bluuebunny/crossref_metadata_2025_split huggingface dataset:
GLOMERULAR PERMEABILITY
Authors: Farquhar Marilyn G. , Wissig Steven L. , Palade George E. 
Published: June 2004

Ferritin was used as a tracer to investigate pathways and mechanisms for transfer across the various layers of the glomerular capillary wall. Kidney tissue, fixed at intervals of 2 minutes to 2 hours following an intravenous injection of ferritin, was examined by electron microscopy.
The observations confirmed the existence of three distinct and successive layers in the glomerular capillary wall (the endothelium, the basement membrane, and the visceral epithelium). In addition, they demonstrated a number of new structural features: namely (a) discrete fibrils in the subendothelial spaces; (b) a characteristic, highly elaborate, cytoplasmic organization in the visceral epithelium; and (c) special structures resembling "desmosomes" in the slits between foot processes.
In animals sacrificed at short time intervals (2 to 15 minutes) following ferritin administration, ferritin molecules were found at high concentration in the lumen and endothelial fenestrae, at low concentration in the basement membrane, and in very small numbers within the epithelium.
Later (1 to 2 hours), the tracer particles were still present in the lumen and within endothelial fenestrae, and, in addition, had accumulated on the luminal side of the basement membrane, especially in the axial regions of the vessels. Larger numbers of ferritin molecules were also found in the epithelium—in invaginations of the cell membrane at the base of the foot processes, and in various membrane-limited bodies (vesicles, multivesicular bodies, vacuoles, and dense bodies) present within the cytoplasm.
These observations suggest that the endothelial fenestrae are patent and that the basement membrane is the main filtration barrier. Since the basement membrane has no demonstrable pores, it is probably not a simple sieve but presumably is a gel-like structure with two fine fibrillar components embedded in an amorphous matrix. Both the epithelium and endothelium may be concerned with building and maintaining this structure. Finally, the intracellular accumulation of particles in the epithelium suggests that the latter acts as a monitor that recovers, at least in part, the small amounts of protein which normally leak through the filter.
EFFECT OF MULTIPLICITY OF INFECTION ON NEWCASTLE DISEASE VIRUS-HELA CELL INTERACTION
Authors: Wheelock E. Frederick , Tamm Igor 
Published: June 2004

The effects of a hundred-fold difference in virus/cell multiplicity on the interaction of Newcastle disease virus (NDV) with HeLa cells were studied, and various phases of the virus reproductive cycle were related to cellular consequences of infection. At both multiplicities used all cells were infected. The following events occurred 1 to 2 hours earlier in cells which were inoculated with the higher multiplicity: (a) first appearance of newly made virus antigen, and the amount present at any time during the period of rapid increase; (b) onset and time course of production of infective virus; (c) development by infected cells of hemadsorbing ability; (d) onset and time course of inhibition of mitosis; and (e) onset and time course of marked cell damage.
Double infection of HeLa cells with NDV and NWS was demonstrated by the fluorescent antibody technique, and was used to show that the establishment of interference against NWS was also dependent upon the multiplicity of NDV.
In cells inoculated at each multiplicity, newly made virus antigen appeared at the same time as the first infective virus particles. Infective virus rapidly reached a peak, and then declined. Viral antigen continued to increase for several hours after the decline in infective virus had begun. Thus, only a small fraction of the virus antigen produced was incorporated into new infective particles. The maximal yield of such particles was only 6 to 11 per HeLa cell. Over 95 per cent of new virus was cell-associated, but could be neutralized by treatment with antiserum before disruption of cells.
Mitosis occurred in cells which had produced and released infective NDV. Progressive inhibition of mitotic activity in infected cells was correlated with continued production of viral antigen. Marked cytopathic changes developed after mitotic activity had decreased to low levels.
The mechanism by which NDV inhibits mitosis in HeLa cells is discussed.
A COMPARATIVE STUDY OF THE GROWTH, NUTRITION, AND METABOLISM OF THE PRIMARY AND THE TRANSFORMED HUMAN CELLS IN VITRO
Authors: Chang R. Shihman 
Published: June 2004

The growth characteristics, nutritional requirements, and metabolic activities of primary explants (chiefly amnion) and transformed human cells (derived from amnion, conjunctiva, and cervical cancer) were compared. Major differences observed are as follows:
1. Five types of human tissue when freshly explanted in vitro were found to have varying but limited growth potential in contrast to the autonomous and apparently unlimited growth of the transformed cell.
2. A requirement for an external source of inositol or glutamine could not be demonstrated for the slowly multiplying primary amnions in contrast to the rapidly growing transformed cells which degenerated in the absence of either metabolite.
3. Unlike the transformed cells, the primary amnion cells fixed an insignificant amount of CO2; when infected by the Coxsackie virus, however, a requirement for CO2 in the formation of more virus became readily demonstrable.
4. The biggest difference in the incorporation of various C14 substrates occurred in the nucleic acid fractions.
5. The difference in the incorporation of glycine into the protein fraction was very small.
6. The utilization of glucose, ribose, and xylose as well as the oxidation of lactic acid into CO2 by the primary amnion cells occurred at a rate much lower than that of the transformed cells.
7. The cytotoxic dose of 5-fluorodeoxyuridine for the primary amnion was at least 100 times that of the transformed cells although growth inhibition was readily demonstrated at 0.1 µg. per ml. for both types of cells.
Based on these observations, several hypotheses are put forth for consideration.
RHEUMATOID FACTOR AND THE PATHOGENESIS OF RHEUMATOID ARTHRITIS
Authors: Mellors Robert C. , Nowoslawski Adam , Korngold Leonhard , Sengson Beth L. 
Published: June 2004

In analogy with the two categories of reactants which are used in the serological tests for the unusual category of macroglobulins called rheumatoid factor, two fluorescent reactants have been prepared for the detection of rheumatoid factor in situ in tissue sections: fluorescent antigen-rabbit antibody (immune) complex, in the present study, and fluorescent aggregated human γ-globulin, in previous work.
Plasma cells in the synovial membrane and germinal center cells and internodular plasma cells in lymph nodes are the sites of origin of rheumatoid factor in active rheumatoid arthritis, whether occurring in adults or children. Plasma cells and germinal center cells which form rheumatoid factor detectable with fluorescent immune complex are less numerous than those which contain factor demonstrable with fluorescent aggregate. In the same tissues, plasma cells and germinal center cells which contain macroglobulin (19S human γ-globulin) detectable with fluorescent antibody—but not showing the reactivity of rheumatoid factor—are more abundant than those containing rheumatoid factor.
While macroglobulin and rheumatoid factor are almost exclusively formed in the cytoplasm, these proteins are also detectable in the nucleus of an occasional plasma cell.
Normal and pathological synovial and capsular tissues, lymph nodes, and connective tissues obtained from individuals without rheumatoid arthritis are not stained with fluorescent immune complex or, except for an unusual example of Waldenstrom's macroglobulinemia, with fluorescent aggregate.
The cellular origin, as well as certain chemical and immunological attributes, of rheumatoid factor suggests an antibody-like nature and function. The observations cited are consistent with the behavior anticipated for cellular rheumatoid factor, were it primarily an antibody direct to an altered human γ-globulin and cross-reacting with rabbit γ-globulin. However, it is also possible that there are two or more cellular rheumatoid factors.
Lesion-associated protein precipitates having the composition anticipated for rheumatoid factor-antigen complex are localized in the amyloid depositions in kidney and spleen of an individual who died with amyloidosis secondary to rheumatoid arthritis.
STUDIES OF ARTHRITIS AND OTHER LESIONS INDUCED IN RATS BY INJECTION OF MYCOBACTERIAL ADJUVANT
Authors: Pearson Carl M. , Waksman Byron H. , Sharp John T. 
Published: June 2004

A generalized disease is induced experimentally in the rat by administration of Freund's adjuvant. The primary clinical and pathologic lesions are arthritis, periarthritis, peritendinitis, and periostitis in the joints of the extremities and tail. Accompanying the arthritis in some cases, and never observed in its absence, are other specific tissue lesions including iridocyclitis, nodular lesions in the glabrous skin (ear, genitalia, feet, tail), transient rashes, a chronic skin disease, genitourinary lesions, and diarrhea. These make up a striking and characteristic picture. The arthritis usually precedes the other lesions and, together with the skin disease may show a prolonged and fluctuating course. Visceral lesions do not occur.
Histologically, the basic lesion is a lymphocytic and histiocytic infiltration, initially perivascular and subsequently more disseminated. In addition, in the region of the joints and in the corpora cavernosa of the penis, there is extensive proliferation of mesenchymal cells, especially fibroblasts. Foci of fibrinoid necrosis are seen in the articular and nodular lesions, and destructive lesions of the joints are common.
Such a combination of tissue lesions has not previously been described in experimental pathology. The experimental disease is shown to have both similarities to and differences from Reiter's syndrome, rheumatoid arthritis, and certain other disorders which occur in man.
CELLULAR SOURCE AND CHARACTER OF A HEAT-STABLE BACTERICIDAL PROPERTY ASSOCIATED WITH RABBIT AND RAT PLATELETS
Authors: Jago Richard , Jacox Ralph F. 
Published: June 2004

Rabbit and rat platelets contain two non-dialyzable components (analogous to Myrvik's components 1 and 2 of serum) which, together with bicarbonate ions, produce a potent bactericidin for B. subtilis. These platelet factors appear to be identical with the serum bactericidal substances, suggesting that disruption of platelets during blood coagulation releases the platelet factors into serum. Normal human platelets contain no measurable component 1 or 2.
Since bovine serum contains component 2 but little or no component 1, estimation of the concentration of component 1 in sera or platelet suspensions of other species can be made by diluting the materials to be tested in bovine serum. The level at which a bactericidal effect is lost represents the end-point of the titration of component 1.
Rabbit serum has a high concentration of component 1 and a lower concentration of component 2. It can be diluted to a point at which bactericidal activity is lost, owing to a depletion of component 2, but at which component 1 is still present in effective concentration. At this point the addition of another serum or a platelet homogenate causes a restoration of the bactericidal activity and permits an estimate of the concentration of component 2 in the added material.
THE ANALYSIS OF STREPTOCOCCAL INFECTIONS
Authors: Halbert S. P. , Bircher R. , Dahle E. 
Published: June 2004

1. The rapid death which occurred after intravenous injection of activated streptolysin O from. Group A or Group C streptococci was always preceded by profound electrocardiographic alterations. After several multiples of the LD50 doses, cardiac electrical arrest or fibrillation could occur within 2 to 4 seconds after completion of the injection.
2. The streptolysin O preparations used were rather highly purified, but were known to be contaminated with small amounts of one or two other immunologically distinct components. Evidence that the observed results were due to streptolysin O was obtained by tests of the reversibly oxidized materials, and by cholesterol inactivation, as well as by in vivo protection with human gamma globulin rich in antistreptolysin antibodies.
3. Four non-streptolysin streptococcal antigens, partially or highly purified, failed to produce similar electrocardiographic changes, and were much less toxic. One of these was 3 X recrystallized and 1 X rechromatographed streptococcal proteinase. Shigella paradysenteriae type III endotoxin also did not produce striking electrocardiographic abnormalities.
4. A working hypothesis has been developed implicating streptolysin O as the etiological streptococcal factor responsible for the pathogenesis of rheumatic fever, which seems to account for the principal features of this illness.
EXPERIMENTAL GLOMERULONEPHRITIS
Authors: Dixon Frank J. , Feldman Joseph D. , Vazquez Jacinto J. 
Published: June 2004

Daily injections of any one of several foreign serum proteins produced in rabbits functional and morphological alterations similar to those seen in acute, subacute, and chronic human glomerulonephritis. The critical factor determining whether a rabbit would develop renal disease and the type of disease developed was the amount of antibody the rabbit formed. Those responding with much antibody were likely to develop an acute, self-limited glomerulonephritis and to be subsequently immune to further renal damage. Those responding with antibody barely sufficient to neutralize the antigen injected developed subacute and chronic glomerulonephritis. In the circulation of the rabbits with chronic glomerulonephritis, there was a daily recurring antigen-antibody reaction in the region of near antigen excess to near antibody excess which presumably led to the disease. Antigen apparently in the form of antigen-antibody complexes was deposited along the renal capillary basement membranes coincident with the development of subacute and chronic glomerulonephritis. Once developed, the morphologic stigmata of chronic glomerulonephritis persisted even after injections of antigen were stopped. However, in milder instances the renal function recovered in part after stopping antigen.
This experimental model has several implications: first, the renal injury is precipitated by antigens with no known affinity for, or immunologic relationship to, kidney; second, antigen antibody complexes localize in the kidney, apparently on the basis of non-immunologic factors, and may be an etiologic agent of renal injury; third, severe hypersensitivity disorders can be related specifically to relatively poor as well as to good antibody responses; and finally, the pathogenesis suggested here offers an alternative to that of nephrotoxic serum nephritis for the experimental approach to the study of human glomerulonephritis.
IMMUNOLOGIC STUDIES WITH ETHYLENE OXIDE-TREATED HUMAN SERUM
Authors: Maurer Paul H. 
Published: June 2004

The antigenicity of an ethylene oxide-treated human serum in humans has been studied. The immune response to the material had many of the characteristics of a delayed cellular skin reaction. Even after repeated immunizations by intradermal skin testing over a period of 1½ years, no detectable antibody could be found in the sera. The antigenicity has been shown to be associated with drastic alteration of the homologous serum proteins as evidenced by (a) the formation of new proteins, and (b) the poor cross-reactions of the modified serum proteins with antisera against normal human serum albumin and normal human gamma globulin.
The delayed hypersensitivity was transferable to normal recipients by either viable or killed leukocytes. The implications of these findings have been discussed with respect to the problem of sterilization of sera, the tuberculin reaction, and autoimmune phenomena.
ANTIGENICITY OF RAT COLLAGEN
Authors: Rothbard Sidney , Watson Robert F. 
Published: June 2004

Rabbit serum or globulin, containing antibody to rat collagen, injected intravenously or intracardially into normal or adjuvant-prepared rats becomes fixed in the basement membranes of renal glomeruli and, to a slight extent, of the tubules. When examined by ultraviolet light, this antibody can be identified in tissue sections by the yellow-green fluorescence occurring where the rabbit globulin, associated with the fixed collagen antibody, has reacted with fluorescein-conjugated anti-rabbit globulin from ducks. The reaction of the antibody to rat collagen with its antigen in the kidney is a primary factor in the production of the renal glomerular injury which occurs in rats prepared with adjuvant. Adjacent control sections failed to fluoresce when pretreated with unlabeled anti-rabbit globulin or when treated with heterologous conjugated anti-duck globulin from rabbits. The antibody to rat collagen remains in the kidney as long as 92 days and has been detected as early as 45 minutes after injection. When normal rabbit serum, rabbit anti-fish collagen serum, or rabbit anti-rat collagen serum absorbed with rat collagen was substituted for the rabbit anti-rat collagen serum, fixed antibody could not be demonstrated by fluorescence; but absorption of the anti-rat collagen serum with fish collagen did not affect the antibody fixation.
This series of immunologic tests indicates that the anti-collagen serum reacts with its homologous antigen, presumably collagen, in the basement membranes of renal glomeruli and tubules, and that specific antibody can be used to identify collagen in other tissues of the animal body.
STUDIES ON BACTERIEMIA
Authors: Derby Bennett M. , Rogers David E. 
Published: June 2004

Observations are presented on the course of experimental bacteriemia in rabbits modified by thorotrast reticuloendothelial "blockade" and mechlorethamine induced leukopenia, given singly and together.
The production of severe granulocytopenia did not impair the clearance of staphylococci from the blood stream and did not enhance the impairment of clearance produced by thorotrast reticuloendothelial "blockade."
Neither severe granulocytopenia nor thorotrast blockade alone produced consistent impairment in the removal of circulating E. coli from the blood stream, whereas when these conditions were present together, the early phases of clearance in these animals were virtually prevented.
These results indicate that the host mechanisms operative in the control of bacteriemia differ for staphylococci and E. coli. It is suggested that the fate of bacteria within polymorphonuclear leukocytes may in part determine the importance of these cells in the removal of bacteria from the blood stream.
BLOOD GROUP ACTIVITY OF GRAM-NEGATIVE BACTERIA
Authors: Springer Georg F. , Williamson Peter , Brandes William C. 
Published: June 2004

Distribution of blood group A, B, and H(O) activities among 282 aerobic Gram-negative bacteria, many isolated from the blood of patients, has been studied. Almost half of these bacteria were found to be blood group active. About 10 per cent of the organisms exhibited high, disproportional activities, which in some instances approached those of crude human blood group mucoids. No significant, specific D (Rho), M, or N activity was found in approximately 70 members of the Enterobacteriaceae.
An attempt was made to correlate the observed activity of a given organism of known O somatic antigen with its monosaccharide components. The presence of those sugars which account for the specificity of human blood group mucoids was noted.
The bearing of these findings on the origin of human anti-A and anti-B isoantibodies has been mentioned.
ENDOTOXIN FEVER IN GRANULOCYTOPENIC ANIMALS
Authors: Herion John C. , Walker Richard I. , Palmer Jeffress G. 
Published: June 2004

The febrile response to bacterial endotoxin was measured in rabbits made leukopenic with nitrogen mustard. A striking increase in susceptibility to the lethal effects of endotoxin occurred in severely leukopenic animals. Animals without circulating granulocytes, or with only basophils, developed no significant fever after endotoxin injection. Animals with circulating granulocytes other than basophils exhibited a biphasic febrile response to endotoxin; this response was significantly less in magnitude than that of control animals. Control animals, severely granulocytopenic animals, and animals with no circulating granulocytes other than basophils showed comparable febrile responses to serum pyrogen.
These results suggest that granulocytes inactivate endotoxin in vivo and support the hypothesis that leukocyte pyrogen is a necessary intermediate in endotoxin fever. Basophils do not appear to participate in this process. These observations also contradict previous studies that were taken to indicate a normal febrile response to endotoxin in leukopenic animals and suggest that those results are related to the persistence of granulocytes.
THE SPECIFICITY OF THE PASSIVE HEMAGGLUTINATION METHODS USED IN SEROLOGY OF TUBERCULOSIS
Authors: Takahashi Yoshio , Fujita Seiichi , Sasaki Akio 
Published: June 2004

The Middlebrook-Dubos hemagglutination test with normal red cells and the Boyden hemagglutination test with red cells tanned with tannic acid were shown to be strictly specific, for tubercle polysaccharide and for the protein antigens. The former test detects polysaccharide antibodies and the latter protein antibodies. Convincing evidence is given that polysaccharide does not adhere to the surface of tanned red cells nor protein to the normal red cell surface. Hemosensitizing ability and in vitro antigenicity were found to be two distinct properties of tubercle polysaccharide and protein antigens.
The phosphatide hemagglutination test with normal red cells sensitized with tubercle phosphatide is also specific; it detects only phosphatide antibodies.
The three different kinds of antibodies, antipolysaccharide, antiprotein, and antiphosphatide, were shown to be completely distinct from each other in tuberculous serum. Each of them can be completely removed from serum by absorption with red cells or kaolin particles coated with its corresponding antigen.
The reliability of the cross-inhibition test is discussed.
THE RENAL LESIONS OF ELECTROLYTE IMBALANCE
Authors: Holliday Malcolm A. , Bright Nancy H. , Schulz Dale , Oliver Jean 
Published: June 2004

Acute chloride depletion in rats is associated with the occurrence of an extensive cell damage in the mid-portion of the proximal convolutions which is followed by an excessive hyperplastic reaction of the renal epithelium; no other significant lesions were found by microdissection in either the tubules of the nephrons or the collecting system.
Potassium deficiency is not essential to the development of this lesion but does increase the severity of the reaction.
As in the case of potassium deficiency, chloride depletion predisposes to or exaggerates the structural alterations that accompany excess phosphate intake.
The relations of the different structural changes in renal architecture that occur in various states of electrolyte imbalance are discussed as well as the relation of the lesions seen experimentally in the rat and monkey and clinically in man.