26 research outputs found
Stroke in women — from evidence to inequalities
Stroke is the second largest cause of disability-adjusted life-years lost worldwide. The prevalence of stroke in women is predicted to rise rapidly, owing to the increasing average age of the global female population. Vascular risk factors differ between women and men in terms of prevalence, and evidence increasingly supports the clinical importance of sex differences in stroke. The influence of some risk factors for stroke — including diabetes mellitus and atrial fibrillation — are stronger in women, and hypertensive disorders of pregnancy also affect the risk of stroke decades after pregnancy. However, in an era of evidence-based medicine, women are notably under-represented in clinical trials — despite governmental actions highlighting the need to include both men and women in clinical trials — resulting in a reduced generalizability of study results to women. The aim of this Review is to highlight new insights into specificities of stroke in women, to plan future research priorities, and to influence public health policies to decrease the worldwide burden of stroke in women
The influence of gender on the short and long-term effects of growth hormone replacement on bone metabolism and bone mineral density in hypopituitary adults: a 5-year study
LACK OF EFFECT OF THE TRH RELATED DIPEPTIDE HISTIDYL-PROLINE DIKETOPIPERAZINE ON TSH AND PRL SECRETION IN NORMAL SUBJECTS, IN PATIENTS WITH MICROPROLACTINOMAS AND IN PRIMARY HYPOTHYROIDISM
INAPPROPRIATE THYROTROPHIN SECRETION, INCREASED DOPAMINERGIC TONE AND PRESERVATION OF THE DIURNAL RHYTHM IN SERUM TSH
Distribution of Melatonin in Different Zones of Lupin and Barley Plants at Different Ages in the Presence and Absence of Light
EFFECT OF LOW-DOSE DOPAMINE INFUSION ON BASAL AND STIMULATED TSH AND PROLACTIN CONCENTRATIONS IN MAN
Thyroid hormone stimulation of Na/Pi-cotransport in opossum kidney cells.
Thyroid hormone (T3), a known stimulator of renal proximal tubular brush border membrane Na-dependent phosphate (Pi) uptake (Na/Pi-cotransport), stimulated Na-dependent Pi transport in opossum kidney (OK) cells. Na/Pi-cotransport was stimulated in a time- and dose-dependent manner with maximal effects (57%) at 24 h and 10(-10) M T3. This stimulation was related to an increase in the apparent capacity (Vmax) of Na/Pi-cotransport. Treatment with T3 had no effect on Na-independent transport of Pi or of L-arginine. The stimulation of Na/Pi-cotransport was paralleled by an increase in the messenger ribonucleic acid (mRNA) encoding the OK cell apical Na/Pi-cotransporter (termed NaPi-4); the mRNA levels related to the activity of Na-independent L-arginine transport (rBAT) were unaffected by T3. Actinomycin D (10(-7) M) completely prevented the stimulatory effect of T3 on OK cell Na/Pi-cotransport and on NaPi-4 mRNA content. In conclusion, T3 stimulates apical Na/Pi-cotransport in OK cells most likely by enhancing its transcription