BACKGROUND AND OBJECTIVES: When nasopharyngeal carcinomas recur after radiotherapy, it becomes difficult to select further treatment modality. We reviewed surgical results of irradiation-failed nasopharyngeal carcinoma patients and investigated the role of salvage surgery. MATERIALS AND METHODS: Surgical results of 10 cases of nasopharyngeal carcinoma were investigated. All of them had a recurrent or residual nasopharyngeal carcinoma after radiation therapy. The medical records of these patients were reviewed retrospectively and the mean survival time was calculated by Kaplan-Meier method. RESULTS: The mean survival time of the irradiation-failed nasopharyngeal carcinoma patients was 21.8 months. The survival times of early staged irradiation-failed tumor were longer than that of the tumor in the advance stage. Among 3 patients whose recurrent tumor stages were T1, two patients had the negative resection margin and they lived without the disease. However, none of the patients whose recurrent tumor stages were beyond T2(n=7) had the negative resection margin and lived without the disease. CONCLUSION: Surgical treatment was an useful treatment modality for improving the survival time of early staged irradiation-failed nasopharyngeal carcinomas.
Humans ; Medical Records ; Radiotherapy ; Retrospective Studies ; Survival Rate

BACKGROUND AND OBJECTIVE: Eosinophil is a major inflammatory cell in allergic diseases and parasitic infestations. Various cytokines such as GM-CSF, IL-3 and IL-5 are known to activate eosinophils and prolong their survival. Among them, IL-5 is the most potent stimulator of eosinophil survival. Recently, it was reported that increased expression of Bcl-2 is related to prolonged survival of IL-5 stimulated eosinophil. Theophylline is a useful drug in bronchial asthma, due not only to bronchial dilation but also to its anti-inflammatory effects. It has been suggested that anti inflammatory action of theophylline derives from the reduction of inflammatory cells in the airways which is mechated by stimulat on of apoptosis of inflammatory cells. In this study, we investigated, by measuring Bcl-2 expression of IL-5 stimulated eosinophil, the effect of theophylline on apoptosis as one of the anti-inflammatory action. MATERIAL AND METHOD: Peripheral eosinophils were isolated from atopic patients by using Perco- 11 discontinuous gradient and purified by negative selection technique using MACS. Eosinophil viability and apoptosis were measured by FACscan. Expression of Bcl-2 protein in eosinophils was detected by Western blot and ELISA. RESULTS: IL-5 increased the percentage of viable eosinophils and reduced the apoptosis of eosinophils in a dose dependent manner. The increased survival of IL-5 stimulated eosinophils was reduced by theophylline via activation of apoptosis. Bcl-2 was increased when eosinophils were cultured with IL-5 only, but when theophylline was cocultured, reduced Bcl-2 was seen with Western blot and ELISA. CONCLUSION: IL-5 increases the survival of eosinophil through the enhanced expression of Bcl- 2. Theophylline has counter action against IL-5 via inhibition of Bcl-2 induced by IL-5. Inhibiting the prolongation of eosinophil survival caused by IL-5 might be one possible mechanism of antiinflammatory effects of theophylline.
Apoptosis ; Asthma ; Blotting, Western ; Cytokines ; Enzyme-Linked Immunosorbent Assay ; Eosinophils* ; Granulocyte-Macrophage Colony-Stimulating Factor ; Humans ; Interleukin-3 ; Interleukin-5 ; Theophylline*

Many intracellular proteins and signaling cascades contribute to the sensitivity of N-methyl-D-aspartate receptors (NMDARs). One such putative contributor is the serine/threonine kinase, protein kinase C (PKC). Activation of PKC by phorbol 12-myristate 13-acetate (PMA) causes activation of extracellular signal-regulated kinase (ERK) and promotes the formation of new spines in cultured hippocampal neurons. The purpose of this study was to examine which PKC isoforms are responsible for the PMA-induced augmentation of long-term potentiation (LTP) in the CA1 stratum radiatum of the hippocampus in vitro and verify that this facilitation requires NMDAR activation. We found that PMA enhanced the induction of LTP by a single episode of theta-burst stimulation in a concentration-dependent manner without affecting to magnitude of baseline field excitatory postsynaptic potentials. Facilitation of LTP by PMA (200 nM) was blocked by the nonspecific PKC inhibitor, Ro 31-8220 (10microM); the selective PKCdelta inhibitor, rottlerin (1microM); and the PKCepsilon inhibitor, TAT-epsilonV1-2 peptide (500 nM). Moreover, the NMDAR blocker DL-APV (50microM) prevented enhancement of LTP by PMA. Our results suggest that PMA contributes to synaptic plasticity in the nervous system via activation of PKCdelta and/or PKCepsilon, and confirm that NMDAR activity is required for this effect.
2-Amino-5-phosphonovalerate ; Acetophenones ; Benzopyrans ; Excitatory Postsynaptic Potentials ; Hippocampus ; Indoles ; Long-Term Potentiation ; Nervous System ; Neurons ; Phorbols ; Phosphotransferases ; Protein Isoforms ; Protein Kinases ; Proteins ; Receptors, N-Methyl-D-Aspartate ; Spine

BACKGROUND: The effect of 3-hydroxy 3-methyl glutaryl CoA reductase inhibitor (statin) on the concentration of lipoprotein (a) [Lp(a)] is controversial. Most studies evaluated the effect of statin administered for less than 2 years. We were to analyze the effect of long-term treatment of statin on the concentration of Lp(a) retrospectively. METHODS: A total 93 cases were enrolled and divided into two groups; statin group (20 mg of lovastatin, n=33) and control group (n=60). Lp(a) and lipid profiles were measured before and after the medication for at least 2 years. RESULTS: Between two groups, there were no differences in baseline clinical variables and in biochemical parameters except total cholesterol and low density lipoprotein-cholesterol (LDL-C) levels. Mean duration of follow-up was similar between control and statin groups (58.7+/-15.0 vs. 54.7+/-16.4 months, p=0.24). Lp(a) levels did not change in both statin group (30.1+/-29.6 mg/dL vs. 28.2+/-23.1 mg/dL, p=0.89) and control group (p=0.49). The change of Lp(a) was not different between two groups (p=0.43). Statin was also ineffective in cases with Lp(a) level over 10 mg/dL. Total cholesterol and LDL-C levels decreased in statin group by 26.4% (p=0.000) and 40.5% (p=0.000) respectively. The elevation of HDL-C was similar between two groups. CONCLUSION: Long-term treatment of lovastatin did not modify Lp(a) level in retrospective study. To clarify the effect of statin precisely, prospective study might be needed.
Cholesterol ; Follow-Up Studies ; Hydroxymethylglutaryl-CoA Reductase Inhibitors ; Lipoprotein(a)* ; Lipoproteins* ; Lovastatin ; Oxidoreductases* ; Retrospective Studies

BACKGROUND: The effect of 3-hydroxy 3-methyl glutaryl CoA reductase inhibitor (statin) on the concentration of lipoprotein (a) [Lp(a)] is controversial. Most studies evaluated the effect of statin administered for less than 2 years. We were to analyze the effect of long-term treatment of statin on the concentration of Lp(a) retrospectively. METHODS: A total 93 cases were enrolled and divided into two groups; statin group (20 mg of lovastatin, n=33) and control group (n=60). Lp(a) and lipid profiles were measured before and after the medication for at least 2 years. RESULTS: Between two groups, there were no differences in baseline clinical variables and in biochemical parameters except total cholesterol and low density lipoprotein-cholesterol (LDL-C) levels. Mean duration of follow-up was similar between control and statin groups (58.7+/-15.0 vs. 54.7+/-16.4 months, p=0.24). Lp(a) levels did not change in both statin group (30.1+/-29.6 mg/dL vs. 28.2+/-23.1 mg/dL, p=0.89) and control group (p=0.49). The change of Lp(a) was not different between two groups (p=0.43). Statin was also ineffective in cases with Lp(a) level over 10 mg/dL. Total cholesterol and LDL-C levels decreased in statin group by 26.4% (p=0.000) and 40.5% (p=0.000) respectively. The elevation of HDL-C was similar between two groups. CONCLUSION: Long-term treatment of lovastatin did not modify Lp(a) level in retrospective study. To clarify the effect of statin precisely, prospective study might be needed.
Cholesterol ; Follow-Up Studies ; Hydroxymethylglutaryl-CoA Reductase Inhibitors ; Lipoprotein(a)* ; Lipoproteins* ; Lovastatin ; Oxidoreductases* ; Retrospective Studies