Total of 125 women, 71 normal and 54 hyperlipidemic subject, were divided into 3 groups, young (students, 19 years old), middle aged (35-45 years old, 39.6 years of average) and senescent (55-82 years old, 59.6 years of average). Serum samples obtained 5 hours after eating of test meal of 439 cal. were fractionated using the purified specific antiserum against human β-lipoprotein.
Cholesterol, Triglyceride and Phospholiped in the serum and in the α fraction were determined by the enzymic methods for each sort of lipids. respectively (TC, TG, PL, αLPC, αLPG and αLPPL). Content of lipids in β fraction, βLPC, βLPG and βLPPL was calculated.
Results:
I. Cases of Normolipemia
a) Contents of each sort of lipids in α and β lipoprotein fractions
Increases of the content of TC and TG in serum were proportional to age, but the content of PL was the highest in the middle aged group. αLPC (=HDL-cholesterol) level was nearly the same in each of three groups, whereas αLPG was the highest in the middle aged. The age-dependent decrease of αLPPL especially in the senescent group and the age-dependent increase of βLPPL and of βLPC were really remarkable.
b) Lipoprotein lipid ratios
The ratios of the same kind of lipids in α and β fraction and those of the different kinds of lipid in α and β fraction were calculated. Each ratio in the young, in the middle aged and in the senescent group was compared with each other. Four ratios among them, βLPC/αLPC, βLPPL/αLPPL, βLPC+βLPPL/βLPC+αLPPL and αLPC+αLPG/αLPPL were age dependent.
II. Cases of Hyperlipidemia
The mild hyperlipidemic subjects, up to 350mg/dl of TC and 250mg/dl of TG were selected and into three groups, hypercholesterolemia, hypertriglyceridemia and hypercholesterol plus hypertriglyceridemia. In young and middle aged groups slight increase of βTLP and slightin crease of αTLP were observed in hyper TC group, whereas decrease of αTLP and the distinct increase of βTLP were clearly demonstrated in hyper TG group. From the results some essential differences may be assumed between senescent and young or middle aged hyperlimidemia.

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A newly established immuno-precipitation method for the fractionation of human serum into α and β lipoprotein fraction using specific goat antiserum (purified γ-globulin fraction of it) against human γ lipoprotein was applied to the serum of the patient of Kawasaki disease.
Cholesterol, triglyceride and phospholipid in the serum and in the α fraction were determined by the enzymic methods for each sort of lipids, respectively (TC, TG, pL, αLpC, αLpG and αLppL). Content of lipids in β fraction, βLpC, βLpG and βLppL was calculated.
Results are as follows.
1) Comparison between the lipids of MCLS at the acute stage and those of normal children. TC and pL in the acute stage were lower than those of normal controls, whereas TG was higher in patients than that in normals. Lipids in α fraction, especially αLpC and αLppL, were distinctly lower in the patient; lipids in β fraction, on the contrary, higher in the patient. Lipoprotein lipid ratios of β/α (total lipid in β fraction/total lipid in α fraction=βTLp/αTLp, in the same manner βLpC/αLpC and βLppL/αLppL) were distinctly elevated in the patient.
2) Comparison of the early stage and the convalescent stage. TC, pL, αLpC, αLpG and αLppL in the convalescence were distinctly higher than those in acute stage. The increase of the content of lipids of α fraction in convalescence of the disease made a dicided contrast with the decrease of those of β fraction in the convalescence in the case of AMI.
3) Resemblance of lipoprotein lipid ratios in viral disease to those in MCLS. There were 14 cases of hypo-α-lipoproteinemia (Hypo-αLpC) in 140 cases of the other disease in this study. In those 14 cases, 7 cases were diagnosed as viral disease; all of 7 cases of the viral disease were Hypo-αLpC. It may be worth noticing, therefore, that the Hypo-αLpC was demonstrated in all viral disease and that the ratios of the lipoprotein lipids of them were closely resembled to those of MCLS.

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Influences of lipid deficiency on cholesterol metabolism in cultured human skin fibroblasts were studied.
Incubation of fibroblasts with lipoprotein-deficient serum (LPDS) for 24hr resulted in a decrease of cellular phospholipids, especially phosphatidylcholine, while cholesterol level was unchanged. The extent of incorporation of ¹⁴C-acetate into sterols was higher than that of fibroblasts cultured in normal medium. These results suggested that at 24hr the fibroblasts were undergoing the destruction of plasma membrane though the cells were still capable of synthesizing cholsterol actively.
After incubation of fibroblasts for 48hr in LPDS, cholesterol content decreased by about 22% and there appeared cholesterol esters in the medium, indicating that the fibroblasts had been exhausted by lipid deficiency and plasma membrane had disintegrated to larger extent.

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Thirty patients with acute cerebral infarction (thrombosis) were studied for. clinical features, brain computed tomograms, serum lipids, and platelet functions before and after treatment with anti-platelet drug acetyl salicylic acid (ASA) for preventing re-infarction. Twenty-four of 30 patients had abnormal low density areas on computed tomograms, but 6 patients did not have such findings.
A statistically significant rise in hematocrits, lipid peroxides and platelet adhesiveness, and a significant fall in HDL-cholesterols and platelet aggregation were observed in these patients as compared with age and sex matched controls. Platelet counts of these patients were moderately lower than those of the normal subjects. At 4 to 8 weeks after onset of these crebral infarctions, there were significant increases in platelet counts and significant decreases in hematocrits. It was suggested that the discrepancy of platelet functions was due to platelet consumption and its consequence in acute cerebral infarction.
The anti-platelet therapy was started with administration of 1gm of ASA once-daily, and the dosage of ASA was regularly checked by measuring the platelet functions with platelet counts, hematocrits, bleeding times, collagen or ADP induced platelet aggregability and platelet adhesiveness. Platelet counts and hematocrits were not affected by ASA. ADP induced platelet aggregation as well as platelet adhesiveness was not always reduced by ASA, and furthermore, there were considerable differences with the effectiveness of ASA on these platelet functions in individuals. However, ASA produced the dose responsive effects on prolongations in the bleeding time and on reductions in the collagen induced aggregation in each patient. Accordingly, the dosage of ASA should be decided by measuring the bleeding time and/or collagen induced platelet aggregation.

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A simple and precise HDL-cholesterol estimation method using precipitation procedure with heparin and Ca⁺⁺ was descrived.
To 0.1ml of serum was added 2.0ml precipitation reagent containing 50ml/dl of heparin and 25mM of CaCl₂. Samples were mixed throughly and allowed to stand at 4°C for 20mim before centrifugation at 4°C and 1, 500 G for 15mim. Cholesterol in the supernate was measured by enzymatic method.
Separation of HDL was examined on the Ouchterlony double diffusion method. A precipitation reaction with anti α-lipiprotein (HDL) antibodies was found only in the supernte and anti β-lipoprotein (LDL plus VLDL) line only in the precipitate.
The precision of the present method appeared excellent (CV, 0.90-1.2%). A regression anlysis of the data obtained using ourmethod (Y) compared to ultracentrifugation method (X): Y=1.017X+0.72(mg/dl), and r=0.986
The heparin-Ca⁺⁺ precipitation method seams feasible in the routine clinical laboratory use.

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The present studies were undertaken in order to elucidate the effects of oxygen inhalation on plasma lipids and atherogenesis.
Eleven male Japanese white rabbits were fed on standard rabbit pellet plus 1% cholesterol. Six among 11 rabbits were exposed to 40% oxygen (hyperoxic) and 5 were exposed to 21% oxygen (control), respectively, for 5 hrs on 5 days of each week for 8 weeks. Obtained results were as follows:
1) Degree of the sudanophilic aortic lesion in hyperoxic rabbits was less than control, especially in the aortic arch and the abdominal aorta.
2) There were no differences of hydroxyproline contents of the aortic intima and media between both groups.
3) Levels of plasma lipids (cholesterool, triglyceride, phospholipid and lipoperoxide) were greatly increased in both groups.
4) A slight increase in HDL cholesterol was seen, but there were no differnces between both groups.
From these results, it is postulated that the progress in atheromatous change of the aorta may be supressed by oxygen inhalation not through the change in pattern of the plasma lipids, but through the direct effect on the aortic wall. We proposed a hypothesis that tissue hypoxia induced by hyperlipidemia might play an important role in the early deposition of lipids in the aortic wall.

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Age- and sex-related characteristics of myocardial infarction were examined with reference to cornary risk factors and coronary arterial lesions. Eightyone patients (male; 70, female; 11 mean age; 53.5 years old) with myocardial infarction were studied by coronary angiogarphy. The results are as follows:
1) Under 39 years old, 36% of this group had nonatherosclerotic artery disease and/or angiographically normal coronary arteries. 64% had coronary atherosclerosis. In this group, patients with coronary atherosclerosis had higher scores of the risk factors compared to the older patients.
2) In the groups aged between 40 to 59 and above 60 years old, the main cause of myocardial infarction was atheromatous coronary disease. Cigarette smoking and hypertension were two main risk factors in these groups.
3) HDL-Cholesterol was lower and T-Cholesterol/HDL-Cholesterol was higher in the group aged below 39 years old with atherosclerotic coronary artery.
4) In old women, two main risk factors were hypertriglyceridemia and hyperbetalipoproteinemia.
5) There were tendencies of higher mean age in the reinfarction group than in the single infarction group. The patients with reinfarction had lesser collateral coronary arteries than single infarction group. Cigarette smoking and hypertension were two dominat risk factors in reinfarction group.

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Serum levels of lipid and lipoprotein fasting triglyceride, total cholesterol and high density cholesterol (HDL-C) in the aorta and the coronary sinus were measured in 40 patients with coronary heart disease (average 56.4y/o) and 10 with noncoronary heart disease (average 49.1y/o) by means of enzyme method, heparin Ca²⁺ and O-phthalaldehyde method. The results were as follows.
1) T-chol. HDL-C and TG concentration of coronary sinus were significantly lowere than that of aorta in both group.
2) Δ TG (aortic TG-coronary sinus TG) was inversely related to severity of coronary artery disease.
3) Δ Fatty acid degradated from triglyceride was about two times higher than that of free fatty acid.

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In order to evaluate the left ventricular function in patients with myocardial infarction, echocardiographic analysis of the left ventricular function was made during ergometer exercise with monitoring heart rate, blood pressue, ECG and Symptom.
The materials consisted of 23 patients with myocardial infarction and 20 normal subjects as a control. The graded exercise was performed in supine position on the bed. Echocardiographic parameters, such as % change in diameter (%ΔD), maximal posterior wall velocity in systole (Max PWV), maximal posterior velocity in diasole (-Max PWV), % change in thickness of the septum (%ΔThs) and that of the posterior wall (%ΔThp), were measured at rest, during and after exercise. In the patients with myocardial infarction, echocardiographic indicies revealed abnormal motions of the wall including infarcted area and impaired left ventricular function after exercise. This tendency was not found out in the control group. Exercise echocardiography appears to be useful to detect wall motion abnormalities and to evaluate cardiac function of the patients with myocardial infarction.

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Serum cholesterol, triglyceride and high density lipoprotein (HDL) cholesterol were measured in 41 consecutive male patients with cineangiogra-phically defined coronary artery disease (CAD). 96 first- and second-degree relatives of 7 patients with type IV hyperlipoproteinemia were also investigated.
The HDL cholesterol was significantly lower in patients and in male relatives of 20-60 years old than in controls, but there was slight decrease in female relatives and children. Serum triglyceride was significantly higher in patients and in male relatives of 20-60 years old than in controls, but there was no increase in other family members. No increase of serum cholesterol was found in patients and relatives.
The results suggest that HDL cholesterol and triglyceride are related not only to genetic factors but also to sex and age factors.

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The immuno-precipitation method for the fractionation of human serum lipoprotein into α and β lipoprotein, using the specific goat antiserum against human α lipoprotein as reported in our 1st report, was used for the present study of adute myocardial infarction (AMI).
Results: Comparison of acute stage and convalescence is follows.
a) Triglyceride was decreased significantly in convalescence.
b) α-lipo-cholesterol (αLpC) and α-lipo-phospholipid (αLppL) were increased significantly in convalescence.
c) αLpC/TC, αLpG/TG and αLppL/PL were significantly higher in convalescence.
d) (αLpC+αLpG)/αLppL was significantly lower in the convalescence than these in the acute stage, whereas the αLppL/(αLpC+αLpG) ratio was nearly the same.
From the results, authors assume that not only HDL-cholesterol (≈LpC) but also the content of lipids in α or β fraction and some of the lipoprotein lipid ratios are available for the research of of the lipid metabolism in the disease.

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The atrial fibrillation is the arrhythmia which is frequently encountered in the valvular disease of the heart. The authors have investigated the conduction system and its supplying arteries by light microscopical study on serial section. The cases subjected for investigation were as follows; Aortic valvular disease (AVD) 4, Mitral valvular disease (MVD) 4, and Combined valvular disease (CVD) 5 cases. A special attention has been paid for the correlation of the ECG findings with histo-pathological observations of conduction system and of its supplying arteries. The histo-pathological study revealed that the extensive loss of conduction cells as well as the sclerotic involvement of the central artery was noted in the cases having atrial fibrillation of the long term duration. Concerning to the Sino-Atrial node, injury to the S-A node and its supplying artery was much more striking in the cases of MVD & CVD rather than ADV. The chages of A-V node and His Bundle were more remarkable in the cases of AVD & CVD compared with MVD. The authors incline to attribute the genesis for these pathological changes of conduction system and of its supplying arteries to the circulatory disturbance involved in the heart valvular disease. The persisting derangement of the circulation in the supplying arteries of these region would result in their sclerotic shanges and in loss of conduction cells. These changes were much more pronounced than those of age matched controls.

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To study about the chemical components of serum glycoprotein (GP) in ischemic heart diseases (IHD), column chromatography of Sephadex G-100 and cellulose electrophoresis were performed on sera in 6 cases of angina pectoris (AP), 10 cases of acute myocardial infarction (AMI), 10 cases of old myocardial infarction (OMI) and 10 cases of Healthy person (PH).
The results as follows
1) Total serum GP is higher in AP, AMI and OMI than in that of HP.
2) Serum GP was fractionated into Fraction I (Fr I) and Fraction II (Fr II) by column chromatography. The molecular size was in order of FrI<Fr II. The concentration of Fr I was higher in AP, AMI and OMI than in that of HP, but the concentration of Fr II was higher only in AMI than in that of HP.
3) Fr I was separated into three fractions of α₂, β-and γ-GP by electrophoresis.
Fr II was separated into four fractions of α₁, α₂-β-and γ-GP by electrophoresis.
4) In AP and OMI, α₂-GP of Fr I, γ-GP of FrI and γ-GP of Fr II were higher than in that of HP
In AMI, α₁-GP of Fr I, α₁-GP of Fr II, β-GP of Fr II and γ-GP of Fr II were higher, and β-GP of Fr I and α₂-GP of Fr II were lower than that of HP.
5) The components of serum GP in IHD were different from those in HP.

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To study the relationships between the daily changes in acute stage of serum glycosidase activity and the prognosis of the stroke, serum N-acetyl-β-D-glucosaminidase (NAGA), β-D-galactosidase and α-L-fucosidase activities were measured in 7 survival cases and 5 death cases, totaling 12 cases.
1. The pattern of the changes of serum NAGA activity in the survival cases was different from those in the death cases, that is, in the former, NAGA activity was most increased in a few days from attack day and the increased enzyme activity continued, but in the latter, the increased enzyme activity reduced at the period of the death. Also, although the other two enzyme activities changed in the course from attack, no differences were showed between the survial cases and the death cases.
2. The measurement of serum NAGA activity is useful in the prognosis of CVD.

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Active substances for lipid metabolism were separated from the extract of Corbicula sandai in organic solvent and identified as α, α′-and α, β-diglycerides of 2-octadecenoic acid.
The synthetic mono-unsaturated fatty acid as well as diglyceride with the same structure to the natural compounds could inhibit the triglyceride accumulation in fatty liver of rats and reduce hypertriglyceridaemia induced by alcohol ingestion.

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Twenty patients with hyperlipidemia (total cholesterol≥220mg/dl) were treated with γ-Oryzanol of 300mg/day for 16 weeks, during which time changes in serum lipid levels were observed.
Both total cholesterol and HDL-cholesterol were reduced significantly within 4 and 12 weeks, respectively, following the treatment with γ-Oryzanol, with the degree of changes in both being almost identical. Therefore, the atherogenic index was not significantly changed.
Levels of triglycerid and β-lipoprotein were significantly reduced at 12 and 16 weeks following medication, respectively, while those of phospholipid and free fatty acid were unchanged.
No complications were found in any of the patients with this medication.

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Pantehtine has been revealed to be effective to reduce serum cholesterol in diabetic patients with hyperlipidemia. The effect of pantethine on lipid metabolism was examined in the hypercholesterolemic rabbits from the view points of prophylactic effect on hyperlipidemia, fatty liver and atherosclerosis.
Fourteen New Zealand white rabbits were divided into two groups. All rabbits were fed with a diet containing 1% cholesterol for 3 months and six out of them were concomitantly administered pantethine 600mg daily by stomach tube.
Serum cholesterol of the pantethine group was 1557mg/dl as compared to 1978mg/dl of the controls, associating with higher alpha and pre beta-lipoproteins and lower beta-lipoprotein in the pantethine group than the control group after three months experiments. The concentration of free cholesterol, phosphilipid and malondialdehyde in the liver homogenate were significantly lower in the pantethine group than in the control. Atheroscelrotic lesion of the aorta was also significantly less in the pantethine group than in the control. These data suggest that pantethine can prevent hypercholesterolemia, fatty liver and atherosclerosis in the experimetal hypercholestrolemic rabbits.

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Fourteen New Zealand white rabbits were divided into two groups. All rabbits fed with a diet containing 1% cholesterol for 3 months and six out of those were concomitantly administered 600mg pantethine daily by stomach tube. Platelet microviscosity, adenine nucleotide content, lipid composition, aggregation and adenine nucleotide release were examined before, the first, the second and the third month of experiments.
The platelets obtained from the hypercholesterolemic rabbits had an increased microviscosity, free cholesterol and phospholipid accompanying with a hyperaggregability induced by ADP, arachidonic acid and collagen in vitro.
Pantethine administered concomitantly protected significantly an increase of microviscosity, free cholesterol and phospholipid of such hypercholesterolemic platelets. The platelets obtained from pantethine treated rabbits had a higher ATP and ADP than either one of normal or hypercholesterolemic rabbits.
These physico-biochemical modification of platelets by pantethine administration corrected the hyperaggregation found in hypercholesterolemic rabbits. These results suggested that pantethine is effective tp prevent the qualitative alterations of platelets provoked in hypercholesterolemic rabbits.

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