Lupus, Latin for “wolf,” is a term used to describe many dermatologic conditions, some of which are related to underlying systemic lupus erythematosus, while others are distinct disease processes. Cutaneous lupus erythematosus includes a wide array of visible skin manifestations and can progress to systemic lupus erythematosus in some cases. Cutaneous lupus can be subdivided into three main categories: acute cutaneous lupus erythematosus, subacute cutaneous lupus erythematosus, and chronic cutaneous lupus erythematosus. Physical exam, laboratory studies, and histopathology enable differentiation of cutaneous lupus subtypes. This differentiation is paramount as the subtype of cutaneous lupus informs upon treatment, disease monitoring, and prognostication. This review outlines the different cutaneous manifestations of lupus erythematosus and provides an update on both topical and systemic treatment options for these patients. Other conditions that utilize the term “lupus” but are not cutaneous lupus erythematosus are also discussed.
The nursing shortage continues to be a significant threat to health care. Creating a culture of professional development in health care institutions is one way to combat this shortage. Professional development refers to a constant commitment to maintain one's knowledge and skill base. Increasing professional development opportunities in the health care setting has been shown to affect nurse retention and satisfaction. Several approaches have been developed to increase professional development among nurses. However, for the most part, these are “one size fits all” approaches that direct nurses to progress in lock step fashion in skill and knowledge acquisition within a specialty. This article introduces a milestone pathway tool for registered nurses designed to enhance professional development that is unique to the individual nurse and the specific nursing unit. This tool provides a unit-specific concept map, a milestone pathway template, and a personal professional development plan. J Contin Educ Nurs 2009;40(11):501–508.
Obesity-induced inflammation has been implicated in the development of iron (Fe) deficiency in non-pregnant populations. Haptoglobin (Hp) is an acute phase protein produced by the liver and adipose tissue and is the primary hemoglobin (Hb) carrier protein in the plasma. Few data are available on adiposity and Fe status during pregnancy. To address these relationships, maternal Hp and maternal and neonatal Fe status are being assessed in 175 pregnant adolescents. Blood Hb, serum Hp, hepcidin, ferritin (SF) and serum transferrin receptor (sTfR) were measured during pregnancy (20–38 wk gestation) and in cord blood at birth (38–42 wk gestation). Preliminary data from 38 pregnant adolescents (14–19 y) found that overweight or obese teens (pre-pregnancy BMI>25 kg/m2) had significantly higher serum Hp than normal weight teens (1.36 ± 0.13 vs. 0.84 ± 0.49 g/L, p=0.002). A positive relationship was observed between maternal Hp and neonatal hepcidin (p=0.01, n=36, R2=0.154). Maternal Hp at mid-gestation was not significantly related to Hb, SF or sTfR in the pregnant teen or the neonate. In conclusion, obese pregnant adolescents had higher serum Hp compared to their lean counterparts supportive of an obesity-inflammation link in pregnancy. The observed association between maternal Hp and neonatal hepcidin suggests a role of Hp-mediated Hb trafficking in determining systemic Fe balance in the neonate. Funded by USDA: 2005-35200 & 2008-0857
Elizabeth Cooper and Paul Twidale discuss the various types of one‑to‑one care, how to decide who should receive it and the implications that affect the provider and the person receiving it.
The long‐acting β 2 ‐adrenoceptor agonist, salmeterol (10 −9 –10 −5 M ), inhibited the IgE‐mediated release of histamine from human lung mast cells (HLMC) in a dose‐dependent fashion. Additional β‐adrenoceptor agonists were studied and the rank order of potency for the inhibition of histamine release from HLMC was isoprenaline>salmeterol>salbutamol. Approximate EC 50 values for the inhibition of histamine release were 10 n M for isoprenaline and 100 n M for salbutamol. An EC 50 value for salmeterol could not be calculated because maximal responses to salmeterol were not observed over the concentration range employed. Both salmeterol and isoprenaline inhibited the generation of sulphopeptidoleukotrienes (sLT) more potently and more efficaciously than the release of histamine from immunologically‐activated HLMC. Salmeterol (EC 50 <0.1 n M ) was more potent than isoprenaline (EC 50 0.4 n M ) at attenuating sLT generation. The β‐adrenoceptor antagonist, propranolol (1 μ M ), and the selective β 2 ‐adrenoceptor antagonist, ICI 118,551 (0.1 μ M ), both caused rightward shifts in the dose‐response curve for the inhibition of histamine release by isoprenaline. The antagonism of salmeterol effects by propranolol and ICI 118,551 was more complex. At lower concentrations (<1 μ M ) of salmeterol, both antagonists shifted the dose‐reponse curve to salmeterol rightward. At a higher concentration (10 μ M ) of salmeterol, neither ICI 118,551 nor propranolol was an effective antagonist of the salmeterol‐mediated inhibition of histamine release. Prolonged exposure (4 h) of HLMC to isoprenaline (1 μ M ) caused an approximately 50% reduction in the effectiveness of a second exposure to isoprenaline (10 μ M ) at inhibiting the release of histamine, whereas this pretreatment did not affect the salmeterol (10 μ M ) inhibition of histamine release. Isoprenaline (10 −9 –10 −5 M ) caused a dose‐dependent increase in total cell cyclicAMP levels in purified HLMC which paralleled the inhibition of histamine release. Salmeterol (10 −9 –10 −5 M ) was considerably less potent than isoprenaline at increasing HLMC cyclicAMP levels. In summary, these data indicate that salmeterol is an effective inhibitor of the stimulated release of mediators from HLMC. The present data also suggest that salmeterol may act to inhibit mediator release from HLMC by β‐adrenoceptor‐dependent and independent mechanisms. British Journal of Pharmacology (1998) 123 , 1009–1015; doi: 10.1038/sj.bjp.0701703
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