New and Recovered Temporary Anchorage Devices, In Vitro Assessment of Structural and Surface Properties.

The orthodontic miniscrew (TADs) is a device that is fixed into bone in the short term for the purpose of enhancing orthodontic anchorage. The aim of our study was to investigate the structural and surface properties of recovered TADs after orthodontic treatment, and compare them to new TADs. TADs (n = 15) from the same manufacturer (Absoanchor; Dentos, Daegu, Korea) were assessed; n = 10 were recovered from patients after orthodontic treatment and n = 5 were new.

State of the art regarding anticoagulant and thrombolytic therapy in dental procedures.

Patients with anticoagulant therapy have a high thromboembolic risk. Due to the rich oro-maxillofacial vasculature and the fact that some dental procedures may cause a bleeding, the physician should be able to correlate this risk with the hemorrhagic risk. Dental procedures are a trigger for psychic stress.

Paradoxical effect of baclofen on social behavior in the fragile X syndrome mouse model.

Introduction: Fragile X syndrome (FXS) is a common monogenetic cause of intellectual disability, autism spectrum features, and a broad range of other psychiatric and medical problems. FXS is caused by the lack of the fragile X mental retardation protein (FMRP), a translational regulator of specific mRNAs at the postsynaptic compartment. The absence of FMRP leads to aberrant synaptic plasticity, which is believed to be caused by an imbalance in excitatory and inhibitory network functioning of the synapse.

Fragile X syndrome: a preclinical review on metabotropic glutamate receptor 5 (mGluR5) antagonists and drug development.

Rationale: Fragile X syndrome (FXS) is considered the leading inherited cause of intellectual disability and autism. In FXS, the fragile X mental retardation 1 (FMR1) gene is silenced and the fragile X mental retardation protein (FMRP) is not expressed, resulting in the characteristic features of the syndrome. Despite recent advances in understanding the pathophysiology of FXS, there is still no cure for this condition; current treatment is symptomatic.

Silencing the majority of cerebellar granule cells uncovers their essential role in motor learning and consolidation.

Cerebellar granule cells (GCs) account for more than half of all neurons in the CNS of vertebrates. Theoretical work has suggested that the abundance of GCs is advantageous for sparse coding during memory formation. Here, we minimized the output of the majority of GCs by selectively eliminating their CaV2.

Rescue of dendritic spine phenotype in Fmr1 KO mice with the mGluR5 antagonist AFQ056/Mavoglurant.

Fragile X syndrome (FXS) is the leading monogenic cause of intellectual disability and autism. The disease is a result of lack of expression of the fragile X mental retardation protein. Brain tissues of patients with FXS and mice with FMRP deficiency have shown an abnormal dendritic spine phenotype.

Chronic administration of AFQ056/Mavoglurant restores social behaviour in Fmr1 knockout mice.

Fragile X syndrome is caused by lack of FMR1 protein (FMRP) leading to severe symptoms, including intellectual disability, hyperactivity and autistic-like behaviour. FMRP is an RNA binding protein involved in the regulation of translation of specific target mRNAs upon stimulation of metabotropic glutamate receptor 5 (mGluR5) at the synapse. The absence of FMRP leads to enhanced activity of mGluR5 signal transduction pathways.

AFQ056, a new mGluR5 antagonist for treatment of fragile X syndrome.

Fragile X syndrome, the most common form of inherited intellectual disability, is caused by a lack of FMRP, which is the product of the Fmr1 gene. FMRP is an RNA-binding protein and a component of RNA-granules found in the dendrites of neurons. At the synapse, FMRP is involved in regulation of translation of specific target mRNAs upon stimulation of mGluR5 receptors.