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periodontitis/tyrosine

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Página 1 a partir de 63 resultados
Tyrosine-protein phosphatase non-receptor type 2 (PTPN2) is an important protection factor for diabetes and periodontitis, but the underlying mechanism remains elusive. This study aimed to identify the substrate of PTPN2 in mediating beneficial effects of 25-Hydroxyvitamin D3

The potential effect of Bruton's tyrosine kinase in refractory periapical periodontitis.

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To determine the expression of Bruton's tyrosine kinase (BTK) in refractory periapical periodontitis and analyze the relationship between BTK and bone resorption in refractory periapical periodontitis. The mechanism of bone resorption is also discussed. The OneArray Plus expression microarray was
Periodontitis is a complication of diabetes mellitus, and the two diseases are highly associated with the dysfunction of inflammatory mediators. 25-hydroxyvitamin D(3) (25(OH)D(3)) plays a pivotal role in inflammatory modulation, but little is known about its effects on the progression of diabetic
Prepubertal periodontitis (PPP) is a rare and rapidly progressive disease of young children that results in destruction of the periodontal support of the primary dentition. The condition may occur as part of a recognised syndrome or may occur as an isolated finding. Both autosomal dominant and

[Effects of Bruton's tyrosine kinase on the proliferation and differentiation of osteoclasts].

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To observe the effect of Bruton's tyrosine kinase (BTK) on the proliferation and differentiation of osteoclasts and to explore the mechanism of BTK on bone destruction in periapical periodontitis.After RAW264.7 cells induced with 100 ng·L⁻¹ receptor

Porphyromonas gingivalis Tyrosine Phosphatase Php1 Promotes Community Development and Pathogenicity.

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Protein-tyrosine phosphorylation in bacteria plays a significant role in multiple cellular functions, including those related to community development and virulence. Metal-dependent protein tyrosine phosphatases that belong to the polymerase and histindinol phosphatase (PHP) family are widespread in
This study assessed the roles of chronic stress (CS) in the stimulation of the sympathetic nervous system and explored the underlying mechanisms of periodontitis. Using an animal model of periodontitis and CS, the expression of tyrosine hydroxylase (TH) and the protein levels of the α1-adrenergic

FcγRIIB-nt645+25A/G gene polymorphism and periodontitis in Japanese women with preeclampsia.

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FcγRIIB contains a unique immunoreceptor tyrosine-based inhibition motif (ITIM) and functions as a negative feedback regulator of leucocyte activation and antibody production. We have previously reported FcγRIIB-nt645+25A/G gene polymorphism to be associated with prevalence and severity of

Tyrosine phosphatase SHP-2 regulates IL-1 signaling in fibroblasts through focal adhesions.

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Interleukin-1beta (IL-1beta) mediates destruction of matrix collagens in diverse inflammatory diseases including arthritis, periodontitis, and pulmonary fibrosis by activating fibroblasts, cells that interact with matrix proteins through integrin-based adhesions. In vitro, IL-1beta signaling is
UNASSIGNED The aim of the present study was to evaluate the gingival crevicular fluid (GCF) levels of YKL-40 acute phase protein in chronic periodontitis (CP) with and without type 2 diabetes and also to assess the effect of periodontal therapy (scaling and root planing [SRP]) on this GCF biomarker

Role of the Btk-PLCγ2 Signaling Pathway in the Bone Destruction of Apical Periodontitis.

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Chronic apical periodontitis is characterized by alveolar bone absorption in the apical region and is the result of the participation of various inflammatory mediators. Studies have shown that the Bruton tyrosine kinase- (Btk-) phospholipase Cγ2 (PLCγ2) signaling pathway plays an

Maternal apical periodontitis is associated with insulin resistance in adult offspring.

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To investigate the plasma concentrations of glucose, insulin and tumour necrosis factor-α (TNF-α) of rats with maternal apical periodontitis (AP) and to explore the effect of maternal inflammation on the initial steps of insulin signalling and the inflammatory pathway in the

BACKGROUND AND OBJECTIVES
Serum 25-hydroxyvitamin D3 (25(OH)D3 ), a newly emerged immune regulator, is considered to be involved in type 2 diabetic periodontitis (T2DCP). However, the risk factors and genes with altered expression that influence the
OBJECTIVE Evaluate the signaling pathways associated with inflammatory mediators activated in two models of experimental periodontitis. METHODS Two models were used: lipopolysaccharide (LPS) injections and ligature placement. Wistar rats were used and 30 microg LPS from Escherichia coli was injected
OBJECTIVE To investigate the expression of protein tyrosine phosphatase non-receptor type 2 (PTPN2) and nuclear factor-kappaB (NF-kappaB), as well as the relationship between their expression and periodontal destruction in mice with diabetic periodontitis. METHODS Four weeks old healthy C57BL/6J
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