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S H Robinson

Publications and source records attributed to S H Robinson.

68 records · Page 4Linked to original sources
PubMed1970

Transfer of bilirubin uridine diphosphate-glucuronyltransferase to enzyme-deficient rats.

Cells from a clonal strain (MH(1)C(1)) of rat hepatoma were transplanted subcutaneously into two homozygous Gunn rats, which are jaundiced because the enzyme bilirubin uridine diphosphate-glucuronyltransferase is absent from the liver. Because of the enzyme activity present in the transplanted cells, the recipient rats developed the capacity to conjugate bilirubin and reverted in large part to a normal pattern of bilirubin excretion.

Animals↗
PubMed1970

Metabolism of bilirubin by a clonal strain of rat hepatoma cells.

These studies demonstrate that the MH(1)C(1) strain of rat hepatoma cells has the ability to take up and conjugate bilirubin and then excrete the conjugated pigment into the culture medium. On incubation with unconjugated bilirubin, the average rate of appearance of conjugated bilirubin in the medium was 4.4 +/- 0.20 microg per mg of cell protein per hour (mean +/- SE). The products formed from bilirubin by MH(1)C(1) cells were chromatographically identical to those found in normal rat bile. Assay of bilirubin UDP glucuronyl transferase activity in homogenates of MH(1)C(1) cells gave a value of 3.3 +/- 0.50 microg of conjugated pigment formed per mg protein per hour, only moderately less than the enzyme activity of liver from normal rats. Rat fibroblasts in culture did not conjugate bilirubin, nor did they contain bilirubin UDP-glucuronyl transferase activity. As in living animals, flavaspidic acid inhibited bilirubin metabolism by MH(1)C(1) cells, suggesting that the mechanism for bilirubin uptake is similar to that of normal liver. In contrast to the findings in animals, however, preincubation of MH(1)C(1) cells with phenobarbital led to only minimal enhancement of pigment conjugation. MH(1)C(1) cells represent the first example of a clonal strain of cells in culture in which many of the pathways of hepatic bilirubin metabolism remain intact. They should, therefore, serve as a useful model for studies of bile pigment metabolism which are not easily performed in the living animal.

Bilirubin↗
PubMed1970

Hemolysis of "stress" reticulocytes: a source of erythropoietic bilirubin formation.

The formation of bilirubin-(14)C was measured in rats given transfusions of red blood cells containing (14)C-labeled hemoglobin heme. Per cent conversion of hemoglobin-(14)C to bilirubin was 4 times greater with transfusion of "stress" reticulocytes from rats responding to hemorrhage than with normal reticulocytes from unstimulated donors. When the increased number of labeled reticulocytes produced by hemorrhaged donors was also considered, the total magnitude of labeled bilirubin formation was almost 20 times higher with stress as compared to normal reticulocytes. The findings were not influenced by splenectomy of either donor or recipient rats, iron loading of donors, or bleeding of recipients. However, bilirubin-(14)C formation fell off progressively as studies were performed at longer intervals after erythroid stimulation. Total bilirubin-(14)C formation in rats transfused with stress reticulocytes was compared to the production of early-labeled bilirubin from all potential sources in intact rats bled according to the same schedule used in the transfusion experiments. It is estimated that degradation of hemoglobin from sress reticulocytes accounts for virtually the entire rise in erythropoietic bilirubin formation from 24 to 96 hr after glycine-2-(14)C administration, but that additional sources make a major contribution before that time. These findings are consistent with the concept that destruction of immature erythroid cells in the peripheral blood, and probably in the bone marrow, accompanies the physiologic response to erythroid stimulation.

Animals↗
PubMedDate not supplied

Does the mean corpuscular volume help physicians evaluate hospitalized patients with anemia?

The authors analyzed the value of using mean corpuscular volume (MCV) as a guide for selecting tests for further evaluation of anemia in hospitalized patients. Of the 2,082 patients with anemia admitted to the medical service of a teaching hospital over one year, 655 (31%) had further diagnostic tests to evaluate the cause of the anemia. Within this group of 655 patients, 399 (61%) had normal MCVs. Over half the patients with abnormal serum vitamin B12, folate, or ferritin levels, or with low serum iron (Fe) levels with elevated total iron-binding capacity (TIBC), did not have the MCVs expected according to the classification of anemia proposed by Wintrobe. Furthermore, 5% of patients with evidence of iron deficiency had high MCVs, and about 12% of patients with decreased vitamin B12 levels had low MCVs. The MCV was quite specific in identifying patients who had low ferritin levels: specificity was 83%; however, sensitivity was only 48%. The MCV was also specific (88%) for identifying patients who had low Fe with elevated TIBC; however, sensitivity was only 43%. The MCV was poor in identifying patients with abnormalities of serum vitamin B12 and folate levels. In this study the MCV did not provide sufficient diagnostic accuracy to be a useful criterion for the selection of more definitive tests in the evaluation of anemia in hospitalized patients.

Aged↗