Healthcare-related carbon footprinting-lower impact of a coronary stenting compared to a coronary surgery pathway.

Healthcare is a major generator of greenhouse gases, so consideration of this contribution to climate change needs to be quantified in ways that can inform models of care. Given the availability of activity-based financial data, environmentally-extended input-output (EEIO) analysis can be employed to calculate systemic carbon footprints for healthcare activities, allowing comparison of different patient care pathways. We thus quantified and compared the carbon footprint of two common care pathways for patients with stable coronary artery disease, with similar clinical outcomes: coronary stenting and coronary artery bypass surgery (CABG).

Memory strength gates the involvement of a CREB-dependent cortical fear engram in remote memory.

Encoding and retrieval of contextual memories is initially mediated by sparsely activated neurons, so-called engram cells, in the hippocampus. Subsequent memory persistence is thought to depend on network-wide changes involving progressive contribution of cortical regions, a process referred to as systems consolidation. Using a viral-based TRAP (targeted recombination in activated populations) approach, we studied whether consolidation of contextual fear memory by neurons in the medial prefrontal cortex (mPFC) is modulated by memory strength and CREB function.

Neurobeachin Regulates Glutamate- and GABA-Receptor Targeting to Synapses via Distinct Pathways.

Neurotransmission and synaptic strength depend on expression of post-synaptic receptors on the cell surface. Post-translational modification of receptors, trafficking to the synapse through the secretory pathway, and subsequent insertion into the synapse involves interaction of the receptor with A-kinase anchor proteins (AKAPs) and scaffolding proteins. Neurobeachin (Nbea), a brain specific AKAP, is required for synaptic surface expression of both glutamate and GABA receptors.

Synapse associated protein 102 (SAP102) binds the C-terminal part of the scaffolding protein neurobeachin.

Neurobeachin (Nbea) is a multidomain scaffold protein abundant in the brain, where it is highly expressed during development. Nbea-null mice have severe defects in neuromuscular synaptic transmission resulting in lethal paralysis of the newborns. Recently, it became clear that Nbea is important also for the functioning of central synapses, where it is suggested to play a role in trafficking membrane proteins to both, the pre- and post-synaptic sites.

Munc18-1 stabilizes syntaxin 1, but is not essential for syntaxin 1 targeting and SNARE complex formation.

Munc18-1, a member of the Sec1/Munc18 (SM) protein family, is essential for synaptic vesicle exocytosis. Munc18-1 binds tightly to the SNARE protein syntaxin 1, but the physiological significance and functional role of this interaction remain unclear. Here we show that syntaxin 1 levels are reduced by 70% in munc18-1 knockout mice.