bluuebunny/crossref_metadata_2025_split huggingface dataset:
ALLOANTIBODY PRODUCTION MEASURED BY PLAQUE ASSAY IN RELATION TO STRONG AND WEAK HISTOINCOMPATIBILITY
Authors: Hildemann W. H. , Pinkerton W. 
Published: June 2004

A plaque technique which provides a sensitive and quantitative determination of allohemolysin (isohemolysin) production by lymphoid cells of mice and Syrian hamsters is described. Much ongoing attention has been given to minimizing sources of spurious plaques while improving the reproducibility of the technique. Primary intravenous immunization with allogeneic blood cells led to the early appearance of plaque-forming spleen cells responding to both strong and weak histocompatibility antigens in inbred strains of mice. The strongest histoincompatibility (A/J → BL/6), characterized by H-2 plus non-H-2 differences and a median skin allograft survival time of 8.2 ± 0.5 days, gave a peak average plaque production of 29.6 per 10 x 106 viable spleen cells after 6 days. At the other extreme with an average allograft survival time of 91 days, C3H(H-1a) → C3H.K(H-1b) showed a feeble production of plaque-forming cells with a peak response of 3.7 per 10 x 106 viable spleen cells at 9 days. Histocompatibility antigens determined by genes at the H-1, H-Y, and H-X loci were demonstrated to be erythrocyte antigens as well. Peak plaque production occurred earlier and reached higher levels across the stronger histocompatibility barriers (H-2 plus non-H-2 or H-2 alone) in temporal accord with the rapidity of skin allograft rejection. Weak H-Y or H-1 differences leading to prolonged allograft survival were associated with moderate, but not commensurate delays in the initial occurrence and recruitment of plaque-forming cells. With one exception (C57BL/10 → B10.A), the average plaque counts found at the peak of the primary responses were inversely proportional to the median survival times of skin allografts in the same strain combinations. Nevertheless, in light of the disparity between the times of allograft rejection and the time course of appearance of plaque-forming cells with the "weaker" congenic combinations, the early 19S antibodies do not appear to be directly involved in allograft rejection.
There appears to be no limitation in the weakness of histocompatibility antigens capable of evoking antibodies detectible by plaque assay. The extent to which molecular species of mouse antibodies other than 19S hemolysins are induced and detected under the conditions employed remains to be determined. The responses in strain combinations involving stronger histocompatibility barriers were characterized by exponential increases in plaque-forming cells, for 2 to 4 days until maximal levels were reached. Repeated immunization in several trials led to substantial increases over the maximum primary response in the number of demonstrable plaque-forming cells. Further preliminary results are reported concerning alloimmune plaque production in three strains of Syrian hamsters exhibiting intermediate to weak histocompatibility differences.
AN ANTIVIRAL SUBSTANCE FROM PENICILLIUM FUNICULOSUM
Authors: Shope Richard E. 
Published: June 2004

Helenine, NDV, and statolon, all known inducers of interferon in mice, all exerted a marked antiviral effect against Semliki Forest virus. This AV effect was, so far as can be demonstrated, mediated through, the induced interferon.
The same three materials also exerted a marked antipassive immunity effect. All the evidence that can be brought to bear indicates that this API effect like the AV effect is mediated through interferon known to be induced by the three materials.
If the API effect does indeed have interferon as its basis, this represents a new and totally unsuspected action of interferon.
STUDIES OF PPLO INFECTION
Authors: Thomas Lewis , Aleu Fernando , Bitensky Mark W. , Davidson Morton , Gesner Bertram 
Published: June 2004

Rolling disease has been produced and studied in rats and mice, using the exotoxin of the A strain of Mycoplasma neurolyticum.
The primary lesion of the brain consists of spongiform degeneration, associated with vesicle formation in the cortex and underlying white matter of the cerebral hemispheres, and in the molecular layer of the cerebellum. The brains of animals surviving 2 days or longer show extensive necrotizing lesions resembling ischemic necrosis, in both cerebral hemispheres.
The brains of rats and mice with rolling disease become deeply stained by intraperitoneally injected trypan blue, indicating early disruption of the blood brain barrier.
The toxin appears to be a thermolabile protein with a molecular weight exceeding 200,000. It is only active when injected by vein, and causes no disease when injected intracerebrally, intraperitoneally or subcutaneously, suggesting the existence of specific receptors within the vascular bed of the central nervous system.
Protection is afforded by rabbit antibody against the toxin, but only when antibody is injected within less than 3 min after intravenous injection of toxin, indicating rapid fixation to receptors in the brain.
The toxin is inactivated by incubation for 10 min at 37°C with suspensions of the sedimentable component of normal brain. The inactivating factor in brain sediment is very thermostable, not affected by trypsin, and eliminated by treatment with periodate. Similar inactivation of toxin is demonstrable with water-soluble gangliosides of brain.
A theoretical concept to explain the action of the toxin is proposed.
STUDIES OF PPLO INFECTION
Authors: Thomas Lewis , Bitensky Mark W. 
Published: June 2004

Concentrated suspensions of washed Mycoplasma neurolyticum produce rolling disease in mice and rats, with neurological manifestations and pathological lesions similar to those seen with the exotoxin of this organism.
Pretreatment of animals with tetracycline protects completely against the toxic effects of washed suspensions of mycoplasmas, while tetracycline affords no protection against the exotoxin. Freeze-thawing disruption of mycoplasma suspensions eliminates their neurotoxicity, while the same treatment does not affect exotoxin. The toxicity of intact organisms is not affected by exposure to the sedimentable component of brain, nor to ganglioside. These observations are interpreted to indicate that the neurotoxicity of living mycoplasmas must be due to their production of toxin after they have been injected into the animal.
Resting mycoplasmas, suspended in Ringer's solution in dialysis sacs submerged in PPLO broth) produce considerable amounts of toxin within 15 min of incubation at 37°C. Toxin is also produced, although in somewhat less amount, by washed organisms suspended in phosphate buffer containing glucose. The formation of toxin is prevented by the presence of puromycin, but not by the aminonucleoside analogue of puromycin, indicating that active protein synthesis is involved in the elaboration of toxin.
The similarities between the neurotoxicity of the intact organisms of M. neurolyticum and Mycoplasma gallisepticum are discussed.
ON THE NATURE OF THE "LIPOVIRUS"
Authors: Chang R. Shihman , Pan I-Hung , Rosenau Barbara J. 
Published: June 2004

Experiments designed to elucidate the nature of the "lipovirus" are described. The development of characteristic nuclear lesions in human cells in vitro depended on the presence of an ameboid cell in the inoculum. The spatial separation of the ameboid cells from the human cells by a membrane filter 150 µ in thickness was sufficient to prevent the development of nuclear lesions. Nuclear lesions appeared to be the primary change of the affected human cells. This development of nuclear lesions was partially suppressed by FUDR and the suppression was reversed by thymidine.
Time-lapse microcinematography showed that a 30 min intermittent contact between an ameboid cell and a human cell resulted in the retraction of both progenies of the human cell after a lapse of about 36 hr. Other human cells not in contact with the ameboid cell remained polygonal and continued to divide.
Radioautography of the ameboid cell revealed the presence in the cytoplasm of thymidine-containing DNAse-sensitive materials.
The development of antigens related to the ameboid cell within the cytoplasm of the human cell is described in the accompanying report (4).
EXPERIMENTAL ALLERGIC GLOMERULONEPHRITIS INDUCED IN THE RABBIT WITH HOMOLOGOUS RENAL ANTIGENS
Authors: Unanue Emil R. , Dixon Frank J. , Feldman Joseph D. 
Published: June 2004

Rabbits immunized to several homologous renal antigens developed a variety of autoantikidney antibodies. Some of these antibodies reacted with the host's glomeruli and appeared to cause glomerulonephritis. Passive transfer of sera from some of these nephritic rabbits into normal, unilaterally nephrectomized rabbits led to the induction of nephritis. The production of autoantibody to glomeruli was transitory in most instances in spite of continued immunization. In some rabbits immunized to whole kidney homogenate, extracts or sediment, antibodies were found fixed to renal tubular basement membranes where an ultrastructural lesion was demonstrated. Rabbits also produced antikidney antibody apparently to tubular cytoplasmic components which did not fix to kidney in vivo and were of no pathogenetic significance.
Immunization with autologous renal basement membranes induced a small autoantibody response in half the rabbits. This response was not associated with detectable renal injury.
EQUINE ANTIHAPTEN ANTIBODY
Authors: Rockey John H. 
Published: June 2004

Eight antigenically unique immunoglobulins have been identified in purified equine anti-p-azophenyl-ß-lactoside (Lac) antibody isolated from a single horse. The Fc fragments of the γGa-, γGb-, γGc-, and -γA-globulins have been shown to possess unique antigenic determinants. Common γG- and γA-Fc fragment antigenic determinants, which were absent from the 10Sγ1- and γM-globulins, have also been observed. All antibody populations share two antigenically distinct light (B, L) chain variants.
The association of anti-Lac antibody with the hapten p-(p-dimethylamino-benzeneazo)-phenyl-ß-lactoside has been measured by equilibrium dialysis and by fluorescence quenching. A variation in the affinity of anti-Lac antibody for hapten has been observed. The affinity of antibody was unaltered by enzymatic removal of the Fc fragments by peptic digestion or dissociation of the two combining sites on the papain 3.5S Fab fragments, indicating that the observed heterogeneity of affinities was not a direct function of the heterogeneity in structure of the Fc fragments. Isolated heavy (A, H) chains of γA-anti-Lac antibody have been shown to have retamed affinity for Lac dye by equilibrium dialysis and by analytical ultracentrifugation, employing a combination of schlieren and absorption optics.
The heavy (A, H) chains from two physically separable, antigenically distinct antibody populations, isolated from the same animal and having affinity for the same haptenic determinant, have been found to differ in their amino acid composition. Anti-Lac antibody light (B, L) chains have also been shown to be chemically heterogeneous, and contained populations of polypeptide chains possessing, and populations lacking methionine.
The relevance of the observed structural heterogeneity of equine anti-Lac antibody to the problem of defining the mechanism of acquisition of immunological specificity is briefly discussed.
BACTERIAL INTERFERENCE IN EXPERIMENTAL BURNS
Authors: Anthony Bascom F. , Wannamaker Lewis W. 
Published: June 2004

A standardized, full thickness, dermal burn in rabbits was used to study interference between strains of Staph. aureus inoculated on the wound surface. Several strains appeared equally capable of colonizing lesions and of preventing superinfection by other staphylococci inoculated at a later time. In addition, cross-infection between rabbits colonized by different strains (502A and Q461) and placed together in cages was prevented, presumably by the same mechanism. Interference appeared to be a strictly local phenomenon, since it did not occur when an animal was colonized by strain 502A at one burn site and subsequently challenged with strain Q461 at a separate lesion.
For interference to occur, a minimal time interval (9 hr) was required between inoculation of the interfering strain and inoculation of the challenge strain. In vivo growth rates indicated rapid growth in the first 24 hr by the interfering strain but no detectable multiplication by the challenge strain. Heat-killed staphylococci, even in large numbers, were incapable of producing interference. Penicillin treatment of animals colonized by strain 502A (penicillin-sensitive) abolished interference with strain Q461 (penicillin-resistant). These findings indicate that bacterial multiplication by the interfering strain is an essential feature of this phenomenon.
The mechanism of interference between strains of Staph. aureus remains obscure. There was no evidence in these studies for direct bacterial antagonism in vitro or in vivo between most of the strains examined; yet, all were capable of producing interference. Attempts to identify antistaphylococcal activity in passively transferred tissue homogenates and serum collected from infected animals were also negative. The ability of large inocula of staphylococci grown in broth to superinfect colonized lesions indicates that the numerical superiority of the interfering strain over the challenge strain is an important aspect of interference. The observation that in vivo-grown organisms may superinfect in significantly smaller quantities is suggestive of a qualitative advantage as well.
ONTOGENY OF MACROPHAGE RESISTANCE TO MOUSE HEPATITIS IN VIVO AND IN VITRO
Authors: Gallily Ruth , Warwick Anne , Bang Frederik B. 
Published: June 2004

Adult or weanling C3H mice were found to be genetically resistant to a strain of mouse hepatitis virus. Infant C3H mice, however, developed infection and died from mouse hepatitis virus when minimal infectious doses of virus were given to them. There was a delay in the time of death compared to that of the genetically susceptible strain, and the virus recovered from these mice had increased pathogenicity for C3H mice.
The ontogeny of resistance to hepatitis in the C3H mice thus progresses from delayed susceptibility to complete resistance as the age of the host increases. It is reflected in increased resistance of macrophages derived in vitro from liver cultures of infant mice of different ages. This increase in resistance with age was reduced by maintaining the cultures for a longer period of time before inoculation, or by increasing the number of explants in a given culture. Resistant cells were uniformly furnished by mice age 16 days, or more. It is concluded that a process of maturation of resistance of the cells takes place after the mice are born, but that this does not continue under in vitro conditions, and that it may be modified by the environment of the cells.
RABBIT MACROPHAGE INTERFERONS
Authors: Smith Thomas J. , Wagner Robert R. 
Published: June 2004

Antiviral factors present in cultures of rabbit peritoneal macrophages or rabbit kidney (RK) cells infected with Newcastle disease virus (NDV) and those in cultures of uninfected macrophages all fulfilled the biological and physicochemical criteria for classification as interferons. Virus-induced macrophage and RK interferons were slightly more stable to heat or acid than "spontaneously produced" or endotoxin-induced macrophage interferon. Interferon activity in serum of NDV-infected rabbits was decidedly more labile than NDV-induced macrophage interferon. However, these differences in lability were too slight to serve as a useful basis for distinguishing one rabbit interferon from another.
Rabbit interferons from various sources could be differentiated by filtration through Sephadex G-100 and their molecular weights estimated by comparison with elution profiles of a series of marker proteins of known molecular weight. Each of four different preparations of rabbit interferons was found to contain more than one molecular component. Elution peaks for three NDV-induced interferons were equivalent to the following molecular weights: RK ≃44,000–45,000 and &gt; 134,000 (variable and &lt; 1% when present); macrophage ≃37,000, 44,000–45,000, and &gt; 134,000 (variable and &lt;1% when present); and serum ≃50,000–52,000 and &gt; 134,000 (∼10% and heat labile). NDV-induced serum interferon may also contain another molecular component of mol wt ≃45,000 represented by a trailing shoulder from the major 51,000 mol wt peak.
Endotoxin-induced macrophage interferon proved to be polydisperse. Sephadex filtration of this interferon did not reveal clear and consistent elution patterns, partially owing to its low initial titer and lability. However, variable peaks of biological activity could be detected in Sephadex fractions equivalent to approximate molecular weight values of &gt; 134,000, 72,000–78,000, 33,000–38,000, 28,000–30,000, and possibly a component of 42,000–45,000. A major component of mol wt ≃37,000 was present in all samples of endotoxin-induced macrophage interferon. The other constituents may be biologically active subunits or polymers.
These data indicate that rabbit macrophages produce two primary kinds of interferon: (a) an RK-like component of mol wt ≃45,000 that is synthesized in greatest amount after viral induction, and (b) a different species of mol wt ≃ 37,000 that can also be synthesized in the absence of viral induction. The presence of major interferon constituents of mol wt ≃51,000 and &gt; 134,000 in rabbit serum after viral induction suggests that macrophages are not the principal interferon-producing cells that respond to intravenous injection of NDV.
BIOLOGICAL ACTIVITY OF THE CLEAVAGE PRODUCT OF HUMAN IMMUNOGLOBULIN G WITH CYANOGEN BROMIDE
Authors: Lahav Mira , Arnon Ruth , Sela Michael 
Published: June 2004

Treatment of human IgG with cyanogen bromide in 0.05 M HCl under specified conditions resulted in the cleavage of about half of its methionyl peptide bonds. A major fragment of about 5S was isolated from the reaction mixture by gel filtration in quantitative yield. The CNBr fragment reacted fully with goat antiserum against human light chain, but its reaction with anti-heavy chain was markedly decreased. The treatment with CNBr caused a drastic decrease in the following biological activities of IgG: complement fixing, skin binding, reaction with antiglobulin factors, and reaction with specific anti-Gm(12) serum. On the other hand, the reaction with serum of anti-Gm(1) or anti-Gm(4) specificity was not impaired and antibody activity, namely antistreptolysin and isohemagglutinin, was retained after the treatment with CNBr.
It is concluded that the CNBr cleaves preferentially the methionyl bonds in the Fc portion of IgG, and that the major fragment obtained, denoted F(ab'')2, has still the combining properties of a divalent antibody. The possible therapeutic uses of F(ab'')2 are discussed.
PERSISTENCE OF GROUP A STREPTOCOCCAL CELL WALLS RELATED TO CHRONIC INFLAMMATION OF RABBIT DERMAL CONNECTIVE TISSUE
Authors: Ohanian Sarkis H. , Schwab John H. 
Published: June 2004

Antibodies specific for the mucopeptide and group-specific C polysaccharide antigens of Group A streptococcal cell walls were prepared by acid dissociation of immune precipitates, and labeled with either fluorescein or 125I.
Employing both fluorescent and radioautographic procedures the persistence of the antigens was followed in skin sites injected with cell wall fragments. Both antigens persisted within macrophages for at least 54 days in those animals which developed no chronic tissue response. In animals which did develop chronic nodular lesions the concentration of antigen decreased as the inflammatory process subsided. Lesion activity was thus associated with the presence of cell wall material.
The fate of these antigens was also determined following the intradermal injection of intact Group A streptococcal cells. Cell wall antigens persisted in the tissue site considerably longer than morphologically identifiable streptococci, indicating that cell wall fragments are released during dismantling of streptococci in phagocytic cells.
GENERATION OF CHEMOTACTIC ACTIVITY IN RABBIT SERUM BY PLASMINOGEN-STREPTOKINASE MIXTURES
Authors: Taylor Fletcher B. , Ward Peter A. 
Published: June 2004

The addition of plasminogen and streptokinase to rabbit serum results in appearance of chemotactic activity which is relatively heat-labile and dialyzable. Generation of this activity requires heat-labile factors in serum, but not the sixth component of complement. The optimal mole ratio for generation of chemotactic activity is 1:1 to 1:3 for plasminogen to streptokinase. Neither material alone is sufficient to generate the activity in fresh serum. Generation of chemotactic activity can be blocked by the presence of ϵ-aminocaproic acid. This plasmin-generated chemotactic factor sediments slowly in a sucrose density gradient during ultracentrifugation.
The addition of plasminogen and streptokinase to rabbit serum containing the preformed chemotactic factor (activated trimolecular complex of C'5, C'6, C'7) causes destruction of the chemotactic factor and loss of hemolytic activity of the sixth component of complement. The same mole ratio of reactants for optimal expression of the phenomenon holds as for plasmin generation of chemotactic activity in untreated serum.
IMMUNOPATHOLOGY OF NZB/BL MICE
Authors: Mellors Robert C. , Huang Chen Ya 
Published: June 2004

Hemolytic disease characterized by slight anemia, reticulocytosis, hemosiderosis, extramedullary hematopoiesis, and positive indirect antiglobulin (Coombs') tests and renal disease with proteinuria, hypoalbuminemia, and glomerular lesions were produced in Swiss mice by neonatal intraperitoneal inoculation of cell-free filtrates prepared from the spleens of old NZB/Bl mice. Lymphoid cell and plasma cell hyperplasia as well as hypergammaglobulinemia occurred in some of these inoculated mice.
Type "C" murine oncogenic virus-like particles, indistinguishable from those previously described (1), were shown by electron microscopic study to be present in distinctive locations, notably in the basal foldings of convoluted tubules in the kidneys of a newborn NZB/Bl mouse, old NZB/Bl mice, a CBA x NZB F1 hybrid mouse, and a Swiss mouse inoculated with NZB/Bl spleen cell-free filtrate.
These observations point to two (perhaps related) circumstances which may be requisites for the pathogenic action of this newly discovered virus within and outside the strain NZB: infection of newborn, or infant, mice; persistent, possibly tolerant, infection of adult mice.
VIRAL ONCOLYSIS: INCREASED IMMUNOGENICITY OF HOST CELL ANTIGEN ASSOCIATED WITH INFLUENZA VIRUS
Authors: Lindenmann Jean , Klein Paul A. 
Published: June 2004

A2G mice could be solidly immunized against the Ehrlich ascites tumor by single intraperitoneal injections of homogenized and lyophilized tumor cells which had been infected with oncolytic strains of influenza A virus. Similar homogenates from noninfected tumor cells were not immunogenic, even when mixed with egg-grown virus.
The immunizing principle in viral oncolysates could not be separated from the oncolytic virus by differential centrifugation or adsorption to and elution from red cells. It could be inhibited by antibody raised in rabbits against the egg-grown oncolytic virus. This reaction showed serologic specificity. Thus, the immunogenicity of an oncolysate produced with the WSA strain of neurotropic influenza virus could be inhibited by rabbit anti-WSA, but not by rabbit antibody to the TUR strain of fowl plague virus. Conversely, the immunogenicity of an oncolysate prepared with the TUR strain could be inhibited by rabbit anti-TUR, but not by anti-WSA.
When mice were preimmunized (primed) with egg-grown WSA virus, their antitumor response to a later injection of WSA oncolysate was of the anamnestic type. Priming with egg-grown influenza B virus had no such effect.
It was concluded that the immunogenicity of certain host cell components was greatly increased by incorporation into the makeup of the oncolytic virus.