporal and limbic regions.
Brain metabolite loss is correlated with deteriorated social functioning
and grey matter losses in schizophrenia, consistent with
A tool has been developed that can be used to characterize or validate a BEOL interconnect technology. It connects various process assumptions directly to electrical parameters including resistance. The resistance of narrow copper lines is becoming a challenging parameter, not only in terms of controlling its value but also understanding the underlying mechanisms. The resistance was measured for 45nm-node interconnects and compared to the theory of electron scattering. This work will demonstrate how valuable it is to directly link the electrical models to the physical on-wafer dimensions and in turn to the process assumptions. For example, one can generate a tolerance pareto for physical and or electrical parameters that immediately identifies those process sectors that have the largest contribution to the overall tolerance. It also can be used to easily generate resistance versus capacitance plots which provide a good BEOL performance gauge. Several examples for 45nm BEOL will be given to demonstrate the value of these tools.
Progressive volumetric changes in the brains of people with schizophrenia have been attributed to a number of factors.
To determine whether glutamatergic changes in patients with schizophrenia correlated with grey-matter losses during the first years of illness.
Left anterior cingulate and thalamic glutamatergic metabolite levels and grey-matter volumes were examined in 16 patients with first-episode schizophrenia before and after 10 months and 30 months of antipsychotic treatment and in 16 healthy participants on two occasions 30 months apart.
Higher than normal glutamine levels were found in the anterior cingulate and thalamus of never-treated patients. Thalamic levels of glutamine were significantly reduced after 30 months. Limited grey-matter reductions were seen in patients at 10 months followed by widespread grey-matter loss at 30 months. Parietal and temporal lobe grey-matter loss was correlated with thalamic glutamine loss.
Elevated glutamine levels in never-treated patients followed by decreased thalamic glutamine and grey-matter loss in connected regions could indicate either neurodegeneration or a plastic response to reduced subcortical activity.
Membrane phospholipid and high-energy abnormalities measured with phosphorus magnetic resonance spectroscopy (31P-MRS) have been reported in patients with schizophrenia in several brain regions.
Using improved imaging techniques, previously inaccessible brain regions were examined in patients with first-episode schizophrenia and healthy volunteers with 4.0 T 31P-MRS.
Brain spectra were collected in vivo from 15 patients with first-episode schizophrenia and 15 healthy volunteers from 15 cm3 effective voxels in the thalamus, cerebellum, hippocampus, anterior/posterior cingulate, prefrontal cortex and parieto-occipital cortex.
People with first-episode schizophrenia showed increased levels of glycerophosphocholine in the anterior cingulate. Inorganic phosphate, phosphocreatine and adenosine triphosphate concentrations were also increased in the anterior cingulate in this group.
The increased phosphodiester and high-energy phosphate levels in the anterior cingulate of brains of people with first-episode schizophrenia may indicate neural overactivity in this region during the early stages of the illness, resulting in increased excitotoxic neural membrane breakdown.
Membrane phospholipid abnormalities in people with schizophrenia, measured with 31P magnetic resonance spectroscopy (31P-MRS), have been previously reported in brain regions involved in this disorder.
In this 4.0 Tesla 31P-MRS study of people with schizophrenia, membrane phospholipid metabolism was examined in brain regions previously inaccessible due to their small volumes.
Three-dimensional chemical-shift imaging (3D–CSI) examined 15 cc volumes in 12 brain regions in 11 people with chronic schizophrenia and 11 healthy control volunteers.
Glycerophosphoethanolamine was decreased in the anterior cingulate, right prefrontal cortex and left thalamus, but increased in the left hippocampus and cerebellum in those with schizophrenia. Phosphoethanolamine and glycerophosphocholine were decreased in the right prefrontal region and phosphocholine was decreased in the anterior cingulate. No significant difference in membrane phospholipid levels existed between groups in the parieto-occipital and posterior cingulate regions.
Altered membrane phospholipid metabolism was demonstrated in all regions implicated in schizophrenia.
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