bluuebunny/crossref_metadata_2025_split huggingface dataset:
IMMUNOLOGICAL STUDIES IN ULCERATIVE COLITIS
Authors: Lagercrantz R. , Hammarström S. , Perlmann P. , Gustafsson B. E. 
Published: June 2004

The incidence and height of antibody titers to colon, assayed by indirect hemagglutination with a heat stable colon extract from germ free rats, is significantly higher in sera from patients with ulcerative colitis than in those from healthy controls or from patients with amebic liver abscess or dysentery. While sera from ulcerative colitis patients and controls are indistinguishable in regard to incidence and height of antibody titers to Forsman antigen, Staphylococcus aureus S 209, Clostridium difficile, and several common strains of E. coli, they have elevated titers and increased incidence of antibodies to a heat stable antigen of E. coli O14. Patients with amebic dysentery have normal titers of such antibodies.
Absorption of patients' sera with E. coli O14 antigen inhibits the colon directed hemagglutination reaction in approximately 30% of the cases tested. Likewise, the anti-E. coli O14 reaction can sometimes be inhibited with the colon extract. Other E. coli strains and other bacteria are inactive or have only weak inhibitory activity. Hemagglutination inhibition experiments show that germ free rat colon and E. coli O14 contain common structures, depicted by antibodies in the patients' sera. This pattern of reactivity closely resembles that seen in rats made autoimmune to colon by injection of newborn rabbit colon.
E. coli O14 is known to carry a heterogenetic antigen present in lower concentration (or activity) in most Enterobacteriaceae. Hemagglutination inhibition experiments with rabbit antisera to E. coli O14 suggest that the antigen common for E. coli O14 and colon is related to this heterogenetic antigen. The findings imply that this antigen, which is constantly present in low concentrations in the human colon, may give rise to anticolon antibody formation in ulcerative colitis through breakage of tolerance. Since this antigen is present in healthy individuals as well, additional factors are required to explain the induction of anti-colon autoimmunity in ulcerative colitis.
ENDOTOXIN AS ADJUVATOR TO THE TRANSPLANTATION OF A MOUSE MAMMARY TUMOR
Authors: Henderson James Stuart 
Published: June 2004

The mouse mammary tumor MT 296 was used in a further series of experiments on the implantation of tumor, plated out in vivo, from suspensions of individual cells.
Lipopolysaccharide from S. typhosa was shown to exert an adjuvator influence. But this adjuvator, an endotoxin, had no direct effect on the suspended tumor cells, unlike the liver preparations previously reported.
Lipopolysaccharide from S. typhosa was shown to act on the host. It made the host's connective tissue expanses more susceptible to successful implantation by the tumor cells. It did this only if present at the time these connective tissue expanses were split. The increased susceptibility, caused by splitting the connective tissue expanses in the presence of lipopolysaccharide, declined quickly after 24 hr.
The structural changes wrought upon the connective tissues by splitting them in the presence of lipopolysaccharide are described. They show kinship to a Schwartzman reaction of the local type. Their possible role in the adjuvator effect on the plating of single cell suspensions of this tumor is discussed.
IMMUNOLOGICAL INDUCTION OF INCREASED VASCULAR PERMEABILITY
Authors: Henson P. M. , Cochrane C. G. 
Published: June 2004

Two mechanisms have been described whereby rabbit platelets in vitro may be induced to release their contained histamine by the reaction of antigen and antibody. Both processes require the participation of the complement system.
In the first, the adherence of platelets to particulate antigens such as zymosan or erythrocytes which have fixed complement through the third component was followed by histamine release. Plasma lacking C6 activity was fully active in this system.
In the second mechanism, the reaction of soluble antigen with antibody in the presence of plasma also caused release of histamine from platelets and platelet clumping was observed. The release process, which appeared to follow the adherence of platelets to the immune complex, required the action of C6 and perhaps the later-acting components. No evidence could be obtained that a soluble factor was produced which caused the release. Instead, an inhibitor of the release process was detected after incubation of antigen, antibody, and plasma.
Antibody preparations capable of giving complement-dependent PCA reactions in rabbits were also shown to induce the release of histamine from platelets in vitro.
THE SERUM BACTERICIDAL SYSTEM: ULTRASTRUCTURAL CHANGES IN NEISSERIA MENINGITIDIS EXPOSED TO NORMAL RAT SERUM
Authors: Swanson John , Goldschneider Irving 
Published: June 2004

Exposure of meningococci to the bactericidal system of normal rat serum initiates a series of ultrastructural changes that accompany death of the organism. These morphological alterations consist of complement-dependent holes in the cell wall outer membrane, edema of the periplasmic space and cytoplasm, and accumulation of fibrillar material in and on the cell wall. Dissolution of the dense line and rupture of the cytoplasmic membrane also occur in meningococci exposed to normal rate serum. These latter two changes, however, are not seen in meningococci that are killed by bentonite-absorbed (lysozyme-deficient) serum, nor are they invariably present when other serum-susceptible organisms (N. catarrhalis and Herellea sp.) are treated with normal rat serum.
The pattern of development of edema in serum-treated meningococci suggests that the cell wall outer membrane, mucopeptide layer, and cytoplasmic membrane act synergistically to maintain osmotic equilibrium of the bacterium. Death of the bacterium seems related to alteration of permeability following injury to the outer membrane.
Holes are demonstrable, by negative straining, in the outer membrane of the meningococcal cell wall after exposure to the bactericidal effects of rat serum. The lesions are 110 A average greatest diameter and depend on the presence of antibody and complement for their formation. In addition, 82 A diameter holes are present in the walls of normal, untreated meningococci. The relation of complement-dependent holes to the smaller, naturally occurring holes is not known.
A NEW METHOD FOR THE ENUMERATION OF ANTIGEN-REACTIVE CELLS RESPONSIVE TO A PURIFIED PROTEIN ANTIGEN
Authors: Armstrong W. D. , Diener E. 
Published: June 2004

A new technique for the enumeration of antigen-reactive cells (ARC) responsive to the polymer antigen of S. adelaide flagellin (POL) is described for two strains of mice. Foci have been shown to be antibody dependent, may be mimicked by IgM as well as IgG antibodies, and contain specific antibody-forming cells (AFC). The use of POL offers a system unencumbered by relatively high numbers of background foci which, when present, appear to be basically different from those found using the SRBC antigen.
The response of 1 antigen-reactive cell (ARC) focus/1 x 106 CBAT6T6 mouse spleen cells is linearly related to the injected number between 1 x 106–3 x 106 donor spleen cells and since 5% of injected cells remain in the spleen, there are an estimated 2400 ARC/spleen.
The number of ARC foci does not increase significantly after the 5th postantigen day, and by the 8th day the AFC progeny of ARC have reached the maximum mean of 280 AFC/ARC focus. In response to increasing antigen concentrations, an initial rise in the number of AFC as well as ARC is observed, resulting in a relatively constant AFC/ARC ratio. This suggests that the number of ARC stimulated determines the total number of AFC produced under these conditions rather than a variable mitotic rate of the ARC offspring. The main significance of this technique is that it will allow a study of the kinetics of the ARC in the primary and secondary immune response as well as in immunological tolerance.
TISSUE INTERACTION IN THE DEVELOPMENT OF THYMUS LYMPHOCYTES
Authors: Owen J. J. T. , Ritter M. A. 
Published: June 2004

Thymic rudiments from chick and mouse embryos have been cultured in diffusion chambers on the chick chorioallantois. In this situation their supply of blood-borne stem cells is cut off. Although rudiments from older embryos become fully lymphoid under these circumstances, primordia from early embryos fail to develop any lymphoid cells. Early chick rudiments will however develop completely if they are grafted directly to the chorioallantois where they receive a vascular supply.
It is concluded that stem cells first enter the chick thymic anlage at between 6 and 7 days' incubation and the mouse thymic rudiment between 10 and 11 days' gestation. During the following few days of development there is a rapid inflow of stem cells to the rudiments. Since it is likely that stem cells, once they have entered the thymic primordium, are capable of only limited proliferation, it must be concluded that an inflow of stem cells continues once full lymphopoiesis has begun, although perhaps at a reduced rate.
Finally, the importance of the interaction between stem cell and organ rudiment to normal thymic development is discussed in relation to the pathogenesis of thymic anomalies.
PATHOGENESIS OF CHRONIC DISEASE ASSOCIATED WITH PERSISTENT LYMPHOCYTIC CHORIOMENINGITIS VIRAL INFECTION
Authors: Oldstone Michael B. A. , Dixon Frank J. 
Published: June 2004

Mice infected shortly after birth with lymphocytic choriomeningitis (LCM) virus are not immunologically tolerant, although they carry the virus throughout life. These LCM carrier mice make anti-LCM antibody, which apparently complexes with viral antigen in the circulation and these complexes accumulate in the glomeruli.
LCM carrier mice of different strains vary significantly as to concentration of detectable infectious virus in their tissue, amount and time of appearance of anti-LCM antibody, and development of an associated chronic disease. The chronic disease consists primarily of glomerulonephritis, focal hepatic necrosis, and disseminated lymphoid infiltrations. LCM carriers of the SWR/J strain contain high tissue concentrations of virus, considerable anti-LCM antibody detectable in the glomeruli by 3 wk to 2 months of age and develop chronic disease within the first 2–3 months of life. In contrast, C3H strain LCM carriers contain 1/1000 as much infectious virus, less detectable anti-LCM antibody, and have not, over a 24 month observation period, developed any detectable disease. B10D2 old and new carrier mice with intermediate amounts of virus develop chronic disease during the latter half of the first year of life.
The pathogenesis of the glomerulonephritis of chronic LCM disease is apparently related to the formation of circulating virus-antibody complexes which are trapped in the glomerular filter. There is no evidence for direct glomerular injury by the virus nor for any autoimmune response by the host.
EFFECT OF ADRENALECTOMY ON BLOOD PRESSURE IN SALT-FED, HYPERTENSION-PRONE RATS
Authors: Iwai Junichi , Knudsen Knud D. , Dahl Lewis K. , Tassinari Lorraine 
Published: June 2004

In adrenalectomized, genetically hypertension-prone rats, a high degree of correlation was found between evidence of functioning adrenal tissue and the development of salt hypertension. There is considerable evidence that some rats have the capacity to regenerate functioning adrenal cortical tissue from accessory glands and microscopic rests, sometimes in remote locations. Therefore, the criteria for continued absence of adrenal function after surgical adrenalectomy are critical. In this study we used three tests to validate the presence, or absence, of adrenal function: (a) a biochemical test, the quantitative, serial measurement of plasma glucocorticoids in individual rats; (b) a physiological test, the ability to survive a virtually sodium-free diet; and (c) the anatomical search for histological evidence of adrenal cortical tissue. Among those animals that developed hypertension after adrenalectomy, the correlation between plasma steroid concentration and blood pressure was statistically significant. We suspect that this correlation exists only during the period when cortical tissue is regenerating; it does not exist among intact animals with and without hypertension induced by salt.
It was concluded that some adrenocortical function is necessary for salt hypertension to develop. The evidence was insufficient to settle the question whether the action of corticosteroids is causative, or whether they play a supporting, although necessary, role for an extraadrenal hypertensinogenic factor to become manifest.
CYSTIC FIBROSIS OF THE PANCREAS
Authors: Danes B. Shannon , Bearn Alexander G. 
Published: June 2004

103 individuals from 16 families with cystic fibrosis and 87 individuals without family history of cystic fibrosis have been studied using the methods of cell culture. Skin fibroblast cultures derived from 19 affected children, and fibroblast cultures from 11 different organs obtained at autopsy from two affected children, showed cellular metachromasia. The morphological appearance and the intracellular mucopolysaccharide content enabled these cultures to be divided into two distinct classes. Class I had discrete cytoplasmic metachromatic vesicles and a mucopolysaccharide content similar to that observed in normal fibroblasts. In class II the metachromasia was present in both vesicles and granules and was evenly distributed throughout the cytoplasm. The mucopolysaccharide content of these cells was markedly increased.
The cultures derived from the parents, presumed heterozygotes, and other members of each family showed cells with the same type of metachromasia as that demonstrated by the propositus. These data strongly suggest that cystic fibrosis is not a homogeneous entity and, moreover, can be caused by homozygosity of genes at two distinct loci.
The recognition of cytoplasmic abnormalities in skin fibroblasts derived from affected individuals and heterozygous carriers for cystic fibrosis should facilitate genetic and biochemical studies on the heterogeneity of this inborn error of metabolism.
EFFECTS OF NEOMYCIN AND PENICILLIN ADMINISTRATION ON MUCOSAL PROLIFERATION OF THE MOUSE SMALL INTESTINE
Authors: Khoury Kenneth A. , Floch Martin H. , Herskovic Teodoro 
Published: June 2004

The effects of an oral neomycin and penicillin regimen on intestinal bacteriology and on morphology and function of the small intestine of mice were investigated. Quantitative and qualitative stool cultures on selective media of the treated animals revealed only growth of yeast organisms. The treated animals developed enlargement of the ceca with fluid contents and watery stools, resembling characteristics of germfree animals.
Radioautography with tritiated thymidine revealed an increased epithelial cell migration rate in the mice treated with the antibiotics for 3 to 5 wk. A slight increase in villus height was also noted. The treated male mice showed greater variance than the treated females in epithelial cell migration rates.
Histochemical staining reactions showed a decrease in nonspecific esterase and in NADH dehydrogenase activity in the proximal gut of the antibiotic animals. Stains of distal gut and those for acid and alkaline phosphatase, NADPH dehydrogenase, lactic dehydrogenase, and succinic dehydrogenase were similar to the controls. A slight increase in sucrase activity and a slight decrease in lactase activity in the antibiotic animals was observed in contrast to control animals. Germfree mice, however, had greater sucrase and lactase activity. Transport of L-methionine was slightly reduced in the distal segment of the treated animals.
Since the direction of these changes is away from the intestinal state observed in germfree animals, they are probably the result of the direct action of the antibiotics on the gut.
THE RENAL HANDLING OF HEMOGLOBIN
Authors: Bunn H. Franklin , Esham William T. , Bull Robert W. 
Published: June 2004

The glomerular filtration of hemoglobin (α2ß2) was studied under conditions in which its dissociation into αß dimers was experimentally altered. Rats receiving hemoglobin treated with the sulfhydryl reagent bis(N-maleimidomethyl) ether (BME) showed a much lower renal excretion and prolonged plasma survival as compared with animals injected with untreated hemoglobin. Plasma disappearance was also prolonged in dogs receiving BME hemoglobin. Gel filtration data indicated that under physiological conditions, BME hemoglobin had impaired subunit dissociation. In addition, BME hemoglobin showed a very high oxygen affinity and a decreased rate of auto-oxidation.
Glomerular filtration was enhanced under conditions which favor the dissociation of hemoglobin into dimers. Cat hemoglobin, which forms subunits much more extensively than canine hemoglobin, was excreted more readily by the rat kidney. The renal uptake of 59Fe hemoglobin injected intra-arterially into rabbits varied inversely with the concentration of the injected dose.
THE EFFECT OF CYTOTOXIC AGENTS ON THE PRIMARY IMMUNE RESPONSE TO LISTERIA MONOCYTOGENES
Authors: Tripathy S. P. , Mackaness G. B. 
Published: June 2004

Four drugs, representing four different categories of cytotoxic agents, were studied for their effect on the immune response to Listeria infection in mice. The development of the host's immune response is revealed by a progressive change in the slope of the bacterial growth curve in spleen and liver. It has its onset at 24 hr in untreated mice, but in the presence of effective immunosuppression the organism multiples uninterruptedly until the animal dies from overwhelming infection. When administered as single injections at the time of infection, cyclophosphamide, vinblastine, and azathioprine all produced an effective immunosuppression, characterized by continuous bacterial multiplication.
Methotrexate was also immunosuppressive, but unlike the others its effects were reversible. They could be sustained, however, by further treatment.
Studies of the time-response relationship indicated that cyclophosphamide was highly active over a broad time-span ranging from 2 days before infection to 4 days after infection. Vinblastine on the other hand was maximally active when given on the day of infection, while methotrexate had its greatest effect when given 48 hr after infection. These differences indicate that these three drugs act on different cell populations involved in the host's immune response. The effects observed have been discussed in relation to what is known of the modes of action of the drugs tested.
An observation of interest was the phenomenon of enhanced immunity in animals treated with cyclophosphamide or vinblastine 7–11 days before, and with methotrexate 4 days before infection; reactive hyperplasia of lymphoid tissue following withdrawal of drug was again advanced as an explanation for the occurrence of this paradoxical effect.
The experimental model employed is simple, requiring only routine bacteriological facilities and minimal equipment. It seems to offer a useful means of assessing the immunosuppressive activity of drugs and of determining the time-course of their action; it could also be of value in the screening of anticancer agents.
THE MECHANISM OF ACTION OF ANTI-LYMPHOCYTE SERUM
Authors: Lance Eugene M. 
Published: June 2004

Studies designed to gain insight into the mechanism of action of the active component of antilymphocyte serum were carried out using an antibody eluate prepared from the IgG fraction of anti-lymphocyte serum by absorption and subsequent elution from thymocyte membrane. The resulting antibody eluate was labeled with radionuclide tracer to determine the fate of the antibody in vivo. The result indicated that anti-lymphocytic antibodies are eliminated from recipients extremely rapidly. The mechanism for this rapid clearance appears to depend upon the absorption of antibody molecules onto lymphocyte surfaces and the subsequent clearing and degradation of the antibody-lymphocyte complexes by the reticuloendothelial system.
Distribution studies confirm that the major site of antibody-lymphocyte interaction occurs in the periphery with relatively little penetration of antibody within lymphoid organs. Radioautographic studies showed that the pattern of localization within lymphoid and other organs is confined to rather specific areas. These observations are believed to offer strong support for the notion that anti-lymphocyte serum achieves its immunosuppressive effect by bringing about a selective ablation of the population of recirculating lymphocytes.
THE ANAMNESTIC ANTIBODY RESPONSE TO TYPE III SPECIFIC PNEUMOCOCCAL POLYSACCHARIDE
Authors: Paul William E. , Benacerraf Baruj , Siskind Gregory W. , Goidl Edmond A. , Reisfeld Ralph A. 
Published: June 2004

Rabbits immunized with killed type III pneumococci respond to anamnestic challenge by type specific polysaccharide (S III) with the synthesis of anti-S III antibody if a long interval is allowed to elapse between primary and secondary immunization. A study of the anti-S III antibody produced early and late in the immune response revealed no change in molecular class, banding pattern of dissociated light chains, or S III binding characteristics as measured under equilibrium conditions or by study of dissociation kinetics utilizing radioiodinated p-OH-benzyl-S III.
Sequential booster injections of S III into rabbits primarily immunized with whole organisms 8 or 9 months earlier led to a progressive decrease in the number of animals showing successful anamnestic responses and in the magnitude of those responses.
It is concluded that S III depletes the antigen sensitive cell population in the secondary response largely because of its limited ability to stimulate sustained proliferation by such cells.
TRANSFER OF EXPERIMENTAL AUTOIMMUNE THYROIDITIS BY SERUM FROM THYROIDECTOMIZED DONORS
Authors: Nakamura R. M. , Weigle W. O. 
Published: June 2004

When rabbits were injected with 10.0 mg rabbit thyroglobulin in complete Freund's adjuvant, the earliest thyroid lesions were seen on day 5 and uniformly severe thyroid lesions were seen by day 14; these observations were not significantly different from the thyroid lesions observed at 1 and 2 months post-immunization. Pooled sera were obtained from immunized, thyroidectomized, and nonthyroidectomized donors on various days and transferred to normal recipient rabbits in different experiments. Successful transfer of thyroid lesions was seen when serum containing early antithyroglobulin antibody obtained from thyroidectomized donor animals at various times after immunization was injected into normal recipients in a sequential manner. Immunofluorescent studies of recipient thyroid glands showed focal fixation of rabbit γ-globulin and ß1C complement in thyroid follicles. When purified antibody to rabbit thyroglobulin obtained from thyroidectomized donor sera was transferred sequentially as above, significant thyroid lesions were seen in recipient rabbits. In contrast, no thyroid lesions were seen in recipient animals injected with rabbit sera containing late antithyroglobulin antibody from thyroidectomized donors or hyperimmune sera from guinea pigs.
No thyroid lesions were seen in recipient animals injected either with sera from donors given complete adjuvant without thyroglobulin or with globulin fraction of pooled sera containing early antithyroglobulin antibody obtained on various days from nonthyroidectomized donors. Similarly, rabbits rendered unresponsive to guinea pig γG-globulin and periodically injected with guinea pig anti-rabbit thyroglobulin showed no thyroid lesions.