Effect of Intracanal Scaffolds on the Success Outcomes of Regenerative Endodontic Therapy - A Systematic Review and Network Meta-analysis.

Introduction: The scaffolds used in regenerative endodontic therapy (RET) provide structural support for cells so that they can adhere to the scaffolds and also are crucial for cellular proliferation and differentiation. The objective of this network meta-analysis was to compare effects of different intracanal scaffolds on success outcomes of RET.

Methods: PubMed/Medline, EMBASE, Cochrane, CINAHL, Scopus, and Web of Science databases were searched.

Exploring the role of the multiple sclerosis susceptibility gene CLEC16A in T cells.

C-type lectin-like domain family 16 member A (CLEC16A) is associated with autoimmune disorders, including multiple sclerosis (MS), but its functional relevance is not completely understood. CLEC16A is expressed in several immune cells, where it affects autophagic processes and receptor expression. Recently, we reported that the risk genotype of an MS-associated single nucleotide polymorphism in CLEC16A intron 19 is associated with higher expression of CLEC16A in CD4 T cells.

CRMP4 Inhibits Bone Formation by Negatively Regulating BMP and RhoA Signaling.

We identified the neuroprotein collapsing response mediator protein-4 (CRMP4) as a noncanonical osteogenic factor that regulates the differentiation of mouse bone marrow skeletal stem cells (bone marrow stromal stem cells [mBMSCs]) into osteoblastic cells. CRMP4 is the only member of the CRMP1-CRMP5 family to be expressed by mBMSCs and in osteoprogenitors of both adult mouse and human bones. In vitro gain-of-function and loss-of-function of CRMP4 in murine stromal cells revealed its inhibitory effect on osteoblast differentiation.

Allelic imbalance of multiple sclerosis susceptibility genes IKZF3 and IQGAP1 in human peripheral blood.

Background: Multiple sclerosis is a chronic inflammatory, demyelinating disease of the central nervous system. Recent genome-wide studies have revealed more than 110 single nucleotide polymorphisms as associated with susceptibility to multiple sclerosis, but their functional contribution to disease development is mostly unknown.

Results: Consistent allelic imbalance was observed for rs907091 in IKZF3 and rs11609 in IQGAP1, which are in strong linkage disequilibrium with the multiple sclerosis associated single nucleotide polymorphisms rs12946510 and rs8042861, respectively.

Multiple Sclerosis Risk Allele in CLEC16A Acts as an Expression Quantitative Trait Locus for CLEC16A and SOCS1 in CD4+ T Cells.

For multiple sclerosis, genome wide association studies and follow up studies have identified susceptibility single nucleotide polymorphisms located in or near CLEC16A at chromosome 16p13.13, encompassing among others CIITA, DEXI and SOCS1 in addition to CLEC16A. These genetic variants are located in intronic or intergenic regions and display strong linkage disequilibrium with each other, complicating the understanding of their functional contribution and the identification of the direct causal variant(s).

Dact1-3 mRNAs exhibit distinct expression domains during tooth development.

Wnt signaling is essential for tooth formation and Dact proteins modulate Wnt signaling by binding to the intracellular protein Dishevelled (Dvl). Comparison of the three known mouse Dact genes, Dact1-3, from the morphological initiation of mandibular first molar development through the onset of root formation using section in situ hybridization showed distinct, complementary and overlapping expression patterns for these genes. Whereas Dact2 expression was restricted to the dental epithelium, including the enamel knot signaling centers and pre-ameloblasts, Dact1 and Dact3 showed developmentally regulated expression in the dental mesenchyme.