Fractionation of the extract of Aspergillus niger. IFB-E003, an endophyte in Cyndon dactylon, gave four known compounds naphtho-gamma-pyrones rubrofusarin B, fonsecinone A, asperpyrone B and aurasperone A, which were further investigated biologically. Rubrofusarin B was shown to be cytotoxic to the colon cancer cell line SW1116 (IC50: 4.5 microgml-1), and aurasperone A inhibitory on XO (xanthine oxidase) (IC50: 10.9 micromoll-1). Moreover, the four naphtho-gamma-pyrones exhibited growth inhibitions against the five test microbes with MICs ranging in between 1.9 and 31.2 microgml(-1). The present recognition of rubrofusarin B and aurasperone A as strong co-inhibitors on XO, colon cancer cell and some microbial pathogens is of significance for the imperative discovery of new relevant therapeutic agents.

Periodontal homeostasis is maintained by the dynamic equilibrium between cell death, differentiation and proliferation of resident cells in the periodontal microenvironment. Loss of resident periodontal ligament fibroblasts (PDLFs) has been a major challenge in the periodontal treatment. This study aimed to investigate the exact role of necroptotic cell death in periodontal diseases. Elevated levels of receptor-interacting protein serine-threonine kinases -1 (RIPK1), phosphorylated RIPK3, mixed lineage kinase domain-like protein (MLKL), phosphorylated MLKL and FLIP L were observed in gingival tissues collected from patients with untreated chronic periodontitis; whereas no difference in caspase 8 was observed between the periodontitis and healthy control group. In contrast to the high incidence of necroptotic cell death in monocytes during live P. gingivalis infection with a low multiplicity of infection (MOI), necroptosis was only observed in PDLFs with a high MOI. Priming PDLFs with frozen thawed monocytes enhanced proinflammatory responses to P. gingivalis infection; moreover, frozen thawed monocytes stimulation triggered RIPK1, RIPK3 and MLKL-mediated-necroptotic cell death in PDLFs. These results indicated that RIPK3 and MLKL-mediated-necroptotic cell death participated in the pathogenesis of periodontitis, and DAMPs released from monocytes after P. gingivalis stimulation by necroptosis triggered not only inflammatory responses, but also necroptosis of PDLFs.

In addition to apoptosis, necroptosis also plays critical roles in pathological changes in mandibular cartilage after compressive mechanical force stimulation, implying RIP1, a master protein that mediates both necroptosis and apoptosis, as a potential therapeutic target in temporal mandibular osteoarthritis.

The nature of the ϳ370-nm ͑3.35-eV͒ photoluminescence ͑PL͒ in Si oxide and nanostructures, which has a PL excitation band at ϳ260 nm, is studied experimentally and theoretically. It is revealed that the PL occurs at the interface between Si structure and its oxide and is closely associated with a characteristic infrared absorption band at ϳ1250 cm −1 . Spectral analyses suggest that the ϳ370-nm PL originates in the -SiO 3 group, which bonds to Si structural surface. The density functional theory calculations are consistent with our experiments. This work clarifies some controversies regarding the ϳ370-nm PL mechanisms in a number of Si oxide and nanostructures.

Fibroblast growth factor receptor 2 ( FGFR2) in craniofacial bones mediates osteoprogenitor proliferation, differentiation, and apoptosis. The distortion of proper craniofacial bone growth may cause class II and class III skeletal malocclusion and result in compromised function and aesthetics. Here, we investigated the association between variations in FGFR2 and skeletal malocclusions. First, 895 subjects were included in a 2-stage case-control study with independent populations (stage 1: n = 138 class I, 111 class II, and 81 class III; stage 2: n = 279 class I, 187 class II, and 99 class III). Eight candidate single-nucleotide polymorphisms (SNPs) in FGFR2 were screened and validated. Five SNPs (rs2162540, rs2981578, rs1078806, rs11200014, and rs10736303) were found to be associated with skeletal malocclusions (all P < 0.05). That is, rs2162540 was significantly associated with skeletal class II malocclusion, while others were associated with skeletal class III malocclusion. Electrophoretic mobility shift assay and chromatin immunoprecipitation analysis showed that the common genotypes of rs2981578 and rs10736303 contained the binding sites of RUNX2 and SMAD4. Compared with the common genotypes, the minor genotypes at these 2 SNPs decreased the binding affinity and enhancer effect of RUNX2 and SMAD4, as well the levels of FGFR2 expression. In addition, FGFR2 expression contributed positively to osteogenic differentiation in vitro. Thus, we identified FGFR2 as a skeletal malocclusion risk gene, and FGFR2 polymorphisms regulated its transcriptional expression and then osteogenic differentiation.