Depending on the duration and severity, psychological tension and physical stress can enhance or suppress the immune system in both humans and animals. Although it is well established that stress alters the release of various hormones and neurotransmitters, the mechanisms by which stress affects immune responses remain elusive. We report here that mice subjected to chronic 12-hour daily physical restraint for two days exhibited a significant reduction in splenocytes, a process likely mediated by apoptosis as demonstrated by the terminal deoxynucleotidyl transferase–mediated deoxyuridine triphosphate nick end labeling assay. CD95 (Fas/APO-1) expression in splenic lymphocytes of stressed mice was substantially increased. Interestingly, Fas-immunoglobulin fusion protein and blocking antibodies against CD95 ligand inhibit stress-induced reduction in lymphocytes. The stress-induced changes in CD95 expression and lymphocyte number could be blocked by naltrexone or naloxone, specific opioid receptor antagonists, indicating a pivotal role of endogenous opioids in this process. In addition, the reduction of splenocytes in this model system seems to be independent of the hypothalamo-pituitary-adrenal axis, as both adrenalectomized and sham-operated mice exhibited similar responses to chronic stress. Moreover, chronic physical restraint failed to induce a decrease in lymphocyte numbers in CD95-deficient (Faslpr/lpr) mice. Therefore, stress modulates the immune system through CD95-mediated apoptosis dependent on endogenous opioids.
It is concerning that 15% of mothers overall could not 'fire' these devices correctly despite a one-to-one demonstration, identifying a need for more user friendly devices and training. Mothers found the Anapen(®) device significantly easier to use, which may have implications for future prescribing. Evaluation of the next generation of autoinjectors and their training packages needs to be performed as important practical differences may be found.
Maternal smoking rates in pregnancy have declined, particularly in the non-manual social classes, and perinatal mortality rates have fallen over the last 20 years. We have therefore re-evaluated the relationship between maternal cigarette smoking and pregnancy outcome against this background. A total of 608 stillbirths and 634 infant deaths were identified using the All Wales Perinatal Survey. The cause of death was classified using the clinicopathological system. Maternal smoking rates and social class groupings were compared with those in a cohort of 16047 survivors born to women resident in South Glamorgan. The smoking rate was 37.8% in mothers of babies who died compared with 27.2% in mothers of survivors, an odds ratio (OR) of 1.63 [95% CI 1.44, 1.84]. The OR for unexplained stillbirth was 1.72 [95% CI 1.38, 2.13], placental abruption 2.07 [95% CI 1.29, 3.31], infection 3.70 [95% CI 2.23, 6.13] and sudden infant death syndrome 4.84 [95% CI 3.05, 7.69]. Maternal smoking was not associated with death due to prematurity or a congenital anomaly. Despite changes in smoking habits and the causes of perinatal death, smoking during pregnancy continues to be strongly associated with fetal and infant mortality. It is important that health promotion activities are effective in reducing smoking during pregnancy.
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