Previous studies on genetic rat hypertension have shown that polymorphism within the alpha-adducin gene may regulate blood pressure. Adducin is a cytoskeletal protein that may be involved in cellular signal transduction and interacts with other membrane-skeleton proteins that affect ion transport across the cell membrane. There is a high homology between rat and human adducin and pathophysiological similarities between the Milan hypertensive rat strain and a subgroup of patients with essential hypertension. Thus, we designed a case-control study to test the possible association between the alpha-adducin locus and hypertension. One hundred ninety primary hypertensive patients were compared with 126 control subjects. All subjects were white and unrelated. Four multiallelic markers surrounding the alpha-adducin locus located in 4p16.3 were selected: D4S125 and D4S95 mapping at 680 and 20 kb centromeric, and D4S43 and D4S228/E24 mapping at 660 and 2500 kb telomeric. Alleles for each marker were pooled into groups. Comparisons between control subjects and hypertensive patients were carried out by testing the allele-disease association relative to the marker genotype. The maximal association occurred for D4S95 (chi 2(1) 13.33), which maps closest to alpha-adducin. These data suggest that a polymorphism within the alpha-adducin gene may affect blood pressure in humans.

There may be a cause-and-effect relationship between early fetal losses and CD36 autoantibodies.

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In order to improve the process control of bedside filtration, a multisampling procedure was evaluated. Serial samples of postfiltration blood were collected, and white blood cells (WBCs) were counted by a microdroplet fluorochromatic assay. The kinetics of the bedside filter efficiency was shown to be nonlinear, with a saturation-like pattern owing to leukocyte escaping mostly during the second half of the filtration procedure. Multisample procedure allows the computation of the actual amount of filter-escaping leukocytes, while evaluation of filter-escaping leukocytes computed on the basis of a single-point sample (postfiltration terminal segment) may give misleading results and an overestimation of the number of filter-escaping WBCs.