bluuebunny/crossref_metadata_2025_split huggingface dataset:
RELATION OF PARTICLE SIZE OF C POLYSACCHARIDE COMPLEXES OF GROUP A STREPTOCOCCI TO TOXIC EFFECTS ON CONNECTIVE TISSUE
Authors: Roberson Bob S. , Schwab John H. , Cromartie William J. 
Published: June 2004

The component of Group A streptococci which is responsible for the chronic, remittent, multinodular lesion of connective tissue is derived from the cell wall. Further evidence is given to support the essential role of the group-specific C polysaccharide in the production of this lesion.
A series of particles containing the group-specific C polysaccharide was prepared, ranging in size from large cell wall fragments to the relatively small hapten. A comparison of the lesion producing capacity of the particles in this spectrum revealed that maximum toxic activity is associated with C polysaccharide complexes of intermediate size. The discussion considers colloidal properties associated with C polysaccharide complexes of a certain size, and the influence particle size has on persistence in tissue, as possible explanations of the relationship between the size of the C polysaccharide complex and its ability to produce the chronic lesion of connective tissue.
ON THE ABSORPTION OF BACTERIAL ENDOTOXIN FROM THE GASTRO-INTESTINAL TRACT OF THE NORMAL AND SHOCKED ANIMAL
Authors: Ravin H. A. , Rowley D. , Jenkins C. , Fine J. 
Published: June 2004

Coliform-free rabbits fed P32 labeled E. coli 0111B4 prior to the induction of experimental hemorrhagic shock were shown to have a substantial amount of the type-specific 0111B4 antigen in the circulating blood, liver, and spleen, whereas normal rabbits fed the same amount of these bacteria and held under identical conditions, but not exposed to shock, have the antigen within the liver, and occasionally in the kidney, but not in the blood.
That the antigen recovered from the blood and tissues was derived from this specific strain of bacteria was demonstrated by the use of the hemagglutination inhibition reaction, by the absence of cross-reacting antigens in appropriate control animals, and by agreement in the amount of antigen as estimated by two different technics.
Transport of bacterial endotoxin across the intestinal membrane appears to be achieved primarily by passive diffusion.
The accumulation of biologically active endotoxin in the blood and tissues of the shocked animal appears to be due to a reduction in the detoxifying potential of the reticulo-endothelial system, and not to a greater than normal absorption of endotoxin from the intestine.
The absence of toxicity in the specific antigen extracted from normal liver demonstrates that the degradation of endotoxic potency can be achieved without altering the chemical integrity of the polysaccharide moiety of the molecule.
The implications of the hypothesis that there is a continuous but fluctuating absorption of bacterial endotoxin from the intestine are briefly discussed, and the contribution of free circulating bacterial endotoxin of intestinal origin to the fate of the shocked animal is noted.
EVIDENCE FOR A LETHAL ENDOTOXEMIA AS THE FUNDAMENTAL FEATURE OF IRREVERSIBILITY IN THREE TYPES OF TRAUMATIC SHOCK
Authors: Schweinburg F. B. , Fine J. 
Published: June 2004

The data here reported (Table I) show that a toxin is present in the blood of animals with two types of irreversible hypovolemic shock. These data also show that although blood volume therapy does not correct the hypovolemia because of continuing loss of plasma at the site of injury, the major factor in the progressive decline and death is the endotoxemia rather than the hypovolemia. This is also true of severe and prolonged hemorrhagic shock that is irreversible to transfusion. The data also show that even when there is bacterial activity at the site of injury, the pool of endotoxin in the intestine is the chief source of the circulating endotoxin.
In all three types of shock, the endotoxemia develops because persisting hypovolemic shock renders the RE system unable to destroy the endotoxin.
The demonstration of an endotoxemia as the cause of irreversibility and death in three types of traumatic shock caused by three different agents suggests that a single pathophysiological mechanism accounts for the phenomenon of irreversibility in all types of traumatic shock.
IN VITRO DETOXIFICATION OF BACTERIAL ENDOTOXIN BY MACROPHAGES
Authors: Rutenburg S. H. , Schweinburg F. B. , Fine J. 
Published: June 2004

In the in vitro model described normal serum or plasma alone does not detoxify endotoxin, as determined by the response of the thorotrast-primed rabbit to the injection of the reaction mixture after 1 hour of incubation at 37°C. Partial detoxification, however, is achieved by serum or plasma after 3 hours of incubation of the same reaction mixture, as determined by the chick embryo test.
Macrophages in serum or plasma do detoxify endotoxin, as determined by both tests. Granulocytes, which are also able to detoxify endotoxin in the presence of serum, are less potent than macrophages.
Immune serum alone is much more potent than normal serum alone. Macrophages in immune serum are more potent than immune serum alone.
The relevance of the anti-endotoxic properties of these in vitro systems to the processes in the living animal are in doubt, and must await the results of comparable observations in the living animal.
ENTEROVIRAL RIBONUCLEIC ACID
Authors: Holland John J. , McLaren Leroy C. , Hoyer Bill H. , Syverton Jerome T. 
Published: June 2004

Chromatographic behavior of whole type 1 poliovirus and phenol-extracted viral RNA on diethylaminoethyl cellulose columns, as revealed by assay of plaque-forming capacity, indicated that infectious RNA had surface properties markedly different from those of the intact virus.
Infectious RNA of type 1 poliovirus and Coxsackie B1 virus was relatively resistant to heat inactivation as compared to intact virus. Kinetics of inactivation at elevated temperatures were multi-hit in character.
The structure of infectious enterovirus RNA was investigated by treatment with chemical inactivating agents. Urea and guanidine as hydrogen bond-disrupting agents, and mercaptoethanol and thioglycolate as disulfide bond-disrupting agents, and combinations of these did not destroy RNA infectivity whereas hydrogen bond-disrupting treatment inactivated intact virus rapidly. RNA infectivity was not reduced by chloroform extraction alone, or by octanol extraction alone, but was reduced by chloroform-octanol extraction which failed to depolymerize RNA to an extent detectable by ultracentrifugal analysis. Infectivity of type 1 poliovirus and Coxsackie B1 virus RNA was destroyed in accordance with first order kinetics by very dilute solutions of pancreatic ribonuclease, and by purified snake venom phosphodiesterase, but not at all by bacterial alkaline phosphatase. Inactivation by venom diesterase was not accelerated by prior treatment of RNA with bacterial alkaline phosphatase. These results indicated that infectivity of enteroviral RNA resided in a single stranded structure, that a single break of a phosphodiester bond anywhere along the structure was sufficient to destroy infectivity, and that infectivity did not require a terminal phosphate group.
Hydroxylamine, but not other carbonyl reagents, rapidly destroyed infectivity of intact type 1 poliovirus viral RNA without depolymerization of RNA-detectable by behavior in the analytical ultracentrifuge.
With S35-methionine-labeled poliovirus a very small fraction of radioactivity remained in RNA preparations following phenol extraction.
No evidence could be obtained to indicate that infectious enteroviral RNA was composed of subunits.
RNA extracted with phenol during the course of infection of HeLa cells with type 1 poliovirus resembled RNA obtained from purified whole virus with respect to heat inactivation, hydroxylamine inactivation, chromatographic separation, susceptibility to protein denaturing agents, and ability to infect productively both naturally susceptible HeLa cells and naturally insusceptible L strain mouse cells. Intracellular production of infectious RNA paralleled intracellular maturation of whole virus and preceded it by a very short interval.
STUDIES OF TWO KINDS OF VIRUS PARTICLES WHICH COMPRISE INFLUENZA A2 VIRUS STRAINS
Authors: Choppin Purnell W. , Tamm Igor 
Published: June 2004

Two kinds of virus particles have been found in varying proportions in influenza A2 strains isolated during the 1957 pandemic. Pure populations of the different particles were obtained, and these substrains were genetically stable on serial passage in the chick embryo.
The two virus particles differ markedly in several biological properties though they are antigenically similar. One kind of particle, designated "+," is relatively sensitive to specific antibody, is highly sensitive to inhibition by serum inhibitors and urinary mucoprotein, fails to elute or elutes very slowly from human erythrocytes, and is capable of agglutinating erythrocytes treated extensively with V. cholerae filtrate. The other particle, designated "-," is relatively insensitive to antibodies and urinary mucoprotein, completely insensitive to serum inhibitors, elutes rapidly from erythrocytes, and can agglutinate erythrocytes treated extensively with V. cholerae filtrate. Both "+" and "-" particles destroy virus receptors on urinary mucoprotein.
The relative proportions of these two particles determine the characteristics of parent strains in reactions with specific antibody, mucoprotein inhibitors, and erythrocytes. The "+" and "-" particles with several easily identifiable markers are well suited for genetic studies.
THE REMOVAL OF CARTILAGE MATRIX BY PAPAIN
Authors: Potter J. L. , McCluskey R. T. , Weissmann G. , Thomas L. 
Published: June 2004

In rabbits, the depletion of cartilage matrix which occurs following intravenous administration of papain treated with iodacetamide is attributable to a portion of the enzyme in the disulfide form which has not undergone alkylation. It is this portion that is reactivated in cartilage in vivo and initiates the enzymatic breakdown of the protein-polysaccharide complex which forms a major component of the matrix. Evidence presented in support of these conclusions indicates that, contrary to an earlier hypothesis, papain acetamide is not reactivated in vivo.
Following intravenous injection in amounts up to 4 mg./kg., active and inactive papain leaves the circulation at a rate proportional to the concentration, and it is likely that the initial rate of disappearance represents equilibration with the extracellular space. Following injection in the active or inactive form, a high proportion of papain in serum is bound to protein in the alpha globulin fraction. It is believed that in the case of fully active papain, the proportion which is not bound to alpha globulin becomes attached to other proteins of serum in extracellular fluid, such as albumin, by a process of enzyme substrate combination, and is thus prevented from diffusing into cartilage. In the case of inactive papain, a comparable excess remains free to enter cartilage, where it initiates depletion of matrix following reactivation within the tissue.
These conclusions provide an explanation for the failure of fully active papain to cause depletion of cartilage matrix in vivo; the widespread changes seen after the injection of papain inactivated by iodoacetamide or by simple reversible oxidation are attributable to a small proportion of the injected material which enters cartilage in the disulfide form in a concentration of approximately 2 micrograms/gm. wet weight. The possibility that such a small amount of protease, when reactivated, can produce changes in cartilage matrix has been confirmed by studies on the effects of papain on isolated cartilage and chondromucoprotein in vitro.
It has been shown that severe local injury results when active papain is injected into the skin of a rabbit in low concentrations. Since a much higher concentration of papain can be attained in the circulation without obvious adverse effects, it is evident that binding of the protease by alpha globulin and possibly other serum proteins may exemplify a mechanism whereby the tissues are protected from injury following entry into the circulation of other potentially harmful agents, such as proteolytic enzymes derived from cells or bacteria.
THE ISOLATION AND PROPERTIES OF THE SPECIFIC CYTOPLASMIC GRANULES OF RABBIT POLYMORPHONUCLEAR LEUCOCYTES
Authors: Cohn Zanvil A. , Hirsch James G. 
Published: June 2004

A method has been described for isolation of the specific cytoplasmic granules of rabbit polymorphonuclear leucocytes. Homogeneous suspensions of leucocytes were disrupted by lysis in 0.34 M sucrose. This procedure liberated the cytoplasmic contents of the cell and dissolved a considerable proportion of the nuclei. Following disruption, the sucrose lysate was separated into three fractions by differential centrifugation, i.e. 400 g or nuclear pellet, 8,200 g or granule pellet and the postgranule supernate. Microscopic examination revealed that the 8,200 g pellet was composed of intact granules as well as occasional mitochondria. The other two fractions were morphologically heterogeneous.
Studies with isolated granules demonstrated their lysis by a variety of weak acids and surface-active agents. When buffered solutions were employed between the ranges of pH 2.0 and 9.0, granule lysis began at pH 5.5 and was complete at pH 4.0.
Chemical analysis disclosed that the granule pellet contained protein and phospholipid with only traces of nucleic acids.
Approximately 70 to 80 per cent of the total cellular antimicrobial agent phagocytin was present in the granule fraction. This material was liberated from the granules by acid (pH 5.0 or lower).
Studies on selected enzymes showed that acid phosphatase, alkaline phosphatase, nucleotidase, ribonuclease, deoxyribonuclease, and beta glucuronidase were predominantly localized in the granule fraction. Approximately 50 per cent of total cellular lysozyme and cathepsin were also present in the 8,200 g pellet. Disruption of the granules was associated with the release of the majority of granule protein and enzymes in a non-sedimentable form. The properties and composition of rabbit polymorphonuclear leucocyte granules seem to be analogous to those of liver lysosomes.
THE USE OF PRECIPITIN ANALYSIS IN AGAR FOR THE STUDY OF HUMAN STREPTOCOCCAL INFECTIONS
Authors: Halbert S. P. , Auerbach T. 
Published: June 2004

Studies on the purification of group A streptococcal extracellular antigens detectable with naturally occurring human antibodies from normal individuals have been extended. It has been shown that streptococcal electrophoretic fractions intermediate between the most rapidly migrating components are quite complex. In the calcium phosphate chromatography of adjacent electrophoretic fractions, particular antigenic components desorbed at similar buffer elution steps.
It is clear from the results obtained that substantially more extracellular antigens than the twelve heretofore recognized are secreted in human beings during infection, as judged by their detection with human antibodies. The precise number is not yet known, but is probably greater than 16.
Of the nine components which thus far have been separated rather well from the others, four were previously identified as streptolysin "O," diphosphopyridine nucleotidase, proteinase precursor, and desoxyribonuclease B. The accumulated data substantiated these previous identifications.
The identity of a fifth antigen has been made as a possible complex of C carbohydrate and protein. Tentative evidence for the relationship of a sixth component to scarlet fever toxin has been presented.
It has been shown that rechromatography of crystalline proteinase precursor and desoxyribonuclease B on calcium phosphate columns resulted in elution principally at the expected stepwise increase in buffer concentration.
Attempts to isolate antigens present as mixtures in some calcium phosphate chromatographic peaks, by rechromatography on DEAE or CM cellulose columns resulted in only limited further purifications.
IMMUNOLOGIC STUDIES OF HEART TISSUE
Authors: Kaplan Melvin H. , Meyeserian Mary , Kushner Irving 
Published: June 2004

Reactions of normal and pathologic sera with heart tissue have been investigated by the immunofluorescent method, with particular reference to presumptive autoantibodies to heart and their differentiation from blood group isoantibodies and Wassermann antibody. In the heart, blood group substances A and B were found distributed in capillary walls, vascular endothelium, and interstitial connective tissue. In surveys of randomly selected sera, isoimmune reactions against tissue blood group substances A and B were noted infrequently. This finding was considered related to the limited sensitivity of fluorescent antibody methods. Heart tissue from blood group O individuals was used for screening of pathologic sera for presence of tissue-reactive factors.
Wassermann antibody was found reactive with constituents of myocardial sarcoplasm, of which the major reactant was cardiolipin. Wassermann-positive sera absorbed with beef cardiolipin gave evidence of reaction with other constituents of myofiber sarcoplasm. Sera of patients with rheumatic fever, rheumatic heart disease, rheumatoid arthritis, disseminated lupus, and liver disease frequently showed a marked reactivity with constituents of myofiber sarcoplasm. These serum factors were differentiated from Wassermann antibody. At least three patterns of immunofluorescent staining could be differentiated by the distribution of reactants in the myofiber sarcoplasm. These reactants were extractable with ethanol and methanol but not by acetone. Sera found reactive by immunofluorescence frequently gave positive flocculation and complement-fixation tests with alcohol extracts of human heart. Immunofluorescent tests were best correlated with flocculation reactions. Sarcoplasmic-reactive factors were associated in some sera with 19S gamma globulin as demonstrated by the use of fluorescent anti-19S gamma globulin. Serologic reactions with homologous or autologous heart were observed particularly frequently with sera from rheumatic patients approximately 2 weeks following cardiac surgery, as well as in some non-rheumatic patients following cardiac or thoracic surgery or acute myocardial infarction. The pathogenetic significance of these presumptive autoantibodies to heart is unknown. As yet, no definite conclusions may be drawn regarding their relationship to bound gamma globulin in rheumatic hearts or to the postcardiotomy and post-infarction syndromes.
STUDIES ON IMMUNE HUMAN HEMOLYSIS
Authors: Hinz Carl F. , Picken Mary E. , Lepow Irwin H. 
Published: June 2004

The Donath-Landsteiner reaction was studied using low and high titer antisera and purified antibody, normal and PNH erythrocytes, and human serum complement.
The requirement for complement in both the cold and warm phases of the reaction depended upon the level of antibody used and the sensitivity of the cells to hemolytic antibodies. Complement was not necessary in the cold phase using PNH cells and a potent source of antibody, but complement was required to be present at some stage if hemolysis were to occur.
Optimal conditions for the cold phase were at 1°C. for 30 minutes at pH 7.4. Ca++ ions were required. Hemolysis in the warm phase occurred within one minute, was optimal at 32°C., and required Mg++.
The relation of these observations to previous reports is discussed with respect to discrepant observations on the nature of the Donath-Landsteiner reaction.
STUDIES ON IMMUNE HUMAN HEMOLYSIS
Authors: Hinz Carl F. , Picken Mary E. , Lepow Irwin H. 
Published: June 2004

1. The inactivation, of C'1 blocks the completion of the cold phase of the Donath-Landsteiner reaction; inactivation of the other components of complement does not interfere with the cold phase of the reaction.
2. C'2, C'3, and C'4 are required for the completion of the hemolytic reaction. C'4 reacts in either the cold or warm phase, but C'2 and C'3 must react in the warm phase.
3. Partially purified C'1 or C'1 esterase can be substituted for whole serum in the cold phase, although neither reagent contains any of the other components of complement
4. Partially purified serum inhibitor of C'1 esterase blocks the effect of C'1 esterase in the cold phase, and reverses the effect of complement, C'1 or C'1 esterase when incubated with "activated" cells after the cold phase.
5. C'1 esterase activity can be eluted from "activated" erythrocytes with Na3EDTA.
6. The components of human complement in this human hemolytic reaction act in the order C'1, C'4, C'2, C'3. Ca++ is required for the reaction with C'1, and Mg++ is required for the reaction with C'2.
7. Accordingly, a functional role of C'1 esterase in a human disease state is demonstrated, and a human model is established for the study of the mechanism of action of complement.
CHANGING VIRAL SUSCEPTIBILITY OF A HUMAN CELL LINE IN CONTINUOUS CULTIVATION
Authors: Wong Sam C. , Kilbourne Edwin D. 
Published: June 2004

During its serial transfer and cultivation in this laboratory, a human conjunctival cell line (Chang) was observed to change in morphology. Concurrently no change was noted in the susceptibility of the cells to viruses capable of infecting the original cell line.
However, it was noted that the derived variant cell line had acquired susceptibility to the induction of cytopathic effects and incomplete virus formation by several strains of influenza viruses.
It was then discovered that swine influenza virus and the N-WS strain of influenza A virus could be serially propagated in the derived cell line with production of infective virus. The swine virus required adaptation, but the N-WS strain did not.
N-WS and swine influenza viruses multiply with infective virus formation only in the variant conjunctival cell and in no other cell line.
Antigenic, cytologic, and virologic evidence is presented that the influenza virus-susceptible variant cell is of human origin and is not a contaminating cell exogenously introduced.
Transition of a cell line from complete insusceptibility to susceptibility to virus infection and multiplication has not been described previously.
STUDIES ON THE PATHOGENESIS OF STAPHYLOCOCCAL INFECTION
Authors: Johnson Joseph E. , Cluff Leighton E. , Goshi Keiichi 
Published: June 2004

The influence of repeated staphylococcal infection of rabbit skin upon the characteristics of the experimentally induced lesion was studied. It was found that the repeated infection was associated with the development of delayed hypersensitivity unaccompanied by the appearance of demonstrable serum antibody. The delayed hypersensitivity to the staphylococcus resulted in an increased infectivity of the organism in skin of the sensitized animal, characterized by intensification of the lesions seen with large bacterial inocula and the induction of abscesses with inocula incapable of producing any lesion in normal rabbit skin. Similarly, the severity of experimentally induced pyoarthrosis was greater in sensitized than in normal rabbits. Induction of delayed hypersensitivity by vaccination of rabbits with washed heat-killed staphylococci resulted in the same increased severity of the infection and an increase in infectivity of the microorganism.
In contrast to the observations of cutaneous and joint infection, the sensitized animals appeared to be less susceptible to severe infection of the anterior chamber of the eye.
The role of immunity and hypersensitivity in staphylococcal infection is discussed and the possibility that non-specific inflammation may influence staphylococcal infection in the same way as specific hypersensitivity is indicated. Studies to further elucidate this are presented in the following pages.