In vivo Regulation of Prolactin Gene Expression in the Male Rat: Role of Sex Steroids and Dopamine

The influence of sex steroids and the dopaminergic system on the in vivo modulation of prolactin (PRL) mRNA levels was investigated by quantitative in situ hybridization in the male rat anterior pituitary gland. In situ hybridization was performed using a [³⁵S]-labeled cDNA probe encoding PRL. Orchiectomy performed 14 days earlier did not modify PRL mRNA levels. In orchiectomized rats treatment with the dopaminergic agonist bromocriptine for 14 days decreased PRL mRNA levels by 30%, while in intact animals the same treatment did not induce any changes in PRL mRNA levels. Administration of the dopamine D₂ receptor antagonist haloperidol in both intact and orchiectomized rats induced a 4-fold increase in mRNA levels. Administration of dihydrotestosterone to orchiectomized animals which had been treated or not with haloperidol or bromocriptine did not modify PRL mRNA levels. In orchiectomized animals administration of 17ß-estradiol (0.25 μg twice daily) for 14 days caused a 4-fold increase in amounts of PRL mRNA. Administration of bromocriptine to 17ß-estradiol-treated animals induced a 15% decrease of PRL mRNA levels compared to those obtained by 17ß-estradiol administered alone. The concomitant administration of 17ß-estradiol and haloperidol resulted in a 50% increase in PRL mRNA levels compared to those measured in animals treated with haloperidol alone. The present results clearly demonstrate that in vivo estrogen as well as dopamine-mediated mechanisms play a regulatory role in PRL mRNA levels in the male rat.     

Treatment of acute cerebral infarction with PGI2--evaluating the clinical effect and observation of dynamic changes in plasma TXB2 and 6-keto PGF1 alpha levels

18 patients with acute cerebral infarction were randomly subdivided into two groups: PGI2-treated group (11 cases) and low-molecular-weight Dextran-treated group (7 cases). Dosage of PGI2 was 2-5 ng/kg/min intravenous drip. Infusion was started within 72 hours after the onset of symptoms. The data showed that the plasma 6-keto-PGF1 alpha levels were increased, the plasma TXB2 levels, MAR as well as the scores of neurological deficit were decreased in the PGI2-treated group. The clinical improvement in PGI2-treated group is better than that in the dextran-treated group.     

Chemical warfare agents

The first 150 words of the full text of this article appear below. Key points

• Chemical personal protective equipment must be wornwhen in contact with contaminated casualties.
• Recognizing theclinical features of chemical warfare agent poisoning allowssupportive treatment and appropriate antidotes to be promptlyadministered.
• The mnemonic DUMBELS describes the muscarinicfeatures of the nerve agent poisoning toxidrome.
• There areeffective antidotes for poisoning with nerve agents, blood agents(metabolic poisons), botulinum toxin and kolokol-1.
• There areno specific antidotes for blistering agents (vesicants) andchoking agents.

  Chemical warfare (CW) agents are chemical substances that havea direct toxic effect on plants, animals and humans. Classifiedaccording to their physiological effects, agents effective againsthumans include nerve agents, blistering agents (vesicants),blood agents, choking agents and toxins. Incapacitating, vomiting,psychoactive and riot control agents (e.g. CS gas) also exist.¹ All personnel in contact with contaminated casualties must wearthe appropriate level of chemical personal protective equipment(CPPE) until adequate decontamination is . . . [Full Text of this Article]