The forkhead transcription factor FOXL2 is expressed in somatic cells of the human ovary prior to follicle formation

Interactions between germ cells and surrounding somatic cells are central to ovarian development as well as later function. Disruption of these interactions arising from abnormalities in either cell type can lead to premature ovarian failure (POF). The forkhead transcription factor FOXL2 is a candidate POF factor, and mutations in the FOXL2 gene are associated with syndromic and non-syndromic ovarian failure. Foxl2-deficient mice display major defects in primordial follicle activation with consequent follicle loss, and earlier roles in gonadal development and sex determination have also been suggested. However, despite its importance no data presently exist on its expression in the developing human ovary. Expression of FOXL2 mRNA was demonstrated in the human fetal ovary between 8 and 19 weeks gestation, thus from soon after sex determination to primordial follicle development. Expression in the ovary was higher after 14 weeks than at earlier gestation weeks and was very low in the fetal testis at all ages examined. Immunolocalization revealed FOXL2 expression to be confined to somatic cells, both adjacent to germ cells and those located in the developing ovarian stroma. These cells are the site of action of oocyte-derived activin signalling, but in vitro treatment of human fetal ovaries with activin failed to reveal any regulation of FOXL2 transcription by this pathway. In summary, the expression of FOXL2 in somatic cells of the developing human ovary before and during follicle formation supports a conserved and continuing role for this factor in somatic/germ cell interactions from the earliest stages of human ovarian development

Human toxocariasis: contribution by Brazilian researchers

In the present paper the main aspects of the natural history of human infection by Toxocara larvae that occasionally result in the occurrence of visceral and/or ocular larva migrans syndrome were reviewed. The contribution by Brazilian researchers was emphasized, especially the staff of the Tropical Medicine Institute of São Paulo (IMT)

Heart rate variability and arrhythmias evaluated with Holter in dogs with degenerative mitral valve disease

Cardiac diseases promote alterations in the autonomic control of the heart, leading to an increase in heart rate and, as a result, a decrease in heart rate variability (HRV).The aim of this study was to evaluate if the development of heart failure secondary to degenerative mitral valve disease (DMVD) concurs with changes in autonomic modulation of heart rhythm which are assessed by long electrocardiography examination (Holter). Dogs were evaluated by clinical examination and echocardiography in order to be categorized into the following groups: Control (healthy; n=6), DMVD (disease without heart failure; n=8), and DMVD heart failure (disease with heart failure; n=13). Arrhythmias and frequency domain HRV were determined by Holter. Diseased animals, when compared to healthy, had significantly lower total power, which indicates overall HRV. DMVD heart failure dogs also showed other disturbances such as high incidence of supraventricular arrhythmias, high heart rate, little amount of pauses (2.0s long between consecutive heartbeats), longer time in tachycardia, shorter time in bradycardia, low high frequency (parasympathetic control), and high low frequency (sympathetic and parasympathetic control) when compared to control (p<0.05). In DMVD dogs, Holter-derived variables changed with the development of heart failure