bluuebunny/crossref_metadata_2025_split huggingface dataset:
STUDIES ON GONOCOCCUS INFECTION
Authors: Swanson John , Kraus Stephen J. , Gotschlich Emil C. 
Published: June 2004

The four colony types of several different strains of gonococci were isolated by selective transfers on agar. These colony variants differed in the degree of autoagglutination which occurred when they were grown in fluid medium. It was found that this clumping behavior was related to the colonial type, with type 2 isolates exhibiting the greatest autoagglutination followed by types 3, 1, and 4.
Electron microscopic examination of thin sections indicated that the clumping in fluid medium was mediated by peculiar zones of adherence of the outer membranes of gonococci. These resembled the gap junctions seen in animal cell systems but differed in that the gonococcal membranes involved in the zone of adherence did not bear typical surface modifications.
Electron microscopic study of negatively stained specimens of gonococci revealed that pili with a diameter of approximately 85 A and a length up to 4 µ were present on the surfaces of all type 1 and type 2 gonococci examined, and were not seen on any type 3 or 4 gonococci. The consistent presence of pili on type 1 and type 2 gonococci which are virulent colony forms and the lack of pili on avirulent colony types 3 and 4 suggests a relationship between the gonococcal pili and pathogenetic potential of the organisms.
THE FIRST COMPONENT OF THE KININ-FORMING SYSTEM IN HUMAN AND RABBIT PLASMA
Authors: Cochrane C. G. , Wuepper K. D. 
Published: June 2004

The isolation and characterization of the first component of the kinin-forming system in human and rabbit plasma are presented. Functionally, the molecule is the precursor of the activator of prekallikrein (Pre-PKA) and evidence is presented that it is identical with Hageman factor (clotting factor XII). The component from each plasma possessed similar characteristics. This molecule was found to have a mol wt of 110,000 and sedimentation rate of 4.6S. It migrated in electrophoresis as a ß-globulin, having an isoelectric point of 6.1. Upon activation with glass, kaolin, diatomaceous earth, ellagic acid, or trypsin, the activated molecule converted purified prekallikrein (prokininogenase) to the active enzyme.
Clot-promoting activity was associated with the capacity to activate prekallikrein through each procedure of isolation. The clot-promoting factor was in precursor form, requiring treatment with kaolin or trypsin to gain activity. Evidence indicated that the protein was Hageman factor (factor XII): it promoted clotting of factor XII-deficient, but not Factor XI- or IX-deficient plasma, and did not convert fibrinogen to fibrin it bound to and was activated by kaolin or other negatively charged particles in the presence of chelating agents; the activation by kaolin could be prevented by pretreating the kaolin with hexadimethrine bromide (H Br); prekallikrein-activating and clot-promoting activities were identical in their physical properties; and the prekallikrein activator could not be detected in Hageman factor-deficient plasma.
Activation of Hageman factor was accompanied by cleavage of the molecule into several fragments, one of which possessed prekallikrein-activating (PKA) and clot-promoting properties. The PKA fragment sedimented at 2.6S and by gel filtration was found to have a molecular weight of 32,000. The PKA possessed only 1/50 the clot-promoting capacity of the freshly activated native molecule.
LYMPHOCYTE-MEDIATED CYTOTOXICITY IN VITRO
Authors: Klein William J. 
Published: June 2004

The ability of antisera to suppress immune responses either in vivo or in vitro is well known. A variety of lymphocyte-target cell systems have been employed to demonstrate inhibition of cell-mediated immunity by antisera in vitro, and skin, tumor, and kidney graft survival have been prolonged by passively administered antiserum in vivo. An in vitro lymphocyte-tumor cell assay system was developed for the purpose of studying the effects of enhancing antisera (in vivo) on lymphocyte-mediated cytotoxicity in vitro. The characteristics of this system with respect to route of immunization, time of harvest of immune cells, lymphocyte:tumor cell ratio, and effect of nonimmune or nonspecifically immune lymphoid cells are presented. Sera capable of enhancement in vivo were tested in this system and shown to inhibit cell-mediated immunity in vitro. Further, in both instances the immunosuppressive effect is mediated by antigen-antibody complexes and not by free antibody alone.
Experiments were also carried out to determine the site of action of these suppressive antigen-antibody complexes. Presensitized lymphocytes were exposed to antigen-antibody complexes, washed, and then allowed to interact with fresh tumor cells (not antibody treated). Lymphocytes treated in this manner are incapable of exhibiting cell-mediated immunity in vitro. This evidence supports the concept that the antigen-antibody complexes have a direct immunosuppressive effect on the lymphocyte.
LYMPHOCYTE MEMBRANE DYNAMICS
Authors: Cone Robert E. , Marchalonis John J. , Rolley Ronald T. 
Published: June 2004

Cell surface proteins of normal and neoplastic lymphocytes were labeled with iodide-125I by lactoperoxidase-catalyzed iodination. Incubation of 125I-labeled iodide cells in vitro resulted in the release of iodinated surface proteins at a rapid rate which was dependent on cellular respiration and protein synthesis.
Comparisons by disc electrophoresis showed a marked similarity between urea-soluble surface proteins extracted from iodinated cells and iodinated material released by the cells during in vitro incubation.
The rate of release of cell surface proteins from thymus cells was three times faster than that of spleen cells or bone marrow-derived thoracic duct lymphocytes. In addition, different proteins were released at different rates as evidenced by the rate of release of 125I of rabbit anti-mouse immunoglobulin specifically bound to mouse spleen cells and comparisons by disc electrophoresis of urea-soluble iodinated surface proteins extracted from cells before and after incubation.
The results suggest that a dynamic state exists at the cell surface. The possible role of the release of cell surface proteins in cell regulation and communication is discussed.
THE INTERACTION IN VITRO BETWEEN POLYMORPHONUCLEAR LEUKOCYTES AND MYCOPLASMA
Authors: Simberkoff Michael S. , Elsbach Peter 
Published: June 2004

The interaction, between mycoplasma (PPLO) and human or rabbit leukocytes was examined in vitro.
Upon incubation of M. hominis or M. arthritidis for 2 hr with rabbit peritoneal exudate granulocytes or leukocytes from human peripheral blood, no killing of mycoplasma was observed either in the presence or absence of type-specific antiserum. However, 14CO2 production from glucose-1-14C was stimulated up to 10-fold in the presence of live or heat-killed PPLO. The extent of stimulation depended upon the number of organisms and the presence of type-specific antiserum. The stimulation of 14CO2 production seems not because of tight adherence of PPLO to the leukocytes, since PPLO were quantitatively recovered in the medium after sedimenting the granulocytes.
The enhanced conversion of medium lysolecithin to cellular lecithin that accompanies phagocytosis of polystyrene particles was significantly reduced when PPLO were also present. Mycoplasma alone elicited no stimulation of lecithin formation.
Killing of E. coli, a microorganism readily engulfed and killed by leukocytes in vitro, was diminished when the leukocytes were preincubated with mycoplasma.
These findings indicate that M. hominis and M. arthritidis are not ingested by granulocytes to any detectable extent, but that these organisms affect the leukocytes' metabolism and also impair phagocytosis of E. coli.
CHOLESTEROL METABOLISM IN THE MACROPHAGE
Authors: Werb Zena , Cohn Zanvil A. 
Published: June 2004

The cholesterol metabolism of homogeneous populations of mouse peritoneal macrophages was evaluated under in vitro conditions. Macrophages are rich in free cholesterol and maintain a constant cholesterol to protein ratio (12 µg cholesterol/mg protein). No detectable cholesterol ester was present within the cell. More than 95% of total cholesterol was membrane associated and the majority was present in subcellular fractions containing lysosomes and plasma membrane. Less than 0.1% of cell cholesterol was synthesized from acetate-1-14C.
During in vitro cultivation, macrophages rapidly exchanged their membrane cholesterol with that of lipoproteins of calf serum. About 30% of the cell cholesterol was exchanged per hour in 20% serum medium, and exchange was nearly complete by 5 hr. Exchange proceeded in a rapid exponential phase followed by a slower phase. Calculations based on a two compartment model indicated that the rapidly exchanging cholesterol compartment represented 60–70% of the total cell cholesterol, and the slowly exchanging compartment accounted for 30–40%. The relationship between serum lipoprotein concentration and exchange rate exhibited first-order kinetics. The rate was determined by thermal energy, in keeping with a Q10 of 2, and an activation energy of 12 kcal/mole. Exchange was independent of bulk transport of lipoproteins by pinocytosis and phagocytosis, and was not linked to energy metabolism. The α-lipoproteins were the major class of proteins of calf serum participating in exchange.
THE ROLE OF PASSENGER LEUKOCYTES IN THE ANOMALOUS SURVIVAL OF NEONATAL SKIN GRAFTS IN MICE
Authors: Wachtel Stephen S. , Silvers Willys K. 
Published: June 2004

The anomalous survival of neonatal C3H skin grafts on CBA mice is correlated with the emigration of passenger leukocytes from the graft vasculature. Thus, newborn homografts whose leukocyte populations are eliminated by X-irradiation or by transient sojourn on an intermediate adult C3H host, do not display prolonged survival. Moreover, the continued presence of the newborn grafts is not requisite to the maintenance of the unresponsive state, an observation consonant with the demonstration that CBA mice bearing long-term neonatal C3H skin grafts are leukocyte chimeras.
In contrast, neonatal male C57 skin grafts may persist on C57 females after heavy irradiation of the donor, or after passage on an intermediate adult male host. In addition, tolerance is broken by removal of long-persistant newborn grafts from hitherto unresponsive females, and chimerism is not detectable in female C57 mice tolerant of infant male isografts.
Finally, leukocytes of neonatal C3H origin, inoculated subcutaneously into CBA males, may occasionally render these animals unresponsive to subsequent adult C3H skin homografts, whereas those taken from infant C57 males usually sensitize their adult female hosts. Thus, passenger leukocytes are implicated in the extended survival of C3H neonatal homografts on CBA recipients, but not in the persistence of H-Y-incompatible neonatal skin isografts on C57 females.
VIRAL AND CELLULAR SURFACE ANTIGENS OF MURINE LEUKEMIAS AND MYELOMAS
Authors: Aoki Tadao , Takahashi Toshitada 
Published: June 2004

Immunoelectron microscopy (IEM) of mouse cells which were productively infected with murine leukemia virus (MuLV) yielded the following conclusions:
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With two exceptions, the alloantigens H-2, θ, Ly-A, and Ly-B were not present on complete or incomplete virions produced by cells bearing these antigens.The exceptions were H-2k (but not H-2b) and θ both appeared on only a minority of virions and never on more than a small part of the circumference.
The incidental discovery of an additional envelope antigen on virions produced by a BALB/c mouse myeloma but lacking from passage A Gross virions distinguishes these two viruses as MuLV subtypes; it also illustrates that IEM can be applied as a primary tool for antigenic analysis, as well as for its usual purpose of finding out where antigens are situated.
STUDIES ON ANTIBODY-PRODUCING CELLS
Authors: Hummeler Klaus , Harris T. N. , Harris Susanna , Farber Miriam B. 
Published: June 2004

Efferent lymph of the popliteal lymph nodes of rabbits was collected 4 days after a single footpad injection of SRBC. Thin-layer agar plating was done to isolate plaque-forming cells of the lymph for electron microscope examination, and the numbers of plaque-forming cells (PFC) in cells from the lymph and lymph nodes were determined.
Of 71 PFC of lymph isolated and examined, 93% were lymphocytes, most of them with signs of substantial levels of physiologic activity. The cytoplasm showed an abundance of free ribosomes and many finger-like projections. The endoplasmic reticulum (ER) was barely detectable in most of the active lymphocytic PFC, and in some, a few short narrow channels of ER could be seen. Approximately one-fifth of the lymphocytic PFC presented an appearance of senescence, with signs of degeneration: rounded cells, with amorphous nuclear chromatin, and very few microvilli. The remaining 7% of the PFC of the lymph showed an unusual combination of features: small round cells with a narrow ring of cytoplasm which, however, contained well-organized channels of ER. Such cells had been found only among PFC of peripheral blood of the rabbit.
The number of PFC per million cells was higher in the lymph than in the suspensions of lymph node cells. In both the contralateral lymph node and its efferent lymph, the number of PFC was less than 1% that of the injected side.
RECEPTORS ON IMMUNOCOMPETENT CELLS
Authors: Davie Joseph M. , Paul William E. 
Published: June 2004

During the course of the immune response to dinitrophenylated guinea pig albumin (DNP-GPA), a striking and parallel increase in avidity for ϵ-DNP-L-lysine occurs in the receptors on antigen-binding lymphocytes, antibody secreted by individual plaque-forming cells, and serum antibody molecules. A detailed analysis of the avidity distribution of antibody produced by plaque-forming cells indicates that this "immunologic maturation" is primarily due to a preservation of the high avidity subpopulation and a striking loss in the low avidity population rather than to sequential appearance of these cells.
Moreover, the demonstration of the increased avidity of receptors of antigen-binding lymphocytes, which appear to be precursors of antibody-synthesizing cells, strongly suggests that the antigen-driven selectional process operates primarily on this cell type.
IMMUNE RESPONSES IN VITRO
Authors: Pierce Carl W. , Solliday Susan M. , Asofsky Richard 
Published: June 2004

The suppressive effects of monospecific goat anti-mouse globulins on primary immunoglobulin class-specific plaque-forming cell responses in mouse spleen cell cultures were investigated. Anti-µ suppressed responses in all immunoglobulin classes, whereas anti-γ1 and anti-γ2 suppressed the γ1 and γ2 responses but not γM or γA responses, and anti-γA suppressed only γA responses. The mechanism of action of the anti-µ was studied in detail because of its suppression of responses in all immunoglobulin classes.
The anti-µ was specific for µ-chain determinants; its activity was dose dependent, but was not mediated by killing cells with surface µ-chain determinants. Free γM but not γG myeloma proteins in solution effectively competed with µ-bearing cells for the anti-µ. An excess of anti-µ was necessary in the cultures for 48 hr to insure complete suppression of 5-day responses. However, after removal of excess anti-µ at 48 hr, responses could be stimulated by newly added antigen in cultures where incubation was prolonged to 7 days. Anti-µ was most effective when added at the initiation of cultures and had no suppressive effect when added at 48 hr. Excess antigen did not effectively compete with anti-µ for antigen receptors. Precursors of antibody-forming cells were shown to be the cell population where the suppressive activity of anti-µ was mediated.
The experiments suggest that anti-µ combines with µ-chain determinants in antigen-specific receptors on the surfaces of antibody-forming cell precursors, prevents effective stimulation by antigen and subsequent antibody production. To explain suppression of responses in all Ig classes by anti-µ, several models were proposed. It is not possible to determine from the data whether stimulation of precursor cells with γG or γA receptors requires concommitant stimulation of separate cells with only γM receptors, or whether cells bearing γM receptors are precommitted to or differentiate into cells capable of synthesis of other Ig classes, or whether receptors of γM and another Ig class are present on some virgin precursors or the second Ig receptor appears after antigenic stimulation.
IMMUNOPATHOGENESIS OF ACUTE CENTRAL NERVOUS SYSTEM DISEASE PRODUCED BY LYMPHOCYTIC CHORIOMENINGITIS VIRUS
Authors: Gilden Donald H. , Cole Gerald A. , Monjan Andrew A. , Nathanson Neal 
Published: June 2004

A single dose of 150 mg/g of cyclophosphamide (CY), given 3 days after intracerebral (i.c.) inoculation of lymphocytic choriomeningitis (LCM) virus, protected over 90% of adult BALB/c mice against acutely fatal choriomeningitis. Surviving mice became persistently infected carriers, with high virus titers in blood and brain.
Immunofluorescent examination of the brain showed that in CY-induced carriers infection was initially confined to the choroid plexus, ependyma, and leptomeninges, but over the next 30 days gradually spread to the neural parenchyma, most notably to the molecular layer of the cerebellum. By contrast, LCM virus-carrier mice produced by neonatal virus injection and examined as adults, showed a much less marked infection of choroid plexus and much more widespread infection of parenchyma, with a different distribution among brain nuclei, including heavy infection of the Purkinje cells of the cerebellum.
ACTIVE SUPPRESSION OF IMMUNOGLOBULIN ALLOTYPE SYNTHESIS
Authors: Jacobson E. B. , Herzenberg Leonore A. 
Published: June 2004

Long-term (chronic) allotype suppression, previously reported only in rabbits, is shown here to occur in at least one strain combination of mice as well. Close to 50% of the offspring of SJL (Igb) males mated to BALB/c (Iga) females immunized against the paternal allotype were found to be suppressed for Ig-1b (γG2a) at 6 months of age. These mice are called "chronically" suppressed.
The percentage of offspring in this strain combination suppressed for the paternal allotype at 8 wk of age is the same as that seen in an earlier strain combination tested, [(C57 x BALB/c)F1], in which all mice recover from suppression by 10–12 wk. After 8 wk, two distinct patterns of long-term (chronic) suppression emerge in (SJL x BALB/c)F1 mice: a small number of these mice never produce detectable amounts of Ig-1b throughout their lives, while the majority produce detectable Ig-1b sporadically, sometimes over a period of several weeks, the level of which eventually falls below detectability.
Attempts to "cure" suppression by destroying the existent lymphoid population and forcing endogenous repopulation in chronically suppressed animals were unsuccessful. Furthermore, attempts to restore Ig-1b production by injection of cells from syngeneic Iga/Igb donors into irradiated, chronically suppressed recipients were also unsuccessful, although the same cell inocula, when injected into irradiated BALB/c (Iga/Iga) mice produced high levels of gamma globulin carrying the allotype. These results suggest that long-term allotype suppression resulting from perinatal exposure of offspring to specific anti-allotype antibody (anti-Ig-1b), is not due merely to an absence of Ig-1b-producing cells or their progenitors, but appears to be an active process, which dominates physiologically over normal production.
ACTIVE SUPPRESSION OF IMMUNOGLOBULIN ALLOTYPE SYNTHESIS
Authors: Jacobson E. B. , Herzenberg Leonore A. , Riblet R. , Herzenberg L. A. 
Published: June 2004

The mechanism of chronic allotype suppression in (SJL x BALB/c)F1 mice has been investigated by means of cell transfer studies.
These mice are phenotypically negative for serum Ig-1b, the paternal allotype determinant on γG2a immunoglubulin, as a result of perinatal exposure to maternal anti-Ig-1b.
When spleen or bone marrow (B) cells from suppressed mice were injected into irradiated BALB/c "indicator" hosts, detectable levels of Ig-1b were demonstrated in the sera of a majority of the recipients early after transfer. These results indicate that Ig-1b-producing cells or their precursors are present in the lymphoid tissues of suppressed mice, even though they are not expressed.
Within 5–7 wk, it was no longer possible to detect Ig-1b in the sera of these hosts, although cells producing another paternal allotype (Ig-4b) were shown to persist. Control BALB/c mice, injected with spleen and B cells from normal mice, continued to produce high levels of immunoglobulin carrying this allotype.
The disappearance of serum, Ig-1b occurred most frequently in the recipients of suppressed spleen cells.
Similar results were obtained using a mixture of spleen cells from normal and suppressed mice. Ig-1b production in the recipient mice ceased within a few weeks, even though the majority of cells in the mixture were obtained from normal (nonsuppressed) donors.
The data are interpreted as evidence that chronic allotype suppression in mice is actively maintained by cells which are resident in the lymphoid tissues, splenic cells being the most effective. These cells are capable of proliferating in a new host and exerting their suppressive influence on Ig-1b-producing cells and/or their precursors.
THE STRUCTURE OF ERYTHROCYTE MEMBRANES STUDIED BY FREEZE-ETCHING
Authors: Tillack Thomas W. , Scott Robert E. , Marchesi Vincent T. 
Published: June 2004

The distribution of specific glycoprotein receptors on the external surfaces of red cells was mapped, by the freeze-etching technique, to determine if the receptors coincided with the underlying 75-A intramembranous particles. Phytohemagglutinin, ferritin-conjugated phytohemagglutinin, and influenza virus were used as labeling agents since they can be seen by freeze-etching techniques and each reacts with a different site on the same glycoprotein molecule. The distribution of these labels was studied on intact human red cells, isolated ghost membranes, and trypsin-treated ghost membranes.
The results show that the receptors for these labels are distributed uniformly over the surfaces of normal red cell membranes in the same apparent distribution as that of the 75-A particles within the membrane. The association between the external receptors and the underlying particles is especially evident when trypsin-treated ghost membranes are labeled: the labeled receptor sites and the intramembranous particles both form sharply defined, reticulated networks, which overlap. These results provide further support for the idea that membrane-bound glycoproteins are oriented so that their carbohydrate-rich segments, which bear the antigenic sites and receptors, are exposed to the external medium, while hydrophobic segments of the same molecules interact with lipids, and possibly other proteins, to form the intramembranous particles.