Open plan offices as sociotechnical systems: What matters and to whom?

Background: Open plan offices have proliferated for the past several decades with more and more workers being concentrated in office buildings. Several studies have identified a number of negative factors associated with open plan offices, and those include noise, speech interference, lack of privacy, and a perceived loss of control over work. While negative factors have been identified several times in the literature, many studies rely on either surveys or highly controlled environments.

Sexual trauma disclosure in clinical settings: addressing diversity.

Although sexual trauma is an experience with wide prevalence, it remains difficult for many individuals to discuss this trauma openly with others. Disclosure of a sexual trauma history to a receptive individual can lead to both emotional and instrumental support. However, a myriad of factors related not only to current circumstances but also to cultural and individual differences determine whether an individual will choose to share his or her trauma history with someone else.

The roles of religion and spirituality among African American survivors of domestic violence.

The investigation examined religious involvement, spirituality, religious coping, and social support as correlates of posttraumatic stress symptoms and depression symptoms in African American survivors of domestic violence. Sixty-five African American women who experienced domestic violence in the past year provided data on demographics, severity and frequency of physical and psychological abuse during the past year, aspects of current social support, types of current coping activities, religious involvement, spiritual experiences, and symptoms related to depression and posttraumatic stress disorder. Women who evinced higher levels of spirituality and greater religious involvement reported fewer depression symptoms.

Are the dissociative criteria in ASD useful?

Acute stress disorder (ASD) is a new DSM-IV diagnostic category, characterized by dissociative, intrusive, avoidance, and hyperarousal symptoms in the first month after a traumatic experience. The goal of the present study was to examine the utility of this diagnosis. In a prospective study, 79 mixed trauma victims who met DSM-IV symptom criteria for PTSD within 1 month following a traumatic event were followed through three months post-event.

A second enzyme protecting mineralocorticoid receptors from glucocorticoid occupancy.

We have confirmed that A6 cells (derived from kidney of Xenopus laevis), which contain both mineralocorticoid and glucocorticoid receptors, do not normally possess 11 beta-hydroxysteroid dehydroxgenase (11 beta-HSD1 or 11 beta-HSD2) enzymatic activity and so are without apparent "protective" enzymes. A6 cells do not convert the glucocorticoid corticosterone to 11-dehydrocorticosterone but do, however, possess steroid 6 beta-hydroxylase that transforms corticosterone to 6 beta-hydroxycorticosterone. This hydroxylase is cytochrome P-450 3A (CYP3A).

Down-regulation of the mineralocorticoid receptor by dexamethasone in an amphibian kidney cell line (A6).

The A6 cell line, derived from Xenopus kidney, is an in vitro model of cortico-steroid mediated transepitheial Na+ transport stimulation. We report the apparent down-regulation of mineralocorticoid receptor levels in A6 cells, in response to the presence of the synthetic glucorticoid dexamethasone in the culture medium. Mineralocorticoid receptor binding was suppressed to approximately 25% of control following 24-hour exposure to 10nM dexamethasone.

Renal and hepatic family 3A cytochromes P450 (CYP3A) in spontaneously hypertensive rats.

Troleandomycin (TAO), a selective family 3A cytochromes P450 (CYP3A) inhibitor, decreases enhanced in vivo corticosterone 6 beta-hydroxylation and blood pressure in spontaneously hypertensive rats (SHR). Corticosterone 6 beta-hydroxylation was measured in liver and kidney microsomes, to determine ontogeny and the effect of TAO on CYP3A activity at the organ level. SHR kidney CYP3A activity increased from 4 to 8 weeks, stabilized at 11 and 16 weeks, and was much higher than in control (Wistar-Kyoto, WKY) rats at all ages.

Maternal environment defines blood pressure and its response to troleandomycin in spontaneously hypertensive rats.

Relationship between family-3A cytochrome P-450-dependent (troleandomycin inhibitable) and maternal environmental-dependent systolic blood pressure (SBP) was investigated in spontaneously hypertensive rats (SHR). Adult SHR nursed by foster or natural SHR mothers had indistinguishable SBP. Troleandomycin reduced 50% of Wistar-Kyoto (WKY)-SHR strain difference in SBP.

Augmented arterial pressure responses to cyclosporine in spontaneously hypertensive rats. Role of cytochrome P-450 3A.

Evidence to support a hypertensinogenic role of family 3A cytochrome P-450 (CYP3A) activity is that troleandomycin, a selective inhibitor of CYP3A, decreases both blood pressure and in vivo corticosterone 6 beta-hydroxylation in spontaneously hypertensive rats (SHR). Renal CYP3A activity is markedly increased in SHR compared with Wistar-Kyoto (WKY) rats. Cyclosporine acutely increases both systolic blood pressure and renal total cytochrome P-450 in SHR.

Effects of corticosteroids on urinary ammonium excretion in humans.

This study was designed to examine the selective effects of glucocorticoid and mineralocorticoid classes of steroid hormones on urinary ammonium excretion in humans. In 22 10-day studies, normal male volunteers received either 9 alpha-fludrohydrocortisone or hydrocortisone, alone or with the receptor antagonist spironolactone or mifepristone. The small but significant increase in ammonium excretion noted with the administration of 9 alpha-fludrohydrocortisone was associated with a significant decrease in serum potassium.

Renal corticosterone 6 beta-hydroxylase in the spontaneously hypertensive rat.

Excess 6 beta-OH-corticosterone production by family 3A cytochromes P-450 may play a role in genesis of hypertension in the spontaneously hypertensive rat (SHR), by producing a renal defect in Na+ excretion. Renal cytochromes P-450 may be a causal factor in this genetic model. Since family 3A P-450 is present in rat kidney (collecting duct), the renal family 3A catalytic (6 beta-OHase) and immunoreactive activities were compared in SHR and normotensive control (Wistar-Kyoto; WKY) rats.

When is cortisol a mineralocorticoid?

(1) Decreased 11 beta-OHSD activity permits binding of cortisol to the Type I (mineralocorticoid) receptor in humans, thereby producing spironolactone-inhibitable Na+ retention, hypokalemia and hypertension, the syndrome of apparent mineralocorticoid excess (AME). (2) Blockade of either the Type I receptor with spironolactone or the Type II (glucocorticoid) receptor with RU-486 does not consistently abolish the effects of stress level cortisol on Na+ retention and hypertension in acute studies in normal humans, suggesting the existence of an additional glucocorticoid receptor. (3) Enhanced glucocorticoid 6 beta-hydroxylation could play an etiologic role in certain hypertensive syndromes.

Corticosterone 6 beta-hydroxylation correlates with blood pressure in spontaneously hypertensive rats.

Evidence for increased glucocorticoid 6 beta-hydroxylation (enhanced family 3A cytochrome P-450 activity) is found in certain reversible forms of human hypertension. This association was investigated in the spontaneously hypertensive rat (SHR). The proportion of injected [3H]corticosterone excreted in urine as 6 beta-[3H]OH-corticosterone was four- to fivefold higher in SHR than in control Wistar-Kyoto rats, before and after development of overt hypertension.

Expression of cytochrome P450 3A in amphibian, rat, and human kidney.

Family 3A mammalian liver cytochromes P450 (3A1, rat; 3A3/4, human) catalyze the 6 beta-hydroxylation of endogenous steroids and are steroid inducible. Our recent finding that A6 cells (a toad kidney epithelial cell line) contain corticosterone 6 beta-hydroxylase activity as a steroid-inducible microsomal cytochrome P450 raised the possibility that corticosterone 6 beta-hydroxylase activity in the A6 cells is catalyzed by a member of the 3A family. We found that incubation of A6 cell microsomes from dexamethasone-induced cells with antibodies against family 3A proteins specifically inhibited corticosterone 6 beta-hydroxylase activity.

Heterogeneity of CYP3A isoforms metabolizing erythromycin and cortisol.

The N-demethylation of erythromycin and 6 beta-hydroxylation of cortisol are both functions of the glucocorticoid-inducible CYP3A in human liver microsomes. To determine whether 6 beta-hydroxylation and erythromycin N-demethylation are catalyzed by similar or distinct CYP3A isoforms, erythromycin N-demethylase activity, as reflected by the recently described 14[C]-erythromycin breath test, was compared with urinary 6 beta-hydroxycortisol/cortisol ratios, a measure of cortisol 6 beta-hydroxylase activity, in nine patients. Erythromycin N-demethylation varied fourfold and 6 beta-hydroxycortisol/cortisol ratios varied sevenfold among the subjects; no correlation was found between these activities (r2 = 0.

11 beta-Hydroxysteroid dehydrogenase activity in the renal target cells of aldosterone.

Aldosterone selectivity in mineralocorticoid target tissues has been suggested to be due to 11 beta-hydroxysteroid dehydrogenase (11-OHSD), which, by inactivating the endogenous glucocorticoids cortisol and corticosterone (CS), would allow aldosterone to bind to the mineralocorticoid receptor that has equal affinity for aldosterone and natural glucocorticoids. However, a recent immunohistochemical study failed to colocalize 11-OHSD and mineralocorticoid receptors in the kidney. The goal of this study was to determine 1) whether metabolism of CS occurs in the renal target cells of aldosterone, i.

Evidence that high dose cortisol-induced Na+ retention in man is not mediated by the mineralocorticoid receptor.

We have previously shown that high dose cortisol (F; 240 mg/day)-induced Na+ retention and systolic blood pressure (BP) increases are not inhibited by the glucocorticoid (type II) receptor antagonist RU486. Adequacy of type II receptor blockade with RU486 was clearly demonstrated, indicating that the Na+ retention was not mediated through the glucocorticoid receptor. Spironolactone (Sp: 400 mg/day), in a preliminary assessment, also did not inhibit F-induced Na+ retention.

Synthesis of 6 beta-hydroxyaldosterone by A6 (toad kidney) cells in culture.

Incubation of aldosterone with confluent layers of A6 (toad kidney) cells leads to its hydroxylation at the 6 beta-position. 6 beta-Hydroxyaldosterone is the major metabolite when the incubation is carried out at pH 6.8, whereas the product comprises 6 beta-hydroxy-17-isoaldosterone accompanied by some 6 beta-hydroxyapoaldosterone at pH 7.

Corticosterone 6 beta-hydroxylase in A6 epithelia: a steroid-inducible cytochrome P-450.

We found microsomal corticosterone 6 beta-hydroxylase (6 beta-OHase) from cultured A6 kidney epithelial cells to be a cytochrome P-450 enzyme with both similarities to and differences from the rat liver steroid 6 beta-OHase P-450p. Enzyme activity was inhibited by CO, alpha-naphthoflavone, metyrapone, and clotrimazole, well-known inhibitors of P-450 enzymes, and increased by known inducers of P-450 enzymes, including dilantin, phenobarbital sodium, and corticosteroids. Moreover, some additional, relatively specific inducers of P-450p (troleandomycin and pregnenolone-16 alpha-carbonitrile) also induced the A6 6 beta-OHase, whereas inducers of other forms of P-450 (aroclor, spironolactone, and isosafrole) appeared to repress the A6 enzyme.

Corticosterone is converted to 6 beta-hydroxycorticosterone in rat: effects of the metabolite on urinary electrolyte excretion.

This study was performed to determine whether corticosterone (B), the major glucocorticoid of rat, is metabolized to its 6 beta-OH derivative (6 beta-OH-B) and whether this derivatives has any effects on Na+ or K+ transport in rat kidney. Normal and adrenalectomized (adx) rats were injected with [3H]B and urine was collected for 5 h and examined for metabolites of B. Metabolites were collected by solid phase extraction on mu Bondapak C18 cartridges and fractionated by reversed phase high performance liquid chromatography.

Corticosterone's metabolite is an agonist for Na+ transport stimulation in A6 cells.

This study tests the hypothesis, in A6 epithelia, that 1) corticosterone stimulates active Na+ transport (short-circuit current, Isc) by an additional receptor mechanism to the type I (mineralocorticoid) and type II (glucocorticoid) mechanisms shared with aldosterone (Aldo) and 2) that the agonist may be 6 beta-OH-corticosterone made in the effector cell. The dose-response relationship of corticosterone at 24 h resolves into two components, by curve fitting, with a 50% effective concentration (EC50) for 10% of maximum Isc stimulation of 2 X 10(-9) M and an EC50 for the other 90% of 3 X 10(-7) M. The EC50 of the smaller component correlates with the apparent dissociation constant (K'd) of corticosterone for high affinity (type II) nuclear binding sites shared with Aldo.

Adrenocorticotropin and cortisol-induced changes in urinary sodium and potassium excretion in man: effects of spironolactone and RU486.

The role of the glucocorticoid (type II) receptor in the Na+ retention induced by cortisol is not known. The relative contribution of mineralocorticoid (type I) and type II receptor activation to changes in urinary Na+ and K+ excretion in man was studied using spironolactone and RU486 to inhibit type I and II receptors, respectively. Normal men eating a constant daily diet received either ACTH or cortisol for 5 days.