Pregnancy-specific stress contributed directly to preterm delivery and indirectly to low birth weight through its association with smoking. Pregnancy-specific stress may be a more powerful contributor to birth outcomes than general stress.

Both aging processes and psychological stress affect the immune system: Each can dysregulate immune function with a potentially substantial impact on physical health. Worse, the effects of stress and age are interactive. Psychological stress can both mimic and exacerbate the effects of aging, with older adults often showing greater immunological impairment to stress than younger adults. In addition, stressful experiences very early in life can alter the responsiveness of the nervous system and immune system. We review the unique impact of aging and stress on immune function, followed by evidence of interactions between age and stress. Further, we suggest that prenatal or early life stress may increase the likelihood of maladaptive immune responses to stress in late life. An understanding of the interactive effects of stress and age is critical to efforts to determine underlying mechanisms, clarify the directionality of effects, and develop effective interventions in early and late life.

This study helps explain how loneliness dynamics relate to poor health and suggests specific points of departure for the development of interventions.

Various in vitro models have been described that emulate one or more of the processes involved in angiogenesis in vivo. In the present study endothelial cells were cultured in three-dimensional type I collagen lattices in the presence of a mixture of basic fibroblast growth factor, vascular endothelial cell growth factor, and phorbol myristate acetate. Under these conditions, the endothelial cells rapidly assemble into an interconnected network of tube-like structures with a high frequency of intercellular canals or lumens. The formation of the networks and lumens was completely blocked by cycloheximide and by actinomycin D. Monoclonal antibodies directed against CD31 or vascular endothelial cadherin (VE-cadherin) inhibited the formation of endothelial tubes. A subtle difference in the morphology of cells treated with anti-CD31 versus anti-VE-cadherin was noted; namely, cells incubated in the presence of CD31 antibodies were rounded or formed attenuated tube-like structures, both of which were characterized by a single, large intra- or intercellular vacuole. In contrast, tube formation by cells incubated in the presence of VE-cadherin antibodies was also impaired and, most notably, demonstrated a reduction in either vacuole formation or vacuole fusion, depending upon the monoclonal antibody used. We suggest that the two endothelial-junction-associated proteins, CD31 and VE-cadherin, play different roles in the process of tube formation. CD31 appears to be required for cell elongation, migration, and/or invasion in the gels as well as for cell-cell association to form the network structures. VE-cadherin also appears to be required for cell-cell association, but additionally appears to play some role in the process of vacuolization or vacuole fusion leading to intercellular lumen formation.

Over the past decade it has become clear that stress can significantly slow wound healing: stressors ranging in magnitude and duration impair healing in humans and animals. For example, in humans, the chronic stress of caregiving as well as the relatively brief stress of academic examinations impedes healing. Similarly, restraint stress slows healing in mice. The interactive effects of glucocorticoids (e.g. cortisol and corticosterone) and proinflammatory cytokines [e.g. interleukin-1β (IL-1β), IL-1α, IL-6, IL-8, and tumor necrosis factor-α] are primary physiological mechanisms underlying the stress and healing connection. The effects of stress on healing have important implications in the context of surgery and naturally occurring wounds, particularly among at-risk and chronically ill populations. In research with clinical populations, greater attention to measurement of health behaviors is needed to better separate behavioral versus direct physiological effects of stress on healing. Recent evidence suggests that interventions designed to reduce stress and its concomitants (e.g., exercise, social support) can prevent stress-induced impairments in healing. Moreover, specific physiological mechanisms are associated with certain types of interventions. In future research, an increased focus on mechanisms will help to more clearly elucidate pathways linking stress and healing processes.

Despite aromatherapy's popularity, efficacy data are scant, and potential mechanisms are controversial. This randomized controlled trial examined the psychological, autonomic, endocrine, and immune consequences of one purported relaxant odor (lavender), one stimulant odor (lemon), and a no-odor control (water), before and after a stressor (cold pressor); 56 healthy men and women were exposed to each of the odors during three separate visits. To assess the effects of expectancies, participants randomized to the "blind" condition were given no information about the odors they would smell; "primed" individuals were told what odors they would smell during the session, and what changes to expect. Experimenters were blind. Self-report and unobtrusive mood measures provided robust evidence that lemon oil reliably enhances positive mood compared to water and lavender regardless of expectancies or previous use of aromatherapy. Moreover, norepinephrine levels following the cold pressor remained elevated when subjects smelled lemon, compared to water or lavender. DTH responses to Candida were larger following inhalation of water than lemon or lavender. Odors did not reliably alter IL-6 and IL-10 production, salivary cortisol, heart rate or blood pressure, skin barrier repair following tape stripping, or pain ratings following the cold pressor.

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