Effect of stem cells and fibrin concentration on the vascularization of the Medpor orbital implant

Background: To determine the effect of adipose‐derived adult stem cells (ADASCs) and optimal concentration of fibrin on fibrovascular ingrowth into porous polyethylene orbital implants (Medpor). Methods: Medpor sheet treated with O.25% fibrin only and ADASCs in mixtures containing fibrin (0.25%, 0.5% or 1.25%) were applied to a Medpor sheet and implanted in the back of each of 20 athymic nude mice. After 10 days, implants were removed and observed for fibrovascularization and stability. Haemoglobin, collagen and cellular DNA content were determined in quantitative assays. Results: Haemoglobin, collagen and cellular DNA levels were significantly higher in ADASC group than in the cell‐free implant (0.25% fibrin only) group (P < 0.01). The level of haemoglobin and collagen content was significantly higher in the ADASC + 0.5% fibrin group among the ADASC and fibrin mixtures (P < 0.01). Conclusion: ADASCs significantly improved fibrovascularization on Medpor compared with implants alone. Fibrin, used together with ADASCs to potentiate fibrovascularization, was most effective at concentrations of 0.5%.     

XPS,AES and SEM analysis of recent dental implants

Today, surface chemistry modifications of titanium implants have become a development strategy for dental implants. The present study investigated the chemistry and morphology of commercially available dental implants (Nobel biocare TiUnite, Astra AB OsseoSpeed, 3i Osseotite, ITI-SLA). X-ray photoelectron spectroscopy (XPS) and auger electron spectroscopy were employed for the analysis of surface chemistry. The morphology was investigated by scanning electron microscopy. The present study demonstrated the major differences of surface properties, mainly dependent on the surface treatment used. The blasting and acid etching technique for the OsseoSpeed, Osseotite and SLA surfaces generally showed mainly TiO₂, but a varying surface morphology. In contrast, the electrochemical oxidation process for TiUnite implants not only produces microporous surface (pore size: 0.5–3.0 μm), but also changes surface chemistry due to incorporation of anions of the used electrolyte. As a result, TiUnite implants contain more than 7 at.% of P in oxide layer and higher amounts of hydroxides compared to the other implants in XPS analysis. F in OsseoSpeed implants was detected at 0.3% before as well as after sputter cleaning.     

Acute myocardial infarction in a young man with sickle cell disease

Sickle cell disease is considered protective against large vessel coronary artery disease. Although sickle cell patients do develop myocardial degeneration and fibrosis at a higher rate than age-matched controls, they rarely suffer from an acute myocardial infarction. We present a case of a 29-year-old man with sickle cell disease who presented with an acute non-ST segment myocardial infarction. In sickle cell patients who present with chest pain as an element of their sickle cell crisis, the clinician must consider acute myocardial infarction in the differential along with more common entities like acute chest syndrome.     

Subacute inhalation toxicity assessment of fly ash from industrial waste incinerators

Fly ash from industrial waste incinerators has been a significant concern because of their constituent toxic heavy metals and organic compounds. The objective of this study was to identify the subacute inhalation toxicity of fly ash from industrial waste incinerators, using whole body inhalation exposure chambers. Male and female groups of Sprague-Dawley rats were exposed to fly ash by inhalation of concentrations of 0, 50, 100, 200?mg/m(3), for 6?h/day, 5 days/week for 4 weeks. There was no significant difference in body weight, and relative organ weight to body weight, between the exposure groups and the control group. Hematological examinations revealed a significant increase of monocyte counts in fly ash exposed rats and brown pigment laden macrophage was found in the lungs of rats exposed to high concentration of fly ash. A decrease of blood glucose levels and an increase in glutamate oxaloacetate transaminase activity were observed in fly ash treated rats. There was also a significant increase of lactate dehydrogenase levels in rat blood exposed fly ash. A significant dose-dependent increase of DNA damage was found in lymphocytes, spleen, bronchoalveolar lavage, liver, lung, and thymus of rats exposed to fly ash. In addition, the level of lipid peroxidation was increased in the plasma of rats exposed to a high concentration of fly ash. These results suggest that inhalation of fly ash from industrial waste incinerators can induce histopathologic, hematological, and serum biochemical changes and oxidative damage.     

Magnolol-Induced Apoptosis in HCT-116 Colon Cancer Cells Is Associated with the AMP-Activated Protein Kinase Signaling Pathway

Colon cancer is the third most common malignancy around the world. Surgery, chemotherapy, and radiotherapy are generally used to treat colon cancer, but no effective therapy for advanced colon carcinoma is available. Therefore, there is a need to identify other therapeutic agents against this disease. Magnolol, a hydroxylated biphenyl compound present in Magnolia officinalis, exerts anticancer potential and low toxicity. Emerging evidence has suggested that activation of AMP-activated protein kinase (AMPK), a potential cancer therapeutic target is involved in apoptosis in colon cancer cells. However, the effects of magnolol on human colon cancer through activation of AMPK remain unexplored. In this study, we explored whether magnolol exerts an antiproliferative effect, and induces apoptosis in HCT-116 human colon cancer cells. Magnolol displayed several apoptotic features, including propidium iodide labeling, DNA fragmentation, and caspase-3 and poly(ADP-ribose) polymerase cleavages. We showed that magnolol induced the phosphorylation of AMPK in dose- and time-dependent manners. The selective AMPK inhibitor compound C abrogated the effect of magnolol on AMPK activation, suppression of proliferation, and caspase-3 cleavage. Magnolol downregulated expression of the antiapoptotic protein Bcl2, upregulated expression of pro-apoptotic protein p53 and Bax, and caused the release of mitochondrial cytochrome c. Magnolol-induced p53 and Bcl2 expression was abolished in the presence of compound C. Magnolol inhibited migration and invasion of HCT-116 cells through AMPK activation. These findings demonstrate that AMPK mediates the anticancer effects of magnolol through apoptosis in HCT-116 cells.     

The roles of surface chemistry and topography in the strength and rate of osseointegration of titanium implants in bone

The present study investigated the effects of surface chemistry and topography on the strength and rate of osseointegration of titanium implants in bone. Three groups of implants were compared: (1) machine-turned implants (turned implants), (2) machine-turned and aluminum oxide-blasted implants (blasted implants), and (3) implants that were machine-turned, aluminum oxide-blasted, and processed with the micro-arc oxidation method (Mg implants). Three and six weeks after implant insertion in rabbit tibiae, the implant osseointegration strength and rate were evaluated. Surface chemistry revealed characteristic differences of nine at.% Mg for Mg implants and 11 at.% Al for blasted implants. In terms of surface roughness, there was no difference between Mg implants and blasted implants in developed surface ratio (Sdr; p = 0.69) or summit density (Sds; p = 0.96), but Mg implants had a significantly lower arithmetic average height deviation (Sa) value than blasted implants (p = 0.007). At both 3 and 6 weeks, Mg implants demonstrated significantly higher osseointegration strength compared with turned (p = 0.0001, p = 0.0001) and blasted (p = 0.0001, p = 0.035) implants, whereas blasted implants showed significantly higher osseointegration than turned implants at 6 weeks (p = 0.02) but not at 3 weeks (p = 0.199). The present results not only support the hypothesis that biochemical bonding facilitates rapid and strong integration of implants in bone, but also provide evidence for biochemical bonding theory previously proposed by Sul.     

An in vitro comparison of possibly bioactive titanium implant surfaces

The aim of the study was to compare Ca and P formation (CaP) and subsequent bone cell response of a blasted and four different possibly bioactive commercially pure (cp) titanium surfaces; 1. Fluoride etched (Fluoride), 2. Alkali-heat treated (AH), 3. Magnesium ion incorporated anodized (TiMgO), and 4. Nano HA coated and heat treated (nano HA) in vitro. Furthermore, to evaluate the significance of the SBF formed CaP coat on bone cell response. The surfaces were characterized by Optical Interferometry, Scanning Electron Microscopy (SEM) and X-ray Photoelectron Spectroscopy (XPS). CaP formation was evaluated after 12, 24 and 72 h in simulated body fluid (SBF). Primary human mandibular osteoblast-like cells were cultured on the various surfaces subjected to SBF for 72 h. Cellular attachment, differentiation (osteocalcin) and protein production (TGF-beta(1)) was evaluated after 3 h and 10 days respectively. Despite different morphological appearances, the roughness of the differently modified surfaces was similar. The possibly bioactive surfaces gave rise to an earlier CaP formation than the blasted surface, however, after 72 h the blasted surface demonstrated increased CaP formation compared to the possibly bioactive surfaces. Subsequent bone cell attachment was correlated to neither surface roughness nor the amount of formed CaP after SBF treatment. In contrast, osteocalcin and TGF-beta(1) production were largely correlated to the amount of CaP formed on the surfaces. However, bone response (cell attachment, osteocalcin and TGF-F production) on the blasted controls were similar or increased compared to the SBF treated fluoridated, AH and TiMgO surface.     

Chrysophanic acid blocks proliferation of colon cancer cells by inhibiting EGFR/mTOR pathway

Inactivation of epidermal growth factor receptor (EGFR) is a prime method used in colon cancer therapy. Here it is shown that chrysophanic acid, a natural anthraquinone, has anticancer activity in EGFR-overexpressing SNU-C5 human colon cancer cells. Chrysophanic acid preferentially blocked proliferation in SNU-C5 cells but not in other cell lines (HT7, HT29, KM12C, SW480, HCT116 and SNU-C4) with low levels of EGFR expression. Chrysophanic acid treatment in SNU-C5 cells inhibited EGF-induced phosphorylation of EGFR and suppressed activation of downstream signaling molecules, such as AKT, extracellular signal-regulated kinase (ERK) and the mammalian target of rapamycin (mTOR)/ribosomal protein S6 kinase (p70S6K). Chrysophanic acid (80 and 120 μm) significantly blocked cell proliferation when combined with the mTOR inhibitor, rapamycin. These findings offer the first evidence of anticancer activity for chrysophanic acid via EGFR/mTOR mediated signaling transduction pathway.