bluuebunny/crossref_metadata_2025_split huggingface dataset:
THE APPLICATION OF TISSUE CULTURE TO THE STUDY OF EXPERIMENTAL ALLERGIC ENCEPHALOMYELITIS
Authors: Appel Stanley H. , Bornstein Murray B. 
Published: June 2004

1. In the presence of a source of complement, the gamma 2 globulin fraction of rabbit EAE serum results in complete demyelination of myelinated cultures of rat cerebellum. Exposure of the serum to homologous or heterologous brain specifically removes the myelinotoxic activity whereas exposure to non-nervous tissue does not. Polylysine has no effect upon the cultures or upon the demyelinative potency of EAE, whereas heparin inhibits activity presumably through an effect on complement.
2. With the fluorescent antibody technique, the EAE globulins are specifically localized to the myelin sheaths and glial cell membranes during the process of demyelination. As demyelination proceeds, the globulins become localized within the neuroglia in a homogeneous manner which contrasts sharply with the punctate pattern observed in control experiments.
3. The "delayed sensitivity" and classical antibody interpretations of experimental allergic encephalomyelitis are discussed. It is suggested that several factors may be responsible for the pathogenesis of EAE, one of which may well be a myelinotoxic antibody.
IMMUNOCHEMICAL IDENTIFICATION OF PARATHYROID HORMONE IN NON-PARATHYROID NEOPLASMS ASSOCIATED WITH HYPERCALCEMIA
Authors: Tashjian Armen H. , Levine Lawrence , Munson Paul L. 
Published: June 2004

1. Immunochemical cross-reactivity, but not identity, has been demonstrated between bovine parathyroid hormone and an antigen in biologically active extracts of human parathyroid tissue by quantitative C' fixation and C' fixation inhibition.
2. An antigen that fixes C' with rabbit antibody to bovine parathyroid hormone has been found in urea extracts of six human non-parathyroid neoplasms associated with a hypercalcemic syndrome mimicking primary hyperparathyroidism. Comparable extracts of control tissues and other tumors were serologically negative.
3. It is concluded that the tumor antigen is parathyroid hormone or a very closely related protein, and that its production by these neoplasms was the cause of the hypercalcemic syndrome in these six patients.
THE HISTOLOGICAL DISTRIBUTION OF THE BLOOD GROUP SUBSTANCES IN MAN AS DISCLOSED BY IMMUNOFLUORESCENCE
Authors: Szulman Aron E. 
Published: June 2004

The ABH antigens have been mapped out in the tissues of embryos and fetuses, 18 to 125 mm crown to rump length, 6 to 14½ weeks ovulation age.
Both the H and A,B antigens have the same distribution, and their spatial and temporal parallel obtains in intrauterine as well as extrauterine phases of life.
The cell wall antigens are present in their maximal distribution in the youngest specimens available. They outline the endothelium of the cardiovascular system, and the cells of most of the epithelia throughout the body. The exceptions are the liver, the adrenal, and the nervous system, presumed to have lost the epithelial antigens at stages antedating the youngest specimens here described.
The antigens of the stratified epithelia (and of the simple epithelia of the renal collecting tubules), together with the endothelial antigens, are permanent and persist into and throughout adult life. All other cell wall antigens disappear at a time characteristic for each organ. The antigenic recession coincides with recognizable steps of morphological advancement and often with assumption of function by the organ concerned; it is completed at about the end of the first trimester of pregnancy.
The secretion-borne antigens first appear at the 35 to 40 mm stage (8 weeks ovulation age) in the salivary glands and in the stomach, to be followed in a constant sequence by the rest of the gastrointestinal tract, respiratory system, and pancreas. The secretion of these antigens persists throughout life.
The early presence and wide distribution of the cell wall A,B antigens render them likely potential targets for maternal anti-A,B antibodies in heterologous pregnancies; the advent of the water-soluble substances at 8 weeks ovulation age may be providing a buffer shielding the fetal cell wall antigens by mopping up the maternal isoagglutinins.
IMMUNE MECHANISMS IN PARABIOSIS INTOXICATION
Authors: Hilgard Henry R. , Cornelius Eugene A. , Dalmasso Agustin P. , Martinez Carlos , Good Robert A. 
Published: June 2004

When A strain mice are placed in parabiotic union with (A x C57Bl/1)F1 hybrid partners, the parental strain partners are polycythemic and the hybrids anemic from the 5th through the 16th parabiosis days. All hybrids develop clinical intoxication between the 7th and the 12th days, and no pairs survive to 1 month.
Long-term survival of parabiotic pairs can be achieved if lethally irradiated or specifically tolerant parental strain mice are united to hybrid partners. Production of tolerance by either of these methods results in elimination of anemia-polycythemia by the 12th parabiosis day and prevents intoxication in the hybrid partners.
Preimmunization of the parental strain partners against the C57Bl/1 component of the hybrid leads to a considerable intensification of day 5 anemia-polycythemia. Intoxication develops in the hybrid partners between the 4th and the 6th days after union. It is concluded that anemia is primarily responsible for the syndrome of clinical intoxication.
Early anemia-polycythemia on day 5 does not depend upon an immunological mechanism, but the late anemia-polycythemia appearing between days 12 and 16 is a function of the ability of the parental strain mouse to react immunologically against its hybrid partner.
When neonatally thymectomized A strain mice are joined to hybrid partners, anemia-polycythemia is sustained through the 16th day and the hybrid partners develop clinical intoxication. On the other hand, when both partners are neonatally thymectomized, late anemia-polycythemia is considerably reduced, and the hybrid partners apparently do not develop clinical intoxication. It is concluded that normal hybrid mice are capable of reconstituting the immunological capacity of their thymectomized partners, whereas thymectomized hybrid mice do not have this restorative capacity.
These findings are discussed in terms of their possible application to the problem of the induction of immunological tolerance in adult mice by the parabiosis procedure.
APPLICATION OF A LOCALIZED HEMOLYSIN REACTION FOR SPECIFIC DETECTION OF INDIVIDUAL ANTIBODY-FORMING CELLS
Authors: Ingraham Joseph S. , Bussard Alain 
Published: June 2004

A technique is described which makes it possible to detect individual antibody-forming cells using a localized hemolysis reaction in a thickened culture medium containing sheep erythrocytes and guinea pig complement. This technique has the advantage over single cell isolation in that it is technically feasible to survey large populations in order to detect a very small active fraction. The cells can be observed continuously during the time of antibody release, and it appears that an estimate of the relative antibody-forming activity can be made from the size of the areas of lysis. Experiments with metabolic inhibitors indicate that active synthesis is occurring rather than release of preformed antibody. Some experiments on the detection of antibody other than anti-red cell antibodies are reported.
This technique has been applied to a study of the induction period of the primary response of rabbits to sheep red blood cells. The results of this experiment are consistent with an induction period of 2 to 3 days during which there is no increase in the number of active cells in spleen and lymph node reflecting the lag in appearance of detectable serum antibody followed by an abrupt rise of 50- to 100-fold between the 3rd and 5th day. However, the present data are not sufficient to exclude various other mechanisms.
STUDIES ON THE PATHOGENESIS OF FEVER
Authors: Berlin Richard D. , Wood W. Barry 
Published: June 2004

1. Phagocytosis promotes the release of endogenous pyrogen from polymorphonuclear leucocytes.
2. The release of pyrogen, though initiated by the phagocytic event, is not synchronous with it.
3. The postphagocytic release mechanism is not inhibited by sodium fluoride and, therefore, appears not to require continued production of energy by the cell.
4. The release process, on the other hand, is inhibited by arsenite, suggesting the participation of one or more sulfhydryl-dependent enzymes in the over-all reaction.
5. Particle for particle, the ingestion of heat-killed rough pneumococci causes the release of approximately 100 times as much pyrogen as the ingestion of polystyrene beads of the same size.
6. The pyrogen release mechanism of polymorphonuclear leucocytes separated directly from blood, unlike that of granulocytes in acute inflammatory exudates, is not readily activated by incubation of the cells in K-free saline. Despite this difference, both blood and exudate leucocytes following phagocytosis release large amounts of pyrogen, even in the presence of K+. The fact that the postphagocytic reaction is uninhibited by the concentrations of K+ which are present in plasma and extracellular fluids, suggests that this mechanism of pyrogen release may well operate in vivo.
7. As might be expected from the foregoing observations, the intravenous injection of a sufficiently large number of heat-killed pneumococci causes fever in the intact host. Intravenously injected polystyrene beads, on the other hand, are significantly less pyrogenic. Evidence is presented to support the conclusion that the fever in both instances is caused by pyrogen released from the circulating leucocytes which have phagocyted the injected particles.
8. The possible relationships of these findings to the pathogenesis of fevers caused by acute bacterial infections are discussed.
IMMUNOLOGIC STUDIES IN HUMAN ORGAN TRANSPLANTATION
Authors: Kirkpatrick Charles H. , Wilson W. E. C. , Talmage David W. 
Published: June 2004

Twenty-eight patients with chronic renal diseases and uremia were investigated with respect to their cutaneous responsiveness to a panel of antigens expected to elicit immediate and delayed hypersensitivity reactions. Compared to a control group, there was a marked decrease in the incidence of responses of both types.
Eighteen patients received renal allografts from members of the control group and were available for restudy in the postoperative period prior to the institution of adrenal steroid therapy. Each recipient acquired delayed responsiveness with specificity identical with that of the kidney donor. The donor group was reactive to 49 antigens to which the recipients were non-reactive preoperatively. Postoperatively, 40 of these reactivities were observed in the recipients.
This successful demonstration of the transfer of immunologically competent tissue in association with renal transplantation indicates that the cause of depressed cutaneous hypersensitivity in uremia is not an inability of the skin per se to react.
STUDIES ON ANTIBODY PRODUCTION
Authors: Sainte-Marie Guy , Coons Albert H. 
Published: June 2004

Cells from lymph nodes of rabbits injected repeatedly with bovine serum albumin were transferred subcutaneously to previously irradiated rabbits, and the recipients were immediately injected with bovine serum albumin. A good antibody response resulted. In a series of such animals killed on successive days, skin samples at sites of cell deposition were removed and examined by immunofluorescence and by light microscopy. In these tissues abundant plasmocytes were found to have multiplied and differentiated in a regular progression from immature, to medium, to mature plasmocytes. During the 6 days of the experiment the small plasmocytes accumulated until they reached 85 per cent of the total plasmocytic population.
The mitotic index of the large and medium plasmocytes averaged 11 per cent, implying a generation time of 6.3 hours on the basis of a 1 hour mitotic time. This rate of growth is sufficiently rapid to account for all the plasmocytes on the 6th day as deriving from less than 1 per cent of the population initially transferred. This rate and the orderly progression in the evolution of the plasmocytic population, make it highly improbable that plasmocytes arise from transformation of lymphocytes, but rather indicate that they spring from specific precursors already present among the transferred cells.
THE ROLE OF IMMUNITY IN THE PATHOGENESIS OF EXPERIMENTAL RETROGRADE PYELONEPHRITIS
Authors: Hunter Betty W. , Akins Lona L. , Sanford Jay P. 
Published: June 2004

Retrograde pyelonephritis was produced in rats by the intravesical injection of Proteus mirabilis. When animals were preimmunized against Proteus mirabilis by (a) prior infection, (b) administration of antigen, or (c) passively transferred antiserum, they were resistant to infection by proteus when challenged by the retrograde route.
The protective effect of specific preimmunization in retrograde pyelonephritis indicates that a major site of action is retardation of bacterial growth within the parenchyma of the kidney.
EFFECT OF ACTINOMYCIN D ON RNA SYNTHESIS AND ANTIBODY FORMATION IN THE ANAMNESTIC RESPONSE IN VITRO
Authors: Smiley J. Donald , Heard John G. , Ziff Morris 
Published: June 2004

Antibody synthesis in anamnestic lymphoid cells, measured by incorporation of leucine-C14 into specific antibody, was inhibited at moderate concentrations of actinomycin D. This was accompanied by marked inhibition of synthesis of RNA as measured by incorporation of H3-cytidine monophosphate. However, at low concentrations of actinomycin D, antibody synthesis was unaffected or even increased while RNA synthesis continued to be inhibited. The results obtained suggest that messenger RNA for antibody synthesis, either because it is relatively stable or present in excess, does not become a limiting factor until its synthesis is maximally inhibited.
Puromycin, an inhibitor of amino acid coupling, abolished antibody synthesis in low concentration. 6-Mercaptopurine had no effect on the synthesis of antibody or RNA even at high concentration.
The data obtained support the view that antibody synthesis follows pathways similar to those utilized for the formation of other types of proteins.
INDUCED PROTECTION OF ADRENAL CORTEX AGAINST 7,12-DIMETHYLBENZ[a]ANTHRACENE
Authors: Huggins Charles , Fukunishi Ryo 
Published: June 2004

7,12-Dimethylbenz[a]anthracene (7,12-DMBA) exerts adrenocorticolytic effects which set it apart from all other polynuclear aromatic hydrocarbons and aromatic amines which have been investigated. Adrenal damage by this compound appears to be due to its steric and electronic properties together with its unusually high solubility in lipides.
Many compounds given prior to 7,12-DMBA induced protection of adrenal. The most efficient inducers of protection are flat condensed aromatics possessing 4 or 5 rings; very small doses of these compounds were required to induce protection. Other compounds devoid of these properties induced protection but large or repeated doses were necessary. All inducers of protection had to be given prior to 7,12-DMBA to prevent adrenal necrosis; when given simultaneously with, or later than, this compound adrenal apoplexy resulted.
Protective aromatics and 7,12-DMBA as well induced synthesis of menadione reductase in liver. 3-Methylcholanthrene (3-MC) induced this enzyme in many normal organs including liver, lung, adrenal, and in mammary cancer as well. dl-Ethionine under appropriate conditions of time and dosage eliminated the adrenal protection induced by aromatics and also delayed the induction of menadione reductase while depressing the amount of this enzyme which was synthesized.
7,12-DMBA caused a greatly reduced incorporation of tritium from thymidine-H3 into washed acid-insoluble residue of adrenal. 3-MC given in advance mitigated the drastic effect of 7,12-DMBA on DNA synthesis and increased considerably the amount of tritium which was incorporated.
The specific damage to adrenal by 7,12-DMBA is a direct effect on cells. Protection of adrenal is a secondary effect which requires induction of protein synthesis and it results in improvement in synthesis of DNA.
SPECIFIC FRACTIONATION OF HUMAN ANTIDEXTRAN ANTIBODIES
Authors: Gelzer Justus , Kabat Elvin A. 
Published: June 2004

Human antidextran of one individual, absorbed specifically on sephadex, was fractionated into two populations of antibody molecules by successive elution with oligosaccharides of the isomaltose series of increasing size. The purified antibody fractions and some whole antidextran sera were found to fix complement with dextrans of molecular weight of 195,000 and above.
It could be demonstrated by quantitative microcomplement fixation inhibition assays that the antibody eluted with isomaltotriose had a higher affinity for smaller oligosaccharides relative to isomaltohexaose, indicating a high content of antibody molecules with smaller combining sites, while with the second fraction, eluted with isomaltohexaose, the small haptens were very poor inhibitors and the larger oligosaccharides inhibited readily, presumably due to a higher proportion of molecules with larger combining site size. Assays of similarly prepared fractions, obtained from earlier bleedings of the same individual (1), with inhibition of complement fixation were in good agreement with those obtained by inhibition of precipitation.
The two purified antidextran fractions were shown to differ with respect to their complement-fixing capacity. The fraction with molecules with smaller size-combining sites fixed only about half as much complement per unit antibody N as did the fraction containing largely molecules with larger combining sites suggesting that the strength of complement fixation is affected by the strength of the antigen-antibody interaction.
PATHOGENESIS OF INFLAMMATION
Authors: Moses John M. , Ebert Robert H. , Graham Richard C. , Brine Katherine L. 
Published: June 2004

Material obtained from the in vitro incubation of granulocytes from saline-induced peritoneal exudates of rabbits has been shown to produce inflammation and fever in rabbits. The supernatant material from cells incubated in saline has been termed granulocytic substance (GS) and is heat-labile. Its production is temperature dependent, occurring at 37°C but not at 4°C, requires viable cells, and is inhibited by potassium ions. A similar material is liberated when cells are incubated in a more physiologic medium. Freezing and thawing of granulocytes does not release GS and the active principle cannot be obtained from the incubation of lymphocytes.
GS produces a delayed inflammatory response as measured by leucocyte sticking and emigration in the rabbit ear chamber and the leakage of protein-conjugated dye at the site of intradermal injection. The former response can be accurately quantitated by calculation of the inflammatory index from reactions observed in the ear chamber. The inflammatory reaction and the properties of GS distinguish it from a variety of previously described mediators of inflammation, but GS appears to be identical with leucocytic pyrogen. The possible role of GS in delayed and protracted inflammation and its relationship to the pathogenesis of fever are discussed.
DETECTION OF SPECIFIC ANTIGEN IN SV40-TRANSFORMED CELLS BY IMMUNOFLUORESCENCE
Authors: Pope John H. , Rowe Wallace P. 
Published: June 2004

With an immunofluorescent technique involving the use of serum of hamsters with SV40 tumors, nuclear fluorescence was detected in each of five cell lines, derived from four mammalian species, transformed by SV40 virus. Essentially all nuclei, including those of multinuclear cells, were fluorescent-stainable. Serum of hamsters bearing SV40 tumors was also found to give nuclear fluorescence in susceptible cells (AGMK or BSC-1) acutely infected with SV40 virus.
These findings provide further evidence that cellular incorporation of the SV40 viral genome, with partial expression of the genome by synthesis of at least one virus-specific antigen, is an integral property of all SV40 transformed cells.
THE IMMUNOGLOBULINS OF MICE
Authors: Fahey John L. , Wunderlich John , Mishell Robert 
Published: June 2004

Two classes of 7S γ-globulins are identified in normal mouse serum and are designated 7S γ2-globulins and 7S γ1-globulins. These two immunoglobulin classes are similar in size. They differ in range of electrophoretic mobility, in specific antigenic determinants, and in genetically determined isoantigens.
Four classes of immunoglobulins in mouse serum, i.e. 7S γ2-, 7S γ1-, γ1A (ß2A), and γM-globulins, were shown to have antibody activity. Each class was characterized and shown to have distinctive immunochemical and physicochemical properties. The genetically determined isoantigens, Iga-1 and Iga-2, were shown to be present only on 7S γ2-globulin molecules.
THE IMMUNOGLOBULINS OF MICE
Authors: Fahey John L. , Wunderlich John , Mishell Robert 
Published: June 2004

Two subclasses of mouse 7S γ2-globulins are identified, and are designated γ2a- and γ2b-globulins. They are distinguished from 7S γ1-globulins, γ1A (ß2A)-globulins, and γ1M-globulins of mouse serum. Antibody activity was detected among the γ2a-globulins and γ2b-globulins of hyperimmune mouse serum.
γ2a- and γ2b-myeloma proteins were identified. The genetically determined isoantigen, Iga-1, was present on γ2a-myeloma proteins, but not on γ2b-myeloma proteins.
These findings indicate a complexity among the 7S γ2-globulins which must be taken into account in structural, functional, and genetic studies of immunoglobulins.
STUDIES ON THE MECHANISMS OF HYPERSENSITIVITY PHENOMENA
Authors: Lichtenstein Lawrence M. , Osler Abraham G. 
Published: June 2004

Human leukocytes, isolated from the blood of ragweed-sensitive donors, release histamine upon reaction with a purified protein antigen derived from this pollen. The release process has been studied with washed cells suspended in a defined, serum-free medium. Physiologic levels of pH, ionic strength, and temperature, as well as both calcium and magnesium, are required for optimal cellular reactivity. The level of cellular sensitivity of approximately 200 ragweed-sensitive donors has been ascertained, and the kinetics of the release process studied. The rate of histamine release is a function of antigen concentration, but even with a large excess of this reagent it is impossible to abolish a lag phase. Chelation of the divalent cations or a decrease in the reaction temperature may be utilized to stop the reaction. These measures are effective both before and after the initiation of histamine release. Diminished cellular reactivity (desensitization) has been achieved by several procedures. These have in common the addition of antigen to cells in an environment deficient in but a single respect, followed by a restoration of optimal conditions.
The significance of these data has been discussed and it has been proposed that immunologically induced histamine release is an active, enzymatically mediated process which occurs as a multistep response of viable cells to a specific antigenic stimulus.