Supine exercise test was done with bicycle ergometer and echocardiography in 28 patients with chronic aortic regurgitation. Ejection fraction was measured before and immediately after exercise from echocardiography, wall stress and radius/thickness ratio was calculated from echocardiography and systolic blood pressure. 1. There was no difference in left ventricular end systolic and diastolic dimension, ejection fraction at rest, radius/thickness ratio, wall stress between NYHA functional class I, II, III. But work capacity was greater in NYHA class I than in class II, III(39712+/-10778 watt-sec, 23766+/-14280 watt-sec, 11968+/-6052 watt-sec respectively). Ejection fraction after exercise was significantly increased in class I(66.3+/-8.9% at rast vs 71.3+/-10.7% after exercise). 2. Ejection fraction was increased more than 5% in 12 patients(group I) and increased less than 5% or decreased in 16 patients(group II). There was no difference in basal E.F., Ded, Des and postexercise heart rate-blod pressure product between group I and II. But between group I and II, there was significant difference in diastolic redius/thickness ratio(2.55+/-0.30 vs 3.00+/-0.51), mean radius/thickness ratio(1.86+/-0.23 vs 2.18+/-0.30), systolic wall stress(192.3+/-38.6mmHg vs 240.2+/-57.7mmHg), mean wall stress(265.8mmHg vs 334.8+/-68.7mmHg) and work capacity(33848+/-12682 watt-sec vs 19210+/-12342 watt-sce). 3. Work capacity was more than 23800 watt-sec in 16 patients(group A), and less than 23800 watt-sec in 12 patients(group B). There was no difference in ejection fraction at rest, radius/thickness ratio, wall stress, and left ventricular dimension. But ejection fraction after exercise was significantly different between group A and B(68.6+/-14.6% vs 55.8+/-14.2%). 4. In nine patients with end systolic dimension greater than 50 mm ejection fraction was decreased or increased less than 5% in 7 patients. So mean ejection fraction was significantly decreased after exercise(56.8+/-7.5% at rest, 51.0+/-16.3% after exercise).
Aortic Valve Insufficiency* ; Blood Pressure ; Echocardiography* ; Exercise Test ; Heart ; Humans

BACKGROUND: The circadian rhythm of circulating melatonin is regulated by the endogenous oscillators, the suprachi-asmatic nuclei, and entrained by the light-dark cycle of the environment, but it seems that the rhythm can be affected by variable lesions outside the retina-pineal pathway. We intended to know how acute cerebral infarction affects on the cir-cadian rhythm of plasma melatonin secretion. METHODS: Plasma melatonin level was measured from 64 patients with acute cerebral infarction. On admission, blood samples were collected by venipuncture at 2AM, 4AM, 10AM, and 2PM and melatonin level was measured by radioimmunoassay. The state of consciousness of each patient was assessed clini-cally and the infarction site and size were evaluated clinically and radiographically. RESULTS: Among 64 patients with acute cerebral infarction, dramatic blunting or obliteration of nocturnal melatonin surge in the blood was found in 29 patients. The circadian rhythm of melatonin secretion was absent in 12 of 35 alert patients, in 10 of 20 drowsy patients, and in 5 of 7 stuporous patients. Melatonin secretion into plasma was markedly decreased in all 2 comatose patients. Of 14 patients with brainstem lesions, 8 patients showed decreased melatonin levels with the absence of a nocturnal rise, although most of them were alert. CONCLUSIONS: This study suggests that brainstem and the initial mental state might contribute to the regulation of the circadian rhythm of plasma melatonin even though the lesion does not involve the retina-pineal pathway, but further extensive study is required to elucidate it. (J Korean Neurol Assoc 19(4):359~363, 2001)
Biological Clocks ; Brain Stem ; Cerebral Infarction* ; Circadian Rhythm* ; Coma ; Consciousness ; Humans ; Infarction ; Melatonin* ; Phlebotomy ; Photoperiod ; Pineal Gland ; Plasma ; Radioimmunoassay ; Stupor

The cDNA nucleotide sequence of genome segment B encoding the VP1 protein was determined for the aquatic birnavirus GC1 isolated from the rockfish Sebastes schlegeli in Korea. The VP1 protein of GC1 contains a 2,538 bp open reading frame, which encodes a protein comprising 846 amino acid residues that has a predicted MW of 94 kDa. The sequence contains 6 potential Asn-X-Ser/Thr motifs. Eight potential Ser phosphorylation sites and 1 potential Tyr phophorylation site were also identified. GC1 contains the Leu-Lys-Asn (LKN) motif instead of the typical Gly-Asp- Asp (GDD) motif found in other aquatic birnaviruses. We also identified the GLPYIGKT motif, the putative GTPbinding site at amino acid position 248. In total, the VP1 regions of 22 birnavirus strains were compared for analyzing the genetic relationship among the family Birnaviridae. Based on the deduced amino acid sequences, GC1 was observed to be more closely related to the infectious pancreatic necrosis virus (IPNV) from the USA, Japan, and Korea than the IPNV from Europe. Further, aquatic birnaviruses containing GC1 and IPNV have genogroups that are distinct from those in the genus Avibirnaviruses and Entomo-birnaviruses. The birnavirusstrains were clustered into 5 genogroups based on their amino acid sequences. The marine aquatic birnaviruses (MABVs) containing GC1 were included in the MABV genogroup; the IPNV strains isolated from Korea, Japan, and the USA were included in genogroup 1 and the IPNV strains isolated primarily from Europe were included in genogroup 2. Avibirnaviruses and entomobirnaviruses were included in genogroup 3 and 4, respectively.
Amino Acid Sequence ; Animals ; Base Sequence ; Birnaviridae/classification/*genetics ; Capsid Proteins/chemistry/*genetics ; Cell Line ; Fishes/*virology ; Korea ; Molecular Sequence Data ; Phylogeny

BACKGROUND AND OBJECTIVES: Airway allergic reactions are induced by infiltrating inflammatory cells into the human airway tissues through interactions between vascular endothelial cells, inflammatory mediators and adhesion molecules. Accordingly, it is important to study the role of adhesion molecules for the evaluation of pathophysiology of allergy. The aim of this study is to investigate the effect of monoclonal antibodies against intercellular adhesion molecule-1 (ICAM-1) and leukocyte function associated molecule-1 (LFA-1) on the pathophysiology of allergy in ovalbumin-sensitized rats. MATERIALS AND METHODS: We developed an allergy model in rat using the intraperitoneal injection and intranasal nebulization of ovalbumine solution. We evaluated in vivo effects of ICAM-1 and LFA-1 monoclonal antibodies on the expression of ICAM-1 and LFA-1 in ovalbumin sensitized rats. RESULTS: Nasal symptoms after allergen challenge were significantly suppressed and the number of eosinophil in nasal mucosa were significantly inhibited by the treatment of adhesion molecule antibodies. Anti-ICAM-1 and anti-LFA-1 monoclonal antibodies suppressed the expression of ICAM-1 and LFA-1 in nasal mucosa of ovalbumin-sensitized rats. CONCLUSION: It is suggested that allergy can be managed by a useful treatment method using adhesion molecule antibody.
Animals ; Antibodies ; Antibodies, Monoclonal ; Endothelial Cells ; Eosinophils ; Humans ; Hypersensitivity ; Injections, Intraperitoneal ; Intercellular Adhesion Molecule-1 ; Leukocytes ; Lymphocyte Function-Associated Antigen-1 ; Nasal Mucosa* ; Ovalbumin ; Rats* ; Rhinitis*

BACKGROUND: Severe graft dysfunction has been occasionally encountered following adult living donor liver transplantation (LDLT). This study intended to assess the effectiveness of plasmapheresis (PP) as a liver supportive measure in LDLT recipients showing severe graft dysfunction. METHODS: During 1 year of 2007, 276 adult LDLTs were performed in our institution. Of them 27 underwent PP therapy as a liver support. RESULTS: Seventeen underwent PP during the first month following LDLT and another 10 underwent PP after that period. The underlying causes of such liver support were acute and chronic rejections, ischemic damage, viral hepatitis recurrence and unknown causes. A total of 329 sessions of PP were performed for these 27 patients, indicating 12.2+/-9.9 times per patient for 28.1+/-32.2 days. Concurrent hemodiafiltration was done in 66.7%. Serum total bilirubin level was significantly reduced following PP therapy: 23.2+/-6.5 mg/dL before PP and 14.4+/-5.6 mg/dL at 1 week after completion of PP (P<0.001). Other biochemical parameters did not significantly affected by PP. Overall 1-year patient survival rate was 63.0%. Six-month graft survival rate after completion of PP was 82.6% in 17 patients undergoing PP during the first posttransplant month and 30% in 10 patients undergoing PP after 1 month (P= 0.013). CONCLUSIONS: The results of this study implicate that PP has a beneficial effect on the recovery of liver graft function, especially during the early posttransplant period. We suggest to perform active application of PP therapy for liver recipients showing severe graft dysfunction of total bilirubin greater than 15~20 mg/dL.
Adult ; Bilirubin ; Graft Survival ; Hemodiafiltration ; Hepatitis ; Humans ; Liver ; Liver Transplantation ; Living Donors ; Plasmapheresis ; Recurrence ; Rejection (Psychology) ; Survival Rate ; Transplants