bluuebunny/crossref_metadata_2025_split huggingface dataset:
THE ROLE OF PENICILLIN-INDUCED BACTERIAL VARIANTS IN EXPERIMENTAL PYELONEPHRITIS
Authors: Winterbauer Richard H. , Gutman Laura T. , Turck Marvin , Wedgwood Ralph J. , Petersdorf Robert G. 
Published: June 2004

1. After injection into the renal medulla of rats Escherichia coli 06 variants reverted rapidly in vivo in the absence of penicillin. These variants had previously been shown to be stable in vitro.
2. Variants failed to survive following intramedullary injection when animals were receiving penicillin.
3. Late reversion of variants also failed to occur in animals treated with penicillin for only 1 or 2 days.
4. Variants survived and reverted more readily when injected in the renal medulla, compared with liver and spleen. Classical bacteria injected into the kidney, liver, and spleen were recovered in approximately equal numbers.
5. The histologic response to nonreverting variants, medium not containing variants, and killed variants was similar and was characterized by a fibrotic reaction with moderate round cell infiltration.
6. In contrast, the histologic response to reverting variants and to classical E. coli was characterized by an intense, acute, polymorphonuclear leukocytosis typical of acute pyelonephritis.
STUDIES ON THE LEUKOCYTOSIS AND LYMPHOCYTOSIS INDUCED BY BORDETELLA PERTUSSIS
Authors: Morse Stephen I. , Riester Sallie K. 
Published: June 2004

The 24 hr volume flow, cell concentration, and total cell output of thoracic duct fluid from mice with pertussis-induced hyperlymphocytosis were markedly reduced when compared with values obtained in normal animals.
An increase in the number of circulating lymphocytes occurred in several of the pertussis-treated mice despite the presence of an indwelling thoracic duct cannula. The drainage from such animals also showed a reduced cell concentration and total cell output.
It is suggested that lymphocyte recirculation may be minimal in pertussis-induced lymphocytosis, and the evidence obtained also suggests that lymphocytes may enter the blood stream by direct routes during the course of the reaction.
IN VITRO TRANSFORMATION BY THE ADENOVIRUS-SV40 HYBRID VIRUSES
Authors: Igel H. J. , Black P. H. 
Published: June 2004

Tumors induced with hamster kidney cells transformed by the adeno 2-, adeno 3-, adeno 7-, and adeno 12-SV40 hybrid viruses, and by adenovirus type 12, were examined histologically. The tumors induced with adeno 2-, adeno 3-, and adeno 7-SV40-transformed cells were similar to tumors induced with SV40-transformed hamster kidney cells but contained cells intermediate in morphology between SV40 and adenovirus tumor cells and occasionally contained nests of adenovirus-like cells. Cells transformed by the adeno 12-SV40 hybrid and by adenovirus type 12 gave rise to morphologically similar tumors.
The results suggest that both viral genomes are operative in hybrid-transformed cells but that one genome is apparently responsible for the predominant morphology of the tumor. Evidence that the morphology of a single transformed target cell is determined by the transforming genome was discussed.
MOUSE COMPLEMENT: THE EFFECT OF SEX HORMONES AND CASTRATION ON TWO OF THE LATE-ACTING COMPONENTS
Authors: Churchill Winthrop H. , Weintraub Ronald M. , Borsos Tibor , Rapp Herbert J. 
Published: June 2004

The titer of late-acting complement components in sera from male mice is 8–10 times higher than the titer of sera from female mice. Using assays developed to measure the serum content of two of the late-acting components, we have shown that this difference is due to the effect of androgen and estrogen on these two late-acting complement components. These two components have been tentatively identified as C'5 and C'6. Androgen and estrogen have greater effect on C'6 than on C'5. The possibility has not been excluded that still other of the late-acting complement components are affected by androgens and estrogens.
The course of homograft rejection was unchanged in mice deficient in C'5 and C'6.
STUDIES ON THE TRANSMISSION OF HUMAN VIRAL HEPATITIS TO MARMOSET MONKEYS
Authors: Deinhardt F. , Holmes A. W. , Capps R. B. , Popper H. 
Published: June 2004

Inoculation of human serums or plasmas obtained during the early acute phase of viral hepatitis induced chemical and morphological hepatic disease in marmosets in two out of five experimental series. The disease was transmissible in series from marmoset to marmoset with an apparent increased virulence of the causative agent in later marmoset passages. The chemical evidence for the disease was elevation of the activity of SGOT and SICD and of serum bilirubin. In serial liver biopsy specimens interpreted under code, a hepatitis, exhibiting some of the characteristics of human viral hepatitis, was readily distinguishable from nonspecific changes. The morphological changes preceded the biochemical alterations and persisted after them.
The data reported in these studies indicate that marmosets may be susceptible to human hepatitis. If these observations are confirmed, these animals may provide good experimental models for this disease. Final proof that the hepatitis observed in marmosets is caused by agents of human viral hepatitis is still lacking.
IMMUNOFLUORESCENT STUDIES OF THE POTENTIATION OF AN ADENOVIRUS-ASSOCIATED VIRUS BY ADENOVIRUS 7
Authors: Blacklow Neil R. , Hoggan M. David , Rowe Wallace P. 
Published: June 2004

A quantitative immunofluorescent procedure for detection of viral antigen was used to study the potentiation of AAV-1 by Ad.7. AAV viral antigen formed only when the cells were also infected with adenovirus, and only in cell culture systems in which the adenovirus infection proceeded to completion. Ad. 7 infection of AGMK. cell cultures did not potentiate AAV unless the Ad. 7 infection was itself potentiated by SV40. Dose-response studies indicated that a single AAV particle and a single infectious Ad. 7 particle sufficed to initiate AAV antigen synthesis.
Sequential inoculation studies showed that AAV antigen formed simultaneously with Ad. 7 viral antigen when the AAV was inoculated any time between 15 hr before to 10 hr after the Ad. 7, both antigens appearing about 15 hr after inoculation of Ad. 7. The AAV-1 antigen formation had a minimum latent period of 5 hr, as seen with Ad. 7 preinfection of 10 hr or more. When UV-irradiated Ad. 7 was used as helper, the AAV antigen still appeared simultaneously with the Ad. 7 viral antigen, even though the latter was delayed by 23 hr compared to nonirradiated virus.
When the early replicative events of both viruses were allowed to proceed in FUDR-inhibited cells, and then the FUDR inhibition was reversed, AAV antigen formed within 2 hr, which was 3 hr before the Ad. 7 viral antigen appeared.
It was inferred that the event in the adenovirus cycle that renders a cell competent to synthesize AAV occurs after the 10th hr and may be temporally associated with replication of the adenovirus DNA.
COMPLEMENT AS A MEDIATOR OF INFLAMMATION
Authors: da Silva W. Dias , Lepow Irwin H. 
Published: June 2004

Interaction in free solution of highly purified preparations of human C'1 esterase, C'4, C'2, and C'3, in the presence of Mg2+, resulted in rapid generation of an activity indistinguishable by biological criteria from anaphylatoxin. The formation of anaphylatoxin was associated with immunoelectrophoretic conversion of C'3 to anodically faster migrating proteins and was unaffected by the presence or absence of added C'5.
The biological properties of human anaphylatoxin prepared in this manner include: contraction and desensitization of isolated guinea pig ileum, failure to contract isolated rat uterus, enhancement of vascular permeability in guinea pig skin, degranulation of mast cells in guinea pig mesentery preparations, and liberation of histamine from suspensions of rat peritoneal mast cells. The smooth muscle-contracting and permeability enhancing properties were fully blocked by an antihistaminic drug, triprolidine. No cross-desensitizing activity on guinea pig ileum was demonstrable between rat and human or guinea pig and human anaphylatoxins but a closer biological relationship between rat and guinea pig anaphylatoxins was observed.
It is concluded that anaphylatoxin is a product of the complement system. Its possible relationship to apparently similar activities currently being obtained in other laboratories has been discussed.
CELLULAR HETEROGENEITY IN THE PRODUCTION OF AN ANTI-HAPTEN ANTIBODY
Authors: Mäkelä O. 
Published: June 2004

Single lymph node cells from rats immunized with a conjugate of 3-iodo-4-hydroxy-5-nitrophenyl acetic acid chloride (NIP) and chicken globulin were tested against either NIP or NNP conjugated with bacteriophage. NNP is related to NIP but has a nitro group instead of iodine. The conjugated phages were still infective but easily inactivated by anti-hapten sera at a serum concentration of 10–7. Phages carrying a related hapten were less sensitive to antibody than phages conjugated with the immunogenic hapten.
When NIP-T2 and NNP-T4 conjugates were incubated in microdrops containing a single lymph node cell from an anti-NIP animal, strong inactivation of either or both phages occurred in some cases. For the reasons given in the text this inactivation was considered to be due to anti-NIP antibody produced by the cell in the microdrop.
Inactivation of the two kinds of phages by the anti-NIP cells was highly nonrandom; some cells inactivated almost all of the 1700 or so NIP-T2 phages in the drop but left almost all NNP-T4 phages viable. Others had a very strong cross-reaction and inactivated equal proportions (up to 75%) of both phages. The remaining active cells exhibited an intermediate degree of cross-reaction.
Control experiments indicated that there was a true cellular heterogeneity in the specificity of the anti-NIP produced by different cells. They suggested that the observed heterogeneity of specificities was limited to the structure of the hapten and was not influenced by the structure of the carrier. As all the cells studied were induced by a single hapten, the observed cellular heterogeneity was probably not caused by a heterogeneous antigen. It seems more likely that latent heterogeneity was present in the cells before they were stimulated by the NIP hapten.
THE ROLE OF THE KIDNEY IN THE CATABOLISM OF BENCE JONES PROTEINS AND IMMUNOGLOBULIN FRAGMENTS
Authors: Wochner R. Dean , Strober Warren , Waldmann Thomas A. 
Published: June 2004

The role of the kidney in the catabolism of Bence Jones proteins, intact IgG molecules, and isolated L chains, Fab and Fc fragments of IgG, was studied. The proteins were purified, radioiodinated, and their survival times measured in nephrectomized, ureter-severed, and control mice.
Active endogenous catabolism was the major factor in overall Bence Jones metabolism since excretion as proteinuria accounted for less than 25% of the total metabolism. The survival times of λ- and κ-type human Bence Jones proteins and the Bence Jones protein produced by mice with MPC-2 plasma cell tumor were exceedingly short in both unoperated and ureter-severed mice, with 50% of the injected protein catabolized in from 0.8–1.6 hr. In contrast, the survival of Bence Jones protein was markedly prolonged in nephrectomized animals, with 50% of the injected dose catabolized in from 9 to 17 hr. This ten-fold decrease in catabolic rate indicates that the kidneys are the major site of breakdown of Bence Jones proteins. Similar studies with other proteins indicated that the kidneys are also the major site for catabolism of isolated L chains but not of intact IgG molecules. The Fc immunoglobulin fragment was not catabolized and the Fab fragment only partially catabolized by the kidney. When ureter-severed animals were allowed to develop advanced uremia before being studied, the survival of Bence Jones protein was greatly prolonged, indicating that the catabolic process is impaired in the presence of uremia. The nature of this renal catabolism remains unknown.
These observations suggest that the Bence Jones proteins and L chains observed in the urine of patients may reflect only a small fraction of such molecules synthesized by these patients. Furthermore, they provide an explanation for the prolongation of Bence Jones protein survival and the development of Bence Jones proteinemia observed in subjects with multiple myeloma and impaired renal function.
STUDIES ON PNEUMONIA VIRUS OF MICE (PVM) IN CELL CULTURE
Authors: Harter Donald H. , Choppin Purnell W. 
Published: June 2004

Pneumonia virus of mice (PVM) has been serially propagated in a line of baby hamster kidney (BHK21) cells. A maximum titer of 6.3 x 106 TCID50 per ml was obtained, and there was little variation in yield on serial passage.
PVM grown in BHK21 cells was antigenically similar to virus obtained from the mouse lung, but was somewhat less virulent for the mouse after 10 serial passages in these cells. Virus produced by BHK21 cells agglutinated mouse erythrocytes without prior heating or other treatment.
Sedimentation of PVM in the ultracentrifuge or precipitation by ammonium sulfate resulted in a loss in infectivity but an increase in hemagglutinating activity, presumably due to disruption of the virus particle. In a potassium tartrate density gradient, the major portion of infective virus sedimented at a density of approximately 1.15, and noninfective hemagglutinin, at a density of approximately 1.13. Stock virus preparations appear to contain a large amount of noninfective hemagglutinin.
The replication of PVM was not inhibited by 5-fluoro-2'-deoxyuridine, 5-bromo-2'-deoxyuridine, or 5-iodo-2'-deoxyuridine. Infected cells contained eosinophilic cytoplasmic inclusions which showed the acridine orange staining characteristic of single-stranded RNA. Foci of viral antigen were observed in the cytoplasm of infected cells by fluorescent antibody staining.
The results suggest that PVM is an RNA virus that replicates in the cytoplasm.
IMMUNOLOGICAL STUDIES CONCERNING THE NEPHRITIS OF SYSTEMIC LUPUS ERYTHEMATOSUS
Authors: Koffler David , Schur Peter H. , Kunkel Henry G. 
Published: June 2004

Antibodies were eluted from the isolated glomeruli prepared from the kidneys of 10 patients with the nephritis of systemic lupus erythematosus. Antibodies reacting primarily with buffer extracts of nuclei were eluted by acid treatment, and antibodies reacting mainly with DNA and nucleoprotein were eluted with deoxyribonuclease. Quantitative immunochemical studies revealed a high concentration of antinuclear antibody per milligram of γ-globulin in glomerular eluates compared with that in the corresponding serums. The γ-globulin of two eluates was found to consist predominantly of antinucleoprotein antibody. The selective elution of antinuclear antibodies was also indicated by the absence of other serum antibodies in the eluates.
DNA antigen was demonstrated in the glomeruli of two kidneys with nephritis by means of isolated anti-DNA antibody labeled with fluorescein. In one of these cases, anti-DNA antibodies were also found concentrated in the glomeruli and, in the second, circulating anti-DNA antibodies were demonstrated in the patient's serum.
The immunochemical evidence for the high specific activity of antinuclear antibodies and the association of DNA antigen with DNA antibody in glomeruli add further support for the antigen-antibody complex hypothesis for renal injury in systemic lupus erythematosus.
HEMOPOIETIC SPLEEN COLONY STUDIES
Authors: Curry J. L. , Trentin J. J. 
Published: June 2004

The effects of phytohemagglutinin (PHA) were studied in irradiated mice to see if a definite myeloproliferative effect could be demonstrated in vivo. The data obtained suggested the following conclusions.
PHA treatment of the bone marrow donor only, causes a consistent but slight reduction in transplantable spleen colony-forming unit (CFU) content of the bone marrow 24 hr after the last PHA injection, but no change was found in the proportion of the various colony types.
PHA treatment of the irradiated recipient of normal bone marrow causes no change in the number of spleen colonies. However, 8-day colonies are only about half normal size, are much more likely to be of mixed cell types, contain many large undifferentiated blastoid cells, but fewer transplantable CFU. The spleen sinusoids are packed with hemopoietic cells.
Spleen colonies developing in hosts receiving daily injections of PHA show, in addition to the usual spectrum of cell types, a high proportion of unusual blastoid cells resembling the PHA transformed peripheral lymphocytes seen in vitro. The function of these cells is not known, but they may represent augmented proliferation and/or transformation of stem cells.
PHA administered after irradiation significantly increased the number of endogenous spleen colonies, and, at certain doses of irradiation, improved postirradiation survival.
PHA administered before irradiation had no effect on the number of endogenous spleen colonies formed, or on postirradiation survival.
On the basis of these and other data, possible modes of action of PHA are discussed.
THE ROLE OF ANTI-GLOMERULAR BASEMENT MEMBRANE ANTIBODY IN THE PATHOGENESIS OF HUMAN GLOMERULONEPHRITIS
Authors: Lerner R. A. , Glassock R. J. , Dixon Frank J. 
Published: June 2004

These observations established the presence of anti-GBM antibodies in the sera and/or kidneys of six humans with glomerulonephritis. Further, it seems clear that these antibodies do combine with the host's glomeruli in vivo and with GBM antigen of several species in vitro.
Transfer of acute glomerulonephritis to normal recipient monkeys was possible with serum or renal eluate IGG from the three patients with anti-GBM antibodies in whom sufficient material was available. Based on this transfer of nephritis and on the presence of these antibodies at the site of injury in the nephritic kidneys of both the patients and the recipient monkeys, it seems likely that they are at least a contributing, if not primary, cause of the glomerular injury.
The frequency of anti-GBM antibodies in human nephritis is not certain, but on the basis of preliminary observations it would appear that they are present in all cases of Goodpasture's nephritis and somewhat less than half of the cases of subacute and chronic glomerulonephritis of adults.
The nature and source of immunogen stimulating the production of anti-GBM antibodies is not known, but the presence of potentially nephritogenic GBM antigens in normal urine raises the question of possible autoimmunization.
From a practical point of view, it appears that patients forming anti-GBM antibodies may not be good candidates for renal transplantation since they are likely to produce in the transplants the nephritic changes already suffered by their own kidneys.
MIGRATION OF LYMPHOCYTES AND THYMOCYTES IN THE RAT
Authors: Goldschneider Irving , McGregor Douglas D. 
Published: June 2004

The cellular deficit in rats thymectomized at birth is primarily one of circulating small lymphocytes. The lymphocyte deficiency is similar to that induced in adult rats by chronic drainage from a thoracic duct fistula. In both cases, the animals show a reduction of small lymphocytes in peripheral blood, thoracic duct lymph, and in circumscribed areas of lymphoid tissue. The lympocyte deficiency in lymphoid tissue can be corrected by an intravenous injection of thoracic duct lymphocytes. The evidence suggests that the deficiency is corrected by small lymphocytes.
Small lymphocytes pass from blood to lymphoid tissue along a route which includes the marginal sinus in splenic white pulp and postcapillary venules in the cortex of lymph nodes and Peyer's patches. Neither the ability of small lymphocytes to colonize lymphoid tissue nor their ability to traverse postcapillary venules are thymus-dependent phenomena. However, movement of small lymphocytes across postcapillary venules appears to modify the structure of endothelium.
Intravenously injected small thymocytes migrate to lymphoid tissue in smaller numbers than small lymphocytes inoculated by the same route. The few thymocytes which localize in lymphoid tissue follow the same pathway as circulating small lymphocytes.
VARIATION IN THE ONCOGENIC POTENTIAL OF HUMAN ADENOVIRUSES CARRYING A DEFECTIVE SV40 GENOME (PARA)
Authors: Rapp Fred , Jerkofsky Maryann , Melnick Joseph L. , Levy Barnet 
Published: June 2004

The acquisition of the defective SV40 genome by a variety of human adenovirus serotypes by the process of transcapsidation has resulted in the addition of oncogenic potential for newborn hamsters to the previously nononcogenic adenovirus types 1, 2, 5, and 6. These serotypes have previously been grouped together by the high GC content of their DNA.
Transcapsidation of the SV40 genome to weakly oncogenic adenovirus types 3, 14, 16, and 21 has failed to increase their oncogenic potential although the parent adenovirus type 7 carrying PARA is highly oncogenic. These serotypes belong to the group possessing a DNA of intermediate GC content.
All the PARA-adenovirus populations, even those that were nononcogenic, were able to induce SV40 transplantation immunity and therefore carry the SV40 transplantation marker as well as the marker for synthesis of SV40 tumor or T antigen.
ULTRASTRUCTURAL STUDIES OF HUMAN AND RABBIT αM-GLOBULINS
Authors: Bloth Björn , Chesebro Bruce , Svehag Sven-Eric 
Published: June 2004

Electron micrographs of isolated human α2M-molecules, obtained by the negative contrast technique, revealed morphologically homogenous structures resembling a graceful monogram of the two letters H and I. The modal values for the length and width of the α2M particles were 170 A and 100 A, respectively. Purified rabbit αmacroglobulins contained about 80% α1M- and 20% α2M-globulins. The isolated rabbit α1M- and α2M-molecules were morphologically indistinguishable from one another and from human α2M-molecules.
Preliminary immunoprecipitation studies demonstrated that the two rabbit αM-globulins were antigenically different. Sedimentation constant determinations gave s20, w values of 18.8 and 18.2 for rabbit α1M and α2M, respectively.
LASTING BIOLOGICAL EFFECTS OF EARLY ENVIRONMENTAL INFLUENCES
Authors: Dubos René , Schaedler Russell W. , Costello Richard 
Published: June 2004

Newborn specific-pathogen-free mice (SPF) were separated from their mothers shortly after birth and immediately reallocated at random to foster mothers, each of which received eight young. Under these conditions, the growth rate and adult size of the young were profoundly and lastingly conditioned by some unidentified influence exerted by the foster mother.
In SPF mice nursed by their own mothers, the diet of the latter during gestation and lactation, or during lactation alone, conditioned the weight of the young at weaning time, and throughout their whole life span.
Lasting depression of growth has been achieved by minor alterations of the dam's diet, for example by lowering its content in magnesium, or in lysine and threonine. The growth-depressing effect so achieved persisted throughout the whole life-span of the young, even though they were given at weaning time and constantly thereafter unlimited amounts of an optimum diet.
In contrast, the weight-depressing effect of a diet deficient in lysine and threonine administered to adult animals was completely and rapidly reversible when a complete diet was later substituted for the deficient one.
Depression of growth resulting from nutritional experiences during gestation or lactation did not seem to affect adversely the health of the young, or to decrease their longevity. In fact, the results of two experiments in which the animals nursed by mothers on different diets, were kept undisturbed and on optimum diets throughout their whole life span, suggest that the smaller animals had a greater average life expectancy than the larger ones.