Peripheral proteins of human erythrocytes.
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Biomedical subjects
Publications and source records attributed to C Howe.
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A series of 58 cases of traumatic diaphragmatic hernia following blunt and penetrating injury is reviewed. The problems of radiodiagnosis are outlined and the need for barium contrast studies of the entire gastrointestinal tract to ensure recognition of isolated small bowel herniation is emphasized. Surgical access via laparotomy is recommended in the immediate post-traumatic presentation, whereas thoracotomy is preferable in cases diagnosed after a latent interval. Penetrating injury resulted in smaller diaphragmatic defects, greater morbidity and higher mortality due mainly to infective complications.
Residual sodium dodecyl sulfate (SDS) introduces artifacts into immuno- and counterimmunoelectrophoretic analysis of proteins which have been eluted from preparative SDS-polyacrylamide gels. Unbound SDS can be removed by electrophoretic passage of eluted solutions through a barrier of Triton X-100 in agarose in which the anionic and non-ionic detergents interact to form micelles.
Convalescent sera from proven cases of infection with Mycoplasma pneumoniae, and rabbit antisera to M. pneumoniae and to human erythrocyte glycoprotein contained cold hemagglutinins which were reactive only for human erythrocytes. Only the human serum cold agglutinins were inhibited by soluble integral glycoproteins derived from human erythrocyte ghosts by treatment with chloroform-methanol. Rabbit antiserum to chloroform-methanol glycoprotein, as well as to M. pneumoniae, fixed complement with either M. pneumoniae or chloroform-methanol glycoprotein antigens. The findings support the hypothesis that the cold agglutinins elicited by M. pneumoniae infection represent a cross-reaction between determinants common to erythrocyte glycoprotein containing I antigen and the membrane of M. pneumoniae.
Trypsinization of BHK-21 cells 72 h after primary infection with pneumonia virus of mice yielded clones of persistently infected cells which specifically adsorbed murine erythrocytes. We describe one clone of cells, the progeny of which, after more than 100 passages, still bore viral antigen demonstrable by immunofluorescence and immune electron microscopy, but produced little or no detectable infectious virus.
Measles viral envelope proteins were immune precipitated from membranes of infected cells and from purified virus and analyzed by polyacrylamide gel electrophoresis. Under reducing conditions, specific precipitates contained two major polypeptide bands, designated virus glycopeptides 1 and 2 (VGP-1 and VGP-2). Both polypeptides appeared to be glycosylated, as indicated by their incorporation of [(14)C]glucosamine in infected cells. VGP-2 appeared as a single band in specific precipitates of infected cells and as a double band in precipitates of purified virus. Trypsin treatment of infected cells showed that reduced VGP-2 may be composed of two unrelated polypeptides. One may be F(1), which is unglycosylated, and the other may correspond to the proteolytic cleavage product of VGP-1, which is glycosylated. The relation of VGP-1 and VGP-2 to smaller surface antigens (X and Y) obtained by tryptic treatment of infected cells remains to be elucidated. In cells taken at various times postinfection and analyzed for viral membrane proteins, VGP-1 was detected at all times, indicating that the input virus VGP-1 was inserted into the cell and could not be differentiated from newly synthesized VGP-1. VGP-2 was not detectable before 24 h postinfection. In precipitates of cells 4 h postinfection and of infected cells incubated at pH 5.8, an additional polypeptide band migrated immediately ahead of VGP-1. We conclude that VGP-2 (molecular weight, 42,000) possibly consists of two components, one of which is the tryptic cleavage product of VGP-1 and the other of which is the unglycosylated polypeptide, F(1).
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Influenza C virus was propagated successfully in primary chicken embryo lung (CEL) and fibroblast cells and in Madin-Darby canine kidney (MDCK) cells. In other cell lines, either no virus or only noninfectious hemagglutinin (HA) was produced. In productively infected cells (CEL), HA and infectious virus appeared by 24 h and reached a maximum by 36 to 48 h, cell-associated virus remaining at a constant low level. Infected Vero cells produced noninfective HA by 24 h which also remained predominantly cell associated until 60 to 72 h, when the cells disintegrated. Viral antigen was demonstrable on membranes of both CEL- and Vero-infected cells at 24 h; Vero cells yielded membrane vesicles containing HA, but none of the spherical or filamentous viral particles synthesized in CEL cells. Influenza C virus produced in cell culture or in eggs differed in several important respects from A and B viruses and from Newcastle diseases virus. All influenza C preparations, regardless of infectivity or source, lacked detectable neuraminidase activity, yet retained the ability specifically to inactivate receptors only for influenza C. Influenza C HA was not inhibited by soluble glycoproteins highly active against HA of A virus. A rat serum glycoprotein uniquely inhibited influenza C by binding to the surface components of virious.
A case of post-traumatic pseudocyst of the pancreas is presented. The elevated and compressed stomach showed an appearance on X-ray film which might be interpreted as free peritoneal air. The term pseudopneumoperitoneum is defined and other causes of this condition are mentioned.
In the present investigation experiments were carried out to determine whether the functionally obscure synaptic rebbons of mammalian pinealocytes can be affected by acute changes in environmental lighting and which chemical processes may be involved in their regulation. Experiments carried out in male guinea-pigs have shown that the amounts of synaptic ribbons are immediately affected by changes in the lighting pattern. Extension of the light period reduced the normally occurring increase, whereas extension of the dark period inhibited the normally occurring decrease in the amount of synaptic ribbons. Results following injections of a number of drugs known to influence pineal function (noradrenaline, L-DOPA, propranolol, reserpine and p-chlorophenylalanine, respectively) suggest that synaptic ribbons may be directly or indirectly regulated by beta-adrenergic mechanisms.
Present knowledge of cell surface receptors for animal viruses is reviewed. The methods used for enumeration and identification of receptors are critically examined with respect to particular advantages and disadvantages. Specific controls and alternative interpretations are suggested in connection with the reactions of lectins which block viral attachment to cells. Currently available information for each group of animal viruses is summarized in order to define the extent to which the corresponding receptors have been identified. It is concluded that the full range of virus-receptor interactions has not yet been explored even for those viruses of which there is the most detailed knowledge. For some groups, moreover, the receptor is totally uncharacterized. Six areas in which future investigative effort might be productive are identified, including the isolation of membrane components and the immunochemical definition of viral receptors.
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The effect of divalent cations on cell fusion by concentrated Sendai virus, inactivated by beta-propiolactone, was investigated using Vero and mouse L-929 cells in monolayers. With both cell lines, which are normally resistant to exogenous viral fusion, Cu(2+) in sublethal concentrations was found to promote polykaryon formation to a marked degree. The simultaneous presence of Cu(2+) and virus was required for this effect, which was thought to be related to the cytotoxic action of Cu(2+) on the cell membrane. Accordingly, under standard conditions and in the absence of virus, leakage of isotopically labeled intracellular protein was shown to bear a quantitative relationship to Cu(2+) concentration. Concomitant changes in the membrane were seen electron microscopically to consist of loss of microvilli and the appearance of numerous vesicles on, or adjacent to, the membrane. The relationship of enhanced fusibility to these toxic changes was not further elucidated. The fusion-promoting effect of Cu(2+) far exceeded that of Ca(2+); and other cations tested had no effect.
Extensive fusion of human erythrocytes agglutinated by Sendai virus was observed after 30 s of incubation at 37 C. Electron microscopy of thin sections failed to reveal the presence of virions, viral fragments, or discrete viral antigens reactive with ferritin-labeled antibody at the sites of fusion. Immuno-freezeetching of membrane surfaces demonstrated the dispersal of viral envelope antigens from what appeared to be original sites of viral attachment. Virus-induced clustering of membrane glycoproteins was interpreted as resulting from interaction of viral antigens with membrane receptor proteins and forming the structural basis for fusion of membranes with one another.