Bone-added osteotome sinus floor elevation with simultaneous placement of non-submerged sand blasted with large grit and acid etched implants: a 5-year radiographic evaluation

PURPOSE: Implant survival rates using a bone-added osteotome sinus floor elevation (BAOSFE) procedure with simultaneous placement of a non-submerged sand blasted with large grit and acid etched (SLA) implant are well documented at sites where native bone height is less than 5 mm. This study evaluated the clinical results of non-submerged SLA Straumann implants placed at the time of the BAOSFE procedure at sites where native bone height was less than 4 mm. Changes in graft height after the BAOSFE procedure were also assessed using radiographs for 5 years after the implant procedure. METHODS: The BAOSFE procedure was performed on 4 patients with atrophic posterior maxillas with simultaneous placement of 7 non-submerged SLA implants. At least 7 standardized radiographs were obtained from each patient as follows: before surgery, immediately after implant placement, 6 months after surgery, every year for the next 3 years, and after more than 5 years had passed. Clinical and radiographic examinations were performed at every visit. Radiographic changes in graft height were calculated with respect to the implant's known length and the original sinus height. RESULTS: All implants were stable functionally, as well as clinically and radiographically, during the follow-up. Most of the radiographic reduction in the grafted bone height occurred in the first 2 years; reduction after 2 years was slight. CONCLUSIONS: The simultaneous placement of non-submerged SLA implants using the BAOSFE procedure is a feasible treatment option for patients with severe atrophic posterior maxillas. However, the grafted bone height is reduced during the healing period, and patients must be selected with care.ope

A mouse polyomavirus-encoded microRNA targets the cellular apoptosis pathway through Smad2 inhibition

AbstractSome viruses and most eukaryotic cells have microRNAs that regulate the expression of many genes. Although many viral miRNAs have been identified, only a few have been included in in vivo functional studies. Here we show that a Py-encoded miRNA downregulates the expression of the pro-apoptotic factor Smad2, resulting in the suppression of the apoptosis pathway. To study the Py miRNA in an in vivo context, a miRNA-deficient mutant virus was created on the background of the LID virus strain which establishes a rapid and lethal infection in newborn mice. Apoptosis analysis on kidney tissues indicates that the pro-apoptotic pathway is targeted in the infected host as well. Suppression of apoptosis through targeting of Smad2 by the Py miRNA is expected to synergize with anti-apoptotic effects previously attributed to the polyoma tumor antigens in support of virus replication in the natural host

Production of a Natural Antibody to the Mouse Polyoma Virus Is a Multigenic Trait

MA/MyJ mice express a natural antibody to the highly oncogenic polyoma virus. C57BR/cdJ mice lack this antibody but mount an adaptive T-cell response to the virus. Analysis of F2 progeny of a cross between these strains reveals a pattern of inheritance of expression of the natural antibody involving two genes in an epistatic relationship

The Polyoma Virus Large T Binding Protein p150 Is a Transcriptional Repressor of c-MYC

p150, product of the SALL2 gene, is a binding partner of the polyoma virus large T antigen and a putative tumor suppressor. p150 binds to the nuclease hypersensitive element of the c-MYC promoter and represses c-MYC transcription. Overexpression of p150 in human ovarian surface epithelial cells leads to decreased expression, and downregulation to increased expression, of c-MYC. c-MYC is repressed upon restoration of p150 to ovarian carcinoma cells. Induction of apoptosis by etoposide results in recruitment of p150 to the c-MYC promoter and to repression of c-MYC. Analysis of data in The Cancer Genome Atlas shows negative correlations between SALL2 and c-MYC expression in four common solid tumor types

Outer membrane protein a of Salmonella enterica serovar Typhimurium activates dendritic cells and enhances Th1 polarization

<p>Abstract</p> <p>Background</p> <p>Typhoid, which is caused by <it>Salmonella enterica </it>serovar Typhimurium, remains a major health concern worldwide. Multidrug-resistant strains of <it>Salmonella </it>have emerged which exhibit increased survivability and virulence, thus leading to increased morbidity. However, little is known about the protective immune response against this microorganism. The outer membrane protein (Omp)A of bacteria plays an important role in pathogenesis.</p> <p>Results</p> <p>We purified OmpA from <it>S. enterica </it>serovar Typhimurium (OmpA-sal) and characterized the role of OmpA-sal in promoting adaptive and innate immune responses. OmpA-sal functionally activated bone marrow-derived dendritic cells by augmenting expression of CD80, CD86, and major histocompatibility complex classes I and II. Interestingly, OmpA-sal induced production of interferon-γ from T cells in mixed lymphocyte reactions, thus indicating Th1-polarizing capacity. The expression of surface markers and cytokine production in dendritic cells was mediated by the TLR4 signaling pathway in a TLR4 Knock-out system.</p> <p>Conclusions</p> <p>Our findings suggest that OmpA-sal modulates the adaptive immune responses to <it>S. enterica </it>serovar Typhimurium by activating dendritic cells and driving Th1 polarization, which are important properties to consider in the development of effective <it>S. enterica </it>serovar Typhimurium vaccines and immunotherapy adjuvant.</p

Rising Incidence of Hip Fracture in Gwangju City and Chonnam Province, Korea

The purpose of study was to determine the incidence of hip fracture in 2001, to compare this with that of 1991, and to identify possible causes of change. Patients aged 50 yr or more living in Gwangju City and Chonnam Province, Korea, and who sustained a fracture of the hip during 2001 were investigated. Only patients who were admitted to hospitals for primary treatment of the first hip fracture were selected. There were 1,152 patients. A comparison of fracture incidences for 1991 and 2001 showed considerable increase during the 10-yr period. The total annual number of hip fractures rose from 247 in 1991 to 1,152 in 2001 and the fracture incidence also increased remarkably from 3.3 persons per 10,000 population in 1991 to 13.3 in 2001, representing a 4-fold increase over 10-yr. The reasons for this rising trend of hip fracture were not fully explained. However, an increase in the elderly population, an increase in osteoporosis, and an increase in injurious falls could partly account for the observed increase

Down-regulation of phosphoglucomutase 3 mediates sulforaphane-induced cell death in LNCaP prostate cancer cells

<p>Abstract</p> <p>Background</p> <p>Sulforaphane (SFN) is an isothiocyanate found in cruciferous vegetables that exerts anti-oxidant, anti-inflammatory, anti-cancer and radio-sensitizing activities. Nonetheless, the mechanism responsible for SFN-induced cell death is not fully understood. In the present study, anti-cancer mechanism of SFN was elucidated in LNCaP prostate cancer cells.</p> <p>Results</p> <p>SFN exerted cytotoxicity and increased TUNEL positive cells in a concentration-dependent manner in LNCaP cells. Proteomics study revealed that levels of nine proteins including tubulin β-2, phosphoglucomutase-3 (PGM3), melanoma-derived leucine zipper containing extra-nuclear factor, activin A type I receptor precursor, smoothelin-A, KIA0073, hypothetical protein LOC57691 and two unnamed proteins were changed over 8 folds in SFN treated LNCaP cells compared to untreated control. We have further confirmed that SFN reduced PGM3 expression with western blotting and showed that PGM3 siRNA enhanced cytotoxicity demonstrated by cell morphology and TUNEL assays in LNCaP cells.</p> <p>Conclusion</p> <p>Taken together, these findings suggest that PGM3 plays a role in mediating SFN-induced cell death in LNCaP cells, and is a potential molecular therapeutic target for prostate cancer.</p

The Mycobacterium avium subsp. paratuberculosis fibronectin attachment protein, a toll-like receptor 4 agonist, enhances dendritic cell-based cancer vaccine potency

In this study, we showed the direct interaction between Mycobacterium avium subsp. paratuberculosis fibronectin attachment protein (FAP) and toll-like receptor4 (TLR4) via co-localization and binding by using confocal microscopy and co-immunoprecipitation assays. FAP triggered the expression of pro- and anti-inflammatory cytokines in a TLR4-dependent manner. In addition, FAP-induced cytokine expression in bone marrow-derived dendritic cells (BMDCs) was modulated in part by glycogen synthase kinase-3 (GSK-3). FAP-induced expression of CD80, CD86, major histocompatibility complex (MHC) class I, and MHC class II in TLR4+/+ BMDCs was not observed in TLR4-/- BMDCs. Furthermore, FAP induced DC-mediated CD8+ T cell proliferation and cytotoxic T lymphocyte (CTL) activity, and suppressed tumor growth with DC-based tumor vaccination in EG7 thymoma murine model. Taken together, these results indicate that the TLR4 agonist, FAP, a potential immunoadjuvant for DC-based cancer vaccination, improves the DC-based immune response via the TLR4 signaling pathway