PubMed · 10444733
The source did not provide an abstract. Follow the original record for more information.
Explore connections, maps & timelines
J L Dhondt, J P Farriaux. 1999. Timely neonatal screening.. https://doi.org/10.1136/jms.6.2.111b
Cite the original work for its findings. Save a collection to share your selection of sources.
KEEP EXPLORING
Naturalized brown trout populations in Chile are a valuable genetic resource with aquaculture potential. The oogenesis of a three-year-old brown trout cultured population was studied in southern Chile. Gonadosomatic index (GSI), oocyte growth, gonadal microscopic characteristics, and plasma levels of estradiol-17beta (E2), testosterone (T), and 17alpha-hydroxyprogesterone (17alpha-HP) were measured bimonthly for a nine-month period before spawning. The maximum GSI level (22%) was similar to that described for other salmonids, although it was reached in May, more than one month before the population started spawning. Oocyte growth increases strongly from January when diameter reaches more than 1 mm. The vitellogenic period (six-seven months) is consistent with the long vitellogenesis, described for salmonid females maturing at three years old. E2 shows a slow increase from November, reaching its peak value in March (65.2+/-0.7 ng/ml), during maximal vitellogenic activity. T increases as oogenesis progresses, reaching a maximum of 90+/-20 ng/ml during May, and falling considerably during ovulation. Following a typical pattern of progestogens in salmonid oogenesis, 17alpha-HP stays at basal levels during most of oogenesis, but experiences a strong surge (2.0+/-0.4 ng/ml) just before ovulation.
OBJECTIVE: New insights into the role of tumor necrosis factor (TNF) in the pathogenesis of rheumatoid arthritis (RA) have expanded our understanding about the possible mechanisms by which anti-TNF antibody therapy reduces local synovial inflammation. Beyond local effects, anti-TNF treatment may modulate systemic antiinflammatory pathways such as the hypothalamic-pituitary-adrenal (HPA) axis. This longitudinal anti-TNF therapy study was designed to assess these effects in RA patients. METHODS: RA patients were given 5 infusions of anti-TNF at weeks 0, 2, 6, 10, and 14, with followup observation until week 16. We measured serum levels of interleukin-6 (IL-6), adrenocorticotropic hormone (ACTH), 17-hydroxyprogesterone (17[OH]progesterone), cortisol, cortisone, androstenedione (ASD), dehydroepiandrosterone (DHEA), and DHEA sulfate in 19 RA patients. RESULTS: Upon treatment with anti-TNF, we observed a fast decrease in the levels of serum IL-6, particularly in RA patients who did not receive parallel prednisolone treatment (P = 0.043). In these RA patients who had not received prednisolone, the mean serum ACTH levels sharply increased after every injection of anti-TNF, which indicates a sensitization of the pituitary gland (not observed for the adrenal gland). During treatment, the ratio of serum cortisol to serum ACTH decreased, which also indicates a sensitization of the pituitary gland (P < 0.001), and which was paralleled by constant cortisol secretion. The adrenal androgen ASD significantly increased relative to its precursor 17(OH)progesterone (P = 0.013) and relative to cortisol (P = 0.009), which indicates a normalization of adrenal androgen production. The comparison of patients previously treated with prednisolone and those without previous prednisolone revealed marked differences in the central and adrenal level of this endocrine axis during long-term anti-TNF therapy. CONCLUSION: Long-term therapy with anti-TNF sensitizes the pituitary gland and improves adrenal androgen secretion in patients who have not previously received prednisolone treatment. These changes are indicative of normalization of the HPA axis and must therefore be considered as evidence of an additional antiinflammatory influence of anti-TNF treatment in patients with RA.
Few and unclear data are available in the literature about the relationship between impairment of GH/IGF-I axis and polycystic ovary syndrome (PCOS). This study was aimed to evaluate the basal GH and IGF- levels, and GH release after challenge test in obese and overweight women with PCOS. Thirty patients with PCOS and other 30 healthy women matched for age, body mass index (BMI) and waist-hip ratio (WHR) were studied. Serum follicle-stimulating hormone (FSH), LH, PRL, E2, P, 17OH-progesterone (17OH-P), total T, delta4, DHEA-S, SHBG, GH and IGF-I levels were evaluated in each subject. A GHRH plus arginine challenge test was performed in all subjects. After provocative test, in PCOS and control women the GH levels were significantly (p<0.05) higher in comparison to basal values from 30 min to 120 min. At the same times, a significant (p<0.05) difference was observed between women with PCOS in comparison to healthy women. The mean peak value of GH resulted significantly (p<0.05) lower in PCOS women in comparison to healthy women. The total GH response (area under curve, AUC) to GHRH plus arginine test resulted significantly (p<0.05) lower in PCOS than in healthy women. These findings were statistically significant (p<0.05) also considering the distinction in obese and overweight women. The AUC for GH secretion was significantly lower (p<0.05) in obese in comparison to overweight subjects in the control group, whereas no significant difference was detected between obese and overweight women in the PCOS group. In conclusion, in PCOS women there is a BMI-independent alteration of the GH levels. Further investigations will be necessary to establish the real cause of these data.