Circumcision--the debate goes on.
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Biomedical subjects
Publications and source records attributed to H Stang.
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Spinal bone mineral density (BMD) is traditionally measured by dual-energy X-ray absorptiometry (DXA) in the anteroposterior (AP) projection which includes both the vertebral body and the posterior elements in the measurement. The posterior elements, however, contribute little to the compressive strength of the spine. It has therefore been suggested that spinal BMD measured in the lateral projection, including only the vertebral body in the measurement, might be more appropriate for the prediction of fracture risk. To date little clinical evidence has been presented to support this assumption. To address the issue, we measured vertebral, hip and forearm BMD in situ in 14 human cadavers and remeasured BMD in vitro in excised vertebrae. Lateral spinal measurements were performed in the decubitus position. Fracture force and other biomechanical measures were determined for 32 vertebrae in a mechanical testing machine and compared with BMD values in situ and in vitro. Correlations of BMD with vertebral fracture force were r = 0.48/0.51 (in situ/in vitro) for the AP spinal measurements, r = 0.45/0.71 (in situ/in vitro) for the lateral spinal measurements, and r = 0.64 and r = 0.53 for total hip and forearm measurements in situ, respectively. Thus, despite an apparent diagnostic advantage in vitro, lateral spinal BMD measurement was not superior to AP measurement when performed in situ. This observation corresponds well with previous clinical findings and is probably due to the larger accuracy error in the lateral than in the AP projection resulting from a lower ratio of bone to soft tissue. The high correlation between hip BMD and vertebral fracture force suggests that hip measurement may prove as useful for vertebral fracture risk assessment as spinal measurement in any projection, especially in the elderly with a high prevalence of degenerative changes in the spine.
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Serum concentrations of conjugated cholic acid determined radioimmunologically were investigated for 3 hours after a test meal in 62 patients with fatty liver, 70 patients with chronic hepatitis and 30 patients with liver cirrhosis. Values were compared with results of further data from chemical pathology. Increased fasting bile acid values were found in 18% of patients with fatty liver, 13% with chronic hepatitis and in 70% with cirrhosis. Following the test meal maximum concentration increase of cholic acid conjugates was obtained after one hour. 70.5% of patients with fatty liver, 80% of patients with chronic hepatitis and 97% of patients with cirrhosis were identifiable by increased bile acid levels. Postprandial serum bile acid levels therefore have a higher sensitivity for diagnosis of liver disease than bilirubin, glutamic-oxaloacetic transaminase, alkaline phosphatase or gamma-glutamyl transferase.
Using commercially available radioimmunoassays, bile acids were measured in the serum of 378 healthy probands. The following values were found: conjugated cholic acid 0.36 +/- 0.38 mumol/l (95% percentile 1.28 mumol/l) (CG-radioimmunoassay from Abbot); sum of the various conjugated cholanic acids 2.8 +/- 1.58 mumol/l (95% percentile 5.98 mumol/l) (CBA-radioimmunoassay from Becton-Dickinson); sulphate glycolithocholic acid 0.57 +/- 0.33 mumol/l (95% percentile 1.23 mumol)l) (SLCG-radioimmunoassay from Abbot). The values showed a normal logarithmic distribution. No sex-specific differences were found between similar age groups of the 207 male and the 171 female probands. In 50 probands, serum concentrations were followed over a period of 3 hours after a standardized meal. Conjugated cholic acid showed a 5-fold postprandial increase, compared with the concentrations measured in fasting probands. In 48% this maximum was reached within 60 minutes, in 32% within 2 hours, and in 20% within 3 hours. The concentrations of sulphate glycolithocholic acid were subject to only slight postprandial variations, which did not appear until the second or third hour.
Aminopyrine breath test was investigated in 268 patients with various liver disease. From the specific activity for six hours after ingestion of a tracer dose the elimination rate in percent per hour is calculated. Comparing to 47 controls the elimination rate is reduced about 20% in patients with chronic persistent hepatitis (49 patients) and fatty liver (84 patients). In 42 patients with chronic active hepatitis the elimination rate is reduced to 48% and in 54 patients with cirrhosis to 64%. Between aminopyrine breath test and indocyaningreen test or cholinesterase and albumin no correlations were found. Aminopyrine breath test is a sensitive, non-invasive test and specific in liver function and therefore useful in the follow up of patients with known liver disease.
The human alpha-globin and phosphoglycollate phosphatase (EC 3.1.3.18) genes have been regionally localized to the short arm of human chromosome 16 (HC16). This was accomplished by fusing mouse fibroblasts (A9) to human fibroblasts that contain a reciprocal translocation between the long arms of chromosomes 16 and 11. The murine A9 cells are deficient in adenine phosphoribosyltransferase (APRT), an enzyme present on the long arm of HC16 (HC16q). Hybrid cells were grown in selection culture medium that required the cells to retain human APRT. Therefore, the hybrids exhibited stable retention of the entire HC16 or the rearranged chromosome containing HC16q. We isolated five independent primary and secondary hybrid cell lines which retained either HC16 or HC16q at a high frequency. The presence of human alpha-globin genes in the various clones was established directly by DNA extraction and hybridization to a cDNA probe for human alpha-globin genes. Autoradiographs showed that hybrid cells containing the long arm, but not the short arm, of HC16 showed only the background mouse bands. Hybrid cells that retained the entire HC16 demonstrated the band(s) containing the human alpha-globin genes. Hybrid cells that contained HC16 with its alpha-globin genes were then placed in culture medium that contained diaminopurine, which is lethal for cells containing APRT. These counter-selected hybrid cells had lost HC16 and also lost the human alpha-globin genes as determined by blot hybridization. The presence of alpha-globin gene sequences in the hybrid clones was concordant with HC16 only and not with any other human chromosome. These results confirm the assignment of alpha-globin genes to HC16 and localize the genes to the short arm. We also assign the locus for phosphoglycollate to the short arm of HC16.
Resistance to methotrexate was induced in bone marrow cells of mice by transformation in vitro with DNA from a drug-resistant cell line. Transformed cells were injected in vivo and haematopoietic cells expressing resistance were selected by drug treatment of recipients. Transformed cells had elevated levels of dihydrofolate reductase and demonstrated a proliferative advantage over untransformed cells, indicating successful gene transfer.