Recent work shows that differing perceptions of stress result in different patterns of neuroendocrine activation. An easily handled challenge elicits norepinephrine and testosterone rises with success. With increasing anxiety, active coping shifts to a more passive mode. Epinephrine, prolactin, renin, and fatty acids increase. As the distress grows, cortisol augments.

Chronic, as well as acute emotional arousal, is a consequence of various types of social interaction, i.e., those between mother and infant and between controlling dominant and less effective subordinate. The neurohumoral accompaniments of this social stress include the sympathetic adrenal medullary and hypothalamic pituitary adrenal responses. A common ensuing pathophysiological state involves a chronic increase of blood pressure. Although Selye's General Adaptation Syndrome presupposed the same response to a variety of stimuli; recent work shows that specific perceptions of control result in different patterns of neuroendocrine activation. A challenge perceived as easy to handle will elicit an active coping response and release of the neurosympathetic system's norepinephrine. Testosterone will rise as the subject savors success. With increasing anxiety this active coping shifts to a more passive mode and the behavior becomes less assured as the animal loses control. The norepinephrine/epinephrine ratio decreases as epinephrine, prolactin, renin and fatty acids rise. As the outcome becomes still less certain and distress grows, adrenocorticotropic hormone and cortisol levels arise. Thus, the effort required on the one hand and the degree of frustration conflict and uncertainty on the other, determine the ratio of catecholamines to corticoids. With severe emotional trauma, brain dysfunction may occur. These effects can be lasting, and corticoids paradoxically return to normal as the behavior changes to that of post-traumatic stress disorder. Repression and denial set in and the organism responds with decreased concern of impaired attachment and increased irritability.

Receptors believed responsible for the diuresis of negative pressure breathing have been located by observing the effect on urine flow of a stepwise engorgement of the intrathoracic vascular bed. Distension of the pulmonary arterial tree (injection of plastic beads) and of the entire pulmonary circulation (snares on the pulmonary veins) were without effect. A diuresis was however elicited by expansion of a balloon in the left atrium. It is concluded that stretch receptors in the left atrium and terminal pulmonary veins are instrumental in a mechanism linking changes in the actively circulating blood volume with homeostatic responses of the kidney.

Despite an increasing knowledge of dandruff and seborrheic dermatitis (D/SD), the pathophysiological understanding is still incomplete but suggests a role of Malassezia yeasts in triggering inflammatory and hyper-proliferative epidermal responses. The objective of this report is to review published literature from in vivo studies of D/SD populations to provide a more complete description of overall scalp health. New biomolecular capabilities establish a depth of pathophysiological understanding not previously achievable with traditional means of investigation. Biomarkers representing inflammation, hyper-proliferation and barrier function are all perturbed by the D/SD condition and robustly respond to therapeutic resolution. These biomarkers can be sampled noninvasively, enabling their use in routine clinical evaluations as either surrogate endpoints or complementary ones to classical signs/symptoms to broaden the etiological learning.

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In addition to repeated reexperiencing of the event, the delayed effects of severe psychological trauma, i.e., post traumatic stress disorder (PTSD), present a paradoxical mix of symptoms. There is enhancement of the self-preservative catecholamine states; anger and fear with a contrasting sense of meaninglessness and a blunting of the emotional responses of the attachment behavior so critical for species preservation. Hormonally, there is a striking separation of the catecholamine response, which stays elevated and that of the hypothalamo-pituitary-adrenal (HPA) axis, which may remain at normal levels. Pathophysiologically, the reexperiencing of the trauma and the arousal may be associated with dysfunction of the locus coeruleus, amygdala and hippocampal systems. This article explores the consequences of an additional dysfunction: a dissociation of the hemispheres that appears to be responsible for the alexithymic avoidance and failure of the cortisol response that so often follow severe psychological trauma. There is neurophysiological evidence that the left and right hemispheres subserve different emotional sets that correspond to "control" and "appraisal," i.e., very approximately to the self and species preservative behavioral complexes, respectively. Several studies point to physiological dissociation of hemispheric functions during alexithymia. This raises the question: What has been lost if in this condition the right side no longer fully contributes to integrated cerebral function? Right hemispheric damaged children lose critical social skills and in adults the related sense of familiarity critical for bonding is lost. Such losses of social sensibilities may account for the lack of empathy and difficulties with bonding found in sociopathy and borderline personality: conditions now believed to result from repeated psychological trauma during development. On the other hand, systems that promote right hemispheric contributions provide solacing access to a "Higher Power." They also appear to protect against socially disordered behavior, substance abuse, the failure of the HPA axis and some aspects of the pathophysiology of chronic disease.