bluuebunny/crossref_metadata_2025_split huggingface dataset:
RENAL GLOMERULAR LESIONS INDUCED BY RABBIT ANTI-RAT COLLAGEN SERUM IN RATS PREPARED WITH ADJUVANT
Authors: Rothbard Sidney , Watson Robert F. 
Published: June 2004

Renal glomerular lesions were induced by rabbit serum containing antibody to rat collagen injected intravenously into rats prepared with subcutaneously administered Freund adjuvant. Neither the anti-collagen serum nor the adjuvant alone induced the lesion. The lesions were characterized by diffuse glomerular injury with swelling, shredding, and fusion of the basement membranes, crescent formation, cellular proliferation, numerous multinuclear giant cells, and capillary hyaline thrombi.
Various rabbit antisera, including those against fish collagen or rat serum failed to induce the renal lesion when substituted for anti-rat collagen serum. Also, anti-rat collagen serum absorbed with its homologous antigen, native rat collagen, failed to induce the lesion. Although complete adjuvant, i.e. with mycobacteria, in which normal serum was incorporated enhanced the glomerular lesion which resulted from intravenous injection of anti-collagen serum, the incomplete adjuvant without serum was sufficient.
Comparison of the renal lesions induced by anti-collagen serum with nephrotoxic nephritis induced in rats by rabbit anti-kidney serum showed that they differ histologically. Also the antisera used to produce these two renal lesions differ immunologically.
Antibodies to normal rabbit serum developed in rats injected intravenously with rabbit anti-rat collagen serum after preparation with adjuvant, but not when adjuvant was omitted. The pathogenesis of the renal injury is discussed as a manifestation of an antigen-antibody reaction, with nephritis occurring only after the adjuvant-stimulated antibody to the rabbit globulin has been formed in the rat and has reacted with the rabbit anti-rat collagen already fixed by its homologous antigen in the kidney.
MACROGLOBULINEMIA
Authors: Korngold Leonhard , van Leeuwen Gerda 
Published: June 2004

The monomers obtained by treating γ1-macroglobulins with mercaptoethanol have proved to be antigenically different from normal 7S 7γ-globulin.
The depolymerization of the macroglobulins resulted in the loss of several antigenic determinants, although the monomers still cross-reacted with antisera against macroglobulins.
Reaggregation of the monomers occasionally resulted in the reconstitution of some or all of the antigenic determinants that were lost during depolymerization.
Repeated freezing and thawing of pathological macroglobulins in iodoacetate resulted in their complete antigenic destruction.
Repeated freezing and thawing of one of the monomers in excess iodoacetate resulted in the degradation to a protein antigenically indistinguishable from Bence Jones protein. The other two monomers studied were stable under these conditions.
EXPERIMENTAL PULMONARY PNEUMOCYSTIS CARINII INFECTION IN RABBITS
Authors: Sheldon Walter H. 
Published: June 2004

Moderate to marked interstitial pneumonitis with many Pneumocystis organisms was found in rabbits treated with cortisone and antibiotics and instilled intranasally with a suspension of lung tissue from either a patient or a rabbit with this infection. Organisms and pulmonary lesions of similar severity and frequency were present in controls treated in the same manner but instilled with either saline or a boiled suspension of normal human lung tissue. The administration of antibiotics and infected rabbit lung suspension only produced less marked lung changes with fewer organisms. Rare organisms and minute foci of pneumonitis were encountered in normal rabbits which had received neither hormone, antibiotics, nor inoculum.
The pulmonary lesions in the cortisone-treated rabbits resembled closely the findings in patients with the subclinical form of Pneumocystis pneumonitis. They did not reproduce the massive lesions of widespread Pneumocystis pneumonia in infants.
The findings indicate that latent pulmonary Pneumocystis infection was widespread in these rabbits but do not establish the transmission of the disease. The activation of latent infection was dependent on an impairment of host resistance which in these experiments was produced most effectively by the administration of cortisone. The differences between the experimental lesions and those of typical Pneumocystis pneumonia in infants suggest that in man an unknown defect of host defenses other than that induced by prolonged hormone administration accounts for the increased susceptibility to the infection. It is concluded that in the presence of widespread latent Pneumocystis infection the development of active disease is a manifestation of altered host resistance.
A QUANTITATIVE STUDY OF THE KINETICS OF BLOOD CLEARANCE OF P32-LABELLED ESCHERICHIA COLI AND STAPHYLOCOCCI BY THE RETICULO-ENDOTHELIAL SYSTEM
Authors: Benacerraf B. , Sebestyen Martha M. , Schlossman Stuart 
Published: June 2004

1. The clearance of P32-labelled heat-killed E. coli and staphylococci from the blood follows an exponential function of the time, and the bacteria are phagocytized principally by the RES of the liver and spleen.
2. The rates of clearance of equivalent number of E. coli from the blood is rapid in rabbits and slow in mice and appears to be related to the level of antibodies in the serum of these animals.
3. Unlike E. coli, staphylococci are cleared rapidly and efficiently by the RES from the blood of mice which have a sufficient level of serum antibody against these bacteria.
4. The numbers of bacteria, phagocytized by the liver or the spleen respectively, depend upon the rate of clearance and the extent of opsonization of the bacteria. Rapidly cleared, well opsonized E. coli are removed almost exclusively by the liver, while less efficiently phagocytized bacteria are also cleared by the spleen in large numbers.
5. The rate of clearance of E. coli and the efficiency with which they are phagocyted by the RES in mice have been shown to be directly related to the level of antibody in the serum.
6. Treatment of mice with S. typhi or Serratia marcescens endotoxins increases the rate of clearance of E. coli from the blood and the level of antibody against E. coli in the serum. The enhanced clearance of E. coli can be transferred to normal mice by the serum of endotoxin-treated mice.
STUDIES OF MOUSE POLYOMA VIRUS INFECTION
Authors: Hartley Janet W. , Rowe Wallace P. , Chanock Robert M. , Andrews Basil E. 
Published: June 2004

Treatment of guinea pig erythrocytes with types A and B influenza viruses rendered them inagglutinable by polyoma virus; also, the inhibitory effect of ovomucin on polyoma virus hemagglutination was destroyed by pretreatment of the ovomucin with various myxoviruses. These results indicate that polyoma virus and myxovirus erythrocyte receptor sites are identical. However, no destruction by polyoma virus of its own or of myxovirus receptors or inhibitors was detected.
No serologic relationship was detected between polyoma virus and members of the myxovirus group; differences in size and stability further indicate their distinctness.
No evidence was found of biologic or serologic relationship of polyoma virus with encephalomyocarditis virus or mouse encephalomyelitis virus.
THE EFFECTS OF BACTERIAL ENDOTOXIN ON LIPIDE METABOLISM
Authors: LeQuire V. S. , Hutcherson J. D. , Hamilton R. L. , Gray M. E. 
Published: June 2004

Single intravenous injections of Shear's polysaccharide in varying dosages invariably produced an elevation in the levels of the total serum lipides 24 hours after injection of endotoxin. The total serum cholesterol and lipide phosphorus were also affected, although they did not change with smaller doses of endotoxin and were rarely elevated to the same degree as were the total serum lipides.
The degree of elevation of the serum lipides was apparently related to the amount of endotoxin injected up to a certain point, beyond which there was no further increase.
There were two types of response to endotoxin by the serum lipides, a moderate increase and an uncontrolled increase. Higher dosages of endotoxin and fasting apparently increased the incidence of the latter response.
No direct correlation could be made between serum lipide responses and histologic evidence typical of the generalized Shwartzman reaction following this regimen of endotoxin injection. The Shwartzman reaction did occur with greater frequency and with lower dosages of endotoxin in fasted animals.
Animals given repeated injections of endotoxin showed an initial increase in serum lipides followed by a progressive decrease to normal levels as tolerance to the febrile action of endotoxin appeared. The febrile tolerance as well as the unresponsiveness of the serum lipides to endotoxin was abolished by thorium dioxide (thorotrast) in these animals. In similar experiments a "breakthrough" of lipide unresponsiveness to endotoxin was obtained by increasing the amount of endotoxin injected.
Some of the implications of these results for the metabolic alterations produced by bacterial endotoxins are discussed.
EFFECTS OF BACTERIAL ENDOTOXIN ON METABOLISM
Authors: Berry L. Joe , Smythe Dorothy S. 
Published: June 2004

Urinary nitrogen excretion over a 17 hour period without food and water was determined for mice poisoned with endotoxin and for control mice with and without the subcutaneous injection of 5 mg. cortisone acetate. Endotoxin did not alter the quantity of nitrogen excreted, compared with that of control mice, but in both groups of animals cortisone increased urinary nitrogen by the same amount.
A balance between the quantity of protein catabolized (as estimated by increased urinary nitrogen excretion) and the total carbohydrate stored as a result of cortisone administration was found in fasted and in fed mice but not in endotoxin-poisoned mice.
Endotoxin inhibited the motility of the gastrointestinal tract and blocked the absorption of food.
Injections of ACTH in normal mice increased protein degradation and carbohydrate synthesis. In endotoxin-poisoned animals, ACTH failed to alter urinary nitrogen excretion and carbohydrate reserves. ACTH increased susceptibility to endotoxin.
The number of heat-killed cells of S. typhimurium required to block the increase in urinary nitrogen caused by an injection of ACTH was found to be 108. A partial block was found with 5 x 107 cells but not with 105 cells.
Mice infected with S. typhimurium excreted less than the normal amount of urinary nitrogen in response to ACTH 6 to 23 hours postinfection while normal amounts of nitrogen were eliminated 54 to 71 hours postinfection. The number of viable cells in the mice during the earlier period was less than the number of dead cells required to alter the nitrogen output, while the reverse was true during the later period.
THE ROLE OF THE RETICULO-ENDOTHELIAL SYSTEM IN HEMORRHAGIC SHOCK
Authors: Fine J. , Rutenburg S. , Schweinburg F. B. 
Published: June 2004

"Blockade" of the RES by thorotrast so lowered the tolerance of hemorrhagic shock in rabbits and dogs that a reversible degree of hemorrhagic shock became irreversible. This was true not only in normal rabbits, but in rabbits made resistant to hemorrhagic shock by producing resistance to endotoxins.
Rabbits which had been pretreated with thorotrast and then subjected to hemorrhagic shock displayed at death the hemorrhagic lesions and the renal cortical necrosis characteristic of the Shwartzman reaction, in addition to the intramural hemorrhages in the gut which are characteristic of animals dying of hemorrhagic or of endotoxic shock. Elimination of the Shwartzman reaction by the prior administration of nitrogen mustard did not prevent the endotoxemia or the death in shock.
Rabbits made more resistant to thorotrast than normal rabbits by prior repeated administration of this substance were also more resistant than normal rabbits to endotoxin, and survived an ordinarily lethal exposure to hemorrhagic shock.
During the first few hours after its administration thorotrast induced excessive vulnerability not only to endotoxin and to hemorrhagic shock, but also to an additional small dose of thorotrast. Moreover, a non-absorbable antibiotic given by gavage shortly after thorotrast produced the same lesions as these other agents; i.e. endotoxic shock, the Shwartzman reaction, and death.
These data indicate that the lesions induced by thorotrast are produced by endotoxins which the injured or blockaded RES cannot inactivate. The presence of endotoxins in the blood of these rabbits was indicated by the lethal effect of this blood in test recipients.
The foregoing observations did not apply to rabbits with an intestinal flora free of coliform bacteria. Over 80 per cent of such rabbits were resistant to an ordinarily lethal exposure to hemorrhagic shock, and they escaped the damage caused by the usual doses of thorotrast. They did, however, develop endotoxic shock and die if given a large dose of thorotrast. These data were taken to indicate that coliform-free rabbits are not entirely free of endotoxins. (In the ordinary environment animals cannot avoid swallowing endotoxin and coliform bacteria.)
The absence of the Shwartzman reaction in the coliform-free rabbits is taken to signify that this reaction requires the participation of the endotoxins derived from the intraintestinal bacteria.
The absence of endotoxic shock in the coliform-free rabbits is taken to signify that the endotoxins of the coliform bacteria are involved in the shock and death of the coliform-bearing rabbits.
Finally the prevention by dibenamine of both the Shwartzman reaction and endotoxic shock and death in rabbits with a normal flora demonstrates that adrenergic activity plays an indispensable role in both phenomena.
The foregoing data provide strong support for the thesis that when the RES is severely disabled by any agent, endotoxins which normally and continuously enter the circulation from the gut will produce endotoxic shock and death.
STUDIES ON THE PATHOGENICITY OF GROUP A STREPTOCOCCI
Authors: Foley Marie Judith , Wood W. Barry 
Published: June 2004

A quantitative study of the combined antiphagocytic effects of the M protein and the hyaluronic acid capsules of four strains of Group A streptococci revealed the following facts relating to their intraperitoneal virulence in mice and rats:
1. The most virulent strain, S23M (matt), produced both a large hyaluronic acid capsule and a full complement of M protein, the combined effects of which rendered the organism highly resistant to surface phagocytosis.
2. The slightly less virulent strain, T14/46 (matt virulent) was somewhat more susceptible to surface phagocytosis owing to the fact that its smaller capsule was less antiphagocytic than that of the S23M organism.
3. The glossy variant of the S23 strain (S23G), which ranked third in virulence, was still more susceptible to surface phagocytosis because of its lack of detectable M substance. Its large hyaluronic acid capsule, however, was capable of protecting it against phagocytosis on glass.
4. The least virulent strain, T14 (matt avirulent), was the most susceptible of all to phagocytosis. Though it possessed both M substance and capsule, which together prevented its phagocytosis on glass, each of them was shown to be quantitatively and functionally deficient as compared to Strain S23M.
The differences in phagocytability, which appear to be directly related to the pathogenicity of the organisms, could be adequately demonstrated in vitro only by phagocytic tests designed to measure surface phagocytosis in the absence of opsonins. This fact is in keeping with the observation, previously reported, that surface phagocytosis plays a critical role in the defense of the host, particularly during the earliest stages of experimental streptococcal infections. Its possible relation to suppuration during the later stages of infection is also discussed.
GAMMA GLOBULIN PRODUCTION IN GERMFREE RATS AFTER BACTERIAL CONTAMINATION
Authors: Gustafsson Bengt E. , Laurell Carl-Bertil 
Published: June 2004

The earlier observed pronounced hypogammaglobulinemia in germfree rats of different ages has been confirmed. Using an immunologic technique the concentration of immunologic gamma globulins were found to vary between 10 and 15 per cent of the values observed in ordinary rats. Upon contamination of germfree rats with the normal microbial flora a pronounced lag phase was noted before the gamma globulin level became normal. This lag phase was most pronounced in growing rats.
Newborn rats seem to start gamma globulin production more rapidly than older germfree rats. The response with regard to gamma globulin production on contamination of germfree rats with different types of bacterial cells through the natural routes is not identical.
ACUTE HEPATIC NECROSIS INDUCED BY BRUCELLA INFECTION IN HYPERTHYROID MICE
Authors: Bradley G. Mary , Spink Wesley W. 
Published: June 2004

When small numbers of Brucella melitensis were inoculated into ABC mice, occasional hepatic granulomas without necrosis were demonstrated. The greatest multiplication of brucellae was detected in the spleens. Because it had been previously observed that ACTH or cortisone markedly accelerated the multiplication of brucellae in the livers of infected mice with destruction of liver cells, it was considered that triiodothyronine might likewise exaggerate a brucella infection by stimulating endogenous adrenal secretion. Although adrenal hypertrophy was produced, infection of mice treated with triiodothyronine resulted in severe hepatic necrosis or infarcts without the multiplication of brucellae in either the livers or spleens. The lesions were not encountered in untreated infected mice or in control mice treated with triiodothyronine. The necrosis was associated with minimal inflammatory reaction. The necrosis was not induced in mice treated with triiodothyronine and given brucella endotoxin. The precise genesis of the acute hepatic necrosis cited in these experiments remains undefined.
Triiodothyronine did not cause deaths in mice infected with Br. melitensis. The infection was neither enhanced nor suppressed.
INFLUENCE OF HORMONES ON LIVER
Authors: Huggins Charles , Yao Fung-O 
Published: June 2004

Modification of the endocrine milieu intérieur by administration or withdrawal of hormones considerably influenced the concentration in liver of lactic dehydrogenase, glucose-6-phosphate dehydrogenase, and 6-phosphogluconic dehydrogenase. Hormones effective in this regard are thyroxine, estradiol-17ß, dihydrotestosterone, and 3α-hydroxysteroids in the androstane series. These hormonal effects are both organ-selective and, in liver, enzyme-selective.
Thyroxine and steroids are not equivalent in their influence on the 3 hepatic dehydrogenases. Thyroxine was preeminent in this regard among hormones investigated in the present experiments.
Each of the pyridine nucleotide-linked dehydrogenases in liver had an individually characteristic response to the administration of various hormones which was reflected in its hepatic level. The concentration in liver of lactic dehydrogenase was profoundly raised or lowered, respectively, by the administration of thyroxine or by thyroidectomy, and injection of steroids had small influence on its level.
The levels of glucose-6-phosphate dehydrogenase and of 6-phosphogluconic dehydrogenase were considerably influenced by injection of thyroxine, estradiol-17ß, or testosterone. Sex steroids did not increase the levels of these enzymes in hypophysectomized or thyroidectomized rats unless thyroxine was administered concurrently.
Under designated conditions, it was found that the concentration of 6-phosphogluconic dehydrogenase was increased by hormonal methods which did not elevate the concentration of glucose-6-phosphate dehydrogenase. But high levels of glucose-6-phosphate dehydrogenase were not achieved without a considerable elevation of 6-phosphogluconic dehydrogenase as well.
EFFECT OF DIETARY PROTEINS AND AMINO ACIDS ON THE SUSCEPTIBILITY OF MICE TO BACTERIAL INFECTIONS
Authors: Schaedler Russell W. , Dubos Rene J. 
Published: June 2004

Young mice were maintained for periods of 1 to 6 weeks on experimental diets containing all known growth factors, but differing in their protein and amino acid contents. All diets were supplemented with L-cystine.
The effect of the nutritional regimen on infection was tested by inoculating the animals with either one of four pathogens (Mycobacterium tuberculosis var. bovis, Mycobacterium fortuitum, Staphylococcus aureus, Klebsiella pneumoniae type C), and by observing the survival time. The infective dose was administered by either one of three routes: intravenous, intraperitoneal, or air-borne (aerosol).
In some experiments, the animals were maintained in groups of five throughout the tests. In other experiments they were housed in individual cages. This difference in housing did not affect the results in a detectable manner.
Mice fed diets containing 5 or 8 per cent casein as sole source of amino acid (except for cystine supplementation) proved more susceptible to the experimental diseases than did mice fed diets containing 15 or 20 per cent of the same protein.
Susceptibility to infection developed when wheat gluten, or soybean α-protein, was substituted for casein—even in high concentrations (15 or 20 per cent).
In one experiment, mice were fed a diet containing as sole source of amino acids a mixture of soybean and rice flour, so designed as to provide a protein concentration of 15 per cent, with an amino acid pattern similar to that of casein. These animals gained weight at the same rate as those fed a diet containing 15 per cent casein and they exhibited a satisfactory level of resistance to bacterial infection.
The infection-enhancing effect of low casein concentration (5 and 8 per cent) could be corrected by supplementing the diet with the proper mixture of amino acids. This could be done using either synthetic or natural amino acids. In contrast, susceptibility to infection developed when low casein diets were supplemented with unbalanced mixtures of amino acids.
The infection-enhancing effect of gluten diets could not be corrected by supplementing the latter with lysine even though this supplementation markedly improved weight gains in uninfected animals.
It appears in conclusion that the relative proportion of the various amino acids in the diet is as important a factor as their total amount in conditioning resistance to bacterial infections. This effect of nutrition on resistance can be detected irrespective of the route of infection: intravenous, intraperitoneal, or air-borne. Moreover, the effect has been observed with two strains of mice differing markedly in their natural resistance to bacterial infection.