Profile of Inflammatory Cytokines in Gingival Crevicular Fluid and Plasma in Patients With Grade C Periodontitis During Orthodontic Treatment: A Longitudinal Case Series Report.

Aim: To examine the immune responses in patients diagnosed as grade C periodontitis during orthodontic treatment.

Materials And Methods: Our study included seven orthodontic patients with grade C periodontitis and measured their levels of inflammatory cytokines in gingival crevicular fluid and plasma before orthodontic treatment, during the alignment and levelling phase, and during the detailing and finishing phase. The key signal pathways in the orthodontic process of patients with periodontitis were detected by KEGG analysis.

M2 exosomes modified by hydrogen sulfide promoted bone regeneration by moesin mediated endocytosis.

Bone defects caused by trauma or tumor led to high medical costs and poor life quality for patients. The exosomes, micro vesicles of 30-150 nm in diameter, derived from macrophages manipulated bone regeneration. However, the role of hydrogen sulfide (HS) in the biogenesis and function of exosomes and its effects on bone regeneration remains elusive.

Adenovirus-mediated overexpression of novel mutated IkappaBalpha inhibits nuclear factor kappaB activation in endothelial cells.

Background: Nuclear factor kappaB (NF-kappaB) overactivation, requiring phosphorylation and degradation of its inhibitor IkappaBalpha, is the basis for chronicity of airway inflammation in asthma. Based on our previous plasmid pShuttle-IkappaBalpha, carrying an IkappaBalpha gene from human placenta, we optimized a novel IkappaBalpha mutant (IkappaBalphaM) gene, constructed and characterized its replication-deficient recombinant adenovirus (AdIkappaBalphaM), and tested whether AdIkappaBalphaM-mediated overexpression of IkappaBalphaM could inhibit the NF-kappaB activation in endothelial cells.

Methods: IkappaBalphaM gene (203 - 1003 bp) encoding 267 amino acids, acquired by site-directed deleting N-terminal phosphorylation sites of serine 32/36, was subcloned into the pShuttle and pGEM-T vectors for further polymerase chain reaction (PCR), restriction digestion, deoxyribonucleic acid (DNA) sequencing and homology analyses.

[Construction of recombinant deltaN IkappaBalpha adenovirus and its suppression of NF-kappaB activity in A549 cells].

Aim: To explore the regulatory effect of deltaN IkappaBalpha gene on the activity of nuclear factor-kappaB(NF-kappaB).

Methods: Ser32-and Ser36-deleted IkappaBalpha gene (deltaN IkappaBalpha) was cloned into adenovirus vector, and a replication-defective recombinant deltaN IkappaBalpha adenovirus(Ad-deltaN IkappaBalpha) was generated. A549 cells were divided into three groups: LPS-stimulated groups, Ad-LacZ+LPS group and Ad-deltaN IkappaBalpha+LPS group.