Weather and the risk of sudden infant death syndrome: the effect of wind

STUDY OBJECTIVE—To examine and identify relations between sudden infant death syndrome (SIDS) and wind, particularly the föhn wind, in Christchurch, New Zealand.
DESIGN—A retrospective epidemiological study combining details of regional hourly meteorological variables and reported SIDS cases.
SETTING—Christchurch, New Zealand, between 1968 and 1997( )inclusively.
PARTICIPANTS—All 646 infants reported as dying from SIDS within the greater Christchurch region.
MAIN RESULTS—Analysis of 1968-1989 data revealed nine wind variables significantly related to SIDS. When compared with corresponding variables calculated over the 1990-1997 period, only the northerly wind on the day of death and the southerly wind three days before a SIDS death had estimated associations with similar effect size and sign. However, both these variables had confidence intervals that included unity.
CONCLUSIONS—No evidence was found to suspect that föhn winds influenced SIDS occurrence. The relations identified between SIDS incidence and wind, after controlling for the effects of temperature and trend, were tenuous and relatively small. More data are necessary to substantiate whether northerly winds on the day of death or southerly winds occurring three days before a death are truly associated with SIDS. It seems that wind has little, if any effect on SIDS incidence in Christchurch.


Keywords: sudden infant death syndrome; weather; föhn win

Acute endocrine profile of sulpiride in the human

Normal men and normally menstruating women received i.m. injections of 0.1 to 4.0 mg/kg sulphide. This psychotropic drug induced a very rapid (already significant after 5 minutes) and sustained (still significant after 7 hours) elevation of prolactin (PRL) concentrations in all subjects with no consistent modification of LH and FSH. After injection of 4.0 mg/kg, there was similarly no modification of mean TSH concentrations in the women tested in the luteal phase, as well as of mean GH levels in men. Sulpiride prevented the inhibitory effect on PRL levels of 500 mg levodopa, administered orally simultaneously; levodopa administered 2 hours prior to sulpiride failed to counteract the PRL-stimulatory effect of sulpiride. Under chronic sulpiride-induced hyperprolactinaemia, levodopa exhibited however a very slight inhibitory effect on PRL concentrations. These data are in agreement with the hypothesis that sulpiride acts mainly at the pituitary level by blocking dopamine receptors of the lactotropes and support the concept that the menstrual cycle perturbations observed under chronic sulpiride administration result from hyperprolactinaemia itself or from a mechanism quite similar to that by which sulpiride induces hyperprolactinaemia.SCOPUS: ar.jFLWNAinfo:eu-repo/semantics/publishe