Ha, Tae-Jin;Kim, Yeong-Mi;Ryu, Je-Ha;Woo, Woon-Tack
Journal of the Institute of Electronics Engineers of Korea CI
/
v.44
no.2
s.314
/
pp.37-46
/
2007
In this paper, we propose technologies for enhancing the immersive realization of virtual objects in AR-based product design. Generally, multimodal senses such as visual/auditory/tactile feedback are well known as a method for enhancing the immersion in case of interaction with virtual objects. By adapting tangible objects we can provide touch sensation to users. A 3D model of the same scale overlays the whole area of the tangible object so the marker area is invisible. This contributes to enhancing immersion. Also, the hand occlusion problem when the virtual objects overlay the user's hands is partially solved, providing more immersive and natural images to users. Finally, multimodal feedback also creates better immersion. In our work, both vibrotactile feedback through page motors, pneumatic tactile feedback, and sound feedback are considered. In our scenario, a game-phone model is selected, by way of proposed augmented vibrotactile feedback, hands occlusion-reduced visual effects and sound feedback are provided to users. These proposed methodologies will contribute to a better immersive realization of the conventional AR system.
This study was carried out to investigate the difference and genetic similarity at the level of molecular genetics. Genomic DNA was extracted from blood of Holstein, Korean cattle, Charolais, and hybrid between Korean cattle and charolais and RAPD(random amplified polymorphic DNAs) was analyzed by PCR(polymerase chain reaction). After genetic similarity value from different breeds are analyzed, genetic similarity was estimated by UPGMA(unweighted pair-group method using average). The results obtained from this study can be summarized as follows: 1. When genomic DNA which was extracted from different breeds was subjected to electrophoresis on 1.5% agarose gel, bigger than 12.2kb was appeared. Ratio by absorbance of $A_{260}/A_{280}$ was 1.75~2.10, indicating that genomic DNA was quite pure for RAPD analysis. 2. Different band patterns by RAPD were appeared according to the breeds in cattle. The best primer used to distinguish Holstein from other breeds was 5'-GAC CGC TTG T-3'. 3. A 340bp fragment was amplified in $33.0^{\circ}C$ of annealing temperature for the Holstein and Charolais breeds, but any amplification was not occurred in this annealing temperature for Korean cattle and hybrid. In addition, a 340bp fragment was amplified in $37.5^{\circ}C$ of annealing temperature for the Holstein and Korean cattle, but any amplification was not occurred in this annealing temperature for Charolais and hybrid. For the reaction of PCR. $37.5^{\circ}C$ and $33.0^{\circ}C$ of annealing temperature was shown to be best for genetic marker identification from Holstein, Charolais, and hybrid between Korean cattle and Charolais. 4. When genetic similarity from different breeds are analyzed at the both temperature of $33.0^{\circ}C$ and $37.5^{\circ}C$, the genetic similarity value of Holstein and Korean cattle, Holstein and Charolais, Korean cattle and Charolais, and Korean cattle and hybrid were 0.666~0.777, 0.615~0.666, 0.400~0.461 and 0.857~0.888, respectively. 5. It could be concluded that different breeds are capable of distinguishing by RAPD used random primer 5'-GAC CGC TTG T-3', genetic similarity from different breeds was appeared the higher genetic similarity value of Korean cattle and Charolais than that of Holstein between Korean cattle and Charolais by UPGMA.
Park, Kye-Young;Yoo, Chul-Gyu;Kim, Young-Whan;Han, Sung-Koo;Shim, Young-Soo;Hyun, In-Gyu
Tuberculosis and Respiratory Diseases
/
v.42
no.4
/
pp.522-534
/
1995
Background: In the pathogenesis of acute lung injury induced by lipopolysaccharide(LPS), oxygen radiclls are known to be involved in one part. Superoxide dismutase(SOD) protects oxygen radical-induced tissue damage by dismutating superoxide to hydrogen peroxide. In eukaryotic cells, two forms of SOD exist intracellularly as a cytosolic, dimeric copper/zinc-containing SOD(CuZnSOD) and a mitochondrial, tetrameric manganese-containing SOD(MnSOD). But there has been little information about SOD gene expression and its regulation in pulmonary alveolar macrophages(PAMs). The objective of this study is to evaluate the SOD gene expression induced by LPS and its regulation in PAMs of rat. Method: In Sprague-Dawley rats, PAMs obtained by broncholaveolar lavage were purified by adherence to plastic plate. To study the effect of LPS on the SOD gene expression of PAMs, they were stimulated with different doses of LPS($0.01{\mu}g/ml{\sim}10{\mu}g/ml$) and for different intervals(0, 2, 4, 8, 24hrs). Also for evaluating the level of SOD gene regulation actinomycin D(AD) or cycloheximide(CHX) were added respectively. To assess whether LPS altered SOD mRNA stability, the rate of mRNA decay was determined in control group and LPS-treated group. Total cellular RNA extraction by guanidinium thiocyanate/phenolfchlorofonn method and Northern blot analysis by using a $^{32}P$-labelled rat MnSOD and CuZnSOD cDNAs were performed. Results: The expression of mRNA in MnSOD increased dose-dependently, but not in CuZnSOD. MnSOD mRNA expression peaked at 8 hours after LPS treatment. Upregulation of MnSOD mRNA expression induced by LPS was suppressed by adding AD or CHX respectively. MnSOD mRNA stability was not altered by LPS. Conclusion: These findings show that PAMs of rat could be an important source of SOD in response to LPS, and suggest that their MnSOD mRNA expression may be regulated transcriptionally and require de novo protein synthesis without affecting mRNA stability.
Background: Tissue-type plasminogen activator is a physiologic activator, which has high affinity for fibrin and is activated by fibrin. Because of these properties, t-PA has the potential to induce effective thrombolysis without producing a systemic lytic state. In practice, however, therapeutically efficacious doses of t-PA has been associated with the development of a systemic lytic state. As experience with t-PA has accumulated, it has suggested that the fibrin selectivity is influenced by the dose and duration of t-PA infusion, and many studies have performed in an attempt to optimize the duration of t-PA regimen. Methods: This study was designed to assess the thrombolytic efficacy of t-PA and the differences of two dosing regimens of t-PA (infusion of 1 mg/kg t-PA over 15 or 180 minutes) in a canine model of pulmonary embolism, induced by injection of radioactive autologous blood clots. By continuously counting over both lung fields with a external gamma counter, we correlated rate and extent of pulmonary thrombolysis with corresponding pulmonary hemodynamics in addition to the gas analyses of arterial and mixed venous blood. Results: 1) While total clot lysis was similar ($36.2{\pm}3.3%$ and $39.6{\pm}2.3%$ respectively, p>0.05) when t-PA was infused over 15 or 180 minutes, the rate of lysis during infusion was markedly increased with the shorter infusion ($81.4{\pm}16.8%/hr$ vs $37.3{\pm}2.4%/hr$, p<0.05). 2) The duration of thrombolysis was $63.3{\pm}22.2$ minutes although t-PA was administered over 15 minutes, and it was only $148.5{\pm}14.0$ minutes in case of the infusion over 180 minutes (p<0.05). 3) The increased rate of thrombolysis with the shorter infusion was accompanied by a faster amelioration of cardiopulmonary impairment from pulmonary embolism (p<0.05). Conclusion: It is concluded that the shorter (15 minutes) infusion of t-PA is superior to the longer (180 minutes) infusion when the dose is equal, in consideration of the faster improvement in cardiopulmonary impairment from pulmonary embolism.
Background: When we define the pressure of pulmonary vasculature in which a recruitment of blood flow occurs as $P_I$ and the proportion of change in pulmonary artery to that in cardiac output as IR and then we compare PI and IR with pulmonary vascular resistance, we would find some problems in pulmonary vascular resistance. In other words, it is the theory that, IR should be increased mainly in pulmonary embolism in which decreases the cross sectional area of pulmonary vasculature. But there are many contradictory reports resulted from various researches and the fact is known widely that any difference exists between PVR and PI, IR. For this reason, the purpose of this study is to observe how PI and IR change at the time of the outbreak and during treatment of the pulmonary embolism, and to find out the meaning of these new indicators and the difference from the pulmonary vascular resistance used generally when we subdivide the pulmonary vascular resistance into PI and IR. Method: After making AV fistula in experimental dog, we controlled cardiac output at the intervals of 15 minute in case of three kinds(all AV fistula are obstructed, only one of fistula is open and all of fistula is open), and after evoking massive pulmonary embolism with radioactive autologous blood clots, we measured the mean pulmonary artery pressure, and calculated PI and IR. We observed the pattern of change in PI and IR, without giving the control group any specific treatment and with injecting intravenously rtPA in the Group 1 and Group 2 at the dose of 1mg per kg, for 15 minutes fot the former and 3 hours for the latter. Result: 1) Pulmonary vascular resistance showed a change similar to that of pulmonary artery pressure and in all three group, PVR increased significantly, but group 1 and group 2 showed tendency that PVR keeps on decreasing after treatment, and the rate of decrease in group 1 is more rapid than group 2 significantly. 2) Both intersection(PI) and degree(IR) are proved statistically significant, in view of the straight line relationship between cardiac output and pulmonary artery pressure, calculated by minimal regression method. 3) PI changed similarly to pulmonary vascular resistance, while in the IR which is theoretically more similar to PVR, there was no significant difference or change after rtPA infusion. Conclusion: In the pulmonary embolism, Both change in IR which means real resistance of pulmonary vasculature and PI which was developed due to secondary vasoconstriction by pulmonary embolism are reflected same time.
Background: Neuron specific enolase (NSE) is a neuronal form of the glycolytic enzyme enolase which was first found in extracts of brain tissue, and later in a variety of APUD cells and neurons of the diffuse endocrine system. SCLC shares many APUD properties with normal neuroendocrine cells. NSE immunostaining and serum NSE measurement may be a useful marker of neuroendocrine differentiation in lung tumors and diagnosis of small cell carcinoma. Methods: NSE immunohistochemical staining was done and at the same time serum NSE levels were measured in 22 small cell lung cancer and 21 non small cell lung cancer which were confirmed histologically. Results: 1) NSE immunoreactivity was detected in 9 of the 18 (50%) small cell lung cancer, in 5 of the 16 non small cell lung cancer. 2) Whereas the mean value in non-small cell lung cancer group was $11.79{\pm}4.47\;ng/ml$, the mean level of serum NSE in small cell lung cancer increased up to $59.3{\pm}77.8\;ng/ml$. In small cell lung cancer patients, mean value of limited disease group was $20.19{\pm}12.91\;ng/ml$, while mean value of extended disease group was $91.9{\pm}94.2\;ng/ml$ showing statistically significant difference. If serum levels above 20 ng/ml were tentatively defined as positive, 16 of 22 (73%) patients with SCLC had positive serum NSE level, but only one patient with NSCLC did. There was no correlation between serum NSE level and immunoreactivity of NSE. Conclusion: These studies indicate that serum NSE measurement may be a useful marker for the diagnosis and disease extent and NSE immunostaining can be used to demonstrate the neuroendocrine components of lung tumor.
Background : Several studies have suggested that impaired mucociliary clearance plays a role in the pathophysiology of bronchial asthma. Cough productive of mucoid sputum is common, and mucous plugs in the airways are frequently observed. These clinical features are in keeping with the histologic lesions of asthma, which involve primarily the epithelial and mucous-producing structures of the conducting airways. Some studies have shown that the mucociliary clearance is impaired in adult asthma, but it has not been studied in childhood asthma. The objectives of this study were to examine whether the mucociliary clearance is impaired in childhood asthma and to estimate the degree of impairment in comparison with that of immotile cilia syndrome. Method : Thirteen children with mild stable asthma and eight patients with immotile cilia syndrome completed this study. Ten healthy children were recruited as a normal control group. The whole-lung mucociliary clearance was measured by the radioaerosol technique. Aerosols, tin colloid particles tagged with the radionuclide technetium-99m($^{99m}Tc$), were generated by means of nebulizer, and inhaled via a mouthpiece. The retention of radioactivity was measured at 30, 60, 90 and 120 minutes by gamma camera, and mucociliary clearance was calculated as percent retention at each time. Results: 1) In each subject, the percent retention decreased variably with the lapse of time. 2) The percent retention of radionuclide decreased at each time in order of normal control, bronchial asthma and immotile cilia syndrome and the percent retention of immotile cilia syndrome was significantly higher than that of normal control at each time(p<0.05). 3) At two hours, the percent retention of bronchial asthma($65.0{\pm}1.8$(SE)%) was significantly higher than that of the normal control($54.4{\pm}3.5%$, p<0.05), and significantly lower than that of immotile cilia syndrome($73.3{\pm}1.4%$, p<0.01). 4) When the percent retention was analyzed according to $PC_{20}$ in the children with bronchial asthma, they had no relationship with each other. Conclusion: Mucociliary clearance in the children with bronchial asthma was significantly lower than normal control. This finding indicates that impaired mucociliary clearance operates in childhood asthma as well, and suggests that it may be one contributing factor in the pathogenesis of asthma. The degree of impairment, however, was not so severe as immotile cilia syndrome.
Kim, Hyun-Jung;Kim, Seong-Keun;Shim, Tae-Sun;Park, Yong-Doo;Park, Mi-Sun
Tuberculosis and Respiratory Diseases
/
v.50
no.1
/
pp.29-41
/
2001
Background : The appearance of multiple-drug-resistant Mycobacterium tuberculosis strains has been seriously compromising successful control of tuberculosis. Rifampin-resistance, caused by mutations in the rpoB gene, can be indicative of multiple-drug-resistance, and its detection is of great importance. The present study aimed to develop an oligonucleotide chip for accurate and convenient screening of drug-resistance. Methods : In order to detect point mutations in the rpoB gene, an oligonucleotide chip was prepared by immobilizing specific probe DNA to a microscopic slide glass by a chemical reaction. The probe DNA that was selected from the 81 bp core region of the rpoB gene was designed to have mutation sites at the center. A total of 17 mutant probes related to rifampin-resistance including 8 rifabutin-sensitive mutant probes were used in this study. For accurate determination, wild type probes were prepared for each mutation position with an equal length, which enabled a direct comparison of the hybridization intensities between the mutant and wild type. Results : Mycobacterial genomic DNA from clinical samples was tested with the oligonucleotide chip and the results were compared with those of the drug-susceptibility test in addition to sequencing and INNO-LiPA Rif. TB kit test in some cases. Out of 15 samples, the oligonucleotide chip results of 13 samples showed good agreement with the rifabutin-sensitivity results. The two samples with conflicting result also showed a discrepancy between the other tests, suggesting such possibilities as existence of mixed strains and difference in drug-sensitivity. Further verification of these samples in addition to more case studies are required before the final evaluation of the oligonucleotide chip can be made. Conlcusion : An oligonucleotide chip was developed for the detection of rpoB gene mutations related to drugsusceptibility. The results to date show the potential for using the oligonucleotide chip for accurate and convenient screening of drug-resistance to provide useful information in antituberculosis drug therapy.
Objective: This study was performed to clarify the role of HomeoboxA (HOXA) and its related signaling molecules in the decidualization of primary cultured endometrial cells. Methods: Human endometrial tissues were obtained by curettage of hysterectomy specimens from patients with conditions other than endometrial diseases. Tissues were minced and digested with Trypsin-EDTA for 20 min, $37^{\circ}C$. Cells were cultured with DMEM/F12 medium in $37^{\circ}C$, 5% $CO_2$ incubator for 24 hrs. Cells were treated with HOXA10 siRNA and added transforming growth factor (TGF)-${\beta}1$ (10 ng/mL) for 48 hrs to induces decidualization in vitro. Reverse transcription polymerase chain reaction analysis was accomplished to observe the expression of HOXA10, prolactin, cyclooxygenase (COX)-2, peroxisome proliferatoractivated receptor (PPAR)-$\gamma$, and wingless-type MMTV integration site family (Wnt). Results: HOXA10 expression was increased (1.8 fold vs. non-treated control) in TGF-${\beta}1$ treated cells. Decidualization marker, prolactin, was significantly increased in TGF-${\beta}1$ treated cells compared with HOXA10 siRNA treated cells. Endometrial cell differentiation marker, COX-2 was down-regulated by HOXA10 siRNA even if cells were treated with TGF-${\beta}1$. Wnt4 was down-regulated by treated with HOXA10 siRNA, this expression patters was not changed by TGF-${\beta}1$. Expression of PPAR-$\gamma$ was down regulated by TGF-${\beta}1$ in regardless of HOXA10 siRNA treatment. Conclusion: TGF-${\beta}1$ which is induced by progesterone in endometrial epithelial cells may induces stromal cell decidualization via HOXA10 and Wnt signaling cascade.
Objective: To evaluate whether T helper 1 (Th1) immune response is predominant in women with reproductive failures (recurrent spontaneous abortion and recurrent implantation failure) and the activation of T cell is related to Th1 propensity. Methods: Women with a history of recurrent implantation failure or recurrent spontaneous abortion comprise the study group (n=37). Controls are normal fertile women without a history of infertility or pregnancy losses (n=11). Th1/Th2 ratios of interferon (INF)-$\gamma$/interleukin (IL)-10 and tumor necrosis factor (TNF)-$\alpha$/IL-10 expression on $CD3^+/4^+$ cells, CD154, and CD69 expression on T cells are measured by flow cytometric analysis. Results: The ratios of TNF-$\alpha$ to IL-10 expressing on $CD3^+/4^+$ cells (Th1/Th2 cell ratios) are significantly higher in study group ($42.1{\pm}2.3$) as compared with that of controls ($28.7{\pm}2.7$) (p=0.002). The overall trend of CD154 and CD69 expression on T cells are elevated in study group than those of controls. The proportion (%) of $CD3^+/4^+/154^+$ cells ($1.7{\pm}0.5$ vs. $0.3{\pm}0.2$, p=0.038) and the % of $CD3^+/8^+/154^+$ cells ($0.6{\pm}0.2$ vs. $0.1{\pm}0.0$, p=0.024) are significantly higher in study group. The % of $CD3^+/69^+$ cells ($5.6{\pm}1.9$ vs. $1.3{\pm}5.4$, p=0.046) and % of $CD3^+/8^+/69^+$ cells ($4.8{\pm}1.3$ vs. $1.8{\pm}0.2$, p=0.035) among $CD3^+/8^+$ cells are significantly increased in study group. Conclusion: Women with reproductive failures have Th1 propensity with increased T cell activation. These finding means that activated T cell has a harmful effect on early pregnancy and implantation by induction of Th1 immunity.
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