bluuebunny/crossref_metadata_2025_split huggingface dataset:
FURTHER STUDIES ON THE ROLE OF PROTEASES IN THE ALLERGIC REACTION
Authors: Ungar Georges , Yamura Takuso , Isola Jacqueline B. , Kobrin Sidney 
Published: June 2004

Protease activity was measured through the hydrolysis of synthetic amino acid esters in body fluids and tissues of guinea pigs, rats, mice, and humans. Significant in vitro activation was observed in serum and lung slices of sensitized guinea pigs on addition of the specific antigen. Increased proteolytic activity was also seen in reverse anaphylaxis. More marked activation occurred when guinea pig serum was treated with peptone and guinea pig or rat serum was treated with agar. Protease activation was demonstrated in specimens of human skin under the influence of a poison ivy extract or croton oil added in vitro.
Urinary protease activity of guinea pigs increased significantly during the first hours of anaphylactic shock and very markedly in peptone shock. Peptone shock, elicited in mice pretreated with H. pertussis, was accompanied by a considerable increase in protease activity in the peritoneal fluid as compared with non-pretreated mice which were insensitive to peptone.
Proteolytic activity resulting from the activation procedures was due to a number of proteases. The dominant substrate affinity and inhibition patterns suggest that serum and urine proteases are similar to but not identical with plasmin. Anaphylactic activation exhibited patterns different from those resulting from the action of anaphylactoid agents. Tissue enzymes are either of cathepsin- or chymotrypsin-type or mixtures of both.
Some of the activated enzymes, although remarkably effective in hydrolyzing amino acid esters, show no activity on protein substrates. This does not justify, however, their designation as "esterases." They probably belong to the class of specific proteases acting only on a single or a small number of functionally significant protein substrates.
There is at present sufficient evidence to prove not only that protease activation does occur in anaphylaxis and anaphylactoid conditions but also that it is an important component of the chain of reactions leading to the allergic response.
THE MAMMALIAN CELL-VIRUS RELATIONSHIP
Authors: Crowell Richard L. , Syverton Jerome T. 
Published: June 2004

Sustained infection of HeLa cells by Coxsackie B3 virus, dependent on presence of viral inhibitor in culture medium, was achieved. Persistent treatment of carrier cultures with anti-Coxsackie B3 hyperimmune monkey serum eventually eliminated virus from carrier cultures indicating that a lysogenic virus-cell relationship was not operative.
Free virus was produced continuously by carrier cultures despite washing and neutralization with antiserum to eliminate free virus temporarily. In carrier cultures, about 1.5 to 1.9 plaque-forming units of virus per cell were cell-associated; approximately 6 per cent of this cell-associated virus was not neutralizable by antiserum. In growth medium containing anti-B3 antibody, cells from carrier cultures formed colonies as efficiently as cells from B3-cured cultures. Assays of carrier cultures for infectious centers indicated that less than 1 per cent of cells produced free infectious virus. The Coxsackie B3 virus-carrier state appeared to represent surface residence of B3 virus on the majority of carrier cells with restriction of productive infection to a small proportion of the population.
Coxsackie B3 carrier HeLa cultures, unlike control cultures, were not destroyed by challenge with Coxsackie B1, B3, or B5 viruses. The B3 carrier state did not interfere with superinfection by herpes, vaccinia, and types 1 to 3 polioviruses. In contrast to parental or B3-cured lines, B3-carrier HeLa cultures superinfected with Coxsackie B1 virus produced no significant virus, and cultures superinfected with B5 viruses produced new virus to a limited extent only.
Specific interference with Coxsackie virus superinfection by the B3-carrier state of HeLa cells was shown to be attributable to failure of attachment in the instance of Coxsackie B1 virus, and failure of penetration and/or eclipse in the instance of B5 virus. The interfering effect was circumvented successfully by superinfection of carrier cells with ribonucleic acid extracted from Coxsackie B1 and B5 viruses.
THE OCCURRENCE OF TWO M ANTIGENS IN CERTAIN GROUP A STREPTOCOCCI RELATED TO TYPE 14
Authors: Wiley Grove G. , Wilson Armine T. 
Published: June 2004

A strain of Group A streptococcus previously considered to belong to Type 14 was shown to have two immunologically distinct M antigens, designated Type 14 and Type 51. Most strains having the Type 14 M antigen were found to have also the Type 51 M antigen, and are considered to belong to Type 14–51. Four strains had the Type 51 M antigen without the Type 14 M antigen and one strain had the Type 14 M antigen without the Type 51 M antigen.
The failure of a variant to produce the known M antigen of the parent strain does not necessarily mean that the strain is M-, because a second M antigen may be present as was the case in several strains described here.
ANAPHYLAXIS IN CHOPPED GUINEA PIG LUNG
Authors: Austen K. F. , Brocklehurst W. E. 
Published: June 2004

The quantitative release of histamine by specific antigen from perfused, chopped, sensitized guinea pig lung has been used to study the effect of peptidase substrates and inhibitors on the anaphylactic reaction.
The anaphylactic release of histamine is prevented by chymotrypsin substrates and inhibitors but not by trypsin, carboxypeptidase, or leucine aminopeptidase substrates or the soybean trypsin inhibitor. The chymotrypsin substrates and inhibitors appear to be acting on an antigen-antibody-activated step because these substances fail to inhibit if the tissue is washed free of them prior to antigen addition, and because there is complete desensitization of the tissue without histamine release when the antigen is added in the presence of these inhibitors. The inhibitors work equally well in tissue from passively sensitized animals or in tissue from animals actively sensitized with either ovalbumin or bovine gamma globulin. These observations suggest that activation of a chymotrypsin-like enzyme is a necessary condition for the anaphylactic release of histamine in guinea pig lung.
Diisopropylfluophosphate is inhibitory when present at the time of antigen addition but not when the tissue is washed free of unfixed diisopropylfluophosphate prior to adding antigen. This indicates that diisopropylfluophosphate must be acting exclusively on an enzyme which exists in lung tissue in a precursor form resistant to diisopropylfluophosphate until activated by the antigen-antibody interaction.
Thiol alkylating or oxidizing agents also prevent the anaphylactic release of histamine, but in contrast to the situation with diisopropylfluophosphate and the other chymotrypsin inhibitors, the phase of the anaphylactic reaction inhibited by N-ethylmaleimide is available prior to the antigen-antibody interaction.
The similarities and differences between immune hemolysis and anaphylaxis in chopped guinea pig lung are considered in detail.
SPECTRUM AND CHARACTERISTICS OF THE VIRUS INHIBITORY ACTION OF 2-(α-HYDROXYBENZYL)-BENZIMIDAZOLE
Authors: Eggers Hans J. , Tamm Igor 
Published: June 2004

2-(α-Hydroxybenzyl)-benzimidazole (HBB) inhibited the cytopathic effects of the following enteroviruses: polio 1 to 3; Coxsackie A9; Coxsackie B 1 to 6; and ECHO virus types 1 to 9, 11 to 21, and 24 to 27. The following enteroviruses were not inhibited: Coxsackie A types 7, 11, 13, 16, and 18; and ECHO types 22, 23, and 28. Other HBB-insusceptible viruses were: arbor B and C, reo 1 to 3; adeno 2 to 4; influenza B; para-influenza 2 and 3; mumps; herpes simplex, and vaccinia.
HBB had no inactivating effect on viral infectivity, but rather inhibited some intracellular step in the reproductive cycle of susceptible viruses. With all viruses examined, inhibition of viral cytopathic effects appeared to be due to inhibition of virus multiplication. Virus inhibition by HBB was demonstrable in monkey kidney, HeLa, and ERK cells.
HBB-susceptible viruses varied quantitatively in their susceptibility to the compound, and different strains of the same virus also exhibited varying susceptibility. No relationship was found between attenuation of polioviruses and their susceptibility to the compound. After passage of HBB-susceptible enteroviruses in the presence of the compound, virus populations with lowered susceptibility to HBB were obtained.
At virus inhibitory concentrations, HBB did not affect the morphology of cells, nor the following cellular metabolic activities: oxygen uptake; glucose utilization; lactic acid production; and incorporation of adenosine into RNA, and of alanine into proteins. The rates of multiplication of HeLa and ERK. cells were not significantly altered by HBB at virus inhibitory concentrations.
TRITON HYPERLIPEMIA IN DOGS
Authors: Scanu Angelo , Oriente Pasquale 
Published: June 2004

Triton WR-1339, a non-ionic detergent, added to canine serum or to ultracentrifugally separated lipoproteins, induced changes in the lipoproteins which were dependent upon concentration of detergent and class of lipoproteins.
D 1.063 to 1.21 lipoprotein (α-LP) was especially sensitive to the action of triton. Addition of 2 mg. of triton to 1 mg. of α-LP (based on protein content), induced only slight changes in the electrophoretic and flotation characteristics of the lipoprotein. With a tenfold increase of the detergent (triton:α-LP, 20:1), the mixture, analyzed by starch gel and paper electrophoresis, yielded a tritonlipid complex which remained close to the origin, and a nearly lipid-free protein with electrophoretic mobility higher (starch gel) or lower (paper) than native α-LP. The splitting of the lipid and protein moieties of α-LP could not be clearly shown when the same mixture was analyzed by free boundary electrophoresis. Triton alone moved only slightly in an electrical field (paper, starch gel, Tiselius); it sedimented during ultracentrifugation at D 1.006 and D 1.063 and floated at D 1.21.
D 1.006 to 1.063 lipoproteins (ß-LP), required larger amounts of triton to show changes. These were evident in 40 to 80:1 mixtures of triton and ß-LP. In starch gel and paper electrophoresis triton retained, in a position close to the origin, part of the lipids of ß-LP; the remaining ß-LP fraction, impoverished of lipids, had electrophoretic mobility similar to native ß-LP. The triton-lipid complex sedimented at D 1.063.
After addition of triton to complexes [chylomicron-α-P-I131] or [lipomul-α-LP-1131], the electrophoretic and ultracentrifugal analyses of these mixtures revealed that the labeled protein was removed from the triglyceride component. Triton also prevented the occurrence of the interaction between lipomul and α-LP and the hydrolysis of both chylomicrons and lipomul-α-LP by lipoprotein lipase.
It is postulated that, if the changes in lipoproteins and chylomicrons observed in vitro occur in vivo, they could account, at least in part, for the hyperlipemia which develops in animals following administration of triton.
STUDIES ON STRUCTURAL UNITS OF THE γ-GLOBULINS
Authors: Edelman G. M. , Poulik M. D. 
Published: June 2004

When human and rabbit 7S γ-globulins were reduced in strong urea solutions by a number of procedures, their molecular weights fell to approximately ⅓ of the original values. Partial separation of the reduction products was achieved using chromatography and starch gel electrophoresis in urea solutions. One of the components of reduced human 7S γ-globulin was isolated by chromatography, identified by starch gel electrophoresis, and subjected to amino acid analyses. The amino acid composition of this component differed from that of the starting material and also from that of the remaining components.
A reduced pathological macroglobulin dissociated to components with an average molecular weight of 41,000. Several reduced human myeloma proteins, when subjected to starch gel electrophoresis, yielded individual patterns that nevertheless had features in common with those of reduced normal γ-globulins. Reduction of normal and abnormal γ-globulins was accompanied by the appearance of titratable sulfhydryl groups. Chemical treatments other than reduction were used to determine the type of bond holding the subunits together. It was tentatively concluded that they were linked by disulfide bonds. An hypothesis is presented to relate the structural features of the various γ-globulins in terms of the multiplicity of polypeptide chains in these molecules.
THE ANALYSIS OF STREPTOCOCCAL INFECTIONS
Authors: Halbert Seymour P. , Keatinge Suzanne L. 
Published: June 2004

It has been found by immunoelectrophoresis, that Group A streptococci release at least 20 distinct extracellular antigens in human tissues, as judged by naturally occurring antibodies present in normal pooled human gamma globulin.
Several of these precipitin arcs have been identified with streptococcal antigens previously purified by electrophoresis and chromatography.
Human gamma globulin, as well as several rheumatic fever sera, were shown to be remarkably potent in antistreptococcal antibodies, when compared to four horse antibody concentrates obtained by hyperimmunization with several streptococcal filtrates.
A Group C streptococcal culture concentrate revealed 8 or 9 antigens for which corresponding antibodies were present in human gamma globulin.
OBSERVATIONS ON THE PRODUCTION OF PYROGENIC SUBSTANCES BY RABBIT AND HUMAN LEUCOCYTES
Authors: Fessler J. H. , Cooper K. E. , Cranston W. I. , Vollum R. L. 
Published: June 2004

1. The mechanism of release of a pyrogen from leucocytes has been studied in cells obtained from sterile rabbit peritoneal exudates and from rabbit blood. Attempts were made to induce human leucocytes—from blood—to release a pyrogen.
2. Rabbit leucocytes, kept below 4°C., were not pyrogenic and did not release any pyrogen when disintegrated. Incubating such cells, in various media, at 37°C. led to the formation of a pyrogen which was heat-labile. The maximum yield was attained after 1½ hours' incubation.
3. The formation of rabbit leucocytic pyrogen was prevented by freezing and thawing the leucocytes, by heating them to 56°C. for half an hour before incubation, and by ageing them in the cold.
4. Nitrofurazone (5-nitro-2-furaldehyde semicarbazone) prevents the formation of leucocytic pyrogen when given by mouth to the cell-donor animals, or when added to leucocytes in intro.
5. Leucocytes from rabbit blood formed leucocytic pyrogen, on incubation in saline, and this formation was also inhibited by nitrofurazone.
6. No leucocytic pyrogen was released from human leucocytes subjected to mechanical, osmotic, or thermal damage, and it was not formed when the cells were incubated in saline.
7. The source of rabbit leucocytic pyrogen, the action of nitrofurazone on leucocytes, and the supposed role of leucocytic pyrogen in fever are discussed.
STUDIES ON THE CHEMICAL STRUCTURE OF THE STREPTOCOCCAL CELL WALL
Authors: Krause Richard M. , McCarty Maclyn 
Published: June 2004

Lysis of trypsinized Group A streptococcal cell walls with phage-associated lysin releases into solution dialyzable and non-dialyzable mucopeptide fractions composed of N-acetylglucosamine, N-acetylmuramic acid and alanine, glutamic acid, lysine, and glycine in addition to the characteristic group-specific carbohydrate. The latter substance contains appreciable amounts of N-acetylmuramic acid and the amino acids as well as N-acetylglucosamine and rhamnose.
Hot formamide extraction of the cell walls results in a soluble fraction of group-specific carbohydrate and an insoluble residue. The Group A carbohydrate in this instance is composed of rhamnose and N-acetylglucosamine. The composition of the insoluble residue is similar to that of the mucopeptide fractions released from the cell wall by phage-associated lysin. This residue was shown by electron microscopy to be composed of discrete discs which appear similar in structure to the intact cell wall.
The specific carbohydrate obtained by hot formamide extraction of Group A-variant cell walls was composed almost exclusively of rhamnose. The residue fraction was similar to that of Group A.
The residue of cell walls extracted with hot formamide is extensively solubilized not only by phage-associated lysin and S. albus enzyme, but also by lysozyme, which has no measurable effect on the intact streptococcal cell wall.
ANAPHYLAXIS IN CHOPPED GUINEA PIG LUNG
Authors: Austen K. F. , Brocklehurst W. E. 
Published: June 2004

The anaphylactic release of histamine from perfused, chopped guinea pig lung is very sensitive to changes in the NaCl concentration of the containing medium, and it is ionic strength rather than particle concentration which is critical. Consequently, in studies with inhibitors care must be taken to avoid inadvertently increasing ionic strength and thereby misinterpreting the cause of the inhibition.
Since immune hemolysis exhibits a similar sensitivity to changes in the NaCl concentration of the suspending medium, salicylaldoxime and phlorizin, which prevent the participation of the third component of complement in immune hemolysis, were investigated for their effect on the anaphylactic reaction. Salicylaldoxime is a potent inhibitor of in vitro anaphylaxis in guinea pig lung, but phlorizin is only a weak inhibitor.
Potassium cyanide, 1 mM, inhibits the anaphylactic release of histamine most effectively if the duration of contact between the tissue and the cyanide prior to antigen addition is minimal; preincubation of the tissue with cyanide prior to antigen addition results in progressive diminution of inhibition even when there is only minimal loss of cyanide from the containing medium.
The anaphylactic release of histamine from perfused whole lungs or suspensions of blood-free chopped lung is not prevented by the cytochrome oxidase inhibitor, carbon monoxide. In addition, 2-heptyl 4 hydroxyquinoline N oxide and malonic acid, which inhibit aerobic metabolism at different sites, do not prevent the reaction. These studies and those with cyanide indicate that the anaphylactic release of histamine in guinea pig lung is not dependent on cytochrome-mediated aerobic metabolism.
FACTORS AFFECTING THE ADHESIVENESS OF HUMAN LEUCOCYTES AND PLATELETS IN VITRO
Authors: Garvin James E. 
Published: June 2004

Some factors affecting the retention of human polymorphonuclear neutrophils (PMN), lymphocytes, and platelets on a siliconized glass bead column were explored.
PMN were more effectively retained when the flow rates were slow and the columns long. They were found largely on the upper portions of the columns except with rapid flow rates when they spread down the columns. PMN retention on the columns was greatest in the range 30°–43°C. Both magnesium and calcium ions were required for full adhesiveness; calcium ions alone were unable to restore adhesiveness to PMN from blood which had been treated with a chelating resin to remove divalent cations. The adhesiveness of the PMN was independent of cyanide and dinitrophenol, but was almost completely eliminated by iodoacetamide. Under all the conditions mentioned above in which adhesiveness was lost there was a concurrent loss of the usual ability of the PMN to migrate, but at least in the presence of EDTA, a capacity to change shape by pseudopod formation remained.
Lymphocytes were retained on the columns to a much lesser extent than the PMN under all conditions and, within limits, this retention was not related to either flow rate or column length. Maximum lymphocyte retention occurred in the range 30°–43°C. No dependence of lymphocyte adhesiveness was shown for divalent cations, cyanide, dinitrophenol, or iodoacetamide, but such dependence is not excluded by the data obtained.
Platelets were largely retained by the glass bead columns under most conditions and this was unrelated to temperature in the range 0°–50°C. Their adhesiveness was found to require either magnesium or calcium ions and to be blocked by iodoacetamide.
THE EFFECT OF AMINOMETHYLPTEROYLGLUTAMIC ACID ON THE DEVELOPMENT OF SKIN HYPERSENSITIVITY AND ON ANTIBODY FORMATION IN GUINEA PIGS
Authors: Friedman Robert M. , Buckler Charles E. , Baron Samuel 
Published: June 2004

1. In guinea pigs, aminomethylpteroylglutamic acid (methotrexate) is capable of blocking the development of delayed skin hypersensitivity, the primary antibody response, and the specific febrile response to ovalbumin and diphtheria toxoid. The primary antibody response is more easily inhibited than is the development of delayed skin hypersensitivity.
2. The effect of methotrexate on immunologic responses depended upon the dose of methotrexate employed and the strength of the antigenic stimulus.
PATHOGENESIS OF EXPERIMENTAL SHOCK
Authors: Nagler Arnold L. , Zweifach Benjamin W. 
Published: June 2004

A series of biological test reactions was used in order to establish the presence of bacterial endotoxins in the blood of rabbits during the progression of hemorrhagic shock.
1. When the shocked animal was used as the test object, it was not possible to induce either the generalized Shwartzman reaction or the dermal Shwartzman phenomenon with exogenous endotoxin (S. enteritidis or E. coli) as one of the two provocative factors.
2. Epinephrine instilled into the skin of rabbits either before, during, or after an episode of hemorrhagic shock did not result in the hemorrhagic skin reaction which occurs in the presence of as little as 1 µg of endotoxin intravenously.
3. Passive transfer from a donor in the irreversible phase of shock of 20 to 25 ml of blood into a primed recipient (B.P. at 40 mm Hg for 1 hour) was uniformly lethal.
4. Similar amounts of blood from such shocked donor failed upon intravenous injection to elicit a protective hemorrhagic reaction in skin sites which were infiltrated with 100 µg of epinephrine. In the same animals 1 µg of endotoxin added to the blood samples caused a positive dermal response.
5. Blood was taken from rabbits which had been pretreated with S. enteritidis endotoxin and then subjected to hemorrhagic shock (35 mm Hg for 2 hours). Such samples upon passive transfer produced positive skin reactions in epinephrine sites but were not lethal to the primed test recipient used in these studies.
It is concluded that the contribution of bacterial endotoxemia to the genesis of hemorrhagic shock remains to be determined.