An, Heesuk;Lee, Jung-Tae;Oh, Seo-Eun;Park, Kyeong-mee;Hu, Kyung-Seok;Kim, Sungtae;Chung, Moon-Kyu
Journal of Periodontal and Implant Science
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v.49
no.1
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pp.2-13
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2019
Purpose: The aim of this study was to conduct a histologic evaluation of irradiated calvarial defects in rats 4 weeks after applying fibroblast growth factor-2 (FGF-2) with hyaluronan or biphasic calcium phosphate (BCP) block in the presence or absence of adjunctive hyperbaric oxygen (HBO) therapy. Methods: Twenty rats were divided into HBO and non-HBO (NHBO) groups, each of which was divided into FGF-2 and BCP-block subgroups according to the grafted material. Localized radiation with a single 12-Gy dose was applied to the calvaria of rats to simulate radiotherapy. Four weeks after applying this radiation, 2 symmetrical circular defects with a diameter of 6 mm were created in the parietal bones of each animal. The right-side defect was filled with the materials mentioned above and the left-side defect was not filled (as a control). All defects were covered with a resorbable barrier membrane. During 4 weeks of healing, 1 hour of HBO therapy was applied to the rats in the HBO groups 5 times a week. The rats were then killed, and the calvarial specimens were harvested for radiographic and histologic analyses. Results: New bone formation was greatest in the FGF-2 subgroup, and improvement was not found in the BCP subgroup. HBO seemed to have a minimal effect on new bone formation. There was tendency for more angiogenesis in the HBO groups than the NHBO groups, but the group with HBO and FGF-2 did not show significantly better outcomes than the HBO-only group or the NHBO group with FGF-2. Conclusions: HBO exerted beneficial effects on angiogenesis in calvarial defects of irradiated rats over a 4-week healing period, but it appeared to have minimal effects on bone regeneration. FGF-2 seemed to enhance new bone formation and angiogenesis, but its efficacy appeared to be reduced when HBO was applied.
The present study was conducted to elucidate whether the expression level of poly(ADP-ribose) polymerase (PARP) is related to the ultraviolet radiation (UV)-induced apoptosis. After treatment of the mammalian cell lines HeLa S3 and Chinese hamster ovary (CHO) with 50 J/m2 UV, induction of apoptosis was determined by several means during 24 h post-incubation. Incidence of apoptosis was much lower in CHO than HeLa S3 cells based on the percentage of apoptotic cells in terms of morphological changes in nucleus or direct counting of viable cells and qualitative or quantitative DNA fragmentation. Interestingly, when the expression level of PARP was measured by western blotting, the amounts of PARP that was retained at each time point inversely correlated with the incidences of apoptosis in these cells. Concomitant with generation of the 85 kDa fragment, 116 kDa PARP disappeared in HeLa S3 within 6 h after UV treatment, whereas a fair amounts of 116 kDa band was still retained in CHO cells at 36 h post-incubation. This inverse relationship was also observed in the adaptive response system, in which cells weve treated with a high dose of UV after pretreatment with a low dose. As expected, typical adaptive responses appeared in CHO cells but not in HeLa cells, showing greater cell viability and lesser DNA fragmentation. During the adaptive response in CHO cells, PARP was expressed at much higher level compared to the single, high dose-treated cells. Interestingly, even though PARP was induced at 6 h post-incubation In both cell types, its expression was more prominent in CHO cells. Thus, our data indicate that the retained level of intact PARP against UV damage inversely correlates with incidence of apoptosis in mammalian cells, and also suggest that a machinery to protect the PARP degradation against UV damage exists in CHO but not in HeLa S3 cells.
Bacterial assimilation of $CO_2$ into stable biomolecules using electrochemical reducing power may be an effective method to reduce atmospheric $CO_2$ without fossil fuel combustion. For the enrichment of the $CO_2$-fixing bacteria using electrochemical reducing power as an energy source, a cylinder-type electrochemical bioreactor with a built-in anode compartment was developed. A graphite felt cathode modified with neutral red (NR-graphite cathode) was used as a solid electron mediator to induce bacterial cells to fix $CO_2$ using electrochemical reducing power. Bacterial $CO_2$ consumption was calculated based on the variation in the ratio of $CO_2$ to $N_2$ in the gas reservoir. $CO_2$ consumed by the bacteria grown in the electrochemical bioreactor (2,000 ml) reached a maximum of approximately 1,500 ml per week. Time-coursed variations in the bacterial community grown with the electrochemical reducing power and $CO_2$ in the mineral-based medium were analyzed via temperature gradient gel electrophoresis (TGGE) of the 16S rDNA variable region. Some of the bacterial community constituents noted at the initial time disappeared completely, but some of them observed as DNA signs at the initial time were clearly enriched in the electrochemical bioreactor during 24 weeks of incubation. Finally, Alcaligenes sp. and Achromobacter sp., which are capable of autotrophically fixing $CO_2$, were enriched to major constituents of the bacterial community in the electrochemical bioreactor.
A pot experiment on the Sr-90 uptake by the barley from a loamy-sandy soil of pH 6.05 treated with Sr-90 and slaked lime was carried out in a green house. The rate of Sr-90 uptake at maturity was, on an average, 0.41% for a naked barley Neolssalbori and 0.23% for a covered one Olbori. Transfer coefficients of Sr-90 for the former were higher than those for the latter by about 30-60% depending on the plant parts. There were, on the whole, not significant differences in the rate and in the coefficient among Sr-90 concentration treatments. Slaked lime addition equivalent to about 94kg/10a was not effective for lessening Sr-90 uptake or diminishing Sr-90 transfer coefficient. As transfer coefficients, 1.51, 4.45, 0.35, and 1.30, on the dry weight basis, could be proposed for the stem, leaf, seed, and whole top of the barley, respectively. Growth inhibition or yield decrease due to Sr-90 uptake was not observed.
$NF-{\kappa}B$ (nuclear factor-kappa B) plays a particularly central role in epidermal biology. It has been established that ultraviolet radiation (UVR) is one of the mechanisms to induce the activation of $NF-{\kappa}B$ in human skin. We previously demonstrated that melanogenic inhibitors may act through the inhibition of $NF-{\kappa}B$ activation in keratinocytes. In order to find another type of melanogenic inhibitors of $NF-{\kappa}B$ activation, various kinds of the extracts from crude drugs $(30\;{\mu}g/ml)$ were preincubated with transfectant HaCaT cells for 3 hrs and then UVR $(60\;mj/cm^2)$ was irradiated. UVR-exposed cells were incubated for another 6 hrs to measure the $NF-{\kappa}B$ activity. $NF-{\kappa}B$ activation was measured with the secreatory alkaline phosphates (SEAP) reporter gene assay using a fluorescence detection method. Among natural products, Lycium chinense, Acanthopanax senticosus, Angelica koreana, Kalopanax pictus and Asparagus cochinchinensis were the most potent inhibitors of $NF-{\kappa}B$ activation by UVR. These observations suggest that some crude drugs might act partially through the modulation of the synthesis of melanotrophic factors to decrease melanogenesis in keratinocytes.
In order to investigate the in vivo effect of $^{60}Co$ radiation on rabbit liver, the uptake ratio and regional excretory value in hepatocytes and Kupffer cells were estimated during acute and chronic hepatic injuries. The left lobe of liver was irradiated at 15 Gy or 30 Gy with a single dose and subsequent changes were analysed with a seial nuclear medicine imaging by using $^{99m}Tc-phytate,\;^{99m}Tc-DISIDA\;and\;^{99m}Tc-HSA$ and resulting data were computerized. The degree of hepatic damage, duration of the injury, and recovery pattern after the irradation were in agreement with the findings of other investigations. However, out values were more quantitative evacuation than those of other publications. Recovery of decreased uptake of $^{99m}Tc-phytate$ was delayed approximately $2{\sim}3$ days later than that of $^{99m}Tc-DISIDA$. In acute radiation induced injury, the results demonstrated that the recovery of Kupffer cells was delayed more than that of hepatocytes. This discrepancy was considered due to the differences in repair activities between these cell types. The decreased of regional excretory value in irradiated area was found to be dose-dependent but had no corelation with regional uptakes of DISIDA and phytate. The decreased of regional excretory value observed in non-irradiated region suggested that irradiated liver might induce an indirect effect.
The present study was aimed at determining the effects of alkylating and oxidative stress inducing agents on a newly identified variant of DNA polymerase beta ($pol{\beta}{\Delta}_{208-304}$) specific for ovarian cancer. $Pol{\beta}{\Delta}_{208-304}$ has a deletion of exons 11-13 which lie in the catalytic part of enzyme. We compared the effect of these chemicals on HeLa cells and HeLa cells stably transfected with this variant cloned into in pcDNAI/neo vector by MTT, colony forming and apoptosis assays. $Pol{\beta}{\Delta}_{208-304}$ cells exhibited greater sensitivity to an alkylating agent and less sensitivity towards $H_2O_2$ and UV when compared with HeLa cells alone. It has been shown that cell death in $Pol{\beta}{\Delta}_{208-304}$ transfected HeLa cells is mediated by the caspase 9 cascade. Exon 11 has nucleotidyl selection activity, while exons 12 and 13 have dNTP selection activity. Hence deletion of this part may affect polymerizing activity although single strand binding and double strand binding activity may remain same. The lack of this part may adversely affect catalytic activity of DNA polymerase beta so that the variant may act as a dominant negative mutant. This would represent clinical significance if translated into a clinical setting because resistance to radiation or chemotherapy during the relapse of the disease could be potentially overcome by this approach.
Oguz, Arzu;Unal, Dilek;Tasdemir, Arzu;Karahan, Samet;Aykas, Fatma;Mutlu, Hasan;Cihan, Yasemin Benderli;Kanbay, Mehmet
Asian Pacific Journal of Cancer Prevention
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v.14
no.1
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pp.453-456
/
2013
Introduction: Lung cancer, the leading cause of cancer deaths, is divided into 2 main classes based on its biology, therapy and prognosis: non-small cell lung cancer (NSCLC) and small cell lung cancer (SCLC). Many cases are at an advanced stage at diagnosis, which is a major obstacle to improving outcomes. It is important to define the high risk group patients for early diagnosis and chance of cure. Blood group antigens are chemical components on erythrocyte membranes but they are also expressed on a variety of epithelial cells. Links between ABO blood groups with benign or malignant diseases, such as gastric and pancreas cancers, have been observed for a long time. In this study, we aimed to investigate any possible relationship between lung cancer histological subtypes and ABO-Rh blood groups. Materials and Methods: The files of 307 pathologically confirmed lung cancer patients were reviewed retrospectively. Cases with a serologically determined blood group and Rh factor were included and those with a history of another primary cancer were excluded, leaving a total of 221. The distribution of blood groups of the lung cancer patients were compared with the distribution of blood groups of healthy donors admitted to the Turkish Red Crescent Blood Service in our city in the year 2012. Results: There was no significant difference between patients with lung cancer of either type and the control group in terms of distribution of ABO blood groups and Rh factor (p: 0.073). There was also no relationship with non small cell cancer histological subtypes. Conclusions: In this study, we found no relationship between the ABO-Rhesus blood groups and NSCLC and SCLC groups. To our knowledge this is the first analysis of ABO blood groups in SCLC patients.
Poly-ADP-ribosylation (PAR) is a post-translational modification of mainly chromosomal proteins. It is known to be strongly involved in several molecular events, including nucleosome-remodelling and carcinogenesis. In this investigation, it was attempted to evaluate PAR level as a reliable biomarker for early detection of cancer in blood lymphocyte histones. PAR of isolated histone proteins was monitored in normal and dimethylnitrosamine (DMN)-exposed mice tissues using a novel ELISA-based immuno-probe assay developed in our laboratory. An inverse relationship was found between the level of PAR and period of DMN exposure in various histone proteins of blood lymphocytes and spleen cells. With the increase in the DMN exposure period, there was reduction in the PAR level of individual histones in both cases. It was also observed that the decrease in the level of PAR of histones resulted in progressive relaxation of genomic DNA, perhaps triggering activation of genes that are involved in initiation of transformation. The observed effect of carcinogen on the PAR of blood lymphocyte histones provided us with a handy tool for monitoring biochemical or physiological status of individuals exposed to carcinogens without obtaining biopsies of cancerous tissues, which involves several medical and ethical issues. Obtaining blood from any patient and separating blood lymphocytes are routine medical practices involving virtually no medical intervention, post-procedure medical care or trauma to a patient. Moreover, the immuno-probe assay is very simple, sensitive, reliable and cost-effective. Therefore, combined with the ease of preparation of blood lymphocytes and the simplicity of the technique, immuno-probe assay of PAR has the potential to be applied for mass screening of cancer. It appears to be a promising step in the ultimate goal of making cancer detection simple, sensitive and reliable in the near future.
Kim, Minjeong;Lim, Sangyong;Kim, Dongho;Choy, Hyon E.;Ryu, Sangryeol
Molecules and Cells
/
v.28
no.4
/
pp.389-395
/
2009
We previously observed that the transcription of some flagellar genes decreased in Salmonella Typhimurium tdcA mutant, which is a gene encoding the transcriptional activator of the tdc operon. Since flagella-mediated bacterial motility accelerates the invasion of Salmonella, we have examined the effect of tdcA mutation on the invasive ability as well as the flagellar biosynthesis in S. Typhimurium. A tdcA mutation caused defects in motility and formation of flagellin protein, FliC in S. Typhimurium. Invasion assays in the presence of a centrifugal force confirmed that the defect of flagellum synthesis decreases the ability of Salmonella to invade into cultured epithelial cells. In addition, we also found that the expression of Salmonella pathogenicity island 1 (SPI1) genes required for Salmonella invasion was down-regulated in the tdcA mutant because of the decreased expression of fliZ, a positive regulator of SPI1 transcriptional activator, hilA. Finally, the virulence of a S. Typhimurium tdcA mutant was attenuated compared to a wild type when administered orally. This study implies the role of tdcA in the invasion process of S. Typhimurium.
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