Biomedical subjects
Publications and source records attributed to R J Price.
Inhibition of cell division by beryllium (Be2+) has been examined in synchronized cultures of a liver-derived cell line (BL9L cells) using cytofluorometric cell cycle analysis. Results show that a selective dose-related block of the G1-pre-S transition is produced, with other periods of the cell cycle appearing relatively insensitive.
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Full-complement component lytic activity was measured in human midcycle cervical mucus, using a sensitive 51Cr release hemolytic assay. The level measured was 11.5% of the activity of complement in an equal volume of undiluted human serum. The relevance of this level of complement to complement-dependent sperm-immobilizing antibody activity was studied. After 1 hour's incubation with mucus levels of complement, immobilization of about 50% of spermatozoa occurred and after 3 hours' incubation, immobilization of about 70% of spermatozoa occurred.
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We demonstrated anticomplementary activity on once-washed human sperm, and in normal and vasectomized seminal plasmas. It was demonstrated to be a normal component of human semen. The origin of the activity is proposed to be the seminal plasma with sperm adsorption of activity. The properties of the seminal anticomplementary factor were characterized further, and the molecular size was shown to be less than 3500 daltons. Reduced anticomplementary activity was found to be associated significantly with abnormal semen profiles and infertility in males. The activity in seminal plasma was shown to have no effect on complement-dependent sperm immobilizing antibodies in the serum of an infertile woman, implicating an effect on the post-C3 components of the complement pathway. The inhibition of complement-dependent haemolysis and the lack of inhibition of complement-dependent sperm immobilization by the anticomplementary factor are considered in the implications of the role of seminal anticomplementary activity in reproduction.
The topological structure of the arteriolar network is an important determinant of microvascular resistance. In several normal and pathological conditions, this network topology is remodeled such that adequate tissue perfusion and oxygenation are maintained. The objective of this study was to quantify the extent of arteriolar remodeling in skeletal muscle of rats chronically exposed to 10% oxygen for 18 +/- 3.6 days. Arcade arteriolar (AA) and transverse arteriolar networks that had been immunofluorescently labeled for smooth muscle alpha-actin and smooth muscle myosin heavy chain were observed in whole-mount gracilis muscles from hypoxic and weight-matched control rats. Eight muscles from 4 animals were used for analysis in each group. The percentage (+/- SD) of terminal arteriolar endings that were positive for smooth muscle alpha-actin, but negative for smooth muscle myosin heavy chain increased significantly (p < 0.05) from 29.2 +/- 8.0 in controls to 70.7 +/- 9.0 in hypoxia, indicating that the rate of terminal arteriolar development was elevated in the hypoxic animals. The number of AA loops/muscle (+/- SD) increased significantly from 9.6 +/- 2.3 in controls to 14.4 +/- 4.6 in hypoxia. This increase in AA loops/muscle was due primarily to a large increase in the number of small-diameter (<15 microm) AA segments/muscle, suggesting that new AA loops were formed via the recent anastomosing of developing small-diameter terminal arterioles. The results demonstrate that exposure to chronic hypoxia stimulates significant remodeling of both the arcade and transverse arteriolar networks in skeletal muscle.