We report a 35-year old female patient with history of seizure and mass which was confirmed as a plasma cell granuloma, arising in the left parietal area. The mass appeared on magnetic resonance imaging as well circumscribed area of decreased signal that markedly enhanced with administration of the contrast. Pathologically, biopsy showed a mixed cellular population with considerable numbers of plasma cells along with eosinophils and lymphocytes and the tumors was characterized immunohistochemically by polyclonal population of lymphoid cells.
Purpose: This study was to find efficacy of integrin alpha2 (${\alpha}_2$) and epidermal growth factor receptor (EGFR) as tumor marker of oral squamous cell carcinoma (SCC) and clarify the selective cell death effect of anti-integrin ${\alpha}_2$ and anti-EGFR on SCC cells, additionally testify conjugated gold nanoparticles (GNP) with air plasma for selective cell death of oral SCC. Methods: Expression of integrin ${\alpha}_2$, EGFR on human SCC cells (SCC25) were examined by western blot. SCC25 cells were treated with anti-integrin ${\alpha}_2$, anti-EGFR and analysed by Hemacolor staining, immunoflorescence staining, FACS flow cytometry. Conjugated GNP with integrin ${\alpha}_2$, EGFR antibody were treated by air plasma on SCC cells. Results: Integrin ${\alpha}_2$ and EGFR were over-expressed on SCC25 cells than normal lung WI-38 cells. The cell viability rate of SCC25 cells treated with anti-integrin ${\alpha}_2$, anti-EGFR was lower than WI-38 cells. The concentration changes of nucleus, releasing cytochrome c and apoptosis inducing factor (AIF) from mitochondria to cytosol were observed. The changes of proteins related with apoptosis were observed. Increase of bax, bcl-xL, activation of caspase-3, -7, -9, and fragmentation of PARP, DFF45 and decrease of lamin A/C in SCC25 cells were observed. In FACS, increase of sub-$G_1$ and S phase was observed. Cell cycle related proteins, Such as cyclin D1, cyclin dependent kinase (CDK) 4, cyclin A, cyclin E, CDK 2, p27 were decreased. After SCC25 cells treated with conjugatged GNP-Integrin ${\alpha}_2$, GNP-EGFR, additionally air plasma, the cell death rate was significantly increased. Conclusion: Integrin ${\alpha}_2$, EGFR were over-expressed in oral SCC cells. Anti-integrin ${\alpha}_2$, anti-EGFR in SCC25 cells induced apoptosis selectively. When GNP-anti integrin ${\alpha}_2$, GNP-anti EGFR were treated with air plasma on SCC25 cells, cancer cells were died more selectively. GNP-anti integrin ${\alpha}_2$, GNP-anti EGFR with air plasma could be treatment choice of oral SCC.
The authors present the fine needle aspiration cytology (FNAC) cytologic findings of a case of extranodal marginal zone B cell lymphoma (MZBCL), which featured abundant plasma cells and eosinophilic histiocytes arising in both parotid glands. A 49-year-old female presented with palpable masses in both parotid glands. She had been suffering from systemic lupus erythematosus and rheumatoid arthritis. The lesions were evaluated by FNAC and smears showed a small number of clusters of oncocytic cells with abundant eosinophilic granular cytoplasm and small nuclei, intermixed with small to medium-sized lymphoid cells containing round to lobulated nuclei, which suggested Warthin's tumor. Some of lymphoid cells had a plasmacytoid appearance, and some scattered large cells contained a large amount of eosinophilic cytoplasm. Bilateral superficial parotidectomy was performed and a histopathologic study indicated MZBCL with abundant plasma cells, intermixed with eosinophilic histiocytes. The presence of oncocytic cells and a mixture of lymphoid and plasma cells indicates Warthin's tumor, but the cytologic features of a relatively monotonous small to medium-sized lymphoid infiltrate suggest the possibility of MZBCL in the clinical setting of an FNAC study performed on a patient suffering from a connective tissue disease.
Promoter hypermethylation of the runt-related transcription factor 3 (RUNX3) gene is associated with increased risk of hepatocellular carcinoma (HCC). Oxidative stress plays a vital role in both carcinogenesis and progression of HCC. However, whether oxidative stress and RUNX3 hypermethylation in HCC have a cause-and-effect relationship is not known. In this study, plasma protein carbonyl and total antioxidant capacity (TAC) in patients with hepatitis B virus (HBV)-associated HCC (n=60) and age-matched healthy subjects (n=80) was determined. RUNX3 methylation in peripheral blood mononuclear cells (PBMC) of subjects was measured by methylation-specific PCR. Effect of reactive oxygen species (ROS) on induction of RUNX3 hypermethylation in HCC cells was investigated. Plasma protein carbonyl content was significantly higher, whereas plasma TAC was significantly lower, in HCC patients than healthy controls. Based on logistic regression, increased plasma protein carbonyl and decreased plasma TAC were independently associated with increased risk for HCC. PBMC RUNX3 methylation in the patient group was significantly greater than in the healthy group. RUNX3 methylation in hydrogen peroxide ($H_2O_2$)-treated HepG2 cells was significantly higher than in untreated control cells. In conclusion, increase in oxidative stress in Thai patients with HBV-associated HCC was demonstrated. This oxidative increment was independently associated with an increased risk for HCC development. RUNX3 in PBMC was found to be hypermethylated in the HCC patients. In vitro, RUNX3 hypermethylation was experimentally induced by $H_2O_2$. Our findings suggest that oxidative stress is a cause of RUNX3 promoter hypermethylation in HCC cells.
Kumar, Naresh;Shaw, Priyanka;Attri, Pankaj;Uhm, Han Sup;Choi, Eun Ha
Proceedings of the Korean Vacuum Society Conference
/
2015.08a
/
pp.158-158
/
2015
Myoblast are myogenic precursors that proliferate, activate, and differentiate on muscle injury to sustain the regenerative capacity of skeletal muscle; The neuronal isoform of nitric oxide synthase (nNOS, termed also NOS-I) is expressed in normal adult skeletal muscle, suggesting important functions for Nitric oxide (NO) in muscle biology1,2,3. However, the expression and subcellular localization of NO in muscle development and myoblast differentiation are largely unknown. In this study, we examined effects of the nitric oxide generated by a microwave plasma torch, on proliferation/differentiation of rat myoblastic L6 cells. Experimental data pertaining to nitric oxide production are presented in terms of the oxygen input in units of cubic centimetres per minute. The various levels of nitric oxide are observed depending on the flow rate of nitrogen gas, the ratio of oxygen gas, and the microwave power4. In order to evaluate the potential of nitric oxide as an activator of cell differentiation, we applied nitric oxide generated from the microwave plasma torch to L6 skeletal muscles. Differentiation of L6 cells into myotubes was significantly enhanced the differentiation after nitric oxide treatment. Nitric oxide treatment also increase the expression of myogenesis marker proteins and mRNA level, such as myogenin and myosin heavy chain (MHC), as well as cyclic guanosine monophosphate (cGMP), However during the myotube differentiation we found that NO activate oxidative stress signaling erks expression. Therefore, these results establish a role of NO and cGMP in regulating myoblast differentiation and elucidate their mechanism of action, providing a direct link with oxidative stress signalling, which is a key player in myogenesis. Based on these findings, nitric oxide generated by plasma can be used as a possible activator of cell differentiation and tissue regeneration.
This study investigated the effects of vitamin C supplementation on immune status in smoking and nonsmoking male college students. Blood samples were obtained from 15 healthy smoking and from 15 healthy nonsmoking volunteers before and 4 weeks after vitamin C supplementation (1000mg/day). Daily nutrient intakes was also calculated. Plasma vitamin C, E, and A concentrations, white blood cells and subpopulations, lymphocytes and subpopulations, NK cell percentage,plasma immunoglobulin A, G, M and complement C3, plasma interleukin-2 , and prostagladin E2 were measured . Daily vitamin C consumption was lower in smokers than in nonsmokers. Vitamin C supplementation significantly increased plasma vitamin C in smokers, and increased NK cell percentage in smokers and nonsmokers. Plasma IL-2 concentrations were significantly increased by vitamin C supplementation in nonsmokers, and decreased helpe $r^pressor T cell ratio were decreased by vitamin C supplementatiion , but the differences were not significant. White blood cells and subpopulation percentage and plasma prostaglandin E2 concentration were not affected by smoking and vitamin C supplementation. These findings as nonsmokers.rs.
In order to investigate whether phospholipase C (PLC) activity in oat celIs is regulated by Gprotein, we have characterized PLC in plasma membranes of oat tissues. To identify the purified plasma membrane, $K^+$-stimulated, $Mg^{2+}$-dependent ATPase activity was measured. The activity of ATPase was shown to be proportional to the concentration of membrane protein. To examine the PLC activity regulated by G-protein, we used the inside-out and outside-out plasma membrane mixture isolated from the oat cells. The plasma membrane mixture showed higher PLC activity than the one of the outside-out plasma membrane. This suggests that PLC activity is located at the cytoplasmic surface of plasma membrane. PLC activity in plasma membrane mixture was dependent on $Ca^{2+}$ with maximum activity at 100 ${\mu}m$$Ca^{2+}$ and it was inhibited by 1 mM EGTA. Using Sep-pak $Accell^{TM}$ Plus QMA chromatography, we found that inositol 1,4,5-trisphosphate ($IP_3$) was produced in the presence of 10 ${\mu}m$$Ca^{2+}$. The PLC activity in the membrane was enhanced by an activator of G-protein ($GTP{\gamma}S$) and not by an inhibitor ($GDP{\beta}S$). This indicates that a G-protein is involved in the activation of PLC in the plasma membrane of oat cells.
The purpose of this study was to investigate the characteristic features of the cells and tissues of the chronic periapical lesions using light microscope and electron microscope. Fifteen dental periapical lesions were obtained from the patients undergoing periapical surgery. Each specimen was divided into two parts along the tooth axis. One part was routinely processed for histopathologic examinations. 12 periapical lesions were diagnosed as granuloma and 3 periapical specimens as periapical cyst. The other part was fixed in 2.5% glutaraldehyde in 0.1M sodium cacodylate buffer at pH 7.4 and 1% osmic acid in same buffer. They were embedded in Epon 812. The semithin sections were used for the orientation of the lesions and the ultrathin sections were stained conventionally and examined with AEI Corynth 500 electron microscope. The results were as follows. 1. PMN and macrophages, which were dominant cell type, were scattered in small or large numbers throughout the central destructive area of granuloma. In the granulomatous area, plasma cells and lymphoytes were found in significant number and a lot of new capillary formation were revealed. Clefts caused by cholesterol were often seen in the connective tissue. Occasionally foam cells became collected in groups and epithelial proliferation were present. 2. In both granuloma and cyst, some plasma cells contained narrow cisternae of granular endoplasmic reticulum of which was tightly packed with electron dense materials, and other cells exhibited dilated profiles of granular endoplasmic reticulum. 3. In the area where plasma cells and lymphocytes were collected in groups, lymphocytes with well developed nucleolus and profuse cytoplasm were found and differentiating plasma cells were also present. 4. In the epithelial strands of the granulomatous area, epithelial cells contained enlarged endoplasmic reticulum, tonofilaments and ribosoms. Toward the intercellular space epithelial cells protruded a few microvilli. In the intercellular space, exudate-like electron dense materials, most of which was attached to the plasma membrane, appeared. 5. Some foam cells filled with numerous lipid droplets and others had lipid droplets and crystal-like structures. 6. Cyst epithelium consisted of bright cells and dark cells. The former had bright cytoplasm and small amounts of ribosoms, and the latter dark cytoplasm, many ribosoms, mitochondria and elongated microvilli. 7. Epithelial cells near the cyst lumen protruded a lot of long microvilli toward intercellular space and cyst lumen.
Folate, a precursor of the coenzyme tetrahydrofolate, plays an important role in DNA replication and cell proliferation, and thus could influence rapidly proliferating immune cells such as leukocytes and splenocytes. The effects of dietary folate on folate concentrations of plasma, thymus, spleen and leukocytes were investigated in rats. The animals were raised for 6 weeks on semipurifed experimental diets containing 0mg, 2mg, 4mg, 8mg folate/kg diet. Folate concentrations were determined microbiologically using Lactobacillus casei(ATCC 7469), and DNA strand breaks produced by alkaline treatment were analyzed fluorometrically. When compared to folate adequate diet, the folate deficient diet(0mg folate/kg diet) resulted in lowest folate levels in plasma, thymus, spleen and leukocytes, and the highest DNA strand breaks in spleen cells and leukocytes. Dietary folate levels significantly increased folate concentrations of immune tissues, leukocytes, and the plasma in a dose dependent manner, folate concentrations being highest with a diet providing 8mg folate/kg diet. The percentages of the double strand DNA remaining in the splenocytes and leukocytes after alkaline treatment were significantly increased with higher amounts of dietary folate in a dose dependent manner. Folate intakes of 8mg than 4mg/kg diet was found to be more effective in the prevention of DNA strand breaks. The results of this study suggest that increased folate above the requirement level could improve DNA stabilities in immune cells.
In this experiment, we have investigated that the transported space charge between sub-pixels in AC-plasma cell discharge. The test pulse 30 V, $5{\mu}s$ was applied to the address electrodes of neighbor cells of discharge occurred cells. And we have measured the transported space charge between sub-pixels in accordance with the various last sustain pulse widths t(time gap between the rising edges of sustain and test pulses) of 0.2 to $3{\mu}s$. It was observed that the peak value of transported space charge has been shown to be 21.5pC at $1.0{\mu}s$. And the IR peak value have been occured after $0.51{\mu}s$ with respect to sustain voltage.
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