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Biomedical subjects

K L Miller

Publications and source records attributed to K L Miller.

At least 91 records · Page 5Linked to original sources
PubMed1985

Interleukin 3 promotes erythroid burst formation in "serum-free" cultures without detectable erythropoietin.

Erythroid burst-forming units (BFU-E) from mouse bone marrow were grown for 7 days in agar or serum-free methylcellulose cultures in the presence or absence of erythropoietin (Ep) and/or interleukin 3 (IL-3). It was found that IL-3, even in the absence of serum and detectable Ep, was able to stimulate the full development of many erythroid bursts. This IL-3 effect was cell-dose dependent and did not appear to correlate with Ep dose. Spontaneous bursts and those stimulated by Ep only were rare and when seen were very small relative to those produced by IL-3 or IL-3 plus Ep. When addition of IL-3 or Ep to 7-day cultures was delayed, IL-3 but not Ep was shown to maintain BFU-E. No evidence was found by radioimmunoassay that Ep was produced or released in 7-day, "serum-free" cultures of bone marrow nor was Ep activity detected in culture media except those to which it had been added deliberately.

Animals↗
PubMed1985

Skin exposure to I blocks thyroid uptake of 131I.

Radioisotopes of I pose an important health risk to man in nuclear accidents associated with electric power generation due to their uptake by the thyroid glands. Topical application of tincture of I or povidone-iodine to the skin of rats has been found to be as effective as oral administration of potassium iodide in blocking thyroid uptake of parenterally administered 131I. If the same effectiveness can be demonstrated in humans, this may be an attractive alternative method of mass protection from radioisotopes of I following nuclear accidents.

Animals↗
PubMed1982

Localized skin changes at the site of immunization with highly irradiated cercariae of Schistosoma mansoni are associated with enhanced resistance to a challenge infection.

The level of immunity to a percutaneous cercarial challenge with Schistosoma mansoni was assayed 4-6 weeks after immunization of mice with highly irradiated (20 krad.) cercariae or schistosomula. When immunization and challenge occurred through the same skin site, resistance, particularly that which occurred in the skin, was greater than that observed when immunization and challenge occurred in different sites. The enhanced resistance is believed to be due to localized changes in the skin; 4 weeks after exposure to irradiated cercariae, abdominal skin is characterized by a thickened epidermis, changes in the ground substance and a cellular infiltration of the dermis. A convenient mouse model is described in which one or both ear pinnae are exposed to irradiated cercariae and a percutaneous challenge is given via the abdomen, thus eliminating the effects of local skin changes. In this model, the majority of the challenge infection which succumbs to the immune response appears to be killed in the skin.

Animals↗
PubMed1981

The response of mice immune to Schistosoma mansoni to a challenge infection which bypasses the skin: evidence for two mechanisms of immunity.

Mice which had developed immunity to reinfection with Schistosoma mansoni following exposure to 20 cercariae and mice which had been immunized against S. mansoni by exposure to 400 highly irradiated (20 krad) cercariae, were tested for their ability to resist a percutaneous cercarial challenge and an intravenous challenge with 5-day-old lung-stage schistosomula derived from the same cercariae. Although both types of immune mice showed a marked resistance to a cercarial challenge, only the infected mice showed a comparable immunity to an intravenous challenge with lung schistosomula. These results confirm earlier studies which suggest that the major attrition of a cercarial challenge in infected mice occurs at the post-lung stage, whilst the attrition of a challenge infection in mice immunized with highly irradiated cercariae takes place in the skin. They provide further evidence for two separate mechanisms of immunity against S. mansoni in mice.

Animals↗
PubMed1981

An added quality-control measurement for fluoroscopic x-ray systems.

Six fluoroscopic systems were evaluated to determine if improvements in imaging could be achieved. In four of the systems, improved contrast perceptibility could be obtained through adjustment and lowering of the image-intensifier input exposure rates (IIIER). The other two systems required no change or an increase in the IIIER.

Evaluation Studies as Topic↗
PubMed1980

The impact of a nuclear crisis on a radiology department.

The experiences of the radiology department at the Milton S. Hershey Medical Center of the Pennsylvania State University College of Medicine during the Three Mile Island Nuclear Power Plant accident are presented. Emergency plans are reviewed.

Decontamination↗
PubMed1980

Protective immunity in murine schistosomiasis mansoni: evidence for two distinct mechanisms.

Techniques for recovering Schistosoma mansoni from the skin, lungs, and liver have enabled us to trace the attrition of a challenge infection in immune mice. Two separate phases of attrition were demonstrated. In mice which had developed immunity following exposure to 20 cercariae a major phase of attrition occurred between days 6 and 13, after the parasites had left the lungs, and only in mice which had been infected for 12 weeks or more did a minor phase of attrition occur in the skin. In contrast, mice which had been immunized by exposure to highly irradiated (20 kr) cercariae destroyed the majority of their reinfecting population in the skin. These results suggest that there are two distinct mechanisms of immunity to S. mansoni in mice. This view was strengthened by experiments in which both types of immune mice were challenged intravenously with 5-day-old lung schistosomula (a challenge which bypassed the skin). While the immunized mice were susceptible to the lung worm challenge, the infected mice were substantially resistant to it.

Animals↗
PubMed1979

Galactosemia: alterations in sulfate metabolism secondary to galactose-1-phosphate uridyltransferase deficiency.

Cultures of nonmutant as well as galactokinase-deficient fibroblasts incorporate 20 percent more [35S]sulfate when galactose is substituted for glucose in the medium; galactose-1-phosphate uridyltransferase-deficient cells incorporate 65.5 percent less. In addition to incorporating less [35S]sulfate, the uridyltransferase-deficient cells showed significant accumulation of intracellular galactose-1-phosphate within 4 hours after galactose exposure. Under the same conditions, no difference in [3H]uridine incorporation was observed. This metabolic alteration, occurring in response to galactose exposure, may be related to the pathophysiology of classical galactosemia.

Cells, Cultured↗
PubMed1978

Immunodepression in Taenia crassiceps infection: restoration of the in vitro response to sheep erythrocytes by activated peritoneal cells.

The in vitro response to sheep erythrocytes of mesenteric lymph node cells from mice infected with the larval cestode Taenia crassiceps is significantly depressed and can be restored to control levels by addition of activated peritoneal cells depleted of functional T or B lymphocytes. Adherent mesenteric lymph node cells from infected mice are unable to reconstitute the in vitro response to sheep erythrocytes of normal nonadherent cells. The responses of mesenteric lymph node cells from infected mice to the T-lymphocyte mitogens concanavalin A and phytohemagglutinin and the B-lymphocyte mitogen lipopolysaccharide are normal. Mesenteric lymph node cells from infected mice do not suppress the in vitro response to sheep erythrocytes of normal mesenteric lymph node cells. These results suggest that the immunodepression in T. crassiceps-infected mice is primarily the result of alterations in functional accessory cells.

Animals↗
PubMed1977

The Philadelphia variant of galactokinase.

We have previously reported the existence of a polymorphism that causes black populations to have lower mean RBC galactokinase activity than comparable white populations. We have designated this allele the Philadelphia variant, GALKP, and have suggested that it is common in blacks and rare in whites. GALKP individuals have normal WBC GALK activity, in contrast to the half normal WBC GALK activities of heterozygotes for the allele (GALKG) that causes the galactokinase-deficient form of galactosemia. In one family, we have presented evidence for the existence of two sisters heterozygous for both GALKG and GALKP alleles. These individuals have 50% normal WBC GALK activity and less than 50% normal red cell activity. The latter finding indicates that the two variant GALK alleles additively affect RBC activity. The WBC results suggest that the low activity of GALK in RBC of individuals with the GALKP allele is due to its relative instability. We could obtain no evidence for such instability from studies of high reticulocyte bloods or RBC fractionation. Furthermore, we could not demonstrate that the GALK in WBC from GALKP individuals has altered electrophoretic migration.

Alleles↗