Browsing by Subject "radiation effects"

Now showing 1 - 6 of 6
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    Laser-treated stainless steel mini-screw implants: 3D surface roughness, bone-implant contact, and fracture resistance analysis
    (Oxford University Press, 2016-04) Kang, He-Kyong; Chu, Tien-Min; Dechow, Paul; Stewart, Kelton; Kyung, Hee-Moon; Liu, Sean Shih-Yao; Department of Orthodontics and Oral Facial Genetics, School of Dentistry
    BACKGROUND/OBJECTIVES: This study investigated the biomechanical properties and bone-implant intersurface response of machined and laser surface-treated stainless steel (SS) mini-screw implants (MSIs). MATERIAL AND METHODS: Forty-eight 1.3mm in diameter and 6mm long SS MSIs were divided into two groups. The control (machined surface) group received no surface treatment; the laser-treated group received Nd-YAG laser surface treatment. Half in each group was used for examining surface roughness (Sa and Sq), surface texture, and facture resistance. The remaining MSIs were placed in the maxilla of six skeletally mature male beagle dogs in a randomized split-mouth design. A pair with the same surface treatment was placed on the same side and immediately loaded with 200 g nickel-titanium coil springs for 8 weeks. After killing, the bone-implant contact (BIC) for each MSI was calculated using micro computed tomography. Analysis of variance model and two-sample t test were used for statistical analysis with a significance level of P <0.05. RESULTS: The mean values of Sa and Sq were significantly higher in the laser-treated group compared with the machined group (P <0.05). There were no significant differences in fracture resistance and BIC between the two groups. LIMITATION: animal study CONCLUSIONS/IMPLICATIONS: Laser treatment increased surface roughness without compromising fracture resistance. Despite increasing surface roughness, laser treatment did not improve BIC. Overall, it appears that medical grade SS has the potential to be substituted for titanium alloy MSIs.
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    Photochemistry and Photobiology of the Spore Photoproduct: A 50-Year Journey
    (Wiley Blackwell (Blackwell Publishing), 2015-11) Setlow, Peter; Li, Lei; Department of Chemistry & Chemical Biology, School of Science
    Fifty years ago, a new thymine dimer was discovered as the dominant DNA photolesion in UV-irradiated bacterial spores [Donnellan, J. E. & Setlow R. B. (1965) Science, 149, 308-310], which was later named the spore photoproduct (SP). Formation of SP is due to the unique environment in the spore core that features low hydration levels favoring an A-DNA conformation, high levels of calcium dipicolinate that acts as a photosensitizer, and DNA saturation with small, acid-soluble proteins that alters DNA structure and reduces side reactions. In vitro studies reveal that any of these factors alone can promote SP formation; however, SP formation is usually accompanied by the production of other DNA photolesions. Therefore, the nearly exclusive SP formation in spores is due to the combined effects of these three factors. Spore photoproduct photoreaction is proved to occur via a unique H-atom transfer mechanism between the two involved thymine residues. Successful incorporation of SP into an oligonucleotide has been achieved via organic synthesis, which enables structural studies that reveal minor conformational changes in the SP-containing DNA. Here, we review the progress on SP photochemistry and photobiology in the past 50 years, which indicates a very rich SP photobiology that may exist beyond endospores.
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    Single-Limb Irradiation Induces Local and Systemic Bone Loss in a Murine Model
    (Wiley Blackwell (John Wiley & Sons), 2015-07) Wright, Laura E.; Buijs, Jeroen T.; Kim, Hun-Soo; Coats, Laura E.; Scheidler, Anne M.; John, Sutha K.; She, Yun; Murthy, Sreemala; Ma, Ning; Chin-Sinex, Helen J.; Bellido, Teresita M.; Bateman, Ted A.; Mendonca, Marc S.; Mohammad, Khalid S.; Guise, Theresa A.; Department of Medicine, IU School of Medicine
    Increased fracture risk is commonly reported in cancer patients receiving radiotherapy, particularly at sites within the field of treatment. The direct and systemic effects of ionizing radiation on bone at a therapeutic dose are not well-characterized in clinically relevant animal models. Using 20-week-old male C57Bl/6 mice, effects of irradiation (right hindlimb; 2 Gy) on bone volume and microarchitecture were evaluated prospectively by microcomputed tomography and histomorphometry and compared to contralateral-shielded bone (left hindlimb) and non-irradiated control bone. One week postirradiation, trabecular bone volume declined in irradiated tibias (-22%; p < 0.0001) and femurs (-14%; p = 0.0586) and microarchitectural parameters were compromised. Trabecular bone volume declined in contralateral tibias (-17%; p = 0.003), and no loss was detected at the femur. Osteoclast number, apoptotic osteocyte number, and marrow adiposity were increased in irradiated bone relative to contralateral and non-irradiated bone, whereas osteoblast number was unchanged. Despite no change in osteoblast number 1 week postirradiation, dynamic bone formation indices revealed a reduction in mineralized bone surface and a concomitant increase in unmineralized osteoid surface area in irradiated bone relative to contralateral and non-irradiated control bone. Further, dose-dependent and time-dependent calvarial culture and in vitro assays confirmed that calvarial osteoblasts and osteoblast-like MC3T3 cells were relatively radioresistant, whereas calvarial osteocyte and osteocyte-like MLO-Y4 cell apoptosis was induced as early as 48 hours postirradiation (4 Gy). In osteoclastogenesis assays, radiation exposure (8 Gy) stimulated murine macrophage RAW264.7 cell differentiation, and coculture of irradiated RAW264.7 cells with MLO-Y4 or murine bone marrow cells enhanced this effect. These studies highlight the multifaceted nature of radiation-induced bone loss by demonstrating direct and systemic effects on bone and its many cell types using clinically relevant doses; they have important implications for bone health in patients treated with radiation therapy.
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    Survival efficacy of the PEGylated G-CSFs Maxy-G34 and neulasta in a mouse model of lethal H-ARS, and residual bone marrow damage in treated survivors
    (Ovid Technologies (Wolters Kluwer) - Lippincott Williams & Wilkins, 2014-01) Chua, Hui Lin; Plett, P. Artur; Sampson, Carol H.; Katz, Barry P.; Carnathan, Gilbert W.; MacVittie, Thomas J.; Lenden, Keith; Orschell, Christie M.; Department of Medicine, IU School of Medicine
    In an effort to expand the worldwide pool of available medical countermeasures (MCM) against radiation, the PEGylated G-CSF (PEG-G-CSF) molecules Neulasta and Maxy-G34, a novel PEG-G-CSF designed for increased half-life and enhanced activity compared to Neulasta, were examined in a murine model of the Hematopoietic Syndrome of the Acute Radiation Syndrome (H-ARS), along with the lead MCM for licensure and stockpiling, G-CSF. Both PEG-G-CSFs were shown to retain significant survival efficacy when administered as a single dose 24 h post-exposure, compared to the 16 daily doses of G-CSF required for survival efficacy. Furthermore, 0.1 mg kg of either PEG-G-CSF affected survival of lethally-irradiated mice that was similar to a 10-fold higher dose. The one dose/low dose administration schedules are attractive attributes of radiation MCM given the logistical challenges of medical care in a mass casualty event. Maxy-G34-treated mice that survived H-ARS were examined for residual bone marrow damage (RBMD) up to 9 mo post-exposure. Despite differences in Sca-1 expression and cell cycle position in some hematopoietic progenitor phenotypes, Maxy-G34-treated mice exhibited the same degree of hematopoietic stem cell (HSC) insufficiency as vehicle-treated H-ARS survivors in competitive transplantation assays of 150 purified Sca-1+cKit+lin-CD150+cells. These data suggest that Maxy-G34, at the dose, schedule, and time frame examined, did not mitigate RBMD but significantly increased survival from H-ARS at one-tenth the dose previously tested, providing strong support for advanced development of Maxy-G34, as well as Neulasta, as MCM against radiation.
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    Topical photodynamic therapy induces systemic immunosuppression via generation of platelet-activating factor receptor ligands
    (Nature Publishing Group, 2015-01) Ferracini, Matheus; Sahu, Ravi P.; Harrison, Kathleen A.; Waeiss, Robert A.; Murphy, Robert C.; Jancar, Sonia; Konger, Raymond L.; Travers, Jeffrey B.; Department of Dermatology, IU School of Medicine
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    Translational Repression Protects Human Keratinocytes from UVB-Induced Apoptosis through a Discordant eIF2 Kinase Stress Response
    (Nature Publishing Group, 2015-10) Collier, Ann E.; Wek, Ronald C.; Spandau, Dan F.; Department of Dermatology, IU School of Medicine
    This study delineates the mechanisms by which UVB regulates protein synthesis in human keratinocytes and the importance of translational control in cell survival. Translation initiation is regulated by phosphorylation of eukaryotic initiation factor 2 (eIF2-P) that causes decreased global protein synthesis coincident with enhanced translation of selected stress-related transcripts, such as activating transcription factor 4 (ATF4). ATF4 is a transcriptional activator of the integrated stress response (ISR) that has cytoprotective functions as well as apoptotic signals through the downstream transcriptional regulator C/EBP homologous protein (CHOP; GADD153/DDIT3). We determined that UVB irradiation is a potent inducer of eIF2-P in keratinocytes, leading to decreased levels of translation initiation. However, expression of ATF4 or CHOP was not induced by UVB as compared with traditional ISR activators. The rationale for this discordant response is that ATF4 mRNA is reduced by UVB, and despite its ability to be preferentially translated, there are diminished levels of available transcript. Forced expression of ATF4 and CHOP protein before UVB irradiation significantly enhanced apoptosis, suggesting that this portion of the ISR is deleterious in keratinocytes following UVB. Inhibition of eIF2-P and translational control reduced viability following UVB that was alleviated by cycloheximide (CHX), indicating that translation repression through eIF2-P is central to keratinocyte survival.