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Biomedical subjects

N Cooper

Publications and source records attributed to N Cooper.

At least 73 records · Page 4Linked to original sources
PubMed1975

Phagocytes and C4 in paraproteinaemia.

Immunological studies were performed on patients with multiple myeloma. A defect in polymorphonuclear leucocyte (PMN) function as evidenced by diminished adherence of these cells to nylon fibre columns was detected in 16, and low levels of the fourth component of complement (C4) were observed in 14, of the 26 patients studied. Twelve of the patients with low C4 exhibited the defect in PMN adhesiveness whereas only four of the 12 patients with normal C4 showed the defect. The PMN defect was not caused solely by the low C4, since PMNs from seven patients with hereditary angioedema, which is associated with low levels of C4, did not show the defect. The low C4 and defect in PMN adhesiveness occurred primarily in patients with IgG myeloma; all but one of the patients with IgA myeloma, macroglobulinaemia, or light chain disease were normal in both parameters. Results of skin window studies indicated that patients with the PMN defect also had a defect in the early PMN inflammatory response. The defect in PMN adhesiveness could be completely corrected by incubating the cells in normal plasma. Binding of the C4 to paraprotein could not be demonstrated, and C1 activation was found to be caused only by one of 10 isolated paraproteins studied. These studies indicate that patients with paraproteinaemia have immunological abnormalities in addition to low immunoglobulin levels and suggest that these abnormalities may be involved in the pathogenesis of the recurrent infections commonly associated with this disease.

Adult↗
PubMed1975

Effects of systemic-pulmonary shunts on regional myocardial blood flow in experimental pulmonary stenosis.

The pulmonary artery of anesthetized dogs was constricted until right ventricular failure occurred (decreased cardiac output and aortic blood pressure; elevated right ventricular end-diastolic pressure). Coronary blood flow distribution was measured by means of an electromagnetic flowmeter and radioactive microspheres. With moderate levels of pulmonary stenosis (right ventricular pressure to 60 per cent of systemic pressure), right ventricular coronary flow increased (30 per cent, p smaller than 0.01) despite a significant fall in right ventricular driving pressure (aorto-right atrial pressure). Right ventricular failure occurred when right ventricular coronary flow did not increase sufficiently to meet raised oxygen requirements. Opening a pulmonary-systemic shunt during right ventricular failure increased pulmonary blood flow but lowered coronary driving pressure further, as blood was diverted into the lungs through the low-resistance fistula. Consequently, right ventricular coronary flow fell 50 per cent (p smaller than 0.01) and right ventricular failure with pulmonary stenosis resulted in a 362 per cent (p smaller than 0.01) increase in right coronary flow plus improved cardiac output. We made the following conclusions: (1) Right ventricular failure with pulmonary stenosis and intact ventricular septum is due to inadequate right ventricular blood flow to meet raised oxygen demands; (2) opening a pulmonary-systemic shunt may potentiate this failure and exaggerate ischemia by lowering coronary driving pressure and reducing right ventricular coronary flow.

Animals↗
PubMed1975

Depressed cardiac performance after mitral valve replacement. A problem of myocardial preservation during operation.

Our experimental studies since 1972 show that the heart is preserved best during cardiopulmonary bypass when it is in the beating, nonworking state. Results after mitral valve replacement (MVR) from 1968 to 1974 using various techniques of cardiac preservation were compared. In group I were 47 patients (1968 to 1972) in which either profound, topical hypothermia with prolonged ischemic arrest (19) or ventricular fibrillation with continuous coronary perfusion (28) was used. In group II there were 22 patients (1972 to 1974) in whom the heart was in a beating, nonworking state between brief periods of ischemic arrest. In group I 55% (25/47) required inotropic support postoperatively, and 17% (8/47) died. In group II 5% (1/22) required inotropic support postoperatively, and this patient died (5% mortality). Extended periods of ischemic arrest were necessary because of intraoperative complications in this patient. These data show that depressed postoperative myocardial performance occurs rarely when the heart is preserved in the beating, nonworking state during MVR and ventricular fibrillation and prolonged topical hypothermic anoxic arrest are avoided.

Extracorporeal Circulation↗
PubMed1974

Regulation of synthesis of two immunologically distinct nucleic acid-dependent nucleoside triphosphate phosphohydrolases in vaccinia virus-infected HeLa cells.

The two nucleic acid-dependent nucleoside triphosphate phosphohydrolases, previously purified from vaccinia virus cores, were shown to be immunologically distinct enzymes. Antiserum prepared against purified phosphohydrolase I and antiserum prepared against purified phosphohydrolase II only neutralized the activity of that enzyme used as antigen. Both enzymes were induced in HeLa cells after vaccinia infection. DNA-cellulose chromatography was used to purify the two phosphohydrolases from the cytoplasms of infected cells. The enzymes were identified by their different substrate specificities, nucleic acid dependence, and neutralization with specific antiserum. A third chromatographically separable nucleic acid-dependent phosphohydrolase similar to phosphohydrolase I in substrate specificity but not neutralizable by antiserum to either phosphohydrolase I or II, was also isolated from infected cells. No nucleic acid-dependent nucleoside triphosphate phosphohydrolase activity was detected by similar methods from uninfected HeLa cells. Formation of these virus-induced enzymes was prevented by actinomycin D and cycloheximide, indicating a requirement for de novo RNA and protein synthesis, respectively. The kinetics of induction and inhibition by cytosine arabinoside, an inhibitor of DNA synthesis, suggested that synthesis of the phosphohydrolases is a late viral function. Rifampin, an inhibitor of vaccinia virus growth which prevents virion assembly, had no inhibitory effect on the induction of the phosphohydrolases. This result was consistent with the finding that these enzymes exist in a soluble as well as in a particulate form in the cytoplasm of infected cells. Addition of another specific anti-poxviral drug, isatin-beta-thiosemicarbazone, to vaccinia-infected cells partially inhibited induction of the phosphohydrolases.

Adenosine Triphosphatases↗