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Biomedical subjects

H Fukuda

Publications and source records attributed to H Fukuda.

At least 1,081 records · Page 60Linked to original sources
PubMed1983

Centrally specific and GABA-insensitive inhibition of benzodiazepine binding by prostaglandins (A1, A2 and B2).

Prostaglandins A1, A2 and B2 (PG A1, A2 and B2) dose-dependently inhibited specific [3H]diazepam binding to rat brain membranes but did not affect specific [3H]Ro 5-4864 binding to kidney membranes. The inhibition of [3H]diazepam binding to brain membranes by benzodiazepine agonists (diazepam and flurazepam) was potentiated by 30 microM GABA, whereas those of prostaglandins were not modified by the same concentration of GABA. These results suggest that PG A1, A2 and B2 specifically interact with central type-benzodiazepine receptors in a manner different from interactions seen with benzodiazepine agonists.

Animals↗
PubMed1983

Effects of zopiclone and benzodiazepines on spinal reflexes, anemic decerebrate rigidity and benzodiazepine binding.

Whether or not zopiclone, a new sleep-inducing drug, exerted a similar effect to that of benzodiazepines was examined. The drug inhibited crossed extensor reflexes in chicks and augmented the dorsal root-dorsal root reflexes in rats without affecting the mono- and polysynaptic reflexes. The site of its action was considered to be located in the spinal cord since the effect on the dorsal root reflex was observed also in the spinal rats. Zopiclone selectively reduced the phasic responses of anemic decerebrate rigidity like benzodiazepines in rats. Despite the structural difference from the benzodiazepines, zopiclone dose-dependently inhibited [3H]flunitrazepam binding in rat brain membranes, although the potency was weaker. These results suggested that zopiclone exerts CNS actions via benzodiazepine receptors.

Animals↗
PubMed1983

Studies on the T3 suppression test by the 24-hour thyroidal 131I uptake in patients with Graves' disease: comparison of the effects of propylthiouracil and methylmercaptoimidazole.

The T3 suppression test by the 24-hr thyroidal 131I uptake was reevaluated in patients with Graves' disease before and after withdrawal of antithyroid drug. Fifty patients had been treated with propylthiouracil (PTU) or methylmercaptoimidazole (MMI) for 12 to 70 months. They were prescribed a maintenance dose of antithyroid drug (PTU, 50 mg/day; MMI, 5 mg/day) at the time of investigation and regarded as euthyroid on the basis of serum T3, T4 and TSH levels. Each patient was given 75 micrograms T3 daily for 8 days in conjunction with PTU or MMI. The 24-hr thyroidal 131I uptake was then measured (post T3 uptake). In 30 patients whose post T3 uptake was below 35%, treatment was stopped and the T3 suppression test was repeated at one and 3 months later. During the two-year follow up, 24 remained well, while 6 relapsed within 4 to 12 months. In patients with sustained remission, the post T3 uptake was significantly lower in the MMI-treated group (13 cases, 7.7 +/- 1.0%) than in the PTU-treated group (11 cases, 18.6 +/- 1.9%). MMI withdrawal produced a marked rebound in the post T3 uptake, whereas none of the patients showed the rebound after PTU withdrawal. In patients who relapsed later, there was no difference in the post T3 uptake during treatment and the rebound occurred in the both groups following goitrogen withdrawal. Serum T3, T4 and TSH levels were within normal ranges at one and 3 months after cessation of antithyroid drug. From the results of the present study, it is concluded that criteria for T3 suppressibility by the 24-hr uptake should be determined by the antithyroid drug employed and by the time of investigation. There is a dissociation in the post T3 uptake values following withdrawal of the two different antithyroid drugs.

Antithyroid Agents↗
PubMed1983

A case of idiopathic hypertrophic obstructive cardiomyopathy causing severe right ventricular outflow tract obstruction in infancy.

An infant with idiopathic hypertrophic obstructive cardiomyopathy, presenting as severe right ventricular outflow obstruction, is described. The nonspecific clinical features and an unexpected angiocardiographic appearance made determining the correct diagnosis difficult. This infant was mistakenly diagnosed as having severe pulmonary stenosis. Attempted surgical correction was unsuccessful and at necropsy this diagnosis was confirmed. It is suggested that cross-sectional echocardiography may be diagnostic for infants with idiopathic hypertrophic obstructive cardiomyopathy.

Cardiac Catheterization↗
PubMed1983

Effects of high-fructose diet on lipogenic enzymes and their substrate and effector levels in diabetic rats.

When rats adapted to a stock diet were fed on various high-carbohydrate diets, the hepatic activities of glucose-6-phosphate dehydrogenase, malic enzyme and acetyl-CoA carboxylase were more greatly increased by fructose than by any other carbohydrate. Even in the diabetic state, the enzyme activities were somewhat increased by fructose feeding. After feeding on the diets for 9 days, the hepatic concentrations of intermediates of carbohydrate metabolism were generally lower in the diabetics than in the normals. Moreover, in both the normal and diabetic rats, the concentrations of fructose-1-phosphate, acetyl-CoA, citrate and malate were increased by fructose as were the enzyme activities. These results suggest that the metabolic pathway of fructose is predominant with respect to that of glucose and consequently lipogenesis may be able to be increased in the fructose-fed rats.

Acetyl Coenzyme A↗
PubMed1983

Cuff-tear arthropathy.

In this report we describe the clinical and pathological findings of cuff-tear arthropathy in twenty-six patients and discuss the differential diagnosis and a hypothesis on the pathomechanics that lead to its development. This lesion is thought to be peculiar to the glenohumeral joint because of the unique anatomy of the rotator cuff. Following a massive tear of the rotator cuff there is inactivity and disuse of the shoulder, leaking of the synovial fluid, and instability of the humeral head. These events in turn result in both nutritional and mechanical factors that cause atrophy of the glenohumeral articular cartilage and osteoporosis of the subchondral bone of the humeral head. A massive tear also allows the humeral head to be displaced upward, causing subacromial impingement that in time erodes the anterior portion of the acromion and the acromioclavicular joint. Eventually the soft, atrophic head collapses, producing the complete syndrome of cuff-tear arthropathy. The incongruous head may eventually erode the glenoid so deeply that the coracoid becomes eroded as well. Although treatment of cuff-tear arthropathy is extremely difficult, the preferred method appears to be a resurfacing total shoulder replacement with rotator-cuff reconstruction and special rehabilitation. We think that it is important to recognize cuff-tear arthropathy as a distinct pathological entity, as such recognition enhances our understanding of the more common impingement lesions. Cuff-tear arthropathy is especially difficult to treat, and although many tears of the rotator cuff do not enlarge sufficiently to allow this condition to develop, it is a factor to consider when deciding whether or not a documented tear of the rotator cuff should be surgically repaired.

Aged↗