BACKGROUND: The central physiological derangement of hemorrhagic fever with renal syndrome (HFRS) caused by hantaan virus (HTNV) is a vascular dysfunction, manifested by hemorrhage, impaired vascular tone and increased vascular permeability. Platelet activating factor (PAF), whose actions are mediated through a specific receptor, is a potent bioactive lipid. PAF has diverse biological functions in the vascular system, such as increasing vascular permeability, adhesion of leukocytes to the endothelium and reduction of cardiac output, which result in hypotension and shock. The goal of the present study was to investigate whether PAF is involved in the pathogenesis of HFRS. For this purpose, we evaluated the effect of HTNV on the expression of PAF receptor (PAF-R) and on the activity of PAF-acetylhydrolase (PAF-AH) instead of PAF because PAF is rapidly degraded by PAF-AH in vivo. MATERIALS AND METHODS: To evaluate the expression of PAF-R, we performed reverse-transcription PCR, western blot and FACS analyses using HTNV-infected human umbilical vein endothelial cells (HUVECs) and non-infected (control) HUVECs. In addition, we measured the activity of plasma PAF-AH in HFRS patients and normal healthy persons. RESULTS: The mRNA and protein expression of PAF-R was increased in HTNV-infected HUVECs compared with control HUVECs at 2 and 3 days post-infection (d.p.i.). FACS analysis showed that HTNV induced the surface expression of PAF-R in HUVECs from 2 d.p.i. The activity of plasma PAF-AH was 2.5-fold lower in HFRS patients than in normal healthy persons. CONCLUSION: Increased PAF-R expression by HTNV might increase the responsiveness to PAF in endothelial cells. Reduced PAF-AH activity in the blood of HFRS patients might delay PAF degradation. These results suggest that changes in PAF-R and PAF-AH by HTNV might influence to PAF activity and might be involved in the vascular dysfunction of HFRS.
Blood Platelets ; Blotting, Western ; Capillary Permeability ; Cardiac Output ; Endothelial Cells ; Endothelium ; Hantaan virus ; Hemorrhage ; Hemorrhagic Fever with Renal Syndrome ; Human Umbilical Vein Endothelial Cells ; Humans ; Hypotension ; Leukocytes ; Plasma ; Platelet Activating Factor ; Platelet Membrane Glycoproteins ; Polymerase Chain Reaction ; Receptors, G-Protein-Coupled ; RNA, Messenger ; Shock

We report herein a case of clear cell hidradenoma in a 65-year-old man, who had a 8-month history of a asymptomatic, smooth-surfaced, round, blue tumor mass with cystic grape-like nature on the left upper chest, measuring 2.0 x 2.0 x 1.5cm in size. A histopathological examination revealed tubular and cystic structures within the intradermal tumor composed of predominant fusiform cells and clear cells, and some transitional cells. The patient remained free of recurrence for a period of one-year follow-up after the excision.
Acrospiroma* ; Aged ; Follow-Up Studies ; Humans ; Recurrence ; Thorax

No abstract available.

BACKGROUND: Thromboembolism is the major complication in patients with the insertion of cardiac prosthetic valves. The purpose of this study is evaluate the risk factors about the formation of left atrial thrombi after cardiac valve replacement. METHOD: Transesophageal(TEE) and transthoracic echocardiography(TTE) were done to evaluate postoperative cardiac condition in 98 patients with cardiac prosthetic valves from Jan. 1991 to Oct 1991. Several clinical and echocardiographic parameters were analyzied to evaluate the relationship with the formation of left atrial thrombi. RESULT: In univariate analysis, important factors related to the formation of left atrial thrombi are type of operation (p=0.027), postoperative left ventricular function(p=0.003), preoperative(p=0.037) and postoperative systolic ventricular size(p=0.024). However, in multivariate analysis postoperative left ventricular size(p=0.017), presence of previous thrombi(p=0.014), preoperative left atrial size(p=0.014) and postoperative left atrial size(p=0.014) are significant factors. CONCLUSION: Patients with high risk and low risk for the formation of left atrial thrombi after valve replacement can be identified by readily available clinical and echocardiographic variables.
Echocardiography ; Heart Valves ; Humans ; Multivariate Analysis ; Risk Factors* ; Thromboembolism

BACKGROUND AND OBJECTIVES: Protein kinase C (PKC) is known to be related with development of various cells. In the heart, each isoform reacts differentially against agonists and the reaction changes during development. In this study, the roles of PKC isoforms (alpha, beta, gamma, delta, epsilon, zeta) were investigated through the localization of mRNA expression in the developing rat heart with in situ hybridization histochemistry. MATERIALS AND METHOD: The mRNA expression pattern of PKC isoforms (alpha, beta, gamma, delta, epsilon, zeta) was investigated with in situ hybridization histochemistry in developing and adult rat hearts. Whole body parasagittal sections were used for embryonal day 14 (E14), E16, E18 and heart sections were used for just born (P0), postnatal day 7 (P7), P14, P21 and adult rat. RESULTS: The expression of PKC alpha was found from E14, peaked at P7, and gradually decreased to adult level. The expression of PKC beta was observed from P14, peaked at P21, and decreased to adult level. The expression of PKC delta in the heart was observed from E14, peaked at P0, and abruptly disappeared at P14. The expression of PKC epsilon was observed from E14, peaked at P0, after that gradually decreased and disappeared at adult rat heart. The expression of PKC gamma and zeta was not found from any stage of developing rat heart. CONCLUSION: From these results, it is suspected that each PKC isoform may be differentially related with development of heart. The strong expression of PKC alpha, delta, epsilon around perinatal period, rapidly developing stage, suggests that PKC alpha, delta, epsilon may be related with rapid development of rat heart. And the late postnatal expression of PKC beta suggests that PKC beta may be related with maturation of rat heart.
Adult ; Animals ; Heart* ; Humans ; In Situ Hybridization ; Protein Isoforms ; Protein Kinase C* ; Protein Kinase C-epsilon ; Protein Kinases* ; Rats* ; RNA, Messenger*

No abstract available.
Extracorporeal Circulation* ; Heart* ; Potassium* ; Thoracic Surgery*

No abstract available.
Electromyography*

No abstract available.
Thrombosis*

No abstract available.
Pneumothorax* ; Thoracotomy*

No Abstract Available.
Hepacivirus* ; Hepatitis C* ; Hepatitis* ; Humans ; Polymerase Chain Reaction*