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The article presents a study regarding DNA encoding of Dictyostelium discoideum β subunit in mitochondrial processing peptidase (Ddβ-MPP). Ddβ-MPP mRNA is down-regulated during early development but remained constant throughout the Dictyostelium life cycle. During life cycle, mitochondria of Dictyostelium exhibited marked morphological changes. Antisense RNA inhibition of Ddβ gene might induce gene expression of mitochondrial proteins in retograde signaling manner.

Objective: Severe combined immunodeficiency (SCID) mice possess neither T nor B lymphocytes and are thus suitable recipients for adoptively transferred lymphocytes. Because autoimmune mechanisms may be involved in the pathogenesis of coxsackievirus B3 (CB3) myocarditis, we attempted to assess the in vitro cellular damage caused by antigen-sensitized lymphocytes and to determine whether splenic lymphocytes from BALB/c mice with chronic CB3 myocarditis could cause myocarditis into SCID mice. Methods and results: Cytotoxic cellular damage against non-myocytes and myocytes was demonstrated using 51Cr-release assay by lymphocytes cultured from myocarditis specimens or splenocytes from mice with chronic CB3 myocarditis. Severe T lymphocyte infiltration with myocardial necrosis was found in adoptively splenocyte-transferred SCID mice, but myocardial necrosis was not defected in wild-type mice by the same procedure. Conclusions: Autoimmune mechanisms might operate in mice with post-CB3 myocarditis and could be transferred in to SCID mice by the antigen-sensitized lymphocytes. An in vivo model of autoimmune post-viral myocarditis in SCID mouse was demonstrated. [Copyright &y& Elsevier]

By using monoclonal antibodies directed against discoidin II, we have isolated cDNA clones from axenically grown Ax-2 cells. On cDNA clone (D2) condtained a 1.2-k.b insert encoding the entire discoidin II protein, which is conposed of 257 amino acid residuces and has a calculated molecular mass of 28,574. The amino acid sequences, determined by Edman degradation of six tryptic peptides of discoidin II, were identical to those deduced from the cDNA sequences. The protein bears no resemblance to any proteins in the data banks, except that its sequence is 49% identical with the amino acid sequence of discoidin I. Discoidin II shares with discoidin I both a carbohydratebinding site and an Arg-Gly-Asp (RGD) sequence, which has been found in fibronectin in mammalian cells. With the onset of aggregation (8 h of development), a 1.3-kb discoidin II mRNA begins to accumulate. A similar pattern of regulation occurs at the protein level. [ABSTRACT FROM AUTHOR]

The cellular slime mold, Polysphondylium pallidum, has two EDTA-resistant types of cell-cell adhesion. The major component of them has been identified as a glycoprotein with a molecular mass of 64 kDa on SDS-PAGE (referred to as gp64). We found that a substantial amount of the gp64 run as dimer, when gp64 was dissolved in SDS-sample buffer without 2-mercaptoethanol and then subjected to electrophoresis. The occurrence of a homophilic dimer was demonstrated by analyzing the dimer-like band on a gel for its amino acid sequence and amino acid composition. The dimer-like band also was analyzed by three sorts of monoclonal antibodies, two of which recognize respectively a conforniational epitope and a denatured epitope of the protein moiety of gp64. The data indicate that the native conformation of gp64 is necessary for dimer formation. [ABSTRACT FROM AUTHOR]

Objective: The aim was to test the role of oxygen derived free radicals in the development of myocarditis. This involved investigating the effects of polyethylene glycol conjugated superoxide dismutase (PEG-SOD, an enzyme catalysing the conversion of O2· − to H2O2) and polyethylene glycol conjugated catalase (PEG-catalase, accelerating the reaction of H2O2 to H2O and O2 upon coxsackievirus B3 (CB3) myocarditis. Methods: Two week old male C3H/He mice were inoculated intraperitoneally with 103 plaque forming units of CB3. PEG-SOD, 1×103 U·kg−1·d−1, and PEG-SOD, 1×103 U·kg−1·d−1, plus PEG-catalase, 1×103 U·kg−1·d−1, were injected subcutaneously daily on days 0 to 14. Treated groups were compared to the infected control. Results: On day 7, there were no significant differences in pathological scores among the three groups. On day 14, the cellular infiltration, myocardial necrosis, and calcification scores were significantly lower in the PEG-SOD group and the PEG-SOD plus PEG-catalase group than in the control. There were no significant differences in pathological scores between the PEG-SOD group and the PEG-SOD plus PEG-catalase group. There were no differences in the myocardial virus titres on day 7 among the three groups. On day 14, virus was not detected from the myocardium in any of the three groups. Conclusions: The results suggest that superoxide anion is mostly responsible for myocyte injury in CB3 myocarditis in mice, and that hydrogen peroxide formed as a result of dismutation of superoxide anion may not play a significant role in the development of myocarditis. Superoxide anion is one of the most important factors in free radical mediated injury in CB3 myocarditis in mice and the administration of PEG-SOD alone has therapeutic potential in clinical CB3 myocarditis.Cardiovascular Research 1993;27:957-961 [ABSTRACT FROM PUBLISHER]

Objective: The aim was to test the efficacy of the immune system modulator lobenzarit disodium in the treatment of coxsackievirus B3 myocarditis. Methods: Two week old C3H/He mice were inoculated with 103 plaque forming units of coxsackievirus B3. Lobenzarit disodium, 25 mg·kg−1·d−1, was given subcutaneously daily on days 0-14 (experiment I; group 2) and days 14-28 (experiment II; group 4). Both treated groups were compared to infected controls for each experiment (groups 1 and 3). For the analysis of splenic lymphocyte subsets, additional mice in untreated and treated groups were killed on d 7, and the percentages of Thy 1.2 (CD3), L3T4 (CD4), Ly 2 (CD8) subsets were analysed by laser flow cytometry (experiment III). Results: In experiment I, the survival rate in the lobenzarit treated group was significantly lower than in the controls (2/11 v 8/11). Cellular infiltration and myocardial necrosis in the lobenzarit group were more severe. Myocardial virus titres and serum neutralising antibody titres did not differ significantly between the two groups. In experiment II, the survival rate (7/9 v 13/13) and cardiac pathology between the two groups did not differ significantly. In experiment III, the percentage of the Thy 1.2 subset (CD3) in the treated group was significantly lower (p<0.05) than in the control group, at 36.0(SD 2.9)% v 42.8(5.8)%. Conclusions: Lobenzarit disodium decreased splenic pan T cells and aggravated both clinical course and cardiac pathology in acute murine coxsackievirus B3 myocarditis.Cardiovascular Research 1993;27:243-248 [ABSTRACT FROM PUBLISHER]

Objective: The aim was to examine the role of oxygen derived free radicals in the development of myocarditis by investigating the effects of polyethylene glycol conjugated superoxide dismutase (PEG-SOD), a potent scavenger of oxygen free radicals, upon coxsackievirus B3 (CB3) myocarditis. Methods: Two week old male C3H/He mice were inoculated intraperitoneally with 103 plaque forming units of CB3. PEG-SOD, 1 × 103, 5 × 103, 1 × 104, and 1 × 105 U·kg−1·d−, was given subcutaneously daily on days 0 to 14. Treated groups were compared to the infected control. Results: The survival rate of the 1 × 105 U·kg−1·d− PEG-SOD group was lower than that of the infected control group (40% v 78%, peO.01). The survival rates of the other treated groups did not differ significantly from the infected control. The myocardial calcification score in the 1 × 105 U·kg−·d−1 PEG-SOD group was higher than in the infected control group on d 7, when myocardial virus titres did not differ significantly among the five groups. The scores for myocardial cellular infiltration and myocardial necrosis in the 1 × 103 and the 5 × 103 U·kg−1·d−1 PEG-SOD groups were significantly lower than in the infected control on d 14, when myocardial viruses were not detected in the five groups. However, the myocardial necrosis and myocardial calcification scores in the 1 × 105 U·kg−1·d− PEG-SOD group were higher than in the infected control.Conclusions: The improvement of cardiac pathology in the 1 × 103 and the 5 × 103 U·kg−1·d−1 PEG-SOD groups seems to have resulted not from reduction in myocardial virus titres but from inhibition of generation of oxygen free radicals. The mechanism of the impaired survival and aggravation of cardiac pathology in the 1 × 105 U·kg−1·d−1 PEG-SOD group is unknown. The results suggest that oxygen free radicals may be involved in the pathogenesis and development of CB3 myocarditis and that appropriate dosages of PEG-SOD have therapeutic potential for clinical CB3 myocarditis, although caution must be paid to the treatment window.Cardiovascular Research 1992;26:956–96 1 [ABSTRACT FROM PUBLISHER]

In an effort to identify and characterize genes expressed during multicellular development in Dictyostelium, we have undertaken a cDNA sequencing project. Using size-fractionated subsets of cDNA from the first finger stage, two sets of gridded libraries were constructed for cDNA sequencing. One, library S, consisting of 9984 clones, carries relatively short inserts, and the other, library L, which consists of 8448 clones, has longer inserts. We sequenced all the selected clones in library S from their 3′-ends, and this generated 3093 non-redundant, expressed sequence tags (ESTs). Among them, 246 ESTs hit known Dictyostelium genes and 910 showed significant similarity to genes of Dictyostelium and other organisms. For library L, 1132 clones were randomly sequenced and 471 non-redundant ESTs were obtained. In combination, the ESTs from the two libraries represent approximately 40% of genes expressed in late development, assuming that the non-redundant ESTs correspond to independent genes. They will provide a useful resource for investigating the genetic networks that regulate multicellular development of this organism. [ABSTRACT FROM PUBLISHER]