Biomedical subjects
R Dimond
Publications and source records attributed to R Dimond.
The effects of pyridoxine on pituitary hormone secretion in amenorrhea-galactorrhea syndromes.
Six patients with amenorrhea, five of whom had galactorrhea and elevated PRL levels, were evaluated on a metabolic ward. All had normal sella tomograms, normal thyroid functions, and routine laboratory evaluations. None of the patients had taken any medication in the previous 6 months. On alternate days, five patients received 500 microgram of TRH iv with the measurement of PRL, TSH, FSh, LH, and hGH; 500 mg L-dopa orally with the measurement of PRL, FSH, and LH; a bolus infusion of 300 mg pyridoxine (B6) with measurement of PRL, hGH, TSH, FSH, and LH; and 25 mg chlorpromazine (CPZ) im with the measurement of PRL, LH, and FSH. The patients were then discharged on 600 mg oral pyridoxine/day and were readmitted for a repeat of the complete protocol 21 days later. The patients were continued on 600 mg oral pyridoxine for 3-4 months with monthly evaluations of serum PRL, LH, and FSH levels. These evaluations continued for 3 months after discontinuing pyridoxine. There was no demonstrable change in serum PRL after acute or chronic B6 therapy, mor was there a significant change in the response of PRL to CPZ, L-dopa, or TRH. The mean basal PRL was 97.5 +/- 9.7 ng/ml and after 3-4 months of oral pyridoxine was 97.1 +/- 14.8. In addition, there was no significant change in LH or FSH levels in response to acute or chronic B6, TRH, L-dopa, or CPZ. Neither acute B6 infusion nor chronic B6 therapy had any effect on TSH or the TSH response to TRH. Finally, acute B6 infusion had no effect on hGH levels and there were no paradoxical hGH responses to TRH. Two patients began having regular menses while on chronic pyridoxine. Their hormonal responses did not differ from those of the group, however.
The role of movement in the development of a digital flexor tendon.
D-tubocurarine was injected into the air sac of 8-day chick embryos to prevent movement of the digits of the hind limb. The embryos were paralyzed from the tenth to the eighteenth day, when the experiment was terminated. The immobilization of the flexor digitorum profundus tendons in the tarsus resulted in a loss of specialized structures around and on this tendon, as determined by light and electron microscopy. Specialized areas observed in the normal chick (synovial cavity, fibrocartilaginous area, and elastic vinculum) failed to form, as a result of the paralysis of the digit. Several authors have shown previously that movement is a requirement for the molding and maintenance of joint cavities in vivo, in ovo and in vitro (see text for references). We have shown that movement of the tendon is required to produce a functional tendon apparatus in the embryo and predict that movement is also required for regeneration after injury.