Neuronal dysfunction caused by FUSR521G promotes ALS-associated phenotypes that are attenuated by NF-κB inhibition.

Amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD) are related neurodegenerative diseases that belong to a common disease spectrum based on overlapping clinical, pathological and genetic evidence. Early pathological changes to the morphology and synapses of affected neuron populations in ALS/FTD suggest a common underlying mechanism of disease that requires further investigation. Fused in sarcoma (FUS) is a DNA/RNA-binding protein with known genetic and pathological links to ALS/FTD.

Restoring glutamate receptosome dynamics at synapses rescues autism-like deficits in Shank3-deficient mice.

Shank3 monogenic mutations lead to autism spectrum disorders (ASD). Shank3 is part of the glutamate receptosome that physically links ionotropic NMDA receptors to metabotropic mGlu5 receptors through interactions with scaffolding proteins PSD95-GKAP-Shank3-Homer. A main physiological function of the glutamate receptosome is to control NMDA synaptic function that is required for plasticity induction.

Benign fibrous histiocytoma of the conjunctiva.

A case is reported on recurrence of a rare conjunctival fibrous histiocytoma (FH) in a 38-year-old man. The lesion was excised and subsequently sent for histopathology and immunostaining resulting in a diagnosis of fibrous histiocytoma (FH). Recurrence was detected 3 months postoperatively requiring a conjunctivosclerokeratomy with cryotherapy and flap.

[Self medication and its limits].

It is necessary to state automedication is an irreversible phenomenon. It is not difficult to show the causes of this but more arduous to demonstrate the dangers involved when it becomes abusive. This report attempts to encompass the practical means of stopping the spread of this phenomenon in all affected instances.