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Biomedical subjects

M Naka

Publications and source records attributed to M Naka.

114 records · Page 7Linked to original sources
PubMed1974

Pleiotropic alteration of activities of several toxins and enzymes in mutants of Staphylococcus aureus.

Pleiotropic alteration of several genetic characters including toxin production was quantitatively shown with a strain of Staphylococcus aureus of phage type 80, 81 which had been given a very specific genetic marker (temperature sensitivity of mannitol fermentation) to avoid confusion by contamination. Thus, alpha-hemolysin hyperproducers obtained by N-methyl-N'-nitro-N-nitrosoguanidine (NTG) mutagenesis were very often hyperproducers of DNase, coagulase, and protease. Their colonies were less yellow than the parent. DNase hyperproducers obtained after NTG mutagenesis were also often hyperproducers of alpha-hemolysin, coagulase, and protease, with colonies less yellow than the parent. Almost all of the revertants obtained by mutagenesis with ethyl methane sulfonate with respect to alpha-hemolysin or DNase were shown to have simultaneously become hypoproducers of alpha-hemolysin, DNase, and protease. Since the pleiotropic alteration of multiple functions was thus quantitatively confirmed, the mechanism underlying this phenomenon should probably be related to a regulatory mechanism common to them.

Alkanesulfonates↗
PubMedDate not supplied

Phorbol ester-induced activation of human platelets is associated with protein kinase C phosphorylation of myosin light chains.

Phosphorylation of the 20,000 molecular weight (MW) light chain of platelet myosin is associated with the activation of platelets and subsequent release of platelet granules, and the protein kinase catalysing this phosphorylation has been identified as the Ca2+/calmodulin-dependent enzyme, myosin light chain kinase. Tumour-promoting phorbol esters such as 12-O-tetradecanoylphorbol-13-acetate (TPA), which activate Ca2+-activated, phospholipid-dependent protein kinase (protein kinase C), can also cause platelet aggregation and phosphorylation of a 20,000-MW peptide in blood platelets. It was therefore of interest to ascertain whether the 20,000-MW peptide phosphorylated in platelets was the light chain of myosin and whether TPA-induced phosphorylation of the 20,000-MW peptide could be differentiated from thrombin-induced phosphorylation. We now report that TPA-induced activation of platelets is associated with the phosphorylation of the 20,000-MW light chain of myosin, that it appears to be mediated mainly through protein kinase C and that the site phosphorylated in the myosin light chain is distinct from that phosphorylated by myosin light chain kinase.

Blood Platelets↗
PubMedDate not supplied

Cardiac abnormalities in ischemic cerebrovascular disease studied by two-dimensional echocardiography.

In the study of cardiac abnormalities responsible for the development of cerebral embolism two-dimensional echocardiography was performed on 350 patients with ischemic cerebrovascular disease. The results were compared with those obtained from 350 controls without any history of stroke. Atrial fibrillation was detected on ECG in 115 cases (33%) of the patients and in 35 cases (10%) of the controls (p less than 0.001). The structural cardiac diseases observed in stroke patients were: rheumatic heart disease (RHD) in 37, congestive cardiomyopathy (CCM) in 7, hypertrophic cardiomyopathy (HCM) in 19, mitral annulus calcification (MAC) in 29, mitral valve prolapse (MVP) in 9, and myocardial infarction (MyI) in 10 patients. Controls were found to have these lesions in 11, 2, 3, 12, 4 and 9 patients respectively. RHD (p less than 0.001), HCM (p less than 0.01) and MAC (p less than 0.01) were significantly more frequent in patients with ischemic cerebrovascular disease, but not MyI, CCM or MVP. Intracardiac thrombi were diagnosed in 29 cases of patients and in 4 cases of controls (p less than 0.001). Our data suggested that nonrheumatic heart diseases such as MAC and HCM could also be considered as causes of embolic stroke. The reasons for the variable frequencies of cardiac abnormalities reported in the literature for stroke patients are discussed.

Adult↗
PubMedDate not supplied

A case of sarcoidosis associated with bronchial asthma.

A 54-year-old woman was treated for bronchial asthma for 14 yr. In March of 1989, chest roentgenography and computed tomography (CT) revealed development of bilateral pulmonary hilar lymph node enlargement. Positive 67Ga uptake was observed in bilateral pulmonary hili. Although levels of serum angiotensin converting enzyme (ACE) and lysozyme were within normal range, biopsy specimen of scalene lymph nodes showed noncaseating epitheloid-cell granuloma, leading to the diagnosis of sarcoidosis. Steroid therapy ameliorated both sarcoidosis and bronchial asthma. Although the association of sarcoidosis and bronchial asthma is uncommon, there may be an etiological relationship between them.

Asthma↗