2,243 publications from this institution
The typical view of seismic performance of structure‐content systems is one of segregation: Contents are assumed to be of low mass relative to the supporting structure, leading to a separate treatment of the two, whereby one first analyzes the structure and then subjects any contents to the resulting peak floor acceleration responses. Racking structures are of the exact opposite persuasion, having massive “palletized” contents that can slide on top of light cold‐formed steel frames, with Content‐Structure‐Sliding Interaction (CSSI) governing global and local response. In support of assessment and design, three approaches are investigated to capture CSSI: (i) introducing friction sliders per pallet and running nonlinear response‐history analysis, (ii) increasing the model viscous damping and using elastic response‐history analysis, and (iii) reducing the horizontal seismic loads in tandem with modal response spectrum analysis. Each comes with its own challenges and modelling/analysis needs, offering different levels of accuracy (or no appreciable capability at all) when assessing the actual sliding displacement of contents. Three case studies are employed to calibrate empirical relationships for damping amplification and seismic load reduction, largely removing the bias of simpler alternatives (ii) and (iii), respectively, to level the ground for future code applications.
Stress may be defined as a threat to homeostasis or the stable internal environment. The physiologic response to stress involves activation of the central nervous system (CNS) with consequent stimulation of the hypothalamic—pituitary—adrenal (HPA) axis and the autonomic nervous system Importantly, these systems respond to hormonal stimulation from the immune system; they also interact with other endocrine systems, such as those controlling gonadal, thyroid, and growth functions. The principal central control loci of the stress system are the corticotropin releasing hormone (CRH) and locus cerulus-norepinephrinergic neurons of the hypothalamus and brainstem; these neurons regulate the HPA axis and the sympathetic nervous system, respectively. The hormone products of these systems, cortisol and the catecholamines, act to maintain cardiovascular, metabolic, and immune homeostasis during stress.
Three families with late-onset 21-hydroxylase deficiency were studied. Homozygous females presented with symptoms of mild hyperandrogenism such as acne, hirsutism, oligomenorrhea and menometrorrhagia. A homozygous male was asymptomatic and had reached normal adult height. The diagnosis of 21-hydroxylase deficiency was based upon markedly elevated responses of plasma 17-hydroxyprogesterone during a short (30-min) ACTH infusion test. The propositi of two of the families were diagnosed despite long-standing glucocorticoid therapy and adrenal suppression by using a prolonged (48-hour) ACTH infusion. Heterozygotes of late-onset 21-hydroxylase deficiency had mildly elevated 17-hydroxy-progesterone responses to ACTH. Late-onset 21-hydroxylase deficiency was inherited as an autosomal recessive trait with close linkage to the histocompatibility leukocyte antigens. The B14 haplotype was present in all affected members. One affected female had a daughter with classic, salt-losing 21-hydroxylase deficiency. Mixed heterozygosity of this patient for a classic and a late-onset 21-hydroxylase deficiency allele may have caused the classic phenotype in her daughter (homozygote for 2 classic alleles).
ABSTRACT. Ten patients with adrenal insufficiency receiving chronic glucocorticoid therapy were studied. All had subnormal plasma cortisol responses to ovine corticotropin-releasing hormone (CRH) (1 ε/kg as an iv bolus) 12–60 h after discontinuation of steroid treatment. Plasma ACTH responses to CRH fell into three different patterns. The first three patients with primary adrenal insufficiency had high basal ACTH levels and augmented ACTH responses to CRH. A fourth such patient, however, treated with pharmacologic doses of prednisone, had a low normal ACTH response. Patients with secondary adrenal insufficiency had either low basal ACTH levels and diminished responses to CRH or low basal ACTH values but prolonged and augmented plasma ACTH responses to CRH with a delayed peak. We postulate that the group of patients with the former pattern have pituitary gland destruction whereas the patients with the latter pattern have hypothalamic CRH deficiency. Thus, CRH may be useful in differentiating between hypothalamic and pituitary causes of adrenal insufficiency.
