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Query: UMLS:C0151744 (myocardial ischemia)
 31,282 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The roles of intracellular naked (INV), cell-associated enveloped (CEV), and extracellular enveloped (EEV) forms of vaccinia virus in cell-to-cell and longer-range spread were investigated by using two closely related strains of vaccinia virus, WR and IHD-J. We confirmed previous results that WR and IHD-J produced similar amounts of INV and formed similar-size primary plaques but that IHD-J produced 10 to 40 times more EEV and spread to distant cells much more efficiently than did WR. Nevertheless, cells infected with WR and IHD-J had similar amounts of CEV, indicating that wrapping and transport of WR virions were unimpaired. A WR mutant with a deletion in VP37, the major outer envelope protein, formed normal amounts of INV; however, the generation of CEV was blocked and plaque formation was inhibited. These results suggested that CEV is the form of virus that mediates cell-to-cell spread. Marker rescue experiments indicated that the differences in EEV production by WR and IHD-J were not due to sequence differences in VP37. The low amount of WR EEV could be attributed to retention of CEV on the cell membrane. In support of this hypothesis, mild treatment with trypsin released as much or more infectious virus from cells infected with WR as it did with cells infected with IHD-J. Most of the virus released by trypsin sedimented with the buoyant density of EEV. Also, addition of trypsin to cells following inoculation with WR led to a comet-shaped distribution of secondary plaques characteristic of IHD-J. These results demonstrated that the release of CEV from the cell surface was limiting for extracellular virus formation and affirmed the role of EEV in long-range spread.
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PMID:Role of cell-associated enveloped vaccinia virus in cell-to-cell spread. 160 40

The vaccinia virus hemagglutinin (HA) has specific affinity for the structural protein, VP37K. The nature of this affinity and its relationship to the function of the HA were analyzed using HA mutants. The VP37K reactive site of the HA molecule is located in its transmembrane region, and the vaccinia virus HA associates with the viral particle via the VP37K-HA affinity. The viruses possessing an HA with fusion inhibitor activity were largely of the low infectivity form, whereas the viruses that associated mutant HAs defective in the activity were of the high infectivity form. D1 mutant virus does not produce HA. When it was incubated with the HA of the IHD-J strain, the HA associated with the virus particle. The HA-loaded D1 mutant virus acquired a high affinity not only for chick erythrocytes but also for KB and Vero cells. At the same time, the infectivity for Vero cells was decreased. The original high infectivity was recovered by treatment with trypsin. The virion-associated vaccinia HA has two functions; the HA protects the infectivity of the virus by the fusion inhibitor activity and exhibits affinity against host cells. Vaccinia virus first adsorbs to the cell via HA, and then proteolysis of the HA activates the second adsorption site which seems to be the fusogenic site of the virus. Proteolytic activation represents removal of the fusion inhibitor activity of the HA.
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PMID:The function of the vaccinia hemagglutinin in the proteolytic activation of infectivity. 234 62

Lipolytic factors associated with myocardial ischemia and factors which activate phospholipase A2 in cells other than heart cells were tested for their actions on the rhythmicity of cultured heart cells. Exogenous triglyceride lipase was without a significant effect on beating while phospholipase A2 produced concentration-related arrhythmias in concentrations as low as 0.0375 U/ml. Quinacrine, a phospholipase inhibitor, demonstrated concentration-dependent inhibition of reoxygenation-induced arrhythmias. Of the compounds known to activate phospholipase only kallikrein and thrombin produced arrhythmias; only bradykinin, thrombin and trypsin depressed beating. Lysophosphatidylcholine, a reaction product of phospholipase A2 on phospholipids, inhibited reoxygenation arrhythmias in a concentration-dependent manner.
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PMID:Arrhythmogenic and antiarrhythmic effects of lipolytic factors on cultured heart cells. 663 27

A vaccinia-specific target antigen for recognition of anti-vaccinia cytotoxic T lymphocytes (CTL) was found to be formed on the surface of infected cells through two distinct processes. In the first phase, the expression of the target antigen was dependent on the dose of inoculated virus, without specific protein synthesis. The target antigen seems to be produced by virus-cell fusion. In the second phase, the expression of the target antigen was accompanied by synthesis of an early protein. In spite of the difference in their mode of expression, the first-phase and the second-phase target antigens were cross-reactive in cytotoxicity inhibition assays. Cowpox virus, CPR Cl strain, brought about a lower response than vaccinia virus, IHD-J strain, in both sensitization of CTL and formation of CTL-susceptible cells at both the first and the second phase. The cross-reactive, but inefficient, recognition of anti-vaccinia CTL for cowpox-infected cells suggested a slight difference in the target antigens of the two viruses. Attempts to identify the target antigen were then made by comparing the polypeptide composition of vaccinia virus, cowpox virus, and their recombinants. SDS-PAGE analysis of trypsin-activated viruses revealed 44K (cowpox)/45K (vaccinia) polypeptides which corresponded to the difference in target cell formation. Trypsinization of the viruses also increased the ability of the virus to induce the production of CTL-susceptible target cells.
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PMID:Target antigen of vaccinia-infected cells recognized by virus-specific cytotoxic T lymphocytes. 697 58

The paper concerns the effect of the diet with a strongly reduced content of carbohydrates, with a restriction of table salt and extractive substances on lipid and carbohydrate metabolism, on catecholamine secretion and exocrine pancreatic function in patients with ischemic heart disease accompanied by overweight and disturbed carbohydrate tolerance. Dietetics has a normalizing action on the body overweight, lipid composition and lipoproteid spectrum, as well as on the enhanced activity of serum trypsin. Moreover, it makes the blood content of immunoreactive insulin return partially to normal.
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PMID:[Effect of a reducing diet on metabolic disorders in ischemic heart disease patients having excess weight]. 740 26

ATP-sensitive K+ (KATP) channels are thought only to open during conditions of metabolic impairment (e.g., myocardial ischemia). However, the regulation of KATP channel opening during ischemia remains poorly understood. We tested whether thiol (SH) group oxidation, which is known to occur during ischemia, may be involved in KATP channel regulation. Inside-out membrane patches were voltage clamped at a constant potential (O mV) in asymmetrical K+ solutions. The effects of compounds that specifically modify SH groups [p-chloromercuri-phenylsulfonic acid (pCMPS), 5-5'-dithio-bis(2-nitrobenzoic acid) [DTNB], and thimerosal] were tested. The membrane-impermeable compound, pCMPS (> or = 5 microM), caused a quick and irreversible inhibition of KATP channel activity. The reducing agent, dl-dithiothreitol (DTT) (3 mM) was able to reverse this inhibition. DTNB (500 microM) caused a rapid, but spontaneously reversible, block of KATP channel activity. After DTNB, no change was observed in single channel conductance. Oxidized glutathione (GSSG, 3 mM) did not block KATP channel activity. Thimerosal (100-500 microM) induced a DTT-reversible block of partially rundown KATP channels, or channels that underwent complete rundown; these channels were reactivated with trypsin (1 mg/ml). Thimerosal did not block KATP channels that had a high degree of activity. However, the ATP sensitivity was decreased; the concentration of ATP needed to half-maximally inhibit the channel (Ki) was increased from 47 +/- 12 to 221 +/- 35 microM (n = 6, P < 0.05). This was not due to a spontaneous change with time.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of thiol-modifying agents on KATP channels in guinea pig ventricular cells. 750 58

Mast cells and their chemical mediators play a role in cardiac and systemic anaphilaxis. Perivascular and cardiac mast cells have been implicated in the pathogenesis of coronary artery spasm, atherosclerosis, myocardial ischemia, and cardiomyopathy. Despite this, nothing is known about the immunological and biochemical characteristics of the human heart mast cell (HHMC). We have isolated and partially purified HHMC and compared them with mast cells isolated from lung (HLMC) and skin (HSMC) tissues. Cross-linking of the high-affinity receptor for IgE (Fc epsilon RI) by a polyclonal anti-Fc epsilon antibody caused the release of preformed (histamine and tryptase) and de novo synthesized mediators [peptide leukotriene C4 (LTC4) and prostaglandin D2 (PGD2)]. The tryptase content of HHMC (19.4 +/- 1.5 micrograms/10(6) cells) was lower than HSMC (33.4 +/- 2.5 micrograms/10(6) cells) and higher than HLMC (10.6 +/- 1.9 micrograms/10(6) cells). Maximal stimulation of HHMC with anti-IgE led to the release of LTC4 (17.5 +/- 5.1 ng/10(6) mast cells) and PGD2 (17.8 +/- 5.0 ng/10(6) mast cells, whereas HSMC synthesized more PGD2 (65.0 +/- 6.8 ng/10(6) mast cells) and much less LTC4 (< 5 ng/10(6) cells). Recombinant human C5a anaphylatoxin and protamine induced histamine release from HHMC and HSMC, but not from HLMC. Substance P and morphine selectively induced the release of histamine from HSMC, but not from HHMC and HLMC. Compound 48/80 caused histamine release from HSMC and HHMC, but not from HLMC. The pattern of mediators synthesized and the responsiveness of HHMC to different secretagogues appear unique providing strong evidence of human mast cell heterogeneity.
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PMID:Human heart mast cells: a definitive case of mast cell heterogeneity. 753 2

A vaccinia virus structural protein responsible for infection was identified by monoclonal antibodies (mAb). Two mAbs (2D5 and 8C2) neutralized the virus at a dilution of about 10(5). The 2D5 mAb reacted with VP29K under standard immunoblotting conditions and with a 23-kDa protein when virus was dissociated under nonreducing conditions. The 8C2 mAb reacted with the 23-kDa protein, but not with VP29K. Two-dimensional electrophoresis demonstrated that the 23-kDa protein was the nonreduced form of VP29K. Since they possess the same N-terminal amino acid sequence, the protein was renamed VP23-29K. The gene that encoded it was HindIII A17L ORF. The VP23-29K-dependent process of infection did not occur during the adsorption phase at 4 degrees, and trypsin-treated virus could complete the process within 10 min at 37 degrees. One half of the trypsin-treated intracellular mature virus (IMV) achieved the process within 20 min, but for normal IMV this time period was 2 hr. VP23-29K had function for the early step of penetration, and the functional site in the nonreduced 23-kDa form was masked to some extent in normal virus. The late cell fusion by the fusion positive (F+) D1 mutant proceeded in neutral pH. Cells infected with F- IHD-J strain virus did not fuse, but a short treatment with pH 5 medium developed cell fusion. Both of the cell fusions were inhibited by the 2D5 and 8C2 mAbs. Virion VP23-29K was suggested to be the fusion protein for the early penetration and the late cell fusion phases of vaccinia infection cycle.
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PMID:Identification of a vaccinia virus penetration protein. 803 Feb 46

The vaccinia virus forms two morphologically distinct infectious virus particles: intracellular mature virus (IMV) and extracellular enveloped virus (EEV). The envelope of EEV is a Golgi-derived membrane (wrapping membrane). A mutant (vRB10) lacks the ability to form the EEV. In medium containing a neutralizing antibody (2D5mAb), the vRB10 mutant was diluted out from infected cells, whereas the IHD-J strain of vaccinia virus replicated well. The result indicated that the 2D5mAb specifically neutralized the IMV. The 2D5-resistant EEV appeared at 6-7 hr postinfection, and over 65% of infectious virus in the culture fluid was EEV at 48 hr after infection. The EEV was resistant not only to the 2D5mAb but also against several neutralizing antibodies, including polyclonal antivaccinia serum reactive with proteins of the wrapping membrane. Freeze-thawing and other procedures that may damage the wrapping membrane converted the EEV to a form susceptible to the antibodies. Since specific infectivity was not affected by the damage or by exposure to antibody against the wrapping membrane proteins, the wrapping membrane did not directly participate in penetration. The infection process of vaccinia virus was analyzed by comparison of responses to acid treatment between normal IMV and trypsin-treated IMV. Proteolytically activated IMV infected rapidly responding to acid. The protected form virus, which was noninfectious under usual conditions, was proteolytically activated on cell membrane then responded to the acid. Proteolysis activated the virus, and an acidic condition accelerated fusion between the activated IMV and plasma membrane. The virus in the EEV wrapping membrane was the activated form that has the capacity to fuse with the cell membrane. However, the infection of intact EEV was more sensitive against lysosomotropic agents (NH4Cl, neutral red) than that of the trypsin-activated IMV. Resistance to the 2D5mAb, sensitivity to lysosomotropic agents, and acceleration of infection by acid suggested that the intact EEV penetrated by virus-endosome membrane fusion. The combined effect of the presence of wrapping membrane and the process of internalization via an endocytic mechanism rendered EEV resistant to neutralizing antibodies.
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PMID:Extracellular enveloped vaccinia virus escapes neutralization. 861 Apr 39

We observed a release of histamine, but not of tryptase, in arterial blood from 64 patients with ischemic heart disease and 24 patients without coronary disease, which was provoked by ioxaglate, a ionic compound, but was not provoked by iomeprol, a non-ionic radiocontrast compound. The release of histamine in arterial blood after ionic contrast medium injection was higher in patients with ischemic heart disease compared with patients without coronary disease, suggesting that an increased release from heart mast cells previously observed exists also for systemic blood basophils.
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PMID:Comparison of effects of ioxaglate versus iomeprol on histamine and tryptase release in patients with ischemic cardiomyopathy. 1144 22


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