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Biomedical subjects

Seok Min Kang

Publications and source records attributed to Seok Min Kang.

8 recordsLinked to original sources

The toxic effects of neem extract and azadirachtin on the brown planthopper, Nilaparvata lugens (Stål) (BPH) (Homoptera: Delphacidae).

Extracts of neem (Azadirachta indica A. Juss) are used in the developing world for many purposes including management of agricultural insect pests. The effects of different neem extracts (aqueous (NSKEaq), ethanol (NSKEeth) and hexane (NSKEhex)) on mortality, survival and weight of the brown planthopper, Nilaparvata lugens (Stål) (BPH) (Homoptera: Delphacidae) third and fourth nymphal instars were investigated. When fed rice plants treated with neem derivatives in bioassays, the survival of BPH nymphs is affected. Comparisons were made with the pure neem limonoid, azadirachtin (AZA) to ascertain its role as a compound responsible for these effects. AZA was most potent in all experiments and produced almost 100% nymphal mortality at 0.5 ppm and higher concentrations. When higher concentrations were applied, the effects appeared shortly after treatment and mortality was higher. Many insects died after remaining inactive for several days or during prolonged moulting. At lower concentrations, if moulting was achieved, disturbed growth and abnormalities were then likely to occur in the moulting process. Nymphs that were chronically exposed to neem extract showed a reduction in weight (45-60%). The results clearly indicate the simple NSKE (aqueous, ethanolic or both), containing low concentrations of AZA, can be used effectively to inhibit the growth and survival of BPH.

Animals↗

Primary idiopathic chylopericardium associated with cervicomediastinal cystic hygroma.

Chylopericardium is a rare clinical entity in which chylous fluid accumulates in the pericardial cavity. We report a case of primary idiopathic chylopericardium associated with multiple, small cervicomediastinal cystic hygromas occurring in an asymptomatic 43-year-old woman with no history of trauma, thoracic surgery, malignancy, infection or tuberculosis. Echocardiography showed a large amount of pericardial effusions and pericardial fluid analysis revealed inappropriately elevated triglyceride. We did not demonstrate communication between the thoracic duct and the pericardial sac by lymphangiography and chest computed tomography. She successfully responded to 30 days of continuous pericardial drainage and 15 days of a medium-chain triglyceride diet after 30 days of total parenteral nutrition. Follow-up echocardiography 6 months after treatment commencement showed a minimal reaccumulation of pericardial fluid without symptom. We conclude that if a patient is asymptomatic and can well tolerate daily life, surgery including pericardiectomy or ligation of the thoracic duct is not necessarily required.

Adult↗

Leptin induces hypertrophy via p38 mitogen-activated protein kinase in rat vascular smooth muscle cells.

The hypertrophy of vascular smooth muscle cells (VSMCs) is critical in vascular remodeling associated with hypertension, atherosclerosis, and restenosis. Recently, leptin has appeared to play a pivotal role in vascular remodeling. However, the mechanism by which leptin induces hypertrophy in vascular smooth muscle cells is still unknown. We studied the role of leptin as a potential hypertrophic factor in rat VSMCs. In the present study, leptin significantly increased [(3)H]leucine incorporation and the total protein/DNA ratio in VSMCs. The maximal hypertrophic effect was at 100ng/ml of leptin. Leptin induced phosphorylation and activation of p38 mitogen-activated protein (p38 MAP) kinase and of signal transducers and activators of transcription 3 in a concentration- and time-dependent manner. A p38 MAP kinase inhibitor SB203580 significantly inhibited leptin-induced hypertrophy, AG490 (a JAK2 inhibitor) partially inhibited it, and other MAP kinase inhibitors, PD98059 (an ERK inhibitor) and SP600125 (a JNK inhibitor), had no effect. These results indicate that leptin directly stimulates cellular hypertrophy via p38 MAP kinase in rat VSMCs.

Animals↗

Subacute bacterial endocarditis associated with upper endoscopy.

Transient bacteremia associated with various endoscopic procedures is a well-documented phenomenon. Clinically important bacteremias are very rarely seen, however, this malady has significant morbidity in susceptible patients with valvular heart disease, liver cirrhosis, malignancy and immune deficiency. This bacteremia is a complication that is generally observed secondary to upper endoscopy and other associated invasive procedures in at risk patients, and the more serious manifestations include spontaneous bacterial peritonitis, septic arthritis, meningitis, brain abscess and infective endocarditis. Infective endocarditis is an extremely rare complication of gastrointestinal endoscopy, and it has been convincingly documented in only seven cases. We report a case of native valve endocarditis due to Streptococcus intermedius in a patient with valvular heart disease as a consequence of routine upper endoscopy.

Endocarditis, Subacute Bacterial↗

Congenital absence of inferior vena cava as a rare cause of pulmonary thromboembolism.

Interruption of the inferior vena cava (IVC) with azygos continuation is an uncommon vascular anomaly that results from aberrant development during embryogenesis. We report a rare case of this anomaly, presenting with massive pulmonary embolism. Subsequent evaluation with abdominal CT scan revealed the congenital absence of retrohepatic IVC. The patient was successfully treated with anticoagulation. When deep venous thrombosis (DVT) develops in patients with no apparent risk factors, the presence of congenital IVC anomalies should be considered.

Adult↗

Clinical and echocardiographic characteristics of pericardial effusion in patients who underwent echocardiographically guided pericardiocentesis: Yonsei Cardiovascular Center experience, 1993-2003.

Percutaneous pericardiocentesis guided by two-dimensional echocardiography was introduced in 1983 as an alternative to electrocardiographically or fluoroscopically guided puncture for the management of pericardial effusion. The objective of this study was to investigate echocardiographically (echo)- guided pericardiocenteses performed at Yonsei Cardiovascular Center from January 1, 1993 to December 31, 2003, and also to determine whether patient profiles, etiology, and practice patterns have changed over this 11-year period. The medical records of 272 patients were examined and a follow-up survey was conducted. Patient clinical profiles, etiology, echocardiographic findings, and procedural details were determined for 2 periods: January, 1993 through December, 1997 (period 1); and January 1998 through December, 2003 (period 2). During the 11-year study period, 291 therapeutic, echo-guided pericardiocenteses with pericardial catheter drainage were performed in 272 patients. The number of pericardiocentesis in period 2 was increased compared with period 1 (191 cases vs. 100 cases). The mean age at pericardiocentesis increased from 49 +/- 17 years in period 1 to 55 +/- 16 years in period 2 (p < 0.05). The procedural success rate was 99% overall with a major complication rate of 0.7% (2 cases of right ventricular free wall perforation which required emergency operation). Only one procedure-related mortality (< 30 days) was noted. Malignancy was the leading cause of a pericardial effusion requiring pericardiocentesis (45.6%). The incidence of pericardial effusion following cardiothoracic surgery and percutaneous coronary intervention procedures accounted for nearly 20% of all pericardiocenteses performed. Echo-guided pericardiocentesis has become a safe, standard practice for clinically significant pericardial effusion, in line with the changes of patients profiles over the 11 years of the study.

Adult↗

Left-ventricular diastolic dysfunction may be prevented by chronic treatment with PPAR-alpha or -gamma agonists in a type 2 diabetic animal model.

OBJECTIVES: The aim of this study was to determine whether the peroxisome proliferator-activated receptor (PPAR) ligands could prevent left-ventricular diastolic dysfunction (LVDD) in rats with advanced diabetes. In addition, this study examined whether the activity of malonyl-CoA decarboxylase (MCD), which is an enzyme related to the degradation of malonyl-CoA that is known to regulate the fatty acid metabolism, is changed by the diabetic state itself or by treatment with the PPAR ligands. METHODS: Male Otsuka Long-Evans Tokushima Fatty (OLETF) rats, a model of type 2 diabetes, aged 28 weeks, were divided into 3 groups: the untreated, pioglitazone-treated (10 mg/kg/d), and fenofibrate-treated (150 mg/kg/d) groups. The rats were treated for 10 weeks. Male Long-Evans Tokushima Otsuka (LETO) rats were used as nondiabetic control. Doppler echocardiography and measurements of the MCD activity at the myocardium were performed. RESULTS: At the age of 38 weeks, the OLETF rats treated with either pioglitazone or fenofibrate showed an improvement in the plasma glucose levels after glucose loading as well as an improvement in the fasting plasma insulin, triglyceride, and FFA levels compared to the untreated OLETF rats. The untreated OLETF rats showed a prolonged deceleration time of the E-wave (DTE) (74.3 +/- 3.7 vs LETO, 56.3 +/- 3.8 ms, P < 0.05) and a reduced ratio of the peak early diastolic velocity wave to the late diastolic wave (E/A ratio) (1.25 +/- 0.06 vs LETO 1.54 +/- 0.08, P < 0.05). Pioglitazone treatment in the OLETF rats improved the DTE (51.6 +/- 1.7 ms, P < 0.05), and the fenofibrate treatment also improved the DTE (61.4 +/- 4.3 ms, P < 0.05) and E/A ratio (1.57 +/- 0.05, P < 0.05) compared to the untreated OLETF rats. The parameters related to the systolic function did not change among the groups at both pre- and post-treatments. The MCD activity of the myocardium was remarkably lower in the OLETF rats compared to the LETO rats (3.26 +/- 0.38 vs 7.76 +/- 0.84 nmol/min/mg protein, P < 0.05). The pioglitazone and fenofibrate treatments resulted in an increase in the MCD activity compared to that in the untreated rats (7.20 +/- 0.74 and 8.33 +/- 0.83 nmol/min/mg protein, P < 0.05, respectively). CONCLUSIONS: The PPAR-alpha or -gamma agonists prevented LVDD in the advanced diabetic rat hearts, possibly through an improvement in the fatty acid metabolism in the myocardium or a correction of the hyperglycemia and/or hyperlipidemia.

Animals↗