Circadian Neurobiology and the Physiologic Regulation of Sleep and Wakefulness

AbstractThe molecular, neurobiological, and physical health impacts of child maltreatment are well established, yet mechanistic pathways remain inadequately defined. Telomere length (TL) decline is an emerging molecular indicator of stress exposure with definitive links to negative health outcomes in maltreated individuals. The multiple confounders endemic to human maltreatment research impede the identification of causal pathways. This study leverages a unique randomized, cross-foster, study design in a naturalistic translational nonhuman primate model of infant maltreatment. At birth, newborn macaques were randomly assigned to either a maltreating or a competent control mother, balancing for sex, biological mother parenting history, and social rank. Offspring TL was measured longitudinally across the first 6 months of life (infancy) from peripheral blood. Hair cortisol accumulation was also determined at 6, 12, and 18 months of age. TL decline was greater in animals randomized to maltreatment, but also interacted with biological mother group. Shorter TL at 6 months was associated with higher mean cortisol levels through 18 months (juvenile period) when controlling for relevant covariates. These results suggest that even under the equivalent social, nutritional, and environmental conditions feasible in naturalistic translational nonhuman primate models, early adverse caregiving results in lasting molecular scars that foreshadow elevated health risk and physiologic dysregulation.

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Preterm infant physiologic regulation during feeding: Dyad and feeding episode predictors of higher oxygen saturation

Infant Behavior and Development ◽

10.1016/s0163-6383(98)91339-x ◽

1998 ◽

Vol 21 ◽

pp. 124

Author(s):

Suzanne Thoyre

Keyword(s):

Oxygen Saturation ◽

Preterm Infant ◽

Physiologic Regulation

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Role of spleen in integrated control of splanchnic vascular tone: physiology and pathophysiologyThis article is part of a Special Issue on Information Transfer in the Microcirculation.

Canadian Journal of Physiology and Pharmacology ◽

10.1139/y08-103 ◽

2009 ◽

Vol 87 (1) ◽

pp. 1-7 ◽

Cited By ~ 32

Author(s):

Shereen M. Hamza ◽

Susan Kaufman

Keyword(s):

Septic Shock ◽

Portal Hypertension ◽

Information Transfer ◽

Integrated Control ◽

Sympathetic Nerves ◽

Preliminary Evidence ◽

Fluid Extravasation ◽

Key Factor ◽

Renal Vascular ◽

Physiologic Regulation

Aside from its established immunologic and hematologic functions, the spleen also plays an important role in cardiovascular regulation. This occurs through changes in intrasplenic microvascular tone, as well as through splenic neurohormonal modulation of the renal and mesenteric vascular beds. Splenic regulation of blood volume occurs predominantly through fluid extravasation from the splenic circulation into lymphatic reservoirs; this is controlled by direct modulation of splenic pre- and postcapillary resistance by established physiologic agents such as atrial natriuretic peptide (ANP), nitric oxide (NO), and adrenomedullin (ADM). In addition to physiologic fluid regulation, splenic extravasation is a key factor in the inability to maintain adequate intravascular volume in septic shock. The spleen also controls renal microvascular tone through reflex activation of the splenic afferent and renal sympathetic nerves. This splenorenal reflex not only contributes to the physiologic regulation of blood pressure, but also contributes to the cardiovascular dysregulation associated with both septic shock and portal hypertension. In septic shock, the splenorenal reflex protectively limits splenic extravasation and potentially promotes renal sodium and water reabsorption and release of the vasoconstrictor angiotensin II; this function is eventually overwhelmed as shock progresses. In portal hypertension, on the other hand, the splenorenal reflex-mediated reduction in renal vascular conductance exacerbates sodium and water retention in the kidneys and may eventually contribute to renal dysfunction. Preliminary evidence suggests that the spleen also may play a role in the hemodynamic complications of portal hypertension via neurohormonal modulation of the mesenteric vascular bed. Lastly, the spleen itself may be a source of a vasoactive factor.

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