Objective:To study the effect of simvastatin on PTHrP stimulated osteoclastic resorption of murine calvarium and bone anabolism in vitro. Methods:Osteoclasts were isolated from bone marrow of Balb/C mice,cultured and identified.Calvaria of the new born Balb/C mice were cultured with PTHrP at 45 ng/ml and/or simvastatin at 10~ -7 -10~ -5 mol/L for 8 d.Ca~ 2+ and ALP in the culture supernatent were measured by atom spectrophotometer and automatic biochemical analyzer respectively.The bones were examined histologically.Results:Simvastatin at 10~ -7 -10~ -5 mol/L inhibited osteoclast formation and the osteoclastic bone resorption stimulated by PTHrP in vitro and reduced the release of Ca~ 2+ from the cultured osteoclasts in a dose-dependent manner. Simvastatin increased the ALP activities and bone mineralization of murines calvaria cultured in vitro. Conclusions:Simvastatin may inhibit the osteoclasric resorption stimulated by PTHrP and promote bone mineralization in vitro.

OBJECTIVE: To observe the effect of Fufang Sishen Decoction (FFSSD) on arrhythmia after virus myocarditis. METHODS: One hundred and two cases of arrhythmia after virus myocarditis were randomly divided into two groups. The treatment group was treated with FFSSD, 6 g, b.i.d.; and the control group with propafenone, 150 mg, q 8 h. The therapeutic effects were observed in 4 weeks. RESULTS: The total anti-arrhythmia effects of FFSSD and propafenone were 71.9% and 78.9% respectively (P>0.05). FFSSD took effects relatively slowly with mild and lasting effect. CONCLUSION: The curative effect of FFSSD in treating arrhythmia after virus myocarditis is confirmed. FFSSD has no obvious side effects.

OBJECTIVETo determine the level of leptin in gingival crevicular fluid (GCF) of patients with aggressive periodontitis (AgP) and to analyze the relationship between leptin and periodontal cilinical parameters.

METHODSFifty-four patients with AgP and 30 healthy controls were recruited. Detailed clinical examinations were conducted, and clinical parameters such as bleeding index (BI), probing depth (PD), attachment loss (AL) were recorded. Two teeth were selected as test teeth in each subject, one from posterior area and the other from anterior region. The level of GCF leptin was measured by enzyme linked immunosorbent assay.

RESULTSThe level of GCF leptin in AgP patients was significantly lower than that of control subjects [(16.5±4.6) ng vs.(26.0±6.0) ng, P < 0.05]. The level of GCF leptin was negatively related to BI (-0.306, P < 0.01), PD (-0.346, P < 0.01) and AL (-0.250, P < 0.01).

CONCLUSIONSAgP patients have significantly decreased level of GCF leptin and the level of leptin was negatively related to BI, PD and AL.

Adult ; Aggressive Periodontitis ; metabolism ; Case-Control Studies ; Enzyme-Linked Immunosorbent Assay ; Female ; Gingival Crevicular Fluid ; chemistry ; Humans ; Leptin ; analysis ; Male ; Periodontal Index

Mitophagy is an essential intracellular process that eliminates dysfunctional mitochondria and maintains cellular homeostasis. Mitophagy is regulated by the post-translational modification of mitophagy receptors. Fun14 domain-containing protein 1 (FUNDC1) was reported to be a new receptor for hypoxia-induced mitophagy in mammalian cells and interact with microtubule-associated protein light chain 3 beta (LC3B) through its LC3 interaction region (LIR). Moreover, the phosphorylation modification of FUNDC1 affects its binding affinity for LC3B and regulates selective mitophagy. However, the structural basis of this regulation mechanism remains unclear. Here, we present the crystal structure of LC3B in complex with a FUNDC1 LIR peptide phosphorylated at Ser17 (pS), demonstrating the key residues of LC3B for the specific recognition of the phosphorylated or dephosphorylated FUNDC1. Intriguingly, the side chain of LC3B Lys49 shifts remarkably and forms a hydrogen bond and electrostatic interaction with the phosphate group of FUNDC1 pS. Alternatively, phosphorylated Tyr18 (pY) and Ser13 (pS) in FUNDC1 significantly obstruct their interaction with the hydrophobic pocket and Arg10 of LC3B, respectively. Structural observations are further validated by mutation and isothermal titration calorimetry (ITC) assays. Therefore, our structural and biochemical results reveal a working model for the specific recognition of FUNDC1 by LC3B and imply that the reversible phosphorylation modification of mitophagy receptors may be a switch for selective mitophagy.
Crystallography, X-Ray ; Membrane Proteins ; chemistry ; metabolism ; Microtubule-Associated Proteins ; chemistry ; metabolism ; Mitochondrial Degradation ; Mitochondrial Proteins ; chemistry ; metabolism ; Peptides ; chemistry ; metabolism ; Phosphorylation ; Protein Structure, Quaternary

Humans ; Models, Molecular ; Repressor Proteins ; chemistry ; metabolism ; Retinoblastoma-Binding Protein 4 ; chemistry ; metabolism