• The Korean Journal of Pain
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• v.19 no.1
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• pp.96-100
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• 2006

Pain control is very important in managing terminal cancer patients and there are several modalities to alleviate their pain. A high dosage of epidural morphine is effective to control terminal cancer pain. Furthermore, to decrease the amount of morphine, adding an alternative adjuvant like ketamine to the morphine regimen is considered helpful for controlling the pain of a terminal cancer patient. A 45 year old male patient with terminal lung cancer had neck pain that was caused by multiple bone metastases. Continuous epidural block was started with 2 mg/day of morphine and the dosage was gradually increased to 90 mg/day in 86 days. 30 mg/day of ketamine was then added to it. Overall, the morphine and ketamine dosages were increased to 564 mg/day and 140 mg/day, respectively, in 11 months until the patient expired. In this case, the high dosage of epidural morphine, 580 mg/day, was administered to control cancer pain without any severe adverse effects.

• Clinical and Experimental Pediatrics
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• v.52 no.9
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• pp.1044-1047
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• 2009

A 13-year-old girl with psoriasis of the elbow, trunk, and face suddenly developed a severe headache followed by left hemiparesis and facial palsy. Brain magnetic resonance imaging showed an acute infarction of the right temporofrontal lobe and basal ganglia on the T2- and diffusion-weighted images. Cerebral angiography showed pre-occlusive irregular scalloped stenosis (99%) in the proximal M1 segment of the right middle cerebral artery and a web-like stenosis at the supraclinoid portion of the right internal carotid artery (ICA) suggestive of a spontaneous intracranial ICA dissection. The patient was administered a low dose of dipyridamole, and a rehabilitation program was initiated. Headache, left motor weakness, and facial droop improved within a week. However, mild left facial palsy and reduced fine motor function of the left hand were still present after 3 weeks. We report a rare case of spontaneous intracranial ICA dissection in a child with psoriasis.

• Journal of Yeungnam Medical Science
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• v.5 no.1
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• pp.153-158
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• 1988

Stomach cancer is the most popular tumor in Korea but the prognosis following extensive surgery and chemotherapy has not improved for many years. Conventional external radiotherapy also has some limitation, namely, a cancerocidal dose can not be delivered to tumors because of low radiation tolerance of adjacent critical sensitive organs. In order to overcome these limitations of curative surgery and external radiotherapy, intraoperative radiotherapy was proposed in many centers and the results were excellent. We treated two cases of locally advanced gastric cancers with IORT by using NEC 18 MeV Linear Accelerator after standard subtotal resection of the stomach. After treatment, the patients are in good conditions so far, but in order to evaluate the effectiveness of IORT, a study will be performed on the survival rates between patients treated by IORT and those treated by surgery alone.

• Journal of Microbiology and Biotechnology
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• v.28 no.9
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• pp.1554-1562
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• 2018

The type I interferons (IFNs) play a vital role in activation of innate immunity in response to viral infection. Accordingly, viruses have evolved to employ various survival strategies to evade innate immune responses induced by type I IFNs. For example, hepatitis E virus (HEV) encoded papain-like cysteine protease (PCP) has been shown to inhibit IFN activation signaling by suppressing K63-linked de-ubiquitination of retinoic acid-inducible gene I (RIG-I) and TANK-binding kinase 1 (TBK1), thus effectively inhibiting down-stream activation of IFN signaling. In the present study, we demonstrated that HEV inhibits polyinosinic-polycytidylic acid (poly(I:C))-induced $IFN-{\beta}$ transcriptional induction. Moreover, by using reporter assay with individual HEV-encoded gene, we showed that HEV methyltransferase (MeT), a non-structural protein, significantly decreases RIG-I-induced $IFN-{\beta}$ induction and $NF-{\kappa}B$ signaling activities in a dose-dependent manner. Taken together, we report here that MeT, along with PCP, is responsible for the inhibition of RIG-I-induced activation of type I IFNs, expanding the list of HEV-encoded antagonists of the host innate immunity.

• Journal of Pharmaceutical Investigation
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• v.32 no.3
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• pp.209-213
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• 2002

Diltiazem inhibits calcium channels and Iεads to vascular smooth muscle rεlaxation and negative inotropic and chronotropic effects in the hεart. Diltiazem is almost completely absorbεd after oral administration, but its extent of absolute oral bioavailability is reduced because of considerable first-pass hepatic metabolism. Diltiazem is able to dilate renal vasculature and can increase the glomerular filtration rate and renal sodium excretion. The purpose of this study was to report the pharmacokinetic changes of diltiazem after oral administration of diltiazem, 20 mg/kg, in rabbits coadministered with cimetidine, 20 mg/kg and pretreated twice per day for 3 days at cimetidine dose of 20 mg/kg. The area under the plasma concentration-time curve (AUC) of diltiazem was significantly higher in rabbits pretreated with cimetidine than that in control rabbits (p<0.01), showing about 149% increased relative bioavailability. The peak plasma concentration $(C_{max})$ and elimination half-life of diltiazem were increased significantly (p<0.05) in rabbits pretreated with cimetidine compared with those in control rabbits. This findings could be due to significant reduction of elimination rate constant by pretreated with cimetidine. The effects of cimetidine on the pharmacokinetics of oral diltiazem were more considerable in rabbits pretreated with cimetidine compared with those in control rabbits. The results suggest that the dosage of diltiazem should be adjusted when the drug would be co-administerεd chronically with cimetidine in a clinical situation.

• The Korean Journal of Pharmacology
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• v.22 no.1 s.38
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• pp.51-59
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• 1986

The effect of metabolic substrate fructose on the force of contraction of isolated rat atria depressed with lidocaine was determined. Fructose produced dose-dependent increase in the force of contraction of isolated atria depressed by substrate-free Krebs-Ringer bicarbonate medium. The maximally effective concentration of fructose was 30 mM. The isolated atria, suspended in Krebs-Ringer bicarbonate glucose medium aerated with 95% $O_2-5%CO_2$at $30^{\circ}C$ and pH 7.4, were depressed 50% by approximately 2.34 mg/100 ml of lidocaine. Addition of 30 mM fructose to these depressed atria resulted in a marked increase in the contractile force similar to that with pyruvate and acetate. Fructose had no significant effect, however, on atria exposed to low-calcium medium. The results are consistent with a previous report suggesting blockade by lidocaine of the uptake or utilization of glucose in the glycolytic pathway, and further pinpoint the blockade as an early step in the glycolytic sequence prior to the phospho-fructokinase step.

• The Korean Journal of Pharmacology
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• v.26 no.1
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• pp.91-100
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• 1990

The benzylacycoluridines (BAU and BBAU) are potent and specific inhibitors of uridine phosphorylase (UrdPase). In contrast to the report that benzylacyclouridines potentiated 5-fluoro-2'-deoxyuridine (FdUrd) cytotoxicity against human solid tumor cells (Cancer Res., 44:1852, 1984), continuous exposure of mouse lymphoma L5178Y cells, to FdURd, 5-fluorouridine (FUrd), 5'-deoxy-5-fluorouridine (5'-dFUrd), or 5-fluorouracil (FUra) showed no potentiation of cytotoxicity by benzylacyclouridines. In fact, under the conditions employed, benzylacycoluridines protected the cells from the cytotoxicity of FdUrd, FUrd, or 5'-dFUrd, but not FUra in a dose dependent manner. Intraperitoneal coadministration of BAU or BBAU and a 5-fluorinated pyrimidine (i.e., FdUrd, FUrd, or FUra), to mice bearing L5178Y cells also did not significantly increase the life span compared to those treated with the antimetabolites alone. Anabolism of these nucleosides through the sequential action of UrdPase and orotate phosphoribosyltransferase (OPRTase), inhibition of nucleoside transport by benzylacyclouridines, or both could be responsible for the ineffectiveness of UrdPase inhibitors to potentiate the antineoplastic activity of fluoropvrimidines in L5178Y cells.

• The Journal of Korean Medicine
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• v.29 no.4
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• pp.171-179
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• 2008

Objective: Bufonis Venenum is the traditional Korean medicine Chan Su, which is obtained from the skin and parotid venom gland of the toads. It has been used for myocardial diseases, inflammation diseases, pain relief, cancer and others. The main components of BV are cinobufotoxin, cinobufalin, bufalin and others. Of these, bufalin, the major active ingredient of BV, has been reported to induce apoptosis and to possess anti-tumor effects. There was no report of anti-tumor screening of BV on hepatic cancer and which signaling pathway can be involved. In order to examine the effect of BV on hepatic cancer and the related signaling pathway with BV-induced apoptosis, human Hep G2 cells were used. Methods: Analysis of apoptosis was confirmed by MTT assay. BV decreased cell viability in a dose and duration dependent manner. To observe which signaling molecules will be activated by BV, phosphorylation of MAPK (p38, ERK, JNK), caspase 8 and caspase 9 were examined by Western blot analysis. Results: The phosphorylation levels of p38 started to increase at 5 min after addition of 5 ${\mu}g$/ml of BV and sustained to increase until 48 hours. The phosphorylation levels of other MAPK (ERK and JNK), caspase 8 and caspase 9 increased in a time-dependent manner. These imply that BV may activate different signaling pathways, MAPK, caspase 8 and caspase 9. These results propose that BV may induce apoptosis on Hep G2 cells through the activation of MAPK, caspase 8 and caspase 9.

• Clinical and Experimental Pediatrics
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• v.46 no.3
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• pp.302-307
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• 2003

The long-term clinical issues in Kawasaki disease are concerned with the coronary artery lesions that result in aneurysmal formation, thrombotic occlusion, progression to ischemic heart disease, and premature atherosclerosis. We here report a 3 month old infant with Kawasaki disease complicated by giant coronary aneurysm with thrombosis. After urokinase(10,000 IU/kg) and heparin(400 IU/kg) were injected for two days as thrombolytic agents, thrombi were successfully dissolved. Even though long-term oral anticoagulation with low-dose aspirin, dipyridamole and coumadin were administered, thrombosis of the left main coronary artery was slowly increased. five years later, coronary angiography showed nearly total occlusion of the left anterior descending artery and collaterals from the right posterior branch and radionuclide scan demonstrated complete reversible perfusion defect of several portions of the left ventricle.

• The Korean Journal of Physiology and Pharmacology
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• v.7 no.6
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• pp.375-379
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• 2003

$Ca^{2+}$ influx appears to be important for triggering myoblast fusion. It remains, however, unclear how $Ca^{2+}$ influx rises prior to myoblast fusion. Recently, several studies suggested that NMDA receptors may be involved in $Ca^{2+}$ mobilization of muscle, and that $Ca^{2+}$ influx is mediated by NMDA receptors in C2C12 myoblasts. Here, we report that other types of ionotropic glutamate receptors, non-NMDA receptors (AMPA and KA receptors), are also involved in $Ca^{2+}$ influx in myoblasts. To explore which subtypes of non-NMDA receptors are expressed in C2C12 myogenic cells, RT-PCR was performed, and the results revealed that KA receptor subunits were expressed in both myoblasts and myotubes. However, AMPA receptor was not detected in myoblasts but expressed in myotubes. Using a $Ca^{2+}$ imaging system, $Ca^{2+}$ influx mediated by these receptors was directly measured in a single myoblast cell. Intracellular $Ca^{2+}$ level was increased by KA, but not by AMPA. These results were consistent with RT-PCR data. In addition, KA-induced intracellular $Ca^{2+}$ increase was completely suppressed by treatment of nifedifine, a L-type $Ca^{2+}$ channel blocker. Furthermore, KA stimulated myoblast fusion in a dose-dependent manner. CNQX inhibited not only KA-induced myoblast fusion but also spontaneous myoblast fusion. Therefore, these results suggest that KA receptors are involved in intracellular $Ca^{2+}$ increase in myoblasts and then may play an important role in myoblast fusion.