Korean Ginseng (Panax C.A. Meyer) has survived empirical efficacy as tonic and geriatric agents for several thousands of years in oriental herbal medicine. But there has been numerous controversial reports about its use in aged hypertensive men due to its allegedly hypertensive effects. Therefore, the author conducted the pharmacological studies of Korean Ginseng extracts on the blood pressure and blood lipid metabolism, during development of hypertension, using SHR(Spontaneously Hypertensive Rat), counterpart model of human essential hypertension. The results obtained were as follows: 1. SHR could be grouped, according to their age, as prehypertensive stage(<6th week after birth), labile hypertensive stage(6th 14th week), early established hypertensive stage(14th-20th week), and late established hypertensive stage(>20th week). 2. Plasma renin activity tended to rise steadily, until established hypertensive stage was reached. Thereafter, plasma renin activity tended to decline. 3. The changes of blood pressure due to Ginseng extract, depended on the amount, route and duration of its administration. Low dose of Ginseng tended to increase blood pressure but high dose of Ginseng tended to decrease blood pressure, until 1 week of intraperitonal administration. But prolonged administration of Ginseng extract beyond 1 week, showed delayed hypertensive effect in the intraperitoneal administration but not in oral administration. 4. SHR seemed to have abnormalities in the lipid metabolism. SHR showed lowered level of serum cholesterol and phospholipid, whereas slightly higher level of triglyceride, and showed lower alpha-lipoprotin fraction but higher pre beta-lipoprotein fraction, as compared with NCR.(=Normal Control Rat). 5. When high fat cholesterol salt diet was fed on, it was possible to indece hyperlidemia and increment of hypertension in SHR. but when high fat cholesterol salt diet and Ginseng extract were fed on concomitantly, Ginseng showed significant inhibiting effect on the development of hyperlidemia and hypertension.
Administration, Oral ; Blood Pressure* ; Cholesterol ; Diet ; Herbal Medicine ; Humans ; Hypertension* ; Lipid Metabolism* ; Male ; Panax* ; Plasma ; Rats, Inbred SHR* ; Renin ; Triglycerides

Preoperative diagnosis of an aneurysm of the right coronary sinus of Valsalve with rupture into the right ventricle was made by echocardiography in a patient who also had a small ventricular septal defect. In this case of ruptured sinus of Valsalva aneurysm, the cardinal echocardiographic finding is a defect in the anterior aortic root through which the right coronary cusp appeared to prolapse. After surgical correction the echo from the herniated right coronary cusp of the aortic valve and discontinuity in the echo from anterior aortic wall disappeared.
Aneurysm ; Aneurysm, Ruptured* ; Aortic Valve ; Coronary Sinus ; Diagnosis ; Echocardiography* ; Heart Septal Defects, Ventricular ; Heart Ventricles ; Humans ; Prolapse ; Rupture ; Sinus of Valsalva*

Preoperative diagnosis of an aneurysm of the right coronary sinus of Valsalve with rupture into the right ventricle was made by echocardiography in a patient who also had a small ventricular septal defect. In this case of ruptured sinus of Valsalva aneurysm, the cardinal echocardiographic finding is a defect in the anterior aortic root through which the right coronary cusp appeared to prolapse. After surgical correction the echo from the herniated right coronary cusp of the aortic valve and discontinuity in the echo from anterior aortic wall disappeared.
Aneurysm ; Aneurysm, Ruptured* ; Aortic Valve ; Coronary Sinus ; Diagnosis ; Echocardiography* ; Heart Septal Defects, Ventricular ; Heart Ventricles ; Humans ; Prolapse ; Rupture ; Sinus of Valsalva*

In order to review the epidemiological data of cardiovascular diseases, statistical observation was made on the 7,271 patients with cardiovascular diseases who were treated in the Department of Internal Medicine, Han-Yang University Hospital during the 10 year period from May 1972 to December 1981. A. General Findings (1) Cardiovascular disease was seen in 18.6% out of a total 39,004 medical inpatients treated during this 10 year time span. (2) Incidences of cardiovascular disease seemed to increase in frequency in consecutive years, especially incidence of coronary heart disease and arrhythmia. (3) Incidence of cardiovascular disease occurred most frequently to patients in their fifth decade, and next most frequently to those in their sixth and fourth decade, in that order. (4) The overall ratio of male to female incidence of cardiovascular disease was 1:1. B. Specific Epidemiology (1) Hypertension was the most common form of cardiovascular problem, accounting for 52.9% of patients with cardiovascular disease and 9.9% of the total medical in-patients population. Incidence of hypertension occured most frequently in the fifth decade of life. It occured next most in the sixth and fourth decades, in that order. The male to female ratio of incidence of hypertension was 1:1. Patients with malignant hypertension made up 5.9% all hypertension patients. (2) Patients with rheumatic heart disease made up 6% of those patients with cardiovascular diseases. Male to female ratio of incidence of rheumatic heart disease was 1:2.4. The most common form of this disease was mitral valvular disease, but isolated aortic valvular disease proved to be rather uncommon in this study in Korea. (3) Coronary heart disease made up 15.5 % of all incidence of cardiovascular diseases. It occured most frequently to patients in their fifth and sixth decades, and in a male to female ratio of 1.5 to 1. (4) Congenital heart disease made of 0.9% of the total incidence of cardiovascular diseases with ventricular septal defect as the most common form of this disease. (5) The remaining forms of cardiovascular diseases diagnosed during the time span of this study were arrhythmia 16.8%, cor pulmonale 1.4%, cardiomyopathy 1.3%, peripheral vascular disease 1.0%, pericarditis 1.0%, thyrotoxic heart disease 0.8%, endocarditis 0.5%, postpartum cardiomyopathy 0.3%, myxedematous heart disease 0.1%, and miscellaneous heart ailments 1.5%.
Arrhythmias, Cardiac ; Cardiomyopathies ; Cardiovascular Diseases* ; Coronary Disease ; Endocarditis ; Epidemiology ; Female ; Heart ; Heart Defects, Congenital ; Heart Diseases ; Heart Septal Defects, Ventricular ; Humans ; Hypertension ; Hypertension, Malignant ; Incidence ; Inpatients ; Internal Medicine ; Korea* ; Male ; Pericarditis ; Peripheral Vascular Diseases ; Postpartum Period ; Pulmonary Heart Disease ; Rheumatic Heart Disease

Mitral valvular heart diseases are known to be one of the easily detectable and the hemodynamic chane to the severity and duration of diseases can directly be described by echocardiography. The objective of this study was to determine the echocardiographic characteristics in 3 groups of mitral valvular diseases, that is mitral stenosis(112 cases), mitral stenoinsufficiency (66 cases). and mitral insufficiency(20 cases). 1) In mitral valve study, closing velocity of anterior leaflet reduced in mitral stenosis than other two groups and DE amplitude was greater in mitral insufficiency but there were no significant differences in 3 groups of mitral valvular diseases. DE and AC slope were slightly more rapid in mitral stenosis group and left ventricular outflow tract was much increased in mitral insufficiency group. 2) In aorta and left atrium study, aortic cusps separation was much increased in mitral insufficiency and left atrium was slightly more dilated in mitral stenoinsufficiency than other two groups. But left atrial dimension in mitral insufficiency was more diminished than that in mitral, stenosis, which is probably due to the short durationn of diseases and small range of materials in mitral insufficiency group. 3) In left ventricle study, thickness of interventricular septem, LSa, Ena, left ventricular dimension, LVPW, LV volume. and stroke volume were more increased in mitral insufficiency than mitral stenosis, because of the left ventricular volume overloading. Vcf and PEP/LVET were higher in mitral insufficiency than other two groups. Ejection fraction and fractional shortening were more diminished in mitral stenoinsufficiency but no significant difference was found. 4) In right ventricle study, there were no remarkable changes in right ventricular dimension and right ventricular internal dimension index in all 3 groups of mitral valvular diseases. 5) Calcification of mitral leaflets was observed in 85.7% of mitral stenosis, 90.9% of mitral stenoinsufficiency and 10% of mitral insufficiency, but heavy calcification was more remarkable in mitral stenosis group(25%). 6) Atrial fibrillation was observed in 47% of total mitral valvular diseases, mitral stenosis being 43.8%, mitral stenoinsufficiency 60.6% and mitral insufficiency 20%. In cases of atrial fibrillation, left atrial dimension was significantly enlarged compared with the group without atrial fibrillation.
Aorta ; Atrial Fibrillation ; Constriction, Pathologic ; Echocardiography* ; Heart Atria ; Heart Valve Diseases* ; Heart Ventricles ; Hemodynamics ; Mitral Valve ; Mitral Valve Insufficiency ; Mitral Valve Stenosis ; Stroke Volume

Naegleria fowleri, a brain-eating amoeba, thrives in lakes and rivers with aquatic vegetation and causes primary amoebic meningoencephalitis (PAM) in humans. Most recently, it has become such a serious problem that N. fowleri was detected in tap water in Houston, USA. Several pathogenic factors are considered very important to destroy target cells in the brain. In particular, the food-cup where N. fowleri antigen-1 (Nfa1) is located, is strongly expressed in pseudopodia involved in the movement of N. fowleri, and is involved in phagocytosis by attaching to target cells. In this article, we reviewed the role of the Nfa1 protein and its associated pathogenicity. The nfa1 gene was cloned by cDNA library immunoscreening using infection serum and immune serum. Nfa1 protein is mainly distributed in pseudopodia important to movement and vacuoles. Moreover, heat shock protein 70, cathepsin-like proteare and Nf-actin are also associated with pseudopodia in which Nfa1 is localized. Interestingly, the amount of the nfa1 gene changed as N. fowleri trophozoites transformed into cysts. Polyclonal antiserum against Nfa1 showed a protective effect against cytotoxicity of approximately 19.7%. Nfa1-specific IgA antibodies prevent N. fowleri trophozoites from adhering to the nasal mucosa, delaying invasion. The nfa1-vaccinated mice showed significantly higher levels of Nfa1-specific antibody. The duration of anti-Nfa1 IgG in the vaccinated mice lasted 12 weeks, strongly suggesting that nfa1 is a significant pathogenic gene and that Nfa1 is a pathogenic protein. Several factors related to pseudopodia and locomotion have been linked to Nfa1. A clearer function of N. fowleri targeting nfa1 with other genes might enable target-based inhibition of N. fowleri pathogenicity.

Naegleria fowleri, a brain-eating amoeba, thrives in lakes and rivers with aquatic vegetation and causes primary amoebic meningoencephalitis (PAM) in humans. Most recently, it has become such a serious problem that N. fowleri was detected in tap water in Houston, USA. Several pathogenic factors are considered very important to destroy target cells in the brain. In particular, the food-cup where N. fowleri antigen-1 (Nfa1) is located, is strongly expressed in pseudopodia involved in the movement of N. fowleri, and is involved in phagocytosis by attaching to target cells. In this article, we reviewed the role of the Nfa1 protein and its associated pathogenicity. The nfa1 gene was cloned by cDNA library immunoscreening using infection serum and immune serum. Nfa1 protein is mainly distributed in pseudopodia important to movement and vacuoles. Moreover, heat shock protein 70, cathepsin-like proteare and Nf-actin are also associated with pseudopodia in which Nfa1 is localized. Interestingly, the amount of the nfa1 gene changed as N. fowleri trophozoites transformed into cysts. Polyclonal antiserum against Nfa1 showed a protective effect against cytotoxicity of approximately 19.7%. Nfa1-specific IgA antibodies prevent N. fowleri trophozoites from adhering to the nasal mucosa, delaying invasion. The nfa1-vaccinated mice showed significantly higher levels of Nfa1-specific antibody. The duration of anti-Nfa1 IgG in the vaccinated mice lasted 12 weeks, strongly suggesting that nfa1 is a significant pathogenic gene and that Nfa1 is a pathogenic protein. Several factors related to pseudopodia and locomotion have been linked to Nfa1. A clearer function of N. fowleri targeting nfa1 with other genes might enable target-based inhibition of N. fowleri pathogenicity.

Naegleria fowleri, a brain-eating amoeba, thrives in lakes and rivers with aquatic vegetation and causes primary amoebic meningoencephalitis (PAM) in humans. Most recently, it has become such a serious problem that N. fowleri was detected in tap water in Houston, USA. Several pathogenic factors are considered very important to destroy target cells in the brain. In particular, the food-cup where N. fowleri antigen-1 (Nfa1) is located, is strongly expressed in pseudopodia involved in the movement of N. fowleri, and is involved in phagocytosis by attaching to target cells. In this article, we reviewed the role of the Nfa1 protein and its associated pathogenicity. The nfa1 gene was cloned by cDNA library immunoscreening using infection serum and immune serum. Nfa1 protein is mainly distributed in pseudopodia important to movement and vacuoles. Moreover, heat shock protein 70, cathepsin-like proteare and Nf-actin are also associated with pseudopodia in which Nfa1 is localized. Interestingly, the amount of the nfa1 gene changed as N. fowleri trophozoites transformed into cysts. Polyclonal antiserum against Nfa1 showed a protective effect against cytotoxicity of approximately 19.7%. Nfa1-specific IgA antibodies prevent N. fowleri trophozoites from adhering to the nasal mucosa, delaying invasion. The nfa1-vaccinated mice showed significantly higher levels of Nfa1-specific antibody. The duration of anti-Nfa1 IgG in the vaccinated mice lasted 12 weeks, strongly suggesting that nfa1 is a significant pathogenic gene and that Nfa1 is a pathogenic protein. Several factors related to pseudopodia and locomotion have been linked to Nfa1. A clearer function of N. fowleri targeting nfa1 with other genes might enable target-based inhibition of N. fowleri pathogenicity.

Naegleria fowleri, a brain-eating amoeba, thrives in lakes and rivers with aquatic vegetation and causes primary amoebic meningoencephalitis (PAM) in humans. Most recently, it has become such a serious problem that N. fowleri was detected in tap water in Houston, USA. Several pathogenic factors are considered very important to destroy target cells in the brain. In particular, the food-cup where N. fowleri antigen-1 (Nfa1) is located, is strongly expressed in pseudopodia involved in the movement of N. fowleri, and is involved in phagocytosis by attaching to target cells. In this article, we reviewed the role of the Nfa1 protein and its associated pathogenicity. The nfa1 gene was cloned by cDNA library immunoscreening using infection serum and immune serum. Nfa1 protein is mainly distributed in pseudopodia important to movement and vacuoles. Moreover, heat shock protein 70, cathepsin-like proteare and Nf-actin are also associated with pseudopodia in which Nfa1 is localized. Interestingly, the amount of the nfa1 gene changed as N. fowleri trophozoites transformed into cysts. Polyclonal antiserum against Nfa1 showed a protective effect against cytotoxicity of approximately 19.7%. Nfa1-specific IgA antibodies prevent N. fowleri trophozoites from adhering to the nasal mucosa, delaying invasion. The nfa1-vaccinated mice showed significantly higher levels of Nfa1-specific antibody. The duration of anti-Nfa1 IgG in the vaccinated mice lasted 12 weeks, strongly suggesting that nfa1 is a significant pathogenic gene and that Nfa1 is a pathogenic protein. Several factors related to pseudopodia and locomotion have been linked to Nfa1. A clearer function of N. fowleri targeting nfa1 with other genes might enable target-based inhibition of N. fowleri pathogenicity.

Naegleria fowleri, a brain-eating amoeba, thrives in lakes and rivers with aquatic vegetation and causes primary amoebic meningoencephalitis (PAM) in humans. Most recently, it has become such a serious problem that N. fowleri was detected in tap water in Houston, USA. Several pathogenic factors are considered very important to destroy target cells in the brain. In particular, the food-cup where N. fowleri antigen-1 (Nfa1) is located, is strongly expressed in pseudopodia involved in the movement of N. fowleri, and is involved in phagocytosis by attaching to target cells. In this article, we reviewed the role of the Nfa1 protein and its associated pathogenicity. The nfa1 gene was cloned by cDNA library immunoscreening using infection serum and immune serum. Nfa1 protein is mainly distributed in pseudopodia important to movement and vacuoles. Moreover, heat shock protein 70, cathepsin-like proteare and Nf-actin are also associated with pseudopodia in which Nfa1 is localized. Interestingly, the amount of the nfa1 gene changed as N. fowleri trophozoites transformed into cysts. Polyclonal antiserum against Nfa1 showed a protective effect against cytotoxicity of approximately 19.7%. Nfa1-specific IgA antibodies prevent N. fowleri trophozoites from adhering to the nasal mucosa, delaying invasion. The nfa1-vaccinated mice showed significantly higher levels of Nfa1-specific antibody. The duration of anti-Nfa1 IgG in the vaccinated mice lasted 12 weeks, strongly suggesting that nfa1 is a significant pathogenic gene and that Nfa1 is a pathogenic protein. Several factors related to pseudopodia and locomotion have been linked to Nfa1. A clearer function of N. fowleri targeting nfa1 with other genes might enable target-based inhibition of N. fowleri pathogenicity.