PubMed · 13948951
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J GOMI. 1963-02-15. [Tuberculosis].. https://pubmed.ncbi.nlm.nih.gov/13948951/
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The risk of cancer of the cervix is linked with sexual behavior. Although infectious agents, such as human papillomaviruses (HPVs) are implicated, these alone may be insufficient to induce the disease. We investigated the potential role of estrogen, androgen, and polyamine metabolism as co-factors in the development of cervical cancer. We obtained urine samples from patients with benign cervical disease (n=18) and cervical cancer (n=18) and from age-matched normal female subjects (n=25). For 11 polyamine determination, an improved and sensitive gas-chromatographic with nitrogen/phosphorus-detection (GC/NPD) procedure was used. The urinary levels of 25 androgens and corticoids and 16 estrogens were quantitatively determined by gas chromatography-mass spectrometry-selected ion-monitoring (GC/MS/SIM). In the patients with cervical cancer, the ratio of 16alpha-hydroxy estrone (16alpha-OH E1)/2-hydroxy estrone (2-OH E1), putrescine (Put)/N(1)-acetylspermidine (N(1)-acSpd) and 5beta-tetrahydrocortisol (THF)/5alpha-tetrahydrocortisol (5alpha-THF) were significantly increased in comparison to the values of the normal controls. These data suggest: (1) an increase of 16alpha-hydroxylation in estrogen metabolism; (2) the high activity of polyamine oxidase (PAO) in polyamine metabolism; and (3) the low activity of 5alpha-reductase in androgen metabolism may play a significant role in the development of cervical cancer. Although additional research is necessary, the combination of 16alpha-OH E1/2-OH E1 and THF/5alpha-THF may provide a dual marker for the discrimination of benign cervical disease and cervical cancer.
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Spontaneous preterm birth due to intrauterine infection is associated with increased concentrations of cytokines in amniotic fluid and in the airways at birth. Intra-amniotic IL-1 induces fetal lung maturity, consistent with the decrease in the incidence of respiratory distress syndrome (RDS) in intrauterine inflammation. On the other hand, antenatal corticosteroid decreases the incidence of RDS in infants born prematurely. The aim of the present study was to investigate the interaction between IL-1 and glucocorticoid in the expression of the surfactant proteins SP-A, -B, and -C. Lung explants from rabbit fetuses at 22 (immature), 27 (transitional), and 30 (mature) d of gestation (term, 30-31 d) and on d 1 after term birth were cultured with dexamethasone (Dx), IL-1alpha, or vehicle in the presence or absence of actinomycin D. According to the present results, IL-1alpha and Dx additively increased the expression of SP-A and SP-B on d 22. Later in gestation, SP-B and SP-C were suppressed by IL-1, whereas glucocorticoid tended to increase the expression of SP-B and SP-C and prevented the IL-1-induced suppression of SP. IL-1alpha and steroid interactively increased the stability of SP mRNA compared with the single agonist, possibly explaining the additive effects on the SP mRNA levels. The present results reveal beneficial additive effects of glucocorticoid and cytokine on lung surfactant. They may explain some of the acute beneficial effects of glucocorticoid therapy in chorioamnionitis before premature birth and in inflammatory lung disease after birth.