The Borrelia burgdorferi infectious cycle requires that the organism adapt to vast differences in environmental conditions found in its tick and mammalian hosts. Previous studies have shown that B. burgdorferi accomplishes this accomodation in part by regulating expression of its surface proteins. Outer surface protein A (OspA) is a borrelial protein important in colonization of the tick midgut. OspA is up-regulated when the organism is in its tick host and down-regulated when it is in a mammalian host. However, little is known about how it is up-regulated again in a mammalian host in preparation for entry into a feeding tick. Here, we report that the host neuroendocrine stress hormones, epinephrine and norepinephrine, are specifically bound by B. burgdorferi and result in increased expression of OspA. This recognition is specific and blocked by competitive inhibitors of human adrenergic receptors. To determine whether recognition of catecholamines, which are likely to be present at the site of a tick bite, may play a role in preparing the organism for reentry into a tick from a mammalian host, we administered a -adrenergic blocker, propranolol, to infected mice. Propranolol significantly reduced uptake of B. burgdorferi by feeding ticks and decreased expression of OspA in B. burgdorferi recovered from ticks that fed on propranolol-treated mice. Our studies suggest that B. burgdorferi may co-opt host neuroendocrine signals to inform the organism of local changes that predict the presence of its next host and allow it to prepare for transition to a new environment.norepinephrine ͉ OspA ͉ transmission ͉ Ixodes ͉ Lyme
Participation in the Special Supplemental Nutrition Program for Women, Infants, and Children (WIC) has been associated with lower rates of breastfeeding; studies have suggested this relationship may be modified by race. The purpose of this study is to examine the association between WIC participation and breastfeeding behaviors among white and black women in Mississippi. Using data from the 2004-2008 Mississippi Pregnancy Risk Assessment Monitoring System, we calculated multivariable prevalence and hazard ratios to assess the relationships among WIC participation during pregnancy and breastfeeding initiation and duration through 10 weeks postpartum. Stratified analyses were performed for white and black women. 52.2 % of white and 82.1 % of black women participated in WIC. 60.4 % of white and 39.7 % of black women initiated breastfeeding, and 26.5 % and 21.9 %, respectively, were breastfeeding at 10 weeks postpartum. WIC participation was negatively associated with breastfeeding initiation among whites (APR: 0.87; 95 % CI 0.77-0.99), but not blacks (APR: 0.99; 95 % CI 0.28-1.21). WIC participation was not associated with breastfeeding duration for women of either race (white: AHR: 1.05, 95 % CI 0.80-1.38; black: AHR: 0.91, 95 % CI 0.65-1.26). The results among white women suggest that Mississippi WIC might benefit from an in depth evaluation of the program's breastfeeding promotional activities to determine if aspects of the program are undermining breastfeeding initiation. High rates of participation in the WIC program among black women, and the overall low rates of breastfeeding in this population point to the potential the program has to increase breastfeeding rates among blacks.
Summary. Oxytocin (10 mi.u./\g=m\1/h) or vehicle (0\m=.\5% chlorobutanol in saline, 1 \g=m\1/h) was chronically infused directly into the corpus luteum of normally cyclic rhesus monkeys, by means of an Alzet pump\p=n-\ovarian cannula system. Infusion of oxytocin (N = 6) or vehicle (N = 5) began 6 days after the preovulatory oestradiol surge, and daily peripheral blood samples were taken. Oxytocin caused a significant (P < 0\m=.\05) decrease in progesterone, beginning 1 day after treatment, and oestradiol after 4 days; progesterone and oestradiol remained significantly depressed until menstruation. However, peripheral LH concentrations remained unchanged. The duration of the luteal phase, menstrual cycle and the onset of menses from the initiation of oxytocin infusion were significantly (P < 0\m=.\01) shorter when compared to those of vehicle\x=req-\ treated controls. These results show that oxytocin can induce functional luteolysis in the primate and supports the hypothesis that oxytocin of luteal origin may play a role in spontaneous luteolysis.
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