bluuebunny/crossref_metadata_2025_split huggingface dataset:
FACTORS INFLUENCING PULMONARY METHANE EXCRETION IN MAN
Authors: Bond John H. , Engel Rolf R. , Levitt Michael D. 
Published: June 2004

Measurements of pulmonary excretion of methane (CH4) were used to obtain information on the CH4-producing bacteria in man. Preliminary studies indicated that (a) all CH4 excreted by man is produced by colonic bacteria, (b) there is no appreciable utilization of CH4 by man, and (c) breath CH4 can serve as a relatively accurate indicator of CH4 production in the intestine.
The rate of pulmonary CH4 excretion varied enormously, ranging from undetectable (&lt;5 x 10–6 ml/min) to 0.66 ml/minute. In general, the CH4 excretion rate for subjects was consistently very low (nonproducers) or relatively large (producers). 33.6% of the adult population were producers of CH4. Whereas diet, age over 10 yr, and sex did not influence the rate of CH4 production, some familial factor appeared to play an important role. 84% of siblings of CH4 producers also were producers, while only 18% of the siblings of nonproducers were found to be CH4 producers. This familial tendency appeared to be determined by early environmental rather than genetic factors.
These studies of CH4 excretion demonstrate that the exposure of individuals to intestinal bacterial metabolites may differ markedly and that these differences may be chronic and determined by familial factors.
STUDIES ON ANTIGEN-ANTIBODY COMPLEXES
Authors: Mannik Mart , Arend William P. , Hall Anthony P. , Gilliland Bruce C. 
Published: June 2004

Solid phase immunoadsorbents were prepared by coupling antigens to agarose. With this technique specific antibodies were easily isolated in large amounts. The γG-globulin class of antibodies isolated in this manner were not denatured as judged by their normal biological half-life in rabbits. Soluble immune complexes at fivefold antigen excess were prepared from isolated specific antibodies and HSA, human λ-chains, human λG-globulins, and a Waldenström's macroglobulin as antigens. In all these preparations a characteristic immune complex was encountered that represented the smallest stable antigen-antibody union. In the HSA-anti-HSA system they were found to be AgAb2 complexes, and Ag2Ab complexes in the γG-anti-γG system. These stable complexes fixed complement ineffectively. Also, a spectrum of larger complexes was present in each system, and these complexes fixed complement effectively.
With intact antibodies the disappearance curves of immune complexes from the circulation were composed of three exponential components. The immune complexes larger than AgAb2 were quickly removed from the circulation with half-lives of 0.09–0.37 hr. Their clearance was not dependent on complement components, in that depletion of complement by cobra venom factor and aggregated γG-globulin did not alter the pattern of their removal from the circulation. However, when the interchain disulfide bonds of antibodies were reduced and alkylated, the removal of the λ-anti-λ, HSA-anti-HSA, and γG-anti-γG complexes was altered. In these experiments the disappearance curves were composed of two exponential components and the rapid removal of the greater than AgAb2 complexes did not occur. The immune complexes prepared from reduced and alkylated antibodies fixed complement ineffectively.
The presented data indicate that the rapid removal of circulating immune complexes, containing γG-globulin molecules as antibodies, depends primarily on the number of antibodies involved. Furthermore, complement fixation is not involved in the rapid removal of such complexes. Nevertheless, the rapid removal of immune complexes and their ability to fix complement have similarities for optimal function in that both processes require intact interchain disulfide bonds of antibodies and complexes that exceed the AgAb2 combination.
ON THE NUMBER AND NATURE OF ANTIGEN-SENSITIVE LYMPHOCYTES IN THE BLOOD OF DELAYED-HYPERSENSITIVE HUMAN DONORS
Authors: Jimenez Luis , Bloom Barry R. , Blume Myron R. , Oettgen Herbert F. 
Published: June 2004

The virus plaque assay has been successfully employed to enumerate antigen-sensitive cells in the peripheral blood lymphocyte populations of tuberculin-hypersensitive human donors. The method is based on the finding that, while resting lymphocytes are unable to produce a variety of viruses upon infection, lymphocytes activated by specific antigens become capable of virus replication. The average number of antigen-sensitive cells detected in cell populations from donors reacting to first test strength or intermediate test strength tuberculin was approximately 3.6/1000 lymphocytes, and the averages for both groups were similar.
Studies on the kinetics of appearance of these virus plaque-forming cells and on the effects of the mitotic inhibitor, vinblastine, indicate that the activation of these antigen-sensitive cells is a linear process and that the cells must be nondividing cells during this process. These qualities contrast markedly with those described for the mitogenic response and the antibody-producing cells which require cell division and increase exponentially. On the basis of these experiments it is suggested that the antigen-sensitive cell measured in the virus plaque assay is the effector cell in delayed-type hypersensitivity reactions and, in addition, may be one of the cells critically involved in antibody formation.
THE ENZYMATIC DEGRADATION OF HEMOGLOBIN TO BILE PIGMENTS BY MACROPHAGES
Authors: Pimstone Neville R. , Tenhunen Raimo , Seitz Paul T. , Marver Harvey S. , Schmid Rudi 
Published: June 2004

Recent studies have identified and characterized the enzymatic mechanism by which hemoglobin-heme is converted to bilirubin. Under physiologic conditions the enzyme system, microsomal heme-oxygenase, is most active in the spleen followed by the liver and bone marrow, all of which are tissues that normally are involved in the sequestration and metabolism of red cells. Indirect evidence suggested that the reticuloendothelial system is important in this process. To test this hypothesis, conversion of heme to bilirubin was studied in macrophages obtained by chemical or immunological means from the peritoneal cavity or from the lungs of rodents. Homogenates of pure populations of these cells were devoid of heme-oxygenase activity, unless before harvesting the macrophages had been exposed to methemalbumin, microcrystalline hemin, or hemoglobin in vivo. In macrophages exposed to heme pigments, the specific activity of heme-oxygenase was far in excess of that in the spleen or liver. Enzyme activity was also present in the granulomatous tissue surrounding subcutaneous hematomas.
The heme-oxygenase system in macrophages resembles that in the spleen and liver in that it is localized in the microsomal fraction, has an absolute requirement for molecular oxygen and NADPH, is inhibited by carbon monoxide, and has a similar Km. These findings indicate that cells of the reticuloendothelial system, presumably including the Kupffer cells of the liver and the macrophages of the spleen, possess the enzymatic machinery for converting hemoglobin-heme to bilirubin. The reaction is a mixed function oxidation, probably involving cytochrome P450 as the terminal oxidase. Enzyme activity in macrophages is capable of regulatory adaptation in response to substrate loads. In the standard assay system for the enzyme, disappearance of heme always was in excess of the amount of bilirubin formed, suggesting the simultaneous presence of alternate routes of heme degradation not involving bilirubin as an end product or intermediate.
IN VITRO STUDIES OF COMPLEMENT FUNCTION IN SERA OF C4-DEFICIENT GUINEA PIGS
Authors: Frank Michael M. , May Joseph , Gaither Thelma , Ellman Leonard 
Published: June 2004

In vitro studies were performed utilizing sera from a strain of guinea pigs with a total absence of hemolytically active C4. Previous studies in these animals have demonstrated normal complement-dependent inflammatory reactions, suggesting that they are able to bypass their deficiency of C4. In vitro studies with C4-deficient serum also indicate normal activation of late-acting C components. Thus, endotoxin was capable of fixing normal amounts of the late components of complement (C3-9) in these sera, but did not fix C1 and C2. Antigen-antibody complexes fixed both early and late components of complement, although components beyond C4 were fixed less efficiently than in normal sera. Therefore, both in vivo and in vitro evidence indicates that the C4-deficient guinea pigs possess an alternate pathway for activation of late-acting complement components.
Antigenic analysis of C4-deficient serum utilizing both guinea pig anti-C4 antibody and rabbit anti-C4 antibody suggests an absolute deficiency of C4-like molecules. Sera from animals with C4-deficiency were found to have one-half the normal level of C2. Sera from five of eight animals tested had 10–20% normal C1 activity. C3-9 assayed as a complex was normal.
CARRIER FUNCTION IN ANTI-HAPTEN ANTIBODY RESPONSES
Authors: Katz David H. , Davie Joseph M. , Paul William E. , Benacerraf Baruj 
Published: June 2004

Administration of nonimmunogenic 2,4-dinitrophenyl (DNP) conjugates of copolymers of D or L-glutamic acid and lysine (GL) induces hapten-specific tolerance in nonimmune and DNP-ovalbumin-primed strain 13 guinea pigs. This tolerant state is evidenced by depressed anti-DNP antibody synthesis in response to challenge with DNP-ovalbumin and by a diminished frequency of DNP-specific antigen-binding cells and of anti-DNP antibody-secreting cells.
Such a nonimmunogenic compound (DNP-D-GL) will nevertheless elicit a DNP-specific anamnestic antibody response when administered at an appropriate time to DNP-ovalbumin-primed guinea pigs undergoing a graft-versus-host reaction. These experiments are discussed in terms of a two-cell theory of stimulation of antibody responses.
IMMUNE RESPONSE TO CHEMICALLY MODIFIED FLAGELLIN
Authors: Parish C. R. 
Published: June 2004

Flagellin (mol.wt. 40,000) from S. adelaide organisms and a series of acetoacetyl derivatives of flagellin were tested for their ability to induce humoral and cell-mediated immunity in adult rats. It was found that unmodified flagellin was an excellent inducer of antibody formation but a poor inducer of delayed-type hypersensitivity. In contrast, increasing acetoacetylation steadily destroyed the ability of flagellin to initiate antibody formation but enhanced the capacity of the molecule to induce flagellin-specific cell-mediated immunity and antibody tolerance. In fact, it appeared that in adult rats antibody formation and cell-mediated immunity may well be opposing immunological processes. Furthermore, the affinity of the acetoacetyl flagellins for anti-flagellin antibodies appeared to determine the type of immune response which predominated. High affinity antigen produced antibody formation whereas low affinity antigen induced cell-mediated immunity and antibody tolerance. The importance of affinity was further evidenced by the fact that a CNBr digest of flagellin induced humoral and cellular immune responses identical to an acetoacetylated flagellin of comparable antigenic activity. From these studies it was proposed that both humoral and cell-mediated immunity can be directed against the same antigenic determinants but that the specificity requirements for delayed hypersensitivity (and antibody tolerance) are less than those required for antibody formation.
Some remarkable immunological features of the flagellin system were revealed. Flagellin induced comparable delayed-type hypersensitivity when injected in either saline or FCA. Furthermore, FCA only slightly enhanced the delayed responses induced by the acetoacetyl flagellins and in fact these preparations produced antibody tolerance whether injected in saline or adjuvant.
Finally, in contrast to the adult tolerance induced by the acetoacetylated flagellins, which existed only at the antibody level, tolerance in neonatal rats existed at the level of both humoral and cell-mediated immunity. This finding is the first indication of a fundamental difference between neonatal and adult tolerance.
The significance of these findings is discussed in the light of current immunological concepts and a hypothesis proposed to explain these phenomena.
THE DISTRIBUTION OF 51CR-LABELED LYMPHOCYTES INTO ANTIGEN-STIMULATED MICE
Authors: Zatz Marion M. , Lance Eugene M. 
Published: June 2004

The localization of syngeneic 51Cr-labeled lymph node cells was investigated in CBA/J mice previously challenged with sheep erythrocytes, Salmonella H antigen, keyhole limpet hemocyanin, C57BL/6J skin, or rat skin. The effect of time, dose, and route of antigen administration on lymphocyte migration was studied in both primary and secondary responses.
When the distribution pattern of lymphocytes was examined after 20–24 hr, it was found that increased localization of labeled cells occurred in spleen after intravenous or intraperitoneal antigen injection, and in draining lymph nodes after subcutaneous antigen injection or skin grafting. Increased localization (trapping) of lymphocytes was antigen dose dependent and could be demonstrated when 1–6 hr had elapsed between intravenous antigen administration, or when 24 hr had elapsed between subcutaneous antigen administration and intravenous cell infusion. Trapping was transient, lasting approximately 24 hr. Maximal trapping of lymphocytes in the draining nodes occurred 9 days after skin grafting in the first-set allograft response, and 3 days after grafting in the second-set allograft and first-set xenograft responses.
The cell type trapped, the specificity and mechanism of action of the trap, and the role of lymphocyte trapping in the initiation of immune responses are discussed.
DEFECTS IN HEMATOPOIETIC DIFFERENTIATION IN NZB AND NZC MICE
Authors: Warner Noel L. , Moore Malcolm A. S. 
Published: June 2004

Hematopoietic stem cell activity in inbred NZB and NZC mice has been determined by transplantation and endogenous spleen colony assays. Whereas NZB mice show normal colony-forming unit (CFU) activity in the transplantation assay, they show markedly elevated endogenous CFU. NZC mice also show this markedly elevated endogenous CFU activity, but in the transplantation assay show only about 5–10% of normal CFU counts. When NZC stem cells are tested for CFU activity in irradiated recipients of the H-2d type, almost normal colony numbers occur. NZB stem cells however also cannot form colonies in NZC mice. These results suggest that NZC mice have a defect in the micro-environment of the spleen which renders them incapable of allowing transplanted CFU to form colonies.
Genetic analysis of both the NZC defect as a CFU recipient, and the elevated endogenous count in NZB and NZC, shows that both are controlled by single recessive genes which are not linked to either coat color, agouti, H-2 or Ig loci. Of even more relevance is the finding that these hematopoietic abnormalities are not linked to the genes involved in controlling autoantibody formation to red cells in the NZB mice. These mice therefore appear to show two distinct hematopoietic abnormalities, the analysis of which may be of considerable value in understanding the detailed events of hematopoietic stem cell differentiation.
SPECIFIC IMMUNE RESPONSE GENES OF THE GUINEA PIG
Authors: Bluestein Harry G. , Green Ira , Benacerraf Baruj 
Published: June 2004

The ability of guinea pigs to make immune responses to GA, a linear random copolymer of L-glutamic acid and L-alanine, GT, a random linear copolymer of L-glutamic acid and L-tyrosine, and PLL, a linear homopolymer of L-lysine, is controlled by different autosomal dominant genes specific for each of those polymers. We have investigated the relationship between the PLL gene and the GA and GT immune response genes by simultaneously immunizing random-bred Hartley strain guinea pigs with GA and PLL, GT and PLL, or GA and GT.
In most Hartley guinea pigs the ability to respond immunologically to GA and to PLL is inherited together; that is, most animals responding to GA respond to PLL and vice versa. However, a few animals respond to either GA or to PLL but not both, demonstrating that the GA and PLL immune response genes are not identical but linked in most Hartley animals. Conversely, when simultaneously immunized with GT and PLL, most Hartley guinea pigs respond to either PLL or GT but not both, indicating that GT and PLL responsiveness tends to segregate away from each other. Thus, the GT and PLL immune response genes also are not inherited independently but, rather, behave as alleles or pseudoalleles. Similar results are observed when Hartley guinea pigs are simultaneously immunized with GA and GT. The ability to respond to GA segregates away from the ability to respond to GT.
Our studies demonstrated that the specific immune response genes thus far identified in guinea pigs controlling the ability to respond to GA, GT, and PLL, respectively, are found on the same chromosome. In most Hartley animals, the GA and PLL immune response genes are often linked, i.e. occur on the same chromosome strand, and tend to behave as alleles or pseudoalleles to the GT immune response gene.
RECEPTORS ON IMMUNOCOMPETENT CELLS
Authors: Davie Joseph M. , Rosenthal Alan S. , Paul William E. 
Published: June 2004

Guinea pigs immunized with 2,4-dinitrophenyl-guinea pig albumin (DNP-GPA) possess lymphocytes which specifically bind sufficient DNP-GPA-125I to their surface to be detected by radioautography. These lymphocytes are present in the draining lymph nodes in a frequency of ∼50/1000 lymphocytes in animals immunized 2–4 wk earlier with DNP-GPA in complete Freund's adjuvant. Nonimmunized animals have ∼0.4 DNP-GPA antigen-binding cells (ABC) per 1000 lymphocytes. An increase in the frequency of DNP-GPA ABC in peripheral blood is detectable by 5 days after immunization, which is before the time that serum anti-DNP antibody is measurable.
The receptors of these ABC are hapten specific in that free ϵ-DNP-L-lysine, at low concentration, inhibits the binding of DNP-GPA-125I; DNP bovine serum alumbin (DNP-BSA) is equivalent to DNP-GPA in the inhibition of binding of DNP-GPA-125I to ABC; and both DNP-GPA agarose beads and DNP-BSA agarose beads specifically adsorb DNP-GPA-125I ABC. Anti-immunoglobulin antisera, particularly anti-γ2 sera, inhibit the binding of DNP-GPA-125I to these cells implying that the receptors are immunoglobulin, primarily of the γ2 heavy chain class.
DNP-GPA-125I ABC appear to represent precursors of antibody-secreting cells and have specificity characteristics which are very different from cells, of similarly immunized guinea pigs, which mediate a cellular immune response to DNP-GPA.
IMMUNOCHEMISTRY OF THE COMMON ANTIGEN OF ENTEROBACTERIACEAE (KUNIN)
Authors: Hammarström Sten , Carlsson Hans Erik , Perlmann Peter , Svensson Sigfrid 
Published: June 2004

Preparations of E. coli 014 lipopolysaccharide (LPS) contain a common enterobacterial antigen (CA) in large amounts or in an immunogenic form. Chemical analysis revealed, in addition to o-acetyl groups, only those sugars which are present in the basal core structure of the E. coli or Salmonella LPS (e.g., galactose, glucose, glucosamine, heptose, and ketodeoxyoctonate). On treatment with acetic acid (pH 3.2) at 100°C for 1.5 hr, a fragment was liberated which after gel filtration on Sephadex G-50 appeared in the molecular weight range of 2–3 x 103. The fragment inhibited precipitation of alkali-treated E. coli 014 LPS by antibodies to CA from anti-E. coli 014 serum. It also inhibited hemagglutination between anti-CA antibodies and red cells coated with E. coli 08 LPS. Chemical analysis of the fragment indicated that it corresponded to the core region of E. coli 014 LPS. It contained a heptose and ketodeoxyoctonate in addition to glucose and galactose. However the fraction lacked glucosamine.
Enterobacterial CA has previously been found to cross-react with colon antigen of ulcerative colitis. These results should provide a chemical basis for further studies of this cross-reactivity.
SURFACE IMMUNOGLOBULINS ON THYMUS AND THYMUS-DERIVED LYMPHOID CELLS
Authors: Bankhurst Arthur D. , Warner Noel L. , Sprent John 
Published: June 2004

Lymphoid cells from thymus, thoracic duct lymph (TDL), and thoracic duct lymph in irradiated animals reconstituted with allogeneic thymus cells (TTDL) were labeled with radioiodinated anti-immunoglobulins using radioautographic techniques. Thymus and TTDL were labeled (14.4 and 37.0%, respectively) with anti-light chain protein after prolonged exposures (30–60 days). No labeling was observed on thymus and TTDL with anti-polyheavy chain globulin. In contrast 18.5–19.0% of TDL labeled on short exposure (6 days) with anti-polyheavy chain and anti-light chain materials. It is proposed that the difference between the labeling observed on short exposures versus long exposures can be related to the difference in surface density of immunoglobulins between nonthymus-derived (B) and thymus-derived (T) cells.
The distribution of labeled cells in the thymus was preferentially among the larger cells (greater than 10 µ diameter). The TTDL population was mostly composed of a larger, blast-like population and the distribution of label was independent of size.
As the thymus and TTDL preparations contain almost exclusively T cells, this represents a direct demonstration of surface immunoglobulin light chains on T lymphoid cells.
THE DEVELOPMENT OF HYPERSENSITIVE LYMPHOCYTES IN CELL CULTURE
Authors: Ginsburg Haim , Hollander Nurit , Feldman Michael 
Published: June 2004

An in vitro cell-mediated immune response to pokeweed mitogen (PWM) is described. Rat lymphocytes were stimulated by PWM, by phytohemagglutinin (PHA), and by concanavalin A (ConA). In the presence of PWM only a fraction of the lymphocytes underwent blastogenesis. This was in contrast to the apparent total blastogenesis obtained in response to PHA or ConA. When blast cells derived from each of the mitogens were plated on rat fibroblast monolayer in the absence of mitogen they differentiated into a distinct type of lymphocyte termed "secondary lymphocyte." Addition of mitogens to cultures of these lymphocytes resulted in a retransformation to blast cells.
The secondary lymphocytes were tested for their ability to effect lysis in the presence of each of the three mitogens. In. the presence of PWM, lysis of fibroblasts produced by PWM-lymphocytes was considerably more efficient than lysis obtained by ConA- or PHA-lymphocytes. No difference in effect on target fibroblasts was obtained when the three types of secondary lymphocytes were tested in the presence of either PHA or ConA. The stimulating action of PWM on lymphocytes was shown to be immunologically specific. No such specificity was found in the case of PHA or ConA.
The results are interpreted to indicate that PWM combines with cell membranes and acts on the lymphocytes as a "transplantation antigen." Lymphocytes capable of responding to "PWM-transplantation antigen" transform to blast cells capable of specifically lysing PWM-conjugated fibroblasts. In the absence of the mitogen, PWM-induced blast cells differentiate to lymphocytes hypersensitive to PWM.