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3.  Consequences of nuclear warfare. 
Western Journal of Medicine  1983;138(2):254-255.
PMCID: PMC1010706  PMID: 11643980
4.  The Enigma of the Eosinophil 
Western Journal of Medicine  1982;137(3):239-240.
PMCID: PMC1274083  PMID: 18749203
5.  Error in drug dosage 
PMCID: PMC1956384  PMID: 20312673
7.  Points of View—II 
British Medical Journal  1974;2(5916):451.
PMCID: PMC1610437
14.  MECHANISM OF EOSINOPHILIA  
The Journal of Experimental Medicine  1970;131(6):1288-1305.
A possible role for the lymphocyte in the mechanism of eosinopoiesis has been examined. Procedures known to deplete or inactivate the pool of recirculating lymphocytes such as neonatal thymectomy, administration of antilymphocyte serum, and prolonged thoracic duct drainage, either singly or in combination, resulted in a highly significant reduction in the eosinophil response to trichinosis. Irradiated animals exposed to parasitic challenge did not develop eosinophilia unless reconstituted with lymphocytes as well as bone marrow cells. When "memory" cells were used instead of normal lymphocytes, a "secondary" type of eosinophil response was observed. Transfer of a primary eosinophilia was achieved adoptively with a population of living large lymphocytes from thoracic duct lymph and peripheral blood, but not with blood plasma or cell-free lymph. The potency of the active lymphocytes was not impaired by enclosing them in cell-tight diffusion chambers, indicating that they exerted an effect on bone marrow by agency of a diffusible factor. The demonstration of a role for lymphocytes in induction of the eosinophil response to this kind of stimulus supports the conclusion that eosinophilia belongs in the category of immunologic phenomena.
PMCID: PMC2138837  PMID: 5419272
15.  MECHANISM OF EOSINOPHILIA  
The Journal of Experimental Medicine  1970;131(6):1271-1287.
The phenomenon of eosinophilia was studied in rats using inoculation with Trichinella larvae as the experimental stimulus. Comparisons were made between the eosinophil response accompanying active infestation via the gastrointestinal tract and that resulting from parenteral inoculation of larvae or their products. A vigorous eosinophilia could be provoked by a single intravenous injection of intact parasites. In this circumstance the larvae lodged in the lungs causing an acute inflammatory reaction which led to their disintegration within 24 hr. Intraaortic injection also produced a significant response, whereas inoculation of the same number of parasites by the intramuscular, intraperitoneal, or subcutaneous routes did not cause eosinophilia. Eosinophilia likewise failed to develop if parasites were homogenized before intravenous injection, so that they were not arrested in the lungs. Antibody levels, as measured by a hemagglutination technique, using whole larval extract as antigen, did not correlate closely with the eosinophil response. The findings are interpreted as suggesting that increased eosinophil production is induced under some circumstances as a consequence of interaction between intact parasites and certain host cells in blood and tissue. No evidence was found for the existence of a specific constituent of the parasite capable of stimulating eosinophil production. Attention is directed to features of eosinophilia which fit with the concept that this phenomenon belongs in the category of immunologic reactions.
PMCID: PMC2138836  PMID: 5419271
20.  THE ANTICOMPLEMENTARY EFFECT OF KIDNEY TISSUE  
In studying the problem of the peculiar susceptibility of the kidney to coliform bacterial infection it was found that kidney tissue, unlike that of other organs, interferes with the ability of normal serum to destroy these organisms. The effect was attributable to strong anticomplementary activity, 5 to 15 times greater than that of other organs. Inactivation of complement by kidney tissue was found to have characteristics of a chemical reaction, the active principle being heat-labile, non-dialysable, and difficult to separate from tissue particles. Attempts to purify it or to obtain it in a soluble form usually resulted in great loss in activity. The component of complement affected was the fourth; i.e., that which is characterized by susceptibility to injury by ammonia. Similarities were found to exist between the conditions of ammonia formation and complement inactivation by kidney homogenates, the most notable being enhancement by phosphate and glutamine. The possibility is suggested that these findings may help to explain the vulnerability of the kidney to certain infections, especially those due to bacteria which are destroyed by the combined action of complement and antibody.
PMCID: PMC2137021  PMID: 13798253
23.  Experimental Pyelonephritis 
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PMCID: PMC2603840  PMID: 13531171
24.  EXPERIMENTAL PYELONEPHRITIS  
A study has been made of the effect of ureteral ligation on the susceptibility of the kidney to pyogenic infection. In most experiments a strain of E. coli was employed as the test organism, being injected intravenously in varying quantity either before or after ureteral ligation. A few experiments were also carried out with S. marcescens. Preliminary observations were made on the distribution and persistence of E. coli following its inoculation into the blood stream of normal rats. Rapid reduction in number of bacteria in the circulation occurred during the first 30 minutes, but bacteriemia persisted at a comparatively low level for at least 48 hours. Large proportions of the inoculated bacteria were arrested and apparently destroyed in the liver, spleen, and lungs. Comparatively small numbers were deposited in the kidneys; nevertheless, these continued to be demonstrable during the 1st week, without notable tendency to increase or decrease, then disappeared during the 2nd week. There was no acceleration in rate of disposal of the bacteria in the kidney when a second injection was made 1 week after the first. In rats with one ureter ligated the number of bacteria lodging in the kidneys after intravenous inoculation did not differ from that found in normal animals. It appears, therefore, that the increased susceptibility of the obstructed kidney to infection via the blood stream is not attributable to an increased trapping of circulating bacteria. 4 to 6 hours after the intravenous injection, however, an increased number of bacteria could be demonstrated in the obstructed kidney, apparently due to local multiplication, and by the end of 24 hours purulent infection was usually obvious. A comparatively large number of bacteria was required to cause infection, even in the kidney with obstruction. This appeared to be related to the small proportion of the intravenous inoculum which lodged in the kidney initially. Although bacteria could be demonstrated in the normal kidney for a week or more following intravenous injection it was not possible to induce active infection with equal regularity by ligating the ureter throughout this time. During the first 3 days the majority of obstructed kidneys developed infection, but after 5 or more days this occurred in only a small proportion of animals so treated. The reason for the difference, in relation to interval between intravenous injection and time of ligation, is not apparent. When the ureter was ligated but no intravenous injection of bacteria was given, staphylococcal infection developed in the obstructed kidney within 2 weeks in about one-third of the animals. Reasons are given for the belief that this was blood-borne infection, and not the result of contamination at the time of operation. Staphylococci were not recovered from the normal rat kidney. These "spontaneous" staphylococcal infections seldom developed when E. coli was injected intravenously at the time of ureteral ligation.
PMCID: PMC2136652  PMID: 13376805

Results 1-25 (36)