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Biomedical subjects

K Kolb

Publications and source records attributed to K Kolb.

10 recordsLinked to original sources
PubMed1996

Using time intervals between expected events to communicate risk magnitudes.

Because members of the public have difficulty understanding risk presented in terms of odds ratios (e.g. 1 in 1000) and in comparing odds ratios from different hazards, we examined the use of time intervals between expected harmful events to communicate risk. Perceptions of the risk from a hypothetical instance of naturally-occurring, cancer-causing arsenic in drinking water supplies was examined with a sample of 705 homeowners. The risk was described as either 1 in 1000 or 1 in 100,000 and as present in a town of 2000 people or a city of 200,000 people. With these parameters, the time intervals ranged from 1 expected death in 3500 years (1 in 100,000 risk, small town) to 1 death every 4 months (1 in 1000 risk, city). The addition of time intervals to the odds ratios significantly decreased perceived threat and perceived need for action in the small town but did not affect response for the city. These framing effects were nearly as large as a 100-fold difference in actual risk. Instances when this communication approach may be useful are discussed.

Communication↗
PubMed1993

Xeroderma pigmentosum-Cockayne syndrome complex in two patients: absence of skin tumors despite severe deficiency of DNA excision repair.

Two brothers had a complex combination of two DNA repair disorders: Cockayne syndrome and xeroderma pigmentosum. This rare combination has previously been observed in only two other patients. The clinical signs shared by these two brothers and the two other previously described patients include severe sun sensitivity, freckling, diminished stature, hearing and movement impairment, and neurologic degeneration. Although defective UV-induced unscheduled DNA synthesis has been demonstrated (5% of normal), no skin cancers have appeared in these 38- and 41-year-old brothers, whereas skin cancers developed at a relatively early age in the two previously described patients who also had defective UV-induced unscheduled DNA synthesis.

Adult↗
PubMed1992

Endogenous intestinal metallothionein possibly contributes to the renal accumulation of cadmium.

At low levels of dietary cadmium chloride, cadmium accumulates directly in the kidneys and not in the liver. As dietary cadmium induces intestinal metallothionein (MT), intestinal CdMT complexes could be at least partly responsible for the renal accumulation of oral cadmium. For this to be possible, however, serosal release of mucosal CdMT would be required. To test this hypothesis, we perfused isolated rat small intestinal segments (Fisher-Parsons method) in an attempt to demonstrate the release of intestinal MT. After two weeks of feeding dietary cadmium chloride, intestinal MT was induced in amounts proportional to the dietary cadmium level. Subsequent in vitro perfusion of the small intestine revealed a concentration-dependent release of intestinal MT on the serosal side. When 109CdCl2 was present in the perfusion medium, 109Cd appeared on the serosal side mainly in the MT fraction. These results indicate that endogenous intestinal MT may deliver CdMT to the organism, thus possibly contributing to the renal accumulation of orally ingested cadmium.

Animals↗
PubMed1987

Metal-metal interactions among dietary toxic and essential trace metals in the rat.

Exposure to toxic and essential metals is thought to be reflected by corresponding metal concentrations in tissues. However, toxic and essential metals may influence each other in regard to their retention in the body. Therefore a basic diet containing four toxic metals (As 7, Cd 9, Ni 13, and Pb 20 ppm) and adequate amounts of essential metals was fed to rats for 2 weeks. Test groups received the basic diet with increasing concentrations of one of the toxic metals (up to 90 ppm As, 180 ppm Cd, 365 ppm Ni, and 394 ppm Pb). As, Cd, Ni, Pb, Cu, Fe, Mn, and Zn were determined by atomic emission spectroscopy in liver, kidney, intestine, brain, muscle, bone, skin, hair, and blood. A linear relationship between diet and tissue concentration is observed for As and Ni in the kidney, for Cd in the liver, and for Pb in the bone. In other tissues saturation was observed. While Cd-Fe interactions were common to most of the tissues, other interactions were detected only in specific tissues, e.g., As-Cu in the kidney, Cd-Zn in the liver, and As-Mn, Cd-Mn, or Ni-Cu in the intestine. Increases of renal Pb and intestinal Cd by dietary Ni, and a decrease in bone As by dietary Pb were the most pronounced interactions between the toxic metals. The results demonstrate that potential target organs for the evaluation of metal exposure need to be carefully analyzed for interfering metal-metal interactions.

Administration, Oral↗
PubMedDate not supplied

The longitudinal distribution of cadmium, zinc, copper, iron, and metallothionein in the small-intestinal mucosa of rats after administration of cadmium chloride.

Different routes of Cd intake may influence the intestinal distribution of Cd, metallothionein (MT), and trace metals differently. Therefore, we compared the effects of parenteral and enteral administration of Cd on the distribution of trace metals and MT along the small intestine. In a first experiment three groups of rats were employed: a control, one receiving CdCl2 within the drinking water, and another receiving sc injections of CdCl2. In a second experiment, rats were fed three different diets with either 0, 0.3, or 1 mmol CdCl2/kg for one and two weeks to study the time- and dose-dependent effects of orally administered Cd. Metal concentrations (Cd, Zn, Cu, Fe) were measured by atomic emission spectrometry and MT was determined by radioimmunoassay. Intestinal MT levels did not show proximodistal gradients in controls or after sc administration of Cd, but orally administered Cd increased mucosal MT levels longitudinally from the duodenum to the ileum. Cd levels paralleled those of MT. Compared with the metal concentrations in the controls, sc administration of Cd did not change intestinal Zn, Cu, and Fe levels. Oral administration of Cd, however, increased Cu and decreased Fe levels in the intestinal mucosa significantly. The second experiment revealed that only high dietary concentrations of Cd increase intestinal Cd and MT levels longitudinally toward the distal parts, whereas at lower dietary concentration the longitudinal distribution was reversed. This shows that different routes and doses of Cd intake lead to a different trace metal and MT distribution and emphasizes the role of dietary Cd in the local induction of small-intestinal MT.

Administration, Oral↗