A patient with femoral osteitis fibrosa cystica mimicking bone neoplasm: a case report.

BACKGROUND: Osteitis fibrosa cystica is a rare, benign and osteolytic lesion attributed to hyperparathyroidism. The high level of parathyroid hormone cause rapid bone loss. CASE PRESENTATION: The patient is a 50-year-old male complaining of severe and persistent pain in the right knee joint. Imaging studies were suspicious for a benign tumor in the right distal femur. Biopsy under CT guidance showed numerous osteoclast aggregation and hemosiderin deposition around the bone trabeculae. Blood tests disclosed significantly elevated parathyroid hormone, serum calcium, serum alkaline phosphatase. Parathyroid ultrasonography and CT scan showed a solid mass in front of the trachea at the thoracic entrance plane. After resection of the mass, the clinical symptoms were relieved and the radiological results were significantly improved, which further confirmed the diagnosis. CONCLUSIONS: Metabolic diseases-associated bone lesions require a comprehensive diagnosis of multiple inspection items. An interprofessional team approach to the diagnosis and treatment of osteitis fibrosa cystica will provide the best outcome.

miR-29a inhibits adhesion, migration, and invasion of osteosarcoma cells by suppressing CDC42.

Osteosarcoma is one of the most common tumors of the bone in children and adolescents worldwide. The relapse and metastasis of osteosarcoma are a major therapeutic challenge. Recently, several metastasis regulators, including miRNAs, kinases, and lncRNAs, were reported in osteosarcoma. Identifying novel regulators of metastasis will be useful to explore novel biomarkers for osteosarcoma. The present study showed miR-29a overexpression significantly inhibited HOS and MG-63 cell adhesion, invasion, and migration. About 70% of the wound area was repaired by migrating cells after 24 h in the control group, and only 50% of the wound area was repaired in the miR-29a overexpression group. The numbers of invading cells were decreased by 40% and 50% in HOS and MG-63 cells transfected with miR-29a, respectively, compared with the negative control group. Moreover, the present study validated that CDC42 was a direct target of miR-29a in OS cells. In conclusion, miR-29a may serve as a therapeutic target for osteosarcoma.

Cimetidine enhances the protective effect of GST DNA vaccine against Schistosoma japonicum.

Cimetidine (CIM), a histamine-2-receptor antagonist, has a long history of safe use in gastric acid-mediated gastrointestinal disorders. In this study, we used CIM, as an adjuvant, with pEGFP-Sj26 GST (the recombinant plasmid containing enhanced green fluorescent protein gene and the gene encoding 26 kDa glutathione S-transferase of Schistosoma japonicum) DNA vaccine to immunized mice and attempted to enhance the protective effect against S. japonicum. The results showed that the reduction rate of worm and egg burdens in the pEGFP-Sj26GST plus CIM group were 79.0% and 68.4%, respectively, significantly higher than that in pEGFP-Sj26GST alone group (27.0% and 22.5%, P<0.01). Compared with the pEGFP-Sj26GST alone group, mice immunized with pEGFP-Sj26GST plus CIM showed an elevated level of IFN-γ and IL-12 and a low level of IL-10 in splenocytes, while the levels of IL-4 and IL-5 showed no difference between the two groups. Our data also demonstrated that the percentage of CD4(+)CD25(+) regulatory T cells (Tregs) was significantly decreased in the spleens of mice immunized with pEGFP-Sj26GST plus CIM. All these findings suggest that CIM as a potential schistosome DNA vaccine adjuvant can enhance the protective effect of pEGFP-Sj26GST vaccine.

[Study on the in vitro effects of dexamethasone at different concentrations on the growth of murine embryonic palatal mesenchymal cell].

OBJECTIVE: To observe the effect of dexamethasone on the proliferation and apoptosis of embryonic palatal mesenchymal (EPM) cells, and chose a proper concentration of dexamethasone which can effect the ordinary growth of embryonic palatal mesenchymal cells. METHODS: The primary EPM cells were isolated and cultured in vitro, then we did biological assay. EPM cells were treated with different concentration dexamethasone (1 x 10(-9), 1 x 10(-8), 1 x 10(-7) and 1 x 10(-6) mol x L(-1)) respectively. The proliferation of EPM cells was evaluated using MTT method. Apoptosis was examined quantitatively with fluorescein stain. RESULTS: In the condition of blood serum's concentration at 10%, optical density step down following the raise of dexamethasone's concentration. The effect of dexamethasone got to a summit at 3 days. Inhibition rate of dexamethasone at 1 x 10(-6) mol x L(-1) was the highest. CONCLUSION: Dexamethasone at 1 x 10(-6) mol x L(-1) can not only inhibit the growth of the EPM cells, but also will not lead to a large number of cells death. Therefore, this concentration can be used as a reference standard in future research. The most significant drug action time of dexamethason appears at the third day after administration, then the effect became weaken following the drug metabolism.

Effect of CD4+ CD25+ regulatory T cells on the immune evasion of Schistosoma japonicum.

It has been known that parasites developed sophisticated strategies to escape from the host immune assault. More recently, one strategy to induce immune evasion involved CD4(+)CD25(+) regulatory T cells (Tregs). Mice were infected with Schistosoma japonicum cercariae and then injected intraperitoneally with anti-CD25 monoclonal antibody (anti-CD25 mAb). The results showed that the percentages of CD4(+)CD25(+) Tregs in mice were expanded by S. japonicum infection, and it could be partially blocked by anti-CD25 mAb. Worm burden in anti-CD25 mAb group (23.17 ± 6.94) was significantly lower than that in infected group (30.17 ± 5.85). The level of interferon gamma was increased with anti-CD25 mAb administration; meanwhile, lower concentration of interleukin 10 was observed in the same group. These results suggest that CD4(+)CD25(+) Tregs contribute to the escape of S. japonicum from the host immune responses, while anti-CD25 mAb can partially block CD4(+)CD25(+) Tregs and enhance the protective immunity to the parasite by Th1-type immune response.

[Effects of dexamethasone and vitamin B12 on expression of fibroblast growth factor 10 and fibroblast growth factor receptor 2b during early palatogenesis].

OBJECTIVE: To observe the alteration of fibroblast growth factor 10 (Fgf10) and fibroblast growth factor receptor 2 (Fgfr2b) signal in mouse embryonic palate after dexamethasone and vitamin B12 exposure. METHODS: Dams were divided teratogenetic group, antagomistic group and control group and were respectively injected dexamethasone, dexamethasone and vitamin B12, and normal sodium. Dams were killed and fetus was collected at embryo 12.5 and 13.5 day. The expression of Fgf10 and Fgfr2b and mesenchymal cells proliferation of mouse embryonic by western blotting and BrdU assay were checked. RESULTS: Fgf10 and Fgfr2b expression was down-regulated and mesenchymal cells proliferation was inhibited significantly after dexamethasone exposure. After vitamin B12 treatment, Fgf10 and Fgfr2b expression did not restore, but cells proliferation was recovered. CONCLUSION: Dexamethasone and vitamin B12 affected the expression of Fgf10 and Fgfr2b of mouse embryonic palate and mesenchyme cells proliferation, but the change was disaccord.

Perturbation of Fgf10 signal pathway in mouse embryonic palate by dexamethasone and vitamin B12 in vivo.

BACKGROUND/PURPOSE: The Fgf10 signaling pathway plays an important role in early stages of mouse embryonic palatal development, which is associated with cell proliferation and differentiation. The objective of this study was to assess whether dexamethasone and vitamin B(12) affected the Fgf10 signal pathway of mouse embryonic palate. MATERIALS AND METHODS: Immunohistochemical studies were performed for expression of Fgf10, Fgfr2b, and sonic hedgehog and for cell proliferation and apoptosis of mouse embryonic palate. RESULTS: The expression of Fgf10, Fgfr2b, and sonic hedgehog was changed in mouse embryonic palate after dexamethasone and vitamin B(12) treatment, resulting in reduced and restored proliferation of mesenchymal cells. CONCLUSIONS: Dexamethasone and vitamin B(12) affected the Fgf10 signaling pathway and cell proliferation of mouse embryonic palate. Cell apoptosis was not altered after dexamethasone and vitamin B(12) exposure.

Vitamin B12 counteracts dexamethasone-induced proliferation and apoptosis during key periods of palatogenesis in mice.

B vitamins rescue cleft palate induced by glucocorticoids in rodents; however, the mechanism of this effect remains largely unknown. The objective of our study was to assess the effect of dexamethasone and Vitamin B12 on cell proliferation and apoptosis during palatogenesis. In our study, mesenchymal cell proliferation in mouse embryonic palates decreased when the subjects were administered dexamethasone at embryo day 13.5 (E 13.5). However, mesenchymal cell proliferation was increased after dexamethasone exposure at E 14.0 and E 14.5 in comparison with the control group. After Vitamin B12 treatment, proliferation of mesenchymal cells was restored. No apoptosis was detected until bilaterial palatal shelves adhered and formed a medial epithelium seam in the control group and Vitamin B12-treated group. However, the apoptotic cells were detected under the medial edge epithelium before the palate contacted after dexamethasone treatment. The results suggested that Vitamin B12 restored proliferation, which had been reduced by dexamethasone via a delayed cellular cycle and apoptosis. This study implies that Vitamin B12 may be used to prevent or alleviate cleft palate induced by dexamethasone during embryonic palatogenesis.

Bis(µ-4-nitro-phthalato)bis-[diaqua-(1,10-phenanthroline)manganese(II)].

In the title compound, [Mn(2)(C(8)H(3)NO(6))(2)(C(12)H(8)N(2))(2)(H(2)O)(4)], the Mn(II) atom in the centrosymmetric binuclear unit has a distorted octa-hedral geometry and is coordinated by a chelating 1,10-phenanthroline ligand, two monodentate carboxyl-ate anions from two 4-nitro-phthalates and two coordinated water mol-ecules. The two Mn(II) ions in the mol-ecule are bridged by two 4-nitro-phthalate anions, both in a bis-monodentate mode, which finally leads to the formation of the binuclear unit. Intra-molecular O-H⋯O hydrogen bonds between the coordinated and uncoordinated O atoms of one monodentate carboxyl-ate group and the corresponding coordinated water mol-ecules result in an eight-membered and two six-membered rings. In the crystal structure, inter-molecular O-H⋯O hydrogen bonds link the dinuclear mol-ecules into supra-molecular chains propagating parallel to [100].

A preliminary study on the teratogenesis of dexamethasone and the preventive effect of vitamin B12 on murine embryonic palatal shelf fusion in vitro.

Excessive dexamethasone (Dex) administrated into pregnant mice during critical periods of palatal development can produce a high incidence of cleft palate. Its mechanisms remain unknown. Vitamin B12 has been shown to antagonize the teratogenic effects of Dex, which, however, remains controversial. In this study, we investigated the effects of Dex and vitamin B12 on murine embryonic palatal shelf fusion using organ culture of murine embryonic shelves. The explanted palatal shelves on embryonic day 14 (E14) were cultured for 24, 48, 72 or 96 h in different concentrations of Dex and/or vitamin B12. The palatal shelves were examined histologically for the morphological alterations on the medial edge epithelium (MEE) and fusion rates among different groups. It was found that the palatal shelves were not fused at 72 h or less of culture in Dex group, while they were completely fused in the control and vitamin B12-treated groups at 72 and 96 h, respectively. The MEE still existed and proliferated. In Dex+vitamin B12 group the palatal shelves were fused at each time point in a similar rate to controls. These results may suggest that Dex causes teratogenesis of murine embryonic palatal shelves and vitamin B12 prevents the teratogenic effect of Dex on palatogenesis on murine embryos in vitro.

Induction of the Epstein-Barr virus latent membrane protein 2 antigen-specific cytotoxic T lymphocytes using human leukocyte antigen tetramer-based artificial antigen-presenting cells.

Cytotoxic T lymphocytes (CTLs) specific for the Epstein-Barr virus (EBV) latent membrane protein 2 (LMP2) antigen are important reagents for the treatment of some EBV-associated malignancies, such as EBV-positive Hodgkin's disease and nasopharyngeal carcinoma. However, the therapeutic amount of CTLs is often hampered by the limited supply of antigen-presenting cells. To address this issue, an artificial antigen-presenting cell (aAPC) was made by coating a human leukocyte antigen (HLA)-pLMP2 tetrameric complex, anti-CD28 antibody and CD54 molecule to a cell-sized latex bead, which provided the dual signals required for T cell activation. By co-culture of the HLA-A2-LMP2 bearing aAPC and peripheral blood mononuclear cells from HLA-A2 positive healthy donors, LMP2 antigen-specific CTLs were induced and expanded in vitro. The specificity of the aAPC-induced CTLs was demonstrated by both HLA-A2-LMP2 tetramer staining and cytotoxicity against HLA-A2-LMP2 bearing T2 cell, the cytotoxicity was inhibited by the anti-HLA class I antibody (W6/32). These results showed that LMP2 antigen-specific CTLs could be induced and expanded in vitro by the HLA-A2-LMP2-bearing aAPC. Thus, aAPCs coated with an HLA-pLMP2 complex, anti-CD28 and CD54 might be promising tools for the enrichment of LMP2-specific CTLs for adoptive immunotherapy.