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Oxidative modification of LDL plays an important role in early atherogenesis but the mechanisms, nonenzymatic and/or enzymatic, by which LDL is oxidized in vivo remain to be established. Several lines of evidence suggest that cellular 15-lipoxygenase (arachidonate 15-oxidoreductase, EC.1.13.11.13) (15-LO) may contribute to oxidative modification of LDL, including recent studies demonstrating that murine fibroblasts overexpressing 15-LO have an enhanced capacity to oxidize LDL in the medium. The present studies were undertaken to better understand the mechanisms by which cells expressing 15-LO bring about oxidative modification of LDL. LDL incubated 1-2 h with the 15-LO-enriched cells showed a much higher lipoperoxide (LOOH) content than did LDL incubated with control cells. By far the largest absolute increase occurred in cholesteryl ester hydroperoxide (CE-OOH), a much lesser increase in free fatty acid hydroperoxides (FFA-OOH), and only a very small increase in phospholipid hydroperoxides (PL-OOH). Addition of EDTA to the medium abolished these increases in LDL lipid hydroperoxides. Enrichment of LDL with probucol or vitamin E also prevented CE-OOH accumulation. Incubation of LDL with linoleic acid hydroperoxide in the absence of cells also caused a significant increase in CE-OOH and this was markedly inhibited by EDTA. These findings provide further evidence for the potential of 15-LO to participate in LDL oxidation by way of a mechanism involving introduction of LOOH into the LDL particle followed by metal-catalyzed propagation.

There is strong experimental evidence that oxidized low density lipoprotein (Ox-LDL) plays an important role in atherosclerosis. However, the mechanisms by which Ox-LDL is formed in vivo are unknown. To test whether 15-lipoxygenase (15-LO) could play a role in oxidation of LDL by cells, we expressed 15-LO activity in murine fibroblasts, which do not normally have 15-LO activity, and tested their ability to modify LDL. Using a retroviral vector, we prepared fibroblasts that expressed 2- to 20-fold more 15-LO activity than control fibroblasts infected with a vector containing beta-galactosidase (lacZ). Compared with LDL incubated with lacZ cells, LDL incubated with 15-LO-containing cells were enriched with lipid hydroperoxides. When these LDL samples were subsequently subjected to oxidative stress, they were more susceptible to further oxidative modification, as judged by increased conjugated diene formation and by increased ability to compete with 125I-Ox-LDL for uptake by macrophages. These findings establish that cellular 15-LO can contribute to oxidative modification of LDL, but the quantitative significance of these findings to the in vivo oxidation of LDL remains to be established.

The effects of hemostatic substances on the vascular tone in porcine coronary arteries and the influence of low density lipoprotein on tension were investigated. Thrombin induced a marked concentration-dependent relaxation in prostaglandin F2 alpha-precontracted strips with intact endothelium, whereas it produced a modest constriction in endothelium-denuded arteries. Methylene blue abolished the relaxation, but indomethacin did not affect it significantly. An exposure of the intact strips to low density lipoprotein resulted in a marked inhibition of the relaxation to thrombin but did not interfere with vasodilation by sodium nitroprusside. The inhibition by low density lipoprotein was reversed completely by washing. In contrast, high density lipoprotein lacked such inhibitory effects. Adenosine diphosphate, calcium ionophore A23187, and platelet-activating factor also produced relaxation in the intact strips. An exposure of the strips to low density lipoprotein almost abolished relaxation to these substances. The inhibition was also reversible. Heat treatment or acid treatment of low density lipoprotein resulted in a complete loss of the inhibitory effects, but diisopropyl fluorophosphate treatment did not alter the effect. It is concluded that low density lipoprotein may play a new pathological role in promotion of coronary vasospasm through rapid and reversible inhibition in endothelium-dependent relaxation to hemostatic substances.

Two cases of Larsen's syndrome, that we have recently experienced, were reported.Case I, a male, aged 10 years, was born via an uncomplicated delivery.Case II, a female, aged 6 years.They had prominent forehead and wide spaced eye.They had bilateral hip, knee and elbow dislocations. In addition, they had foot deformity.Radiographic studies showed abnormalities.They had extra calcaneal ossification, short metacarpals, supernumerary carpal bones and anormalous segmentation of vertebrae.

In treating cervical spondylosis, we first, chose concervative therapy such as head halter traction, cervical brace and medication.In 14 cases not improved by these conservative metods we, after determining the exact level of the spondylosis, performed the operation of “anterior cervical fusion”.One of the most important factors in performing anterior cervical fusion is to decide the correct level of the spondylosis as this procedure affects the success of the operation.It is relatively easy to decide the level if the plain-X ray shows the degeneration in only one vertebra. However, if it reveals degenerative findings in more than one, it becomes necessaary to perform further investigations such as Musle Testig, EMG, Myelography, and Discography, during operation, in addtion to the clinical neurogical examinations. We did not perform fusion of more than two intervertebral spaces.

We report the four cases of the spinal cord tumor which we have experienced recently.Case 1. female … aged fifty was a neurinoma occured in the canda equina.Case 2. female … aged thiry five was a epidermal cyst occured in the nineth thoracic vertebral region.Case 3. male … aged fifty seven intramedullary astrocytoma which occured in the region of the fourth thoracic vertebrae.Case 4. female … aged eighteen was a meningioma occured in the extradural space of the fourth and fifth thoracic vertebrae.In the case 1. 2. 4. tumors were operatively almost completely resected, but in the case 3. unable to resect. Consequently in the former, symptom (sensory and motor disturbance) has obviously improved and deminished, but in the latter not improved and deteriorated.

Primary hyperparathyroydism in childhood is a rare occurence.The present report is of a 13-year-old girl who explained of pain and varus deformity of the hip joint for 2 years.On the laboratory examinations, hypercalcemia, hypophosphatemia, hypercalciuria, hyperposphaturia and increased serum alkaline phosphatase were found.Parathyroid gland function tests were of its hyperfunction.On the radiographic examination of long bones, skull and fingers, diffuse resorption and cystic areas wewe seen. A small tumor was found at the right lower pole of the thyroid.A diagnosis of primary hyperparathyroidism was made and surgical exstirpation was performed. The histological diagnosis was a chief cell adenoma of parathyroid gland.After exstirpation, serum calcium and phosphorous concentration gradually become within normal limmits and hip pain was diminished. Lately we performed valgus osteotomy of the Femur, for its varus deformity.