IL-1Ra regulates IL-1 activity and appears to reduce the levels of other inflammatory cytokines, including TNF-α and IL-6, while it also reduces expression of the EP4 receptor related to prostanoid sensitivity and osteoclast formation. These results suggest that IL-1Ra is an important molecule for inhibition of inflammatory periodontal bone resorption.

This study analyzes the effect of interleukin-15 (IL-15) on osteoclast formation using a coculture of mouse osteoblasts and bone marrow cells (BMCs) stimulated with prostaglandin E2 (PGE2), which both have important role in rheumatoid arthritis (RA) and periodontal disease (PD). BMCs isolate lacking T (BM(T-)) or NK (BM(NK-)) cells, BMCs with no cells removed (BM(T+NK+)), purified NK cells, and purified T cells were each cocultured with osteoblasts in the presence or absence of PGE2 and/or IL-15. The number of both osteoclasts and osteoblasts was decreased by IL-15 in a dose-dependent manner in BM(T+NK+), BM(T-). However, the reductions were improved in BM(NK-). The expression of caspase3 in osteoblasts cocultured with NK cells was increased in a dose-dependent manner by IL-15. IL-15 stimulates apoptosis of osteoblasts via activation of NK cells. Since osteoblasts have an important role in bone formation, IL-15 may be an inflammatory bone destructive factor in RA and PD.

cThe interleukin-1 receptor antagonist (IL-1Ra) binds to IL-1 receptors and inhibits IL-1 activity. However, it is not clear whether IL-1Ra plays a protective role in periodontal disease. This study was undertaken to compare experimental periodontitis induced by Aggregatibacter actinomycetemcomitans in IL-1Ra knockout (KO) mice and wild-type (WT) mice. Computed tomography (CT) analysis and hematoxylin-and-eosin (H&E) and tartrate-resistant acid phosphatase (TRAP) staining were performed. In addition, osteoblasts were isolated; the mRNA expression of relevant genes was assessed by real-time quantitative PCR (qPCR); and calcification was detected by Alizarin Red staining. Infected IL-1Ra KO mice exhibited elevated (P, <0.05) levels of antibody against A. actinomycetemcomitans, bone loss in furcation areas, and alveolar fenestrations. Moreover, protein for tumor necrosis factor alpha (TNF-␣) and IL-6, mRNA for macrophage colony-stimulating factor (M-CSF), and receptor activator of NF-B ligand (RANKL) in IL-1Ra KO mouse osteoblasts stimulated with A. actinomycetemcomitans were increased (P, <0.05) compared to in WT mice. Alkaline phosphatase (ALP), bone sialoprotein (BSP), osteocalcin (OCN)/bone gla protein (BGP), and runt-related gene 2 (Runx2) mRNA levels were decreased (P, <0.05). IL-1␣ mRNA expression was increased, and calcification was not observed, in IL-1 Ra KO mouse osteoblasts. In brief, IL-1Ra deficiency promoted the expression of inflammatory cytokines beyond IL-1 and altered the expression of genes involved in bone resorption in A. actinomycetemcomitans-infected osteoblasts. Alterations consistent with rapid bone loss in infected IL-Ra KO mice were also observed for genes expressed in bone formation and calcification. In short, these data suggest that IL-1Ra may serve as a potential therapeutic drug for periodontal disease.

We investigate high-order harmonic generation from D 2 /H 2 molecules with intense multi-cycle pulses centred both at 1300 nm (60 fs) and at 800 nm (50 fs) together with that from N 2 /Ar as a reference. The experimental observations with 1300 nm pulses are different from those with 800 nm pulses both in spectral shapes and in intensity ratios I D 2 /I H 2 . The effect of nuclear motion in D 2 and H 2 is more distinctive for 1300 nm pulses than for 800 nm pulses. With multi-cycle pulses of 50-60 fs, the intensity ratios I D 2 /I H 2 are found to be higher for both 800 nm and 1300 nm pulses than those with few-cycle pulses of 8 fs, which is attributed partly to the contribution of the coupling between the 1sσ g and 2pσ u states in D + 2 and H + 2 molecular ions during the higher order returns of the electron wave packets.

(1) Objective: hypercoagulability in patients with malignant neoplasm were evaluated to examine the relationship with thrombosis. (2) Methods: clot waveform analysis (CWA)—activated partial thromboplastin time (APTT) and CWA—small amount of tissue factor induced FIX activation (sTF/FIXa) assays were performed in 92 patients with malignant neoplasm and the relationship between hypercoagulability and thrombosis was retrospectively examined. (3) Results: The study population included 92 patients with malignant neoplasms. Twenty-six (28.3%) had thrombotic diseases and 9 (9.8%) patients died within 28 days after the CWA. The peak time of the CWA-APTT could not show hypercoagulability in patients with malignant neoplasms. There were almost no significant differences in the peak times of the sTF/FIXa among patients with malignant neoplasms and healthy volunteers. In contrast, the peak heights of the CWA-sTF/FIXa in patients with various malignant neoplasms were significantly higher than those in healthy volunteers. Furthermore, among patients with malignant neoplasms, the peak heights of the sTF/FIXa in patients with thrombosis were significantly higher than those in patients without thrombosis. (4) Conclusions: although the routine APTT cannot evaluate the hypercoagulability, the peak heights of CWA-sTF/FIXa were significantly high in patients with malignant neoplasms, especially in those with thrombosis, suggesting that an elevated peak height of the CWA-sTF/FIXa may be a risk factor for thrombosis.