• Asian Pacific Journal of Cancer Prevention
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• v.15 no.20
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• pp.8793-8796
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• 2014

Objective: To explore the influence of serum vascular endothelial growth factor (VEGF) level on therapeutic outcome and diagnosis/prognostic value in patients with cervical cancer. Materials and Methods: A total of 37 patients diagnosed with cervical cancer by biopsy were selected and treated with concurrent chemoradiotherapy. Double-antibody sandwich enzyme-linked immunosorbent assay (ELISA) was adopted before treatment to assess VEGF levels, and its relationships with clinicopathological features and short-term therapeutic effects were analyzed. Results: The median VEGF level in 37 patients before treatment was 647.15 (393.35~1125.16) pg/mL. Serum VEGF levels in patients aged <50 years, in International Federation of Gynecology and Obstetrics (FIGO) stage IIIa~IVa, with lymph node metastasis and tumor size >4 cm were significantly increased (P<0.05). The complete remission (CR) rate was 48.7% (18/37), partial remission (PR) rate was 35.1% (13/37), stable disease (SD) rate was 13.5% (5/37) and progressive disease (PD) rate was 2.70% (1/37), so the objective remission rate (ORR) after treatment was 83.8% (31/37). Logistic regression analysis showed that tumor size and serum VEGF level before treatment were independent risk factors affecting the therapeutic outcome, and the higher the level of serum VEGF, the worse the prognosis when tumor size>4 cm. Some 56.8% of patients manifested with myelosuppression, 37.8% with leucopenia, 24.3% with thrombocytopenia, 5.41% with diarrhea, 46.0% with nausea and vomiting, 21.6% with hair loss and 8.11% with hepatic and renal injury during the treatment. Conclusions: Serum VEGF level may reflect the degree of malignancy of cervical cancer and predict therapeutic effect, which is of great importance to cancer diagnosis and prognosis.

• Korean Journal of Medicinal Crop Science
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• v.20 no.1
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• pp.27-35
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• 2012

This study was conducted to investigate changes in composition of ginsenosides and color of processed ginsengs prepared by different steaming-drying times. Processed ginsengs were prepared from white ginseng with skin by 9-time repeated steaming at $96^{\circ}C$ for 3 hours and followed by hot air-drying at $50^{\circ}C$ for 24 hours. As the times of steaming processes increased, lightness (L value) decreased and redness (a value) increased in color of ginseng powders. Crude saponin contents and ginsenosides compositions in processed ginsengs prepared by different steaming-drying times were investigated using the HPLC method, respecively. Crude saponin contents according to increasing steaming-drying times decreased in some degree. In the case of major ginsenosides, the contents of $Rb_1$, $Rb_2$, Rc, Rd, Rf, Re, $RG_1$, Re were decreased with increase in steamimg times, but those of $Rh_1$, $Rg_3$, $Rk_1$ were increased after especially 3 times of steaming processes. Interestingly, in black ginseng were prepared by 9 times steaming processes, the content of ginsenoside $Rg_3$ was 8.20 mg/g, approximately 18 times higher than that (0.46 mg/g) in red ginseng. In addition, the ratio of the protopanaxadiol group and protopanaxatiol group (PD/PT) were increased from 1.9 to 8.4 due to increasing times of steamming process.

• Hanyang Medical Reviews
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• v.33 no.1
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• pp.10-16
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• 2013

Follicular helper T cells (Tfh) play a significant role in providing T cell help to B cells during the germinal center reaction, where somatic hypermutation, affinity maturation, isotype class switching, and the differentiation of memory B cells and long-lived plasma cells occur. Antigen-specific T cells with IL-6 and IL-21 upregulate CXCR5, which is required for the migration of T cells into B cell follicles, where these T cells mature into Tfh. The surface markers including PD-1, ICOS, and CD40L play a significant role in providing T cell help to B cells. The upregulation of transcription factor Bcl-6 induces the expression of CXCR5, which is an important factor for Tfh differentiation, by inhibiting the expression of other lineage-specific transcription factors such as T-bet, GATA3, and RORγt. Surprisingly, recent evidence suggests that CD4 T cells already committed to Th1, Th2, and Th17 cells obtain flexibility in their differentiation programs by downregulating T-bet, GATA3, and RORγt, upregulating Bcl-6 and thus convert into Tfh. Limiting the numbers of Tfh within germinal centers is important in the regulation of the autoantibody production that is central to autoimmune diseases. Recently, it was revealed that the germinal center reaction and the size of the Tfh population are also regulated by thymus-derived follicular regulatory T cells (Tfr) expressing CXCR5 and Foxp3. Dysregulation of Tfh appears to be a pathogenic cause of autoimmune disease suggesting that tight regulation of Tfh and germinal center reaction by Tfr is essential for maintaining immune tolerance. Therefore, the balance between Tfh and Tfr appears to be a critical peripheral tolerance mechanism that can inhibit autoimmune disorders.

• Parasites, Hosts and Diseases
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• v.62 no.1
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• pp.30-41
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• 2024

The dense granule protein of Toxoplasma gondii, inhibitor of signal transducer and activator of transcription 1 (IST) is an inhibitor of signal transducer and activator of transcription 1 (STAT1) transcriptional activity that binds to STAT1 and regulates the expression of inflammatory molecules in host cells. A sterile inflammatory liver injury in pathological acute liver failures occurs when excessive innate immune function, such as the massive release of IFN-γ and TNF-α, is activated without infection. In relation to inflammatory liver injury, we hypothesized that Toxoplasma gondii inhibitor of STAT1 transcription (TgIST) can inhibit the inflammatory response induced by activating the STAT1/IRF-1 mechanism in liver inflammation. This study used IFN-γ and TNF-α as inflammatory inducers at the cellular level of murine hepatocytes (Hepa-1c1c7) to determine whether TgIST inhibits the STAT1/IRF-1 axis. In stable cells transfected with TgIST, STAT1 expression decreased with a decrease in interferon regulatory factor (IRF)-1 levels. Furthermore, STAT1 inhibition of TgIST resulted in lower levels of NF-κB and COX2, as well as significantly lower levels of class II transactivator (CIITA), iNOS, and chemokines (CLXCL9/10/11). TgIST also significantly reduced the expression of hepatocyte proapoptotic markers (Caspase3/8/9, P53, and BAX), which are linked to sterile inflammatory liver injury. TgIST also reduced the expression of adhesion (ICAM-1 and VCAM-1) and infiltration markers of programmed death-ligand 1 (PD-L1) induced by hepatocyte and tissue damage. TgIST restored the cell apoptosis induced by IFN-γ/TNF-α stimulation. These results suggest that TgIST can inhibit STAT1-mediated inflammatory and apoptotic responses in hepatocytes stimulated with proinflammatory cytokines.

• Clinical and Experimental Pediatrics
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• v.46 no.9
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• pp.883-888
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• 2003

Purpose : The etiology of hemolytic anemia can be classified as either cellular or extracellular defects of red blood cells. The aim of this study was to investigate the clinical and laboratory findings of hemolytic anemia concerning its etiological classification. Methods : Clinical and laboratory findings of the patients with hemolytic anemia treated from January 1987 to May 2002 at Severance Hospital were analyzed retrospectively. They were divided into two groups based on the types of red cell defects(group I : erythrocytic defect, group II : extraerythrocytic defect). Results : Twenty one cases were included in group I, thirty four cases in group II, and three cases were unclassified. In group I, nineteen cases(90.5%) were diagnosed as hereditary spherocytosis and were proved to have red cell membrane disorders while two cases(9.5%) were shown to have red cell enzyme deficiencies. In group II, thirteen cases(38.2%) were noted as autoimmune hemolytic anemia, eleven cases(32.4%) as traumatic or microangiopathic hemolytic anemia, four cases(11.8%) as drug induced hemolytic anemia, two cases(5.9%) were related with systemic lupus erythematosus and one case(2.9%) with malignancy. Hemoglobin at the time of diagnosis(7.5 g/dL vs. 6.2 g/dL, P<0.05) and the incidence of splenomegaly(85.7% vs. 18.2%, P<0.05) were higher in group I though blood urea nitrogen(9.0/0.4 mg/dL vs. 27.8/1.6 mg/dL, P<0.05) was higher in group II. Conclusion : Comparing the clinical features of pediatric hemolytic anemia, we concluded as following : In cases associated with extraerythrocytic defect, blood tests revealed significant initial lower hematocrit with higher level of BUN and Cr while cases with erythrocytic defect, splenomegaly were more common noted.

• Journal of Food Hygiene and Safety
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• v.35 no.4
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• pp.382-390
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• 2020

This study was carried out to evaluate the antimicrobial effect of red ginseng (Panax ginseng C.A. Meyer) against several foodborne pathogens including Staphylococcus aureus, Escherichia coli, Candida albicans and Aspergillus niger. The antimicrobial effect was determined by agar diffusion method using red ginseng extract, crude saponin and non-water-soluble fractions. Red ginseng extract showed antimicrobial effect against S. aureus, but not C. albicans or A. niger. The extract showed anti-bacterial activity at concentration above 30% against S. aureus, which cause both food poisoning and atophic dermatitis. Crude saponin showed antibacterial activity above 7.5% against the bacterium. However, the ginsenosides purified from crude saponin showed no antimicrobial activities at 100-200 ㎍/mL. To investigate the mode of growth inhibition, red ginseng extract and crude saponin were added to 0.85% NaCl solution containing S. aureus and then incubated at 35℃ for 12 h. The results showed that viable cells were rapidly reduced in above 10% concentration of red ginseng extract and above 2% of crude saponin, respectively. However, the crude saponin and red ginseng extract did not inhibit the bacterial cells completely at those same concentrations. On the other hand, whereas all non-water-soluble fractions showed inhibition zones above 10 mm against S. aureus, they showed no inhibition effects against E. coli, C. albicans or A. niger. The methanol fraction-1 (MF-1) showed the highest antibacterial activity against S. aureus, and the MIC (minimal inhibitory concentration) was 0.625 mg/mL. These results suggest that red ginseng extract, crude saponin and non-water-soluble fractions show selective antibacterial activity against S. aureus, and non-water-soluble fractions might be used as natural antibacterial agents.

• Economic and Environmental Geology
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• v.44 no.5
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• pp.373-386
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• 2011

Geochemical study was performed on black slates and interbedded U-bearing coaly slates in Deokpyeongri area, the representative uranium mineralized district of the Ogcheon Metamorphic Belt, to discuss the genetic environments of the uranium deposit. REE concentration (254 ppm) of the black slates is higher than that (169 ppm) of the coaly slates and NASC-normalized REE patterns of the coaly slates show remarkable positive Eu anomaly. l11e redox-sensitive trace elements such as V, Cr, Co, Ni, Mo and U in the coaly slates are highly enriched compared to the black slates, especially for V of 24 times, Mo of 62 times, and U of 60 times. In additions, Pd and Pt are also enriched in the coaly slates. Positive Eu anomaly and the noticeable enrichment of the elements listed above compared to those of NASC indicate that those elements were not derived from common seawater but deposited under high temperature and reducing environment of submarine hydrothermal activities. Wide compositional ranges of major elements ($SiO_2/Al_2O_3$: 3.98~11.88, $Al_2O_3/Na_2O$: 25.6~139.06, $K_2O/Na_2O$: 6.80~46.85) also suggest that the source rocks of the sediments are mixtures of sedimentary rocks and igneous rocks. Higher sulfur contents in the coaly slates, 2.6 wt.%, than those in the black slates, 0.6 wt.% also indicates that the former was influenced by hydrothermal activities containing much sulfur. These geochemical characteristics are similar to the genetic environments of South China type PGE deposits (Mo-Ni-Zn-PGE) which is geotectonically correlated with the Ogcheon Metamorphic Belt and is known as sedimentary-exhalative deposits. In conclusions, the uranium and other metallic elements mineralization seems to have occurred in the sedimentary basin that was affected by submarine hydrothermal activities and rich in organic materials under oxygen-poor environments as well.

• The Journal of Korean Academy of Prosthodontics
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• v.23 no.1
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• pp.39-59
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• 1985

The purpose of this study was to investigate how gap distances of 0.13mm, 0.15mm, 0.20mm, and 0.30mm affects solder joint strength from gold alloys and nickel-chromium base alloys and to examine the composition of solder gold, the solder joint of gold alloys and nickel-chromium base alloys. The tensile test specimens were prepared in the split stainless steel mold with a half dumbbell shape 2.5mm in diameter and l2mm in length. 6 pairs of specimens of each gap distance group of gold alloys and nickel-chromium base alloys were made and 48 pairs of all specimens were soldered with solder gold of 666 fineness. All soldered specimens were machined to a uniform diameter and then a tensile load was applied at a cross-head speed of 0.10mm/min using Instron Universal Testing Machine, Model 1115. The fractured specimens at solder gold of solder joint fracture with each gap distance of 0.13mm, 0.15mm, 0.20mm, and 0.30mm were examined under the Scanning Electron Microscope, JSM-35c and the composition of solder gold, the solder joint of gold alloys and nickel-chromium base alloys was analyzed by Electron Probe Micro Analyzer. The results of this study were obtained as follows: 1. In case of soldering of gold alloys, the tensile strength between gold alloys showed $37.33{\pm}2.52kg/mm^2$ at 0.13, $39.14{\pm}3.35kg/mm^2$ at 0.15mm, $43.76{\pm}2.97kg/mm^2$ at 0.20mm, and $49.18{\pm}4.60kg/mm^2$ at 0.30mm. There was statistically significant difference at each gap distance, and so the greater increase of gap distance showed the greater tensile strength. 2. In case of soldering of nickel-chromium base alloys, the tensile strength between nickel-chromium base alloys showed $34.84{\pm}4.26kg/mm^2$ at 0.13mm, $37.25{\pm}2.49kg/mm^2$ at 0.15mm, $42.91{\pm}4.32kg/mm^2$ at 0.20mm, and $46.93{\pm}4.21kg/mm^2$ at 0.30mm. There was not statistically significant difference only between 0.13mm and 0.15mm and bet ween 0.20 mm and 0.30mm, but generally the greater increase of gap distance showed the greater tensile strength. 3. The greater increase of gap distance shoed less porosities in solder gold at solder joint fracture. 4. In solder gold Au, Cu, Ag, Zn, and Sn were composed and Au and Cu were mostly distributed uniformly. 5. In solder joints of solder gold and gold alloys Au, Cu, Ag, Zn, and Sn were composed in solder gold and Au, Cu, Ag, Pt, and Pd were composed in gold alloys. Au and Cu of solder gold and gold alloys were mostly distributed uniformly and the diffusion of other elements except Pt and Pd around the solder joint was not almost found. In solder joints of solder gold and nickel-chromium base alloys Au, Cu, Ag, Zn, and Sn were composed in solder gold and Ni, Cr, and Al were composed in nickel-chromium base alloys. Au and Cu of solder gold and Ni and Cr of nickel-chromium base alloys were mostly distributed uniformly and the diffusion of other elements except Cr around the solder joint was not almost found.

• The Korean Journal of Nuclear Medicine
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• v.39 no.1
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• pp.9-14
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• 2005

Purpose: Abnormal myocardial perfusion may be caused by ventricular preexcitation, but its location, extent, severity and correlation with accessory pathway (AP) are not established. We evaluated perfusion patterns on myocardial perfusion SPECT and location of AP in patients with WPW (Wolff-Parkinson-White) syndrome. Materials and Methods: Adenosine Tc-99m MIBI or Tl-201 myocardial perfusion SPECT was performed in 11 patients with WPW syndrome. Perfusion defects (PD) were compared to AP location based on ECG with Fitzpatrick's algorithm or electrophysiologic study and radiofrequency catheter ablation. Results: Patients had atypical chest discomfort or no symptom. Risk of coronary artery disease (CAD) was below 0.1 in 11 patients using the nomogram to estimate the probability of CAD. Coronary angiography was performed in 4 patients (mid-LAD 50% in one, normal in others). In 4 patients, AP localization was done by electrophysiologic study and radiofrequency catheter ablation (RFCA). Small to large extent ($11.0{\pm}8.5%$, range:$3{\sim}35%$) and mild to moderate severity ($-71{\pm}42.7%$, range:$-2l7{\sim}-39%$) of reversible (n=9) or fixed (n=1) perfusion defects were noted. One patient with right free wall (right lateral) AP showed normal. PD locations were variable following the location of AP. One patient with left lateral wall AP was followed 6 weeks after RFCA and showed significantly decreased PD on SPECT with successful ablation. Conclusion: Myocardial perfusion defect showed variable extent, severity and location in patients with WPW syndrome. Abnormal perfusion defect showed in most of all patients, but it did not seem to be correlated specifically with location of accessory pathway and coronary artery disease. Therefore myocardial perfusion SPECT should be interpreted carefully in patients with WPW syndrome.

• The Korean Journal of Physiology and Pharmacology
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• v.20 no.1
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• pp.101-109
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• 2016

Reducing $[Mg^{2+}]_o$ to 0.1 mM can evoke repetitive $[Ca^{2+}]_i$ spikes and seizure activity, which induces neuronal cell death in a process called excitotoxicity. We examined the issue of whether cultured rat hippocampal neurons preconditioned by a brief exposure to 0.1 mM $[Mg^{2+}]_o$ are rendered resistant to excitotoxicity induced by a subsequent prolonged exposure and whether $Ca^{2+}$ spikes are involved in this process. Preconditioning by an exposure to 0.1 mM $[Mg^{2+}]_o$ for 5 min inhibited significantly subsequent 24 h exposure-induced cell death 24 h later (tolerance). Such tolerance was prevented by both the NMDA receptor antagonist D-AP5 and the L-type $Ca^{2+}$ channel antagonist nimodipine, which blocked 0.1 mM $[Mg^{2+}]_o$-induced $[Ca^{2+}]_i$ spikes. The AMPA receptor antagonist NBQX significantly inhibited both the tolerance and the $[Ca^{2+}]_i$ spikes. The intracellular $Ca^{2+}$ chelator BAPTA-AM significantly prevented the tolerance. The nonspecific PKC inhibitor staurosporin inhibited the tolerance without affecting the $[Ca^{2+}]_i$ spikes. While $G{\ddot{o}}6976$, a specific inhibitor of $PKC{\alpha}$ had no effect on the tolerance, both the $PKC{\varepsilon}$ translocation inhibitor and the $PKC{\zeta}$ pseudosubstrate inhibitor significantly inhibited the tolerance without affecting the $[Ca^{2+}]_i$ spikes. Furthermore, JAK-2 inhibitor AG490, MAPK kinase inhibitor PD98059, and CaMKII inhibitor KN-62 inhibited the tolerance, but PI-3 kinase inhibitor LY294,002 did not. The protein synthesis inhibitor cycloheximide significantly inhibited the tolerance. Collectively, these results suggest that low $[Mg^{2+}]_o$ preconditioning induced excitotoxic tolerance was directly or indirectly mediated through the $[Ca^{2+}]_i$ spike-induced activation of $PKC{\varepsilon}$ and $PKC{\xi}$, JAK-2, MAPK kinase, CaMKII and the de novo synthesis of proteins.