Five families with familial inherited TSH deficiency, reported to date, were examined for the TSH beta gene at the nucleotide level. The first family carries a single base substitution in the 29th codon which lies in the so-called CAGYC region; GCA (glycine) is replaced by AGA (arginine). This substitution induces conformational changes of the beta-polypeptide which make it unable to associate with the alpha-subunit. This mutation generates a new cleavage site for a restriction endonuclease MaeI, a new marker that can be used for DNA diagnosis. The second and third families were found to carry the same nucleotide substitution. Also, all three families were associated with an additional single base substitution in intron 2 as a polymorphic change, suggesting that these three families may have originated from the same single founder from Shikoku Island in Japan. The nucleotide sequence from the fourth and fifth families showed no alterations in the TSH beta gene from the about -200 basepair up-stream region to the polyadenylation site.
Immobilization stress had a biphasic effect on serum prolactin levels: the early short stimulatory phase followed by a long inhibitory phase in male rats. Stress induced the rise in serum prolactin without concomitant increase in serum TSH levels which declined during the immobilization for 300 min. Other stressors, ether inhalation or formalin s.c. injection, or TSH i.v. injection, which were effective in controls failed to elevate serum prolactin after the 300-min immobilization. Serum TSH responded to TRH after the stress as well. Pimozide, dopamine receptor blocker, was effective in increase of serum prolactin in the stressed rats as well as in controls. In pimozide pretreated rats, elevated serum prolactin levels decrease in 10 min by the immobilization and returned to the preimmobilization levels thereafter which were higher than those in stressed animals without pimozide treatment. It is suggested that TRH is not a physiological PRF in the stress-induced prolactin release and that the dopaminergic system may be activated by the immobilization stress, resulting in decrease of the prolactin-releasing activity of the pituitary.
We studied the immunomodulatory role of growth hormone (GH) treatment in GH‐deficient children. CH potentiated natural killer (NK)cell activity and the PHA and Con‐A lymphocytoproliferative response. Two‐color fluorescence using monoclonal antibodies (CLM, 2H4, CD8 and CD11) showed a moderate reduction of the helper T cells and NK cells, but no changes of suppressor T cells or cytotoxic T‐cells during GH therapy. Cancer and slow viral infection in GH‐deficient children have been watched for carefully before and after GH therapy.
Ova are captured by the oviductal fimbria and rapidly transported to the ampullary-isthmic junction of the fallopian tube. Fertilized ova and oviductal fluids are then carried medially in the fallopian tube, while undergoing maturation in preparation for entering the uterine cavity, where nidation and further development take place. This movement of oviductal fluids was visualized in a rabbit model with human chorionic gonadotropin-induced ovulation, by injection of a contrast medium into the ampulla region of the oviduct. In the ampulla, the opaque medium was observed to oscillate at 0-85.4 mm/s. This medial transport of the fluid towards the uterus decreased to 0-9.6 mm/s in the isthmic portion of the tube. This decrease substantiates previous findings that the transport of material in the isthmic portion of the oviduct is more strongly under the control of ciliary action than under peristaltic activity.
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