Acute massive rise in the capture threshold: successful management with long-term oral prednisolone.
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Aged↗
Biomedical subjects
Jong-Chun Park
Publications and source records attributed to Jong-Chun Park.
Modulation of cell death sensitivity by mutant p53 in HCV core-expressing cells.
The hepatitis C virus (HCV) core protein plays important roles in hepatocarcinogenesis through modulation of cellular proliferation, apoptosis, and immunological responses. The roles of core protein in apoptosis have been conflicting; both proapoptotic and anti-apoptotic roles have been reported from different experimental conditions. Nonetheless, the overcoming apoptosis is a key molecular event to development of hepatocellular carcinoma. We investigated whether the HCV core-expressing cells are susceptible to apoptosis after cellular stress. Furthermore, we focused on the possibility that the presence of mutant p53 can render cells resistant to apoptosis. Our data clearly indicated that core-expressing cells showed increased apoptotic cell death through caspase-3 activation pathways after genotoxic stress without modulation of Bcl-2 family proteins. However, core-expressing cells, when transiently transfected with mutant p53, showed markedly increased resistance upon apoptosis after genotoxic stress. Thus, our data suggest that even though HCV core-expressing cells are susceptible to apoptosis after genotoxic stress, cells are resistant to apoptosis under mutant p53, implying a functional abnormality of p53 giving a chance to overcome apoptosis and ultimately cells develop into hepatocellular cell carcinoma.
Animals↗
Clinical characteristics of hypervagotonic sinus node dysfunction.
BACKGROUND: Sinus node dysfunction (SND) is caused not only by intrinsic sinus node disease, but also by the extrinsic factors. Among the extrinsic factors, autonomic imbalance is most common. Symptomatic SND usually requires permanent pacemaker therapy. However, the clinical characteristics and patient response to medical therapy for hypervagotonic SND have not been properly clarified. MATERIALS AND METHODS: Thirty two patients (14 men, 18 women, 51 +/- 14 years) with hypervagotonic SND were included in this study, but those patients who had taken calcium antagonists, beta-blockers or other antiarrhythmic drugs were excluded. Hypervagotonic SND was diagnosed if the abnormal electrophysiologic properties of the sinus node were normalized after the administration of atropine (0.04 mg/kg). RESULTS: The presenting arrhythmias were 16 cases of sinus bradycardia (50.0%), 12 of sinus pause (37.5%), 3 of sinoatrial block (9.4%) and 1 of tachy-bradycardia (3.1%). Nine (28.1%) patients had hypertension, 7 (21.9%) smoked, 2 (6.3%) had diabetes mellitus, and 1 (3.1%) had hypercholesterolemia. Among the patients, 3 had no remarkable symptoms, 13 had dizziness, 7 had syncope, 3 had weakness and 6 had shortness of breath. Twenty five (78.1%) patients were treated with theophylline, 1 patient with tachy-bradycardia syndrome was treated with digoxin and propafenone, and 6 (18.8%) were treated with no medication. During the 43 +/- 28 month follow-up, 25 patients remained asymptomatic, but 6 who took no medication developed mild dizziness. One patient needed permanent pacemaker implantation owing to recurrent syncope despite of theophylline treatment. CONCLUSION: These results show that hypervagotonic SND has a benign course and most of the patients can be managed safely without implanting a pacemaker. (Ed note: I like the abstract. It is short and direct, as it should be.)
Dizziness↗
Exogenous wild-type p16INK4A gene induces delayed cell proliferation and promotes chemosensitivity through decreased pRB and increased E2F-1 expressions.
Human gastric cancer SNU 484 cells express mutant p16, which migrates slower than the wild-type p16. We constructed an expression vector containing human p16 cDNA to evaluate the cytotoxic effects of exogenous p16 expression on SNU 484 cell proliferation and to explore the potential use of p16 in cancer gene therapy. The stable transfectant expressing wild-type p16, showed a 2-fold slower growth rate than mock and non-infected cells through down-regulation of CDK4-dependent kinase activity. When cells were transiently transfected with mock or p16 encoded vector, the mock cells showed larger survival colonies than those of wild-type p16. Furthermore, p16-expressing stable transfectant was readily progressed into cell death by combination with treatment of chemotherapeutic drug in a dose-dependent manner. According to western blot analysis, both decreased expression of pRB and increased expression of E2F-1 may contribute to the susceptibility of cell death. Our data indicate that exogenous wild-type p16 induces delayed cell proliferation and promotes chemo-sensitivity in the gastric cancer cell line, implying the promise of p16 in cancer gene therapy.
Antimetabolites, Antineoplastic↗
A case of secondary myocardial lymphoma presenting with ventricular tachycardia.
Malignant lymphoma can involve the cardiac cavity or myocardium as a mass. Clinical symptoms of its cardiac involvement are usually absent or nonspecific, making the diagnosis of the cardiac involvement very difficult before death. We experienced a patient with secondary myocardial non-Hodgkin's lymphoma presenting with sustained ventricular tachycardia (VT) as a primary clinical problem. A 39-yr-old woman visited our hospital because of dyspnea and palpitation for 7 days. Physical examination revealed rapid heart beat with variable intensity of the first heart sound and soft mass in the lower abdomen. VT with a cycle length of 480 msec was recorded in resting 12-lead electrocardiogram. Two well-circumscribed hypo-echogenic round masses were demonstrated in the interventricular septum and left ventricular posterior wall. Cytological examination of aspirated pericardial fluid and percutaneous needle biopsy of the abdominal mass revealed a diffuse large cell type non-Hodgkin's lymphoma. Myocardial masses and ventricular tachycardia resolved with chemotherapy using cyclophosphamide, adriamycin, vincristine and prednisone regimen. To our best knowledge, the same case as ours has not been reported previously.
Abdominal Neoplasms↗