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Biomedical subjects

R A Roberts

Publications and source records attributed to R A Roberts.

99 records · Page 6Linked to original sources
PubMedDate not supplied

Results following trapeziometacarpal arthroplasty of the thumb.

A retrospective follow-up study was performed on patients with degenerative joint disease (DJD) who underwent trapeziometacarpal arthroplasty of the thumb with 3-week immobilization and without the use of K-wire fixation. Pre- and post-operative pain, activities of daily living (ADLs), grip strength, and pinch strength were compared. Data were collected on 25 hands in 23 patients, 7 hands with full trapezium resections and 18 with hemi-trapezium resections. The median age was 60 years, with a range of 39 to 73 years, and the median follow-up period was 1 year 11 months, with a range of 3 months to 11 years. Grip and pinch strength were measured pre- and postoperatively. Pain was assessed on a visual analog scale (VAS), and ADLs were assessed by means of a 15-item survey. Both pain and ADLs were evaluated postoperatively with recall of preoperative status. Following surgery, all thumbs were immobilized in a static splint for 3 weeks and then allowed progressive use. Median improvements in hemi-trapezium resections included grip, 22.5 lb; pinch, 4.7 lb; and ADLs, 33%. Pain was reduced a median of 7.0 cm on the VAS. Median improvements in full trapezium resection included grip, 29.5 lb; pinch, 0 lb; ADLs, 60%; and pain reduction, 8 cm on the VAS. This follow-up study suggests that satisfactory results can be achieved in pain reduction, strength, and ADLs with an immobilization period of only 3 weeks and without the use of K-wires following carpometacarpal (CMC) arthroplasty.

Activities of Daily Living↗
PubMedDate not supplied

Plasma transferrin receptor levels and indices of erythropoiesis and iron status in healthy term infants.

PURPOSE: The goal of this study was to determine if the postnatal changes in plasma transferrin receptor (TfR) levels in healthy infants were associated with changes in erythropoiesis or iron status. SUBJECTS AND METHODS: Longitudinal blood samples were obtained monthly from healthy term infants fed iron-fortified formula for the first 7 months and analyzed for plasma TfR and indices of erythropoiesis and iron status. RESULTS: Plasma TfR level rose during the first 2 months of life (p < 0.002). When examined for its association with indices of erythropoiesis, plasma TfR was negatively associated with hemoglobin (Hb) (p < 0.01), and positively associated with plasma erythropoietin (EPO) concentration (p < 0.005) and absolute reticulocyte count (p < 0.005). Plasma TfR was not associated with erythrocyte protoporphyrin. Although indices of iron status were not suggestive of iron deficiency, plasma TfR was negatively associated with plasma ferritin, Tf saturation, and plasma iron, and positively associated with total iron binding capacity (TIBC) (p < 0.0001 for all). CONCLUSIONS: Increases in plasma TfR levels were observed during normal infancy. The increases in plasma TfR levels correlate with increases in erythropoiesis without evidence for functional iron deficiency.

Birth Weight↗
PubMedDate not supplied

The nongenotoxic hepatocarcinogens diethylhexylphthalate and methylclofenapate induce DNA synthesis preferentially in octoploid rat hepatocytes.

Diethylhexylphthalate (DEHP), a rodent carcinogen, and 1,4-dichlorobenzene (DCB), a noncarcinogen in rat liver, are potent hepatomitogens. We have reported previously that 7-day dosing with DEHP induced a higher bromodeoxyuridine labeling index (LI) in binuclear octoploid (2x4N) rat hepatocytes than did DCB, suggesting that induction of DNA synthesis in 2x4N hepatocytes might represent a more substantial carcinogenic risk. We compared 2 additional rodent hepatocarcinogens, methylclofenapate (MCP) and phenobarbitone, with ethylene thiourea (ETU), a noncarcinogenic hepatomitogen in rat. All 3 chemicals increased hepatic LI; the 8N population had the highest LI, but only the carcinogens increased LI in the 2x4N and 4N populations. To identify the target population for induction of DNA synthesis, we used a 1-hour pulse label at the peak of induction. The results were consistent with the 7-day data, and again the highest LI was in the 8N population. The nongenotoxic rodent carcinogens MCP and DEHP induced a significant increase in the LI in the 2x4N population, whereas ETU and DCB did not. These data support the hypothesis that increased DNA synthesis within the minority 2x4N population may be more significant for subsequent hepatocarcinogenesis.

Animals↗
PubMedDate not supplied

Quantitation of apoptotic bodies in rat liver by in situ end labelling (ISEL): correlation with morphology.

Nongenotoxic hepatocarcinogens have been proposed to inhibit hepatocyte apoptosis, preventing the removal of DNA-damaged cells. Conclusive proof of this hypothesis has been hindered by the lack of a marker or stain for apoptosis suitable for high throughput counting. A method is described for the detection of apoptotic bodies (AB) in paraffin sections of rat liver using an in situ end labeling (ISEL) technique that detects DNA damage. Results of this AB quantitation were compared with routine hematoxylin-eosin (H&E)-stained sections. The number of apoptotic bodies was enhanced by the withdrawal of the rodent nongenotoxic hepatocarcinogens and hepatomitogens nafenopin (naf) or cyproterone acetate (CPA) after 7 days of daily dosing. In rat livers 24-96 hr after cessation of dosing with naf, and in control livers, an AB index of approximately 0.1% of hepatocyte nuclei was seen when stained by H&E or ISEL. However, livers examined 48 hr after cessation of 7 days of daily dosing with CPA had an AB index of approximately 1% hepatocyte nuclei when stained with H&E, but only approximately 0.4% hepatocyte nuclei using the ISEL technique. Thus, CPA withdrawal from the hyperplastic liver generated a wave of apoptosis in contrast to naf withdrawal where little was seen up to 96 hr after withdrawal. The differing kinetics of CPA and naf clearance may explain this discrepancy. Less apoptosis was detected by the ISEL method following CPA withdrawal; this could arise if the stage of apoptosis labeled by ISEL is shorter than the morphologically recognizable stages (using H&E). The ISEL method for the evaluation of AB indices is useful in parallel with H&E, although more validation is required before it can be used routinely for the quantitation of AB in tissue sections.

Animals↗
PubMedDate not supplied

Perturbation of rodent hepatocyte growth control by nongenotoxic hepatocarcinogens: mechanisms and lack of relevance for human health (review).

During the development of new industrial and pharmaceutical chemicals, it is necessary to determine whether they are potential carcinogens. However, there are no short-term tests available for nongenotoxic carcinogens that do not damage DNA yet cause tumours in rodent bioassays. The peroxisome proliferators (PPs) constitute a diverse class of nongenotoxic carcinogens that include chemicals of therapeutic, industrial and environmental importance such as hypolipidaemic fibrate drugs, clingwrap/medical tubing plasticizers and certain pesticides and solvents. PPs induce DNA synthesis and suppress apoptosis in rat and mouse hepatocytes, leading to tumour formation. In addition to altering hepatocyte growth and survival, PPs cause peroxisome proliferation and the induction of enzymes of the beta-oxidation pathway. PPs mediate their biological responses in rodents via activation of the nuclear hormone receptor PPARalpha (peroxisome proliferator activated receptor alpha) which regulates expression of the genes associated with response to PPs. The mechanisms through which normally quiescent hepatocytes are recruited into the cell cycle currently remain obscure. However, it is probable that expression of hepatic cytokines by hepatic macrophages (Kupffer cells) may be involved. In common with other classes of nongenotoxic carcinogen, there are remarkable species differences in response to PPs; humans respond to the fibrate hypolipidaemic PPs via a reduction in serum cholesterol but appear refractory to the adverse effects of PPs such as hepatic peroxisome proliferation, DNA synthesis and tumour formation. The molecular basis of the observed species differences in response to PPs is unclear at present, but recent data support a quantitative hypothesis wherein PPARalpha expression levels are sufficient in humans to mediate hypolipidaemia, but too low for transcriptional regulation of the full battery of genes associated with the adverse effects seen in rodents such as peroxisome proliferation, liver enlargement and tumours. A more detailed understanding of the mechanisms through which these chemicals cause tumours in rodents and how humans may differ will assist in extrapolation of rodent data to human risk assessment.

Animals↗